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Foxg1 suppresses early cortical cell fate
Carina Hanashima1, Suzanne C Li, Lijian Shen
1Developmental 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.
Science (New York, N.Y.)
|January 6, 2004
Summary
The transcription factor Foxg1 suppresses the generation of early-born Cajal-Retzius neurons during mammalian brain development. Loss of Foxg1 leads to an overproduction of these crucial neurons.
Area of Science:
- Neuroscience
- Developmental Biology
- Genetics
Background:
- Mammalian cerebral corticogenesis involves progenitor cells progressively restricting neuronal output.
- The molecular mechanisms governing the fate of early-born versus late-born neurons remain unclear.
Purpose of the Study:
- To investigate the molecular regulation of early-born neuron production during corticogenesis.
- To identify the role of the transcription factor Foxg1 in determining neuronal fate.
Main Methods:
- Utilized Foxg1 null mutant mice to observe effects on Cajal-Retzius neuron production.
- Employed conditional inactivation of Foxg1 in specific cortical progenitor populations.
Main Results:
- Foxg1 null mutants exhibited an excess of Cajal-Retzius neuron production in the cortex.
- Constitutive requirement of Foxg1 for suppressing Cajal-Retzius cell fate demonstrated via conditional inactivation.
Conclusions:
- The transcription factor Foxg1 actively suppresses Cajal-Retzius cell fate during corticogenesis.
- The potential to generate early-born neurons is actively repressed, not lost, during later cortical development.
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