Abstract: |
During corticogenesis, the balance between the self-renewal of radial glial stem cells and the production of their descendent progenitor cells is essential in generating the correct size and cell composition of the neocortex. How the stem-to-progenitor cell transition is regulated is poorly understood. FGFs are commonly implicated in promoting proliferation of neural precursor cells, but it is unclear how they exert their effects on stem cells, progenitor cells, or both in vivo. Here, three FGF receptor genes are simultaneously deleted during cortical neurogenesis. In these mutants, radial glia are depleted due to an increased transition from an uncommitted state to a more differentiated one, initially causing an increase in progenitors, but ultimately resulting in a smaller cortex. The proliferation rate of progenitors themselves, however, is unchanged. These results indicate that FGFs normally repress the radial glia to progenitor cell transition during corticogenesis. Copyright © 2009 Society for Neuroscience. |
Keywords: |
signal transduction; controlled study; gene deletion; nonhuman; cell proliferation; animal cell; mouse; animals; mice; mice, knockout; animal tissue; cell survival; embryo; brain cortex; cell renewal; neural stem cell; cell differentiation; fibroblast growth factor receptor 3; mice, transgenic; cell transformation; glia cell; neuroglia; stem cells; pregnancy; cerebral cortex; nerve cell differentiation; nervous system development; neurogenesis; receptor gene; receptor, fibroblast growth factor, type 1; fibroblast growth factor receptor 1; fibroblast growth factor receptor 2; receptor, fibroblast growth factor, type 2; receptor, fibroblast growth factor, type 3
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