---
_id: '14794'
abstract:
- lang: eng
text: "Mosaic analysis with double markers (MADM) technology enables the sparse
labeling of genetically defined neurons. We present a protocol for time-lapse
imaging of cortical projection neuron migration in mice using MADM. We describe
steps for the isolation, culturing, and 4D imaging of neuronal dynamics in MADM-labeled
brain tissue. While this protocol is compatible with other single-cell labeling
methods, the MADM approach provides a genetic platform for the functional assessment
of cell-autonomous candidate gene function and the relative contribution of non-cell-autonomous
effects.\r\n\r\nFor complete details on the use and execution of this protocol,
please refer to Hansen et al. (2022),1 Contreras et al. (2021),2 and Amberg and
Hippenmeyer (2021).3"
acknowledged_ssus:
- _id: Bio
- _id: PreCl
acknowledgement: We thank Florian Pauler for discussion and his expert technical support.
This research was supported by the Scientific Service Units (SSU) at IST Austria
through resources provided by the Imaging and Optics Facility (IOF) and Preclinical
Facility (PCF). A.H.H. was a recipient of a DOC Fellowship (24812) of the Austrian
Academy of Sciences.
article_number: '102795'
article_processing_charge: Yes
article_type: review
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. Time-lapse imaging of cortical projection neuron
migration in mice using mosaic analysis with double markers. STAR Protocols.
2024;5(1). doi:10.1016/j.xpro.2023.102795
apa: Hansen, A. H., & Hippenmeyer, S. (2024). Time-lapse imaging of cortical
projection neuron migration in mice using mosaic analysis with double markers.
STAR Protocols. Elsevier. https://doi.org/10.1016/j.xpro.2023.102795
chicago: Hansen, Andi H, and Simon Hippenmeyer. “Time-Lapse Imaging of Cortical
Projection Neuron Migration in Mice Using Mosaic Analysis with Double Markers.”
STAR Protocols. Elsevier, 2024. https://doi.org/10.1016/j.xpro.2023.102795.
ieee: A. H. Hansen and S. Hippenmeyer, “Time-lapse imaging of cortical projection
neuron migration in mice using mosaic analysis with double markers,” STAR Protocols,
vol. 5, no. 1. Elsevier, 2024.
ista: Hansen AH, Hippenmeyer S. 2024. Time-lapse imaging of cortical projection
neuron migration in mice using mosaic analysis with double markers. STAR Protocols.
5(1), 102795.
mla: Hansen, Andi H., and Simon Hippenmeyer. “Time-Lapse Imaging of Cortical Projection
Neuron Migration in Mice Using Mosaic Analysis with Double Markers.” STAR Protocols,
vol. 5, no. 1, 102795, Elsevier, 2024, doi:10.1016/j.xpro.2023.102795.
short: A.H. Hansen, S. Hippenmeyer, STAR Protocols 5 (2024).
date_created: 2024-01-14T23:00:56Z
date_published: 2024-01-01T00:00:00Z
date_updated: 2024-01-17T10:32:31Z
day: '01'
department:
- _id: SiHi
doi: 10.1016/j.xpro.2023.102795
external_id:
pmid:
- '38165800'
intvolume: ' 5'
issue: '1'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1016/j.xpro.2023.102795
month: '01'
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
publication: STAR Protocols
publication_identifier:
eissn:
- 2666-1667
publication_status: epub_ahead
publisher: Elsevier
quality_controlled: '1'
related_material:
link:
- relation: software
url: http://github.com/hippenmeyerlab
scopus_import: '1'
status: public
title: Time-lapse imaging of cortical projection neuron migration in mice using mosaic
analysis with double markers
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 5
year: '2024'
...
---
_id: '12875'
abstract:
- lang: eng
text: The superior colliculus (SC) in the mammalian midbrain is essential for multisensory
integration and is composed of a rich diversity of excitatory and inhibitory neurons
and glia. However, the developmental principles directing the generation of SC
cell-type diversity are not understood. Here, we pursued systematic cell lineage
tracing in silico and in vivo, preserving full spatial information, using genetic
mosaic analysis with double markers (MADM)-based clonal analysis with single-cell
sequencing (MADM-CloneSeq). The analysis of clonally related cell lineages revealed
that radial glial progenitors (RGPs) in SC are exceptionally multipotent. Individual
resident RGPs have the capacity to produce all excitatory and inhibitory SC neuron
types, even at the stage of terminal division. While individual clonal units show
no pre-defined cellular composition, the establishment of appropriate relative
proportions of distinct neuronal types occurs in a PTEN-dependent manner. Collectively,
our findings provide an inaugural framework at the single-RGP/-cell level of the
mammalian SC ontogeny.
