---
_id: '6995'
abstract:
- lang: eng
text: Human brain organoids represent a powerful tool for the study of human neurological
diseases particularly those that impact brain growth and structure. However, many
neurological diseases lack obvious anatomical abnormalities, yet significantly
impact neural network functions, raising the question of whether organoids possess
sufficient neural network architecture and complexity to model these conditions.
Here, we explore the network level functions of brain organoids using calcium
sensor imaging and extracellular recording approaches that together reveal the
existence of complex oscillatory network behaviors reminiscent of intact brain
preparations. We further demonstrate strikingly abnormal epileptiform network
activity in organoids derived from a Rett Syndrome patient despite only modest
anatomical differences from isogenically matched controls, and rescue with an
unconventional neuromodulatory drug Pifithrin-α. Together, these findings provide
an essential foundation for the utilization of human brain organoids to study
intact and disordered human brain network formation and illustrate their utility
in therapeutic discovery.
acknowledgement: We thank S. Butler, T. Carmichael and members of the laboratory of
B.G.N. for helpful discussions and comments on the manuscript; N. Vishlaghi and
F. Turcios-Hernandez for technical assistance, and J. Lee, S.-K. Lee, H. Shinagawa
and K. Yoshikawa for valuable reagents. We also thank the UCLA Eli and Edythe Broad
Stem Cell Research Center (BSCRC) and Intellectual and Developmental Disabilities
Research Center microscopy cores for access to imaging facilities. This work was
supported by grants from the California Institute for Regenerative Medicine (CIRM)
(DISC1-08819 to B.G.N.), the National Institute of Health (R01NS089817, R01DA051897
and P50HD103557 to B.G.N.; K08NS119747 to R.A.S.; K99HD096105 to M.W.; R01MH123922,
R01MH121521 and P50HD103557 to M.J.G.; R01GM099134 to K.P.; R01NS103788 to W.E.L.;
R01NS088571 to J.M.P.; R01NS030549 and R01AG050474 to I.M.), and research awards
from the UCLA Jonsson Comprehensive Cancer Center and BSCRC Ablon Scholars Program
(to B.G.N.), the BSCRC Innovation Program (to B.G.N., K.P. and W.E.L.), the UCLA
BSCRC Steffy Brain Aging Research Fund (to B.G.N. and W.E.L.) and the UCLA Clinical
and Translational Science Institute (to B.G.N.), Paul Allen Family Foundation Frontiers
Group (to K.P. and W.E.L.), the March of Dimes Foundation (to W.E.L.) and the Simons
Foundation Autism Research Initiative Bridge to Independence Program (to R.A.S.
and M.J.G.). R.A.S. was also supported by the UCLA/NINDS Translational Neuroscience
Training Grant (R25NS065723), a Research and Training Fellowship from the American
Epilepsy Society, a Taking Flight Award from CURE Epilepsy and a Clinician Scientist
training award from the UCLA BSCRC. J.E.B. was supported by the UCLA BSCRC Rose
Hills Foundation Graduate Scholarship Training Program. M.W. was supported by postdoctoral
training awards provided by the UCLA BSCRC and the Uehara Memorial Foundation. O.A.M.
and A.K. were supported in part by the UCLA-California State University Northridge
CIRM-Bridges training program (EDUC2-08411). We also acknowledge the support of
the IDDRC Cells, Circuits and Systems Analysis, Microscopy and Genetics and Genomics
Cores of the Semel Institute of Neuroscience at UCLA, which are supported by the
NICHD (U54HD087101 and P50HD10355701). We lastly acknowledge support from a Quantitative
and Computational Biosciences Collaboratory Postdoctoral Fellowship to S.M. and
the Quantitative and Computational Biosciences Collaboratory community, directed
by M. Pellegrini.
alternative_title:
- Nature Neuroscience
article_processing_charge: Yes
author:
- first_name: Ranmal A.
full_name: Samarasinghe, Ranmal A.
last_name: Samarasinghe
- first_name: Osvaldo
full_name: Miranda, Osvaldo
id: 862A3C56-A8BF-11E9-B4FA-D9E3E5697425
last_name: Miranda
orcid: 0000-0001-6618-6889
- first_name: Jessie E.
full_name: Buth, Jessie E.
last_name: Buth
- first_name: Simon
full_name: Mitchell, Simon
last_name: Mitchell
- first_name: Isabella
full_name: Ferando, Isabella
last_name: Ferando
- first_name: Momoko
full_name: Watanabe, Momoko
last_name: Watanabe
- first_name: Arinnae
full_name: Kurdian, Arinnae
last_name: Kurdian
- first_name: Peyman
full_name: Golshani, Peyman
last_name: Golshani
- first_name: Kathrin
full_name: Plath, Kathrin
last_name: Plath
- first_name: William E.
full_name: Lowry, William E.
last_name: Lowry
- first_name: Jack M.
full_name: Parent, Jack M.
last_name: Parent
- first_name: Istvan
full_name: Mody, Istvan
last_name: Mody
- first_name: Bennett G.
full_name: Novitch, Bennett G.
last_name: Novitch
citation:
ama: Samarasinghe RA, Miranda O, Buth JE, et al. Identification of Neural Oscillations
and Epileptiform Changes in Human Brain Organoids. Vol 24. Springer Nature;
2021. doi:10.1038/s41593-021-00906-5
apa: Samarasinghe, R. A., Miranda, O., Buth, J. E., Mitchell, S., Ferando, I., Watanabe,
M., … Novitch, B. G. (2021). Identification of neural oscillations and epileptiform
changes in human brain organoids (Vol. 24). Springer Nature. https://doi.org/10.1038/s41593-021-00906-5
chicago: Samarasinghe, Ranmal A., Osvaldo Miranda, Jessie E. Buth, Simon Mitchell,
Isabella Ferando, Momoko Watanabe, Arinnae Kurdian, et al. Identification of
Neural Oscillations and Epileptiform Changes in Human Brain Organoids. Vol.
24. Springer Nature, 2021. https://doi.org/10.1038/s41593-021-00906-5.
ieee: R. A. Samarasinghe et al., Identification of neural oscillations
and epileptiform changes in human brain organoids, vol. 24. Springer Nature,
2021.
ista: Samarasinghe RA, Miranda O, Buth JE, Mitchell S, Ferando I, Watanabe M, Kurdian
A, Golshani P, Plath K, Lowry WE, Parent JM, Mody I, Novitch BG. 2021. Identification
of neural oscillations and epileptiform changes in human brain organoids, Springer
Nature, 32p.
mla: Samarasinghe, Ranmal A., et al. Identification of Neural Oscillations and
Epileptiform Changes in Human Brain Organoids. Vol. 24, Springer Nature, 2021,
doi:10.1038/s41593-021-00906-5.
short: R.A. Samarasinghe, O. Miranda, J.E. Buth, S. Mitchell, I. Ferando, M. Watanabe,
A. Kurdian, P. Golshani, K. Plath, W.E. Lowry, J.M. Parent, I. Mody, B.G. Novitch,
Identification of Neural Oscillations and Epileptiform Changes in Human Brain
Organoids, Springer Nature, 2021.
date_created: 2019-11-10T11:23:58Z
date_published: 2021-08-23T00:00:00Z
date_updated: 2023-08-04T10:49:44Z
day: '23'
department:
- _id: GradSch
- _id: SiHi
doi: 10.1038/s41593-021-00906-5
external_id:
isi:
- '000687516300001'
pmid:
- '34426698 '
intvolume: ' 24'
isi: 1
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1038/s41593-021-00906-5
month: '08'
oa: 1
oa_version: Published Version
page: '32'
pmid: 1
publication_identifier:
eissn:
- 1546-1726
issn:
- 1097-6256
publication_status: published
publisher: Springer Nature
status: public
title: Identification of neural oscillations and epileptiform changes in human brain
organoids
type: technical_report
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 24
year: '2021'
...
---
_id: '8546'
abstract:
- lang: eng
text: Brain neurons arise from relatively few progenitors generating an enormous
diversity of neuronal types. Nonetheless, a cardinal feature of mammalian brain
neurogenesis is thought to be that excitatory and inhibitory neurons derive from
separate, spatially segregated progenitors. Whether bi-potential progenitors with
an intrinsic capacity to generate both lineages exist and how such a fate decision
may be regulated are unknown. Using cerebellar development as a model, we discover
that individual progenitors can give rise to both inhibitory and excitatory lineages.
Gradations of Notch activity determine the fates of the progenitors and their
daughters. Daughters with the highest levels of Notch activity retain the progenitor
fate, while intermediate levels of Notch activity generate inhibitory neurons,
and daughters with very low levels of Notch signaling adopt the excitatory fate.
Therefore, Notch-mediated binary cell fate choice is a mechanism for regulating
the ratio of excitatory to inhibitory neurons from common progenitors.
acknowledgement: This work was supported by the program “Investissements d’avenir”
ANR-10-IAIHU-06 , ICM , a Sorbonne Université Emergence grant, an Allen Distinguished
Investigator Award , and the Roger De Spoelberch Foundation Prize (to B.A.H.); Armenise-Harvard
Foundation , AIRC , and CARITRO (to L.T.); and the European Research Council under
the European Union’s Horizon 2020 research and innovation programme grant agreement
no. 725780 LinPro (to S.H.). T.Z. and T.L. were supported by doctoral fellowships
from the China Scholarship Council and A.H.H. by a doctoral DOC fellowship of the
Austrian Academy of Sciences ( 24812 ). All animal work was conducted at the PHENO-ICMice
facility. The Core is supported by 2 “Investissements d’avenir” (ANR-10- IAIHU-06
and ANR-11-INBS-0011-NeurATRIS) and the “Fondation pour la Recherche Médicale.”
Light microscopy work was carried out at ICM’s imaging core facility, ICM.Quant,
and analysis of scRNA-seq data was carried out at ICM’s bioinformatics core facility,
iCONICS. We thank Paulina Ejsmont, Natalia Danda, and Nathalie De Geest for technical
support. We are grateful to Dr. Shahragim TAJBAKHSH for providing R26Rstop-NICD-nGFP
transgenic mice, Dr. Bart De Strooper for Psn1-deficient mice, Dr. Jean-Christophe
Marine for Gt(ROSA)26SortdTom reporter mice, and Dr. Martinez Barbera for Sox2CreERT2
mice. We also give thanks to Dr. Mikio Hoshino for providing Atoh1 and Ptf1a antibodies.
B.A.H. is an Einstein Visiting Fellow of the Berlin Institute of Health .
article_number: '109208'
article_processing_charge: No
article_type: original
author:
- first_name: Tingting
full_name: Zhang, Tingting
last_name: Zhang
- first_name: Tengyuan
full_name: Liu, Tengyuan
last_name: Liu
- first_name: Natalia
full_name: Mora, Natalia
last_name: Mora
- first_name: Justine
full_name: Guegan, Justine
last_name: Guegan
- first_name: Mathilde
full_name: Bertrand, Mathilde
last_name: Bertrand
- first_name: Ximena
full_name: Contreras, Ximena
id: 475990FE-F248-11E8-B48F-1D18A9856A87
last_name: Contreras
- first_name: Andi H
full_name: Hansen, Andi H
id: 38853E16-F248-11E8-B48F-1D18A9856A87
last_name: Hansen
- first_name: Carmen
full_name: Streicher, Carmen
id: 36BCB99C-F248-11E8-B48F-1D18A9856A87
last_name: Streicher
- first_name: Marica
full_name: Anderle, Marica
last_name: Anderle
- first_name: Natasha
full_name: Danda, Natasha
last_name: Danda
- first_name: Luca
full_name: Tiberi, Luca
last_name: Tiberi
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Bassem A.
full_name: Hassan, Bassem A.
last_name: Hassan
citation:
ama: Zhang T, Liu T, Mora N, et al. Generation of excitatory and inhibitory neurons
from common progenitors via Notch signaling in the cerebellum. Cell Reports.
2021;35(10). doi:10.1016/j.celrep.2021.109208
apa: Zhang, T., Liu, T., Mora, N., Guegan, J., Bertrand, M., Contreras, X., … Hassan,
B. A. (2021). Generation of excitatory and inhibitory neurons from common progenitors
via Notch signaling in the cerebellum. Cell Reports. Elsevier. https://doi.org/10.1016/j.celrep.2021.109208
chicago: Zhang, Tingting, Tengyuan Liu, Natalia Mora, Justine Guegan, Mathilde Bertrand,
Ximena Contreras, Andi H Hansen, et al. “Generation of Excitatory and Inhibitory
Neurons from Common Progenitors via Notch Signaling in the Cerebellum.” Cell
Reports. Elsevier, 2021. https://doi.org/10.1016/j.celrep.2021.109208.
ieee: T. Zhang et al., “Generation of excitatory and inhibitory neurons from
common progenitors via Notch signaling in the cerebellum,” Cell Reports,
vol. 35, no. 10. Elsevier, 2021.
ista: Zhang T, Liu T, Mora N, Guegan J, Bertrand M, Contreras X, Hansen AH, Streicher
C, Anderle M, Danda N, Tiberi L, Hippenmeyer S, Hassan BA. 2021. Generation of
excitatory and inhibitory neurons from common progenitors via Notch signaling
in the cerebellum. Cell Reports. 35(10), 109208.
mla: Zhang, Tingting, et al. “Generation of Excitatory and Inhibitory Neurons from
Common Progenitors via Notch Signaling in the Cerebellum.” Cell Reports,
vol. 35, no. 10, 109208, Elsevier, 2021, doi:10.1016/j.celrep.2021.109208.
short: T. Zhang, T. Liu, N. Mora, J. Guegan, M. Bertrand, X. Contreras, A.H. Hansen,
C. Streicher, M. Anderle, N. Danda, L. Tiberi, S. Hippenmeyer, B.A. Hassan, Cell
Reports 35 (2021).
date_created: 2020-09-21T12:00:48Z
date_published: 2021-06-08T00:00:00Z
date_updated: 2023-08-04T11:00:48Z
day: '08'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1016/j.celrep.2021.109208
ec_funded: 1
external_id:
isi:
- '000659894300001'
pmid:
- '34107249 '
file:
- access_level: open_access
checksum: 7def3d42ebc8f5675efb6f38819e3e2e
content_type: application/pdf
creator: cziletti
date_created: 2021-06-15T14:01:35Z
date_updated: 2021-06-15T14:01:35Z
file_id: '9554'
file_name: 2021_CellReports_Zhang.pdf
file_size: 8900385
relation: main_file
success: 1
file_date_updated: 2021-06-15T14:01:35Z
has_accepted_license: '1'
intvolume: ' 35'
isi: 1
issue: '10'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
- _id: 2625A13E-B435-11E9-9278-68D0E5697425
grant_number: '24812'
name: Molecular Mechanisms of Radial Neuronal Migration
publication: Cell Reports
publication_identifier:
eissn:
- ' 22111247'
publication_status: published
publisher: Elsevier
quality_controlled: '1'
related_material:
link:
- relation: earlier_version
url: https://doi.org/10.1101/2020.03.18.997205
scopus_import: '1'
status: public
title: Generation of excitatory and inhibitory neurons from common progenitors via
Notch signaling in the cerebellum
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 35
year: '2021'
...
---
_id: '9188'
abstract:
- lang: eng
text: Genomic imprinting is an epigenetic mechanism that results in parental allele-specific
expression of ~1% of all genes in mouse and human. Imprinted genes are key developmental
regulators and play pivotal roles in many biological processes such as nutrient
transfer from the mother to offspring and neuronal development. Imprinted genes
are also involved in human disease, including neurodevelopmental disorders, and
often occur in clusters that are regulated by a common imprint control region
(ICR). In extra-embryonic tissues ICRs can act over large distances, with the
largest surrounding Igf2r spanning over 10 million base-pairs. Besides classical
imprinted expression that shows near exclusive maternal or paternal expression,
widespread biased imprinted expression has been identified mainly in brain. In
this review we discuss recent developments mapping cell type specific imprinted
expression in extra-embryonic tissues and neocortex in the mouse. We highlight
the advantages of using an inducible uniparental chromosome disomy (UPD) system
to generate cells carrying either two maternal or two paternal copies of a specific
chromosome to analyze the functional consequences of genomic imprinting. Mosaic
Analysis with Double Markers (MADM) allows fluorescent labeling and concomitant
induction of UPD sparsely in specific cell types, and thus to over-express or
suppress all imprinted genes on that chromosome. To illustrate the utility of
this technique, we explain how MADM-induced UPD revealed new insights about the
function of the well-studied Cdkn1c imprinted gene, and how MADM-induced UPDs
led to identification of highly cell type specific phenotypes related to perturbed
imprinted expression in the mouse neocortex. Finally, we give an outlook on how
MADM could be used to probe cell type specific imprinted expression in other tissues
in mouse, particularly in extra-embryonic tissues.
acknowledgement: We thank Melissa Stouffer for critically reading the manuscript.
This work was supported by IST Austria institutional funds; NÖ Forschung und Bildung
n[f + b] life science call grant (C13-002) to S.H. and the European Research Council
(ERC) under the European Union's Horizon 2020 research and innovation program (grant
agreement 725780 LinPro) to S.H.
article_number: '104986'
article_processing_charge: Yes (via OA deal)
article_type: original
author:
- first_name: Florian
full_name: Pauler, Florian
id: 48EA0138-F248-11E8-B48F-1D18A9856A87
last_name: Pauler
- first_name: Quanah
full_name: Hudson, Quanah
last_name: Hudson
- first_name: Susanne
full_name: Laukoter, Susanne
id: 2D6B7A9A-F248-11E8-B48F-1D18A9856A87
last_name: Laukoter
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Pauler F, Hudson Q, Laukoter S, Hippenmeyer S. Inducible uniparental chromosome
disomy to probe genomic imprinting at single-cell level in brain and beyond. Neurochemistry
International. 2021;145(5). doi:10.1016/j.neuint.2021.104986
apa: Pauler, F., Hudson, Q., Laukoter, S., & Hippenmeyer, S. (2021). Inducible
uniparental chromosome disomy to probe genomic imprinting at single-cell level
in brain and beyond. Neurochemistry International. Elsevier. https://doi.org/10.1016/j.neuint.2021.104986
chicago: Pauler, Florian, Quanah Hudson, Susanne Laukoter, and Simon Hippenmeyer.
“Inducible Uniparental Chromosome Disomy to Probe Genomic Imprinting at Single-Cell
Level in Brain and Beyond.” Neurochemistry International. Elsevier, 2021.
https://doi.org/10.1016/j.neuint.2021.104986.
ieee: F. Pauler, Q. Hudson, S. Laukoter, and S. Hippenmeyer, “Inducible uniparental
chromosome disomy to probe genomic imprinting at single-cell level in brain and
beyond,” Neurochemistry International, vol. 145, no. 5. Elsevier, 2021.
ista: Pauler F, Hudson Q, Laukoter S, Hippenmeyer S. 2021. Inducible uniparental
chromosome disomy to probe genomic imprinting at single-cell level in brain and
beyond. Neurochemistry International. 145(5), 104986.
mla: Pauler, Florian, et al. “Inducible Uniparental Chromosome Disomy to Probe Genomic
Imprinting at Single-Cell Level in Brain and Beyond.” Neurochemistry International,
vol. 145, no. 5, 104986, Elsevier, 2021, doi:10.1016/j.neuint.2021.104986.
short: F. Pauler, Q. Hudson, S. Laukoter, S. Hippenmeyer, Neurochemistry International
145 (2021).
date_created: 2021-02-23T12:31:43Z
date_published: 2021-05-01T00:00:00Z
date_updated: 2023-08-07T13:48:26Z
day: '01'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1016/j.neuint.2021.104986
ec_funded: 1
external_id:
isi:
- '000635575000005'
pmid:
- '33600873'
file:
- access_level: open_access
checksum: c6d7a40089cd29e289f9b22e75768304
content_type: application/pdf
creator: kschuh
date_created: 2021-08-11T12:30:38Z
date_updated: 2021-08-11T12:30:38Z
file_id: '9883'
file_name: 2021_NCI_Pauler.pdf
file_size: 7083499
relation: main_file
success: 1
file_date_updated: 2021-08-11T12:30:38Z
has_accepted_license: '1'
intvolume: ' 145'
isi: 1
issue: '5'
keyword:
- Cell Biology
- Cellular and Molecular Neuroscience
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
- _id: 25D92700-B435-11E9-9278-68D0E5697425
grant_number: LS13-002
name: Mapping Cell-Type Specificity of the Genomic Imprintome in the Brain
publication: Neurochemistry International
publication_identifier:
issn:
- 0197-0186
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Inducible uniparental chromosome disomy to probe genomic imprinting at single-cell
level in brain and beyond
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 145
year: '2021'
...
---
_id: '9601'
abstract:
- lang: eng
text: 'In mammalian genomes, differentially methylated regions (DMRs) and histone
marks including trimethylation of histone 3 lysine 27 (H3K27me3) at imprinted
genes are asymmetrically inherited to control parentally-biased gene expression.
However, neither parent-of-origin-specific transcription nor imprints have been
comprehensively mapped at the blastocyst stage of preimplantation development.
Here, we address this by integrating transcriptomic and epigenomic approaches
in mouse preimplantation embryos. We find that seventy-one genes exhibit previously
unreported parent-of-origin-specific expression in blastocysts (nBiX: novel blastocyst-imprinted
expressed). Uniparental expression of nBiX genes disappears soon after implantation.
Micro-whole-genome bisulfite sequencing (µWGBS) of individual uniparental blastocysts
detects 859 DMRs. We further find that 16% of nBiX genes are associated with a
DMR, whereas most are associated with parentally-biased H3K27me3, suggesting a
role for Polycomb-mediated imprinting in blastocysts. nBiX genes are clustered:
five clusters contained at least one published imprinted gene, and five clusters
exclusively contained nBiX genes. These data suggest that early development undergoes
a complex program of stage-specific imprinting involving different tiers of regulation.'
acknowledgement: The authors thank Robert Feil and Anton Wutz for helpful discussions
and comments, Samuel Collombet and Peter Fraser for sharing embryo TAD coordinates,
and Andy Riddel at the Cambridge Stem Cell Institute and Thomas Sauer at the Max
Perutz Laboratories FACS facility for flow-sorting. We thank the team of the Biomedical
Sequencing Facility at the CeMM and the Vienna Biocenter Core Facilities (VBCF)
for support with next-generation sequencing. We are grateful to animal care teams
at the University of Bath and MRC Harwell. A.C.F.P. acknowledges support from the
UK Medical Research Council (MR/N000080/1 and MR/N020294/1) and Biotechnology and
Biological Sciences Research Council (BB/P009506/1). L.S. is part of the FWF doctoral
programme SMICH and supported by an Austrian Academy of Sciences DOC Fellowship.
M.L. is funded by a Vienna Research Group for Young Investigators grant (VRG14-006)
by the Vienna Science and Technology Fund (WWTF) and by the Austrian Science Fund
FWF (I3786 and P31334).
article_number: '3804'
article_processing_charge: No
article_type: original
author:
- first_name: Laura
full_name: Santini, Laura
last_name: Santini
- first_name: Florian
full_name: Halbritter, Florian
last_name: Halbritter
- first_name: Fabian
full_name: Titz-Teixeira, Fabian
last_name: Titz-Teixeira
- first_name: Toru
full_name: Suzuki, Toru
last_name: Suzuki
- first_name: Maki
full_name: Asami, Maki
last_name: Asami
- first_name: Xiaoyan
full_name: Ma, Xiaoyan
last_name: Ma
- first_name: Julia
full_name: Ramesmayer, Julia
last_name: Ramesmayer
- first_name: Andreas
full_name: Lackner, Andreas
last_name: Lackner
- first_name: Nick
full_name: Warr, Nick
last_name: Warr
- first_name: Florian
full_name: Pauler, Florian
id: 48EA0138-F248-11E8-B48F-1D18A9856A87
last_name: Pauler
orcid: 0000-0002-7462-0048
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Ernest
full_name: Laue, Ernest
last_name: Laue
- first_name: Matthias
full_name: Farlik, Matthias
last_name: Farlik
- first_name: Christoph
full_name: Bock, Christoph
last_name: Bock
- first_name: Andreas
full_name: Beyer, Andreas
last_name: Beyer
- first_name: Anthony C.F.
full_name: Perry, Anthony C.F.
last_name: Perry
- first_name: Martin
full_name: Leeb, Martin
last_name: Leeb
citation:
ama: Santini L, Halbritter F, Titz-Teixeira F, et al. Genomic imprinting in mouse
blastocysts is predominantly associated with H3K27me3. Nature Communications.
2021;12(1). doi:10.1038/s41467-021-23510-4
apa: Santini, L., Halbritter, F., Titz-Teixeira, F., Suzuki, T., Asami, M., Ma,
X., … Leeb, M. (2021). Genomic imprinting in mouse blastocysts is predominantly
associated with H3K27me3. Nature Communications. Springer Nature. https://doi.org/10.1038/s41467-021-23510-4
chicago: Santini, Laura, Florian Halbritter, Fabian Titz-Teixeira, Toru Suzuki,
Maki Asami, Xiaoyan Ma, Julia Ramesmayer, et al. “Genomic Imprinting in Mouse
Blastocysts Is Predominantly Associated with H3K27me3.” Nature Communications.
Springer Nature, 2021. https://doi.org/10.1038/s41467-021-23510-4.
ieee: L. Santini et al., “Genomic imprinting in mouse blastocysts is predominantly
associated with H3K27me3,” Nature Communications, vol. 12, no. 1. Springer
Nature, 2021.
ista: Santini L, Halbritter F, Titz-Teixeira F, Suzuki T, Asami M, Ma X, Ramesmayer
J, Lackner A, Warr N, Pauler F, Hippenmeyer S, Laue E, Farlik M, Bock C, Beyer
A, Perry ACF, Leeb M. 2021. Genomic imprinting in mouse blastocysts is predominantly
associated with H3K27me3. Nature Communications. 12(1), 3804.
mla: Santini, Laura, et al. “Genomic Imprinting in Mouse Blastocysts Is Predominantly
Associated with H3K27me3.” Nature Communications, vol. 12, no. 1, 3804,
Springer Nature, 2021, doi:10.1038/s41467-021-23510-4.
short: L. Santini, F. Halbritter, F. Titz-Teixeira, T. Suzuki, M. Asami, X. Ma,
J. Ramesmayer, A. Lackner, N. Warr, F. Pauler, S. Hippenmeyer, E. Laue, M. Farlik,
C. Bock, A. Beyer, A.C.F. Perry, M. Leeb, Nature Communications 12 (2021).
date_created: 2021-06-27T22:01:46Z
date_published: 2021-07-12T00:00:00Z
date_updated: 2023-08-10T13:53:23Z
day: '12'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1038/s41467-021-23510-4
external_id:
isi:
- '000667248600005'
file:
- access_level: open_access
checksum: 75dd89d09945185b2d14b2434a0bcb50
content_type: application/pdf
creator: asandaue
date_created: 2021-06-28T08:04:22Z
date_updated: 2021-06-28T08:04:22Z
file_id: '9608'
file_name: 2021_NatureCommunications_Santini.pdf
file_size: 2156554
relation: main_file
success: 1
file_date_updated: 2021-06-28T08:04:22Z
has_accepted_license: '1'
intvolume: ' 12'
isi: 1
issue: '1'
language:
- iso: eng
month: '07'
oa: 1
oa_version: Published Version
publication: Nature Communications
publication_identifier:
eissn:
- '20411723'
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Genomic imprinting in mouse blastocysts is predominantly associated with H3K27me3
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 12
year: '2021'
...
---
_id: '9603'
abstract:
- lang: eng
text: Mosaic analysis with double markers (MADM) offers one approach to visualize
and concomitantly manipulate genetically defined cells in mice with single-cell
resolution. MADM applications include the analysis of lineage, single-cell morphology
and physiology, genomic imprinting phenotypes, and dissection of cell-autonomous
gene functions in vivo in health and disease. Yet, MADM can only be applied to
<25% of all mouse genes on select chromosomes to date. To overcome this limitation,
we generate transgenic mice with knocked-in MADM cassettes near the centromeres
of all 19 autosomes and validate their use across organs. With this resource,
>96% of the entire mouse genome can now be subjected to single-cell genetic mosaic
analysis. Beyond a proof of principle, we apply our MADM library to systematically
trace sister chromatid segregation in distinct mitotic cell lineages. We find
striking chromosome-specific biases in segregation patterns, reflecting a putative
mechanism for the asymmetric segregation of genetic determinants in somatic stem
cell division.
acknowledged_ssus:
- _id: Bio
- _id: LifeSc
- _id: PreCl
acknowledgement: We thank the Bioimaging, Life Science, and Pre-Clinical Facilities
at IST Austria; M.P. Postiglione, C. Simbriger, K. Valoskova, C. Schwayer, T. Hussain,
M. Pieber, and V. Wimmer for initial experiments, technical support, and/or assistance;
R. Shigemoto for sharing iv (Dnah11 mutant) mice; and M. Sixt and all members of
the Hippenmeyer lab for discussion. This work was supported by National Institutes
of Health grants ( R01-NS050580 to L.L. and F32MH096361 to L.A.S.). L.L. is an investigator
of HHMI. N.A. received support from FWF Firnberg-Programm ( T 1031 ). A.H.H. is
a recipient of a DOC Fellowship (24812) of the Austrian Academy of Sciences . This
work also received support from IST Austria institutional funds , FWF SFB F78 to
S.H., the People Programme (Marie Curie Actions) of the European Union’s Seventh
Framework Programme ( FP7/2007-2013 ) under REA grant agreement no 618444 to S.H.,
and the European Research Council (ERC) under the European Union’s Horizon 2020
Research and Innovation Programme (grant agreement no. 725780 LinPro ) to S.H.
article_number: '109274'
article_processing_charge: No
article_type: original
author:
- first_name: Ximena
full_name: Contreras, Ximena
id: 475990FE-F248-11E8-B48F-1D18A9856A87
last_name: Contreras
- first_name: Nicole
full_name: Amberg, Nicole
id: 4CD6AAC6-F248-11E8-B48F-1D18A9856A87
last_name: Amberg
orcid: 0000-0002-3183-8207
- first_name: Amarbayasgalan
full_name: Davaatseren, Amarbayasgalan
id: 70ADC922-B424-11E9-99E3-BA18E6697425
last_name: Davaatseren
- first_name: Andi H
full_name: Hansen, Andi H
id: 38853E16-F248-11E8-B48F-1D18A9856A87
last_name: Hansen
- first_name: Johanna
full_name: Sonntag, Johanna
id: 32FE7D7C-F248-11E8-B48F-1D18A9856A87
last_name: Sonntag
- first_name: Lill
full_name: Andersen, Lill
last_name: Andersen
- first_name: Tina
full_name: Bernthaler, Tina
last_name: Bernthaler
- first_name: Carmen
full_name: Streicher, Carmen
id: 36BCB99C-F248-11E8-B48F-1D18A9856A87
last_name: Streicher
- first_name: Anna-Magdalena
full_name: Heger, Anna-Magdalena
id: 4B76FFD2-F248-11E8-B48F-1D18A9856A87
last_name: Heger
- first_name: Randy L.
full_name: Johnson, Randy L.
last_name: Johnson
- first_name: Lindsay A.
full_name: Schwarz, Lindsay A.
last_name: Schwarz
- first_name: Liqun
full_name: Luo, Liqun
last_name: Luo
- first_name: Thomas
full_name: Rülicke, Thomas
last_name: Rülicke
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Contreras X, Amberg N, Davaatseren A, et al. A genome-wide library of MADM
mice for single-cell genetic mosaic analysis. Cell Reports. 2021;35(12).
doi:10.1016/j.celrep.2021.109274
apa: Contreras, X., Amberg, N., Davaatseren, A., Hansen, A. H., Sonntag, J., Andersen,
L., … Hippenmeyer, S. (2021). A genome-wide library of MADM mice for single-cell
genetic mosaic analysis. Cell Reports. Cell Press. https://doi.org/10.1016/j.celrep.2021.109274
chicago: Contreras, Ximena, Nicole Amberg, Amarbayasgalan Davaatseren, Andi H Hansen,
Johanna Sonntag, Lill Andersen, Tina Bernthaler, et al. “A Genome-Wide Library
of MADM Mice for Single-Cell Genetic Mosaic Analysis.” Cell Reports. Cell
Press, 2021. https://doi.org/10.1016/j.celrep.2021.109274.
ieee: X. Contreras et al., “A genome-wide library of MADM mice for single-cell
genetic mosaic analysis,” Cell Reports, vol. 35, no. 12. Cell Press, 2021.
ista: Contreras X, Amberg N, Davaatseren A, Hansen AH, Sonntag J, Andersen L, Bernthaler
T, Streicher C, Heger A-M, Johnson RL, Schwarz LA, Luo L, Rülicke T, Hippenmeyer
S. 2021. A genome-wide library of MADM mice for single-cell genetic mosaic analysis.
Cell Reports. 35(12), 109274.
mla: Contreras, Ximena, et al. “A Genome-Wide Library of MADM Mice for Single-Cell
Genetic Mosaic Analysis.” Cell Reports, vol. 35, no. 12, 109274, Cell Press,
2021, doi:10.1016/j.celrep.2021.109274.
short: X. Contreras, N. Amberg, A. Davaatseren, A.H. Hansen, J. Sonntag, L. Andersen,
T. Bernthaler, C. Streicher, A.-M. Heger, R.L. Johnson, L.A. Schwarz, L. Luo,
T. Rülicke, S. Hippenmeyer, Cell Reports 35 (2021).
date_created: 2021-06-27T22:01:48Z
date_published: 2021-06-22T00:00:00Z
date_updated: 2023-08-10T13:55:00Z
day: '22'
ddc:
- '570'
department:
- _id: SiHi
- _id: LoSw
- _id: PreCl
doi: 10.1016/j.celrep.2021.109274
ec_funded: 1
external_id:
isi:
- '000664463600016'
file:
- access_level: open_access
checksum: d49520fdcbbb5c2f883bddb67cee5d77
content_type: application/pdf
creator: asandaue
date_created: 2021-06-28T14:06:24Z
date_updated: 2021-06-28T14:06:24Z
file_id: '9613'
file_name: 2021_CellReports_Contreras.pdf
file_size: 7653149
relation: main_file
success: 1
file_date_updated: 2021-06-28T14:06:24Z
has_accepted_license: '1'
intvolume: ' 35'
isi: 1
issue: '12'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
project:
- _id: 2625A13E-B435-11E9-9278-68D0E5697425
grant_number: '24812'
name: Molecular Mechanisms of Radial Neuronal Migration
- _id: 25D61E48-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '618444'
name: Molecular Mechanisms of Cerebral Cortex Development
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
publication: Cell Reports
publication_identifier:
eissn:
- '22111247'
publication_status: published
publisher: Cell Press
quality_controlled: '1'
related_material:
link:
- description: News on IST Homepage
relation: press_release
url: https://ist.ac.at/en/news/boost-for-mouse-genetic-analysis/
scopus_import: '1'
status: public
title: A genome-wide library of MADM mice for single-cell genetic mosaic analysis
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 35
year: '2021'
...
---
_id: '9906'
abstract:
- lang: eng
text: Endometriosis is a common gynecological disorder characterized by ectopic
growth of endometrium outside the uterus and is associated with chronic pain and
infertility. We investigated the role of the long intergenic noncoding RNA 01133
(LINC01133) in endometriosis, an lncRNA that has been implicated in several types
of cancer. We found that LINC01133 is upregulated in ectopic endometriotic lesions.
As expression appeared higher in the epithelial endometrial layer, we performed
a siRNA knockdown of LINC01133 in an endometriosis epithelial cell line. Phenotypic
assays indicated that LINC01133 may promote proliferation and suppress cellular
migration, and affect the cytoskeleton and morphology of the cells. Gene ontology
analysis of differentially expressed genes indicated that cell proliferation and
migration pathways were affected in line with the observed phenotype. We validated
upregulation of p21 and downregulation of Cyclin A at the protein level, which
together with the quantification of the DNA content using fluorescence-activated
cell sorting (FACS) analysis indicated that the observed effects on cellular proliferation
may be due to changes in cell cycle. Further, we found testis-specific protein
kinase 1 (TESK1) kinase upregulation corresponding with phosphorylation and inactivation
of actin severing protein Cofilin, which could explain changes in the cytoskeleton
and cellular migration. These results indicate that endometriosis is associated
with LINC01133 upregulation, which may affect pathogenesis via the cellular proliferation
and migration pathways.
acknowledgement: "Open access funding provided by Medical University of Vienna. The
authors would like to thank all the participants and health professionals involved
in the present study. We want to thank our technical assistants Barbara Widmar and
Matthias Witzmann-Stern for their diligent work and constant assistance. We would
like to thank Simon Hippenmeyer for access to\r\nbioinformatic infrastructure and
resources."
article_number: '8385'
article_processing_charge: Yes
article_type: original
author:
- first_name: Iveta
full_name: Yotova, Iveta
last_name: Yotova
- first_name: Quanah J.
full_name: Hudson, Quanah J.
last_name: Hudson
- first_name: Florian
full_name: Pauler, Florian
id: 48EA0138-F248-11E8-B48F-1D18A9856A87
last_name: Pauler
orcid: 0000-0002-7462-0048
- first_name: Katharina
full_name: Proestling, Katharina
last_name: Proestling
- first_name: Isabella
full_name: Haslinger, Isabella
last_name: Haslinger
- first_name: Lorenz
full_name: Kuessel, Lorenz
last_name: Kuessel
- first_name: Alexandra
full_name: Perricos, Alexandra
last_name: Perricos
- first_name: Heinrich
full_name: Husslein, Heinrich
last_name: Husslein
- first_name: René
full_name: Wenzl, René
last_name: Wenzl
citation:
ama: Yotova I, Hudson QJ, Pauler F, et al. LINC01133 inhibits invasion and promotes
proliferation in an endometriosis epithelial cell line. International Journal
of Molecular Sciences. 2021;22(16). doi:10.3390/ijms22168385
apa: Yotova, I., Hudson, Q. J., Pauler, F., Proestling, K., Haslinger, I., Kuessel,
L., … Wenzl, R. (2021). LINC01133 inhibits invasion and promotes proliferation
in an endometriosis epithelial cell line. International Journal of Molecular
Sciences. MDPI. https://doi.org/10.3390/ijms22168385
chicago: Yotova, Iveta, Quanah J. Hudson, Florian Pauler, Katharina Proestling,
Isabella Haslinger, Lorenz Kuessel, Alexandra Perricos, Heinrich Husslein, and
René Wenzl. “LINC01133 Inhibits Invasion and Promotes Proliferation in an Endometriosis
Epithelial Cell Line.” International Journal of Molecular Sciences. MDPI,
2021. https://doi.org/10.3390/ijms22168385.
ieee: I. Yotova et al., “LINC01133 inhibits invasion and promotes proliferation
in an endometriosis epithelial cell line,” International Journal of Molecular
Sciences, vol. 22, no. 16. MDPI, 2021.
ista: Yotova I, Hudson QJ, Pauler F, Proestling K, Haslinger I, Kuessel L, Perricos
A, Husslein H, Wenzl R. 2021. LINC01133 inhibits invasion and promotes proliferation
in an endometriosis epithelial cell line. International Journal of Molecular Sciences.
22(16), 8385.
mla: Yotova, Iveta, et al. “LINC01133 Inhibits Invasion and Promotes Proliferation
in an Endometriosis Epithelial Cell Line.” International Journal of Molecular
Sciences, vol. 22, no. 16, 8385, MDPI, 2021, doi:10.3390/ijms22168385.
short: I. Yotova, Q.J. Hudson, F. Pauler, K. Proestling, I. Haslinger, L. Kuessel,
A. Perricos, H. Husslein, R. Wenzl, International Journal of Molecular Sciences
22 (2021).
date_created: 2021-08-15T22:01:27Z
date_published: 2021-08-04T00:00:00Z
date_updated: 2023-08-11T10:34:13Z
day: '04'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.3390/ijms22168385
external_id:
isi:
- '000689147400001'
file:
- access_level: open_access
checksum: be7f0042607ca60549cb27513c19c6af
content_type: application/pdf
creator: asandaue
date_created: 2021-08-16T09:29:17Z
date_updated: 2021-08-16T09:29:17Z
file_id: '9922'
file_name: 2021_InternationalJournalOfMolecularSciences_Yotova.pdf
file_size: 2646018
relation: main_file
success: 1
file_date_updated: 2021-08-16T09:29:17Z
has_accepted_license: '1'
intvolume: ' 22'
isi: 1
issue: '16'
language:
- iso: eng
month: '08'
oa: 1
oa_version: Published Version
publication: International Journal of Molecular Sciences
publication_identifier:
eissn:
- '14220067'
issn:
- '16616596'
publication_status: published
publisher: MDPI
quality_controlled: '1'
scopus_import: '1'
status: public
title: LINC01133 inhibits invasion and promotes proliferation in an endometriosis
epithelial cell line
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 22
year: '2021'
...
