A conserved molecular logic for neurogenesis to gliogenesis switch in the cerebral cortex.
Animals
Neurogenesis
/ physiology
Cerebral Cortex
/ metabolism
Basic Helix-Loop-Helix Transcription Factors
/ metabolism
ErbB Receptors
/ metabolism
Mice
Oligodendrocyte Transcription Factor 2
/ metabolism
Nerve Tissue Proteins
/ metabolism
Hedgehog Proteins
/ metabolism
PAX6 Transcription Factor
/ metabolism
Neural Stem Cells
/ metabolism
Homeodomain Proteins
/ metabolism
Zinc Finger Protein Gli3
/ metabolism
Eye Proteins
/ metabolism
Repressor Proteins
/ metabolism
Paired Box Transcription Factors
/ metabolism
Neuroglia
/ metabolism
Gene Expression Regulation, Developmental
Signal Transduction
Olfactory Bulb
/ metabolism
Cell Lineage
Humans
Olig2
enhancer
gliogenesis
lineage switch
neurogenesis
Journal
Proceedings of the National Academy of Sciences of the United States of America
ISSN: 1091-6490
Titre abrégé: Proc Natl Acad Sci U S A
Pays: United States
ID NLM: 7505876
Informations de publication
Date de publication:
14 May 2024
14 May 2024
Historique:
medline:
7
5
2024
pubmed:
7
5
2024
entrez:
7
5
2024
Statut:
ppublish
Résumé
During development, neural stem cells in the cerebral cortex, also known as radial glial cells (RGCs), generate excitatory neurons, followed by production of cortical macroglia and inhibitory neurons that migrate to the olfactory bulb (OB). Understanding the mechanisms for this lineage switch is fundamental for unraveling how proper numbers of diverse neuronal and glial cell types are controlled. We and others recently showed that Sonic Hedgehog (Shh) signaling promotes the cortical RGC lineage switch to generate cortical oligodendrocytes and OB interneurons. During this process, cortical RGCs generate intermediate progenitor cells that express critical gliogenesis genes
Identifiants
pubmed: 38713624
doi: 10.1073/pnas.2321711121
doi:
Substances chimiques
Basic Helix-Loop-Helix Transcription Factors
0
ErbB Receptors
EC 2.7.10.1
Oligodendrocyte Transcription Factor 2
0
Nerve Tissue Proteins
0
Hedgehog Proteins
0
PAX6 Transcription Factor
0
Ascl1 protein, mouse
0
Olig2 protein, mouse
0
Pax6 protein, mouse
0
Homeodomain Proteins
0
Zinc Finger Protein Gli3
0
Eye Proteins
0
Repressor Proteins
0
Paired Box Transcription Factors
0
EGFR protein, mouse
EC 2.7.10.1
Gli3 protein, mouse
0
Shh protein, mouse
0
PAX6 protein, human
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e2321711121Subventions
Organisme : NIMH NIH HHS
ID : R01 MH094589
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS089777
Pays : United States
Organisme : NIMH NIH HHS
ID : R01 MH117106
Pays : United States
Organisme : NIDCR NIH HHS
ID : R01 DE028599
Pays : United States
Organisme : NIMH NIH HHS
ID : R01 MH129419
Pays : United States
Organisme : NIDA NIH HHS
ID : U01 DA052713
Pays : United States
Organisme : NIDA NIH HHS
ID : U01 DA052713
Pays : United States
Déclaration de conflit d'intérêts
Competing interests statement:The authors declare no competing interest.