acknowledged_ssus:
- _id: Bio
- _id: M-Shop
- _id: LifeSc
- _id: PreCl
acknowledgement: "We thank Liqun Luo for his continued support, for providing essential
resources for generating Fzd10-CreER mice which were generated in his laboratory,
and for comments on the manuscript; W. Zhong for providing Nestin-Cre transgenic
mouse line for this study; A. Heger for mouse colony management; R. Beattie and
T. Asenov for designing and producing components of acute slice recovery chamber
for MADM-CloneSeq experiments; and K. Leopold, J. Rodarte and N. Amberg for initial
experiments, technical support and/or assistance. This study was supported by the
Scientific Service Units (SSU) of IST Austria through resources provided by the
Imaging & Optics Facility (IOF), Laboratory Support Facility (LSF), Miba Machine
Shop, and Pre-clinical Facility (PCF). G.C. received funding from European Commission
(IST plus postdoctoral fellowship). This work was supported by ISTA institutional\r\nfunds;
the Austrian Science Fund Special Research Programmes (FWF SFB F78 Neuro Stem Modulation)
to S.H. "
article_processing_charge: Yes (via OA deal)
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: Florian
full_name: Pauler, Florian
id: 48EA0138-F248-11E8-B48F-1D18A9856A87
last_name: Pauler
orcid: 0000-0002-7462-0048
- first_name: Peter
full_name: Koppensteiner, Peter
id: 3B8B25A8-F248-11E8-B48F-1D18A9856A87
last_name: Koppensteiner
orcid: 0000-0002-3509-1948
- first_name: Thomas
full_name: Krausgruber, Thomas
last_name: Krausgruber
- first_name: Carmen
full_name: Streicher, Carmen
id: 36BCB99C-F248-11E8-B48F-1D18A9856A87
last_name: Streicher
- first_name: Martin
full_name: Schrammel, Martin
id: f13e7cae-e8bd-11ed-841a-96dedf69f46d
last_name: Schrammel
- first_name: Natalie Y
full_name: Özgen, Natalie Y
id: e68ece33-f6e0-11ea-865d-ae1031dcc090
last_name: Özgen
- first_name: Alexis
full_name: Ivec, Alexis
id: 1d144691-e8be-11ed-9b33-bdd3077fad4c
last_name: Ivec
- first_name: Christoph
full_name: Bock, Christoph
last_name: Bock
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Cheung GT, Pauler F, Koppensteiner P, et al. Multipotent progenitors instruct
ontogeny of the superior colliculus. Neuron. 2024;112(2):230-246.e11. doi:10.1016/j.neuron.2023.11.009
apa: Cheung, G. T., Pauler, F., Koppensteiner, P., Krausgruber, T., Streicher, C.,
Schrammel, M., … Hippenmeyer, S. (2024). Multipotent progenitors instruct ontogeny
of the superior colliculus. Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2023.11.009
chicago: Cheung, Giselle T, Florian Pauler, Peter Koppensteiner, Thomas Krausgruber,
Carmen Streicher, Martin Schrammel, Natalie Y Özgen, et al. “Multipotent Progenitors
Instruct Ontogeny of the Superior Colliculus.” Neuron. Elsevier, 2024.
https://doi.org/10.1016/j.neuron.2023.11.009.
ieee: G. T. Cheung et al., “Multipotent progenitors instruct ontogeny of
the superior colliculus,” Neuron, vol. 112, no. 2. Elsevier, p. 230–246.e11,
2024.
ista: Cheung GT, Pauler F, Koppensteiner P, Krausgruber T, Streicher C, Schrammel
M, Özgen NY, Ivec A, Bock C, Shigemoto R, Hippenmeyer S. 2024. Multipotent progenitors
instruct ontogeny of the superior colliculus. Neuron. 112(2), 230–246.e11.
mla: Cheung, Giselle T., et al. “Multipotent Progenitors Instruct Ontogeny of the
Superior Colliculus.” Neuron, vol. 112, no. 2, Elsevier, 2024, p. 230–246.e11,
doi:10.1016/j.neuron.2023.11.009.
short: G.T. Cheung, F. Pauler, P. Koppensteiner, T. Krausgruber, C. Streicher, M.
Schrammel, N.Y. Özgen, A. Ivec, C. Bock, R. Shigemoto, S. Hippenmeyer, Neuron
112 (2024) 230–246.e11.
date_created: 2023-04-27T09:41:48Z
date_published: 2024-01-17T00:00:00Z
date_updated: 2024-03-05T09:43:02Z
day: '17'
ddc:
- '570'
department:
- _id: SiHi
- _id: RySh
doi: 10.1016/j.neuron.2023.11.009
external_id:
pmid:
- '38096816'
file:
- access_level: open_access
checksum: 32b3788f7085cf44a84108d8faaff3ce
content_type: application/pdf
creator: dernst
date_created: 2024-02-06T13:56:15Z
date_updated: 2024-02-06T13:56:15Z
file_id: '14944'
file_name: 2024_Neuron_Cheung.pdf
file_size: 5942467
relation: main_file
success: 1
file_date_updated: 2024-02-06T13:56:15Z
has_accepted_license: '1'
intvolume: ' 112'
issue: '2'
language:
- iso: eng
month: '01'
oa: 1
oa_version: Published Version
page: 230-246.e11
pmid: 1
project:
- _id: 059F6AB4-7A3F-11EA-A408-12923DDC885E
grant_number: F07805
name: Molecular Mechanisms of Neural Stem Cell Lineage Progression
publication: Neuron
publication_identifier:
issn:
- 0896-6273
publication_status: published
publisher: Elsevier
quality_controlled: '1'
related_material:
link:
- description: News on ISTA Website
relation: press_release
url: https://ista.ac.at/en/news/the-pedigree-of-brain-cells/
scopus_import: '1'
status: public
title: Multipotent progenitors instruct ontogeny of the superior colliculus
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: 112
year: '2024'
...
---
_id: '12542'
abstract:
- lang: eng
text: In this issue of Neuron, Espinosa-Medina et al.1 present the TEMPO (Temporal
Encoding and Manipulation in a Predefined Order) system, which enables the marking
and genetic manipulation of sequentially generated cell lineages in vertebrate
species in vivo.
article_processing_charge: No
article_type: letter_note
author:
- first_name: Ana
full_name: Villalba Requena, Ana
id: 68cb85a0-39f7-11eb-9559-9aaab4f6a247
last_name: Villalba Requena
orcid: 0000-0002-5615-5277
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Villalba Requena A, Hippenmeyer S. Going back in time with TEMPO. Neuron.
2023;111(3):291-293. doi:10.1016/j.neuron.2023.01.006
apa: Villalba Requena, A., & Hippenmeyer, S. (2023). Going back in time with
TEMPO. Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2023.01.006
chicago: Villalba Requena, Ana, and Simon Hippenmeyer. “Going Back in Time with
TEMPO.” Neuron. Elsevier, 2023. https://doi.org/10.1016/j.neuron.2023.01.006.
ieee: A. Villalba Requena and S. Hippenmeyer, “Going back in time with TEMPO,” Neuron,
vol. 111, no. 3. Elsevier, pp. 291–293, 2023.
ista: Villalba Requena A, Hippenmeyer S. 2023. Going back in time with TEMPO. Neuron.
