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Previous Article | Next Article
The Journal of Neuroscience, August 1, 2002, 22(15):6526-6536
Brain Factor-1 Controls the Proliferation and Differentiation of Neocortical Progenitor Cells through Independent Mechanisms
Carina Hanashima1, *, Lijian Shen1, 2, *, Suzanne C. Li1, and Eseng Lai1 1 Cell Biology Program, Memorial Sloan-Kettering Cancer Center, New York, New York 10021, and 2 Program of Physiology, Biophysics and Molecular Medicine, Graduate School of Medical Sciences, Weill Medical College, Cornell University, New York, New York 10021
The winged helix gene Brain factor-1 (BF1) has a pleiotropic role in the development of the cerebral hemispheres of the brain. Mice lacking BF1 have defects in the morphogenesis of the structures of the dorsal telencephalon (e.g., neocortex) and the ventral telencephalon (e.g., the basal ganglia). This study focuses on the functions of BF1 in the dorsal telencephalon. We showed previously that telencephalic progenitor cells lacking BF1 differentiate into neurons prematurely. Here, we demonstrate that the loss of BF1 also results in an early lengthening of the cell cycle in neocortical progenitors. To investigate the mechanisms by which BF1 regulates progenitor cell proliferation and differentiation in the developing brain, we have replaced the endogenous BF1 protein with a DNA binding defective form of BF1 in mice, BF1NHAA. The BF1NHAA protein restores the growth of the dorsal telencephalon, by improving the proliferation of progenitor cells. However, the BF1NHAA protein does not correct the early neuronal differentiation associated with the loss of BF1. In contrast, replacement of endogenous BF1 with wild-type BF1 corrects the defects in both the proliferation and differentiation of neocortical progenitors. These results demonstrate that BF1 controls progenitor cell proliferation and differentiation in the neocortex through distinct DNA binding-independent and binding-dependent mechanisms.
Key words: BF1; foxg1; winged helix; neocortex; brain development; telencephalon; neurogenesis
* C.H. and L.S. contributed equally to this work.
Copyright © 2002 Society for Neuroscience 0270-6474/02/22156526-11$05.00/0
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