NDLI: Progression from mitotic catastrophe to germ cell death in C. elegans lis-1 mutants requires the spindle checkpoint

Content Provider	PubMed Central
Author	Buttner, Edgar (ned) A. Gil-krzewska, Aleksandra J. Rajpurohit, Anandita K. Hunter, Craig P.
Abstract	Deletion of the lissencephaly disease gene LIS-1 in humans causes an extreme disorganization of the brain associated with significant reduction in cortical neurons. Here we show that deletion or RNA interference (RNAi) of Caenorhabditis elegans lis-1 results in a reduction in germline nuclei and causes a variety of cellular, developmental, and neurological defects throughout development. Our analysis of the germline defects suggests that the reduction in nuclei number stems from dysfunctional mitotic spindles resulting in cell cycle arrest and eventually programmed cell death (apoptosis). Deletion of the spindle checkpoint gene mdf-1 blocks lis-1(lf)-induced cell cycle arrest and germline apoptosis, placing the spindle checkpoint pathway upstream of the programmed cell death pathway. These results suggest that apoptosis may contribute to the cell-sparse pathology of lissencephaly.
Related Links	http://dx.doi.org/10.1016/j.ydbio.2007.02.024
Ending Page	410
Page Count	14
Starting Page	397
File Format	PDF
ISSN	00121606
e-ISSN	1095564X
Journal	Developmental biology
Issue Number	2
Volume Number	305
Language	English
Publisher Date	2007-05-01
Access Restriction	Open
Subject Keyword	Developmental Biology Cell Biology Molecular Biology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Cell Biology Developmental Biology Molecular Biology

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Progression from mitotic catastrophe to germ cell death in C. elegans lis-1 mutants requires the spindle checkpoint