Regulation of neurogenesis by interkinetic nuclear migration through an apical-basal notch gradient. Cell 2008 Sep 19;134(6):1055-65
Date
09/23/2008Pubmed ID
18805097Pubmed Central ID
PMC2628487DOI
10.1016/j.cell.2008.07.017Scopus ID
2-s2.0-51749083057 (requires institutional sign-in at Scopus site) 258 CitationsAbstract
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.
Author List
Del Bene F, Wehman AM, Link BA, Baier HAuthor
Brian A. Link PhD Professor in the Cell Biology, Neurobiology and Anatomy department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsBody Patterning
Cell Cycle
Cell Differentiation
Cell Nucleus
Dynactin Complex
Embryo, Nonmammalian
Gene Expression Regulation, Developmental
Microtubule-Associated Proteins
Mutation
Neuroepithelial Cells
Organogenesis
Receptors, Notch
Retina
Retinal Ganglion Cells
Stem Cells
Zebrafish
Zebrafish Proteins