---
_id: '9073'
abstract:
- lang: eng
text: The sensory and cognitive abilities of the mammalian neocortex are underpinned
by intricate columnar and laminar circuits formed from an array of diverse neuronal
populations. One approach to determining how interactions between these circuit
components give rise to complex behavior is to investigate the rules by which
cortical circuits are formed and acquire functionality during development. This
review summarizes recent research on the development of the neocortex, from genetic
determination in neural stem cells through to the dynamic role that specific neuronal
populations play in the earliest circuits of neocortex, and how they contribute
to emergent function and cognition. While many of these endeavors take advantage
of model systems, consideration will also be given to advances in our understanding
of activity in nascent human circuits. Such cross-species perspective is imperative
when investigating the mechanisms underlying the dysfunction of early neocortical
circuits in neurodevelopmental disorders, so that one can identify targets amenable
to therapeutic intervention.
acknowledgement: Work in the I.L.H.-O. laboratory was supported by European Research
Council Grant ERC-2015-CoG 681577 and German Research Foundation Ha 4466/10-1, Ha4466/11-1,
Ha4466/12-1, SPP 1665, and SFB 936B5. Work in the S.J.B.B. laboratory was supported
by Biotechnology and Biological Sciences Research Council BB/P003796/1, Medical
Research Council MR/K004387/1 and MR/T033320/1, Wellcome Trust 215199/Z/19/Z and
102386/Z/13/Z, and John Fell Fund. Work in the S.H. laboratory was supported by
European Research Council Grants ERC-2016-CoG 725780 LinPro and FWF SFB F78. This
work was supported by National Institutes of Health Grant NIMH 1R01MH110553 to N.V.D.M.G.
Work in the J.A.C. laboratory was supported by the Ludwig Family Foundation, Simons
Foundation SFARI Research Award, and National Institutes of Health/National Institute
of Mental Health R01 MH102365 and R01MH113852. The B.V. laboratory was supported
by Whitehall Foundation 2017-12-73, National Science Foundation 1736028, National
Institutes of Health, National Institute of General Medical Sciences R01GM134363-01,
and Halıcıoğlu Data Science Institute Fellowship. This work was supported by the
University of California San Diego School of Medicine.
article_processing_charge: No
article_type: original
author:
- first_name: Ileana L.
full_name: Hanganu-Opatz, Ileana L.
last_name: Hanganu-Opatz
- first_name: Simon J. B.
full_name: Butt, Simon J. B.
last_name: Butt
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Natalia V.
full_name: De Marco García, Natalia V.
last_name: De Marco García
- first_name: Jessica A.
full_name: Cardin, Jessica A.
last_name: Cardin
- first_name: Bradley
full_name: Voytek, Bradley
last_name: Voytek
- first_name: Alysson R.
full_name: Muotri, Alysson R.
last_name: Muotri
citation:
ama: Hanganu-Opatz IL, Butt SJB, Hippenmeyer S, et al. The logic of developing neocortical
circuits in health and disease. The Journal of Neuroscience. 2021;41(5):813-822.
doi:10.1523/jneurosci.1655-20.2020
apa: Hanganu-Opatz, I. L., Butt, S. J. B., Hippenmeyer, S., De Marco García, N.
V., Cardin, J. A., Voytek, B., & Muotri, A. R. (2021). The logic of developing
neocortical circuits in health and disease. The Journal of Neuroscience.
Society for Neuroscience. https://doi.org/10.1523/jneurosci.1655-20.2020
chicago: Hanganu-Opatz, Ileana L., Simon J. B. Butt, Simon Hippenmeyer, Natalia
V. De Marco García, Jessica A. Cardin, Bradley Voytek, and Alysson R. Muotri.
“The Logic of Developing Neocortical Circuits in Health and Disease.” The Journal
of Neuroscience. Society for Neuroscience, 2021. https://doi.org/10.1523/jneurosci.1655-20.2020.
ieee: I. L. Hanganu-Opatz et al., “The logic of developing neocortical circuits
in health and disease,” The Journal of Neuroscience, vol. 41, no. 5. Society
for Neuroscience, pp. 813–822, 2021.
ista: Hanganu-Opatz IL, Butt SJB, Hippenmeyer S, De Marco García NV, Cardin JA,
Voytek B, Muotri AR. 2021. The logic of developing neocortical circuits in health
and disease. The Journal of Neuroscience. 41(5), 813–822.
mla: Hanganu-Opatz, Ileana L., et al. “The Logic of Developing Neocortical Circuits
in Health and Disease.” The Journal of Neuroscience, vol. 41, no. 5, Society
for Neuroscience, 2021, pp. 813–22, doi:10.1523/jneurosci.1655-20.2020.
short: I.L. Hanganu-Opatz, S.J.B. Butt, S. Hippenmeyer, N.V. De Marco García, J.A.
Cardin, B. Voytek, A.R. Muotri, The Journal of Neuroscience 41 (2021) 813–822.
date_created: 2021-02-03T12:23:51Z
date_published: 2021-02-03T00:00:00Z
date_updated: 2023-09-05T14:03:17Z
day: '03'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1523/jneurosci.1655-20.2020
ec_funded: 1
external_id:
isi:
- '000616763400002'
pmid:
- '33431633'
file:
- access_level: open_access
checksum: 578fd7ed1a0aef74bce61bea2d987b33
content_type: application/pdf
creator: dernst
date_created: 2022-05-27T06:59:55Z
date_updated: 2022-05-27T06:59:55Z
file_id: '11414'
file_name: 2021_JourNeuroscience_Hanganu.pdf
file_size: 1031150
relation: main_file
success: 1
file_date_updated: 2022-05-27T06:59:55Z
has_accepted_license: '1'
intvolume: ' 41'
isi: 1
issue: '5'
keyword:
- General Neuroscience
language:
- iso: eng
month: '02'
oa: 1
oa_version: Published Version
page: 813-822
pmid: 1
project:
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
- _id: 059F6AB4-7A3F-11EA-A408-12923DDC885E
grant_number: F07805
name: Molecular Mechanisms of Neural Stem Cell Lineage Progression
publication: The Journal of Neuroscience
publication_identifier:
eissn:
- 1529-2401
issn:
- 0270-6474
publication_status: published
publisher: Society for Neuroscience
quality_controlled: '1'
scopus_import: '1'
status: public
title: The logic of developing neocortical circuits in health and disease
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 41
year: '2021'
...
---
_id: '9793'
abstract:
- lang: eng
text: Astrocytes extensively infiltrate the neuropil to regulate critical aspects
of synaptic development and function. This process is regulated by transcellular
interactions between astrocytes and neurons via cell adhesion molecules. How astrocytes
coordinate developmental processes among one another to parse out the synaptic
neuropil and form non-overlapping territories is unknown. Here we identify a molecular
mechanism regulating astrocyte-astrocyte interactions during development to coordinate
astrocyte morphogenesis and gap junction coupling. We show that hepaCAM, a disease-linked,
astrocyte-enriched cell adhesion molecule, regulates astrocyte competition for
territory and morphological complexity in the developing mouse cortex. Furthermore,
conditional deletion of Hepacam from developing astrocytes significantly impairs
gap junction coupling between astrocytes and disrupts the balance between synaptic
excitation and inhibition. Mutations in HEPACAM cause megalencephalic leukoencephalopathy
with subcortical cysts in humans. Therefore, our findings suggest that disruption
of astrocyte self-organization mechanisms could be an underlying cause of neural
pathology.
acknowledgement: This work was supported by the National Institutes of Health (R01
DA047258 and R01 NS102237 to C.E., F32 NS100392 to K.T.B.) and the Holland-Trice
Brain Research Award (to C.E.). K.T.B. was supported by postdoctoral fellowships
from the Foerster-Bernstein Family and The Hartwell Foundation. The Hippenmeyer
lab was supported by the European Research Council (ERC) under the European Union’s
Horizon 2020 research and innovations program (725780 LinPro) to S.H. R.E. was supported
by Ministerio de Ciencia y Tecnología (RTI2018-093493-B-I00). We thank the Duke
Light Microscopy Core Facility, the Duke Transgenic Mouse Facility, Dr. U. Schulte
for assistance with proteomic experiments, and Dr. D. Silver for critical review
of the manuscript. Cartoon elements of figure panels were created using BioRender.com.
article_processing_charge: No
article_type: original
author:
- first_name: Katherine T.
full_name: Baldwin, Katherine T.
last_name: Baldwin
- first_name: Christabel X.
full_name: Tan, Christabel X.
last_name: Tan
- first_name: Samuel T.
full_name: Strader, Samuel T.
last_name: Strader
- first_name: Changyu
full_name: Jiang, Changyu
last_name: Jiang
- first_name: Justin T.
full_name: Savage, Justin T.
last_name: Savage
- first_name: Xabier
full_name: Elorza-Vidal, Xabier
last_name: Elorza-Vidal
- first_name: Ximena
full_name: Contreras, Ximena
id: 475990FE-F248-11E8-B48F-1D18A9856A87
last_name: Contreras
- first_name: Thomas
full_name: Rülicke, Thomas
last_name: Rülicke
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Raúl
full_name: Estévez, Raúl
last_name: Estévez
- first_name: Ru-Rong
full_name: Ji, Ru-Rong
last_name: Ji
- first_name: Cagla
full_name: Eroglu, Cagla
last_name: Eroglu
citation:
ama: Baldwin KT, Tan CX, Strader ST, et al. HepaCAM controls astrocyte self-organization
and coupling. Neuron. 2021;109(15):2427-2442.e10. doi:10.1016/j.neuron.2021.05.025
apa: Baldwin, K. T., Tan, C. X., Strader, S. T., Jiang, C., Savage, J. T., Elorza-Vidal,
X., … Eroglu, C. (2021). HepaCAM controls astrocyte self-organization and coupling.
Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2021.05.025
chicago: Baldwin, Katherine T., Christabel X. Tan, Samuel T. Strader, Changyu Jiang,
Justin T. Savage, Xabier Elorza-Vidal, Ximena Contreras, et al. “HepaCAM Controls
Astrocyte Self-Organization and Coupling.” Neuron. Elsevier, 2021. https://doi.org/10.1016/j.neuron.2021.05.025.
ieee: K. T. Baldwin et al., “HepaCAM controls astrocyte self-organization
and coupling,” Neuron, vol. 109, no. 15. Elsevier, p. 2427–2442.e10, 2021.
ista: Baldwin KT, Tan CX, Strader ST, Jiang C, Savage JT, Elorza-Vidal X, Contreras
X, Rülicke T, Hippenmeyer S, Estévez R, Ji R-R, Eroglu C. 2021. HepaCAM controls
astrocyte self-organization and coupling. Neuron. 109(15), 2427–2442.e10.
mla: Baldwin, Katherine T., et al. “HepaCAM Controls Astrocyte Self-Organization
and Coupling.” Neuron, vol. 109, no. 15, Elsevier, 2021, p. 2427–2442.e10,
doi:10.1016/j.neuron.2021.05.025.
short: K.T. Baldwin, C.X. Tan, S.T. Strader, C. Jiang, J.T. Savage, X. Elorza-Vidal,
X. Contreras, T. Rülicke, S. Hippenmeyer, R. Estévez, R.-R. Ji, C. Eroglu, Neuron
109 (2021) 2427–2442.e10.
date_created: 2021-08-06T09:08:25Z
date_published: 2021-08-04T00:00:00Z
date_updated: 2023-09-27T07:46:09Z
day: '04'
department:
- _id: SiHi
doi: 10.1016/j.neuron.2021.05.025
ec_funded: 1
external_id:
isi:
- '000692851900010'
pmid:
- '34171291'
intvolume: ' 109'
isi: 1
issue: '15'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1016/j.neuron.2021.05.025
month: '08'
oa: 1
oa_version: Published Version
page: 2427-2442.e10
pmid: 1
project:
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
publication: Neuron
publication_identifier:
eissn:
- 1097-4199
issn:
- 0896-6273
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: HepaCAM controls astrocyte self-organization and coupling
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 109
year: '2021'
...
---
_id: '10655'
abstract:
- lang: eng
text: "Adeno-associated viruses (AAVs) are widely used to deliver genetic material
in vivo to distinct cell types such as neurons or glial cells, allowing for targeted
manipulation. Transduction of microglia is mostly excluded from this strategy,
likely due to the cells’ heterogeneous state upon environmental changes, which
makes AAV design challenging. Here, we established the retina as a model system
for microglial AAV validation and optimization. First, we show that AAV2/6 transduced
microglia in both synaptic layers, where layer preference corresponds to the intravitreal
or subretinal delivery method. Surprisingly, we observed significantly enhanced
microglial transduction during photoreceptor degeneration. Thus, we modified the
AAV6 capsid to reduce heparin binding by introducing four point mutations (K531E,
R576Q, K493S, and K459S), resulting in increased microglial transduction in the
outer plexiform layer. Finally, to improve microglial-specific transduction, we
validated a Cre-dependent transgene delivery cassette for use in combination with
the Cx3cr1CreERT2 mouse line. Together, our results provide a foundation for future
studies optimizing AAV-mediated microglia transduction and highlight that environmental
conditions influence microglial transduction efficiency.\r\n"
acknowledged_ssus:
- _id: Bio
- _id: LifeSc
- _id: PreCl
acknowledgement: This project has received funding from the European Research Council
(ERC) under the European Union’s Horizon 2020 research and innovation programme
(grant agreement no. 715571). The research was supported by the Scientific Service
Units (SSU) of IST Austria through resources provided by the Bioimaging Facility,
the Life Science Facility, and the Pre-Clinical Facility, namely Sonja Haslinger
and Michael Schunn for their animal colony management and support. We would also
like to thank Chakrabarty Lab for sharing the plasmids for AAV2/6 production. Finally,
we would like to thank the Siegert team members for discussion about the manuscript.
article_processing_charge: Yes
article_type: original
author:
- first_name: Margaret E
full_name: Maes, Margaret E
id: 3838F452-F248-11E8-B48F-1D18A9856A87
last_name: Maes
orcid: 0000-0001-9642-1085
- first_name: Gabriele M.
full_name: Wögenstein, Gabriele M.
last_name: Wögenstein
- first_name: Gloria
full_name: Colombo, Gloria
id: 3483CF6C-F248-11E8-B48F-1D18A9856A87
last_name: Colombo
orcid: 0000-0001-9434-8902
- first_name: Raquel
full_name: Casado Polanco, Raquel
id: 15240fc1-dbcd-11ea-9d1d-ac5a786425fd
last_name: Casado Polanco
orcid: 0000-0001-8293-4568
- first_name: Sandra
full_name: Siegert, Sandra
id: 36ACD32E-F248-11E8-B48F-1D18A9856A87
last_name: Siegert
orcid: 0000-0001-8635-0877
citation:
ama: Maes ME, Wögenstein GM, Colombo G, Casado Polanco R, Siegert S. Optimizing
AAV2/6 microglial targeting identified enhanced efficiency in the photoreceptor
degenerative environment. Molecular Therapy - Methods and Clinical Development.
2021;23:210-224. doi:10.1016/j.omtm.2021.09.006
apa: Maes, M. E., Wögenstein, G. M., Colombo, G., Casado Polanco, R., & Siegert,
S. (2021). Optimizing AAV2/6 microglial targeting identified enhanced efficiency
in the photoreceptor degenerative environment. Molecular Therapy - Methods
and Clinical Development. Elsevier. https://doi.org/10.1016/j.omtm.2021.09.006
chicago: Maes, Margaret E, Gabriele M. Wögenstein, Gloria Colombo, Raquel Casado
Polanco, and Sandra Siegert. “Optimizing AAV2/6 Microglial Targeting Identified
Enhanced Efficiency in the Photoreceptor Degenerative Environment.” Molecular
Therapy - Methods and Clinical Development. Elsevier, 2021. https://doi.org/10.1016/j.omtm.2021.09.006.
ieee: M. E. Maes, G. M. Wögenstein, G. Colombo, R. Casado Polanco, and S. Siegert,
“Optimizing AAV2/6 microglial targeting identified enhanced efficiency in the
photoreceptor degenerative environment,” Molecular Therapy - Methods and Clinical
Development, vol. 23. Elsevier, pp. 210–224, 2021.
ista: Maes ME, Wögenstein GM, Colombo G, Casado Polanco R, Siegert S. 2021. Optimizing
AAV2/6 microglial targeting identified enhanced efficiency in the photoreceptor
degenerative environment. Molecular Therapy - Methods and Clinical Development.
23, 210–224.
mla: Maes, Margaret E., et al. “Optimizing AAV2/6 Microglial Targeting Identified
Enhanced Efficiency in the Photoreceptor Degenerative Environment.” Molecular
Therapy - Methods and Clinical Development, vol. 23, Elsevier, 2021, pp. 210–24,
doi:10.1016/j.omtm.2021.09.006.
short: M.E. Maes, G.M. Wögenstein, G. Colombo, R. Casado Polanco, S. Siegert, Molecular
Therapy - Methods and Clinical Development 23 (2021) 210–224.
date_created: 2022-01-23T23:01:28Z
date_published: 2021-12-10T00:00:00Z
date_updated: 2023-11-16T13:12:03Z
day: '10'
ddc:
- '570'
department:
- _id: SaSi
- _id: SiHi
doi: 10.1016/j.omtm.2021.09.006
ec_funded: 1
external_id:
isi:
- '000748748500019'
file:
- access_level: open_access
checksum: 77dc540e8011c5475031bdf6ccef20a6
content_type: application/pdf
creator: cchlebak
date_created: 2022-01-24T07:43:09Z
date_updated: 2022-01-24T07:43:09Z
file_id: '10657'
file_name: 2021_MolTherMethodsClinDev_Maes.pdf
file_size: 4794147
relation: main_file
success: 1
file_date_updated: 2022-01-24T07:43:09Z
has_accepted_license: '1'
intvolume: ' 23'
isi: 1
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
page: 210-224
project:
- _id: 25D4A630-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '715571'
name: Microglia action towards neuronal circuit formation and function in health
and disease
publication: Molecular Therapy - Methods and Clinical Development
publication_identifier:
eissn:
- 2329-0501
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Optimizing AAV2/6 microglial targeting identified enhanced efficiency in the
photoreceptor degenerative environment
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 23
year: '2021'
...
---
_id: '10321'
abstract:
- lang: eng
text: Mosaic analysis with double markers (MADM) technology enables the generation
of genetic mosaic tissue in mice. MADM enables concomitant fluorescent cell labeling
and introduction of a mutation of a gene of interest with single-cell resolution.
This protocol highlights major steps for the generation of genetic mosaic tissue
and the isolation and processing of respective tissues for downstream histological
analysis. For complete details on the use and execution of this protocol, please
refer to Contreras et al. (2021).
acknowledged_ssus:
- _id: Bio
- _id: PreCl
acknowledgement: This research was supported by the Scientific Service Units (SSU)
at IST Austria through resources provided by the Bioimaging (BIF) and Preclinical
Facilities (PCF). We particularly thank Mohammad Goudarzi for assistance with photography
of mouse perfusion and dissection. N.A. received support from FWF Firnberg-Programm
(T 1031). This work was also supported by IST Austria institutional funds; FWF SFB
F78 to S.H.; and the European Research Council (ERC) under the European Union’s
Horizon 2020 research and innovation programme (grant agreement no. 725780 LinPro)
to S.H.
article_number: '100939'
article_processing_charge: Yes
article_type: original
author:
- first_name: Nicole
full_name: Amberg, Nicole
id: 4CD6AAC6-F248-11E8-B48F-1D18A9856A87
last_name: Amberg
orcid: 0000-0002-3183-8207
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Amberg N, Hippenmeyer S. Genetic mosaic dissection of candidate genes in mice
using mosaic analysis with double markers. STAR Protocols. 2021;2(4). doi:10.1016/j.xpro.2021.100939
apa: Amberg, N., & Hippenmeyer, S. (2021). Genetic mosaic dissection of candidate
genes in mice using mosaic analysis with double markers. STAR Protocols.
Cell Press. https://doi.org/10.1016/j.xpro.2021.100939
chicago: Amberg, Nicole, and Simon Hippenmeyer. “Genetic Mosaic Dissection of Candidate
Genes in Mice Using Mosaic Analysis with Double Markers.” STAR Protocols.
Cell Press, 2021. https://doi.org/10.1016/j.xpro.2021.100939.
ieee: N. Amberg and S. Hippenmeyer, “Genetic mosaic dissection of candidate genes
in mice using mosaic analysis with double markers,” STAR Protocols, vol.
2, no. 4. Cell Press, 2021.
ista: Amberg N, Hippenmeyer S. 2021. Genetic mosaic dissection of candidate genes
in mice using mosaic analysis with double markers. STAR Protocols. 2(4), 100939.
mla: Amberg, Nicole, and Simon Hippenmeyer. “Genetic Mosaic Dissection of Candidate
Genes in Mice Using Mosaic Analysis with Double Markers.” STAR Protocols,
vol. 2, no. 4, 100939, Cell Press, 2021, doi:10.1016/j.xpro.2021.100939.
short: N. Amberg, S. Hippenmeyer, STAR Protocols 2 (2021).
date_created: 2021-11-21T23:01:28Z
date_published: 2021-11-10T00:00:00Z
date_updated: 2023-11-16T13:08:03Z
day: '10'
ddc:
- '573'
department:
- _id: SiHi
doi: 10.1016/j.xpro.2021.100939
ec_funded: 1
file:
- access_level: open_access
checksum: 9e3f6d06bf583e7a8b6a9e9a60500a28
content_type: application/pdf
creator: cchlebak
date_created: 2021-11-22T08:23:58Z
date_updated: 2021-11-22T08:23:58Z
file_id: '10329'
file_name: 2021_STARProtocols_Amberg.pdf
file_size: 7309464
relation: main_file
success: 1
file_date_updated: 2021-11-22T08:23:58Z
has_accepted_license: '1'
intvolume: ' 2'
issue: '4'
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
project:
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
- _id: 268F8446-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: T0101031
name: Role of Eed in neural stem cell lineage progression
- _id: 059F6AB4-7A3F-11EA-A408-12923DDC885E
grant_number: F07805
name: Molecular Mechanisms of Neural Stem Cell Lineage Progression
publication: STAR Protocols
publication_identifier:
eissn:
- 2666-1667
publication_status: published
publisher: Cell Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: Genetic mosaic dissection of candidate genes in mice using mosaic analysis
with double markers
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 2
year: '2021'
...
---
_id: '8544'
abstract:
- lang: eng
text: The synaptotrophic hypothesis posits that synapse formation stabilizes dendritic
branches, yet this hypothesis has not been causally tested in vivo in the mammalian
brain. Presynaptic ligand cerebellin-1 (Cbln1) and postsynaptic receptor GluD2
mediate synaptogenesis between granule cells and Purkinje cells in the molecular
layer of the cerebellar cortex. Here we show that sparse but not global knockout
of GluD2 causes under-elaboration of Purkinje cell dendrites in the deep molecular
layer and overelaboration in the superficial molecular layer. Developmental, overexpression,
structure-function, and genetic epistasis analyses indicate that dendrite morphogenesis
defects result from competitive synaptogenesis in a Cbln1/GluD2-dependent manner.
A generative model of dendritic growth based on competitive synaptogenesis largely
recapitulates GluD2 sparse and global knockout phenotypes. Our results support
the synaptotrophic hypothesis at initial stages of dendrite development, suggest
a second mode in which cumulative synapse formation inhibits further dendrite
growth, and highlight the importance of competition in dendrite morphogenesis.
acknowledgement: We thank M. Mishina for GluD2fl frozen embryos, T.C. Südhof and J.I.
Morgan for Cbln1fl mice, L. Anderson for help in generating the MADM alleles, W.
Joo for a previously unpublished construct, M. Yuzaki, K. Shen, J. Ding, and members
of the Luo lab, including J.M. Kebschull, H. Li, J. Li, T. Li, C.M. McLaughlin,
D. Pederick, J. Ren, D.C. Wang and C. Xu for discussions and critiques of the manuscript,
and M. Yuzaki for supporting Y.H.T. during the final phase of this project. Y.H.T.
was supported by a JSPS fellowship; S.A.S. was supported by a Stanford Graduate
Fellowship and an NSF Predoctoral Fellowship; L.J. is supported by a Stanford Graduate
Fellowship and an NSF Predoctoral Fellowship; M.J.W. is supported by a Burroughs
Wellcome Fund CASI Award. This work was supported by an NIH grant (R01-NS050538)
to L.L.; the European Research Council (ERC) under the European Union's Horizon
2020 research and innovations programme (No. 725780 LinPro) to S.H.; and Simons
and James S. McDonnell Foundations and an NSF CAREER award to S.G.; L.L. is an HHMI
investigator.
article_processing_charge: No
article_type: original
author:
- first_name: Yukari H.
full_name: Takeo, Yukari H.
last_name: Takeo
- first_name: S. Andrew
full_name: Shuster, S. Andrew
last_name: Shuster
- first_name: Linnie
full_name: Jiang, Linnie
last_name: Jiang
- first_name: Miley
full_name: Hu, Miley
last_name: Hu
- first_name: David J.
full_name: Luginbuhl, David J.
last_name: Luginbuhl
- first_name: Thomas
full_name: Rülicke, Thomas
last_name: Rülicke
- first_name: Ximena
full_name: Contreras, Ximena
id: 475990FE-F248-11E8-B48F-1D18A9856A87
last_name: Contreras
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Mark J.
full_name: Wagner, Mark J.
last_name: Wagner
- first_name: Surya
full_name: Ganguli, Surya
last_name: Ganguli
- first_name: Liqun
full_name: Luo, Liqun
last_name: Luo
citation:
ama: Takeo YH, Shuster SA, Jiang L, et al. GluD2- and Cbln1-mediated competitive
synaptogenesis shapes the dendritic arbors of cerebellar Purkinje cells. Neuron.
2021;109(4):P629-644.E8. doi:10.1016/j.neuron.2020.11.028
apa: Takeo, Y. H., Shuster, S. A., Jiang, L., Hu, M., Luginbuhl, D. J., Rülicke,
T., … Luo, L. (2021). GluD2- and Cbln1-mediated competitive synaptogenesis shapes
the dendritic arbors of cerebellar Purkinje cells. Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2020.11.028
chicago: Takeo, Yukari H., S. Andrew Shuster, Linnie Jiang, Miley Hu, David J. Luginbuhl,
Thomas Rülicke, Ximena Contreras, et al. “GluD2- and Cbln1-Mediated Competitive
Synaptogenesis Shapes the Dendritic Arbors of Cerebellar Purkinje Cells.” Neuron.
Elsevier, 2021. https://doi.org/10.1016/j.neuron.2020.11.028.
ieee: Y. H. Takeo et al., “GluD2- and Cbln1-mediated competitive synaptogenesis
shapes the dendritic arbors of cerebellar Purkinje cells,” Neuron, vol.
109, no. 4. Elsevier, p. P629–644.E8, 2021.
ista: Takeo YH, Shuster SA, Jiang L, Hu M, Luginbuhl DJ, Rülicke T, Contreras X,
Hippenmeyer S, Wagner MJ, Ganguli S, Luo L. 2021. GluD2- and Cbln1-mediated competitive
synaptogenesis shapes the dendritic arbors of cerebellar Purkinje cells. Neuron.
109(4), P629–644.E8.
mla: Takeo, Yukari H., et al. “GluD2- and Cbln1-Mediated Competitive Synaptogenesis
Shapes the Dendritic Arbors of Cerebellar Purkinje Cells.” Neuron, vol.
109, no. 4, Elsevier, 2021, p. P629–644.E8, doi:10.1016/j.neuron.2020.11.028.
short: Y.H. Takeo, S.A. Shuster, L. Jiang, M. Hu, D.J. Luginbuhl, T. Rülicke, X.
Contreras, S. Hippenmeyer, M.J. Wagner, S. Ganguli, L. Luo, Neuron 109 (2021)
P629–644.E8.
date_created: 2020-09-21T11:59:47Z
date_published: 2021-02-17T00:00:00Z
date_updated: 2024-03-06T12:12:48Z
day: '17'
department:
- _id: SiHi
doi: 10.1016/j.neuron.2020.11.028
ec_funded: 1
intvolume: ' 109'
issue: '4'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1101/2020.06.14.151258
month: '02'
oa: 1
oa_version: Preprint
page: P629-644.E8
project:
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
publication: Neuron
publication_identifier:
eissn:
- 1097-4199
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: GluD2- and Cbln1-mediated competitive synaptogenesis shapes the dendritic arbors
of cerebellar Purkinje cells
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 109
year: '2021'
...
---
_id: '9962'
abstract:
- lang: eng
text: The brain is one of the largest and most complex organs and it is composed
of billions of neurons that communicate together enabling e.g. consciousness.
The cerebral cortex is the largest site of neural integration in the central nervous
system. Concerted radial migration of newly born cortical projection neurons,
from their birthplace to their final position, is a key step in the assembly of
the cerebral cortex. The cellular and molecular mechanisms regulating radial neuronal
migration in vivo are however still unclear. Recent evidence suggests that distinct
signaling cues act cell-autonomously but differentially at certain steps during
the overall migration process. Moreover, functional analysis of genetic mosaics
(mutant neurons present in wild-type/heterozygote environment) using the MADM
(Mosaic Analysis with Double Markers) analyses in comparison to global knockout
also indicate a significant degree of non-cell-autonomous and/or community effects
in the control of cortical neuron migration. The interactions of cell-intrinsic
(cell-autonomous) and cell-extrinsic (non-cell-autonomous) components are largely
unknown. In part of this thesis work we established a MADM-based experimental
strategy for the quantitative analysis of cell-autonomous gene function versus
non-cell-autonomous and/or community effects. The direct comparison of mutant
neurons from the genetic mosaic (cell-autonomous) to mutant neurons in the conditional
and/or global knockout (cell-autonomous + non-cell-autonomous) allows to quantitatively
analyze non-cell-autonomous effects. Such analysis enable the high-resolution
analysis of projection neuron migration dynamics in distinct environments with
concomitant isolation of genomic and proteomic profiles. Using these experimental
paradigms and in combination with computational modeling we show and characterize
the nature of non-cell-autonomous effects to coordinate radial neuron migration.
Furthermore, this thesis discusses recent developments in neurodevelopment with
focus on neuronal polarization and non-cell-autonomous mechanisms in neuronal
migration.
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Andi H
full_name: Hansen, Andi H
id: 38853E16-F248-11E8-B48F-1D18A9856A87
last_name: Hansen
citation:
ama: Hansen AH. Cell-autonomous gene function and non-cell-autonomous effects in
radial projection neuron migration. 2021. doi:10.15479/at:ista:9962
apa: Hansen, A. H. (2021). Cell-autonomous gene function and non-cell-autonomous
effects in radial projection neuron migration. Institute of Science and Technology
Austria. https://doi.org/10.15479/at:ista:9962
chicago: Hansen, Andi H. “Cell-Autonomous Gene Function and Non-Cell-Autonomous
Effects in Radial Projection Neuron Migration.” Institute of Science and Technology
Austria, 2021. https://doi.org/10.15479/at:ista:9962.
ieee: A. H. Hansen, “Cell-autonomous gene function and non-cell-autonomous effects
in radial projection neuron migration,” Institute of Science and Technology Austria,
2021.
ista: Hansen AH. 2021. Cell-autonomous gene function and non-cell-autonomous effects
in radial projection neuron migration. Institute of Science and Technology Austria.
mla: Hansen, Andi H. Cell-Autonomous Gene Function and Non-Cell-Autonomous Effects
in Radial Projection Neuron Migration. Institute of Science and Technology
Austria, 2021, doi:10.15479/at:ista:9962.
short: A.H. Hansen, Cell-Autonomous Gene Function and Non-Cell-Autonomous Effects
in Radial Projection Neuron Migration, Institute of Science and Technology Austria,
2021.
date_created: 2021-08-29T12:36:50Z
date_published: 2021-09-02T00:00:00Z
date_updated: 2023-09-22T09:58:30Z
day: '02'
ddc:
- '570'
degree_awarded: PhD
department:
- _id: GradSch
- _id: SiHi
doi: 10.15479/at:ista:9962
file:
- access_level: closed
checksum: 66b56f5b988b233dc66a4f4b4fb2cdfe
content_type: application/vnd.openxmlformats-officedocument.wordprocessingml.document
creator: ahansen
date_created: 2021-08-30T09:17:39Z
date_updated: 2022-09-03T22:30:04Z
embargo_to: open_access
file_id: '9971'
file_name: Thesis_Hansen.docx
file_size: 10629190
relation: source_file
- access_level: open_access
checksum: 204fa40321a1c6289b68c473634c4bf3
content_type: application/pdf
creator: ahansen
date_created: 2021-08-30T09:29:44Z
date_updated: 2022-09-03T22:30:04Z
embargo: 2022-09-02
file_id: '9972'
file_name: Thesis_Hansen_PDFA-1a.pdf
file_size: 13457469
relation: main_file
file_date_updated: 2022-09-03T22:30:04Z
has_accepted_license: '1'
keyword:
- Neuronal migration
- Non-cell-autonomous
- Cell-autonomous
- Neurodevelopmental disease
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
page: '182'
project:
- _id: 2625A13E-B435-11E9-9278-68D0E5697425
grant_number: '24812'
name: Molecular Mechanisms of Radial Neuronal Migration
publication_identifier:
issn:
- 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
related_material:
record:
- id: '8569'
relation: part_of_dissertation
status: public
- id: '960'
relation: part_of_dissertation
status: public
status: public
supervisor:
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
title: Cell-autonomous gene function and non-cell-autonomous effects in radial projection
neuron migration
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: dissertation
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
year: '2021'
...
---
_id: '7814'
abstract:
- lang: eng
text: 'Scientific research is to date largely restricted to wealthy laboratories
in developed nations due to the necessity of complex and expensive equipment.
This inequality limits the capacity of science to be used as a diplomatic channel.
Maker movements use open-source technologies including additive manufacturing
(3D printing) and laser cutting, together with low-cost computers for developing
novel products. This movement is setting the groundwork for a revolution, allowing
scientific equipment to be sourced at a fraction of the cost and has the potential
to increase the availability of equipment for scientists around the world. Science
education is increasingly recognized as another channel for science diplomacy.
In this perspective, we introduce the idea that the Maker movement and open-source
technologies have the potential to revolutionize science, technology, engineering
and mathematics (STEM) education worldwide. We present an open-source STEM didactic
tool called SCOPES (Sparking Curiosity through Open-source Platforms in Education
and Science). SCOPES is self-contained, independent of local resources, and cost-effective.
SCOPES can be adapted to communicate complex subjects from genetics to neurobiology,
perform real-world biological experiments and explore digitized scientific samples.
We envision such platforms will enhance science diplomacy by providing a means
for scientists to share their findings with classrooms and for educators to incorporate
didactic concepts into STEM lessons. By providing students the opportunity to
design, perform, and share scientific experiments, students also experience firsthand
the benefits of a multinational scientific community. We provide instructions
on how to build and use SCOPES on our webpage: http://scopeseducation.org.'
acknowledged_ssus:
- _id: Bio
- _id: LifeSc
- _id: PreCl
- _id: EM-Fac
article_number: '48'
article_processing_charge: No
article_type: original
author:
- first_name: Robert J
full_name: Beattie, Robert J
id: 2E26DF60-F248-11E8-B48F-1D18A9856A87
last_name: Beattie
orcid: 0000-0002-8483-8753
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Florian
full_name: Pauler, Florian
id: 48EA0138-F248-11E8-B48F-1D18A9856A87
last_name: Pauler
citation:
ama: 'Beattie RJ, Hippenmeyer S, Pauler F. SCOPES: Sparking curiosity through Open-Source
platforms in education and science. Frontiers in Education. 2020;5. doi:10.3389/feduc.2020.00048'
apa: 'Beattie, R. J., Hippenmeyer, S., & Pauler, F. (2020). SCOPES: Sparking
curiosity through Open-Source platforms in education and science. Frontiers
in Education. Frontiers Media. https://doi.org/10.3389/feduc.2020.00048'
chicago: 'Beattie, Robert J, Simon Hippenmeyer, and Florian Pauler. “SCOPES: Sparking
Curiosity through Open-Source Platforms in Education and Science.” Frontiers
in Education. Frontiers Media, 2020. https://doi.org/10.3389/feduc.2020.00048.'
ieee: 'R. J. Beattie, S. Hippenmeyer, and F. Pauler, “SCOPES: Sparking curiosity
through Open-Source platforms in education and science,” Frontiers in Education,
vol. 5. Frontiers Media, 2020.'
ista: 'Beattie RJ, Hippenmeyer S, Pauler F. 2020. SCOPES: Sparking curiosity through
Open-Source platforms in education and science. Frontiers in Education. 5, 48.'
mla: 'Beattie, Robert J., et al. “SCOPES: Sparking Curiosity through Open-Source
Platforms in Education and Science.” Frontiers in Education, vol. 5, 48,
Frontiers Media, 2020, doi:10.3389/feduc.2020.00048.'
short: R.J. Beattie, S. Hippenmeyer, F. Pauler, Frontiers in Education 5 (2020).
date_created: 2020-05-11T08:18:48Z
date_published: 2020-05-08T00:00:00Z
date_updated: 2021-01-12T08:15:42Z
day: '08'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.3389/feduc.2020.00048
ec_funded: 1
file:
- access_level: open_access
checksum: a24ec24e38d843341ae620ec76c53688
content_type: application/pdf
creator: dernst
date_created: 2020-05-11T11:34:08Z
date_updated: 2020-07-14T12:48:03Z
file_id: '7818'
file_name: 2020_FrontiersEduc_Beattie.pdf
file_size: 1402146
relation: main_file
file_date_updated: 2020-07-14T12:48:03Z
has_accepted_license: '1'
intvolume: ' 5'
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
project:
- _id: 264E56E2-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: M02416
name: Molecular Mechanisms Regulating Gliogenesis in the Cerebral Cortex
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
publication: Frontiers in Education
publication_identifier:
issn:
- 2504-284X
publication_status: published
publisher: Frontiers Media
quality_controlled: '1'
status: public
title: 'SCOPES: Sparking curiosity through Open-Source platforms in education and
science'
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 5
year: '2020'
...
---
_id: '8616'
abstract:
- lang: eng
text: The brain vasculature supplies neurons with glucose and oxygen, but little
is known about how vascular plasticity contributes to brain function. Using longitudinal
in vivo imaging, we reported that a substantial proportion
of blood vessels in the adult brain sporadically occluded and regressed. Their
regression proceeded through sequential stages of blood-flow occlusion, endothelial
cell collapse, relocation or loss of pericytes, and retraction of glial endfeet.
Regressing vessels were found to be widespread in mouse, monkey and human brains.
Both brief occlusions of the middle cerebral artery and lipopolysaccharide-mediated
inflammation induced an increase of vessel regression. Blockage of leukocyte adhesion
to endothelial cells alleviated LPS-induced vessel regression. We further revealed
that blood vessel regression caused a reduction of neuronal activity due to a
dysfunction in mitochondrial metabolism and glutamate production. Our results
elucidate the mechanism of vessel regression and its role in neuronal function
in the adult brain.
acknowledgement: 'The project was initiated in the Jan lab at UCSF. We thank Lily
Jan and Yuh-Nung Jan’s generous support. We thank Liqun Luo’s lab for providing
MADM-7 mice and Rolf A Brekken for VEGF-antibodies. Drs. Yuanquan Song (UPenn),
Zhaozhu Hu (JHU), Ji Hu (ShanghaiTech), Yang Xiang (U. Mass), Hao Wang (Zhejiang
U.) and Ruikang Wang (U. Washington) for critical input, colleagues at Children’s
Research Institute, Departments of Neuroscience, Neurology and Neurotherapeutics,
Pediatrics from UT Southwestern, and colleagues from the Jan lab for discussion.
Dr. Bridget Samuels, Sean Morrison (UT Southwestern), and Nannan Lu (Zhejiang U.)
for critical reading. We acknowledge the assistance of the CIBR Imaging core. We
also thank UT Southwestern Live Cell Imaging Facility, a Shared Resource of the
Harold C. Simmons Cancer Center, supported in part by an NCI Cancer Center Support
Grant, P30 CA142543K. This work is supported by CIBR funds and the American Heart
Association AWRP Summer 2016 Innovative Research Grant (17IRG33410377) to W-P.G.;
National Natural Science Foundation of China (No.81370031) to Z.Z.;National Key
Research and Development Program of China (2016YFE0125400)to F.H.;National Natural
Science Foundations of China (No. 81473202) to Y.L.; National Natural Science Foundation
of China (No.31600839) and Shenzhen Science and Technology Research Program (JCYJ20170818163320865)
to B.P.; National Natural Science Foundation of China (No. 31800864) and Westlake
University start-up funds to J-M. J. NIH R01NS088627 to W.L.J.; NIH: R01 AG020670
and RF1AG054111 to H.Z.; R01 NS088555 to A.M.S., and European Research Council No.725780
to S.H.;W-P.G. was a recipient of Bugher-American Heart Association Dan Adams Thinking
Outside the Box Award.'
article_processing_charge: No
author:
- first_name: Xiaofei
full_name: Gao, Xiaofei
last_name: Gao
- first_name: Jun-Liszt
full_name: Li, Jun-Liszt
last_name: Li
- first_name: Xingjun
full_name: Chen, Xingjun
last_name: Chen
- first_name: Bo
full_name: Ci, Bo
last_name: Ci
- first_name: Fei
full_name: Chen, Fei
last_name: Chen
- first_name: Nannan
full_name: Lu, Nannan
last_name: Lu
- first_name: Bo
full_name: Shen, Bo
last_name: Shen
- first_name: Lijun
full_name: Zheng, Lijun
last_name: Zheng
- first_name: Jie-Min
full_name: Jia, Jie-Min
last_name: Jia
- first_name: Yating
full_name: Yi, Yating
last_name: Yi
- first_name: Shiwen
full_name: Zhang, Shiwen
last_name: Zhang
- first_name: Ying-Chao
full_name: Shi, Ying-Chao
last_name: Shi
- first_name: Kaibin
full_name: Shi, Kaibin
last_name: Shi
- first_name: Nicholas E
full_name: Propson, Nicholas E
last_name: Propson
- first_name: Yubin
full_name: Huang, Yubin
last_name: Huang
- first_name: Katherine
full_name: Poinsatte, Katherine
last_name: Poinsatte
- first_name: Zhaohuan
full_name: Zhang, Zhaohuan
last_name: Zhang
- first_name: Yuanlei
full_name: Yue, Yuanlei
last_name: Yue
- first_name: Dale B
full_name: Bosco, Dale B
last_name: Bosco
- first_name: Ying-mei
full_name: Lu, Ying-mei
last_name: Lu
- first_name: Shi-bing
full_name: Yang, Shi-bing
last_name: Yang
- first_name: Ralf H.
full_name: Adams, Ralf H.
last_name: Adams
- first_name: Volkhard
full_name: Lindner, Volkhard
last_name: Lindner
- first_name: Fen
full_name: Huang, Fen
last_name: Huang
- first_name: Long-Jun
full_name: Wu, Long-Jun
last_name: Wu
- first_name: Hui
full_name: Zheng, Hui
last_name: Zheng
- first_name: Feng
full_name: Han, Feng
last_name: Han
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Ann M.
full_name: Stowe, Ann M.
last_name: Stowe
- first_name: Bo
full_name: Peng, Bo
last_name: Peng
- first_name: Marta
full_name: Margeta, Marta
last_name: Margeta
- first_name: Xiaoqun
full_name: Wang, Xiaoqun
last_name: Wang
- first_name: Qiang
full_name: Liu, Qiang
last_name: Liu
- first_name: Jakob
full_name: Körbelin, Jakob
last_name: Körbelin
- first_name: Martin
full_name: Trepel, Martin
last_name: Trepel
- first_name: Hui
full_name: Lu, Hui
last_name: Lu
- first_name: Bo O.
full_name: Zhou, Bo O.
last_name: Zhou
- first_name: Hu
full_name: Zhao, Hu
last_name: Zhao
- first_name: Wenzhi
full_name: Su, Wenzhi
last_name: Su
- first_name: Robert M.
full_name: Bachoo, Robert M.
last_name: Bachoo
- first_name: Woo-ping
full_name: Ge, Woo-ping
last_name: Ge
citation:
ama: Gao X, Li J-L, Chen X, et al. Reduction of neuronal activity mediated by blood-vessel
regression in the brain. bioRxiv. doi:10.1101/2020.09.15.262782
apa: Gao, X., Li, J.-L., Chen, X., Ci, B., Chen, F., Lu, N., … Ge, W. (n.d.). Reduction
of neuronal activity mediated by blood-vessel regression in the brain. bioRxiv.