111(3), 291–293.
mla: Villalba Requena, Ana, and Simon Hippenmeyer. “Going Back in Time with TEMPO.”
Neuron, vol. 111, no. 3, Elsevier, 2023, pp. 291–93, doi:10.1016/j.neuron.2023.01.006.
short: A. Villalba Requena, S. Hippenmeyer, Neuron 111 (2023) 291–293.
date_created: 2023-02-12T23:00:58Z
date_published: 2023-02-01T00:00:00Z
date_updated: 2023-08-01T13:10:27Z
day: '01'
department:
- _id: SiHi
doi: 10.1016/j.neuron.2023.01.006
external_id:
isi:
- '000994473300001'
intvolume: ' 111'
isi: 1
issue: '3'
language:
- iso: eng
month: '02'
oa_version: None
page: 291-293
publication: Neuron
publication_identifier:
eissn:
- 1097-4199
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Going back in time with TEMPO
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 111
year: '2023'
...
---
_id: '12679'
abstract:
- lang: eng
text: How to generate a brain of correct size and with appropriate cell-type diversity
during development is a major question in Neuroscience. In the developing neocortex,
radial glial progenitor (RGP) cells are the main neural stem cells that produce
cortical excitatory projection neurons, glial cells, and establish the prospective
postnatal stem cell niche in the lateral ventricles. RGPs follow a tightly orchestrated
developmental program that when disrupted can result in severe cortical malformations
such as microcephaly and megalencephaly. The precise cellular and molecular mechanisms
instructing faithful RGP lineage progression are however not well understood.
This review will summarize recent conceptual advances that contribute to our understanding
of the general principles of RGP lineage progression.
acknowledgement: "I wish to thank all current and past members of the Hippenmeyer
laboratory at ISTA for exciting discussions on the subject of this review. I apologize
to colleagues whose work I could not cite and/or discuss in the frame of the available
space. Work in the Hippenmeyer laboratory on the\r\ndiscussed topic is supported
by ISTA 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 agree-ment no. 725780 LinPro) to SH."
article_number: '102695'
article_processing_charge: Yes (via OA deal)
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. Principles of neural stem cell lineage progression: Insights
from developing cerebral cortex. Current Opinion in Neurobiology. 2023;79(4).
doi:10.1016/j.conb.2023.102695'
apa: 'Hippenmeyer, S. (2023). Principles of neural stem cell lineage progression:
Insights from developing cerebral cortex. Current Opinion in Neurobiology.
Elsevier. https://doi.org/10.1016/j.conb.2023.102695'
chicago: 'Hippenmeyer, Simon. “Principles of Neural Stem Cell Lineage Progression:
Insights from Developing Cerebral Cortex.” Current Opinion in Neurobiology.
Elsevier, 2023. https://doi.org/10.1016/j.conb.2023.102695.'
ieee: 'S. Hippenmeyer, “Principles of neural stem cell lineage progression: Insights
from developing cerebral cortex,” Current Opinion in Neurobiology, vol.
79, no. 4. Elsevier, 2023.'
ista: 'Hippenmeyer S. 2023. Principles of neural stem cell lineage progression:
Insights from developing cerebral cortex. Current Opinion in Neurobiology. 79(4),
102695.'
mla: 'Hippenmeyer, Simon. “Principles of Neural Stem Cell Lineage Progression: Insights
from Developing Cerebral Cortex.” Current Opinion in Neurobiology, vol.
79, no. 4, 102695, Elsevier, 2023, doi:10.1016/j.conb.2023.102695.'
short: S. Hippenmeyer, Current Opinion in Neurobiology 79 (2023).
date_created: 2023-02-26T12:24:21Z
date_published: 2023-04-01T00:00:00Z
date_updated: 2023-08-16T12:30:25Z
day: '01'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1016/j.conb.2023.102695
ec_funded: 1
external_id:
isi:
- '000953497700001'
pmid:
- '36842274'
file:
- access_level: open_access
checksum: 4d11c4ca87e6cbc4d2ac46d3225ea615
content_type: application/pdf
creator: dernst
date_created: 2023-08-16T12:29:06Z
date_updated: 2023-08-16T12:29:06Z
file_id: '14071'
file_name: 2023_CurrentOpinionNeurobio_Hippenmeyer.pdf
file_size: 1787894
relation: main_file
success: 1
file_date_updated: 2023-08-16T12:29:06Z
has_accepted_license: '1'
intvolume: ' 79'
isi: 1
issue: '4'
keyword:
- General Neuroscience
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 059F6AB4-7A3F-11EA-A408-12923DDC885E
grant_number: F07805
name: Molecular Mechanisms of Neural Stem Cell Lineage Progression
- _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: Current Opinion in Neurobiology
publication_identifier:
issn:
- 0959-4388
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'Principles of neural stem cell lineage progression: Insights from 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: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 79
year: '2023'
...
---
_id: '12562'
abstract:
- lang: eng
text: Presynaptic inputs determine the pattern of activation of postsynaptic neurons
in a neural circuit. Molecular and genetic pathways that regulate the selective
formation of subsets of presynaptic inputs are largely unknown, despite significant
understanding of the general process of synaptogenesis. In this study, we have
begun to identify such factors using the spinal monosynaptic stretch reflex circuit
as a model system. In this neuronal circuit, Ia proprioceptive afferents establish
monosynaptic connections with spinal motor neurons that project to the same muscle
(termed homonymous connections) or muscles with related or synergistic function.
However, monosynaptic connections are not formed with motor neurons innervating
muscles with antagonistic functions. The ETS transcription factor ER81 (also known
as ETV1) is expressed by all proprioceptive afferents, but only a small set of
motor neuron pools in the lumbar spinal cord of the mouse. Here we use conditional
mouse genetic techniques to eliminate Er81 expression selectively from motor neurons.
