Journal
CELL
Volume 132, Issue 3, Pages 474-486Publisher
CELL PRESS
DOI: 10.1016/j.cell.2008.01.026
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Funding
- NICHD NIH HHS [HD047380, R01 HD047380-03, R01 HD047380-01A1, R01 HD047380, R01 HD047380-02] Funding Source: Medline
- NINDS NIH HHS [NS041310, R01 NS041030, R01 NS041030-05, R01 NS041030-04, P30 NS047101, R01 NS041030-06, R01 NS041030-02, R01 NS041310, R01 NS041030-01A2, R01 NS041030-03] Funding Source: Medline
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Mitotic spindle orientation and plane of cleavage in mammals is a determinant of whether division yields progenitor expansion and/or birth of new neurons during radial glial progenitor cell (RGPC) neurogenesis, but its role earlier in neuroepithelial stem cells is poorly understood. Here we report that Lis1 is essential for precise control of mitotic spindle orientation in both neuroepithelial stem cells and radial glial progenitor cells. Controlled gene deletion of Lis1 in vivo in neuroepithelial stem cells, where cleavage is uniformly vertical and symmetrical, provokes rapid apoptosis of those cells, while radial glial progenitors are less affected. Impaired cortical microtubule capture via loss of cortical dynein causes astral and cortical microtubules to be greatly reduced in Lis1-deficient cells. Increased expression of the LIS/dynein binding partner NDEL1 restores cortical microtubule and dynein localization in Lis1-deficient cells. Thus, control of symmetric division, essential for neuroepithelial stem cell proliferation, is mediated through spindle orientation determined via LIS1/NDEL1/dynein-mediated cortical microtubule capture.
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