Cold Spring Harbor Laboratory. https://doi.org/10.1101/2020.09.15.262782
chicago: Gao, Xiaofei, Jun-Liszt Li, Xingjun Chen, Bo Ci, Fei Chen, Nannan Lu, Bo
Shen, et al. “Reduction of Neuronal Activity Mediated by Blood-Vessel Regression
in the Brain.” BioRxiv. Cold Spring Harbor Laboratory, n.d. https://doi.org/10.1101/2020.09.15.262782.
ieee: X. Gao et al., “Reduction of neuronal activity mediated by blood-vessel
regression in the brain,” bioRxiv. Cold Spring Harbor Laboratory.
ista: Gao X, Li J-L, Chen X, Ci B, Chen F, Lu N, Shen B, Zheng L, Jia J-M, Yi Y,
Zhang S, Shi Y-C, Shi K, Propson NE, Huang Y, Poinsatte K, Zhang Z, Yue Y, Bosco
DB, Lu Y, Yang S, Adams RH, Lindner V, Huang F, Wu L-J, Zheng H, Han F, Hippenmeyer
S, Stowe AM, Peng B, Margeta M, Wang X, Liu Q, Körbelin J, Trepel M, Lu H, Zhou
BO, Zhao H, Su W, Bachoo RM, Ge W. Reduction of neuronal activity mediated by
blood-vessel regression in the brain. bioRxiv, 10.1101/2020.09.15.262782.
mla: Gao, Xiaofei, et al. “Reduction of Neuronal Activity Mediated by Blood-Vessel
Regression in the Brain.” BioRxiv, Cold Spring Harbor Laboratory, doi:10.1101/2020.09.15.262782.
short: X. Gao, J.-L. Li, X. Chen, B. Ci, F. Chen, N. Lu, B. Shen, L. Zheng, J.-M.
Jia, Y. Yi, S. Zhang, Y.-C. Shi, K. Shi, N.E. Propson, Y. Huang, K. Poinsatte,
Z. Zhang, Y. Yue, D.B. Bosco, Y. Lu, S. Yang, R.H. Adams, V. Lindner, F. Huang,
L.-J. Wu, H. Zheng, F. Han, S. Hippenmeyer, A.M. Stowe, B. Peng, M. Margeta, X.
Wang, Q. Liu, J. Körbelin, M. Trepel, H. Lu, B.O. Zhou, H. Zhao, W. Su, R.M. Bachoo,
W. Ge, BioRxiv (n.d.).
date_created: 2020-10-06T08:58:59Z
date_published: 2020-09-15T00:00:00Z
date_updated: 2021-01-12T08:20:19Z
day: '15'
department:
- _id: SiHi
doi: 10.1101/2020.09.15.262782
ec_funded: 1
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1101/2020.09.15.262782
month: '09'
oa: 1
oa_version: Preprint
project:
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
publication: bioRxiv
publication_status: submitted
publisher: Cold Spring Harbor Laboratory
status: public
title: Reduction of neuronal activity mediated by blood-vessel regression in the brain
type: preprint
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2020'
...
---
_id: '8978'
abstract:
- lang: eng
text: "Mosaic analysis with double markers (MADM) technology enables concomitant
fluorescent cell labeling and induction of uniparental chromosome disomy (UPD)
with single-cell resolution. In UPD, imprinted genes are either overexpressed
2-fold or are not expressed. Here, the MADM platform is utilized to probe imprinting
phenotypes at the transcriptional level. This protocol highlights major steps
for the generation and isolation of projection neurons and astrocytes with MADM-induced
UPD from mouse cerebral cortex for downstream single-cell and low-input sample
RNA-sequencing experiments.\r\n\r\nFor complete details on the use and execution
of this protocol, please refer to Laukoter et al. (2020b)."
acknowledged_ssus:
- _id: Bio
- _id: PreCl
acknowledgement: This research was supported by the Scientific Service Units (SSU)
at IST Austria through resources provided by the Bioimaging (BIF) and Preclinical
Facilities (PCF). N.A received support from the FWF Firnberg-Programm (T 1031).
This work was also supported by IST Austria institutional funds; FWF SFB F78 to
S.H.; NÖ Forschung und Bildung n[f+b] life science call grant (C13-002) to S.H.;
the People Programme (Marie Curie Actions) of the European Union’s Seventh Framework
Programme (FP7/2007-2013) under REA grant agreement no. 618444 to S.H.; and the
European Research Council (ERC) under the European Union’s Horizon 2020 research
and innovation programme (grant agreement no. 725780 LinPro) to S.H.
article_number: '100215'
article_processing_charge: No
article_type: original
author:
- first_name: Susanne
full_name: Laukoter, Susanne
id: 2D6B7A9A-F248-11E8-B48F-1D18A9856A87
last_name: Laukoter
- first_name: Nicole
full_name: Amberg, Nicole
id: 4CD6AAC6-F248-11E8-B48F-1D18A9856A87
last_name: Amberg
orcid: 0000-0002-3183-8207
- first_name: Florian
full_name: Pauler, Florian
id: 48EA0138-F248-11E8-B48F-1D18A9856A87
last_name: Pauler
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Laukoter S, Amberg N, Pauler F, Hippenmeyer S. Generation and isolation of
single cells from mouse brain with mosaic analysis with double markers-induced
uniparental chromosome disomy. STAR Protocols. 2020;1(3). doi:10.1016/j.xpro.2020.100215
apa: Laukoter, S., Amberg, N., Pauler, F., & Hippenmeyer, S. (2020). Generation
and isolation of single cells from mouse brain with mosaic analysis with double
markers-induced uniparental chromosome disomy. STAR Protocols. Elsevier.
https://doi.org/10.1016/j.xpro.2020.100215
chicago: Laukoter, Susanne, Nicole Amberg, Florian Pauler, and Simon Hippenmeyer.
“Generation and Isolation of Single Cells from Mouse Brain with Mosaic Analysis
with Double Markers-Induced Uniparental Chromosome Disomy.” STAR Protocols.
Elsevier, 2020. https://doi.org/10.1016/j.xpro.2020.100215.
ieee: S. Laukoter, N. Amberg, F. Pauler, and S. Hippenmeyer, “Generation and isolation
of single cells from mouse brain with mosaic analysis with double markers-induced
uniparental chromosome disomy,” STAR Protocols, vol. 1, no. 3. Elsevier,
2020.
ista: Laukoter S, Amberg N, Pauler F, Hippenmeyer S. 2020. Generation and isolation
of single cells from mouse brain with mosaic analysis with double markers-induced
uniparental chromosome disomy. STAR Protocols. 1(3), 100215.
mla: Laukoter, Susanne, et al. “Generation and Isolation of Single Cells from Mouse
Brain with Mosaic Analysis with Double Markers-Induced Uniparental Chromosome
Disomy.” STAR Protocols, vol. 1, no. 3, 100215, Elsevier, 2020, doi:10.1016/j.xpro.2020.100215.
short: S. Laukoter, N. Amberg, F. Pauler, S. Hippenmeyer, STAR Protocols 1 (2020).
date_created: 2020-12-30T10:17:07Z
date_published: 2020-12-18T00:00:00Z
date_updated: 2021-01-12T08:21:36Z
day: '18'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1016/j.xpro.2020.100215
ec_funded: 1
external_id:
pmid:
- '33377108'
file:
- access_level: open_access
checksum: f1e9a433e9cb0f41f7b6df6b76db1f6e
content_type: application/pdf
creator: dernst
date_created: 2021-01-07T15:57:27Z
date_updated: 2021-01-07T15:57:27Z
file_id: '8996'
file_name: 2020_STARProtocols_Laukoter.pdf
file_size: 4031449
relation: main_file
success: 1
file_date_updated: 2021-01-07T15:57:27Z
has_accepted_license: '1'
intvolume: ' 1'
issue: '3'
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 268F8446-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: T0101031
name: Role of Eed in neural stem cell lineage progression
- _id: 059F6AB4-7A3F-11EA-A408-12923DDC885E
grant_number: F07805
name: Molecular Mechanisms of Neural Stem Cell Lineage Progression
- _id: 25D92700-B435-11E9-9278-68D0E5697425
grant_number: LS13-002
name: Mapping Cell-Type Specificity of the Genomic Imprintome in the Brain
- _id: 25D61E48-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '618444'
name: Molecular Mechanisms of Cerebral Cortex Development
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
publication: STAR Protocols
publication_identifier:
issn:
- 2666-1667
publication_status: published
publisher: Elsevier
quality_controlled: '1'
status: public
title: Generation and isolation of single cells from mouse brain with mosaic analysis
with double markers-induced uniparental chromosome disomy
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 1
year: '2020'
...
---
_id: '7253'
abstract:
- lang: eng
text: The cyclin-dependent kinase inhibitor p57KIP2 is encoded by the imprinted
Cdkn1c locus, exhibits maternal expression, and is essential for cerebral cortex
development. How Cdkn1c regulates corticogenesis is however not clear. To this
end we employ Mosaic Analysis with Double Markers (MADM) technology to genetically
dissect Cdkn1c gene function in corticogenesis at single cell resolution. We find
that the previously described growth-inhibitory Cdkn1c function is a non-cell-autonomous
one, acting on the whole organism. In contrast we reveal a growth-promoting cell-autonomous
Cdkn1c function which at the mechanistic level mediates radial glial progenitor
cell and nascent projection neuron survival. Strikingly, the growth-promoting
function of Cdkn1c is highly dosage sensitive but not subject to genomic imprinting.
Collectively, our results suggest that the Cdkn1c locus regulates cortical development
through distinct cell-autonomous and non-cell-autonomous mechanisms. More generally,
our study highlights the importance to probe the relative contributions of cell
intrinsic gene function and tissue-wide mechanisms to the overall phenotype.
acknowledged_ssus:
- _id: PreCl
article_number: '195'
article_processing_charge: No
article_type: original
author:
- first_name: Susanne
full_name: Laukoter, Susanne
id: 2D6B7A9A-F248-11E8-B48F-1D18A9856A87
last_name: Laukoter
orcid: 0000-0002-7903-3010
- first_name: Robert J
full_name: Beattie, Robert J
id: 2E26DF60-F248-11E8-B48F-1D18A9856A87
last_name: Beattie
orcid: 0000-0002-8483-8753
- first_name: Florian
full_name: Pauler, Florian
id: 48EA0138-F248-11E8-B48F-1D18A9856A87
last_name: Pauler
orcid: 0000-0002-7462-0048
- first_name: Nicole
full_name: Amberg, Nicole
id: 4CD6AAC6-F248-11E8-B48F-1D18A9856A87
last_name: Amberg
orcid: 0000-0002-3183-8207
- first_name: Keiichi I.
full_name: Nakayama, Keiichi I.
last_name: Nakayama
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Laukoter S, Beattie RJ, Pauler F, Amberg N, Nakayama KI, Hippenmeyer S. Imprinted
Cdkn1c genomic locus cell-autonomously promotes cell survival in cerebral cortex
development. Nature Communications. 2020;11. doi:10.1038/s41467-019-14077-2
apa: Laukoter, S., Beattie, R. J., Pauler, F., Amberg, N., Nakayama, K. I., &
Hippenmeyer, S. (2020). Imprinted Cdkn1c genomic locus cell-autonomously promotes
cell survival in cerebral cortex development. Nature Communications. Springer
Nature. https://doi.org/10.1038/s41467-019-14077-2
chicago: Laukoter, Susanne, Robert J Beattie, Florian Pauler, Nicole Amberg, Keiichi
I. Nakayama, and Simon Hippenmeyer. “Imprinted Cdkn1c Genomic Locus Cell-Autonomously
Promotes Cell Survival in Cerebral Cortex Development.” Nature Communications.
Springer Nature, 2020. https://doi.org/10.1038/s41467-019-14077-2.
ieee: S. Laukoter, R. J. Beattie, F. Pauler, N. Amberg, K. I. Nakayama, and S. Hippenmeyer,
“Imprinted Cdkn1c genomic locus cell-autonomously promotes cell survival in cerebral
cortex development,” Nature Communications, vol. 11. Springer Nature, 2020.
ista: Laukoter S, Beattie RJ, Pauler F, Amberg N, Nakayama KI, Hippenmeyer S. 2020.
Imprinted Cdkn1c genomic locus cell-autonomously promotes cell survival in cerebral
cortex development. Nature Communications. 11, 195.
mla: Laukoter, Susanne, et al. “Imprinted Cdkn1c Genomic Locus Cell-Autonomously
Promotes Cell Survival in Cerebral Cortex Development.” Nature Communications,
vol. 11, 195, Springer Nature, 2020, doi:10.1038/s41467-019-14077-2.
short: S. Laukoter, R.J. Beattie, F. Pauler, N. Amberg, K.I. Nakayama, S. Hippenmeyer,
Nature Communications 11 (2020).
date_created: 2020-01-11T10:42:48Z
date_published: 2020-01-10T00:00:00Z
date_updated: 2023-08-17T14:23:41Z
day: '10'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1038/s41467-019-14077-2
ec_funded: 1
external_id:
isi:
- '000551459000005'
file:
- access_level: open_access
checksum: ebf1ed522f4e0be8d94c939c1806a709
content_type: application/pdf
creator: dernst
date_created: 2020-01-13T07:42:31Z
date_updated: 2020-07-14T12:47:54Z
file_id: '7261'
file_name: 2020_NatureComm_Laukoter.pdf
file_size: 8063333
relation: main_file
file_date_updated: 2020-07-14T12:47:54Z
has_accepted_license: '1'
intvolume: ' 11'
isi: 1
language:
- iso: eng
month: '01'
oa: 1
oa_version: Published Version
project:
- _id: 268F8446-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: T0101031
name: Role of Eed in neural stem cell lineage progression
- _id: 264E56E2-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: M02416
name: Molecular Mechanisms Regulating Gliogenesis in the Cerebral Cortex
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
- _id: 25D92700-B435-11E9-9278-68D0E5697425
grant_number: LS13-002
name: Mapping Cell-Type Specificity of the Genomic Imprintome in the Brain
publication: Nature Communications
publication_identifier:
issn:
- 2041-1723
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
related_material:
link:
- description: News on IST Homepage
relation: press_release
url: https://ist.ac.at/en/news/new-function-for-potential-tumour-suppressor-in-brain-development/
scopus_import: '1'
status: public
title: Imprinted Cdkn1c genomic locus cell-autonomously promotes cell survival in
cerebral cortex development
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 11
year: '2020'
...
---
_id: '7593'
abstract:
- lang: eng
text: Heterozygous loss of human PAFAH1B1 (coding for LIS1) results in the disruption
of neurogenesis and neuronal migration via dysregulation of microtubule (MT) stability
and dynein motor function/localization that alters mitotic spindle orientation,
chromosomal segregation, and nuclear migration. Recently, human induced pluripotent
stem cell (iPSC) models revealed an important role for LIS1 in controlling the
length of terminal cell divisions of outer radial glial (oRG) progenitors, suggesting
cellular functions of LIS1 in regulating neural progenitor cell (NPC) daughter
cell separation. Here we examined the late mitotic stages NPCs in vivo and mouse
embryonic fibroblasts (MEFs) in vitro from Pafah1b1-deficient mutants. Pafah1b1-deficient
neocortical NPCs and MEFs similarly exhibited cleavage plane displacement with
mislocalization of furrow-associated markers, associated with actomyosin dysfunction
and cell membrane hyper-contractility. Thus, it suggests LIS1 acts as a key molecular
link connecting MTs/dynein and actomyosin, ensuring that cell membrane contractility
is tightly controlled to execute proper daughter cell separation.
article_number: '51512'
article_processing_charge: No
article_type: original
author:
- first_name: Hyang Mi
full_name: Moon, Hyang Mi
last_name: Moon
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Liqun
full_name: Luo, Liqun
last_name: Luo
- first_name: Anthony
full_name: Wynshaw-Boris, Anthony
last_name: Wynshaw-Boris
citation:
ama: Moon HM, Hippenmeyer S, Luo L, Wynshaw-Boris A. LIS1 determines cleavage plane
positioning by regulating actomyosin-mediated cell membrane contractility. eLife.
2020;9. doi:10.7554/elife.51512
apa: Moon, H. M., Hippenmeyer, S., Luo, L., & Wynshaw-Boris, A. (2020). LIS1
determines cleavage plane positioning by regulating actomyosin-mediated cell membrane
contractility. ELife. eLife Sciences Publications. https://doi.org/10.7554/elife.51512
chicago: Moon, Hyang Mi, Simon Hippenmeyer, Liqun Luo, and Anthony Wynshaw-Boris.
“LIS1 Determines Cleavage Plane Positioning by Regulating Actomyosin-Mediated
Cell Membrane Contractility.” ELife. eLife Sciences Publications, 2020.
https://doi.org/10.7554/elife.51512.
ieee: H. M. Moon, S. Hippenmeyer, L. Luo, and A. Wynshaw-Boris, “LIS1 determines
cleavage plane positioning by regulating actomyosin-mediated cell membrane contractility,”
eLife, vol. 9. eLife Sciences Publications, 2020.
ista: Moon HM, Hippenmeyer S, Luo L, Wynshaw-Boris A. 2020. LIS1 determines cleavage
plane positioning by regulating actomyosin-mediated cell membrane contractility.
eLife. 9, 51512.
mla: Moon, Hyang Mi, et al. “LIS1 Determines Cleavage Plane Positioning by Regulating
Actomyosin-Mediated Cell Membrane Contractility.” ELife, vol. 9, 51512,
eLife Sciences Publications, 2020, doi:10.7554/elife.51512.
short: H.M. Moon, S. Hippenmeyer, L. Luo, A. Wynshaw-Boris, ELife 9 (2020).
date_created: 2020-03-20T13:16:41Z
date_published: 2020-03-11T00:00:00Z
date_updated: 2023-08-18T07:06:31Z
day: '11'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.7554/elife.51512
external_id:
isi:
- '000522835800001'
pmid:
- '32159512'
file:
- access_level: open_access
checksum: 396ceb2dd10b102ef4e699666b9342c3
content_type: application/pdf
creator: dernst
date_created: 2020-09-24T07:03:20Z
date_updated: 2020-09-24T07:03:20Z
file_id: '8567'
file_name: 2020_elife_Moon.pdf
file_size: 15089438
relation: main_file
success: 1
file_date_updated: 2020-09-24T07:03:20Z
has_accepted_license: '1'
intvolume: ' 9'
isi: 1
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1101/751958
month: '03'
oa: 1
oa_version: Published Version
pmid: 1
publication: eLife
publication_identifier:
issn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: LIS1 determines cleavage plane positioning by regulating actomyosin-mediated
cell membrane contractility
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 9
year: '2020'
...
---
_id: '8093'
abstract:
- lang: eng
text: "Background: The activation of the EGFR/Ras-signalling pathway in tumour cells
induces a distinct chemokine repertoire, which in turn modulates the tumour microenvironment.\r\nMethods:
The effects of EGFR/Ras on the expression and translation of CCL20 were analysed
in a large set of epithelial cancer cell lines and tumour tissues by RT-qPCR and
ELISA in vitro. CCL20 production was verified by immunohistochemistry in different
tumour tissues and correlated with clinical data. The effects of CCL20 on endothelial
cell migration and tumour-associated vascularisation were comprehensively analysed
with chemotaxis assays in vitro and in CCR6-deficient mice in vivo.\r\nResults:
Tumours facilitate progression by the EGFR/Ras-induced production of CCL20. Expression
of the chemokine CCL20 in tumours correlates with advanced tumour stage, increased
lymph node metastasis and decreased survival in patients. Microvascular endothelial
cells abundantly express the specific CCL20 receptor CCR6. CCR6 signalling in
endothelial cells induces angiogenesis. CCR6-deficient mice show significantly
decreased tumour growth and tumour-associated vascularisation. The observed phenotype
is dependent on CCR6 deficiency in stromal cells but not within the immune system.\r\nConclusion:
We propose that the chemokine axis CCL20–CCR6 represents a novel and promising
target to interfere with the tumour microenvironment, and opens an innovative
multimodal strategy for cancer therapy."
acknowledgement: "The authors would like to thank A. van Lierop for technical assistance.
In addition, we thank C. Dullin, J. Missbach-Güntner and S. Greco for advice and
assistance with fpVCT imaging. Furthermore, the authors would like to thank H. K.
Horst for advice on performing matrigel plug assays. This study has also been partially
presented in A. Schorr’s doctoral thesis and the funding report of the SPP 1190
‘The tumor-vessel interface’ of the ‘Deutsche Forschungsgemeinschaft’ (DFG).\r\nThis
project was funded by the SPP 1190 “The tumor-vessel interface” and HO 2092/8-1
of the ‘Deutsche Forschungsgemeinschaft’ (DFG) to B. Homey. In addition, it was
supported by grants from the Austrian Science Fund (FWF, W1212 to N. Amberg and
J. Klufa and I4300-B to T. Bauer), the WWTF project LS16-025 and the European Research
Council (ERC) Advanced grant (ERC-2015-AdG TNT-Tumors 694883) to M. Sibilia."
article_processing_charge: No
article_type: original
author:
- first_name: Andreas
full_name: Hippe, Andreas
last_name: Hippe
- first_name: Stephan Alexander
full_name: Braun, Stephan Alexander
last_name: Braun
- first_name: Péter
full_name: Oláh, Péter
last_name: Oláh
- first_name: Peter Arne
full_name: Gerber, Peter Arne
last_name: Gerber
- first_name: Anne
full_name: Schorr, Anne
last_name: Schorr
- first_name: Stephan
full_name: Seeliger, Stephan
last_name: Seeliger
- first_name: Stephanie
full_name: Holtz, Stephanie
last_name: Holtz
- first_name: Katharina
full_name: Jannasch, Katharina
last_name: Jannasch
- first_name: Andor
full_name: Pivarcsi, Andor
last_name: Pivarcsi
- first_name: Bettina
full_name: Buhren, Bettina
last_name: Buhren
- first_name: Holger
full_name: Schrumpf, Holger
last_name: Schrumpf
- first_name: Andreas
full_name: Kislat, Andreas
last_name: Kislat
- first_name: Erich
full_name: Bünemann, Erich
last_name: Bünemann
- first_name: Martin
full_name: Steinhoff, Martin
last_name: Steinhoff
- first_name: Jens
full_name: Fischer, Jens
last_name: Fischer
- first_name: Sérgio A.
full_name: Lira, Sérgio A.
last_name: Lira
- first_name: Petra
full_name: Boukamp, Petra
last_name: Boukamp
- first_name: Peter
full_name: Hevezi, Peter
last_name: Hevezi
- first_name: Nikolas Hendrik
full_name: Stoecklein, Nikolas Hendrik
last_name: Stoecklein
- first_name: Thomas
full_name: Hoffmann, Thomas
last_name: Hoffmann
- first_name: Frauke
full_name: Alves, Frauke
last_name: Alves
- first_name: Jonathan
full_name: Sleeman, Jonathan
last_name: Sleeman
- first_name: Thomas
full_name: Bauer, Thomas
last_name: Bauer
- first_name: Jörg
full_name: Klufa, Jörg
last_name: Klufa
- first_name: Nicole
full_name: Amberg, Nicole
id: 4CD6AAC6-F248-11E8-B48F-1D18A9856A87
last_name: Amberg
orcid: 0000-0002-3183-8207
- first_name: Maria
full_name: Sibilia, Maria
last_name: Sibilia
- first_name: Albert
full_name: Zlotnik, Albert
last_name: Zlotnik
- first_name: Anja
full_name: Müller-Homey, Anja
last_name: Müller-Homey
- first_name: Bernhard
full_name: Homey, Bernhard
last_name: Homey
citation:
ama: Hippe A, Braun SA, Oláh P, et al. EGFR/Ras-induced CCL20 production modulates
the tumour microenvironment. British Journal of Cancer. 2020;123:942-954.
doi:10.1038/s41416-020-0943-2
apa: Hippe, A., Braun, S. A., Oláh, P., Gerber, P. A., Schorr, A., Seeliger, S.,
… Homey, B. (2020). EGFR/Ras-induced CCL20 production modulates the tumour microenvironment.
British Journal of Cancer. Springer Nature. https://doi.org/10.1038/s41416-020-0943-2
chicago: Hippe, Andreas, Stephan Alexander Braun, Péter Oláh, Peter Arne Gerber,
Anne Schorr, Stephan Seeliger, Stephanie Holtz, et al. “EGFR/Ras-Induced CCL20
Production Modulates the Tumour Microenvironment.” British Journal of Cancer.
Springer Nature, 2020. https://doi.org/10.1038/s41416-020-0943-2.
ieee: A. Hippe et al., “EGFR/Ras-induced CCL20 production modulates the tumour
microenvironment,” British Journal of Cancer, vol. 123. Springer Nature,
pp. 942–954, 2020.
ista: Hippe A, Braun SA, Oláh P, Gerber PA, Schorr A, Seeliger S, Holtz S, Jannasch
K, Pivarcsi A, Buhren B, Schrumpf H, Kislat A, Bünemann E, Steinhoff M, Fischer
J, Lira SA, Boukamp P, Hevezi P, Stoecklein NH, Hoffmann T, Alves F, Sleeman J,
Bauer T, Klufa J, Amberg N, Sibilia M, Zlotnik A, Müller-Homey A, Homey B. 2020.
EGFR/Ras-induced CCL20 production modulates the tumour microenvironment. British
Journal of Cancer. 123, 942–954.
mla: Hippe, Andreas, et al. “EGFR/Ras-Induced CCL20 Production Modulates the Tumour
Microenvironment.” British Journal of Cancer, vol. 123, Springer Nature,
2020, pp. 942–54, doi:10.1038/s41416-020-0943-2.
short: A. Hippe, S.A. Braun, P. Oláh, P.A. Gerber, A. Schorr, S. Seeliger, S. Holtz,
K. Jannasch, A. Pivarcsi, B. Buhren, H. Schrumpf, A. Kislat, E. Bünemann, M. Steinhoff,
J. Fischer, S.A. Lira, P. Boukamp, P. Hevezi, N.H. Stoecklein, T. Hoffmann, F.
Alves, J. Sleeman, T. Bauer, J. Klufa, N. Amberg, M. Sibilia, A. Zlotnik, A. Müller-Homey,
B. Homey, British Journal of Cancer 123 (2020) 942–954.
date_created: 2020-07-05T22:00:46Z
date_published: 2020-09-15T00:00:00Z
date_updated: 2023-08-22T07:51:12Z
day: '15'
ddc:
- '610'
department:
- _id: SiHi
doi: 10.1038/s41416-020-0943-2
external_id:
isi:
- '000544152500001'
pmid:
- '32601464'
file:
- access_level: open_access
checksum: 05a8e65d49c3f5b8e37ac4afe68287e2
content_type: application/pdf
creator: cchlebak
date_created: 2021-12-02T12:35:12Z
date_updated: 2021-12-02T12:35:12Z
file_id: '10398'
file_name: 2020_BrJournalCancer_Hippe.pdf
file_size: 3620691
relation: main_file
success: 1
file_date_updated: 2021-12-02T12:35:12Z
has_accepted_license: '1'
intvolume: ' 123'
isi: 1
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
page: 942-954
pmid: 1
publication: British Journal of Cancer
publication_identifier:
eissn:
- 1532-1827
issn:
- 0007-0920
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
related_material:
link:
- relation: erratum
url: https://doi.org/10.1038/s41416-021-01563-y
record:
- id: '10170'
relation: later_version
status: deleted
scopus_import: '1'
status: public
title: EGFR/Ras-induced CCL20 production modulates the tumour microenvironment
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 123
year: '2020'
...
---
_id: '8162'
abstract:
- lang: eng
text: In mammalian genomes, a subset of genes is regulated by genomic imprinting,
resulting in silencing of one parental allele. Imprinting is essential for cerebral
cortex development, but prevalence and functional impact in individual cells is
unclear. Here, we determined allelic expression in cortical cell types and established
a quantitative platform to interrogate imprinting in single cells. We created
cells with uniparental chromosome disomy (UPD) containing two copies of either
the maternal or the paternal chromosome; hence, imprinted genes will be 2-fold
overexpressed or not expressed. By genetic labeling of UPD, we determined cellular
phenotypes and transcriptional responses to deregulated imprinted gene expression
at unprecedented single-cell resolution. We discovered an unexpected degree of
cell-type specificity and a novel function of imprinting in the regulation of
cortical astrocyte survival. More generally, our results suggest functional relevance
of imprinted gene expression in glial astrocyte lineage and thus for generating
cortical cell-type diversity.
acknowledged_ssus:
- _id: Bio
- _id: LifeSc
- _id: PreCl
acknowledgement: We thank A. Heger (IST Austria Preclinical Facility), A. Sommer and
C. Czepe (VBCF GmbH, NGS Unit), and A. Seitz and P. Moll (Lexogen GmbH) for technical
support; G. Arque, S. Resch, C. Igler, C. Dotter, C. Yahya, Q. Hudson, and D. Andergassen
for initial experiments and/or assistance; D. Barlow, O. Bell, and all members of
the Hippenmeyer lab for discussion; and N. Barton, B. Vicoso, M. Sixt, and L. Luo
for comments on earlier versions of the manuscript. This research was supported
by the Scientific Service Units (SSU) of IST Austria through resources provided
by the Bioimaging Facilities (BIF), Life Science Facilities (LSF), and Preclinical
Facilities (PCF). A.H.H. is a recipient of a DOC fellowship (24812) of the Austrian
Academy of Sciences. N.A. received support from the FWF Firnberg-Programm (T 1031).
R.B. received support from the FWF Meitner-Programm (M 2416). This work was also
supported by IST Austria institutional funds; a NÖ Forschung und Bildung n[f+b]
life science call grant (C13-002) to S.H.; a program grant from the Human Frontiers
Science Program (RGP0053/2014) to S.H.; the People Programme (Marie Curie Actions)
of the European Union’s Seventh Framework Programme (FP7/2007-2013) under REA grant
agreement 618444 to S.H.; and the European Research Council (ERC) under the European
Union’s Horizon 2020 research and innovation program (grant agreement 725780 LinPro)
to S.H.
article_processing_charge: No
article_type: original
author:
- first_name: Susanne
full_name: Laukoter, Susanne
id: 2D6B7A9A-F248-11E8-B48F-1D18A9856A87
last_name: Laukoter
orcid: 0000-0002-7903-3010
- first_name: Florian
full_name: Pauler, Florian
id: 48EA0138-F248-11E8-B48F-1D18A9856A87
last_name: Pauler
orcid: 0000-0002-7462-0048
- first_name: Robert J
full_name: Beattie, Robert J
id: 2E26DF60-F248-11E8-B48F-1D18A9856A87
last_name: Beattie
orcid: 0000-0002-8483-8753
- first_name: Nicole
full_name: Amberg, Nicole
id: 4CD6AAC6-F248-11E8-B48F-1D18A9856A87
last_name: Amberg
orcid: 0000-0002-3183-8207
- first_name: Andi H
full_name: Hansen, Andi H
id: 38853E16-F248-11E8-B48F-1D18A9856A87
last_name: Hansen
- first_name: Carmen
full_name: Streicher, Carmen
id: 36BCB99C-F248-11E8-B48F-1D18A9856A87
last_name: Streicher
- first_name: Thomas
full_name: Penz, Thomas
last_name: Penz
- first_name: Christoph
full_name: Bock, Christoph
last_name: Bock
orcid: 0000-0001-6091-3088
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Laukoter S, Pauler F, Beattie RJ, et al. Cell-type specificity of genomic imprinting
in cerebral cortex. Neuron. 2020;107(6):1160-1179.e9. doi:10.1016/j.neuron.2020.06.031
apa: Laukoter, S., Pauler, F., Beattie, R. J., Amberg, N., Hansen, A. H., Streicher,
C., … Hippenmeyer, S. (2020). Cell-type specificity of genomic imprinting in cerebral
cortex. Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2020.06.031
chicago: Laukoter, Susanne, Florian Pauler, Robert J Beattie, Nicole Amberg, Andi
H Hansen, Carmen Streicher, Thomas Penz, Christoph Bock, and Simon Hippenmeyer.
“Cell-Type Specificity of Genomic Imprinting in Cerebral Cortex.” Neuron.
Elsevier, 2020. https://doi.org/10.1016/j.neuron.2020.06.031.
ieee: S. Laukoter et al., “Cell-type specificity of genomic imprinting in
cerebral cortex,” Neuron, vol. 107, no. 6. Elsevier, p. 1160–1179.e9, 2020.
ista: Laukoter S, Pauler F, Beattie RJ, Amberg N, Hansen AH, Streicher C, Penz T,
Bock C, Hippenmeyer S. 2020. Cell-type specificity of genomic imprinting in cerebral
cortex. Neuron. 107(6), 1160–1179.e9.
mla: Laukoter, Susanne, et al. “Cell-Type Specificity of Genomic Imprinting in Cerebral
Cortex.” Neuron, vol. 107, no. 6, Elsevier, 2020, p. 1160–1179.e9, doi:10.1016/j.neuron.2020.06.031.
short: S. Laukoter, F. Pauler, R.J. Beattie, N. Amberg, A.H. Hansen, C. Streicher,
T. Penz, C. Bock, S. Hippenmeyer, Neuron 107 (2020) 1160–1179.e9.
date_created: 2020-07-23T16:03:12Z
date_published: 2020-09-23T00:00:00Z
date_updated: 2023-08-22T08:20:11Z
day: '23'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1016/j.neuron.2020.06.031
ec_funded: 1
external_id:
isi:
- '000579698700006'
file:
- access_level: open_access
checksum: 7becdc16a6317304304631087ae7dd7f
content_type: application/pdf
creator: dernst
date_created: 2020-12-02T09:26:46Z
date_updated: 2020-12-02T09:26:46Z
file_id: '8828'
file_name: 2020_Neuron_Laukoter.pdf
file_size: 8911830
relation: main_file
success: 1
file_date_updated: 2020-12-02T09:26:46Z
has_accepted_license: '1'
intvolume: ' 107'
isi: 1
issue: '6'
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
page: 1160-1179.e9
project:
- _id: 2625A13E-B435-11E9-9278-68D0E5697425
grant_number: '24812'
name: Molecular Mechanisms of Radial Neuronal Migration
- _id: 268F8446-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: T0101031
name: Role of Eed in neural stem cell lineage progression
- _id: 264E56E2-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: M02416
name: Molecular Mechanisms Regulating Gliogenesis in the Cerebral Cortex
- _id: 25D92700-B435-11E9-9278-68D0E5697425
grant_number: LS13-002
name: Mapping Cell-Type Specificity of the Genomic Imprintome in the Brain
- _id: 25D7962E-B435-11E9-9278-68D0E5697425
grant_number: RGP0053/2014
name: Quantitative Structure-Function Analysis of Cerebral Cortex Assembly at Clonal
Level
- _id: 25D61E48-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '618444'
name: Molecular Mechanisms of Cerebral Cortex Development
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
publication: Neuron
publication_identifier:
issn:
- 0896-6273
publication_status: published
publisher: Elsevier
quality_controlled: '1'
related_material:
link:
- description: News on IST Website
relation: press_release
url: https://ist.ac.at/en/news/cells-react-differently-to-genomic-imprinting/
scopus_import: '1'
status: public
title: Cell-type specificity of genomic imprinting in cerebral cortex
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 107
year: '2020'
...
---
_id: '8592'
abstract:
- lang: eng
text: Glioblastoma is the most malignant cancer in the brain and currently incurable.
It is urgent to identify effective targets for this lethal disease. Inhibition
of such targets should suppress the growth of cancer cells and, ideally also precancerous
cells for early prevention, but minimally affect their normal counterparts. Using
genetic mouse models with neural stem cells (NSCs) or oligodendrocyte precursor
cells (OPCs) as the cells‐of‐origin/mutation, it is shown that the susceptibility
of cells within the development hierarchy of glioma to the knockout of insulin‐like
growth factor I receptor (IGF1R) is determined not only by their oncogenic states,
but also by their cell identities/states. Knockout of IGF1R selectively disrupts
the growth of mutant and transformed, but not normal OPCs, or NSCs. The desirable
outcome of IGF1R knockout on cell growth requires the mutant cells to commit to
the OPC identity regardless of its development hierarchical status. At the molecular
level, oncogenic mutations reprogram the cellular network of OPCs and force them
to depend more on IGF1R for their growth. A new‐generation brain‐penetrable, orally
available IGF1R inhibitor harnessing tumor OPCs in the brain is also developed.
The findings reveal the cellular window of IGF1R targeting and establish IGF1R
as an effective target for the prevention and treatment of glioblastoma.
acknowledgement: The authors thank Drs. J. Eisen, QR. Lu, S. Duan, Z‐H. Li, W. Mo,
and Q. Wu for their critical comments on the manuscript. They also thank Dr. H.
Zong for providing the CKO_NG2‐CreER model. This work is supported by the National
Key Research and Development Program of China, Stem Cell and Translational Research
(2016YFA0101201 to C.L., 2016YFA0100303 to Y.J.W.), the National Natural Science
Foundation of China (81673035 and 81972915 to C.L., 81472722 to Y.J.W.), the Science
Foundation for Distinguished Young Scientists of Zhejiang Province (LR17H160001
to C.L.), Fundamental Research Funds for the Central Universities (2016QNA7023 and
2017QNA7028 to C.L.) and the Thousand Talent Program for Young Outstanding Scientists,
China (to C.L.), IST Austria institutional funds (to S.H.), European Research Council
(ERC) under the European Union's Horizon 2020 research and innovation programme
(725780 LinPro to S.H.). C.L. is a scholar of K. C. Wong Education Foundation.
article_number: '2001724'
article_processing_charge: No
article_type: original
author:
- first_name: Anhao
full_name: Tian, Anhao
last_name: Tian
- first_name: Bo
full_name: Kang, Bo
last_name: Kang
- first_name: Baizhou
full_name: Li, Baizhou
last_name: Li
- first_name: Biying
full_name: Qiu, Biying
last_name: Qiu
- first_name: Wenhong
full_name: Jiang, Wenhong
last_name: Jiang
- first_name: Fangjie
full_name: Shao, Fangjie
last_name: Shao
- first_name: Qingqing
full_name: Gao, Qingqing
last_name: Gao
- first_name: Rui
full_name: Liu, Rui
last_name: Liu
- first_name: Chengwei
full_name: Cai, Chengwei
last_name: Cai
- first_name: Rui
full_name: Jing, Rui
last_name: Jing
- first_name: Wei
full_name: Wang, Wei
last_name: Wang
- first_name: Pengxiang
full_name: Chen, Pengxiang
last_name: Chen
- first_name: Qinghui
full_name: Liang, Qinghui
last_name: Liang
- first_name: Lili
full_name: Bao, Lili
last_name: Bao
- first_name: Jianghong
full_name: Man, Jianghong
last_name: Man
- first_name: Yan
full_name: Wang, Yan
last_name: Wang
- first_name: Yu
full_name: Shi, Yu
last_name: Shi
- first_name: Jin
full_name: Li, Jin
last_name: Li
- first_name: Minmin
full_name: Yang, Minmin
last_name: Yang
- first_name: Lisha
full_name: Wang, Lisha
last_name: Wang
- first_name: Jianmin
full_name: Zhang, Jianmin
last_name: Zhang
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Junming
full_name: Zhu, Junming
last_name: Zhu
- first_name: Xiuwu
full_name: Bian, Xiuwu
last_name: Bian
- first_name: Ying‐Jie
full_name: Wang, Ying‐Jie
last_name: Wang
- first_name: Chong
full_name: Liu, Chong
last_name: Liu
citation:
ama: Tian A, Kang B, Li B, et al. Oncogenic state and cell identity combinatorially
dictate the susceptibility of cells within glioma development hierarchy to IGF1R
targeting. Advanced Science. 2020;7(21). doi:10.1002/advs.202001724
apa: Tian, A., Kang, B., Li, B., Qiu, B., Jiang, W., Shao, F., … Liu, C. (2020).
