---
_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: 2024-03-27T23:30:40Z
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: 2024-03-27T23:30:41Z
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'
...