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Cell Cycle. 2011 Jun 15;10(12):1916-20. Epub 2011 Jun 15.

An extracellular matrix protein prevents cytokinesis failure and aneuploidy in the C. elegans germline.

Author information

1
Center for Biomedical Engineering and Technology and Department of Physiology, University of Maryland at Baltimore, Baltimore, MD, USA. bvogel@umaryland.edu

Abstract

Interactions between extracellular matrix (ECM) proteins and their transmembrane receptors mediate cytoskeletal reorganization and corresponding changes in cell shape during cell migration, adhesion, differentiation and polarization. Cytokinesis is the final step in cell division as cells employ a contractile ring composed of actin and myosin to partition one cell into two. Cells undergo dramatic changes in cell shape during the division process, creating new membrane and forming an extracellular invagination called the cleavage furrow. However, existing models of cytokinesis include no role for the ECM. In a recent paper, we demonstrate that depletion of a large secreted protein, hemicentin, results in membrane destabilization, cleavage furrow retraction and cytokinesis failure in C. elegans germ cells and in pre-implantation mouse embryos. Here, we demonstrate that cytokinesis failure produces tetraploid intermediate cells with multipolar spindles, providing a potential explanation for the large number of aneuploid progeny observed among C. elegans hemicentin mutant hermaphrodites.

PMID:
21558805
PMCID:
PMC3154414
DOI:
10.4161/cc.10.12.15896
[Indexed for MEDLINE]
Free PMC Article

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