Oncogenic state and cell identity combinatorially dictate the susceptibility of
cells within glioma development hierarchy to IGF1R targeting. Advanced Science.
Wiley. https://doi.org/10.1002/advs.202001724
chicago: Tian, Anhao, Bo Kang, Baizhou Li, Biying Qiu, Wenhong Jiang, Fangjie Shao,
Qingqing Gao, et al. “Oncogenic State and Cell Identity Combinatorially Dictate
the Susceptibility of Cells within Glioma Development Hierarchy to IGF1R Targeting.”
Advanced Science. Wiley, 2020. https://doi.org/10.1002/advs.202001724.
ieee: A. Tian et al., “Oncogenic state and cell identity combinatorially
dictate the susceptibility of cells within glioma development hierarchy to IGF1R
targeting,” Advanced Science, vol. 7, no. 21. Wiley, 2020.
ista: Tian A, Kang B, Li B, Qiu B, Jiang W, Shao F, Gao Q, Liu R, Cai C, Jing R,
Wang W, Chen P, Liang Q, Bao L, Man J, Wang Y, Shi Y, Li J, Yang M, Wang L, Zhang
J, Hippenmeyer S, Zhu J, Bian X, Wang Y, Liu C. 2020. Oncogenic state and cell
identity combinatorially dictate the susceptibility of cells within glioma development
hierarchy to IGF1R targeting. Advanced Science. 7(21), 2001724.
mla: Tian, Anhao, et al. “Oncogenic State and Cell Identity Combinatorially Dictate
the Susceptibility of Cells within Glioma Development Hierarchy to IGF1R Targeting.”
Advanced Science, vol. 7, no. 21, 2001724, Wiley, 2020, doi:10.1002/advs.202001724.
short: A. Tian, B. Kang, B. Li, B. Qiu, W. Jiang, F. Shao, Q. Gao, R. Liu, C. Cai,
R. Jing, W. Wang, P. Chen, Q. Liang, L. Bao, J. Man, Y. Wang, Y. Shi, J. Li, M.
Yang, L. Wang, J. Zhang, S. Hippenmeyer, J. Zhu, X. Bian, Y. Wang, C. Liu, Advanced
Science 7 (2020).
date_created: 2020-10-01T09:44:13Z
date_published: 2020-11-04T00:00:00Z
date_updated: 2023-08-22T09:53:01Z
day: '04'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1002/advs.202001724
ec_funded: 1
external_id:
isi:
- '000573860700001'
file:
- access_level: open_access
checksum: 92818c23ecc70e35acfa671f3cfb9909
content_type: application/pdf
creator: dernst
date_created: 2020-12-10T14:07:24Z
date_updated: 2020-12-10T14:07:24Z
file_id: '8938'
file_name: 2020_AdvScience_Tian.pdf
file_size: 7835833
relation: main_file
success: 1
file_date_updated: 2020-12-10T14:07:24Z
has_accepted_license: '1'
intvolume: ' 7'
isi: 1
issue: '21'
keyword:
- General Engineering
- General Physics and Astronomy
- General Materials Science
- Medicine (miscellaneous)
- General Chemical Engineering
- Biochemistry
- Genetics and Molecular Biology (miscellaneous)
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
project:
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
publication: Advanced Science
publication_identifier:
issn:
- 2198-3844
publication_status: published
publisher: Wiley
quality_controlled: '1'
status: public
title: Oncogenic state and cell identity combinatorially dictate the susceptibility
of cells within glioma development hierarchy to IGF1R targeting
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 7
year: '2020'
...
---
_id: '8949'
abstract:
- lang: eng
text: Development of the nervous system undergoes important transitions,
including one from neurogenesis to gliogenesis which occurs late during embryonic
gestation. Here we report on clonal analysis of gliogenesis in mice using Mosaic
Analysis with Double Markers (MADM) with quantitative and computational methods.
Results reveal that developmental gliogenesis in the cerebral cortex occurs in
a fraction of earlier neurogenic clones, accelerating around E16.5, and giving
rise to both astrocytes and oligodendrocytes. Moreover, MADM-based genetic deletion
of the epidermal growth factor receptor (Egfr) in gliogenic clones revealed that
Egfr is cell autonomously required for gliogenesis in the mouse dorsolateral cortices.
A broad range in the proliferation capacity, symmetry of clones, and competitive
advantage of MADM cells was evident in clones that contained one cellular lineage
with double dosage of Egfr relative to their environment, while their sibling
Egfr-null cells failed to generate glia. Remarkably, the total numbers of glia
in MADM clones balance out regardless of significant alterations in clonal symmetries.
The variability in glial clones shows stochastic patterns that we define mathematically,
which are different from the deterministic patterns in neuronal clones. This study
sets a foundation for studying the biological significance of stochastic and deterministic
clonal principles underlying tissue development, and identifying mechanisms that
differentiate between neurogenesis and gliogenesis.
acknowledgement: This research was funded by grants from the National Institutes of
Health to H.T.G. (R01NS098370 and R01NS089795). C.V.M. was supported by a National
Science Foundation Graduate Research Fellowship (DGE-1746939). R.B. was supported
by the FWF Lise-Meitner program (M 2416), and S.H. was supported by the European
Research Council (ERC) under the European Union’s Horizon 2020 research and innovation
programme (grant agreement No 725780 LinPro).The authors thank members of the Ghashghaei
lab for discussions, technical support, and help with preparation of the manuscript.
article_number: '2662'
article_processing_charge: No
article_type: original
author:
- first_name: Xuying
full_name: Zhang, Xuying
last_name: Zhang
- first_name: Christine V.
full_name: Mennicke, Christine V.
last_name: Mennicke
- first_name: Guanxi
full_name: Xiao, Guanxi
last_name: Xiao
- first_name: Robert J
full_name: Beattie, Robert J
id: 2E26DF60-F248-11E8-B48F-1D18A9856A87
last_name: Beattie
orcid: 0000-0002-8483-8753
- first_name: Mansoor
full_name: Haider, Mansoor
last_name: Haider
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: H. Troy
full_name: Ghashghaei, H. Troy
last_name: Ghashghaei
citation:
ama: Zhang X, Mennicke CV, Xiao G, et al. Clonal analysis of gliogenesis in the
cerebral cortex reveals stochastic expansion of glia and cell autonomous responses
to Egfr dosage. Cells. 2020;9(12). doi:10.3390/cells9122662
apa: Zhang, X., Mennicke, C. V., Xiao, G., Beattie, R. J., Haider, M., Hippenmeyer,
S., & Ghashghaei, H. T. (2020). Clonal analysis of gliogenesis in the cerebral
cortex reveals stochastic expansion of glia and cell autonomous responses to Egfr
dosage. Cells. MDPI. https://doi.org/10.3390/cells9122662
chicago: Zhang, Xuying, Christine V. Mennicke, Guanxi Xiao, Robert J Beattie, Mansoor
Haider, Simon Hippenmeyer, and H. Troy Ghashghaei. “Clonal Analysis of Gliogenesis
in the Cerebral Cortex Reveals Stochastic Expansion of Glia and Cell Autonomous
Responses to Egfr Dosage.” Cells. MDPI, 2020. https://doi.org/10.3390/cells9122662.
ieee: X. Zhang et al., “Clonal analysis of gliogenesis in the cerebral cortex
reveals stochastic expansion of glia and cell autonomous responses to Egfr dosage,”
Cells, vol. 9, no. 12. MDPI, 2020.
ista: Zhang X, Mennicke CV, Xiao G, Beattie RJ, Haider M, Hippenmeyer S, Ghashghaei
HT. 2020. Clonal analysis of gliogenesis in the cerebral cortex reveals stochastic
expansion of glia and cell autonomous responses to Egfr dosage. Cells. 9(12),
2662.
mla: Zhang, Xuying, et al. “Clonal Analysis of Gliogenesis in the Cerebral Cortex
Reveals Stochastic Expansion of Glia and Cell Autonomous Responses to Egfr Dosage.”
Cells, vol. 9, no. 12, 2662, MDPI, 2020, doi:10.3390/cells9122662.
short: X. Zhang, C.V. Mennicke, G. Xiao, R.J. Beattie, M. Haider, S. Hippenmeyer,
H.T. Ghashghaei, Cells 9 (2020).
date_created: 2020-12-14T08:04:03Z
date_published: 2020-12-11T00:00:00Z
date_updated: 2023-08-24T10:57:48Z
day: '11'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.3390/cells9122662
ec_funded: 1
external_id:
isi:
- '000601787300001'
file:
- access_level: open_access
checksum: 5095cbdc728c9a510c5761cf60a8861c
content_type: application/pdf
creator: dernst
date_created: 2020-12-14T08:09:43Z
date_updated: 2020-12-14T08:09:43Z
file_id: '8950'
file_name: 2020_Cells_Zhang.pdf
file_size: 3504525
relation: main_file
success: 1
file_date_updated: 2020-12-14T08:09:43Z
has_accepted_license: '1'
intvolume: ' 9'
isi: 1
issue: '12'
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
project:
- _id: 264E56E2-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: M02416
name: Molecular Mechanisms Regulating Gliogenesis in the Cerebral Cortex
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
publication: Cells
publication_identifier:
issn:
- 2073-4409
publication_status: published
publisher: MDPI
quality_controlled: '1'
status: public
title: Clonal analysis of gliogenesis in the cerebral cortex reveals stochastic expansion
of glia and cell autonomous responses to Egfr dosage
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 9
year: '2020'
...
---
_id: '8813'
abstract:
- lang: eng
text: 'In mammals, chromatin marks at imprinted genes are asymmetrically inherited
to control parentally-biased gene expression. This control is thought predominantly
to involve parent-specific differentially methylated regions (DMR) in genomic
DNA. However, neither parent-of-origin-specific transcription nor DMRs have been
comprehensively mapped. We here address this by integrating transcriptomic and
epigenomic approaches in mouse preimplantation embryos (blastocysts). Transcriptome-analysis
identified 71 genes expressed with previously unknown parent-of-origin-specific
expression in blastocysts (nBiX: novel blastocyst-imprinted expression). Uniparental
expression of nBiX genes disappeared soon after implantation. Micro-whole-genome
bisulfite sequencing (μWGBS) of individual uniparental blastocysts detected 859
DMRs. Only 18% of nBiXs were associated with a DMR, whereas 60% were associated
with parentally-biased H3K27me3. This suggests a major role for Polycomb-mediated
imprinting in blastocysts. Five nBiX-clusters contained at least one known imprinted
gene, and five novel clusters contained exclusively nBiX-genes. These data suggest
a complex program of stage-specific imprinting involving different tiers of regulation.'
article_processing_charge: No
author:
- first_name: Laura
full_name: Santini, Laura
last_name: Santini
- first_name: Florian
full_name: Halbritter, Florian
last_name: Halbritter
- first_name: Fabian
full_name: Titz-Teixeira, Fabian
last_name: Titz-Teixeira
- first_name: Toru
full_name: Suzuki, Toru
last_name: Suzuki
- first_name: Maki
full_name: Asami, Maki
last_name: Asami
- first_name: Julia
full_name: Ramesmayer, Julia
last_name: Ramesmayer
- first_name: Xiaoyan
full_name: Ma, Xiaoyan
last_name: Ma
- first_name: Andreas
full_name: Lackner, Andreas
last_name: Lackner
- first_name: Nick
full_name: Warr, Nick
last_name: Warr
- first_name: Florian
full_name: Pauler, Florian
id: 48EA0138-F248-11E8-B48F-1D18A9856A87
last_name: Pauler
orcid: 0000-0002-7462-0048
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Ernest
full_name: Laue, Ernest
last_name: Laue
- first_name: Matthias
full_name: Farlik, Matthias
last_name: Farlik
- first_name: Christoph
full_name: Bock, Christoph
last_name: Bock
- first_name: Andreas
full_name: Beyer, Andreas
last_name: Beyer
- first_name: Anthony C. F.
full_name: Perry, Anthony C. F.
last_name: Perry
- first_name: Martin
full_name: Leeb, Martin
last_name: Leeb
citation:
ama: Santini L, Halbritter F, Titz-Teixeira F, et al. Novel imprints in mouse blastocysts
are predominantly DNA methylation independent. bioRxiv. doi:10.1101/2020.11.03.366948
apa: Santini, L., Halbritter, F., Titz-Teixeira, F., Suzuki, T., Asami, M., Ramesmayer,
J., … Leeb, M. (n.d.). Novel imprints in mouse blastocysts are predominantly DNA
methylation independent. bioRxiv. Cold Spring Harbor Laboratory. https://doi.org/10.1101/2020.11.03.366948
chicago: Santini, Laura, Florian Halbritter, Fabian Titz-Teixeira, Toru Suzuki,
Maki Asami, Julia Ramesmayer, Xiaoyan Ma, et al. “Novel Imprints in Mouse Blastocysts
Are Predominantly DNA Methylation Independent.” BioRxiv. Cold Spring Harbor
Laboratory, n.d. https://doi.org/10.1101/2020.11.03.366948.
ieee: L. Santini et al., “Novel imprints in mouse blastocysts are predominantly
DNA methylation independent,” bioRxiv. Cold Spring Harbor Laboratory.
ista: Santini L, Halbritter F, Titz-Teixeira F, Suzuki T, Asami M, Ramesmayer J,
Ma X, Lackner A, Warr N, Pauler F, Hippenmeyer S, Laue E, Farlik M, Bock C, Beyer
A, Perry ACF, Leeb M. Novel imprints in mouse blastocysts are predominantly DNA
methylation independent. bioRxiv, 10.1101/2020.11.03.366948.
mla: Santini, Laura, et al. “Novel Imprints in Mouse Blastocysts Are Predominantly
DNA Methylation Independent.” BioRxiv, Cold Spring Harbor Laboratory, doi:10.1101/2020.11.03.366948.
short: L. Santini, F. Halbritter, F. Titz-Teixeira, T. Suzuki, M. Asami, J. Ramesmayer,
X. Ma, A. Lackner, N. Warr, F. Pauler, S. Hippenmeyer, E. Laue, M. Farlik, C.
Bock, A. Beyer, A.C.F. Perry, M. Leeb, BioRxiv (n.d.).
date_created: 2020-11-26T07:17:19Z
date_published: 2020-11-05T00:00:00Z
date_updated: 2023-09-12T11:05:28Z
day: '05'
department:
- _id: SiHi
doi: 10.1101/2020.11.03.366948
external_id:
pmid:
- 'PPR234457 '
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1101/2020.11.03.366948
month: '11'
oa: 1
oa_version: Preprint
pmid: 1
publication: bioRxiv
publication_status: submitted
publisher: Cold Spring Harbor Laboratory
status: public
title: Novel imprints in mouse blastocysts are predominantly DNA methylation independent
type: preprint
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2020'
...
---
_id: '8569'
abstract:
- lang: eng
text: Concerted radial migration of newly born cortical projection neurons, from
their birthplace to their final target lamina, is a key step in the assembly of
the cerebral cortex. The cellular and molecular mechanisms regulating the specific
sequential steps of radial neuronal migration in vivo are however still unclear,
let alone the effects and interactions with the extracellular environment. In
any in vivo context, cells will always be exposed to a complex extracellular environment
consisting of (1) secreted factors acting as potential signaling cues, (2) the
extracellular matrix, and (3) other cells providing cell–cell interaction through
receptors and/or direct physical stimuli. Most studies so far have described and
focused mainly on intrinsic cell-autonomous gene functions in neuronal migration
but there is accumulating evidence that non-cell-autonomous-, local-, systemic-,
and/or whole tissue-wide effects substantially contribute to the regulation of
radial neuronal migration. These non-cell-autonomous effects may differentially
affect cortical neuron migration in distinct cellular environments. However, the
cellular and molecular natures of such non-cell-autonomous mechanisms are mostly
unknown. Furthermore, physical forces due to collective migration and/or community
effects (i.e., interactions with surrounding cells) may play important roles in
neocortical projection neuron migration. In this concise review, we first outline
distinct models of non-cell-autonomous interactions of cortical projection neurons
along their radial migration trajectory during development. We then summarize
experimental assays and platforms that can be utilized to visualize and potentially
probe non-cell-autonomous mechanisms. Lastly, we define key questions to address
in the future.
acknowledgement: AH was a recipient of a DOC Fellowship (24812) of the Austrian Academy
of Sciences. This work also received support from IST Austria institutional funds;
the People Programme (Marie Curie Actions) of the European Union’s Seventh Framework
Programme (FP7/2007–2013) under REA Grant Agreement No. 618444 to SH.
article_number: '574382'
article_processing_charge: Yes (via OA deal)
article_type: original
author:
- first_name: Andi H
full_name: Hansen, Andi H
id: 38853E16-F248-11E8-B48F-1D18A9856A87
last_name: Hansen
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Hansen AH, Hippenmeyer S. Non-cell-autonomous mechanisms in radial projection
neuron migration in the developing cerebral cortex. Frontiers in Cell and Developmental
Biology. 2020;8(9). doi:10.3389/fcell.2020.574382
apa: Hansen, A. H., & Hippenmeyer, S. (2020). Non-cell-autonomous mechanisms
in radial projection neuron migration in the developing cerebral cortex. Frontiers
in Cell and Developmental Biology. Frontiers. https://doi.org/10.3389/fcell.2020.574382
chicago: Hansen, Andi H, and Simon Hippenmeyer. “Non-Cell-Autonomous Mechanisms
in Radial Projection Neuron Migration in the Developing Cerebral Cortex.” Frontiers
in Cell and Developmental Biology. Frontiers, 2020. https://doi.org/10.3389/fcell.2020.574382.
ieee: A. H. Hansen and S. Hippenmeyer, “Non-cell-autonomous mechanisms in radial
projection neuron migration in the developing cerebral cortex,” Frontiers in
Cell and Developmental Biology, vol. 8, no. 9. Frontiers, 2020.
ista: Hansen AH, Hippenmeyer S. 2020. Non-cell-autonomous mechanisms in radial projection
neuron migration in the developing cerebral cortex. Frontiers in Cell and Developmental
Biology. 8(9), 574382.
mla: Hansen, Andi H., and Simon Hippenmeyer. “Non-Cell-Autonomous Mechanisms in
Radial Projection Neuron Migration in the Developing Cerebral Cortex.” Frontiers
in Cell and Developmental Biology, vol. 8, no. 9, 574382, Frontiers, 2020,
doi:10.3389/fcell.2020.574382.
short: A.H. Hansen, S. Hippenmeyer, Frontiers in Cell and Developmental Biology
8 (2020).
date_created: 2020-09-26T06:11:07Z
date_published: 2020-09-25T00:00:00Z
date_updated: 2024-03-29T23:30:40Z
day: '25'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.3389/fcell.2020.574382
ec_funded: 1
external_id:
isi:
- '000577915900001'
pmid:
- '33102480'
file:
- access_level: open_access
checksum: 01f731824194c94c81a5da360d997073
content_type: application/pdf
creator: dernst
date_created: 2020-09-28T13:11:17Z
date_updated: 2020-09-28T13:11:17Z
file_id: '8584'
file_name: 2020_Frontiers_Hansen.pdf
file_size: 5527139
relation: main_file
success: 1
file_date_updated: 2020-09-28T13:11:17Z
has_accepted_license: '1'
intvolume: ' 8'
isi: 1
issue: '9'
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 2625A13E-B435-11E9-9278-68D0E5697425
grant_number: '24812'
name: Molecular Mechanisms of Radial Neuronal Migration
- _id: 25D61E48-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '618444'
name: Molecular Mechanisms of Cerebral Cortex Development
publication: Frontiers in Cell and Developmental Biology
publication_identifier:
issn:
- 2296-634X
publication_status: published
publisher: Frontiers
quality_controlled: '1'
related_material:
record:
- id: '9962'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Non-cell-autonomous mechanisms in radial projection neuron migration in the
developing cerebral cortex
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 8
year: '2020'
...
---
_id: '7815'
abstract:
- lang: eng
text: Beginning from a limited pool of progenitors, the mammalian cerebral cortex
forms highly organized functional neural circuits. However, the underlying cellular
and molecular mechanisms regulating lineage transitions of neural stem cells (NSCs)
and eventual production of neurons and glia in the developing neuroepithelium
remains unclear. Methods to trace NSC division patterns and map the lineage of
clonally related cells have advanced dramatically. However, many contemporary
lineage tracing techniques suffer from the lack of cellular resolution of progeny
cell fate, which is essential for deciphering progenitor cell division patterns.
Presented is a protocol using mosaic analysis with double markers (MADM) to perform
in vivo clonal analysis. MADM concomitantly manipulates individual progenitor
cells and visualizes precise division patterns and lineage progression at unprecedented
single cell resolution. MADM-based interchromosomal recombination events during
the G2-X phase of mitosis, together with temporally inducible CreERT2, provide
exact information on the birth dates of clones and their division patterns. Thus,
MADM lineage tracing provides unprecedented qualitative and quantitative optical
readouts of the proliferation mode of stem cell progenitors at the single cell
level. MADM also allows for examination of the mechanisms and functional requirements
of candidate genes in NSC lineage progression. This method is unique in that comparative
analysis of control and mutant subclones can be performed in the same tissue environment
in vivo. Here, the protocol is described in detail, and experimental paradigms
to employ MADM for clonal analysis and lineage tracing in the developing cerebral
cortex are demonstrated. Importantly, this protocol can be adapted to perform
MADM clonal analysis in any murine stem cell niche, as long as the CreERT2 driver
is present.
acknowledged_ssus:
- _id: Bio
- _id: LifeSc
- _id: PreCl
article_number: e61147
article_processing_charge: No
article_type: original
author:
- first_name: Robert J
full_name: Beattie, Robert J
id: 2E26DF60-F248-11E8-B48F-1D18A9856A87
last_name: Beattie
orcid: 0000-0002-8483-8753
- first_name: Carmen
full_name: Streicher, Carmen
id: 36BCB99C-F248-11E8-B48F-1D18A9856A87
last_name: Streicher
- first_name: Nicole
full_name: Amberg, Nicole
id: 4CD6AAC6-F248-11E8-B48F-1D18A9856A87
last_name: Amberg
orcid: 0000-0002-3183-8207
- first_name: Giselle T
full_name: Cheung, Giselle T
id: 471195F6-F248-11E8-B48F-1D18A9856A87
last_name: Cheung
orcid: 0000-0001-8457-2572
- first_name: Ximena
full_name: Contreras, Ximena
id: 475990FE-F248-11E8-B48F-1D18A9856A87
last_name: Contreras
- first_name: Andi H
full_name: Hansen, Andi H
id: 38853E16-F248-11E8-B48F-1D18A9856A87
last_name: Hansen
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Beattie RJ, Streicher C, Amberg N, et al. Lineage tracing and clonal analysis
in developing cerebral cortex using mosaic analysis with double markers (MADM).
Journal of Visual Experiments. 2020;(159). doi:10.3791/61147
apa: Beattie, R. J., Streicher, C., Amberg, N., Cheung, G. T., Contreras, X., Hansen,
A. H., & Hippenmeyer, S. (2020). Lineage tracing and clonal analysis in developing
cerebral cortex using mosaic analysis with double markers (MADM). Journal of
Visual Experiments. MyJove Corporation. https://doi.org/10.3791/61147
chicago: Beattie, Robert J, Carmen Streicher, Nicole Amberg, Giselle T Cheung, Ximena
Contreras, Andi H Hansen, and Simon Hippenmeyer. “Lineage Tracing and Clonal Analysis
in Developing Cerebral Cortex Using Mosaic Analysis with Double Markers (MADM).”
Journal of Visual Experiments. MyJove Corporation, 2020. https://doi.org/10.3791/61147.
ieee: R. J. Beattie et al., “Lineage tracing and clonal analysis in developing
cerebral cortex using mosaic analysis with double markers (MADM),” Journal
of Visual Experiments, no. 159. MyJove Corporation, 2020.
ista: Beattie RJ, Streicher C, Amberg N, Cheung GT, Contreras X, Hansen AH, Hippenmeyer
S. 2020. Lineage tracing and clonal analysis in developing cerebral cortex using
mosaic analysis with double markers (MADM). Journal of Visual Experiments. (159),
e61147.
mla: Beattie, Robert J., et al. “Lineage Tracing and Clonal Analysis in Developing
Cerebral Cortex Using Mosaic Analysis with Double Markers (MADM).” Journal
of Visual Experiments, no. 159, e61147, MyJove Corporation, 2020, doi:10.3791/61147.
short: R.J. Beattie, C. Streicher, N. Amberg, G.T. Cheung, X. Contreras, A.H. Hansen,
S. Hippenmeyer, Journal of Visual Experiments (2020).
date_created: 2020-05-11T08:31:20Z
date_published: 2020-05-08T00:00:00Z
date_updated: 2024-03-29T23:30:41Z
day: '08'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.3791/61147
ec_funded: 1
external_id:
isi:
- '000546406600043'
file:
- access_level: open_access
checksum: 3154ea7f90b9fb45e084cd1c2770597d
content_type: application/pdf
creator: rbeattie
date_created: 2020-05-11T08:28:38Z
date_updated: 2020-07-14T12:48:03Z
file_id: '7816'
file_name: jove-protocol-61147-lineage-tracing-clonal-analysis-developing-cerebral-cortex-using.pdf
file_size: 1352186
relation: main_file
file_date_updated: 2020-07-14T12:48:03Z
has_accepted_license: '1'
isi: 1
issue: '159'
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
project:
- _id: 264E56E2-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: M02416
name: Molecular Mechanisms Regulating Gliogenesis in the Cerebral Cortex
- _id: 268F8446-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: T0101031
name: Role of Eed in neural stem cell lineage progression
- _id: 260C2330-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '754411'
name: ISTplus - Postdoctoral Fellowships
- _id: 2625A13E-B435-11E9-9278-68D0E5697425
grant_number: '24812'
name: Molecular Mechanisms of Radial Neuronal Migration
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
publication: Journal of Visual Experiments
publication_identifier:
issn:
- 1940-087X
publication_status: published
publisher: MyJove Corporation
quality_controlled: '1'
related_material:
record:
- id: '7902'
relation: part_of_dissertation
status: public
scopus_import: '1'
status: public
title: Lineage tracing and clonal analysis in developing cerebral cortex using mosaic
analysis with double markers (MADM)
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2020'
...
---
_id: '7902'
abstract:
- lang: eng
text: "Mosaic genetic analysis has been widely used in different model organisms
such as the fruit fly to study gene-function in a cell-autonomous or tissue-specific
fashion. More recently, and less easily conducted, mosaic genetic analysis in
mice has also been enabled with the ambition to shed light on human gene function
and disease. These genetic tools are of particular interest, but not restricted
to, the study of the brain. Notably, the MADM technology offers a genetic approach
in mice to visualize and concomitantly manipulate small subsets of genetically
defined cells at a clonal level and single cell resolution. MADM-based analysis
has already advanced the study of genetic mechanisms regulating brain development
and is expected that further MADM-based analysis of genetic alterations will continue
to reveal important insights on the fundamental principles of development and
disease to potentially assist in the development of new therapies or treatments.\r\nIn
summary, this work completed and characterized the necessary genome-wide genetic
tools to perform MADM-based analysis at single cell level of the vast majority
of mouse genes in virtually any cell type and provided a protocol to perform lineage
tracing using the novel MADM resource. Importantly, this work also explored and
revealed novel aspects of biologically relevant events in an in vivo context,
such as the chromosome-specific bias of chromatid sister segregation pattern,
the generation of cell-type diversity in the cerebral cortex and in the cerebellum
and finally, the relevance of the interplay between the cell-autonomous gene function
and cell-non-autonomous (community) effects in radial glial progenitor lineage
progression.\r\nThis work provides a foundation and opens the door to further
elucidating the molecular mechanisms underlying neuronal diversity and astrocyte
generation."
acknowledged_ssus:
- _id: PreCl
- _id: Bio
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Ximena
full_name: Contreras, Ximena
id: 475990FE-F248-11E8-B48F-1D18A9856A87
last_name: Contreras
citation:
ama: Contreras X. Genetic dissection of neural development in health and disease
at single cell resolution. 2020. doi:10.15479/AT:ISTA:7902
apa: Contreras, X. (2020). Genetic dissection of neural development in health
and disease at single cell resolution. Institute of Science and Technology
Austria. https://doi.org/10.15479/AT:ISTA:7902
chicago: Contreras, Ximena. “Genetic Dissection of Neural Development in Health
and Disease at Single Cell Resolution.” Institute of Science and Technology Austria,
2020. https://doi.org/10.15479/AT:ISTA:7902.
ieee: X. Contreras, “Genetic dissection of neural development in health and disease
at single cell resolution,” Institute of Science and Technology Austria, 2020.
ista: Contreras X. 2020. Genetic dissection of neural development in health and
disease at single cell resolution. Institute of Science and Technology Austria.
mla: Contreras, Ximena. Genetic Dissection of Neural Development in Health and
Disease at Single Cell Resolution. Institute of Science and Technology Austria,
2020, doi:10.15479/AT:ISTA:7902.
short: X. Contreras, Genetic Dissection of Neural Development in Health and Disease
at Single Cell Resolution, Institute of Science and Technology Austria, 2020.
date_created: 2020-05-29T08:27:32Z
date_published: 2020-06-05T00:00:00Z
date_updated: 2023-10-18T08:45:16Z
day: '05'
ddc:
- '570'
degree_awarded: PhD
department:
- _id: SiHi
doi: 10.15479/AT:ISTA:7902
ec_funded: 1
file:
- access_level: closed
checksum: 43c172bf006c95b65992d473c7240d13
content_type: application/vnd.openxmlformats-officedocument.wordprocessingml.document
creator: xcontreras
date_created: 2020-06-05T08:18:08Z
date_updated: 2021-06-07T22:30:03Z
embargo_to: open_access
file_id: '7927'
file_name: PhDThesis_Contreras.docx
file_size: 53134142
relation: source_file
- access_level: open_access
checksum: addfed9128271be05cae3608e03a6ec0
content_type: application/pdf
creator: xcontreras
date_created: 2020-06-05T08:18:07Z
date_updated: 2021-06-07T22:30:03Z
embargo: 2021-06-06
file_id: '7928'
file_name: PhDThesis_Contreras.pdf
file_size: 35117191
relation: main_file
file_date_updated: 2021-06-07T22:30:03Z
has_accepted_license: '1'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
page: '214'
project:
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
publication_identifier:
issn:
- 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
related_material:
record:
- id: '6830'
relation: dissertation_contains
status: public
- id: '28'
relation: dissertation_contains
status: public
- id: '7815'
relation: dissertation_contains
status: public
status: public
supervisor:
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
title: Genetic dissection of neural development in health and disease at single cell
resolution
type: dissertation
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2020'
...
---
_id: '6091'
abstract:
- lang: eng
text: Cortical networks are characterized by sparse connectivity, with synapses
found at only a subset of axo-dendritic contacts. Yet within these networks, neurons
can exhibit high connection probabilities, suggesting that cell-intrinsic factors,
not proximity, determine connectivity. Here, we identify ephrin-B3 (eB3) as a
factor that determines synapse density by mediating a cell-cell competition that
requires ephrin-B-EphB signaling. In a microisland culture system designed to
isolate cell-cell competition, we find that eB3 determines winning and losing
neurons in a contest for synapses. In a Mosaic Analysis with Double Markers (MADM)
genetic mouse model system in vivo the relative levels of eB3 control spine density
in layer 5 and 6 neurons. MADM cortical neurons in vitro reveal that eB3 controls
synapse density independently of action potential-driven activity. Our findings
illustrate a new class of competitive mechanism mediated by trans-synaptic organizing
proteins which control the number of synapses neurons receive relative to neighboring
neurons.
article_number: e41563
article_processing_charge: No
author:
- first_name: Nathan T.
full_name: Henderson, Nathan T.
last_name: Henderson
- first_name: Sylvain J.
full_name: Le Marchand, Sylvain J.
last_name: Le Marchand
- first_name: Martin
full_name: Hruska, Martin
last_name: Hruska
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Liqun
full_name: Luo, Liqun
last_name: Luo
- first_name: Matthew B.
full_name: Dalva, Matthew B.
last_name: Dalva
citation:
ama: Henderson NT, Le Marchand SJ, Hruska M, Hippenmeyer S, Luo L, Dalva MB. Ephrin-B3
controls excitatory synapse density through cell-cell competition for EphBs. eLife.
2019;8. doi:10.7554/eLife.41563
apa: Henderson, N. T., Le Marchand, S. J., Hruska, M., Hippenmeyer, S., Luo, L.,
& Dalva, M. B. (2019). Ephrin-B3 controls excitatory synapse density through
cell-cell competition for EphBs. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.41563
chicago: Henderson, Nathan T., Sylvain J. Le Marchand, Martin Hruska, Simon Hippenmeyer,
Liqun Luo, and Matthew B. Dalva. “Ephrin-B3 Controls Excitatory Synapse Density
through Cell-Cell Competition for EphBs.” ELife. eLife Sciences Publications,
2019. https://doi.org/10.7554/eLife.41563.
ieee: N. T. Henderson, S. J. Le Marchand, M. Hruska, S. Hippenmeyer, L. Luo, and
M. B. Dalva, “Ephrin-B3 controls excitatory synapse density through cell-cell
competition for EphBs,” eLife, vol. 8. eLife Sciences Publications, 2019.
ista: Henderson NT, Le Marchand SJ, Hruska M, Hippenmeyer S, Luo L, Dalva MB. 2019.
Ephrin-B3 controls excitatory synapse density through cell-cell competition for
EphBs. eLife. 8, e41563.
mla: Henderson, Nathan T., et al. “Ephrin-B3 Controls Excitatory Synapse Density
through Cell-Cell Competition for EphBs.” ELife, vol. 8, e41563, eLife
Sciences Publications, 2019, doi:10.7554/eLife.41563.
short: N.T. Henderson, S.J. Le Marchand, M. Hruska, S. Hippenmeyer, L. Luo, M.B.
Dalva, ELife 8 (2019).
date_created: 2019-03-10T22:59:20Z
date_published: 2019-02-21T00:00:00Z
date_updated: 2023-08-24T14:50:50Z
day: '21'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.7554/eLife.41563
external_id:
isi:
- '000459380600001'
pmid:
- '30789343'
file:
- access_level: open_access
checksum: 7b0800d003f14cd06b1802dea0c52941
content_type: application/pdf
creator: dernst
date_created: 2019-03-11T16:15:37Z
date_updated: 2020-07-14T12:47:19Z
file_id: '6098'
file_name: 2019_eLife_Henderson.pdf
file_size: 7260753
relation: main_file
file_date_updated: 2020-07-14T12:47:19Z
has_accepted_license: '1'
intvolume: ' 8'
isi: 1
language:
- iso: eng
month: '02'
oa: 1
oa_version: Published Version
pmid: 1
publication: eLife
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: Ephrin-B3 controls excitatory synapse density through cell-cell competition
for EphBs
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 8
year: '2019'
...
---
_id: '6844'
abstract:
- lang: eng
text: Studying the progression of the proliferative and differentiative patterns
of neural stem cells at the individual cell level is crucial to the understanding
of cortex development and how the disruption of such patterns can lead to malformations
and neurodevelopmental diseases. However, our understanding of the precise lineage
progression programme at single-cell resolution is still incomplete due to the
technical variations in lineage- tracing approaches. One of the key challenges
involves developing a robust theoretical framework in which we can integrate experimental
observations and introduce correction factors to obtain a reliable and representative
description of the temporal modulation of proliferation and differentiation. In
order to obtain more conclusive insights, we carry out virtual clonal analysis
using mathematical modelling and compare our results against experimental data.
Using a dataset obtained with Mosaic Analysis with Double Markers, we illustrate
how the theoretical description can be exploited to interpret and reconcile the
disparity between virtual and experimental results.
article_processing_charge: No
article_type: original
author:
- first_name: Noemi
full_name: Picco, Noemi
last_name: Picco
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Julio
full_name: Rodarte, Julio
id: 3C70A038-F248-11E8-B48F-1D18A9856A87
last_name: Rodarte
- first_name: Carmen
full_name: Streicher, Carmen
id: 36BCB99C-F248-11E8-B48F-1D18A9856A87
last_name: Streicher
- first_name: Zoltán
full_name: Molnár, Zoltán
last_name: Molnár
- first_name: Philip K.
full_name: Maini, Philip K.
last_name: Maini
- first_name: Thomas E.
full_name: Woolley, Thomas E.
last_name: Woolley
citation:
ama: Picco N, Hippenmeyer S, Rodarte J, et al. A mathematical insight into cell
labelling experiments for clonal analysis. Journal of Anatomy. 2019;235(3):686-696.
doi:10.1111/joa.13001
apa: Picco, N., Hippenmeyer, S., Rodarte, J., Streicher, C., Molnár, Z., Maini,
P. K., & Woolley, T. E. (2019). A mathematical insight into cell labelling
experiments for clonal analysis. Journal of Anatomy. Wiley. https://doi.org/10.1111/joa.13001
chicago: Picco, Noemi, Simon Hippenmeyer, Julio Rodarte, Carmen Streicher, Zoltán
Molnár, Philip K. Maini, and Thomas E. Woolley. “A Mathematical Insight into Cell
Labelling Experiments for Clonal Analysis.” Journal of Anatomy. Wiley,
2019. https://doi.org/10.1111/joa.13001.
ieee: N. Picco et al., “A mathematical insight into cell labelling experiments
for clonal analysis,” Journal of Anatomy, vol. 235, no. 3. Wiley, pp. 686–696,
2019.
ista: Picco N, Hippenmeyer S, Rodarte J, Streicher C, Molnár Z, Maini PK, Woolley
TE. 2019. A mathematical insight into cell labelling experiments for clonal analysis.
Journal of Anatomy. 235(3), 686–696.
mla: Picco, Noemi, et al. “A Mathematical Insight into Cell Labelling Experiments
for Clonal Analysis.” Journal of Anatomy, vol. 235, no. 3, Wiley, 2019,
pp. 686–96, doi:10.1111/joa.13001.
short: N. Picco, S. Hippenmeyer, J. Rodarte, C. Streicher, Z. Molnár, P.K. Maini,
T.E. Woolley, Journal of Anatomy 235 (2019) 686–696.
date_created: 2019-09-02T11:57:28Z
date_published: 2019-09-01T00:00:00Z
date_updated: 2023-08-29T07:19:39Z
day: '01'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1111/joa.13001
ec_funded: 1
external_id:
isi:
- '000482426800017'
file:
- access_level: open_access
checksum: 160f960844b204057f20896e0e1f8ee7
content_type: application/pdf
creator: dernst
date_created: 2019-09-02T12:05:18Z
date_updated: 2020-07-14T12:47:42Z
file_id: '6845'
file_name: 2019_JournalAnatomy_Picco.pdf
file_size: 1192994
relation: main_file
file_date_updated: 2020-07-14T12:47:42Z
has_accepted_license: '1'
intvolume: ' 235'
isi: 1
issue: '3'
language:
- iso: eng
license: https://creativecommons.org/licenses/by-nc/4.0/
month: '09'
oa: 1
oa_version: Published Version
page: 686-696
project:
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
publication: Journal of Anatomy
publication_identifier:
eissn:
- 1469-7580
issn:
- 0021-8782
publication_status: published
publisher: Wiley
quality_controlled: '1'
scopus_import: '1'
status: public
title: A mathematical insight into cell labelling experiments for clonal analysis
tmp:
image: /images/cc_by_nc.png
legal_code_url: https://creativecommons.org/licenses/by-nc/4.0/legalcode
name: Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)
short: CC BY-NC (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 235
year: '2019'
...
---
_id: '7005'
abstract:
- lang: eng
text: Activity-dependent bulk endocytosis generates synaptic vesicles (SVs) during
intense neuronal activity via a two-step process. First, bulk endosomes are formed
direct from the plasma membrane from which SVs are then generated. SV generation
from bulk endosomes requires the efflux of previously accumulated calcium and
activation of the protein phosphatase calcineurin. However, it is still unknown
how calcineurin mediates SV generation. We addressed this question using a series
of acute interventions that decoupled the generation of SVs from bulk endosomes
in rat primary neuronal culture. This was achieved by either disruption of protein–protein
interactions via delivery of competitive peptides, or inhibition of enzyme activity
by known inhibitors. SV generation was monitored using either a morphological
horseradish peroxidase assay or an optical assay that monitors the replenishment
of the reserve SV pool. We found that SV generation was inhibited by, (i) peptides
that disrupt calcineurin interactions, (ii) an inhibitor of dynamin I GTPase activity
and (iii) peptides that disrupt the phosphorylation-dependent dynamin I–syndapin
I interaction. Peptides that disrupted syndapin I interactions with eps15 homology
domain-containing proteins had no effect. This revealed that (i) calcineurin must
be localized at bulk endosomes to mediate its effect, (ii) dynamin I GTPase activity
is essential for SV fission and (iii) the calcineurin-dependent interaction between
dynamin I and syndapin I is essential for SV generation. We therefore propose
that a calcineurin-dependent dephosphorylation cascade that requires both dynamin
I GTPase and syndapin I lipid-deforming activity is essential for SV generation
from bulk endosomes.
article_processing_charge: No
article_type: original
author:
- first_name: Giselle T
full_name: Cheung, Giselle T
id: 471195F6-F248-11E8-B48F-1D18A9856A87
last_name: Cheung
orcid: 0000-0001-8457-2572
- first_name: Michael A.
full_name: Cousin, Michael A.
last_name: Cousin
citation:
ama: Cheung GT, Cousin MA. Synaptic vesicle generation from activity‐dependent bulk
endosomes requires a dephosphorylation‐dependent dynamin–syndapin interaction.