We find that ablation of Er81 in motor neurons reduces synaptic inputs from proprioceptive
afferents conveying information from homonymous and synergistic muscles, with
no change observed in the connectivity pattern from antagonistic proprioceptive
afferents. In summary, these findings suggest a role for ER81 in defined motor
neuron pools to control the assembly of specific presynaptic inputs and thereby
influence the profile of activation of these motor neurons.
acknowledgement: The authors gratefully thank Dr. Silvia Arber, University of Basel
and Friedrich Miescher Institute for Biomedical Research, for support and in whose
lab the data were collected. For advice on statistical analysis, we thank Michael
Bottomley from the Statistical Consulting Center, College of Science and Mathematics,
Wright State University.
article_processing_charge: No
article_type: original
author:
- first_name: David R.
full_name: Ladle, David R.
last_name: Ladle
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Ladle DR, Hippenmeyer S. Loss of ETV1/ER81 in motor neurons leads to reduced
monosynaptic inputs from proprioceptive sensory neurons. Journal of Neurophysiology.
2023;129(3):501-512. doi:10.1152/jn.00172.2022
apa: Ladle, D. R., & Hippenmeyer, S. (2023). Loss of ETV1/ER81 in motor neurons
leads to reduced monosynaptic inputs from proprioceptive sensory neurons. Journal
of Neurophysiology. American Physiological Society. https://doi.org/10.1152/jn.00172.2022
chicago: Ladle, David R., and Simon Hippenmeyer. “Loss of ETV1/ER81 in Motor Neurons
Leads to Reduced Monosynaptic Inputs from Proprioceptive Sensory Neurons.” Journal
of Neurophysiology. American Physiological Society, 2023. https://doi.org/10.1152/jn.00172.2022.
ieee: D. R. Ladle and S. Hippenmeyer, “Loss of ETV1/ER81 in motor neurons leads
to reduced monosynaptic inputs from proprioceptive sensory neurons,” Journal
of Neurophysiology, vol. 129, no. 3. American Physiological Society, pp. 501–512,
2023.
ista: Ladle DR, Hippenmeyer S. 2023. Loss of ETV1/ER81 in motor neurons leads to
reduced monosynaptic inputs from proprioceptive sensory neurons. Journal of Neurophysiology.
129(3), 501–512.
mla: Ladle, David R., and Simon Hippenmeyer. “Loss of ETV1/ER81 in Motor Neurons
Leads to Reduced Monosynaptic Inputs from Proprioceptive Sensory Neurons.” Journal
of Neurophysiology, vol. 129, no. 3, American Physiological Society, 2023,
pp. 501–12, doi:10.1152/jn.00172.2022.
short: D.R. Ladle, S. Hippenmeyer, Journal of Neurophysiology 129 (2023) 501–512.
date_created: 2023-02-15T14:46:14Z
date_published: 2023-03-01T00:00:00Z
date_updated: 2023-09-05T12:13:34Z
day: '01'
department:
- _id: SiHi
doi: 10.1152/jn.00172.2022
external_id:
isi:
- '000957721600001'
pmid:
- '36695533'
intvolume: ' 129'
isi: 1
issue: '3'
keyword:
- Physiology
- General Neuroscience
language:
- iso: eng
month: '03'
oa_version: None
page: 501-512
pmid: 1
publication: Journal of Neurophysiology
publication_identifier:
eissn:
- 1522-1598
issn:
- 0022-3077
publication_status: published
publisher: American Physiological Society
quality_controlled: '1'
status: public
title: Loss of ETV1/ER81 in motor neurons leads to reduced monosynaptic inputs from
proprioceptive sensory neurons
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 129
year: '2023'
...
---
_id: '14647'
abstract:
- lang: eng
text: In the developing vertebrate central nervous system, neurons and glia typically
arise sequentially from common progenitors. Here, we report that the transcription
factor Forkhead Box G1 (Foxg1) regulates gliogenesis in the mouse neocortex via
distinct cell-autonomous roles in progenitors and in postmitotic neurons that
regulate different aspects of the gliogenic FGF signalling pathway. We demonstrate
that loss of Foxg1 in cortical progenitors at neurogenic stages causes premature
astrogliogenesis. We identify a novel FOXG1 target, the pro-gliogenic FGF pathway
component Fgfr3, which is suppressed by FOXG1 cell-autonomously to maintain neurogenesis.
Furthermore, FOXG1 can also suppress premature astrogliogenesis triggered by the
augmentation of FGF signalling. We identify a second novel function of FOXG1 in
regulating the expression of gliogenic ligand FGF18 in new born neocortical upper-layer
neurons. Loss of FOXG1 in postmitotic neurons increases Fgf18 expression and enhances
gliogenesis in the progenitors. These results fit well with the model that new
born neurons secrete cues that trigger progenitors to produce the next wave of
cell types, astrocytes. If FGF signalling is attenuated in Foxg1 null progenitors,
they progress to oligodendrocyte production. Therefore, loss of FOXG1 transitions
the progenitor to a gliogenic state, producing either astrocytes or oligodendrocytes
depending on FGF signalling levels. Our results uncover how FOXG1 integrates extrinsic
signalling via the FGF pathway to regulate the sequential generation of neurons,
astrocytes, and oligodendrocytes in the cerebral cortex.
acknowledgement: "We thank Dr. Shital Suryavanshi and the animal house staff of the
Tata Institute of\r\nFundamental Research (TIFR) for their excellent support; Gord
Fishell and Goichi Miyoshi for\r\nthe Foxg1 floxed mouse line; Hiroshi Kawasaki
for the plasmids pCAG-FGF8 and pCAGsFGFR3c. We thank Prof. S.K. Lee for the Foxg1lox/lox
genotyping primers and protocol. We thank Dr. Deepak Modi and Dr. Vainav Patel for
allowing us to use the NIRRCH FACS Facility and the staff of the NIRRCH and TIFR
FACS facilities for their assistance.\r\nWe thank Denis Jabaudon for his critical
comments on the manuscript and members of the\r\nJabaudon lab for helpful discussions.
