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Science 2 January 2004:
Vol. 303. no. 5654, pp. 56 - 59
DOI: 10.1126/science.1090674
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Research Articles

Foxg1 Suppresses Early Cortical Cell Fate

Carina Hanashima,1,2 Suzanne C. Li,2* Lijian Shen,3 Eseng Lai,2{dagger}{ddagger} Gord Fishell1{ddagger}

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.

1 Developmental Genetics Program and the Department of Cell Biology, The Skirball Institute of Biomolecular Medicine, New York University Medical Center, 540 First Avenue, New York, NY 10016, USA.
2 Cell Biology Program, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, NY 10021, USA.
3 Department of Physiology and Biophysics, Weill Medical College of Cornell University, New York, NY 10021, USA.



* Present address: Hackensack University Medical Center, 30 Prospect Avenue, Hackensack, NJ 07601, USA.

{dagger} Present address: Clinical Pharmacology, Merck Research Labs, RY34-A-428, 126 East Lincoln Avenue, Rahway, NJ 07065–0900, USA.

{ddagger} To whom correspondence should be addressed. E-mail: fishell{at}saturn.med.nyu.edu (G.F.); eseng_lai{at}merck.com (E.L.)

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