Journal of Neurochemistry. 2019;151(5):570-583. doi:10.1111/jnc.14862
apa: Cheung, G. T., & Cousin, M. A. (2019). Synaptic vesicle generation from
activity‐dependent bulk endosomes requires a dephosphorylation‐dependent dynamin–syndapin
interaction. Journal of Neurochemistry. Wiley. https://doi.org/10.1111/jnc.14862
chicago: Cheung, Giselle T, and Michael A. Cousin. “Synaptic Vesicle Generation
from Activity‐dependent Bulk Endosomes Requires a Dephosphorylation‐dependent
Dynamin–Syndapin Interaction.” Journal of Neurochemistry. Wiley, 2019.
https://doi.org/10.1111/jnc.14862.
ieee: G. T. Cheung and M. A. Cousin, “Synaptic vesicle generation from activity‐dependent
bulk endosomes requires a dephosphorylation‐dependent dynamin–syndapin interaction,”
Journal of Neurochemistry, vol. 151, no. 5. Wiley, pp. 570–583, 2019.
ista: Cheung GT, Cousin MA. 2019. Synaptic vesicle generation from activity‐dependent
bulk endosomes requires a dephosphorylation‐dependent dynamin–syndapin interaction.
Journal of Neurochemistry. 151(5), 570–583.
mla: Cheung, Giselle T., and Michael A. Cousin. “Synaptic Vesicle Generation from
Activity‐dependent Bulk Endosomes Requires a Dephosphorylation‐dependent Dynamin–Syndapin
Interaction.” Journal of Neurochemistry, vol. 151, no. 5, Wiley, 2019,
pp. 570–83, doi:10.1111/jnc.14862.
short: G.T. Cheung, M.A. Cousin, Journal of Neurochemistry 151 (2019) 570–583.
date_created: 2019-11-12T14:37:08Z
date_published: 2019-12-01T00:00:00Z
date_updated: 2023-08-30T07:21:50Z
day: '01'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1111/jnc.14862
external_id:
isi:
- '000490703100001'
pmid:
- '31479508'
file:
- access_level: open_access
checksum: ec1fb2aebb874009bc309adaada6e1d7
content_type: application/pdf
creator: dernst
date_created: 2020-02-05T10:30:02Z
date_updated: 2020-07-14T12:47:47Z
file_id: '7452'
file_name: 2019_JournNeurochemistry_Cheung.pdf
file_size: 4334962
relation: main_file
file_date_updated: 2020-07-14T12:47:47Z
has_accepted_license: '1'
intvolume: ' 151'
isi: 1
issue: '5'
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
page: 570-583
pmid: 1
publication: Journal of Neurochemistry
publication_identifier:
eissn:
- 1471-4159
issn:
- 0022-3042
publication_status: published
publisher: Wiley
quality_controlled: '1'
scopus_import: '1'
status: public
title: Synaptic vesicle generation from activity‐dependent bulk endosomes requires
a dephosphorylation‐dependent dynamin–syndapin interaction
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 151
year: '2019'
...
---
_id: '6455'
abstract:
- lang: eng
text: During corticogenesis, distinct subtypes of neurons are sequentially born
from ventricular zone progenitors. How these cells are molecularly temporally
patterned is poorly understood. We used single-cell RNA sequencing at high temporal
resolution to trace the lineage of the molecular identities of successive generations
of apical progenitors (APs) and their daughter neurons in mouse embryos. We identified
a core set of evolutionarily conserved, temporally patterned genes that drive
APs from internally driven to more exteroceptive states. We found that the Polycomb
repressor complex 2 (PRC2) epigenetically regulates AP temporal progression. Embryonic
age–dependent AP molecular states are transmitted to their progeny as successive
ground states, onto which essentially conserved early postmitotic differentiation
programs are applied, and are complemented by later-occurring environment-dependent
signals. Thus, epigenetically regulated temporal molecular birthmarks present
in progenitors act in their postmitotic progeny to seed adult neuronal diversity.
article_number: eaav2522
article_processing_charge: No
article_type: original
author:
- first_name: L
full_name: Telley, L
last_name: Telley
- first_name: G
full_name: Agirman, G
last_name: Agirman
- first_name: J
full_name: Prados, J
last_name: Prados
- first_name: Nicole
full_name: Amberg, Nicole
id: 4CD6AAC6-F248-11E8-B48F-1D18A9856A87
last_name: Amberg
orcid: 0000-0002-3183-8207
- first_name: S
full_name: Fièvre, S
last_name: Fièvre
- first_name: P
full_name: Oberst, P
last_name: Oberst
- first_name: G
full_name: Bartolini, G
last_name: Bartolini
- first_name: I
full_name: Vitali, I
last_name: Vitali
- first_name: C
full_name: Cadilhac, C
last_name: Cadilhac
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: L
full_name: Nguyen, L
last_name: Nguyen
- first_name: A
full_name: Dayer, A
last_name: Dayer
- first_name: D
full_name: Jabaudon, D
last_name: Jabaudon
citation:
ama: Telley L, Agirman G, Prados J, et al. Temporal patterning of apical progenitors
and their daughter neurons in the developing neocortex. Science. 2019;364(6440).
doi:10.1126/science.aav2522
apa: Telley, L., Agirman, G., Prados, J., Amberg, N., Fièvre, S., Oberst, P., …
Jabaudon, D. (2019). Temporal patterning of apical progenitors and their daughter
neurons in the developing neocortex. Science. AAAS. https://doi.org/10.1126/science.aav2522
chicago: Telley, L, G Agirman, J Prados, Nicole Amberg, S Fièvre, P Oberst, G Bartolini,
et al. “Temporal Patterning of Apical Progenitors and Their Daughter Neurons in
the Developing Neocortex.” Science. AAAS, 2019. https://doi.org/10.1126/science.aav2522.
ieee: L. Telley et al., “Temporal patterning of apical progenitors and their
daughter neurons in the developing neocortex,” Science, vol. 364, no. 6440.
AAAS, 2019.
ista: Telley L, Agirman G, Prados J, Amberg N, Fièvre S, Oberst P, Bartolini G,
Vitali I, Cadilhac C, Hippenmeyer S, Nguyen L, Dayer A, Jabaudon D. 2019. Temporal
patterning of apical progenitors and their daughter neurons in the developing
neocortex. Science. 364(6440), eaav2522.
mla: Telley, L., et al. “Temporal Patterning of Apical Progenitors and Their Daughter
Neurons in the Developing Neocortex.” Science, vol. 364, no. 6440, eaav2522,
AAAS, 2019, doi:10.1126/science.aav2522.
short: L. Telley, G. Agirman, J. Prados, N. Amberg, S. Fièvre, P. Oberst, G. Bartolini,
I. Vitali, C. Cadilhac, S. Hippenmeyer, L. Nguyen, A. Dayer, D. Jabaudon, Science
364 (2019).
date_created: 2019-05-14T13:07:47Z
date_published: 2019-05-10T00:00:00Z
date_updated: 2023-09-05T11:51:09Z
day: '10'
department:
- _id: SiHi
doi: 10.1126/science.aav2522
ec_funded: 1
external_id:
isi:
- '000467631800034'
pmid:
- '31073041'
intvolume: ' 364'
isi: 1
issue: '6440'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://orbi.uliege.be/bitstream/2268/239604/1/Telley_Agirman_Science2019.pdf
month: '05'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
- _id: 268F8446-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: T0101031
name: Role of Eed in neural stem cell lineage progression
publication: Science
publication_identifier:
eissn:
- 1095-9203
issn:
- 0036-8075
publication_status: published
publisher: AAAS
quality_controlled: '1'
related_material:
link:
- description: News on IST Homepage
relation: press_release
url: https://ist.ac.at/en/news/how-to-generate-a-brain-of-correct-size-and-composition/
scopus_import: '1'
status: public
title: Temporal patterning of apical progenitors and their daughter neurons in the
developing neocortex
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 364
year: '2019'
...
---
_id: '6454'
abstract:
- lang: eng
text: 'Adult neural stem cells and multiciliated ependymalcells are glial cells
essential for neurological func-tions. Together, they make up the adult neurogenicniche.
Using both high-throughput clonal analysisand single-cell resolution of progenitor
division pat-terns and fate, we show that these two componentsof the neurogenic
niche are lineally related: adult neu-ral stem cells are sister cells to ependymal
cells,whereas most ependymal cells arise from the termi-nal symmetric divisions
of the lineage. Unexpectedly,we found that the antagonist regulators of DNA repli-cation,
GemC1 and Geminin, can tune the proportionof neural stem cells and ependymal cells.
Our find-ings reveal the controlled dynamic of the neurogenicniche ontogeny and
identify the Geminin familymembers as key regulators of the initial pool of adultneural
stem cells.'
article_processing_charge: No
author:
- first_name: G
full_name: Ortiz-Álvarez, G
last_name: Ortiz-Álvarez
- first_name: M
full_name: Daclin, M
last_name: Daclin
- first_name: A
full_name: Shihavuddin, A
last_name: Shihavuddin
- first_name: P
full_name: Lansade, P
last_name: Lansade
- first_name: A
full_name: Fortoul, A
last_name: Fortoul
- first_name: M
full_name: Faucourt, M
last_name: Faucourt
- first_name: S
full_name: Clavreul, S
last_name: Clavreul
- first_name: ME
full_name: Lalioti, ME
last_name: Lalioti
- first_name: S
full_name: Taraviras, S
last_name: Taraviras
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: J
full_name: Livet, J
last_name: Livet
- first_name: A
full_name: Meunier, A
last_name: Meunier
- first_name: A
full_name: Genovesio, A
last_name: Genovesio
- first_name: N
full_name: Spassky, N
last_name: Spassky
citation:
ama: Ortiz-Álvarez G, Daclin M, Shihavuddin A, et al. Adult neural stem cells and
multiciliated ependymal cells share a common lineage regulated by the Geminin
family members. Neuron. 2019;102(1):159-172.e7. doi:10.1016/j.neuron.2019.01.051
apa: Ortiz-Álvarez, G., Daclin, M., Shihavuddin, A., Lansade, P., Fortoul, A., Faucourt,
M., … Spassky, N. (2019). Adult neural stem cells and multiciliated ependymal
cells share a common lineage regulated by the Geminin family members. Neuron.
Elsevier. https://doi.org/10.1016/j.neuron.2019.01.051
chicago: Ortiz-Álvarez, G, M Daclin, A Shihavuddin, P Lansade, A Fortoul, M Faucourt,
S Clavreul, et al. “Adult Neural Stem Cells and Multiciliated Ependymal Cells
Share a Common Lineage Regulated by the Geminin Family Members.” Neuron.
Elsevier, 2019. https://doi.org/10.1016/j.neuron.2019.01.051.
ieee: G. Ortiz-Álvarez et al., “Adult neural stem cells and multiciliated
ependymal cells share a common lineage regulated by the Geminin family members,”
Neuron, vol. 102, no. 1. Elsevier, p. 159–172.e7, 2019.
ista: Ortiz-Álvarez G, Daclin M, Shihavuddin A, Lansade P, Fortoul A, Faucourt M,
Clavreul S, Lalioti M, Taraviras S, Hippenmeyer S, Livet J, Meunier A, Genovesio
A, Spassky N. 2019. Adult neural stem cells and multiciliated ependymal cells
share a common lineage regulated by the Geminin family members. Neuron. 102(1),
159–172.e7.
mla: Ortiz-Álvarez, G., et al. “Adult Neural Stem Cells and Multiciliated Ependymal
Cells Share a Common Lineage Regulated by the Geminin Family Members.” Neuron,
vol. 102, no. 1, Elsevier, 2019, p. 159–172.e7, doi:10.1016/j.neuron.2019.01.051.
short: G. Ortiz-Álvarez, M. Daclin, A. Shihavuddin, P. Lansade, A. Fortoul, M. Faucourt,
S. Clavreul, M. Lalioti, S. Taraviras, S. Hippenmeyer, J. Livet, A. Meunier, A.
Genovesio, N. Spassky, Neuron 102 (2019) 159–172.e7.
date_created: 2019-05-14T13:06:30Z
date_published: 2019-04-03T00:00:00Z
date_updated: 2023-09-05T13:02:21Z
day: '03'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1016/j.neuron.2019.01.051
ec_funded: 1
external_id:
isi:
- '000463337900018'
pmid:
- '30824354'
file:
- access_level: open_access
checksum: 1fb6e195c583eb0c5cabf26f69ff6675
content_type: application/pdf
creator: dernst
date_created: 2019-05-15T09:28:41Z
date_updated: 2020-07-14T12:47:30Z
file_id: '6457'
file_name: 2019_Neuron_Ortiz.pdf
file_size: 7288572
relation: main_file
file_date_updated: 2020-07-14T12:47:30Z
has_accepted_license: '1'
intvolume: ' 102'
isi: 1
issue: '1'
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
page: 159-172.e7
pmid: 1
project:
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
publication: Neuron
publication_identifier:
eissn:
- 1097-4199
issn:
- 0896-6273
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Adult neural stem cells and multiciliated ependymal cells share a common lineage
regulated by the Geminin family members
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 102
year: '2019'
...
---
_id: '7202'
abstract:
- lang: eng
text: The cerebral cortex contains multiple areas with distinctive cytoarchitectonical
patterns, but the cellular mechanisms underlying the emergence of this diversity
remain unclear. Here, we have investigated the neuronal output of individual progenitor
cells in the developing mouse neocortex using a combination of methods that together
circumvent the biases and limitations of individual approaches. Our experimental
results indicate that progenitor cells generate pyramidal cell lineages with a
wide range of sizes and laminar configurations. Mathematical modelling indicates
that these outcomes are compatible with a stochastic model of cortical neurogenesis
in which progenitor cells undergo a series of probabilistic decisions that lead
to the specification of very heterogeneous progenies. Our findings support a mechanism
for cortical neurogenesis whose flexibility would make it capable to generate
the diverse cytoarchitectures that characterize distinct neocortical areas.
article_number: e51381
article_processing_charge: No
article_type: original
author:
- first_name: Alfredo
full_name: Llorca, Alfredo
last_name: Llorca
- first_name: Gabriele
full_name: Ciceri, Gabriele
last_name: Ciceri
- first_name: Robert J
full_name: Beattie, Robert J
id: 2E26DF60-F248-11E8-B48F-1D18A9856A87
last_name: Beattie
orcid: 0000-0002-8483-8753
- first_name: Fong Kuan
full_name: Wong, Fong Kuan
last_name: Wong
- first_name: Giovanni
full_name: Diana, Giovanni
last_name: Diana
- first_name: Eleni
full_name: Serafeimidou-Pouliou, Eleni
last_name: Serafeimidou-Pouliou
- first_name: Marian
full_name: Fernández-Otero, Marian
last_name: Fernández-Otero
- first_name: Carmen
full_name: Streicher, Carmen
id: 36BCB99C-F248-11E8-B48F-1D18A9856A87
last_name: Streicher
- first_name: Sebastian J.
full_name: Arnold, Sebastian J.
last_name: Arnold
- first_name: Martin
full_name: Meyer, Martin
last_name: Meyer
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Miguel
full_name: Maravall, Miguel
last_name: Maravall
- first_name: Oscar
full_name: Marín, Oscar
last_name: Marín
citation:
ama: Llorca A, Ciceri G, Beattie RJ, et al. A stochastic framework of neurogenesis
underlies the assembly of neocortical cytoarchitecture. eLife. 2019;8.
doi:10.7554/eLife.51381
apa: Llorca, A., Ciceri, G., Beattie, R. J., Wong, F. K., Diana, G., Serafeimidou-Pouliou,
E., … Marín, O. (2019). A stochastic framework of neurogenesis underlies the assembly
of neocortical cytoarchitecture. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.51381
chicago: Llorca, Alfredo, Gabriele Ciceri, Robert J Beattie, Fong Kuan Wong, Giovanni
Diana, Eleni Serafeimidou-Pouliou, Marian Fernández-Otero, et al. “A Stochastic
Framework of Neurogenesis Underlies the Assembly of Neocortical Cytoarchitecture.”
ELife. eLife Sciences Publications, 2019. https://doi.org/10.7554/eLife.51381.
ieee: A. Llorca et al., “A stochastic framework of neurogenesis underlies
the assembly of neocortical cytoarchitecture,” eLife, vol. 8. eLife Sciences
Publications, 2019.
ista: Llorca A, Ciceri G, Beattie RJ, Wong FK, Diana G, Serafeimidou-Pouliou E,
Fernández-Otero M, Streicher C, Arnold SJ, Meyer M, Hippenmeyer S, Maravall M,
Marín O. 2019. A stochastic framework of neurogenesis underlies the assembly of
neocortical cytoarchitecture. eLife. 8, e51381.
mla: Llorca, Alfredo, et al. “A Stochastic Framework of Neurogenesis Underlies the
Assembly of Neocortical Cytoarchitecture.” ELife, vol. 8, e51381, eLife
Sciences Publications, 2019, doi:10.7554/eLife.51381.
short: A. Llorca, G. Ciceri, R.J. Beattie, F.K. Wong, G. Diana, E. Serafeimidou-Pouliou,
M. Fernández-Otero, C. Streicher, S.J. Arnold, M. Meyer, S. Hippenmeyer, M. Maravall,
O. Marín, ELife 8 (2019).
date_created: 2019-12-22T23:00:42Z
date_published: 2019-11-18T00:00:00Z
date_updated: 2023-09-06T14:38:39Z
day: '18'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.7554/eLife.51381
ec_funded: 1
external_id:
isi:
- '000508156800001'
pmid:
- '31736464'
file:
- access_level: open_access
checksum: b460ecc33e1a68265e7adea775021f3a
content_type: application/pdf
creator: dernst
date_created: 2020-02-18T15:19:26Z
date_updated: 2020-07-14T12:47:53Z
file_id: '7503'
file_name: 2019_eLife_Llorca.pdf
file_size: 2960543
relation: main_file
file_date_updated: 2020-07-14T12:47:53Z
has_accepted_license: '1'
intvolume: ' 8'
isi: 1
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
- _id: 264E56E2-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: M02416
name: Molecular Mechanisms Regulating Gliogenesis in the Cerebral Cortex
publication: eLife
publication_identifier:
eissn:
- 2050084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: A stochastic framework of neurogenesis underlies the assembly of neocortical
cytoarchitecture
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 8
year: '2019'
...
---
_id: '6451'
abstract:
- lang: eng
text: Epidermal growth factor receptor (EGFR) signaling controls skin development
and homeostasis inmice and humans, and its deficiency causes severe skin inflammation,
which might affect epidermalstem cell behavior. Here, we describe the inflammation-independent
effects of EGFR deficiency dur-ing skin morphogenesis and in adult hair follicle
stem cells. Expression and alternative splicing analysisof RNA sequencing data
from interfollicular epidermis and outer root sheath indicate that EGFR con-trols
genes involved in epidermal differentiation and also in centrosome function, DNA
damage, cellcycle, and apoptosis. Genetic experiments employingp53deletion in
EGFR-deficient epidermis revealthat EGFR signaling exhibitsp53-dependent functions
in proliferative epidermal compartments, aswell asp53-independent functions in
differentiated hair shaft keratinocytes. Loss of EGFR leads toabsence of LEF1
protein specifically in the innermost epithelial hair layers, resulting in disorganizationof
medulla cells. Thus, our results uncover important spatial and temporal features
of cell-autonomousEGFR functions in the epidermis.
article_processing_charge: No
author:
- first_name: Nicole
full_name: Amberg, Nicole
id: 4CD6AAC6-F248-11E8-B48F-1D18A9856A87
last_name: Amberg
orcid: 0000-0002-3183-8207
- first_name: Panagiota A.
full_name: Sotiropoulou, Panagiota A.
last_name: Sotiropoulou
- first_name: Gerwin
full_name: Heller, Gerwin
last_name: Heller
- first_name: Beate M.
full_name: Lichtenberger, Beate M.
last_name: Lichtenberger
- first_name: Martin
full_name: Holcmann, Martin
last_name: Holcmann
- first_name: Bahar
full_name: Camurdanoglu, Bahar
last_name: Camurdanoglu
- first_name: Temenuschka
full_name: Baykuscheva-Gentscheva, Temenuschka
last_name: Baykuscheva-Gentscheva
- first_name: Cedric
full_name: Blanpain, Cedric
last_name: Blanpain
- first_name: Maria
full_name: Sibilia, Maria
last_name: Sibilia
citation:
ama: Amberg N, Sotiropoulou PA, Heller G, et al. EGFR controls hair shaft differentiation
in a p53-independent manner. iScience. 2019;15:243-256. doi:10.1016/j.isci.2019.04.018
apa: Amberg, N., Sotiropoulou, P. A., Heller, G., Lichtenberger, B. M., Holcmann,
M., Camurdanoglu, B., … Sibilia, M. (2019). EGFR controls hair shaft differentiation
in a p53-independent manner. IScience. Elsevier. https://doi.org/10.1016/j.isci.2019.04.018
chicago: Amberg, Nicole, Panagiota A. Sotiropoulou, Gerwin Heller, Beate M. Lichtenberger,
Martin Holcmann, Bahar Camurdanoglu, Temenuschka Baykuscheva-Gentscheva, Cedric
Blanpain, and Maria Sibilia. “EGFR Controls Hair Shaft Differentiation in a P53-Independent
Manner.” IScience. Elsevier, 2019. https://doi.org/10.1016/j.isci.2019.04.018.
ieee: N. Amberg et al., “EGFR controls hair shaft differentiation in a p53-independent
manner,” iScience, vol. 15. Elsevier, pp. 243–256, 2019.
ista: Amberg N, Sotiropoulou PA, Heller G, Lichtenberger BM, Holcmann M, Camurdanoglu
B, Baykuscheva-Gentscheva T, Blanpain C, Sibilia M. 2019. EGFR controls hair shaft
differentiation in a p53-independent manner. iScience. 15, 243–256.
mla: Amberg, Nicole, et al. “EGFR Controls Hair Shaft Differentiation in a P53-Independent
Manner.” IScience, vol. 15, Elsevier, 2019, pp. 243–56, doi:10.1016/j.isci.2019.04.018.
short: N. Amberg, P.A. Sotiropoulou, G. Heller, B.M. Lichtenberger, M. Holcmann,
B. Camurdanoglu, T. Baykuscheva-Gentscheva, C. Blanpain, M. Sibilia, IScience
15 (2019) 243–256.
date_created: 2019-05-14T11:47:40Z
date_published: 2019-05-31T00:00:00Z
date_updated: 2023-09-08T11:38:04Z
day: '31'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1016/j.isci.2019.04.018
external_id:
isi:
- '000470104600022'
file:
- access_level: open_access
checksum: a9ad2296726c9474ad5860c9c2f53622
content_type: application/pdf
creator: dernst
date_created: 2019-05-14T11:51:51Z
date_updated: 2020-07-14T12:47:30Z
file_id: '6452'
file_name: 2019_iScience_Amberg.pdf
file_size: 8365970
relation: main_file
file_date_updated: 2020-07-14T12:47:30Z
has_accepted_license: '1'
intvolume: ' 15'
isi: 1
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
page: 243-256
publication: iScience
publication_identifier:
issn:
- 2589-0042
publication_status: published
publisher: Elsevier
quality_controlled: '1'
status: public
title: EGFR controls hair shaft differentiation in a p53-independent manner
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 15
year: '2019'
...
---
_id: '27'
abstract:
- lang: eng
text: The cerebral cortex is composed of a large variety of distinct cell-types
including projection neurons, interneurons and glial cells which emerge from distinct
neural stem cell (NSC) lineages. The vast majority of cortical projection neurons
and certain classes of glial cells are generated by radial glial progenitor cells
(RGPs) in a highly orchestrated manner. Recent studies employing single cell analysis
and clonal lineage tracing suggest that NSC and RGP lineage progression are regulated
in a profound deterministic manner. In this review we focus on recent advances
based mainly on correlative phenotypic data emerging from functional genetic studies
in mice. We establish hypotheses to test in future research and outline a conceptual
framework how epigenetic cues modulate the generation of cell-type diversity during
cortical development. This article is protected by copyright. All rights reserved.
acknowledgement: " This work was supported by IST Austria institutional funds; NÖ
Forschung und Bildung \r\nn[f+b] (C13-002) to SH; a program grant from
\ the Human Frontiers Science Program (RGP0053/2014) to SH; the People
\ Programme (Marie Curie Actions) of the European Union’s Seventh Framework
Programme (FP7/2007-2013) under REA grant agreement No 618444 to SH, and the European
\ Research Council (ERC) under the European Union’s Horizon 2020 research
\ and innovation programme (grant agreement No 725780 LinPro)to SH.\r\n"
article_processing_charge: Yes (via OA deal)
article_type: review
author:
- first_name: Nicole
full_name: Amberg, Nicole
id: 4CD6AAC6-F248-11E8-B48F-1D18A9856A87
last_name: Amberg
orcid: 0000-0002-3183-8207
- first_name: Susanne
full_name: Laukoter, Susanne
id: 2D6B7A9A-F248-11E8-B48F-1D18A9856A87
last_name: Laukoter
orcid: 0000-0002-7903-3010
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Amberg N, Laukoter S, Hippenmeyer S. Epigenetic cues modulating the generation
of cell type diversity in the cerebral cortex. Journal of Neurochemistry.
2019;149(1):12-26. doi:10.1111/jnc.14601
apa: Amberg, N., Laukoter, S., & Hippenmeyer, S. (2019). Epigenetic cues modulating
the generation of cell type diversity in the cerebral cortex. Journal of Neurochemistry.
Wiley. https://doi.org/10.1111/jnc.14601
chicago: Amberg, Nicole, Susanne Laukoter, and Simon Hippenmeyer. “Epigenetic Cues
Modulating the Generation of Cell Type Diversity in the Cerebral Cortex.” Journal
of Neurochemistry. Wiley, 2019. https://doi.org/10.1111/jnc.14601.
ieee: N. Amberg, S. Laukoter, and S. Hippenmeyer, “Epigenetic cues modulating the
generation of cell type diversity in the cerebral cortex,” Journal of Neurochemistry,
vol. 149, no. 1. Wiley, pp. 12–26, 2019.
ista: Amberg N, Laukoter S, Hippenmeyer S. 2019. Epigenetic cues modulating the
generation of cell type diversity in the cerebral cortex. Journal of Neurochemistry.
149(1), 12–26.
mla: Amberg, Nicole, et al. “Epigenetic Cues Modulating the Generation of Cell Type
Diversity in the Cerebral Cortex.” Journal of Neurochemistry, vol. 149,
no. 1, Wiley, 2019, pp. 12–26, doi:10.1111/jnc.14601.
short: N. Amberg, S. Laukoter, S. Hippenmeyer, Journal of Neurochemistry 149 (2019)
12–26.
date_created: 2018-12-11T11:44:14Z
date_published: 2019-04-01T00:00:00Z
date_updated: 2023-09-11T13:40:26Z
day: '01'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1111/jnc.14601
ec_funded: 1
external_id:
isi:
- '000462680200002'
file:
- access_level: open_access
checksum: db027721a95d36f5de36aadcd0bdf7e6
content_type: application/pdf
creator: kschuh
date_created: 2020-01-07T13:35:52Z
date_updated: 2020-07-14T12:45:45Z
file_id: '7239'
file_name: 2019_Wiley_Amberg.pdf
file_size: 889709
relation: main_file
file_date_updated: 2020-07-14T12:45:45Z
has_accepted_license: '1'
intvolume: ' 149'
isi: 1
issue: '1'
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
page: 12-26
project:
- _id: 25D92700-B435-11E9-9278-68D0E5697425
grant_number: LS13-002
name: Mapping Cell-Type Specificity of the Genomic Imprintome in the Brain
- _id: 25D7962E-B435-11E9-9278-68D0E5697425
grant_number: RGP0053/2014
name: Quantitative Structure-Function Analysis of Cerebral Cortex Assembly at Clonal
Level
- _id: 25D61E48-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '618444'
name: Molecular Mechanisms of Cerebral Cortex Development
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
publication: Journal of Neurochemistry
publication_status: published
publisher: Wiley
quality_controlled: '1'
scopus_import: '1'
status: public
title: Epigenetic cues modulating the generation of cell type diversity in the cerebral
cortex
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 149
year: '2019'
...
---
_id: '7399'
abstract:
- lang: eng
text: Long non-coding (lnc) RNAs are numerous and found throughout the mammalian
genome, and many are thought to be involved in the regulation of gene expression.
However, the majority remain relatively uncharacterised and of uncertain function
making the use of model systems to uncover their mode of action valuable. Imprinted
lncRNAs target and recruit epigenetic silencing factors to a cluster of imprinted
genes on the same chromosome, making them one of the best characterized lncRNAs
for silencing distant genes in cis. In this study we examined silencing of the
distant imprinted gene Slc22a3 by the lncRNA Airn in the Igf2r imprinted cluster
in mouse. Previously we proposed that imprinted lncRNAs may silence distant imprinted
genes by disrupting promoter-enhancer interactions by being transcribed through
the enhancer, which we called the enhancer interference hypothesis. Here we tested
this hypothesis by first using allele-specific chromosome conformation capture
(3C) to detect interactions between the Slc22a3 promoter and the locus of the
Airn lncRNA that silences it on the paternal chromosome. In agreement with the
model, we found interactions enriched on the maternal allele across the entire
Airn gene consistent with multiple enhancer-promoter interactions. Therefore,
to test the enhancer interference hypothesis we devised an approach to delete
the entire Airn gene. However, the deletion showed that there are no essential
enhancers for Slc22a2, Pde10a and Slc22a3 within the Airn gene, strongly indicating
that the Airn RNA rather than its transcription is responsible for silencing distant
imprinted genes. Furthermore, we found that silent imprinted genes were covered
with large blocks of H3K27me3 on the repressed paternal allele. Therefore we propose
an alternative hypothesis whereby the chromosome interactions may initially guide
the lncRNA to target imprinted promoters and recruit repressive chromatin, and
that these interactions are lost once silencing is established.
article_number: e1008268
article_processing_charge: No
article_type: original
author:
- first_name: Daniel
full_name: Andergassen, Daniel
last_name: Andergassen
- first_name: Markus
full_name: Muckenhuber, Markus
last_name: Muckenhuber
- first_name: Philipp C.
full_name: Bammer, Philipp C.
last_name: Bammer
- first_name: Tomasz M.
full_name: Kulinski, Tomasz M.
last_name: Kulinski
- first_name: Hans-Christian
full_name: Theussl, Hans-Christian
last_name: Theussl
- first_name: Takahiko
full_name: Shimizu, Takahiko
last_name: Shimizu
- first_name: Josef M.
full_name: Penninger, Josef M.
last_name: Penninger
- first_name: Florian
full_name: Pauler, Florian
id: 48EA0138-F248-11E8-B48F-1D18A9856A87
last_name: Pauler
orcid: 0000-0002-7462-0048
- first_name: Quanah J.
full_name: Hudson, Quanah J.
last_name: Hudson
citation:
ama: Andergassen D, Muckenhuber M, Bammer PC, et al. The Airn lncRNA does not require
any DNA elements within its locus to silence distant imprinted genes. PLoS
Genetics. 2019;15(7). doi:10.1371/journal.pgen.1008268
apa: Andergassen, D., Muckenhuber, M., Bammer, P. C., Kulinski, T. M., Theussl,
H.-C., Shimizu, T., … Hudson, Q. J. (2019). The Airn lncRNA does not require any
DNA elements within its locus to silence distant imprinted genes. PLoS Genetics.
Public Library of Science. https://doi.org/10.1371/journal.pgen.1008268
chicago: Andergassen, Daniel, Markus Muckenhuber, Philipp C. Bammer, Tomasz M. Kulinski,
Hans-Christian Theussl, Takahiko Shimizu, Josef M. Penninger, Florian Pauler,
and Quanah J. Hudson. “The Airn LncRNA Does Not Require Any DNA Elements within
Its Locus to Silence Distant Imprinted Genes.” PLoS Genetics. Public Library
of Science, 2019. https://doi.org/10.1371/journal.pgen.1008268.
ieee: D. Andergassen et al., “The Airn lncRNA does not require any DNA elements
within its locus to silence distant imprinted genes,” PLoS Genetics, vol.
15, no. 7. Public Library of Science, 2019.
ista: Andergassen D, Muckenhuber M, Bammer PC, Kulinski TM, Theussl H-C, Shimizu
T, Penninger JM, Pauler F, Hudson QJ. 2019. The Airn lncRNA does not require any
DNA elements within its locus to silence distant imprinted genes. PLoS Genetics.
15(7), e1008268.
mla: Andergassen, Daniel, et al. “The Airn LncRNA Does Not Require Any DNA Elements
within Its Locus to Silence Distant Imprinted Genes.” PLoS Genetics, vol.
15, no. 7, e1008268, Public Library of Science, 2019, doi:10.1371/journal.pgen.1008268.
short: D. Andergassen, M. Muckenhuber, P.C. Bammer, T.M. Kulinski, H.-C. Theussl,
T. Shimizu, J.M. Penninger, F. Pauler, Q.J. Hudson, PLoS Genetics 15 (2019).
date_created: 2020-01-29T16:14:07Z
date_published: 2019-07-22T00:00:00Z
date_updated: 2023-10-17T12:30:27Z
day: '22'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1371/journal.pgen.1008268
external_id:
isi:
- '000478689100025'
pmid:
- '31329595'
file:
- access_level: open_access
checksum: 2f51fc91e4a4199827adc51d432ad864
content_type: application/pdf
creator: dernst
date_created: 2020-02-04T10:11:55Z
date_updated: 2020-07-14T12:47:57Z
file_id: '7446'
file_name: 2019_PlosGenetics_Andergassen.pdf
file_size: 2302307
relation: main_file
file_date_updated: 2020-07-14T12:47:57Z
has_accepted_license: '1'
intvolume: ' 15'
isi: 1
issue: '7'
language:
- iso: eng
month: '07'
oa: 1
oa_version: Published Version
pmid: 1
publication: PLoS Genetics
publication_identifier:
issn:
- 1553-7404
publication_status: published
publisher: Public Library of Science
quality_controlled: '1'
scopus_import: '1'
status: public
title: The Airn lncRNA does not require any DNA elements within its locus to silence
distant imprinted genes
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 15
year: '2019'
...
---
_id: '6830'
article_processing_charge: No
article_type: letter_note
author:
- first_name: Ximena
full_name: Contreras, Ximena
id: 475990FE-F248-11E8-B48F-1D18A9856A87
last_name: Contreras
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Contreras X, Hippenmeyer S. Memo1 tiles the radial glial cell grid. Neuron.
2019;103(5):750-752. doi:10.1016/j.neuron.2019.08.021
apa: Contreras, X., & Hippenmeyer, S. (2019). Memo1 tiles the radial glial cell
grid. Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2019.08.021
chicago: Contreras, Ximena, and Simon Hippenmeyer. “Memo1 Tiles the Radial Glial
Cell Grid.” Neuron. Elsevier, 2019. https://doi.org/10.1016/j.neuron.2019.08.021.
ieee: X. Contreras and S. Hippenmeyer, “Memo1 tiles the radial glial cell grid,”
Neuron, vol. 103, no. 5. Elsevier, pp. 750–752, 2019.
ista: Contreras X, Hippenmeyer S. 2019. Memo1 tiles the radial glial cell grid.
Neuron. 103(5), 750–752.
mla: Contreras, Ximena, and Simon Hippenmeyer. “Memo1 Tiles the Radial Glial Cell
Grid.” Neuron, vol. 103, no. 5, Elsevier, 2019, pp. 750–52, doi:10.1016/j.neuron.2019.08.021.
short: X. Contreras, S. Hippenmeyer, Neuron 103 (2019) 750–752.
date_created: 2019-08-25T22:00:50Z
date_published: 2019-09-04T00:00:00Z
date_updated: 2024-03-29T23:30:41Z
day: '04'
department:
- _id: SiHi
doi: 10.1016/j.neuron.2019.08.021
external_id:
isi:
- '000484400200002'
pmid:
- '31487522'
intvolume: ' 103'
isi: 1
issue: '5'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1016/j.neuron.2019.08.021
month: '09'
oa: 1
oa_version: Published Version
page: 750-752
pmid: 1
publication: Neuron
publication_identifier:
eissn:
- '10974199'
issn:
- '08966273'
publication_status: published
publisher: Elsevier
quality_controlled: '1'
related_material:
record:
- id: '7902'
relation: part_of_dissertation
status: public
scopus_import: '1'
status: public
title: Memo1 tiles the radial glial cell grid
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 103
year: '2019'
...
---
_id: '8547'
abstract:
- lang: eng
text: The cerebral cortex contains multiple hierarchically organized areas with
distinctive cytoarchitectonical patterns, but the cellular mechanisms underlying
the emergence of this diversity remain unclear. Here, we have quantitatively investigated
the neuronal output of individual progenitor cells in the ventricular zone of
the developing mouse neocortex using a combination of methods that together circumvent
the biases and limitations of individual approaches. We found that individual
cortical progenitor cells show a high degree of stochasticity and generate pyramidal
cell lineages that adopt a wide range of laminar configurations. Mathematical
modelling these lineage data suggests that a small number of progenitor cell populations,
each generating pyramidal cells following different stochastic developmental programs,
suffice to generate the heterogenous complement of pyramidal cell lineages that
collectively build the complex cytoarchitecture of the neocortex.
acknowledgement: We thank I. Andrew and S.E. Bae for excellent technical assistance,
F. Gage for plasmids, and K. Nave (Nex-Cre) for mouse colonies. We thank members
of the Marín and Rico laboratories for stimulating discussions and ideas. Our research
on this topic is supported by grants from the European Research Council (ERC-2017-AdG
787355 to O.M and ERC2016-CoG 725780 to S.H.) and Wellcome Trust (103714MA) to O.M.
L.L. was the recipient of an EMBO long-term postdoctoral fellowship, R.B. received
support from FWF Lise-Meitner program (M 2416) and F.K.W. was supported by an EMBO
postdoctoral fellowship and is currently a Marie Skłodowska-Curie Fellow from the
European Commission under the H2020 Programme.
article_processing_charge: No
author:
- first_name: Alfredo
full_name: Llorca, Alfredo
last_name: Llorca
- first_name: Gabriele
full_name: Ciceri, Gabriele
last_name: Ciceri
- first_name: Robert J
full_name: Beattie, Robert J
id: 2E26DF60-F248-11E8-B48F-1D18A9856A87
last_name: Beattie
orcid: 0000-0002-8483-8753
- first_name: Fong K.
full_name: Wong, Fong K.
last_name: Wong
- first_name: Giovanni
full_name: Diana, Giovanni
last_name: Diana
- first_name: Eleni
full_name: Serafeimidou, Eleni
last_name: Serafeimidou
- first_name: Marian
full_name: Fernández-Otero, Marian
last_name: Fernández-Otero
- first_name: Carmen
full_name: Streicher, Carmen
id: 36BCB99C-F248-11E8-B48F-1D18A9856A87
last_name: Streicher
- first_name: Sebastian J.
full_name: Arnold, Sebastian J.
last_name: Arnold
- first_name: Martin
full_name: Meyer, Martin
last_name: Meyer
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Miguel
full_name: Maravall, Miguel
last_name: Maravall
- first_name: Oscar
full_name: Marín, Oscar
last_name: Marín
citation:
ama: Llorca A, Ciceri G, Beattie RJ, et al. Heterogeneous progenitor cell behaviors
underlie the assembly of neocortical cytoarchitecture. bioRxiv. doi:10.1101/494088
apa: Llorca, A., Ciceri, G., Beattie, R. J., Wong, F. K., Diana, G., Serafeimidou,
E., … Marín, O. (n.d.). Heterogeneous progenitor cell behaviors underlie the assembly
of neocortical cytoarchitecture. bioRxiv. Cold Spring Harbor Laboratory.
https://doi.org/10.1101/494088
chicago: Llorca, Alfredo, Gabriele Ciceri, Robert J Beattie, Fong K. Wong, Giovanni
Diana, Eleni Serafeimidou, Marian Fernández-Otero, et al. “Heterogeneous Progenitor
Cell Behaviors Underlie the Assembly of Neocortical Cytoarchitecture.” BioRxiv.
Cold Spring Harbor Laboratory, n.d. https://doi.org/10.1101/494088.
ieee: A. Llorca et al., “Heterogeneous progenitor cell behaviors underlie
the assembly of neocortical cytoarchitecture,” bioRxiv. Cold Spring Harbor
Laboratory.
ista: Llorca A, Ciceri G, Beattie RJ, Wong FK, Diana G, Serafeimidou E, Fernández-Otero
M, Streicher C, Arnold SJ, Meyer M, Hippenmeyer S, Maravall M, Marín O. Heterogeneous
progenitor cell behaviors underlie the assembly of neocortical cytoarchitecture.
bioRxiv, 10.1101/494088.
mla: Llorca, Alfredo, et al. “Heterogeneous Progenitor Cell Behaviors Underlie the
Assembly of Neocortical Cytoarchitecture.” BioRxiv, Cold Spring Harbor
Laboratory, doi:10.1101/494088.
short: A. Llorca, G. Ciceri, R.J. Beattie, F.K. Wong, G. Diana, E. Serafeimidou,
M. Fernández-Otero, C. Streicher, S.J. Arnold, M. Meyer, S. Hippenmeyer, M. Maravall,
O. Marín, BioRxiv (n.d.).
date_created: 2020-09-21T12:01:50Z
date_published: 2018-12-13T00:00:00Z
date_updated: 2021-01-12T08:20:00Z
day: '13'
department:
- _id: SiHi
doi: 10.1101/494088
ec_funded: 1
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1101/494088
month: '12'
oa: 1
oa_version: Preprint
project:
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
- _id: 264E56E2-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: M02416
name: Molecular Mechanisms Regulating Gliogenesis in the Cerebral Cortex
publication: bioRxiv
publication_status: submitted
publisher: Cold Spring Harbor Laboratory
status: public
title: Heterogeneous progenitor cell behaviors underlie the assembly of neocortical
cytoarchitecture
type: preprint
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2018'
...
