Journal
CELL
Volume 134, Issue 6, Pages 1055-1065Publisher
CELL PRESS
DOI: 10.1016/j.cell.2008.07.017
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Funding
- NEI NIH HHS [EY012406, R01 EY013855-04, EY01467, EY013855, R01 EY013855, R01 EY012406-09, R01 EY012406-05, R01 EY012406, R01 EY013855-06] Funding Source: Medline
- NINDS NIH HHS [R01 NS053358, R01 NS053358-02] Funding Source: Medline
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The different cell types in the central nervous system develop from a common pool of progenitor cells. The nuclei of progenitors move between the apical and basal surfaces of the neuroepithelium in phase with their cell cycle, a process termed interkinetic nuclear migration (INM). In the retina of zebrafish mikre oko (mok) mutants, in which the motor protein Dynactin-1 is disrupted, interkinetic nuclei migrate more rapidly and deeply to the basal side and more slowly to the apical side. We found that Notch signaling is predominantly activated on the apical side in both mutants and wild-type. Mutant progenitors are, thus, less exposed to Notch and exit the cell cycle prematurely. This leads to an overproduction of early-born retinal ganglion cells (RGCs) at the expense of later-born interneurons and glia. Our data indicate that the function of INM is to balance the exposure of progenitor nuclei to neurogenic versus proliferative signals.
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