This work was funded by the Department of Atomic\r\nEnergy (DAE), Govt. of India
(Project Identification no. RTI4003, DAE OM no.\r\n1303/2/2019/R&D-II/DAE/2079)."
article_processing_charge: No
author:
- first_name: Mahima
full_name: Bose, Mahima
last_name: Bose
- first_name: Varun
full_name: Suresh, Varun
last_name: Suresh
- first_name: Urvi
full_name: Mishra, Urvi
last_name: Mishra
- first_name: Ishita
full_name: Talwar, Ishita
last_name: Talwar
- first_name: Anuradha
full_name: Yadav, Anuradha
last_name: Yadav
- first_name: Shiona
full_name: Biswas, Shiona
last_name: Biswas
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Shubha
full_name: Tole, Shubha
last_name: Tole
citation:
ama: Bose M, Suresh V, Mishra U, et al. Dual role of FOXG1 in regulating gliogenesis
in the developing neocortex via the FGF signalling pathway. bioRxiv. doi:10.1101/2023.11.30.569337
apa: Bose, M., Suresh, V., Mishra, U., Talwar, I., Yadav, A., Biswas, S., … Tole,
S. (n.d.). Dual role of FOXG1 in regulating gliogenesis in the developing neocortex
via the FGF signalling pathway. bioRxiv. Cold Spring Harbor Laboratory.
https://doi.org/10.1101/2023.11.30.569337
chicago: Bose, Mahima, Varun Suresh, Urvi Mishra, Ishita Talwar, Anuradha Yadav,
Shiona Biswas, Simon Hippenmeyer, and Shubha Tole. “Dual Role of FOXG1 in Regulating
Gliogenesis in the Developing Neocortex via the FGF Signalling Pathway.” BioRxiv.
Cold Spring Harbor Laboratory, n.d. https://doi.org/10.1101/2023.11.30.569337.
ieee: M. Bose et al., “Dual role of FOXG1 in regulating gliogenesis in the
developing neocortex via the FGF signalling pathway,” bioRxiv. Cold Spring
Harbor Laboratory.
ista: Bose M, Suresh V, Mishra U, Talwar I, Yadav A, Biswas S, Hippenmeyer S, Tole
S. Dual role of FOXG1 in regulating gliogenesis in the developing neocortex via
the FGF signalling pathway. bioRxiv, 10.1101/2023.11.30.569337.
mla: Bose, Mahima, et al. “Dual Role of FOXG1 in Regulating Gliogenesis in the Developing
Neocortex via the FGF Signalling Pathway.” BioRxiv, Cold Spring Harbor
Laboratory, doi:10.1101/2023.11.30.569337.
short: M. Bose, V. Suresh, U. Mishra, I. Talwar, A. Yadav, S. Biswas, S. Hippenmeyer,
S. Tole, BioRxiv (n.d.).
date_created: 2023-12-06T13:07:01Z
date_published: 2023-12-01T00:00:00Z
date_updated: 2023-12-11T07:37:17Z
day: '01'
department:
- _id: SiHi
doi: 10.1101/2023.11.30.569337
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1101/2023.11.30.569337
month: '12'
oa: 1
oa_version: Preprint
publication: bioRxiv
publication_status: submitted
publisher: Cold Spring Harbor Laboratory
status: public
title: Dual role of FOXG1 in regulating gliogenesis in the developing neocortex via
the FGF signalling pathway
type: preprint
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2023'
...
---
_id: '14683'
abstract:
- lang: eng
text: "Mosaic analysis with double markers (MADM) technology enables the generation
of genetic mosaic tissue in mice and high-resolution phenotyping at the individual
cell level. Here, we present a protocol for isolating MADM-labeled cells with
high yield for downstream molecular analyses using fluorescence-activated cell
sorting (FACS). We describe steps for generating MADM-labeled mice, perfusion,
single-cell suspension, and debris removal. We then detail procedures for cell
sorting by FACS and downstream analysis. This protocol is suitable for embryonic
to adult mice.\r\nFor complete details on the use and execution of this protocol,
please refer to Contreras et al. (2021).1"
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 Imaging & Optics Facility (IOF)
and Preclinical Facilities (PCF). N.A. received support from FWF Firnberg-Programme
(T 1031). G.C. received support from the European Union’s Horizon 2020 research
and innovation programme under the Marie Skłodowska-Curie grant agreement no. 754411
as an ISTplus postdoctoral fellow. 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: '102771'
article_processing_charge: No
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: Giselle T
full_name: Cheung, Giselle T
id: 471195F6-F248-11E8-B48F-1D18A9856A87
last_name: Cheung
orcid: 0000-0001-8457-2572
- 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, Cheung GT, Hippenmeyer S. Protocol for sorting cells from mouse brains
labeled with mosaic analysis with double markers by flow cytometry. STAR Protocols.
2023;5(1). doi:10.1016/j.xpro.2023.102771
apa: Amberg, N., Cheung, G. T., & Hippenmeyer, S. (2023). Protocol for sorting
cells from mouse brains labeled with mosaic analysis with double markers by flow
cytometry. STAR Protocols. Elsevier. https://doi.org/10.1016/j.xpro.2023.102771
chicago: Amberg, Nicole, Giselle T Cheung, and Simon Hippenmeyer. “Protocol for
Sorting Cells from Mouse Brains Labeled with Mosaic Analysis with Double Markers
by Flow Cytometry.” STAR Protocols. Elsevier, 2023. https://doi.org/10.1016/j.xpro.2023.102771.
ieee: N. Amberg, G. T. Cheung, and S. Hippenmeyer, “Protocol for sorting cells from
mouse brains labeled with mosaic analysis with double markers by flow cytometry,”
STAR Protocols, vol. 5, no. 1. Elsevier, 2023.
ista: Amberg N, Cheung GT, Hippenmeyer S. 2023. Protocol for sorting cells from
mouse brains labeled with mosaic analysis with double markers by flow cytometry.