---
_id: '20'
abstract:
- lang: eng
text: 'Background: Norepinephrine (NE) signaling has a key role in white adipose
tissue (WAT) functions, including lipolysis, free fatty acid liberation and, under
certain conditions, conversion of white into brite (brown-in-white) adipocytes.
However, acute effects of NE stimulation have not been described at the transcriptional
network level. Results: We used RNA-seq to uncover a broad transcriptional response.
The inference of protein-protein and protein-DNA interaction networks allowed
us to identify a set of immediate-early genes (IEGs) with high betweenness, validating
our approach and suggesting a hierarchical control of transcriptional regulation.
In addition, we identified a transcriptional regulatory network with IEGs as master
regulators, including HSF1 and NFIL3 as novel NE-induced IEG candidates. Moreover,
a functional enrichment analysis and gene clustering into functional modules suggest
a crosstalk between metabolic, signaling, and immune responses. Conclusions: Altogether,
our network biology approach explores for the first time the immediate-early systems
level response of human adipocytes to acute sympathetic activation, thereby providing
a first network basis of early cell fate programs and crosstalks between metabolic
and transcriptional networks required for proper WAT function.'
acknowledgement: This work was funded by the German Centre for Diabetes Research (DZD)
and the Austrian Science Fund (FWF, P25729-B19).
article_processing_charge: No
article_type: original
author:
- first_name: Juan
full_name: Higareda Almaraz, Juan
last_name: Higareda Almaraz
- first_name: Michael
full_name: Karbiener, Michael
last_name: Karbiener
- first_name: Maude
full_name: Giroud, Maude
last_name: Giroud
- first_name: Florian
full_name: Pauler, Florian
id: 48EA0138-F248-11E8-B48F-1D18A9856A87
last_name: Pauler
orcid: 0000-0002-7462-0048
- first_name: Teresa
full_name: Gerhalter, Teresa
last_name: Gerhalter
- first_name: Stephan
full_name: Herzig, Stephan
last_name: Herzig
- first_name: Marcel
full_name: Scheideler, Marcel
last_name: Scheideler
citation:
ama: Higareda Almaraz J, Karbiener M, Giroud M, et al. Norepinephrine triggers an
immediate-early regulatory network response in primary human white adipocytes.
BMC Genomics. 2018;19(1). doi:10.1186/s12864-018-5173-0
apa: Higareda Almaraz, J., Karbiener, M., Giroud, M., Pauler, F., Gerhalter, T.,
Herzig, S., & Scheideler, M. (2018). Norepinephrine triggers an immediate-early
regulatory network response in primary human white adipocytes. BMC Genomics.
BioMed Central. https://doi.org/10.1186/s12864-018-5173-0
chicago: Higareda Almaraz, Juan, Michael Karbiener, Maude Giroud, Florian Pauler,
Teresa Gerhalter, Stephan Herzig, and Marcel Scheideler. “Norepinephrine Triggers
an Immediate-Early Regulatory Network Response in Primary Human White Adipocytes.”
BMC Genomics. BioMed Central, 2018. https://doi.org/10.1186/s12864-018-5173-0.
ieee: J. Higareda Almaraz et al., “Norepinephrine triggers an immediate-early
regulatory network response in primary human white adipocytes,” BMC Genomics,
vol. 19, no. 1. BioMed Central, 2018.
ista: Higareda Almaraz J, Karbiener M, Giroud M, Pauler F, Gerhalter T, Herzig S,
Scheideler M. 2018. Norepinephrine triggers an immediate-early regulatory network
response in primary human white adipocytes. BMC Genomics. 19(1).
mla: Higareda Almaraz, Juan, et al. “Norepinephrine Triggers an Immediate-Early
Regulatory Network Response in Primary Human White Adipocytes.” BMC Genomics,
vol. 19, no. 1, BioMed Central, 2018, doi:10.1186/s12864-018-5173-0.
short: J. Higareda Almaraz, M. Karbiener, M. Giroud, F. Pauler, T. Gerhalter, S.
Herzig, M. Scheideler, BMC Genomics 19 (2018).
date_created: 2018-12-11T11:44:12Z
date_published: 2018-11-03T00:00:00Z
date_updated: 2023-09-13T09:10:47Z
day: '03'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1186/s12864-018-5173-0
external_id:
isi:
- '000450976700002'
file:
- access_level: open_access
checksum: a56516e734dab589dc7f3e1915973b4d
content_type: application/pdf
creator: dernst
date_created: 2018-12-17T14:52:57Z
date_updated: 2020-07-14T12:45:23Z
file_id: '5712'
file_name: 2018_BMCGenomics_Higareda.pdf
file_size: 4629784
relation: main_file
file_date_updated: 2020-07-14T12:45:23Z
has_accepted_license: '1'
intvolume: ' 19'
isi: 1
issue: '1'
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
publication: BMC Genomics
publication_identifier:
issn:
- 1471-2164
publication_status: published
publisher: BioMed Central
publist_id: '8035'
quality_controlled: '1'
related_material:
record:
- id: '9807'
relation: research_data
status: public
- id: '9808'
relation: research_data
status: public
scopus_import: '1'
status: public
title: Norepinephrine triggers an immediate-early regulatory network response in primary
human white adipocytes
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 19
year: '2018'
...
---
_id: '9807'
abstract:
- lang: eng
text: Table S1. Genes with highest betweenness. Table S2. Local and Master regulators
up-regulated. Table S3. Local and Master regulators down-regulated (XLSX 23 kb).
article_processing_charge: No
author:
- first_name: Juan
full_name: Higareda Almaraz, Juan
last_name: Higareda Almaraz
- first_name: Michael
full_name: Karbiener, Michael
last_name: Karbiener
- first_name: Maude
full_name: Giroud, Maude
last_name: Giroud
- first_name: Florian
full_name: Pauler, Florian
id: 48EA0138-F248-11E8-B48F-1D18A9856A87
last_name: Pauler
orcid: 0000-0002-7462-0048
- first_name: Teresa
full_name: Gerhalter, Teresa
last_name: Gerhalter
- first_name: Stephan
full_name: Herzig, Stephan
last_name: Herzig
- first_name: Marcel
full_name: Scheideler, Marcel
last_name: Scheideler
citation:
ama: 'Higareda Almaraz J, Karbiener M, Giroud M, et al. Additional file 1: Of Norepinephrine
triggers an immediate-early regulatory network response in primary human white
adipocytes. 2018. doi:10.6084/m9.figshare.7295339.v1'
apa: 'Higareda Almaraz, J., Karbiener, M., Giroud, M., Pauler, F., Gerhalter, T.,
Herzig, S., & Scheideler, M. (2018). Additional file 1: Of Norepinephrine
triggers an immediate-early regulatory network response in primary human white
adipocytes. Springer Nature. https://doi.org/10.6084/m9.figshare.7295339.v1'
chicago: 'Higareda Almaraz, Juan, Michael Karbiener, Maude Giroud, Florian Pauler,
Teresa Gerhalter, Stephan Herzig, and Marcel Scheideler. “Additional File 1: Of
Norepinephrine Triggers an Immediate-Early Regulatory Network Response in Primary
Human White Adipocytes.” Springer Nature, 2018. https://doi.org/10.6084/m9.figshare.7295339.v1.'
ieee: 'J. Higareda Almaraz et al., “Additional file 1: Of Norepinephrine
triggers an immediate-early regulatory network response in primary human white
adipocytes.” Springer Nature, 2018.'
ista: 'Higareda Almaraz J, Karbiener M, Giroud M, Pauler F, Gerhalter T, Herzig
S, Scheideler M. 2018. Additional file 1: Of Norepinephrine triggers an immediate-early
regulatory network response in primary human white adipocytes, Springer Nature,
10.6084/m9.figshare.7295339.v1.'
mla: 'Higareda Almaraz, Juan, et al. Additional File 1: Of Norepinephrine Triggers
an Immediate-Early Regulatory Network Response in Primary Human White Adipocytes.
Springer Nature, 2018, doi:10.6084/m9.figshare.7295339.v1.'
short: J. Higareda Almaraz, M. Karbiener, M. Giroud, F. Pauler, T. Gerhalter, S.
Herzig, M. Scheideler, (2018).
date_created: 2021-08-06T12:26:53Z
date_published: 2018-11-03T00:00:00Z
date_updated: 2023-09-13T09:10:47Z
day: '03'
department:
- _id: SiHi
doi: 10.6084/m9.figshare.7295339.v1
main_file_link:
- open_access: '1'
url: https://doi.org/10.6084/m9.figshare.7295339.v1
month: '11'
oa: 1
oa_version: Published Version
publisher: Springer Nature
related_material:
record:
- id: '20'
relation: used_in_publication
status: public
status: public
title: 'Additional file 1: Of Norepinephrine triggers an immediate-early regulatory
network response in primary human white adipocytes'
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
year: '2018'
...
---
_id: '9808'
abstract:
- lang: eng
text: Table S4. Counts per Gene per Million Reads Mapped. (XLSX 2751 kb).
article_processing_charge: No
author:
- first_name: Juan
full_name: Higareda Almaraz, Juan
last_name: Higareda Almaraz
- first_name: Michael
full_name: Karbiener, Michael
last_name: Karbiener
- first_name: Maude
full_name: Giroud, Maude
last_name: Giroud
- first_name: Florian
full_name: Pauler, Florian
id: 48EA0138-F248-11E8-B48F-1D18A9856A87
last_name: Pauler
orcid: 0000-0002-7462-0048
- first_name: Teresa
full_name: Gerhalter, Teresa
last_name: Gerhalter
- first_name: Stephan
full_name: Herzig, Stephan
last_name: Herzig
- first_name: Marcel
full_name: Scheideler, Marcel
last_name: Scheideler
citation:
ama: 'Higareda Almaraz J, Karbiener M, Giroud M, et al. Additional file 3: Of Norepinephrine
triggers an immediate-early regulatory network response in primary human white
adipocytes. 2018. doi:10.6084/m9.figshare.7295369.v1'
apa: 'Higareda Almaraz, J., Karbiener, M., Giroud, M., Pauler, F., Gerhalter, T.,
Herzig, S., & Scheideler, M. (2018). Additional file 3: Of Norepinephrine
triggers an immediate-early regulatory network response in primary human white
adipocytes. Springer Nature. https://doi.org/10.6084/m9.figshare.7295369.v1'
chicago: 'Higareda Almaraz, Juan, Michael Karbiener, Maude Giroud, Florian Pauler,
Teresa Gerhalter, Stephan Herzig, and Marcel Scheideler. “Additional File 3: Of
Norepinephrine Triggers an Immediate-Early Regulatory Network Response in Primary
Human White Adipocytes.” Springer Nature, 2018. https://doi.org/10.6084/m9.figshare.7295369.v1.'
ieee: 'J. Higareda Almaraz et al., “Additional file 3: Of Norepinephrine
triggers an immediate-early regulatory network response in primary human white
adipocytes.” Springer Nature, 2018.'
ista: 'Higareda Almaraz J, Karbiener M, Giroud M, Pauler F, Gerhalter T, Herzig
S, Scheideler M. 2018. Additional file 3: Of Norepinephrine triggers an immediate-early
regulatory network response in primary human white adipocytes, Springer Nature,
10.6084/m9.figshare.7295369.v1.'
mla: 'Higareda Almaraz, Juan, et al. Additional File 3: Of Norepinephrine Triggers
an Immediate-Early Regulatory Network Response in Primary Human White Adipocytes.
Springer Nature, 2018, doi:10.6084/m9.figshare.7295369.v1.'
short: J. Higareda Almaraz, M. Karbiener, M. Giroud, F. Pauler, T. Gerhalter, S.
Herzig, M. Scheideler, (2018).
date_created: 2021-08-06T12:31:57Z
date_published: 2018-11-03T00:00:00Z
date_updated: 2023-09-13T09:10:47Z
day: '03'
department:
- _id: SiHi
doi: 10.6084/m9.figshare.7295369.v1
main_file_link:
- open_access: '1'
url: https://doi.org/10.6084/m9.figshare.7295369.v1
month: '11'
oa: 1
oa_version: Published Version
publisher: Springer Nature
related_material:
record:
- id: '20'
relation: used_in_publication
status: public
status: public
title: 'Additional file 3: Of Norepinephrine triggers an immediate-early regulatory
network response in primary human white adipocytes'
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
year: '2018'
...
---
_id: '10'
abstract:
- lang: eng
text: Genomic imprinting is an epigenetic process that leads to parent of origin-specific
gene expression in a subset of genes. Imprinted genes are essential for brain
development, and deregulation of imprinting is associated with neurodevelopmental
diseases and the pathogenesis of psychiatric disorders. However, the cell-type
specificity of imprinting at single cell resolution, and how imprinting and thus
gene dosage regulates neuronal circuit assembly is still largely unknown. Here,
MADM (Mosaic Analysis with Double Markers) technology was employed to assess genomic
imprinting at single cell level. By visualizing MADM-induced uniparental disomies
(UPDs) in distinct colors at single cell level in genetic mosaic animals, this
experimental paradigm provides a unique quantitative platform to systematically
assay the UPD-mediated imbalances in imprinted gene expression at unprecedented
resolution. An experimental pipeline based on FACS, RNA-seq and bioinformatics
analysis was established and applied to systematically map cell-type-specific
‘imprintomes’ in the mouse brain. The results revealed that parental-specific
expression of imprinted genes per se is rarely cell-type-specific even at the
individual cell level. Conversely, when we extended the comparison to downstream
responses resulting from imbalanced imprinted gene expression, we discovered an
unexpectedly high degree of cell-type specificity. Furthermore, we determined
a novel function of genomic imprinting in cortical astrocyte production and in
olfactory bulb (OB) granule cell generation. These results suggest important functional
implication of genomic imprinting for generating cell-type diversity in the brain.
In addition, MADM provides a powerful tool to study candidate genes by concomitant
genetic manipulation and fluorescent labelling of single cells. MADM-based candidate
gene approach was utilized to identify potential imprinted genes involved in the
generation of cortical astrocytes and OB granule cells. We investigated p57Kip2,
a maternally expressed gene and known cell cycle regulator. Although we found
that p57Kip2 does not play a role in these processes, we detected an unexpected
function of the paternal allele previously thought to be silent. Finally, we took
advantage of a key property of MADM which is to allow unambiguous investigation
of environmental impact on single cells. The experimental pipeline based on FACS
and RNA-seq analysis of MADM-labeled cells was established to probe the functional
differences of single cell loss of gene function compared to global loss of function
on a transcriptional level. With this method, both common and distinct responses
were isolated due to cell-autonomous and non-autonomous effects acting on genotypically
identical cells. As a result, transcriptional changes were identified which result
solely from the surrounding environment. Using the MADM technology to study genomic
imprinting at single cell resolution, we have identified cell-type-specific gene
expression, novel gene function and the impact of environment on single cell transcriptomes.
Together, these provide important insights to the understanding of mechanisms
regulating cell-type specificity and thus diversity in the brain.
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Susanne
full_name: Laukoter, Susanne
id: 2D6B7A9A-F248-11E8-B48F-1D18A9856A87
last_name: Laukoter
orcid: 0000-0002-7903-3010
citation:
ama: Laukoter S. Role of genomic imprinting in cerebral cortex development. 2018:1-139.
doi:10.15479/AT:ISTA:th1057
apa: Laukoter, S. (2018). Role of genomic imprinting in cerebral cortex development.
Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:th1057
chicago: Laukoter, Susanne. “Role of Genomic Imprinting in Cerebral Cortex Development.”
Institute of Science and Technology Austria, 2018. https://doi.org/10.15479/AT:ISTA:th1057.
ieee: S. Laukoter, “Role of genomic imprinting in cerebral cortex development,”
Institute of Science and Technology Austria, 2018.
ista: Laukoter S. 2018. Role of genomic imprinting in cerebral cortex development.
Institute of Science and Technology Austria.
mla: Laukoter, Susanne. Role of Genomic Imprinting in Cerebral Cortex Development.
Institute of Science and Technology Austria, 2018, pp. 1–139, doi:10.15479/AT:ISTA:th1057.
short: S. Laukoter, Role of Genomic Imprinting in Cerebral Cortex Development, Institute
of Science and Technology Austria, 2018.
date_created: 2018-12-11T11:44:08Z
date_published: 2018-11-21T00:00:00Z
date_updated: 2023-09-07T12:40:44Z
day: '21'
ddc:
- '570'
degree_awarded: PhD
department:
- _id: SiHi
doi: 10.15479/AT:ISTA:th1057
file:
- access_level: closed
checksum: 41fdbf5fdce312802935d88a8ad9932c
content_type: application/vnd.openxmlformats-officedocument.wordprocessingml.document
creator: dernst
date_created: 2019-05-10T07:47:04Z
date_updated: 2019-11-23T23:30:03Z
embargo_to: open_access
file_id: '6396'
file_name: Thesis_LaukoterSusanne_FINAL.docx
file_size: 17949175
relation: source_file
- access_level: open_access
checksum: 53001a9a0c9e570e598d861bb0af28aa
content_type: application/pdf
creator: dernst
date_created: 2019-05-10T07:47:04Z
date_updated: 2021-02-11T11:17:16Z
embargo: 2019-11-21
file_id: '6397'
file_name: Thesis_LaukoterSusanne_FINAL.pdf
file_size: 21187245
relation: main_file
file_date_updated: 2021-02-11T11:17:16Z
has_accepted_license: '1'
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
page: 1 - 139
publication_identifier:
issn:
- 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
publist_id: '8046'
pubrep_id: '1057'
status: public
supervisor:
- first_name: Beatriz
full_name: Vicoso, Beatriz
id: 49E1C5C6-F248-11E8-B48F-1D18A9856A87
last_name: Vicoso
orcid: 0000-0002-4579-8306
title: Role of genomic imprinting in cerebral cortex development
type: dissertation
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
year: '2018'
...
---
_id: '28'
abstract:
- lang: eng
text: 'This scientific commentary refers to ‘NEGR1 and FGFR2 cooperatively regulate
cortical development and core behaviours related to autism disorders in mice’
by Szczurkowska et al. '
article_processing_charge: No
author:
- first_name: Ximena
full_name: Contreras, Ximena
id: 475990FE-F248-11E8-B48F-1D18A9856A87
last_name: Contreras
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Contreras X, Hippenmeyer S. Incorrect trafficking route leads to autism. Brain
a journal of neurology. 2018;141(9):2542-2544. doi:10.1093/brain/awy218
apa: Contreras, X., & Hippenmeyer, S. (2018). Incorrect trafficking route leads
to autism. Brain a Journal of Neurology. Oxford University Press. https://doi.org/10.1093/brain/awy218
chicago: Contreras, Ximena, and Simon Hippenmeyer. “Incorrect Trafficking Route
Leads to Autism.” Brain a Journal of Neurology. Oxford University Press,
2018. https://doi.org/10.1093/brain/awy218.
ieee: X. Contreras and S. Hippenmeyer, “Incorrect trafficking route leads to autism,”
Brain a journal of neurology, vol. 141, no. 9. Oxford University Press,
pp. 2542–2544, 2018.
ista: Contreras X, Hippenmeyer S. 2018. Incorrect trafficking route leads to autism.
Brain a journal of neurology. 141(9), 2542–2544.
mla: Contreras, Ximena, and Simon Hippenmeyer. “Incorrect Trafficking Route Leads
to Autism.” Brain a Journal of Neurology, vol. 141, no. 9, Oxford University
Press, 2018, pp. 2542–44, doi:10.1093/brain/awy218.
short: X. Contreras, S. Hippenmeyer, Brain a Journal of Neurology 141 (2018) 2542–2544.
date_created: 2018-12-11T11:44:14Z
date_published: 2018-09-01T00:00:00Z
date_updated: 2024-03-29T23:30:41Z
day: '01'
department:
- _id: SiHi
doi: 10.1093/brain/awy218
external_id:
isi:
- '000446548100012'
intvolume: ' 141'
isi: 1
issue: '9'
language:
- iso: eng
month: '09'
oa_version: None
page: 2542 - 2544
publication: Brain a journal of neurology
publication_status: published
publisher: Oxford University Press
quality_controlled: '1'
related_material:
record:
- id: '7902'
relation: part_of_dissertation
status: public
scopus_import: '1'
status: public
title: Incorrect trafficking route leads to autism
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 141
year: '2018'
...
---
_id: '713'
abstract:
- lang: eng
text: To determine the dynamics of allelic-specific expression during mouse development,
we analyzed RNA-seq data from 23 F1 tissues from different developmental stages,
including 19 female tissues allowing X chromosome inactivation (XCI) escapers
to also be detected. We demonstrate that allelic expression arising from genetic
or epigenetic differences is highly tissue-specific. We find that tissue-specific
strain-biased gene expression may be regulated by tissue-specific enhancers or
by post-transcriptional differences in stability between the alleles. We also
find that escape from X-inactivation is tissue-specific, with leg muscle showing
an unexpectedly high rate of XCI escapers. By surveying a range of tissues during
development, and performing extensive validation, we are able to provide a high
confidence list of mouse imprinted genes including 18 novel genes. This shows
that cluster size varies dynamically during development and can be substantially
larger than previously thought, with the Igf2r cluster extending over 10 Mb in
placenta.
article_number: e25125
author:
- first_name: Daniel
full_name: Andergassen, Daniel
last_name: Andergassen
- first_name: Christoph
full_name: Dotter, Christoph
id: 4C66542E-F248-11E8-B48F-1D18A9856A87
last_name: Dotter
- first_name: Dyniel
full_name: Wenzel, Dyniel
last_name: Wenzel
- first_name: Verena
full_name: Sigl, Verena
last_name: Sigl
- first_name: Philipp
full_name: Bammer, Philipp
last_name: Bammer
- first_name: Markus
full_name: Muckenhuber, Markus
last_name: Muckenhuber
- first_name: Daniela
full_name: Mayer, Daniela
last_name: Mayer
- first_name: Tomasz
full_name: Kulinski, Tomasz
last_name: Kulinski
- first_name: Hans
full_name: Theussl, Hans
last_name: Theussl
- first_name: Josef
full_name: Penninger, Josef
last_name: Penninger
- first_name: Christoph
full_name: Bock, Christoph
last_name: Bock
- first_name: Denise
full_name: Barlow, Denise
last_name: Barlow
- first_name: Florian
full_name: Pauler, Florian
id: 48EA0138-F248-11E8-B48F-1D18A9856A87
last_name: Pauler
- first_name: Quanah
full_name: Hudson, Quanah
last_name: Hudson
citation:
ama: Andergassen D, Dotter C, Wenzel D, et al. Mapping the mouse Allelome reveals
tissue specific regulation of allelic expression. eLife. 2017;6. doi:10.7554/eLife.25125
apa: Andergassen, D., Dotter, C., Wenzel, D., Sigl, V., Bammer, P., Muckenhuber,
M., … Hudson, Q. (2017). Mapping the mouse Allelome reveals tissue specific regulation
of allelic expression. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.25125
chicago: Andergassen, Daniel, Christoph Dotter, Dyniel Wenzel, Verena Sigl, Philipp
Bammer, Markus Muckenhuber, Daniela Mayer, et al. “Mapping the Mouse Allelome
Reveals Tissue Specific Regulation of Allelic Expression.” ELife. eLife
Sciences Publications, 2017. https://doi.org/10.7554/eLife.25125.
ieee: D. Andergassen et al., “Mapping the mouse Allelome reveals tissue specific
regulation of allelic expression,” eLife, vol. 6. eLife Sciences Publications,
2017.
ista: Andergassen D, Dotter C, Wenzel D, Sigl V, Bammer P, Muckenhuber M, Mayer
D, Kulinski T, Theussl H, Penninger J, Bock C, Barlow D, Pauler F, Hudson Q. 2017.
Mapping the mouse Allelome reveals tissue specific regulation of allelic expression.
eLife. 6, e25125.
mla: Andergassen, Daniel, et al. “Mapping the Mouse Allelome Reveals Tissue Specific
Regulation of Allelic Expression.” ELife, vol. 6, e25125, eLife Sciences
Publications, 2017, doi:10.7554/eLife.25125.
short: D. Andergassen, C. Dotter, D. Wenzel, V. Sigl, P. Bammer, M. Muckenhuber,
D. Mayer, T. Kulinski, H. Theussl, J. Penninger, C. Bock, D. Barlow, F. Pauler,
Q. Hudson, ELife 6 (2017).
date_created: 2018-12-11T11:48:05Z
date_published: 2017-08-14T00:00:00Z
date_updated: 2021-01-12T08:11:57Z
day: '14'
ddc:
- '576'
department:
- _id: GaNo
- _id: SiHi
doi: 10.7554/eLife.25125
file:
- access_level: open_access
checksum: 1ace3462e64a971b9ead896091829549
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:13:36Z
date_updated: 2020-07-14T12:47:50Z
file_id: '5020'
file_name: IST-2017-885-v1+1_elife-25125-figures-v2.pdf
file_size: 6399510
relation: main_file
- access_level: open_access
checksum: 6241dc31eeb87b03facadec3a53a6827
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:13:36Z
date_updated: 2020-07-14T12:47:50Z
file_id: '5021'
file_name: IST-2017-885-v1+2_elife-25125-v2.pdf
file_size: 4264398
relation: main_file
file_date_updated: 2020-07-14T12:47:50Z
has_accepted_license: '1'
intvolume: ' 6'
language:
- iso: eng
month: '08'
oa: 1
oa_version: Published Version
project:
- _id: 25E9AF9E-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P27201-B22
name: Revealing the mechanisms underlying drug interactions
publication: eLife
publication_identifier:
issn:
- 2050084X
publication_status: published
publisher: eLife Sciences Publications
publist_id: '6971'
pubrep_id: '885'
quality_controlled: '1'
scopus_import: 1
status: public
title: Mapping the mouse Allelome reveals tissue specific regulation of allelic expression
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 6
year: '2017'
...
---
_id: '9707'
abstract:
- lang: eng
text: Branching morphogenesis of the epithelial ureteric bud forms the renal collecting
duct system and is critical for normal nephron number, while low nephron number
is implicated in hypertension and renal disease. Ureteric bud growth and branching
requires GDNF signaling from the surrounding mesenchyme to cells at the ureteric
bud tips, via the Ret receptor tyrosine kinase and coreceptor Gfrα1; Ret signaling
up-regulates transcription factors Etv4 and Etv5, which are also critical for
branching. Despite extensive knowledge of the genetic control of these events,
it is not understood, at the cellular level, how renal branching morphogenesis
is achieved or how Ret signaling influences epithelial cell behaviors to promote
this process. Analysis of chimeric embryos previously suggested a role for Ret
signaling in promoting cell rearrangements in the nephric duct, but this method
was unsuited to study individual cell behaviors during ureteric bud branching.
Here, we use Mosaic Analysis with Double Markers (MADM), combined with organ culture
and time-lapse imaging, to trace the movements and divisions of individual ureteric
bud tip cells. We first examine wild-type clones and then Ret or Etv4 mutant/wild-type
clones in which the mutant and wild-type sister cells are differentially and heritably
marked by green and red fluorescent proteins. We find that, in normal kidneys,
most individual tip cells behave as self-renewing progenitors, some of whose progeny
remain at the tips while others populate the growing UB trunks. In Ret or Etv4
MADM clones, the wild-type cells generated at a UB tip are much more likely to
remain at, or move to, the new tips during branching and elongation, while their
Ret−/− or Etv4−/− sister cells tend to lag behind and contribute only to the trunks.
By tracking successive mitoses in a cell lineage, we find that Ret signaling has
little effect on proliferation, in contrast to its effects on cell movement. Our
results show that Ret/Etv4 signaling promotes directed cell movements in the ureteric
bud tips, and suggest a model in which these cell movements mediate branching
morphogenesis.
article_processing_charge: No
author:
- first_name: Paul
full_name: Riccio, Paul
last_name: Riccio
- first_name: Christina
full_name: Cebrián, Christina
last_name: Cebrián
- first_name: Hui
full_name: Zong, Hui
last_name: Zong
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Frank
full_name: Costantini, Frank
last_name: Costantini
citation:
ama: 'Riccio P, Cebrián C, Zong H, Hippenmeyer S, Costantini F. Data from: Ret and
Etv4 promote directed movements of progenitor cells during renal branching morphogenesis.
2017. doi:10.5061/dryad.pk16b'
apa: 'Riccio, P., Cebrián, C., Zong, H., Hippenmeyer, S., & Costantini, F. (2017).
Data from: Ret and Etv4 promote directed movements of progenitor cells during
renal branching morphogenesis. Dryad. https://doi.org/10.5061/dryad.pk16b'
chicago: 'Riccio, Paul, Christina Cebrián, Hui Zong, Simon Hippenmeyer, and Frank
Costantini. “Data from: Ret and Etv4 Promote Directed Movements of Progenitor
Cells during Renal Branching Morphogenesis.” Dryad, 2017. https://doi.org/10.5061/dryad.pk16b.'
ieee: 'P. Riccio, C. Cebrián, H. Zong, S. Hippenmeyer, and F. Costantini, “Data
from: Ret and Etv4 promote directed movements of progenitor cells during renal
branching morphogenesis.” Dryad, 2017.'
ista: 'Riccio P, Cebrián C, Zong H, Hippenmeyer S, Costantini F. 2017. Data from:
Ret and Etv4 promote directed movements of progenitor cells during renal branching
morphogenesis, Dryad, 10.5061/dryad.pk16b.'
mla: 'Riccio, Paul, et al. Data from: Ret and Etv4 Promote Directed Movements
of Progenitor Cells during Renal Branching Morphogenesis. Dryad, 2017, doi:10.5061/dryad.pk16b.'
short: P. Riccio, C. Cebrián, H. Zong, S. Hippenmeyer, F. Costantini, (2017).
date_created: 2021-07-23T09:39:34Z
date_published: 2017-01-14T00:00:00Z
date_updated: 2022-08-25T13:34:55Z
day: '14'
department:
- _id: SiHi
doi: 10.5061/dryad.pk16b
main_file_link:
- open_access: '1'
url: https://doi.org/10.5061/dryad.pk16b
month: '01'
oa: 1
oa_version: Published Version
publisher: Dryad
related_material:
record:
- id: '9702'
relation: used_in_publication
status: deleted
status: public
title: 'Data from: Ret and Etv4 promote directed movements of progenitor cells during
renal branching morphogenesis'
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
year: '2017'
...
---
_id: '1017'
abstract:
- lang: eng
text: The development of the vertebrate central nervous system is reliant on a complex
cascade of biological processes that include mitotic division, relocation of migrating
neurons, and the extension of dendritic and axonal processes. Each of these cellular
events requires the diverse functional repertoire of the microtubule cytoskeleton
for the generation of forces, assembly of macromolecular complexes and transport
of molecules and organelles. The tubulins are a multi-gene family that encode
for the constituents of microtubules, and have been implicated in a spectrum of
neurological disorders. Evidence is building that different tubulins tune the
functional properties of the microtubule cytoskeleton dependent on the cell type,
developmental profile and subcellular localisation. Here we review of the origins
of the functional specification of the tubulin gene family in the developing brain
at a transcriptional, translational, and post-transcriptional level. We remind
the reader that tubulins are not just loading controls for your average Western
blot.
article_processing_charge: No
author:
- first_name: Martin
full_name: Breuss, Martin
last_name: Breuss
- first_name: Ines
full_name: Leca, Ines
last_name: Leca
- first_name: Thomas
full_name: Gstrein, Thomas
last_name: Gstrein
- first_name: Andi H
full_name: Hansen, Andi H
id: 38853E16-F248-11E8-B48F-1D18A9856A87
last_name: Hansen
- first_name: David
full_name: Keays, David
last_name: Keays
citation:
ama: 'Breuss M, Leca I, Gstrein T, Hansen AH, Keays D. Tubulins and brain development:
The origins of functional specification. Molecular and Cellular Neuroscience.
2017;84:58-67. doi:10.1016/j.mcn.2017.03.002'
apa: 'Breuss, M., Leca, I., Gstrein, T., Hansen, A. H., & Keays, D. (2017).
Tubulins and brain development: The origins of functional specification. Molecular
and Cellular Neuroscience. Academic Press. https://doi.org/10.1016/j.mcn.2017.03.002'
chicago: 'Breuss, Martin, Ines Leca, Thomas Gstrein, Andi H Hansen, and David Keays.
“Tubulins and Brain Development: The Origins of Functional Specification.” Molecular
and Cellular Neuroscience. Academic Press, 2017. https://doi.org/10.1016/j.mcn.2017.03.002.'
ieee: 'M. Breuss, I. Leca, T. Gstrein, A. H. Hansen, and D. Keays, “Tubulins and
brain development: The origins of functional specification,” Molecular and
Cellular Neuroscience, vol. 84. Academic Press, pp. 58–67, 2017.'
ista: 'Breuss M, Leca I, Gstrein T, Hansen AH, Keays D. 2017. Tubulins and brain
development: The origins of functional specification. Molecular and Cellular Neuroscience.
84, 58–67.'
mla: 'Breuss, Martin, et al. “Tubulins and Brain Development: The Origins of Functional
Specification.” Molecular and Cellular Neuroscience, vol. 84, Academic
Press, 2017, pp. 58–67, doi:10.1016/j.mcn.2017.03.002.'
short: M. Breuss, I. Leca, T. Gstrein, A.H. Hansen, D. Keays, Molecular and Cellular
Neuroscience 84 (2017) 58–67.
date_created: 2018-12-11T11:49:42Z
date_published: 2017-10-01T00:00:00Z
date_updated: 2023-09-22T09:42:15Z
day: '01'
ddc:
- '571'
department:
- _id: SiHi
doi: 10.1016/j.mcn.2017.03.002
external_id:
isi:
- '000415140700007'
file:
- access_level: open_access
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:09:19Z
date_updated: 2018-12-12T10:09:19Z
file_id: '4742'
file_name: IST-2017-806-v1+2_1-s2.0-S1044743116302500-main_1_.pdf
file_size: 1436377
relation: main_file
file_date_updated: 2018-12-12T10:09:19Z
has_accepted_license: '1'
intvolume: ' 84'
isi: 1
language:
- iso: eng
month: '10'
oa: 1
oa_version: Published Version
page: 58 - 67
publication: Molecular and Cellular Neuroscience
publication_identifier:
issn:
- '10447431'
publication_status: published
publisher: Academic Press
publist_id: '6377'
pubrep_id: '806'
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'Tubulins and brain development: The origins of functional specification'
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 84
year: '2017'
...
---
_id: '1016'
abstract:
- lang: eng
text: The integrity and dynamic properties of the microtubule cytoskeleton are indispensable
for the development of the mammalian brain. Consequently, mutations in the genes
that encode the structural component (the α/β-tubulin heterodimer) can give rise
to severe, sporadic neurodevelopmental disorders. These are commonly referred
to as the tubulinopathies. Here we report the addition of recessive quadrupedalism,
also known as Uner Tan syndrome (UTS), to the growing list of diseases caused
by tubulin variants. Analysis of a consanguineous UTS family identified a biallelic
TUBB2B mutation, resulting in a p.R390Q amino acid substitution. In addition to
the identifying quadrupedal locomotion, all three patients showed severe cerebellar
hypoplasia. None, however, displayed the basal ganglia malformations typically
associated with TUBB2B mutations. Functional analysis of the R390Q substitution
revealed that it did not affect the ability of β-tubulin to fold or become assembled
into the α/β-heterodimer, nor did it influence the incorporation of mutant-containing
heterodimers into microtubule polymers. The 390Q mutation in S. cerevisiae TUB2
did not affect growth under basal conditions, but did result in increased sensitivity
to microtubule-depolymerizing drugs, indicative of a mild impact of this mutation
on microtubule function. The TUBB2B mutation described here represents an unusual
recessive mode of inheritance for missense-mediated tubulinopathies and reinforces
the sensitivity of the developing cerebellum to microtubule defects.
article_processing_charge: No
author:
- first_name: Martin
full_name: Breuss, Martin
last_name: Breuss
- first_name: Thai
full_name: Nguyen, Thai
last_name: Nguyen
- first_name: Anjana
full_name: Srivatsan, Anjana
last_name: Srivatsan
- first_name: Ines
full_name: Leca, Ines
last_name: Leca
- first_name: Guoling
full_name: Tian, Guoling
last_name: Tian
- first_name: Tanja
full_name: Fritz, Tanja
last_name: Fritz
- first_name: Andi H
full_name: Hansen, Andi H
id: 38853E16-F248-11E8-B48F-1D18A9856A87
last_name: Hansen
- first_name: Damir
full_name: Musaev, Damir
last_name: Musaev
- first_name: Jennifer
full_name: Mcevoy Venneri, Jennifer
last_name: Mcevoy Venneri
- first_name: James
full_name: Kiely, James
last_name: Kiely
- first_name: Rasim
full_name: Rosti, Rasim
last_name: Rosti
- first_name: Eric
full_name: Scott, Eric
last_name: Scott
- first_name: Uner
full_name: Tan, Uner
last_name: Tan
- first_name: Richard
full_name: Kolodner, Richard
last_name: Kolodner
- first_name: Nicholas
full_name: Cowan, Nicholas
last_name: Cowan
- first_name: David
full_name: Keays, David
last_name: Keays
- first_name: Joseph
full_name: Gleeson, Joseph
last_name: Gleeson
citation:
ama: Breuss M, Nguyen T, Srivatsan A, et al. Uner Tan syndrome caused by a homozygous
TUBB2B mutation affecting microtubule stability. Human Molecular Genetics.
2017;26(2):258-269. doi:10.1093/hmg/ddw383
apa: Breuss, M., Nguyen, T., Srivatsan, A., Leca, I., Tian, G., Fritz, T., … Gleeson,
J. (2017). Uner Tan syndrome caused by a homozygous TUBB2B mutation affecting
microtubule stability. Human Molecular Genetics. Oxford University Press.
https://doi.org/10.1093/hmg/ddw383
chicago: Breuss, Martin, Thai Nguyen, Anjana Srivatsan, Ines Leca, Guoling Tian,
Tanja Fritz, Andi H Hansen, et al. “Uner Tan Syndrome Caused by a Homozygous TUBB2B
Mutation Affecting Microtubule Stability.” Human Molecular Genetics. Oxford
University Press, 2017. https://doi.org/10.1093/hmg/ddw383.
ieee: M. Breuss et al., “Uner Tan syndrome caused by a homozygous TUBB2B
mutation affecting microtubule stability,” Human Molecular Genetics, vol.
26, no. 2. Oxford University Press, pp. 258–269, 2017.
ista: Breuss M, Nguyen T, Srivatsan A, Leca I, Tian G, Fritz T, Hansen AH, Musaev
D, Mcevoy Venneri J, Kiely J, Rosti R, Scott E, Tan U, Kolodner R, Cowan N, Keays
D, Gleeson J. 2017. Uner Tan syndrome caused by a homozygous TUBB2B mutation affecting
microtubule stability. Human Molecular Genetics. 26(2), 258–269.
mla: Breuss, Martin, et al. “Uner Tan Syndrome Caused by a Homozygous TUBB2B Mutation
Affecting Microtubule Stability.” Human Molecular Genetics, vol. 26, no.
2, Oxford University Press, 2017, pp. 258–69, doi:10.1093/hmg/ddw383.
short: M. Breuss, T. Nguyen, A. Srivatsan, I. Leca, G. Tian, T. Fritz, A.H. Hansen,
D. Musaev, J. Mcevoy Venneri, J. Kiely, R. Rosti, E. Scott, U. Tan, R. Kolodner,
N. Cowan, D. Keays, J. Gleeson, Human Molecular Genetics 26 (2017) 258–269.
date_created: 2018-12-11T11:49:42Z
date_published: 2017-01-01T00:00:00Z
date_updated: 2023-09-22T09:42:42Z
day: '01'
department:
- _id: SiHi
doi: 10.1093/hmg/ddw383
external_id:
isi:
- '000397066400002'
intvolume: ' 26'
isi: 1
issue: '2'
language:
- iso: eng
month: '01'
oa_version: None
page: 258 - 269
publication: Human Molecular Genetics
publication_identifier:
issn:
- '09646906'
publication_status: published
publisher: Oxford University Press
publist_id: '6379'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Uner Tan syndrome caused by a homozygous TUBB2B mutation affecting microtubule
stability
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 26
year: '2017'
...
