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Published online September 22, 2008
doi:10.1083/jcb.200803071
The Journal of Cell Biology, Vol. 182, No. 6, 1063-1071
The Rockefeller University Press, 0021-9525 $30.00
© 2008 Hebbar et al.
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 Lis1 and Ndel1 influence the timing of nuclear envelope breakdown in neural stem cells

Sachin Hebbar1, Mariano T. Mesngon1, Aimee M. Guillotte1, Bhavim Desai1, Ramses Ayala2, and Deanna S. Smith1

1 Department of Biological Sciences, University of South Carolina, Columbia, SC 29208
2 Neurology Department, Mass General Institute for Neurodegenerative Disease, Charlestown, MA 02120

Correspondence to Deanna S. Smith: deannasm{at}biol.sc.edu

Lis1 and Ndel1 are essential for animal development. They interact directly with one another and with cytoplasmic dynein. The developing brain is especially sensitive to reduced Lis1 or Ndel1 levels, as both proteins influence spindle orientation, neural cell fate decisions, and neuronal migration. We report here that Lis1 and Ndel1 reduction in a mitotic cell line impairs prophase nuclear envelope (NE) invagination (PNEI). This dynein-dependent process facilitates NE breakdown (NEBD) and occurs before the establishment of the bipolar spindle. Ndel1 phosphorylation is important for this function, regulating binding to both Lis1 and dynein. Prophase cells in the ventricular zone (VZ) of embryonic day 13.5 Lis1+/– mouse brains show reduced PNEI, and the ratio of prophase to prometaphase cells is increased, suggesting an NEBD delay. Moreover, prophase cells in the VZ contain elevated levels of Ndel1 phosphorylated at a key cdk5 site. Our data suggest that a delay in NEBD in the VZ could contribute to developmental defects associated with Lis1–Ndel1 disruption.

Abbreviations used in this paper: BP, basal progenitor; co-IP, coimmunoprecipitation; DHC, dynein heavy chain; DIC, dynein intermediate chain; LAP2, lamin-associated protein 2; NE, nuclear envelope; NEBD, NE breakdown; NRK, normal rat kidney; PNEI, prophase NE invagination; RG, radial glia; shRNA, short hairpin RNA; S/T-P, Ser/Thr-Pro; VZ, ventricular zone.

© 2008 Hebbar et al. This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jcb.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).


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