RGD Reference Report - Lis1 and Ndel1 influence the timing of nuclear envelope breakdown in neural stem cells. - Rat Genome Database

Send us a Message



Submit Data |  Help |  Video Tutorials |  News |  Publications |  Download |  REST API |  Citing RGD |  Contact   

Lis1 and Ndel1 influence the timing of nuclear envelope breakdown in neural stem cells.

Authors: Hebbar, S  Mesngon, MT  Guillotte, AM  Desai, B  Ayala, R  Smith, DS 
Citation: Hebbar S, etal., J Cell Biol. 2008 Sep 22;182(6):1063-71. doi: 10.1083/jcb.200803071.
RGD ID: 8554736
Pubmed: PMID:18809722   (View Abstract at PubMed)
PMCID: PMC2542469   (View Article at PubMed Central)
DOI: DOI:10.1083/jcb.200803071   (Journal Full-text)

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.



Gene Ontology Annotations    

Biological Process

Cellular Component
nuclear envelope  (IDA,IMP)

Objects Annotated

Genes (Rattus norvegicus)
Ndel1  (nudE neurodevelopment protein 1-like 1)
Pafah1b1  (platelet-activating factor acetylhydrolase 1b, regulatory subunit 1)


Additional Information