---
_id: '944'
abstract:
- lang: eng
text: The concerted production of neurons and glia by neural stem cells (NSCs) is
essential for neural circuit assembly. In the developing cerebral cortex, radial
glia progenitors (RGPs) generate nearly all neocortical neurons and certain glia
lineages. RGP proliferation behavior shows a high degree of non-stochasticity,
thus a deterministic characteristic of neuron and glia production. However, the
cellular and molecular mechanisms controlling RGP behavior and proliferation dynamics
in neurogenesis and glia generation remain unknown. By using mosaic analysis with
double markers (MADM)-based genetic paradigms enabling the sparse and global knockout
with unprecedented single-cell resolution, we identified Lgl1 as a critical regulatory
component. We uncover Lgl1-dependent tissue-wide community effects required for
embryonic cortical neurogenesis and novel cell-autonomous Lgl1 functions controlling
RGP-mediated glia genesis and postnatal NSC behavior. These results suggest that
NSC-mediated neuron and glia production is tightly regulated through the concerted
interplay of sequential Lgl1-dependent global and cell intrinsic mechanisms.
acknowledged_ssus:
- _id: Bio
- _id: PreCl
article_processing_charge: No
author:
- first_name: Robert J
full_name: Beattie, Robert J
id: 2E26DF60-F248-11E8-B48F-1D18A9856A87
last_name: Beattie
orcid: 0000-0002-8483-8753
- first_name: Maria P
full_name: Postiglione, Maria P
id: 2C67902A-F248-11E8-B48F-1D18A9856A87
last_name: Postiglione
- first_name: Laura
full_name: Burnett, Laura
id: 3B717F68-F248-11E8-B48F-1D18A9856A87
last_name: Burnett
orcid: 0000-0002-8937-410X
- first_name: Susanne
full_name: Laukoter, Susanne
id: 2D6B7A9A-F248-11E8-B48F-1D18A9856A87
last_name: Laukoter
orcid: 0000-0002-7903-3010
- first_name: Carmen
full_name: Streicher, Carmen
id: 36BCB99C-F248-11E8-B48F-1D18A9856A87
last_name: Streicher
- first_name: Florian
full_name: Pauler, Florian
id: 48EA0138-F248-11E8-B48F-1D18A9856A87
last_name: Pauler
orcid: 0000-0002-7462-0048
- first_name: Guanxi
full_name: Xiao, Guanxi
last_name: Xiao
- first_name: Olga
full_name: Klezovitch, Olga
last_name: Klezovitch
- first_name: Valeri
full_name: Vasioukhin, Valeri
last_name: Vasioukhin
- first_name: Troy
full_name: Ghashghaei, Troy
last_name: Ghashghaei
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Beattie RJ, Postiglione MP, Burnett L, et al. Mosaic analysis with double markers
reveals distinct sequential functions of Lgl1 in neural stem cells. Neuron.
2017;94(3):517-533.e3. doi:10.1016/j.neuron.2017.04.012
apa: Beattie, R. J., Postiglione, M. P., Burnett, L., Laukoter, S., Streicher, C.,
Pauler, F., … Hippenmeyer, S. (2017). Mosaic analysis with double markers reveals
distinct sequential functions of Lgl1 in neural stem cells. Neuron. Cell
Press. https://doi.org/10.1016/j.neuron.2017.04.012
chicago: Beattie, Robert J, Maria P Postiglione, Laura Burnett, Susanne Laukoter,
Carmen Streicher, Florian Pauler, Guanxi Xiao, et al. “Mosaic Analysis with Double
Markers Reveals Distinct Sequential Functions of Lgl1 in Neural Stem Cells.” Neuron.
Cell Press, 2017. https://doi.org/10.1016/j.neuron.2017.04.012.
ieee: R. J. Beattie et al., “Mosaic analysis with double markers reveals
distinct sequential functions of Lgl1 in neural stem cells,” Neuron, vol.
94, no. 3. Cell Press, p. 517–533.e3, 2017.
ista: Beattie RJ, Postiglione MP, Burnett L, Laukoter S, Streicher C, Pauler F,
Xiao G, Klezovitch O, Vasioukhin V, Ghashghaei T, Hippenmeyer S. 2017. Mosaic
analysis with double markers reveals distinct sequential functions of Lgl1 in
neural stem cells. Neuron. 94(3), 517–533.e3.
mla: Beattie, Robert J., et al. “Mosaic Analysis with Double Markers Reveals Distinct
Sequential Functions of Lgl1 in Neural Stem Cells.” Neuron, vol. 94, no.
3, Cell Press, 2017, p. 517–533.e3, doi:10.1016/j.neuron.2017.04.012.
short: R.J. Beattie, M.P. Postiglione, L. Burnett, S. Laukoter, C. Streicher, F.
Pauler, G. Xiao, O. Klezovitch, V. Vasioukhin, T. Ghashghaei, S. Hippenmeyer,
Neuron 94 (2017) 517–533.e3.
date_created: 2018-12-11T11:49:20Z
date_published: 2017-05-03T00:00:00Z
date_updated: 2023-09-26T15:37:02Z
day: '03'
department:
- _id: SiHi
- _id: MaJö
doi: 10.1016/j.neuron.2017.04.012
ec_funded: 1
external_id:
isi:
- '000400466700011'
intvolume: ' 94'
isi: 1
issue: '3'
language:
- iso: eng
month: '05'
oa_version: None
page: 517 - 533.e3
project:
- _id: 25D61E48-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '618444'
name: Molecular Mechanisms of Cerebral Cortex Development
- _id: 25D7962E-B435-11E9-9278-68D0E5697425
grant_number: RGP0053/2014
name: Quantitative Structure-Function Analysis of Cerebral Cortex Assembly at Clonal
Level
publication: Neuron
publication_identifier:
issn:
- '08966273'
publication_status: published
publisher: Cell Press
publist_id: '6473'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Mosaic analysis with double markers reveals distinct sequential functions of
Lgl1 in neural stem cells
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 94
year: '2017'
...
---
_id: '805'
abstract:
- lang: eng
text: During corticogenesis, distinct classes of neurons are born from progenitor
cells located in the ventricular and subventricular zones, from where they migrate
towards the pial surface to assemble into highly organized layer-specific circuits.
However, the precise and coordinated transcriptional network activity defining
neuronal identity is still not understood. Here, we show that genetic depletion
of the basic helix-loop-helix (bHLH) transcription factor E2A splice variant E47
increased the number of Tbr1-positive deep layer and Satb2-positive upper layer
neurons at E14.5, while depletion of the alternatively spliced E12 variant did
not affect layer-specific neurogenesis. While ChIP-Seq identified a big overlap
for E12- and E47-specific binding sites in embryonic NSCs, including sites at
the cyclin-dependent kinase inhibitor (CDKI) Cdkn1c gene locus, RNA-Seq revealed
a unique transcriptional regulation by each splice variant. E47 activated the
expression of the CDKI Cdkn1c through binding to a distal enhancer. Finally, overexpression
of E47 in embryonic NSCs in vitro impaired neurite outgrowth and E47 overexpression
in vivo by in utero electroporation disturbed proper layer-specific neurogenesis
and upregulated p57(KIP2) expression. Overall, this study identified E2A target
genes in embryonic NSCs and demonstrates that E47 regulates neuronal differentiation
via p57(KIP2).
article_processing_charge: No
author:
- first_name: Sabrina
full_name: Pfurr, Sabrina
last_name: Pfurr
- first_name: Yu
full_name: Chu, Yu
last_name: Chu
- first_name: Christian
full_name: Bohrer, Christian
last_name: Bohrer
- first_name: Franziska
full_name: Greulich, Franziska
last_name: Greulich
- first_name: Robert J
full_name: Beattie, Robert J
id: 2E26DF60-F248-11E8-B48F-1D18A9856A87
last_name: Beattie
orcid: 0000-0002-8483-8753
- first_name: Könül
full_name: Mammadzada, Könül
last_name: Mammadzada
- first_name: Miriam
full_name: Hils, Miriam
last_name: Hils
- first_name: Sebastian
full_name: Arnold, Sebastian
last_name: Arnold
- first_name: Verdon
full_name: Taylor, Verdon
last_name: Taylor
- first_name: Kristina
full_name: Schachtrup, Kristina
last_name: Schachtrup
- first_name: N Henriette
full_name: Uhlenhaut, N Henriette
last_name: Uhlenhaut
- first_name: Christian
full_name: Schachtrup, Christian
last_name: Schachtrup
citation:
ama: Pfurr S, Chu Y, Bohrer C, et al. The E2A splice variant E47 regulates the differentiation
of projection neurons via p57(KIP2) during cortical development. Development.
2017;144:3917-3931. doi:10.1242/dev.145698
apa: Pfurr, S., Chu, Y., Bohrer, C., Greulich, F., Beattie, R. J., Mammadzada, K.,
… Schachtrup, C. (2017). The E2A splice variant E47 regulates the differentiation
of projection neurons via p57(KIP2) during cortical development. Development.
Company of Biologists. https://doi.org/10.1242/dev.145698
chicago: Pfurr, Sabrina, Yu Chu, Christian Bohrer, Franziska Greulich, Robert J
Beattie, Könül Mammadzada, Miriam Hils, et al. “The E2A Splice Variant E47 Regulates
the Differentiation of Projection Neurons via P57(KIP2) during Cortical Development.”
Development. Company of Biologists, 2017. https://doi.org/10.1242/dev.145698.
ieee: S. Pfurr et al., “The E2A splice variant E47 regulates the differentiation
of projection neurons via p57(KIP2) during cortical development,” Development,
vol. 144. Company of Biologists, pp. 3917–3931, 2017.
ista: Pfurr S, Chu Y, Bohrer C, Greulich F, Beattie RJ, Mammadzada K, Hils M, Arnold
S, Taylor V, Schachtrup K, Uhlenhaut NH, Schachtrup C. 2017. The E2A splice variant
E47 regulates the differentiation of projection neurons via p57(KIP2) during cortical
development. Development. 144, 3917–3931.
mla: Pfurr, Sabrina, et al. “The E2A Splice Variant E47 Regulates the Differentiation
of Projection Neurons via P57(KIP2) during Cortical Development.” Development,
vol. 144, Company of Biologists, 2017, pp. 3917–31, doi:10.1242/dev.145698.
short: S. Pfurr, Y. Chu, C. Bohrer, F. Greulich, R.J. Beattie, K. Mammadzada, M.
Hils, S. Arnold, V. Taylor, K. Schachtrup, N.H. Uhlenhaut, C. Schachtrup, Development
144 (2017) 3917–3931.
date_created: 2018-12-11T11:48:36Z
date_published: 2017-10-31T00:00:00Z
date_updated: 2023-09-26T16:20:09Z
day: '31'
department:
- _id: SiHi
doi: 10.1242/dev.145698
external_id:
isi:
- '000414025600007'
intvolume: ' 144'
isi: 1
language:
- iso: eng
month: '10'
oa_version: None
page: 3917 - 3931
publication: Development
publication_status: published
publisher: Company of Biologists
publist_id: '6846'
quality_controlled: '1'
scopus_import: '1'
status: public
title: The E2A splice variant E47 regulates the differentiation of projection neurons
via p57(KIP2) during cortical development
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 144
year: '2017'
...
---
_id: '621'
abstract:
- lang: eng
text: The mammalian cerebral cortex is responsible for higher cognitive functions
such as perception, consciousness, and acquiring and processing information. The
neocortex is organized into six distinct laminae, each composed of a rich diversity
of cell types which assemble into highly complex cortical circuits. Radial glia
progenitors (RGPs) are responsible for producing all neocortical neurons and certain
glia lineages. Here, we discuss recent discoveries emerging from clonal lineage
analysis at the single RGP cell level that provide us with an inaugural quantitative
framework of RGP lineage progression. We further discuss the importance of the
relative contribution of intrinsic gene functions and non-cell-autonomous or community
effects in regulating RGP proliferation behavior and lineage progression.
article_processing_charge: Yes (in subscription journal)
author:
- first_name: Robert J
full_name: Beattie, Robert J
id: 2E26DF60-F248-11E8-B48F-1D18A9856A87
last_name: Beattie
orcid: 0000-0002-8483-8753
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Beattie RJ, Hippenmeyer S. Mechanisms of radial glia progenitor cell lineage
progression. FEBS letters. 2017;591(24):3993-4008. doi:10.1002/1873-3468.12906
apa: Beattie, R. J., & Hippenmeyer, S. (2017). Mechanisms of radial glia progenitor
cell lineage progression. FEBS Letters. Wiley-Blackwell. https://doi.org/10.1002/1873-3468.12906
chicago: Beattie, Robert J, and Simon Hippenmeyer. “Mechanisms of Radial Glia Progenitor
Cell Lineage Progression.” FEBS Letters. Wiley-Blackwell, 2017. https://doi.org/10.1002/1873-3468.12906.
ieee: R. J. Beattie and S. Hippenmeyer, “Mechanisms of radial glia progenitor cell
lineage progression,” FEBS letters, vol. 591, no. 24. Wiley-Blackwell,
pp. 3993–4008, 2017.
ista: Beattie RJ, Hippenmeyer S. 2017. Mechanisms of radial glia progenitor cell
lineage progression. FEBS letters. 591(24), 3993–4008.
mla: Beattie, Robert J., and Simon Hippenmeyer. “Mechanisms of Radial Glia Progenitor
Cell Lineage Progression.” FEBS Letters, vol. 591, no. 24, Wiley-Blackwell,
2017, pp. 3993–4008, doi:10.1002/1873-3468.12906.
short: R.J. Beattie, S. Hippenmeyer, FEBS Letters 591 (2017) 3993–4008.
date_created: 2018-12-11T11:47:32Z
date_published: 2017-12-01T00:00:00Z
date_updated: 2024-02-14T12:02:08Z
day: '01'
ddc:
- '571'
- '610'
department:
- _id: SiHi
doi: 10.1002/1873-3468.12906
ec_funded: 1
external_id:
pmid:
- '29121403'
file:
- access_level: open_access
checksum: a46dadc84e0c28d389dd3e9e954464db
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:16:24Z
date_updated: 2020-07-14T12:47:24Z
file_id: '5211'
file_name: IST-2018-928-v1+1_Beattie_et_al-2017-FEBS_Letters.pdf
file_size: 644149
relation: main_file
file_date_updated: 2020-07-14T12:47:24Z
has_accepted_license: '1'
intvolume: ' 591'
issue: '24'
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
page: 3993 - 4008
pmid: 1
project:
- _id: 25D7962E-B435-11E9-9278-68D0E5697425
grant_number: RGP0053/2014
name: Quantitative Structure-Function Analysis of Cerebral Cortex Assembly at Clonal
Level
- _id: 25D61E48-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '618444'
name: Molecular Mechanisms of Cerebral Cortex Development
publication: FEBS letters
publication_identifier:
issn:
- '00145793'
publication_status: published
publisher: Wiley-Blackwell
publist_id: '7183'
pubrep_id: '928'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Mechanisms of radial glia progenitor cell lineage progression
tmp:
image: /images/cc_by_nc.png
legal_code_url: https://creativecommons.org/licenses/by-nc/4.0/legalcode
name: Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)
short: CC BY-NC (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 591
year: '2017'
...
---
_id: '960'
abstract:
- lang: eng
text: The human cerebral cortex is the seat of our cognitive abilities and composed
of an extraordinary number of neurons, organized in six distinct layers. The establishment
of specific morphological and physiological features in individual neurons needs
to be regulated with high precision. Impairments in the sequential developmental
programs instructing corticogenesis lead to alterations in the cortical cytoarchitecture
which is thought to represent the major underlying cause for several neurological
disorders including neurodevelopmental and psychiatric diseases. In this review
we discuss the role of cell polarity at sequential stages during cortex development.
We first provide an overview of morphological cell polarity features in cortical
neural stem cells and newly-born postmitotic neurons. We then synthesize a conceptual
molecular and biochemical framework how cell polarity is established at the cellular
level through a break in symmetry in nascent cortical projection neurons. Lastly
we provide a perspective how the molecular mechanisms applying to single cells
could be probed and integrated in an in vivo and tissue-wide context.
article_number: '176'
article_processing_charge: Yes
author:
- first_name: Andi H
full_name: Hansen, Andi H
id: 38853E16-F248-11E8-B48F-1D18A9856A87
last_name: Hansen
- first_name: Christian F
full_name: Düllberg, Christian F
id: 459064DC-F248-11E8-B48F-1D18A9856A87
last_name: Düllberg
orcid: 0000-0001-6335-9748
- first_name: Christine
full_name: Mieck, Christine
id: 34CAE85C-F248-11E8-B48F-1D18A9856A87
last_name: Mieck
orcid: 0000-0003-1919-7416
- first_name: Martin
full_name: Loose, Martin
id: 462D4284-F248-11E8-B48F-1D18A9856A87
last_name: Loose
orcid: 0000-0001-7309-9724
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Hansen AH, Düllberg CF, Mieck C, Loose M, Hippenmeyer S. Cell polarity in cerebral
cortex development - cellular architecture shaped by biochemical networks. Frontiers
in Cellular Neuroscience. 2017;11. doi:10.3389/fncel.2017.00176
apa: Hansen, A. H., Düllberg, C. F., Mieck, C., Loose, M., & Hippenmeyer, S.
(2017). Cell polarity in cerebral cortex development - cellular architecture shaped
by biochemical networks. Frontiers in Cellular Neuroscience. Frontiers
Research Foundation. https://doi.org/10.3389/fncel.2017.00176
chicago: Hansen, Andi H, Christian F Düllberg, Christine Mieck, Martin Loose, and
Simon Hippenmeyer. “Cell Polarity in Cerebral Cortex Development - Cellular Architecture
Shaped by Biochemical Networks.” Frontiers in Cellular Neuroscience. Frontiers
Research Foundation, 2017. https://doi.org/10.3389/fncel.2017.00176.
ieee: A. H. Hansen, C. F. Düllberg, C. Mieck, M. Loose, and S. Hippenmeyer, “Cell
polarity in cerebral cortex development - cellular architecture shaped by biochemical
networks,” Frontiers in Cellular Neuroscience, vol. 11. Frontiers Research
Foundation, 2017.
ista: Hansen AH, Düllberg CF, Mieck C, Loose M, Hippenmeyer S. 2017. Cell polarity
in cerebral cortex development - cellular architecture shaped by biochemical networks.
Frontiers in Cellular Neuroscience. 11, 176.
mla: Hansen, Andi H., et al. “Cell Polarity in Cerebral Cortex Development - Cellular
Architecture Shaped by Biochemical Networks.” Frontiers in Cellular Neuroscience,
vol. 11, 176, Frontiers Research Foundation, 2017, doi:10.3389/fncel.2017.00176.
short: A.H. Hansen, C.F. Düllberg, C. Mieck, M. Loose, S. Hippenmeyer, Frontiers
in Cellular Neuroscience 11 (2017).
date_created: 2018-12-11T11:49:25Z
date_published: 2017-06-28T00:00:00Z
date_updated: 2024-03-29T23:30:40Z
day: '28'
ddc:
- '570'
department:
- _id: SiHi
- _id: MaLo
doi: 10.3389/fncel.2017.00176
ec_funded: 1
external_id:
isi:
- '000404486700001'
file:
- access_level: open_access
checksum: dc1f5a475b918d09a0f9f587400b1626
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:09:40Z
date_updated: 2020-07-14T12:48:16Z
file_id: '4764'
file_name: IST-2017-830-v1+1_2017_Hansen_CellPolarity.pdf
file_size: 2153858
relation: main_file
file_date_updated: 2020-07-14T12:48:16Z
has_accepted_license: '1'
intvolume: ' 11'
isi: 1
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
project:
- _id: 25D61E48-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '618444'
name: Molecular Mechanisms of Cerebral Cortex Development
- _id: 25D7962E-B435-11E9-9278-68D0E5697425
grant_number: RGP0053/2014
name: Quantitative Structure-Function Analysis of Cerebral Cortex Assembly at Clonal
Level
- _id: 25681D80-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '291734'
name: International IST Postdoc Fellowship Programme
- _id: 25985A36-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: T00817-B21
name: The biochemical basis of PAR polarization
publication: Frontiers in Cellular Neuroscience
publication_identifier:
issn:
- '16625102'
publication_status: published
publisher: Frontiers Research Foundation
publist_id: '6445'
pubrep_id: '830'
quality_controlled: '1'
related_material:
record:
- id: '9962'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Cell polarity in cerebral cortex development - cellular architecture shaped
by biochemical networks
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 11
year: '2017'
...
---
_id: '1181'
abstract:
- lang: eng
text: 'This review accompanies a 2016 SFN mini-symposium presenting examples of
current studies that address a central question: How do neural stem cells (NSCs)
divide in different ways to produce heterogeneous daughter types at the right
time and in proper numbers to build a cerebral cortex with the appropriate size
and structure? We will focus on four aspects of corticogenesis: cytokinesis events
that follow apical mitoses of NSCs; coordinating abscission with delamination
from the apical membrane; timing of neurogenesis and its indirect regulation through
emergence of intermediate progenitors; and capacity of single NSCs to generate
the correct number and laminar fate of cortical neurons. Defects in these mechanisms
can cause microcephaly and other brain malformations, and understanding them is
critical to designing diagnostic tools and preventive and corrective therapies.'
acknowledgement: This work was supported by National Institutes of Health Grants R01NS089795
and R01NS098370 to H.T.G., R01NS076640 to N.D.D., and R01MH094589 and R01NS089777
to B.C., Academia Sinica AS-104-TPB09-2 to S.-J.C, European Union FP7-CIG618444
and Human Frontiers Science Program RGP0053 to S.H., and Fonds Léon Fredericq, from
the Fondation Médicale Reine Elisabeth, and from the Fonation Simone et Pierre Clerdent
to L.N. The authors apologize to colleagues whose work could not be cited due to
space limitations.
author:
- first_name: Noelle
full_name: Dwyer, Noelle
last_name: Dwyer
- first_name: Bin
full_name: Chen, Bin
last_name: Chen
- first_name: Shen
full_name: Chou, Shen
last_name: Chou
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Laurent
full_name: Nguyen, Laurent
last_name: Nguyen
- first_name: Troy
full_name: Ghashghaei, Troy
last_name: Ghashghaei
citation:
ama: 'Dwyer N, Chen B, Chou S, Hippenmeyer S, Nguyen L, Ghashghaei T. Neural stem
cells to cerebral cortex: Emerging mechanisms regulating progenitor behavior and
productivity. Journal of Neuroscience. 2016;36(45):11394-11401. doi:10.1523/JNEUROSCI.2359-16.2016'
apa: 'Dwyer, N., Chen, B., Chou, S., Hippenmeyer, S., Nguyen, L., & Ghashghaei,
T. (2016). Neural stem cells to cerebral cortex: Emerging mechanisms regulating
progenitor behavior and productivity. Journal of Neuroscience. Society
for Neuroscience. https://doi.org/10.1523/JNEUROSCI.2359-16.2016'
chicago: 'Dwyer, Noelle, Bin Chen, Shen Chou, Simon Hippenmeyer, Laurent Nguyen,
and Troy Ghashghaei. “Neural Stem Cells to Cerebral Cortex: Emerging Mechanisms
Regulating Progenitor Behavior and Productivity.” Journal of Neuroscience.
Society for Neuroscience, 2016. https://doi.org/10.1523/JNEUROSCI.2359-16.2016.'
ieee: 'N. Dwyer, B. Chen, S. Chou, S. Hippenmeyer, L. Nguyen, and T. Ghashghaei,
“Neural stem cells to cerebral cortex: Emerging mechanisms regulating progenitor
behavior and productivity,” Journal of Neuroscience, vol. 36, no. 45. Society
for Neuroscience, pp. 11394–11401, 2016.'
ista: 'Dwyer N, Chen B, Chou S, Hippenmeyer S, Nguyen L, Ghashghaei T. 2016. Neural
stem cells to cerebral cortex: Emerging mechanisms regulating progenitor behavior
and productivity. Journal of Neuroscience. 36(45), 11394–11401.'
mla: 'Dwyer, Noelle, et al. “Neural Stem Cells to Cerebral Cortex: Emerging Mechanisms
Regulating Progenitor Behavior and Productivity.” Journal of Neuroscience,
vol. 36, no. 45, Society for Neuroscience, 2016, pp. 11394–401, doi:10.1523/JNEUROSCI.2359-16.2016.'
short: N. Dwyer, B. Chen, S. Chou, S. Hippenmeyer, L. Nguyen, T. Ghashghaei, Journal
of Neuroscience 36 (2016) 11394–11401.
date_created: 2018-12-11T11:50:35Z
date_published: 2016-11-09T00:00:00Z
date_updated: 2021-01-12T06:48:54Z
day: '09'
department:
- _id: SiHi
doi: 10.1523/JNEUROSCI.2359-16.2016
intvolume: ' 36'
issue: '45'
language:
- iso: eng
month: '11'
oa_version: None
page: 11394 - 11401
project:
- _id: 25D7962E-B435-11E9-9278-68D0E5697425
grant_number: RGP0053/2014
name: Quantitative Structure-Function Analysis of Cerebral Cortex Assembly at Clonal
Level
publication: Journal of Neuroscience
publication_status: published
publisher: Society for Neuroscience
publist_id: '6172'
quality_controlled: '1'
scopus_import: 1
status: public
title: 'Neural stem cells to cerebral cortex: Emerging mechanisms regulating progenitor
behavior and productivity'
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 36
year: '2016'
...
---
_id: '1488'
abstract:
- lang: eng
text: Branching morphogenesis of the epithelial ureteric bud forms the renal collecting
duct system and is critical for normal nephron number, while low nephron number
is implicated in hypertension and renal disease. Ureteric bud growth and branching
requires GDNF signaling from the surrounding mesenchyme to cells at the ureteric
bud tips, via the Ret receptor tyrosine kinase and coreceptor Gfrα1; Ret signaling
up-regulates transcription factors Etv4 and Etv5, which are also critical for
branching. Despite extensive knowledge of the genetic control of these events,
it is not understood, at the cellular level, how renal branching morphogenesis
is achieved or how Ret signaling influences epithelial cell behaviors to promote
this process. Analysis of chimeric embryos previously suggested a role for Ret
signaling in promoting cell rearrangements in the nephric duct, but this method
was unsuited to study individual cell behaviors during ureteric bud branching.
Here, we use Mosaic Analysis with Double Markers (MADM), combined with organ culture
and time-lapse imaging, to trace the movements and divisions of individual ureteric
bud tip cells. We first examine wild-type clones and then Ret or Etv4 mutant/wild-type
clones in which the mutant and wild-type sister cells are differentially and heritably
marked by green and red fluorescent proteins. We find that, in normal kidneys,
most individual tip cells behave as self-renewing progenitors, some of whose progeny
remain at the tips while others populate the growing UB trunks. In Ret or Etv4
MADM clones, the wild-type cells generated at a UB tip are much more likely to
remain at, or move to, the new tips during branching and elongation, while their
Ret−/− or Etv4−/− sister cells tend to lag behind and contribute only to the trunks.
By tracking successive mitoses in a cell lineage, we find that Ret signaling has
little effect on proliferation, in contrast to its effects on cell movement. Our
results show that Ret/Etv4 signaling promotes directed cell movements in the ureteric
bud tips, and suggest a model in which these cell movements mediate branching
morphogenesis.
acknowledgement: We thank Silvia Arber, Thomas Jessell, Kenneth M. Murphy, Carlton
Bates, Hideki Enomoto, Liqun Luo and Andrew McMahon for mouse strains; Thomas Jessell
for antibodies; and Laura Martinez Prat for experimental assistance.
article_number: e1002382
author:
- first_name: Paul
full_name: Riccio, Paul
last_name: Riccio
- first_name: Cristina
full_name: Cebrián, Cristina
last_name: Cebrián
- first_name: Hui
full_name: Zong, Hui
last_name: Zong
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Frank
full_name: Costantini, Frank
last_name: Costantini
citation:
ama: Riccio P, Cebrián C, Zong H, Hippenmeyer S, Costantini F. Ret and Etv4 promote
directed movements of progenitor cells during renal branching morphogenesis. PLoS
Biology. 2016;14(2). doi:10.1371/journal.pbio.1002382
apa: Riccio, P., Cebrián, C., Zong, H., Hippenmeyer, S., & Costantini, F. (2016).
Ret and Etv4 promote directed movements of progenitor cells during renal branching
morphogenesis. PLoS Biology. Public Library of Science. https://doi.org/10.1371/journal.pbio.1002382
chicago: Riccio, Paul, Cristina Cebrián, Hui Zong, Simon Hippenmeyer, and Frank
Costantini. “Ret and Etv4 Promote Directed Movements of Progenitor Cells during
Renal Branching Morphogenesis.” PLoS Biology. Public Library of Science,
2016. https://doi.org/10.1371/journal.pbio.1002382.
ieee: P. Riccio, C. Cebrián, H. Zong, S. Hippenmeyer, and F. Costantini, “Ret and
Etv4 promote directed movements of progenitor cells during renal branching morphogenesis,”
PLoS Biology, vol. 14, no. 2. Public Library of Science, 2016.
ista: Riccio P, Cebrián C, Zong H, Hippenmeyer S, Costantini F. 2016. Ret and Etv4
promote directed movements of progenitor cells during renal branching morphogenesis.
PLoS Biology. 14(2), e1002382.
mla: Riccio, Paul, et al. “Ret and Etv4 Promote Directed Movements of Progenitor
Cells during Renal Branching Morphogenesis.” PLoS Biology, vol. 14, no.
2, e1002382, Public Library of Science, 2016, doi:10.1371/journal.pbio.1002382.
short: P. Riccio, C. Cebrián, H. Zong, S. Hippenmeyer, F. Costantini, PLoS Biology
14 (2016).
date_created: 2018-12-11T11:52:19Z
date_published: 2016-02-19T00:00:00Z
date_updated: 2023-02-23T10:01:08Z
day: '19'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1371/journal.pbio.1002382
file:
- access_level: open_access
checksum: 7f8fa1b3a29f94c0a14dd4465278cdbc
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:13:42Z
date_updated: 2020-07-14T12:44:57Z
file_id: '5027'
file_name: IST-2016-517-v1+1_journal.pbio.1002382_1_.PDF
file_size: 5904773
relation: main_file
file_date_updated: 2020-07-14T12:44:57Z
has_accepted_license: '1'
intvolume: ' 14'
issue: '2'
language:
- iso: eng
month: '02'
oa: 1
oa_version: Published Version
publication: PLoS Biology
publication_status: published
publisher: Public Library of Science
publist_id: '5699'
pubrep_id: '517'
quality_controlled: '1'
related_material:
record:
- id: '9703'
relation: research_data
status: deleted
scopus_import: 1
status: public
title: Ret and Etv4 promote directed movements of progenitor cells during renal branching
morphogenesis
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 14
year: '2016'
...
---
_id: '1550'
abstract:
- lang: eng
text: The medial ganglionic eminence (MGE) gives rise to the majority of mouse forebrain
interneurons. Here, we examine the lineage relationship among MGE-derived interneurons
using a replication-defective retroviral library containing a highly diverse set
of DNA barcodes. Recovering the barcodes from the mature progeny of infected progenitor
cells enabled us to unambiguously determine their respective lineal relationship.
We found that clonal dispersion occurs across large areas of the brain and is
not restricted by anatomical divisions. As such, sibling interneurons can populate
the cortex, hippocampus striatum, and globus pallidus. The majority of interneurons
appeared to be generated from asymmetric divisions of MGE progenitor cells, followed
by symmetric divisions within the subventricular zone. Altogether, our findings
uncover that lineage relationships do not appear to determine interneuron allocation
to particular regions. As such, it is likely that clonally related interneurons
have considerable flexibility as to the particular forebrain circuits to which
they can contribute.
acknowledgement: "Research in the G.F. laboratory is supported by NIH (NS 081297,
MH095147, and P01NS074972) and the Simons Foundation. Research in the S.H. laboratory
is supported by the European Union (FP7-CIG618444). C.M. is supported by EMBO ALTF
(1295-2012). X.H.J. is supported by EMBO (ALTF 303-2010) and HFSP (LT000078/2011-L).\r\n\r\n"
author:
- first_name: Christian
full_name: Mayer, Christian
last_name: Mayer
- first_name: Xavier
full_name: Jaglin, Xavier
last_name: Jaglin
- first_name: Lucy
full_name: Cobbs, Lucy
last_name: Cobbs
- first_name: Rachel
full_name: Bandler, Rachel
last_name: Bandler
- first_name: Carmen
full_name: Streicher, Carmen
id: 36BCB99C-F248-11E8-B48F-1D18A9856A87
last_name: Streicher
- first_name: Constance
full_name: Cepko, Constance
last_name: Cepko
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Gord
full_name: Fishell, Gord
last_name: Fishell
citation:
ama: Mayer C, Jaglin X, Cobbs L, et al. Clonally related forebrain interneurons
disperse broadly across both functional areas and structural boundaries. Neuron.
2015;87(5):989-998. doi:10.1016/j.neuron.2015.07.011
apa: Mayer, C., Jaglin, X., Cobbs, L., Bandler, R., Streicher, C., Cepko, C., …
Fishell, G. (2015). Clonally related forebrain interneurons disperse broadly across
both functional areas and structural boundaries. Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2015.07.011
chicago: Mayer, Christian, Xavier Jaglin, Lucy Cobbs, Rachel Bandler, Carmen Streicher,
Constance Cepko, Simon Hippenmeyer, and Gord Fishell. “Clonally Related Forebrain
Interneurons Disperse Broadly across Both Functional Areas and Structural Boundaries.”
Neuron. Elsevier, 2015. https://doi.org/10.1016/j.neuron.2015.07.011.
ieee: C. Mayer et al., “Clonally related forebrain interneurons disperse
broadly across both functional areas and structural boundaries,” Neuron,
vol. 87, no. 5. Elsevier, pp. 989–998, 2015.
ista: Mayer C, Jaglin X, Cobbs L, Bandler R, Streicher C, Cepko C, Hippenmeyer S,
Fishell G. 2015. Clonally related forebrain interneurons disperse broadly across
both functional areas and structural boundaries. Neuron. 87(5), 989–998.
mla: Mayer, Christian, et al. “Clonally Related Forebrain Interneurons Disperse
Broadly across Both Functional Areas and Structural Boundaries.” Neuron,
vol. 87, no. 5, Elsevier, 2015, pp. 989–98, doi:10.1016/j.neuron.2015.07.011.
short: C. Mayer, X. Jaglin, L. Cobbs, R. Bandler, C. Streicher, C. Cepko, S. Hippenmeyer,
G. Fishell, Neuron 87 (2015) 989–998.
date_created: 2018-12-11T11:52:40Z
date_published: 2015-09-02T00:00:00Z
date_updated: 2021-01-12T06:51:32Z
day: '02'
department:
- _id: SiHi
doi: 10.1016/j.neuron.2015.07.011
external_id:
pmid:
- '26299473'
intvolume: ' 87'
issue: '5'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4560602/
month: '09'
oa: 1
oa_version: Submitted Version
page: 989 - 998
pmid: 1
publication: Neuron
publication_status: published
publisher: Elsevier
publist_id: '5621'
quality_controlled: '1'
scopus_import: 1
status: public
title: Clonally related forebrain interneurons disperse broadly across both functional
areas and structural boundaries
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 87
year: '2015'
...
---
_id: '1899'
abstract:
- lang: eng
text: Asymmetric cell divisions allow stem cells to balance proliferation and differentiation.
During embryogenesis, murine epidermis expands rapidly from a single layer of
unspecified basal layer progenitors to a stratified, differentiated epithelium.
Morphogenesis involves perpendicular (asymmetric) divisions and the spindle orientation
protein LGN, but little is known about how the apical localization of LGN is regulated.
Here, we combine conventional genetics and lentiviral-mediated in vivo RNAi to
explore the functions of the LGN-interacting proteins Par3, mInsc and Gα i3. Whereas
loss of each gene alone leads to randomized division angles, combined loss of
Gnai3 and mInsc causes a phenotype of mostly planar divisions, akin to loss of
LGN. These findings lend experimental support for the hitherto untested model
that Par3-mInsc and Gα i3 act cooperatively to polarize LGN and promote perpendicular
divisions. Finally, we uncover a developmental switch between delamination-driven
early stratification and spindle-orientation-dependent differentiation that occurs
around E15, revealing a two-step mechanism underlying epidermal maturation.
article_processing_charge: No
article_type: original
author:
- first_name: Scott
full_name: Williams, Scott
last_name: Williams
- first_name: Lyndsay
full_name: Ratliff, Lyndsay
last_name: Ratliff
- first_name: Maria P
full_name: Postiglione, Maria P
id: 2C67902A-F248-11E8-B48F-1D18A9856A87
last_name: Postiglione
- first_name: Juergen
full_name: Knoblich, Juergen
last_name: Knoblich
- first_name: Elaine
full_name: Fuchs, Elaine
last_name: Fuchs
citation:
ama: Williams S, Ratliff L, Postiglione MP, Knoblich J, Fuchs E. Par3-mInsc and
Gα i3 cooperate to promote oriented epidermal cell divisions through LGN. Nature
Cell Biology. 2014;16(8):758-769. doi:10.1038/ncb3001
apa: Williams, S., Ratliff, L., Postiglione, M. P., Knoblich, J., & Fuchs, E.
(2014). Par3-mInsc and Gα i3 cooperate to promote oriented epidermal cell divisions
through LGN. Nature Cell Biology. Nature Publishing Group. https://doi.org/10.1038/ncb3001
chicago: Williams, Scott, Lyndsay Ratliff, Maria P Postiglione, Juergen Knoblich,
and Elaine Fuchs. “Par3-MInsc and Gα I3 Cooperate to Promote Oriented Epidermal
Cell Divisions through LGN.” Nature Cell Biology. Nature Publishing Group,
2014. https://doi.org/10.1038/ncb3001.
ieee: S. Williams, L. Ratliff, M. P. Postiglione, J. Knoblich, and E. Fuchs, “Par3-mInsc
and Gα i3 cooperate to promote oriented epidermal cell divisions through LGN,”
Nature Cell Biology, vol. 16, no. 8. Nature Publishing Group, pp. 758–769,
2014.
ista: Williams S, Ratliff L, Postiglione MP, Knoblich J, Fuchs E. 2014. Par3-mInsc
and Gα i3 cooperate to promote oriented epidermal cell divisions through LGN.
Nature Cell Biology. 16(8), 758–769.
mla: Williams, Scott, et al. “Par3-MInsc and Gα I3 Cooperate to Promote Oriented
Epidermal Cell Divisions through LGN.” Nature Cell Biology, vol. 16, no.
8, Nature Publishing Group, 2014, pp. 758–69, doi:10.1038/ncb3001.
short: S. Williams, L. Ratliff, M.P. Postiglione, J. Knoblich, E. Fuchs, Nature
Cell Biology 16 (2014) 758–769.
date_created: 2018-12-11T11:54:36Z
date_published: 2014-07-13T00:00:00Z
date_updated: 2021-01-12T06:53:55Z
day: '13'
department:
- _id: SiHi
doi: 10.1038/ncb3001
external_id:
pmid:
- '25016959'
intvolume: ' 16'
issue: '8'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4159251/
month: '07'
oa: 1
oa_version: Submitted Version
page: 758 - 769
pmid: 1
publication: Nature Cell Biology
publication_status: published
publisher: Nature Publishing Group
publist_id: '5196'
quality_controlled: '1'
scopus_import: 1
status: public
title: Par3-mInsc and Gα i3 cooperate to promote oriented epidermal cell divisions
through LGN
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 16
year: '2014'
...
---
_id: '2022'
abstract:
- lang: eng
text: Radial glial progenitors (RGPs) are responsible for producing nearly all neocortical
neurons. To gain insight into the patterns of RGP division and neuron production,
we quantitatively analyzed excitatory neuron genesis in the mouse neocortex using
Mosaic Analysis with Double Markers, which provides single-cell resolution of
progenitor division patterns and potential in vivo. We found that RGPs progress
through a coherent program in which their proliferative potential diminishes in
a predictable manner. Upon entry into the neurogenic phase, individual RGPs produce
∼8–9 neurons distributed in both deep and superficial layers, indicating a unitary
output in neuronal production. Removal of OTX1, a transcription factor transiently
expressed in RGPs, results in both deep- and superficial-layer neuron loss and
a reduction in neuronal unit size. Moreover, ∼1/6 of neurogenic RGPs proceed to
produce glia. These results suggest that progenitor behavior and histogenesis
in the mammalian neocortex conform to a remarkably orderly and deterministic program.
author:
- first_name: Peng
full_name: Gao, Peng
last_name: Gao
- first_name: Maria P
full_name: Postiglione, Maria P
id: 2C67902A-F248-11E8-B48F-1D18A9856A87
last_name: Postiglione
- first_name: Teresa
full_name: Krieger, Teresa
last_name: Krieger
- first_name: Luisirene
full_name: Hernandez, Luisirene
last_name: Hernandez
- first_name: Chao
full_name: Wang, Chao
last_name: Wang
- first_name: Zhi
full_name: Han, Zhi
last_name: Han
- first_name: Carmen
full_name: Streicher, Carmen
id: 36BCB99C-F248-11E8-B48F-1D18A9856A87
last_name: Streicher
- first_name: Ekaterina
full_name: Papusheva, Ekaterina
id: 41DB591E-F248-11E8-B48F-1D18A9856A87
last_name: Papusheva
- first_name: Ryan
full_name: Insolera, Ryan
last_name: Insolera
- first_name: Kritika
full_name: Chugh, Kritika
last_name: Chugh
- first_name: Oren
full_name: Kodish, Oren
last_name: Kodish
- first_name: Kun
full_name: Huang, Kun
last_name: Huang
- first_name: Benjamin
full_name: Simons, Benjamin
last_name: Simons
- first_name: Liqun
full_name: Luo, Liqun
last_name: Luo
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Song
full_name: Shi, Song
last_name: Shi
citation:
ama: Gao P, Postiglione MP, Krieger T, et al. Deterministic progenitor behavior
and unitary production of neurons in the neocortex. Cell. 2014;159(4):775-788.
doi:10.1016/j.cell.2014.10.027
apa: Gao, P., Postiglione, M. P., Krieger, T., Hernandez, L., Wang, C., Han, Z.,
… Shi, S. (2014). Deterministic progenitor behavior and unitary production of
neurons in the neocortex. Cell. Cell Press. https://doi.org/10.1016/j.cell.2014.10.027
chicago: Gao, Peng, Maria P Postiglione, Teresa Krieger, Luisirene Hernandez, Chao
Wang, Zhi Han, Carmen Streicher, et al. “Deterministic Progenitor Behavior and
Unitary Production of Neurons in the Neocortex.” Cell. Cell Press, 2014.
https://doi.org/10.1016/j.cell.2014.10.027.
ieee: P. Gao et al., “Deterministic progenitor behavior and unitary production
of neurons in the neocortex,” Cell, vol. 159, no. 4. Cell Press, pp. 775–788,
2014.
ista: Gao P, Postiglione MP, Krieger T, Hernandez L, Wang C, Han Z, Streicher C,
Papusheva E, Insolera R, Chugh K, Kodish O, Huang K, Simons B, Luo L, Hippenmeyer
S, Shi S. 2014. Deterministic progenitor behavior and unitary production of neurons
in the neocortex. Cell. 159(4), 775–788.
mla: Gao, Peng, et al. “Deterministic Progenitor Behavior and Unitary Production
of Neurons in the Neocortex.” Cell, vol. 159, no. 4, Cell Press, 2014,
pp. 775–88, doi:10.1016/j.cell.2014.10.027.
short: P. Gao, M.P. Postiglione, T. Krieger, L. Hernandez, C. Wang, Z. Han, C. Streicher,
E. Papusheva, R. Insolera, K. Chugh, O. Kodish, K. Huang, B. Simons, L. Luo, S.
Hippenmeyer, S. Shi, Cell 159 (2014) 775–788.
date_created: 2018-12-11T11:55:16Z
date_published: 2014-11-06T00:00:00Z
date_updated: 2021-01-12T06:54:47Z
day: '06'
ddc:
- '570'
department:
- _id: SiHi
- _id: Bio
doi: 10.1016/j.cell.2014.10.027
ec_funded: 1
file:
- access_level: open_access
checksum: 6c5de8329bb2ffa71cba9fda750f14ce
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:08:47Z
date_updated: 2020-07-14T12:45:25Z
file_id: '4709'
file_name: IST-2016-423-v1+1_1-s2.0-S0092867414013154-main.pdf
file_size: 4435787
relation: main_file
file_date_updated: 2020-07-14T12:45:25Z
has_accepted_license: '1'
intvolume: ' 159'
issue: '4'
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
page: 775 - 788
project:
- _id: 25D61E48-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '618444'
name: Molecular Mechanisms of Cerebral Cortex Development
- _id: 25D7962E-B435-11E9-9278-68D0E5697425
grant_number: RGP0053/2014
name: Quantitative Structure-Function Analysis of Cerebral Cortex Assembly at Clonal
Level
publication: Cell
publication_status: published
publisher: Cell Press
publist_id: '5050'
pubrep_id: '423'
quality_controlled: '1'
scopus_import: 1
status: public
title: Deterministic progenitor behavior and unitary production of neurons in the
neocortex
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 159
year: '2014'
...
