Extracellular matrix-inducing Sox9 promotes both basal progenitor proliferation and gliogenesis in developing neocortex.


Journal

eLife
ISSN: 2050-084X
Titre abrégé: Elife
Pays: England
ID NLM: 101579614

Informations de publication

Date de publication:
19 03 2020
Historique:
received: 30 06 2019
accepted: 18 03 2020
pubmed: 20 3 2020
medline: 31 3 2021
entrez: 20 3 2020
Statut: epublish

Résumé

Neocortex expansion is largely based on the proliferative capacity of basal progenitors (BPs), which is increased by extracellular matrix (ECM) components via integrin signaling. Here we show that the transcription factor Sox9 drives expression of ECM components and that laminin 211 increases BP proliferation in embryonic mouse neocortex. We show that Sox9 is expressed in human and ferret BPs and is required for BP proliferation in embryonic ferret neocortex. Conditional Sox9 expression in the mouse BP lineage, where it normally is not expressed, increases BP proliferation, reduces Tbr2 levels and induces Olig2 expression, indicative of premature gliogenesis. Conditional Sox9 expression also results in cell-non-autonomous stimulation of BP proliferation followed by increased upper-layer neuron production. Our findings demonstrate that Sox9 exerts concerted effects on transcription, BP proliferation, neuron production, and neurogenic vs. gliogenic BP cell fate, suggesting that Sox9 may have contributed to promote neocortical expansion.

Identifiants

pubmed: 32191207
doi: 10.7554/eLife.49808
pii: 49808
pmc: PMC7105383
doi:
pii:

Substances chimiques

SOX9 Transcription Factor 0
SOX9 protein, human 0

Banques de données

GEO
['GSE134162', 'GSE38805', 'GSE65000']

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : Medical Research Council
ID : G0701018
Pays : United Kingdom
Organisme : Medical Research Council
ID : G1100578
Pays : United Kingdom
Organisme : Medical Research Council
ID : MR/N004272/1
Pays : United Kingdom
Organisme : Deutsche Forschungsgemeinschaft
ID : SFB 655
Organisme : Deutsche Forschungsgemeinschaft
ID : SFB 655,A2
Organisme : European Research Council
ID : 250197
Pays : International
Organisme : Medical Research Council
ID : MR/R006237/1
Pays : United Kingdom
Organisme : Deutsche Forschungsgemeinschaft
ID : A2

Informations de copyright

© 2020, Güven et al.

Déclaration de conflit d'intérêts

AG, NK, KL, MF, SV, HB, DS, WH No competing interests declared

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Auteurs

Ayse Güven (A)

Max Planck Institute of Molecular Cell Biology and Genetics, Dresden, Germany.

Nereo Kalebic (N)

Max Planck Institute of Molecular Cell Biology and Genetics, Dresden, Germany.
Human Technopole, Milan, Italy.

Katherine R Long (KR)

Max Planck Institute of Molecular Cell Biology and Genetics, Dresden, Germany.

Marta Florio (M)

Max Planck Institute of Molecular Cell Biology and Genetics, Dresden, Germany.

Samir Vaid (S)

Max Planck Institute of Molecular Cell Biology and Genetics, Dresden, Germany.

Holger Brandl (H)

Max Planck Institute of Molecular Cell Biology and Genetics, Dresden, Germany.

Denise Stenzel (D)

Max Planck Institute of Molecular Cell Biology and Genetics, Dresden, Germany.

Wieland B Huttner (WB)

Max Planck Institute of Molecular Cell Biology and Genetics, Dresden, Germany.

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