STAR Protocols. 5(1), 102771.
mla: Amberg, Nicole, et al. “Protocol for Sorting Cells from Mouse Brains Labeled
with Mosaic Analysis with Double Markers by Flow Cytometry.” STAR Protocols,
vol. 5, no. 1, 102771, Elsevier, 2023, doi:10.1016/j.xpro.2023.102771.
short: N. Amberg, G.T. Cheung, S. Hippenmeyer, STAR Protocols 5 (2023).
date_created: 2023-12-13T11:48:05Z
date_published: 2023-12-08T00:00:00Z
date_updated: 2023-12-18T08:06:14Z
day: '08'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1016/j.xpro.2023.102771
ec_funded: 1
external_id:
pmid:
- '38070137'
intvolume: ' 5'
issue: '1'
keyword:
- General Immunology and Microbiology
- General Biochemistry
- Genetics and Molecular Biology
- General Neuroscience
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1016/j.xpro.2023.102771
month: '12'
oa: 1
oa_version: Submitted 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: 260C2330-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '754411'
name: ISTplus - Postdoctoral Fellowships
- _id: 059F6AB4-7A3F-11EA-A408-12923DDC885E
grant_number: F07805
name: Molecular Mechanisms of Neural Stem Cell Lineage Progression
- _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: epub_ahead
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Protocol for sorting cells from mouse brains labeled with mosaic analysis with
double markers by flow cytometry
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: '2023'
...
---
_id: '14757'
abstract:
- lang: eng
text: The cerebral cortex is comprised of a vast cell-type diversity sequentially
generated by cortical progenitor cells. Faithful progenitor lineage progression
requires the tight orchestration of distinct molecular and cellular mechanisms
regulating proper progenitor proliferation behavior and differentiation. Correct
execution of developmental programs involves a complex interplay of cell intrinsic
and tissue-wide mechanisms. Many studies over the past decades have been able
to determine a plethora of genes critically involved in cortical development.
However, only a few made use of genetic paradigms with sparse and global gene
deletion to probe cell-autonomous vs. tissue-wide contribution. In this chapter,
we will elaborate on the importance of dissecting the cell-autonomous and tissue-wide
mechanisms to gain a precise understanding of gene function during radial glial
progenitor lineage progression.
article_processing_charge: No
author:
- first_name: Ana
full_name: Villalba Requena, Ana
id: 68cb85a0-39f7-11eb-9559-9aaab4f6a247
last_name: Villalba Requena
orcid: 0000-0002-5615-5277
- 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: 'Villalba Requena A, Amberg N, Hippenmeyer S. Interplay of Cell‐autonomous
Gene Function and Tissue‐wide Mechanisms Regulating Radial Glial Progenitor Lineage
Progression. In: Huttner W, ed. Neocortical Neurogenesis in Development and
Evolution. Wiley; 2023:169-191. doi:10.1002/9781119860914.ch10'
apa: Villalba Requena, A., Amberg, N., & Hippenmeyer, S. (2023). Interplay of
Cell‐autonomous Gene Function and Tissue‐wide Mechanisms Regulating Radial Glial
Progenitor Lineage Progression. In W. Huttner (Ed.), Neocortical Neurogenesis
in Development and Evolution (pp. 169–191). Wiley. https://doi.org/10.1002/9781119860914.ch10
chicago: Villalba Requena, Ana, Nicole Amberg, and Simon Hippenmeyer. “Interplay
of Cell‐autonomous Gene Function and Tissue‐wide Mechanisms Regulating Radial
Glial Progenitor Lineage Progression.” In Neocortical Neurogenesis in Development
and Evolution, edited by Wieland Huttner, 169–91. Wiley, 2023. https://doi.org/10.1002/9781119860914.ch10.
ieee: A. Villalba Requena, N. Amberg, and S. Hippenmeyer, “Interplay of Cell‐autonomous
Gene Function and Tissue‐wide Mechanisms Regulating Radial Glial Progenitor Lineage
Progression,” in Neocortical Neurogenesis in Development and Evolution,
W. Huttner, Ed. Wiley, 2023, pp. 169–191.
ista: 'Villalba Requena A, Amberg N, Hippenmeyer S. 2023.Interplay of Cell‐autonomous
Gene Function and Tissue‐wide Mechanisms Regulating Radial Glial Progenitor Lineage
Progression. In: Neocortical Neurogenesis in Development and Evolution. , 169–191.'
mla: Villalba Requena, Ana, et al. “Interplay of Cell‐autonomous Gene Function and
Tissue‐wide Mechanisms Regulating Radial Glial Progenitor Lineage Progression.”
Neocortical Neurogenesis in Development and Evolution, edited by Wieland
Huttner, Wiley, 2023, pp. 169–91, doi:10.1002/9781119860914.ch10.
short: A. Villalba Requena, N. Amberg, S. Hippenmeyer, in:, W. Huttner (Ed.), Neocortical
Neurogenesis in Development and Evolution, Wiley, 2023, pp. 169–191.
date_created: 2024-01-08T13:16:36Z
date_published: 2023-08-08T00:00:00Z
date_updated: 2024-01-09T09:46:57Z
day: '08'
department:
- _id: SiHi
doi: 10.1002/9781119860914.ch10
editor:
- first_name: Wieland
full_name: Huttner, Wieland
last_name: Huttner
language:
- iso: eng
month: '08'
oa_version: None
page: 169-191
publication: Neocortical Neurogenesis in Development and Evolution
publication_identifier:
eisbn:
- '9781119860914'
publication_status: published
publisher: Wiley
quality_controlled: '1'
scopus_import: '1'
status: public
title: Interplay of Cell‐autonomous Gene Function and Tissue‐wide Mechanisms Regulating
Radial Glial Progenitor Lineage Progression
type: book_chapter
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2023'
...
