Excess FoxG1 causes overgrowth of the neural tube

Authors

  • Sara Ahlgren,

    Corresponding author
    1. Division of Biology 139-74, California Institute of Technology, Pasadena, California 91125
    Current affiliation:
    1. Developmental Systems Biology Program, Department of Pediatrics, Feinberg School of Medicine, Northwestern University, Children's Memorial Institute for Education and Research, 2300 Children's Plaza, Box 204, Chicago, IL 60614-3394
    • Division of Biology 139-74, California Institute of Technology, Pasadena, California 91125
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  • Peter Vogt,

    1. Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, California 92037
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  • Marianne Bronner-Fraser

    1. Division of Biology 139-74, California Institute of Technology, Pasadena, California 91125
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Abstract

The winged helix transcription factor FoxG1 (Bf-1, qin) plays multiple roles in the development of the telencephalon, with different parts of the protein affecting either proliferation or differentiation. We examined the consequences of over-expression, via retroviral expression, of FoxG1 on the growth of different regions of the chicken brain. Excess expression of FoxG1 caused a thickening of the neuroepithelium, and ultimately large outgrowths of the telencephalon and mesencephalon. In contrast, the myelencephalon appeared unaffected, exhibiting normal apoptosis and growth characteristics. A DNA binding defective form of FoxG1 did not exhibit these abnormalities, suggesting that these effects are due to FoxG1's function as a transcriptional repressor. To examine the means by which excess FoxG1caused overgrowth of the brain, we examined alterations in cell proliferation and death. No increase in proliferation was noted in any portion of the neural tube, rather a significant decrease in neuroepithelial apoptosis was seen. These results demonstrate a previously unrecognized role for winged helix factors in the regulation of neural cell apoptosis. © 2003 Wiley Periodicals, Inc. J Neurobiol 57: 337–349, 2003

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