Foxg1 suppresses early cortical cell fate Journal Article


Authors: Hanashima, C.; Li, S. C.; Shen, L.; Lai, E.; Fishell, G.
Article Title: Foxg1 suppresses early cortical cell fate
Abstract: During mammalian cerebral corticogenesis, progenitor cells become progressively restricted in the types of neurons they can produce. The molecular mechanism that determines earlier versus later born neuron fate is unknown. We demonstrate here that the generation of the earliest born neurons, the Cajal-Retzius cells, is suppressed by the telencephalic transcription factor Foxg1. In Foxg1 null mutants, we observed an excess of Cajal-Retzius neuron production in the cortex. By conditionally inactivating Foxg1 in cortical progenitors that normally produce deep-layer cortical neurons, we demonstrate that Foxg1 is constitutively required to suppress Cajal-Retzius cell fate. Hence, the competence to generate the earliest born neurons during later cortical development is actively suppressed but not lost.
Keywords: mutation; dna-binding proteins; nonhuman; forkhead transcription factors; mammalia; animals; mice; gene; biology; nerve tissue proteins; transcription factor; cell fate; gene function; cell differentiation; neurons; time factors; cell lineage; mice, transgenic; transcription factors; stem cell; gene expression regulation, developmental; serine endopeptidases; brain development; mammal; stem cells; gene control; foxg1 gene; molecular biology; cerebral cortex; doxycycline; nerve cell differentiation; neurology; cells; telencephalon; crosses, genetic; brain cell; extracellular matrix proteins; male; female; priority journal; article; cell adhesion molecules, neuronal; protoplasmatic astrocyte
Journal Title: Science
Volume: 303
Issue: 5654
ISSN: 0036-8075
Publisher: American Association for the Advancement of Science  
Date Published: 2004-01-02
Start Page: 56
End Page: 59
Language: English
DOI: 10.1126/science.1090674
PROVIDER: scopus
PUBMED: 14704420
DOI/URL:
Notes: Science -- Cited By (since 1996):174 -- Export Date: 16 June 2014 -- CODEN: SCIEA -- Source: Scopus
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  1. Eseng Lai
    45 Lai
  2. Suzanne C Li
    6 Li