---
_id: '2020'
abstract:
- lang: eng
text: The mammalian heart has long been considered a postmitotic organ, implying
that the total number of cardiomyocytes is set at birth. Analysis of cell division
in the mammalian heart is complicated by cardiomyocyte binucleation shortly after
birth, which makes it challenging to interpret traditional assays of cell turnover
[Laflamme MA, Murray CE (2011) Nature 473(7347):326–335; Bergmann O, et al. (2009)
Science 324(5923):98–102]. An elegant multi-isotope imaging-mass spectrometry
technique recently calculated the low, discrete rate of cardiomyocyte generation
in mice [Senyo SE, et al. (2013) Nature 493(7432):433–436], yet our cellular-level
understanding of postnatal cardiomyogenesis remains limited. Herein, we provide
a new line of evidence for the differentiated α-myosin heavy chain-expressing
cardiomyocyte as the cell of origin of postnatal cardiomyogenesis using the “mosaic
analysis with double markers” mouse model. We show limited, life-long, symmetric
division of cardiomyocytes as a rare event that is evident in utero but significantly
diminishes after the first month of life in mice; daughter cardiomyocytes divide
very seldom, which this study is the first to demonstrate, to our knowledge. Furthermore,
ligation of the left anterior descending coronary artery, which causes a myocardial
infarction in the mosaic analysis with double-marker mice, did not increase the
rate of cardiomyocyte division above the basal level for up to 4 wk after the
injury. The clonal analysis described here provides direct evidence of postnatal
mammalian cardiomyogenesis.
author:
- first_name: Shah
full_name: Ali, Shah
last_name: Ali
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Lily
full_name: Saadat, Lily
last_name: Saadat
- first_name: Liqun
full_name: Luo, Liqun
last_name: Luo
- first_name: Irving
full_name: Weissman, Irving
last_name: Weissman
- first_name: Reza
full_name: Ardehali, Reza
last_name: Ardehali
citation:
ama: Ali S, Hippenmeyer S, Saadat L, Luo L, Weissman I, Ardehali R. Existing cardiomyocytes
generate cardiomyocytes at a low rate after birth in mice. PNAS. 2014;111(24):8850-8855.
doi:10.1073/pnas.1408233111
apa: Ali, S., Hippenmeyer, S., Saadat, L., Luo, L., Weissman, I., & Ardehali,
R. (2014). Existing cardiomyocytes generate cardiomyocytes at a low rate after
birth in mice. PNAS. National Academy of Sciences. https://doi.org/10.1073/pnas.1408233111
chicago: Ali, Shah, Simon Hippenmeyer, Lily Saadat, Liqun Luo, Irving Weissman,
and Reza Ardehali. “Existing Cardiomyocytes Generate Cardiomyocytes at a Low Rate
after Birth in Mice.” PNAS. National Academy of Sciences, 2014. https://doi.org/10.1073/pnas.1408233111.
ieee: S. Ali, S. Hippenmeyer, L. Saadat, L. Luo, I. Weissman, and R. Ardehali, “Existing
cardiomyocytes generate cardiomyocytes at a low rate after birth in mice,” PNAS,
vol. 111, no. 24. National Academy of Sciences, pp. 8850–8855, 2014.
ista: Ali S, Hippenmeyer S, Saadat L, Luo L, Weissman I, Ardehali R. 2014. Existing
cardiomyocytes generate cardiomyocytes at a low rate after birth in mice. PNAS.
111(24), 8850–8855.
mla: Ali, Shah, et al. “Existing Cardiomyocytes Generate Cardiomyocytes at a Low
Rate after Birth in Mice.” PNAS, vol. 111, no. 24, National Academy of
Sciences, 2014, pp. 8850–55, doi:10.1073/pnas.1408233111.
short: S. Ali, S. Hippenmeyer, L. Saadat, L. Luo, I. Weissman, R. Ardehali, PNAS
111 (2014) 8850–8855.
date_created: 2018-12-11T11:55:15Z
date_published: 2014-06-17T00:00:00Z
date_updated: 2021-01-12T06:54:46Z
day: '17'
department:
- _id: SiHi
doi: 10.1073/pnas.1408233111
intvolume: ' 111'
issue: '24'
language:
- iso: eng
month: '06'
oa_version: None
page: 8850 - 8855
publication: PNAS
publication_status: published
publisher: National Academy of Sciences
publist_id: '5052'
quality_controlled: '1'
scopus_import: 1
status: public
title: Existing cardiomyocytes generate cardiomyocytes at a low rate after birth in
mice
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 111
year: '2014'
...
---
_id: '2021'
abstract:
- lang: eng
text: Neurotrophins regulate diverse aspects of neuronal development and plasticity,
but their precise in vivo functions during neural circuit assembly in the central
brain remain unclear. We show that the neurotrophin receptor tropomyosin-related
kinase C (TrkC) is required for dendritic growth and branching of mouse cerebellar
Purkinje cells. Sparse TrkC knockout reduced dendrite complexity, but global Purkinje
cell knockout had no effect. Removal of the TrkC ligand neurotrophin-3 (NT-3)
from cerebellar granule cells, which provide major afferent input to developing
Purkinje cell dendrites, rescued the dendrite defects caused by sparse TrkC disruption
in Purkinje cells. Our data demonstrate that NT-3 from presynaptic neurons (granule
cells) is required for TrkC-dependent competitive dendrite morphogenesis in postsynaptic
neurons (Purkinje cells)—a previously unknown mechanism of neural circuit development.
author:
- first_name: Joo
full_name: William, Joo
last_name: William
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Liqun
full_name: Luo, Liqun
last_name: Luo
citation:
ama: William J, Hippenmeyer S, Luo L. Dendrite morphogenesis depends on relative
levels of NT-3/TrkC signaling. Science. 2014;346(6209):626-629. doi:10.1126/science.1258996
apa: William, J., Hippenmeyer, S., & Luo, L. (2014). Dendrite morphogenesis
depends on relative levels of NT-3/TrkC signaling. Science. American Association
for the Advancement of Science. https://doi.org/10.1126/science.1258996
chicago: William, Joo, Simon Hippenmeyer, and Liqun Luo. “Dendrite Morphogenesis
Depends on Relative Levels of NT-3/TrkC Signaling.” Science. American Association
for the Advancement of Science, 2014. https://doi.org/10.1126/science.1258996.
ieee: J. William, S. Hippenmeyer, and L. Luo, “Dendrite morphogenesis depends on
relative levels of NT-3/TrkC signaling,” Science, vol. 346, no. 6209. American
Association for the Advancement of Science, pp. 626–629, 2014.
ista: William J, Hippenmeyer S, Luo L. 2014. Dendrite morphogenesis depends on relative
levels of NT-3/TrkC signaling. Science. 346(6209), 626–629.
mla: William, Joo, et al. “Dendrite Morphogenesis Depends on Relative Levels of
NT-3/TrkC Signaling.” Science, vol. 346, no. 6209, American Association
for the Advancement of Science, 2014, pp. 626–29, doi:10.1126/science.1258996.
short: J. William, S. Hippenmeyer, L. Luo, Science 346 (2014) 626–629.
date_created: 2018-12-11T11:55:15Z
date_published: 2014-10-31T00:00:00Z
date_updated: 2021-01-12T06:54:47Z
day: '31'
department:
- _id: SiHi
doi: 10.1126/science.1258996
intvolume: ' 346'
issue: '6209'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4631524/
month: '10'
oa: 1
oa_version: Submitted Version
page: 626 - 629
publication: Science
publication_status: published
publisher: American Association for the Advancement of Science
publist_id: '5051'
quality_controlled: '1'
scopus_import: 1
status: public
title: Dendrite morphogenesis depends on relative levels of NT-3/TrkC signaling
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 346
year: '2014'
...
---
_id: '2261'
abstract:
- lang: eng
text: To reveal the full potential of human pluripotent stem cells, new methods
for rapid, site-specific genomic engineering are needed. Here, we describe a system
for precise genetic modification of human embryonic stem cells (ESCs) and induced
pluripotent stem cells (iPSCs). We identified a novel human locus, H11, located
in a safe, intergenic, transcriptionally active region of chromosome 22, as the
recipient site, to provide robust, ubiquitous expression of inserted genes. Recipient
cell lines were established by site-specific placement of a ‘landing pad’ cassette
carrying attP sites for phiC31 and Bxb1 integrases at the H11 locus by spontaneous
or TALEN-assisted homologous recombination. Dual integrase cassette exchange (DICE)
mediated by phiC31 and Bxb1 integrases was used to insert genes of interest flanked
by phiC31 and Bxb1 attB sites at the H11 locus, replacing the landing pad. This
system provided complete control over content, direction and copy number of inserted
genes, with a specificity of 100%. A series of genes, including mCherry and various
combinations of the neural transcription factors LMX1a, FOXA2 and OTX2, were inserted
in recipient cell lines derived from H9 ESC, as well as iPSC lines derived from
a Parkinson’s disease patient and a normal sibling control. The DICE system offers
rapid, efficient and precise gene insertion in ESC and iPSC and is particularly
well suited for repeated modifications of the same locus.
acknowledgement: "California Institute for Regenerative Medicine [RT2-01880 and TR2-01756].
Funding for open access charge: California Institute for Regenerative Medicine [RT2-01880
and TR2-01756]\r\nCC BY 3,0"
article_number: e34
author:
- first_name: Fangfang
full_name: Zhu, Fangfang
last_name: Zhu
- first_name: Matthew
full_name: Gamboa, Matthew
last_name: Gamboa
- first_name: Alfonso
full_name: Farruggio, Alfonso
last_name: Farruggio
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Bosiljka
full_name: Tasic, Bosiljka
last_name: Tasic
- first_name: Birgitt
full_name: Schüle, Birgitt
last_name: Schüle
- first_name: Yanru
full_name: Chen Tsai, Yanru
last_name: Chen Tsai
- first_name: Michele
full_name: Calos, Michele
last_name: Calos
citation:
ama: Zhu F, Gamboa M, Farruggio A, et al. DICE, an efficient system for iterative
genomic editing in human pluripotent stem cells. Nucleic Acids Research.
2014;42(5). doi:10.1093/nar/gkt1290
apa: Zhu, F., Gamboa, M., Farruggio, A., Hippenmeyer, S., Tasic, B., Schüle, B.,
… Calos, M. (2014). DICE, an efficient system for iterative genomic editing in
human pluripotent stem cells. Nucleic Acids Research. Oxford University
Press. https://doi.org/10.1093/nar/gkt1290
chicago: Zhu, Fangfang, Matthew Gamboa, Alfonso Farruggio, Simon Hippenmeyer, Bosiljka
Tasic, Birgitt Schüle, Yanru Chen Tsai, and Michele Calos. “DICE, an Efficient
System for Iterative Genomic Editing in Human Pluripotent Stem Cells.” Nucleic
Acids Research. Oxford University Press, 2014. https://doi.org/10.1093/nar/gkt1290.
ieee: F. Zhu et al., “DICE, an efficient system for iterative genomic editing
in human pluripotent stem cells,” Nucleic Acids Research, vol. 42, no.
5. Oxford University Press, 2014.
ista: Zhu F, Gamboa M, Farruggio A, Hippenmeyer S, Tasic B, Schüle B, Chen Tsai
Y, Calos M. 2014. DICE, an efficient system for iterative genomic editing in human
pluripotent stem cells. Nucleic Acids Research. 42(5), e34.
mla: Zhu, Fangfang, et al. “DICE, an Efficient System for Iterative Genomic Editing
in Human Pluripotent Stem Cells.” Nucleic Acids Research, vol. 42, no.
5, e34, Oxford University Press, 2014, doi:10.1093/nar/gkt1290.
short: F. Zhu, M. Gamboa, A. Farruggio, S. Hippenmeyer, B. Tasic, B. Schüle, Y.
Chen Tsai, M. Calos, Nucleic Acids Research 42 (2014).
date_created: 2018-12-11T11:56:38Z
date_published: 2014-03-05T00:00:00Z
date_updated: 2021-01-12T06:56:22Z
day: '05'
ddc:
- '571'
- '610'
department:
- _id: SiHi
doi: 10.1093/nar/gkt1290
file:
- access_level: open_access
checksum: e9268f5f96a820f04d7ebbf85927c3cb
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:09:15Z
date_updated: 2020-07-14T12:45:35Z
file_id: '4738'
file_name: IST-2018-961-v1+1_2014_Hippenmeyer_DICE.pdf
file_size: 11044478
relation: main_file
file_date_updated: 2020-07-14T12:45:35Z
has_accepted_license: '1'
intvolume: ' 42'
issue: '5'
language:
- iso: eng
month: '03'
oa: 1
oa_version: Preprint
publication: Nucleic Acids Research
publication_status: published
publisher: Oxford University Press
publist_id: '4684'
pubrep_id: '961'
quality_controlled: '1'
scopus_import: 1
status: public
title: DICE, an efficient system for iterative genomic editing in human pluripotent
stem cells
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 42
year: '2014'
...
---
_id: '2265'
abstract:
- lang: eng
text: Coordinated migration of newly-born neurons to their target territories is
essential for correct neuronal circuit assembly in the developing brain. Although
a cohort of signaling pathways has been implicated in the regulation of cortical
projection neuron migration, the precise molecular mechanisms and how a balanced
interplay of cell-autonomous and non-autonomous functions of candidate signaling
molecules controls the discrete steps in the migration process, are just being
revealed. In this chapter, I will focally review recent advances that improved
our understanding of the cell-autonomous and possible cell-nonautonomous functions
of the evolutionarily conserved LIS1/NDEL1-complex in regulating the sequential
steps of cortical projection neuron migration. I will then elaborate on the emerging
concept that the Reelin signaling pathway, acts exactly at precise stages in the
course of cortical projection neuron migration. Lastly, I will discuss how finely
tuned transcriptional programs and downstream effectors govern particular aspects
in driving radial migration at discrete stages and how they regulate the precise
positioning of cortical projection neurons in the developing cerebral cortex.
alternative_title:
- Advances in Experimental Medicine and Biology
author:
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: 'Hippenmeyer S. Molecular pathways controlling the sequential steps of cortical
projection neuron migration. In: Nguyen L, ed. Cellular and Molecular Control
of Neuronal Migration. Vol 800. Springer; 2014:1-24. doi:10.1007/978-94-007-7687-6_1'
apa: Hippenmeyer, S. (2014). Molecular pathways controlling the sequential steps
of cortical projection neuron migration. In L. Nguyen (Ed.), Cellular and
Molecular Control of Neuronal Migration (Vol. 800, pp. 1–24). Springer. https://doi.org/10.1007/978-94-007-7687-6_1
chicago: Hippenmeyer, Simon. “Molecular Pathways Controlling the Sequential Steps
of Cortical Projection Neuron Migration.” In Cellular and Molecular Control
of Neuronal Migration, edited by Laurent Nguyen, 800:1–24. Springer, 2014.
https://doi.org/10.1007/978-94-007-7687-6_1.
ieee: S. Hippenmeyer, “Molecular pathways controlling the sequential steps of cortical
projection neuron migration,” in Cellular and Molecular Control of Neuronal
Migration, vol. 800, L. Nguyen, Ed. Springer, 2014, pp. 1–24.
ista: 'Hippenmeyer S. 2014.Molecular pathways controlling the sequential steps of
cortical projection neuron migration. In: Cellular and Molecular Control of Neuronal
Migration. Advances in Experimental Medicine and Biology, vol. 800, 1–24.'
mla: Hippenmeyer, Simon. “Molecular Pathways Controlling the Sequential Steps of
Cortical Projection Neuron Migration.” Cellular and Molecular Control of Neuronal
Migration, edited by Laurent Nguyen, vol. 800, Springer, 2014, pp. 1–24, doi:10.1007/978-94-007-7687-6_1.
short: S. Hippenmeyer, in:, L. Nguyen (Ed.), Cellular and Molecular Control of
Neuronal Migration, Springer, 2014, pp. 1–24.
date_created: 2018-12-11T11:56:39Z
date_published: 2014-01-01T00:00:00Z
date_updated: 2021-01-12T06:56:23Z
day: '01'
department:
- _id: SiHi
doi: 10.1007/978-94-007-7687-6_1
editor:
- first_name: Laurent
full_name: Nguyen, Laurent
last_name: Nguyen
intvolume: ' 800'
language:
- iso: eng
month: '01'
oa_version: None
page: 1 - 24
publication: ' Cellular and Molecular Control of Neuronal Migration'
publication_status: published
publisher: Springer
publist_id: '4679'
quality_controlled: '1'
scopus_import: 1
status: public
title: Molecular pathways controlling the sequential steps of cortical projection
neuron migration
type: book_chapter
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 800
year: '2014'
...
---
_id: '2175'
abstract:
- lang: eng
text: The cerebral cortex, the seat of our cognitive abilities, is composed of an
intricate network of billions of excitatory projection and inhibitory interneurons.
Postmitotic cortical neurons are generated by a diverse set of neural stem cell
progenitors within dedicated zones and defined periods of neurogenesis during
embryonic development. Disruptions in neurogenesis can lead to alterations in
the neuronal cytoarchitecture, which is thought to represent a major underlying
cause for several neurological disorders, including microcephaly, autism and epilepsy.
Although a number of signaling pathways regulating neurogenesis have been described,
the precise cellular and molecular mechanisms regulating the functional neural
stem cell properties in cortical neurogenesis remain unclear. Here, we discuss
the most up-to-date strategies to monitor the fundamental mechanistic parameters
of neuronal progenitor proliferation, and recent advances deciphering the logic
and dynamics of neurogenesis.
article_processing_charge: No
author:
- first_name: Maria P
full_name: Postiglione, Maria P
id: 2C67902A-F248-11E8-B48F-1D18A9856A87
last_name: Postiglione
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: 'Postiglione MP, Hippenmeyer S. Monitoring neurogenesis in the cerebral cortex:
an update. Future Neurology. 2014;9(3):323-340. doi:10.2217/fnl.14.18'
apa: 'Postiglione, M. P., & Hippenmeyer, S. (2014). Monitoring neurogenesis
in the cerebral cortex: an update. Future Neurology. Future Science Group.
https://doi.org/10.2217/fnl.14.18'
chicago: 'Postiglione, Maria P, and Simon Hippenmeyer. “Monitoring Neurogenesis
in the Cerebral Cortex: An Update.” Future Neurology. Future Science Group,
2014. https://doi.org/10.2217/fnl.14.18.'
ieee: 'M. P. Postiglione and S. Hippenmeyer, “Monitoring neurogenesis in the cerebral
cortex: an update,” Future Neurology, vol. 9, no. 3. Future Science Group,
pp. 323–340, 2014.'
ista: 'Postiglione MP, Hippenmeyer S. 2014. Monitoring neurogenesis in the cerebral
cortex: an update. Future Neurology. 9(3), 323–340.'
mla: 'Postiglione, Maria P., and Simon Hippenmeyer. “Monitoring Neurogenesis in
the Cerebral Cortex: An Update.” Future Neurology, vol. 9, no. 3, Future
Science Group, 2014, pp. 323–40, doi:10.2217/fnl.14.18.'
short: M.P. Postiglione, S. Hippenmeyer, Future Neurology 9 (2014) 323–340.
date_created: 2018-12-11T11:56:09Z
date_published: 2014-05-01T00:00:00Z
date_updated: 2023-10-17T08:34:27Z
day: '01'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.2217/fnl.14.18
ec_funded: 1
file:
- access_level: open_access
checksum: ba06659ecadabceec9a37dd8c4586dce
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:10:25Z
date_updated: 2020-07-14T12:45:31Z
file_id: '4812'
file_name: IST-2016-528-v1+1_fnl.14.18.pdf
file_size: 3848424
relation: main_file
file_date_updated: 2020-07-14T12:45:31Z
has_accepted_license: '1'
intvolume: ' 9'
issue: '3'
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
page: 323 - 340
project:
- _id: 25D61E48-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '618444'
name: Molecular Mechanisms of Cerebral Cortex Development
publication: Future Neurology
publication_identifier:
eissn:
- 1748-6971
issn:
- 1479-6708
publication_status: published
publisher: Future Science Group
publist_id: '4806'
pubrep_id: '528'
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'Monitoring neurogenesis in the cerebral cortex: an update'
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 9
year: '2014'
...
---
_id: '2264'
abstract:
- lang: eng
text: Faithful progression through the cell cycle is crucial to the maintenance
and developmental potential of stem cells. Here, we demonstrate that neural stem
cells (NSCs) and intermediate neural progenitor cells (NPCs) employ a zinc-finger
transcription factor specificity protein 2 (Sp2) as a cell cycle regulator in
two temporally and spatially distinct progenitor domains. Differential conditional
deletion of Sp2 in early embryonic cerebral cortical progenitors, and perinatal
olfactory bulb progenitors disrupted transitions through G1, G2 and M phases,
whereas DNA synthesis appeared intact. Cell-autonomous function of Sp2 was identified
by deletion of Sp2 using mosaic analysis with double markers, which clearly established
that conditional Sp2-null NSCs and NPCs are M phase arrested in vivo. Importantly,
conditional deletion of Sp2 led to a decline in the generation of NPCs and neurons
in the developing and postnatal brains. Our findings implicate Sp2-dependent mechanisms
as novel regulators of cell cycle progression, the absence of which disrupts neurogenesis
in the embryonic and postnatal brain.
article_processing_charge: No
author:
- first_name: Huixuan
full_name: Liang, Huixuan
last_name: Liang
- first_name: Guanxi
full_name: Xiao, Guanxi
last_name: Xiao
- first_name: Haifeng
full_name: Yin, Haifeng
last_name: Yin
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Jonathan
full_name: Horowitz, Jonathan
last_name: Horowitz
- first_name: Troy
full_name: Ghashghaei, Troy
last_name: Ghashghaei
citation:
ama: Liang H, Xiao G, Yin H, Hippenmeyer S, Horowitz J, Ghashghaei T. Neural development
is dependent on the function of specificity protein 2 in cell cycle progression.
Development. 2013;140(3):552-561. doi:10.1242/dev.085621
apa: Liang, H., Xiao, G., Yin, H., Hippenmeyer, S., Horowitz, J., & Ghashghaei,
T. (2013). Neural development is dependent on the function of specificity protein
2 in cell cycle progression. Development. Company of Biologists. https://doi.org/10.1242/dev.085621
chicago: Liang, Huixuan, Guanxi Xiao, Haifeng Yin, Simon Hippenmeyer, Jonathan Horowitz,
and Troy Ghashghaei. “Neural Development Is Dependent on the Function of Specificity
Protein 2 in Cell Cycle Progression.” Development. Company of Biologists,
2013. https://doi.org/10.1242/dev.085621.
ieee: H. Liang, G. Xiao, H. Yin, S. Hippenmeyer, J. Horowitz, and T. Ghashghaei,
“Neural development is dependent on the function of specificity protein 2 in cell
cycle progression,” Development, vol. 140, no. 3. Company of Biologists,
pp. 552–561, 2013.
ista: Liang H, Xiao G, Yin H, Hippenmeyer S, Horowitz J, Ghashghaei T. 2013. Neural
development is dependent on the function of specificity protein 2 in cell cycle
progression. Development. 140(3), 552–561.
mla: Liang, Huixuan, et al. “Neural Development Is Dependent on the Function of
Specificity Protein 2 in Cell Cycle Progression.” Development, vol. 140,
no. 3, Company of Biologists, 2013, pp. 552–61, doi:10.1242/dev.085621.
short: H. Liang, G. Xiao, H. Yin, S. Hippenmeyer, J. Horowitz, T. Ghashghaei, Development
140 (2013) 552–561.
date_created: 2018-12-11T11:56:39Z
date_published: 2013-02-01T00:00:00Z
date_updated: 2021-01-12T06:56:23Z
day: '01'
department:
- _id: SiHi
doi: 10.1242/dev.085621
external_id:
pmid:
- '23293287'
intvolume: ' 140'
issue: '3'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3561788/
month: '02'
oa: 1
oa_version: Submitted Version
page: 552 - 561
pmid: 1
publication: Development
publication_status: published
publisher: Company of Biologists
publist_id: '4681'
quality_controlled: '1'
scopus_import: 1
status: public
title: Neural development is dependent on the function of specificity protein 2 in
cell cycle progression
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 140
year: '2013'
...
---
_id: '2303'
abstract:
- lang: eng
text: MADM (Mosaic Analysis with Double Markers) technology offers a genetic approach
in mice to visualize and concomitantly manipulate genetically defined cells at
clonal level and single cell resolution. MADM employs Cre recombinase/loxP-dependent
interchromosomal mitotic recombination to reconstitute two split marker genes—green
GFP and red tdTomato—and can label sparse clones of homozygous mutant cells in
one color and wild-type cells in the other color in an otherwise unlabeled background.
At present, major MADM applications include lineage tracing, single cell labeling,
conditional knockouts in small populations of cells and induction of uniparental
chromosome disomy to assess effects of genomic imprinting. MADM can be applied
universally in the mouse with the sole limitation being the specificity of the
promoter controlling Cre recombinase expression. Here I review recent developments
and extensions of the MADM technique and give an overview of the major discoveries
and progresses enabled by the implementation of the novel genetic MADM tools.
acknowledgement: This work was supported by IST Austria institutional funds.
article_type: review
author:
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Hippenmeyer S. Dissection of gene function at clonal level using mosaic analysis
with double markers. Frontiers in Biology. 2013;8(6):557-568. doi:10.1007/s11515-013-1279-6
apa: Hippenmeyer, S. (2013). Dissection of gene function at clonal level using mosaic
analysis with double markers. Frontiers in Biology. Springer. https://doi.org/10.1007/s11515-013-1279-6
chicago: Hippenmeyer, Simon. “Dissection of Gene Function at Clonal Level Using
Mosaic Analysis with Double Markers.” Frontiers in Biology. Springer, 2013.
https://doi.org/10.1007/s11515-013-1279-6.
ieee: S. Hippenmeyer, “Dissection of gene function at clonal level using mosaic
analysis with double markers,” Frontiers in Biology, vol. 8, no. 6. Springer,
pp. 557–568, 2013.
ista: Hippenmeyer S. 2013. Dissection of gene function at clonal level using mosaic
analysis with double markers. Frontiers in Biology. 8(6), 557–568.
mla: Hippenmeyer, Simon. “Dissection of Gene Function at Clonal Level Using Mosaic
Analysis with Double Markers.” Frontiers in Biology, vol. 8, no. 6, Springer,
2013, pp. 557–68, doi:10.1007/s11515-013-1279-6.
short: S. Hippenmeyer, Frontiers in Biology 8 (2013) 557–568.
date_created: 2018-12-11T11:56:52Z
date_published: 2013-09-03T00:00:00Z
date_updated: 2021-01-12T06:56:39Z
day: '03'
department:
- _id: SiHi
doi: 10.1007/s11515-013-1279-6
intvolume: ' 8'
issue: '6'
language:
- iso: eng
month: '09'
oa_version: None
page: 557 - 568
publication: Frontiers in Biology
publication_status: published
publisher: Springer
publist_id: '4624'
quality_controlled: '1'
scopus_import: 1
status: public
title: Dissection of gene function at clonal level using mosaic analysis with double
markers
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 8
year: '2013'
...
---
_id: '2838'
abstract:
- lang: eng
text: Individuals with Down syndrome (DS) present important motor deficits that
derive from altered motor development of infants and young children. DYRK1A, a
candidate gene for DS abnormalities has been implicated in motor function due
to its expression in motor nuclei in the adult brain, and its overexpression in
DS mouse models leads to hyperactivity and altered motor learning. However, its
precise role in the adult motor system, or its possible involvement in postnatal
locomotor development has not yet been clarified. During the postnatal period
we observed time-specific expression of Dyrk1A in discrete subsets of brainstem
nuclei and spinal cord motor neurons. Interestingly, we describe for the first
time the presence of Dyrk1A in the presynaptic terminal of the neuromuscular junctions
and its axonal transport from the facial nucleus, suggesting a function for Dyrk1A
in these structures. Relevant to DS, Dyrk1A overexpression in transgenic mice
(TgDyrk1A) produces motor developmental alterations possibly contributing to DS
motor phenotypes and modifies the numbers of motor cholinergic neurons, suggesting
that the kinase may have a role in the development of the brainstem and spinal
cord motor system.
article_number: e54285
author:
- first_name: Gloria
full_name: Arquè Fuste, Gloria
id: 3CF33908-F248-11E8-B48F-1D18A9856A87
last_name: Arquè Fuste
- first_name: Anna
full_name: Casanovas, Anna
last_name: Casanovas
- first_name: Mara
full_name: Dierssen, Mara
last_name: Dierssen
citation:
ama: 'Arquè Fuste G, Casanovas A, Dierssen M. Dyrk1A is dynamically expressed on
subsets of motor neurons and in the neuromuscular junction: Possible role in Down
syndrome. PLoS One. 2013;8(1). doi:10.1371/journal.pone.0054285'
apa: 'Arquè Fuste, G., Casanovas, A., & Dierssen, M. (2013). Dyrk1A is dynamically
expressed on subsets of motor neurons and in the neuromuscular junction: Possible
role in Down syndrome. PLoS One. Public Library of Science. https://doi.org/10.1371/journal.pone.0054285'
chicago: 'Arquè Fuste, Gloria, Anna Casanovas, and Mara Dierssen. “Dyrk1A Is Dynamically
Expressed on Subsets of Motor Neurons and in the Neuromuscular Junction: Possible
Role in Down Syndrome.” PLoS One. Public Library of Science, 2013. https://doi.org/10.1371/journal.pone.0054285.'
ieee: 'G. Arquè Fuste, A. Casanovas, and M. Dierssen, “Dyrk1A is dynamically expressed
on subsets of motor neurons and in the neuromuscular junction: Possible role in
Down syndrome,” PLoS One, vol. 8, no. 1. Public Library of Science, 2013.'
ista: 'Arquè Fuste G, Casanovas A, Dierssen M. 2013. Dyrk1A is dynamically expressed
on subsets of motor neurons and in the neuromuscular junction: Possible role in
Down syndrome. PLoS One. 8(1), e54285.'
mla: 'Arquè Fuste, Gloria, et al. “Dyrk1A Is Dynamically Expressed on Subsets of
Motor Neurons and in the Neuromuscular Junction: Possible Role in Down Syndrome.”
PLoS One, vol. 8, no. 1, e54285, Public Library of Science, 2013, doi:10.1371/journal.pone.0054285.'
short: G. Arquè Fuste, A. Casanovas, M. Dierssen, PLoS One 8 (2013).
date_created: 2018-12-11T11:59:52Z
date_published: 2013-01-16T00:00:00Z
date_updated: 2021-01-12T07:00:07Z
day: '16'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1371/journal.pone.0054285
file:
- access_level: open_access
checksum: 512733b21419574a45f10cabef3d7f81
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:15:38Z
date_updated: 2020-07-14T12:45:50Z
file_id: '5160'
file_name: IST-2016-407-v1+1_journal.pone.0054285.pdf
file_size: 4795977
relation: main_file
file_date_updated: 2020-07-14T12:45:50Z
has_accepted_license: '1'
intvolume: ' 8'
issue: '1'
language:
- iso: eng
month: '01'
oa: 1
oa_version: Published Version
publication: PLoS One
publication_status: published
publisher: Public Library of Science
publist_id: '3960'
pubrep_id: '407'
quality_controlled: '1'
scopus_import: 1
status: public
title: 'Dyrk1A is dynamically expressed on subsets of motor neurons and in the neuromuscular
junction: Possible role in Down syndrome'
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 8
year: '2013'
...
---
_id: '2855'
abstract:
- lang: eng
text: Genomic imprinting leads to preferred expression of either the maternal or
paternal alleles of a subset of genes. Imprinting is essential for mammalian development,
and its deregulation causes many diseases. However, the functional relevance of
imprinting at the cellular level is poorly understood for most imprinted genes.
We used mosaic analysis with double markers (MADM) in mice to create uniparental
disomies (UPDs) and to visualize imprinting effects with single-cell resolution.
Although chromosome 12 UPD did not produce detectable phenotypes, chromosome 7
UPD caused highly significant paternal growth dominance in the liver and lung,
but not in the brain or heart. A single gene on chromosome 7, encoding the secreted
insulin-like growth factor 2 (IGF2), accounts for most of the paternal dominance
effect. Mosaic analyses implied additional imprinted loci on chromosome 7 acting
cell autonomously to transmit the IGF2 signal. Our study reveals chromosome- and
cell-type specificity of genomic imprinting effects.
author:
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Randy
full_name: Johnson, Randy
last_name: Johnson
- first_name: Liqun
full_name: Luo, Liqun
last_name: Luo
citation:
ama: Hippenmeyer S, Johnson R, Luo L. Mosaic analysis with double markers reveals
cell type specific paternal growth dominance. Cell Reports. 2013;3(3):960-967.
doi:10.1016/j.celrep.2013.02.002
apa: Hippenmeyer, S., Johnson, R., & Luo, L. (2013). Mosaic analysis with double
markers reveals cell type specific paternal growth dominance. Cell Reports.
Cell Press. https://doi.org/10.1016/j.celrep.2013.02.002
chicago: Hippenmeyer, Simon, Randy Johnson, and Liqun Luo. “Mosaic Analysis with
Double Markers Reveals Cell Type Specific Paternal Growth Dominance.” Cell
Reports. Cell Press, 2013. https://doi.org/10.1016/j.celrep.2013.02.002.
ieee: S. Hippenmeyer, R. Johnson, and L. Luo, “Mosaic analysis with double markers
reveals cell type specific paternal growth dominance,” Cell Reports, vol.
3, no. 3. Cell Press, pp. 960–967, 2013.
ista: Hippenmeyer S, Johnson R, Luo L. 2013. Mosaic analysis with double markers
reveals cell type specific paternal growth dominance. Cell Reports. 3(3), 960–967.
mla: Hippenmeyer, Simon, et al. “Mosaic Analysis with Double Markers Reveals Cell
Type Specific Paternal Growth Dominance.” Cell Reports, vol. 3, no. 3,
Cell Press, 2013, pp. 960–67, doi:10.1016/j.celrep.2013.02.002.
short: S. Hippenmeyer, R. Johnson, L. Luo, Cell Reports 3 (2013) 960–967.
date_created: 2018-12-11T11:59:57Z
date_published: 2013-03-28T00:00:00Z
date_updated: 2021-01-12T07:00:16Z
day: '28'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1016/j.celrep.2013.02.002
file:
- access_level: open_access
checksum: 6e977b918e81384cd571ec5a9d812289
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:17:20Z
date_updated: 2020-07-14T12:45:51Z
file_id: '5274'
file_name: IST-2016-405-v1+1_1-s2.0-S2211124713000612-main.pdf
file_size: 1907211
relation: main_file
file_date_updated: 2020-07-14T12:45:51Z
has_accepted_license: '1'
intvolume: ' 3'
issue: '3'
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
page: 960 - 967
publication: Cell Reports
publication_status: published
publisher: Cell Press
publist_id: '3937'
pubrep_id: '405'
quality_controlled: '1'
scopus_import: 1
status: public
title: Mosaic analysis with double markers reveals cell type specific paternal growth
dominance
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 3
year: '2013'
...
---
_id: '2263'
abstract:
- lang: eng
text: Nestin-cre transgenic mice have been widely used to direct recombination to
neural stem cells (NSCs) and intermediate neural progenitor cells (NPCs). Here
we report that a readily utilized, and the only commercially available, Nestin-cre
line is insufficient for directing recombination in early embryonic NSCs and NPCs.
Analysis of recombination efficiency in multiple cre-dependent reporters and a
genetic mosaic line revealed consistent temporal and spatial patterns of recombination
in NSCs and NPCs. For comparison we utilized a knock-in Emx1cre line and found
robust recombination in NSCs and NPCs in ventricular and subventricular zones
of the cerebral cortices as early as embryonic day 12.5. In addition we found
that the rate of Nestin-cre driven recombination only reaches sufficiently high
levels in NSCs and NPCs during late embryonic and early postnatal periods. These
findings are important when commercially available cre lines are considered for
directing recombination to embryonic NSCs and NPCs.
author:
- first_name: Huixuan
full_name: Liang, Huixuan
last_name: Liang
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: H.
full_name: Ghashghaei, H.
last_name: Ghashghaei
citation:
ama: Liang H, Hippenmeyer S, Ghashghaei H. A Nestin-cre transgenic mouse is insufficient
for recombination in early embryonic neural progenitors. Biology open.
2012;1(12):1200-1203. doi:10.1242/bio.20122287
apa: Liang, H., Hippenmeyer, S., & Ghashghaei, H. (2012). A Nestin-cre transgenic
mouse is insufficient for recombination in early embryonic neural progenitors.
Biology Open. The Company of Biologists. https://doi.org/10.1242/bio.20122287
chicago: Liang, Huixuan, Simon Hippenmeyer, and H. Ghashghaei. “A Nestin-Cre Transgenic
Mouse Is Insufficient for Recombination in Early Embryonic Neural Progenitors.”
Biology Open. The Company of Biologists, 2012. https://doi.org/10.1242/bio.20122287.
ieee: H. Liang, S. Hippenmeyer, and H. Ghashghaei, “A Nestin-cre transgenic mouse
is insufficient for recombination in early embryonic neural progenitors,” Biology
open, vol. 1, no. 12. The Company of Biologists, pp. 1200–1203, 2012.
ista: Liang H, Hippenmeyer S, Ghashghaei H. 2012. A Nestin-cre transgenic mouse
is insufficient for recombination in early embryonic neural progenitors. Biology
open. 1(12), 1200–1203.
mla: Liang, Huixuan, et al. “A Nestin-Cre Transgenic Mouse Is Insufficient for Recombination
in Early Embryonic Neural Progenitors.” Biology Open, vol. 1, no. 12, The
Company of Biologists, 2012, pp. 1200–03, doi:10.1242/bio.20122287.
short: H. Liang, S. Hippenmeyer, H. Ghashghaei, Biology Open 1 (2012) 1200–1203.
date_created: 2018-12-11T11:56:38Z
date_published: 2012-12-15T00:00:00Z
date_updated: 2021-01-12T06:56:23Z
day: '15'
ddc:
- '576'
department:
- _id: SiHi
doi: 10.1242/bio.20122287
file:
- access_level: open_access
checksum: 605a1800b81227848c361fd6ba7d22ba
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:13:09Z
date_updated: 2020-07-14T12:45:35Z
file_id: '4990'
file_name: IST-2015-387-v1+1_1200.full.pdf
file_size: 726695
relation: main_file
file_date_updated: 2020-07-14T12:45:35Z
has_accepted_license: '1'
intvolume: ' 1'
issue: '12'
language:
- iso: eng
license: https://creativecommons.org/licenses/by-nc-sa/4.0/
month: '12'
oa: 1
oa_version: Published Version
page: 1200 - 1203
publication: Biology open
publication_status: published
publisher: The Company of Biologists
publist_id: '4682'
pubrep_id: '387'
quality_controlled: '1'
scopus_import: 1
status: public
title: A Nestin-cre transgenic mouse is insufficient for recombination in early embryonic
neural progenitors
tmp:
image: /images/cc_by_nc_sa.png
legal_code_url: https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC
BY-NC-SA 4.0)
short: CC BY-NC-SA (4.0)
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 1
year: '2012'
...