---
_id: '14783'
abstract:
- lang: eng
text: Connexin 43, an astroglial gap junction protein, is enriched in perisynaptic
astroglial processes and plays major roles in synaptic transmission. We have previously
found that astroglial Cx43 controls synaptic glutamate levels and allows for activity-dependent
glutamine release to sustain physiological synaptic transmissions and cognitiogns.
However, whether Cx43 is important for the release of synaptic vesicles, which
is a critical component of synaptic efficacy, remains unanswered. Here, using
transgenic mice with a glial conditional knockout of Cx43 (Cx43−/−), we investigate
whether and how astrocytes regulate the release of synaptic vesicles from hippocampal
synapses. We report that CA1 pyramidal neurons and their synapses develop normally
in the absence of astroglial Cx43. However, a significant impairment in synaptic
vesicle distribution and release dynamics were observed. In particular, the FM1-43
assays performed using two-photon live imaging and combined with multi-electrode
array stimulation in acute hippocampal slices, revealed a slower rate of synaptic
vesicle release in Cx43−/− mice. Furthermore, paired-pulse recordings showed that
synaptic vesicle release probability was also reduced and is dependent on glutamine
supply via Cx43 hemichannel (HC). Taken together, we have uncovered a role for
Cx43 in regulating presynaptic functions by controlling the rate and probability
of synaptic vesicle release. Our findings further highlight the significance of
astroglial Cx43 in synaptic transmission and efficacy.
acknowledgement: 'This research was funded by grants from the European Research Council
(Consolidator grant #683154) and European Union’s Horizon 2020 research and innovation
program (Marie Sklodowska-Curie Innovative Training Networks, grant #722053, EU-GliaPhD)
to N.R., as well as from FP7-PEOPLE Marie Curie Intra-European Fellowship for career
development (grant #622289) to G.C. We thank Elena Dossi, Grégory Ghézali, and Jérémie
Teillon for support with setting up the MEA system for the two-photon microscope.
We would also like to thank Tayfun Palaz for their technical assistance with the
EM preparations.'
article_number: '1133'
article_processing_charge: Yes
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: Oana
full_name: Chever, Oana
last_name: Chever
- first_name: Astrid
full_name: Rollenhagen, Astrid
last_name: Rollenhagen
- first_name: Nicole
full_name: Quenech’du, Nicole
last_name: Quenech’du
- first_name: Pascal
full_name: Ezan, Pascal
last_name: Ezan
- first_name: Joachim H. R.
full_name: Lübke, Joachim H. R.
last_name: Lübke
- first_name: Nathalie
full_name: Rouach, Nathalie
last_name: Rouach
citation:
ama: Cheung GT, Chever O, Rollenhagen A, et al. Astroglial connexin 43 regulates
synaptic vesicle release at hippocampal synapses. Cells. 2023;12(8). doi:10.3390/cells12081133
apa: Cheung, G. T., Chever, O., Rollenhagen, A., Quenech’du, N., Ezan, P., Lübke,
J. H. R., & Rouach, N. (2023). Astroglial connexin 43 regulates synaptic vesicle
release at hippocampal synapses. Cells. MDPI. https://doi.org/10.3390/cells12081133
chicago: Cheung, Giselle T, Oana Chever, Astrid Rollenhagen, Nicole Quenech’du,
Pascal Ezan, Joachim H. R. Lübke, and Nathalie Rouach. “Astroglial Connexin 43
Regulates Synaptic Vesicle Release at Hippocampal Synapses.” Cells. MDPI,
2023. https://doi.org/10.3390/cells12081133.
ieee: G. T. Cheung et al., “Astroglial connexin 43 regulates synaptic vesicle
release at hippocampal synapses,” Cells, vol. 12, no. 8. MDPI, 2023.
ista: Cheung GT, Chever O, Rollenhagen A, Quenech’du N, Ezan P, Lübke JHR, Rouach
N. 2023. Astroglial connexin 43 regulates synaptic vesicle release at hippocampal
synapses. Cells. 12(8), 1133.
mla: Cheung, Giselle T., et al. “Astroglial Connexin 43 Regulates Synaptic Vesicle
Release at Hippocampal Synapses.” Cells, vol. 12, no. 8, 1133, MDPI, 2023,
doi:10.3390/cells12081133.
short: G.T. Cheung, O. Chever, A. Rollenhagen, N. Quenech’du, P. Ezan, J.H.R. Lübke,
N. Rouach, Cells 12 (2023).
date_created: 2024-01-10T09:46:35Z
date_published: 2023-04-11T00:00:00Z
date_updated: 2024-01-16T09:29:35Z
day: '11'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.3390/cells12081133
external_id:
isi:
- '000977445700001'
pmid:
- '37190042'
file:
- access_level: open_access
checksum: 6798cd75d8857976fbc58a43fd173d68
content_type: application/pdf
creator: dernst
date_created: 2024-01-16T09:26:52Z
date_updated: 2024-01-16T09:26:52Z
file_id: '14808'
file_name: 2023_Cells_Cheung.pdf
file_size: 7931643
relation: main_file
success: 1
file_date_updated: 2024-01-16T09:26:52Z
has_accepted_license: '1'
intvolume: ' 12'
isi: 1
issue: '8'
keyword:
- General Medicine
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
pmid: 1
publication: Cells
publication_identifier:
issn:
- 2073-4409
publication_status: published
publisher: MDPI
quality_controlled: '1'
status: public
title: Astroglial connexin 43 regulates synaptic vesicle release at hippocampal synapses
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: 12
year: '2023'
...
---
_id: '12802'
abstract:
- lang: eng
text: Little is known about the critical metabolic changes that neural cells have
to undergo during development and how temporary shifts in this program can influence
brain circuitries and behavior. Inspired by the discovery that mutations in SLC7A5,
a transporter of metabolically essential large neutral amino acids (LNAAs), lead
to autism, we employed metabolomic profiling to study the metabolic states of
the cerebral cortex across different developmental stages. We found that the forebrain
undergoes significant metabolic remodeling throughout development, with certain
groups of metabolites showing stage-specific changes, but what are the consequences
of perturbing this metabolic program? By manipulating Slc7a5 expression in neural
cells, we found that the metabolism of LNAAs and lipids are interconnected in
the cortex. Deletion of Slc7a5 in neurons affects the postnatal metabolic state,
leading to a shift in lipid metabolism. Additionally, it causes stage- and cell-type-specific
alterations in neuronal activity patterns, resulting in a long-term circuit dysfunction.
acknowledged_ssus:
- _id: PreCl
- _id: EM-Fac
- _id: Bio
- _id: LifeSc
acknowledgement: We thank A. Freeman and V. Voronin for technical assistance, S. Deixler,
A. Stichelberger, M. Schunn, and the Preclinical Facility for managing our animal
colony. We thank L. Andersen and J. Sonntag, who were involved in generating the
MADM lines. We thank the ISTA LSF Mass Spectrometry Core Facility for assistance
with the proteomic analysis, as well as the ISTA electron microscopy and Imaging
and Optics facility for technical support. Metabolomics LC-MS/MS analysis was performed
by the Metabolomics Facility at Vienna BioCenter Core Facilities (VBCF). We acknowledge
the support of the EMBL Metabolomics Core Facility (MCF) for lipidomics and intracellular
metabolomics mass spectrometry data acquisition and analysis. RNA sequencing was
performed by the Next Generation Sequencing Facility at VBCF. Schematics were generated
using Biorender.com. This work was supported by the Austrian Science Fund (FWF,
DK W1232-B24) and by the European Union’s Horizon 2020 research and innovation program
(ERC) grant 725780 (LinPro) to S.H. and 715508 (REVERSEAUTISM) to G.N.
article_processing_charge: Yes (via OA deal)
article_type: original
author:
- first_name: Lisa
full_name: Knaus, Lisa
id: 3B2ABCF4-F248-11E8-B48F-1D18A9856A87
last_name: Knaus
- first_name: Bernadette
full_name: Basilico, Bernadette
id: 36035796-5ACA-11E9-A75E-7AF2E5697425
last_name: Basilico
orcid: 0000-0003-1843-3173
- first_name: Daniel
full_name: Malzl, Daniel
last_name: Malzl
- first_name: Maria
full_name: Gerykova Bujalkova, Maria
last_name: Gerykova Bujalkova
- first_name: Mateja
full_name: Smogavec, Mateja
last_name: Smogavec
- first_name: Lena A.
full_name: Schwarz, Lena A.
last_name: Schwarz
- first_name: Sarah
full_name: Gorkiewicz, Sarah
id: f141a35d-15a9-11ec-9fb2-fef6becc7b6f
last_name: Gorkiewicz
- 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
orcid: 0000-0002-7462-0048
- first_name: Christian
full_name: Knittl-Frank, Christian
last_name: Knittl-Frank
- first_name: Marianna
full_name: Tassinari, Marianna
id: 7af593f1-d44a-11ed-bf94-a3646a6bb35e
last_name: Tassinari
- first_name: Nuno
full_name: Maulide, Nuno
last_name: Maulide
- first_name: Thomas
full_name: Rülicke, Thomas
last_name: Rülicke
- first_name: Jörg
full_name: Menche, Jörg
last_name: Menche
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Gaia
full_name: Novarino, Gaia
id: 3E57A680-F248-11E8-B48F-1D18A9856A87
last_name: Novarino
orcid: 0000-0002-7673-7178
citation:
ama: Knaus L, Basilico B, Malzl D, et al. Large neutral amino acid levels tune perinatal
neuronal excitability and survival. Cell. 2023;186(9):1950-1967.e25. doi:10.1016/j.cell.2023.02.037
apa: Knaus, L., Basilico, B., Malzl, D., Gerykova Bujalkova, M., Smogavec, M., Schwarz,
L. A., … Novarino, G. (2023). Large neutral amino acid levels tune perinatal neuronal
excitability and survival. Cell. Elsevier. https://doi.org/10.1016/j.cell.2023.02.037
chicago: Knaus, Lisa, Bernadette Basilico, Daniel Malzl, Maria Gerykova Bujalkova,
Mateja Smogavec, Lena A. Schwarz, Sarah Gorkiewicz, et al. “Large Neutral Amino
Acid Levels Tune Perinatal Neuronal Excitability and Survival.” Cell. Elsevier,
2023. https://doi.org/10.1016/j.cell.2023.02.037.
ieee: L. Knaus et al., “Large neutral amino acid levels tune perinatal neuronal
excitability and survival,” Cell, vol. 186, no. 9. Elsevier, p. 1950–1967.e25,
2023.
ista: Knaus L, Basilico B, Malzl D, Gerykova Bujalkova M, Smogavec M, Schwarz LA,
Gorkiewicz S, Amberg N, Pauler F, Knittl-Frank C, Tassinari M, Maulide N, Rülicke
T, Menche J, Hippenmeyer S, Novarino G. 2023. Large neutral amino acid levels
tune perinatal neuronal excitability and survival. Cell. 186(9), 1950–1967.e25.
mla: Knaus, Lisa, et al. “Large Neutral Amino Acid Levels Tune Perinatal Neuronal
Excitability and Survival.” Cell, vol. 186, no. 9, Elsevier, 2023, p. 1950–1967.e25,
doi:10.1016/j.cell.2023.02.037.
short: L. Knaus, B. Basilico, D. Malzl, M. Gerykova Bujalkova, M. Smogavec, L.A.
Schwarz, S. Gorkiewicz, N. Amberg, F. Pauler, C. Knittl-Frank, M. Tassinari, N.
Maulide, T. Rülicke, J. Menche, S. Hippenmeyer, G. Novarino, Cell 186 (2023) 1950–1967.e25.
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title: Large neutral amino acid levels tune perinatal neuronal excitability and survival
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