Document Detail

Regulation of myosin activation during cell-cell contact formation by Par3-Lgl antagonism: entosis without matrix detachment.
MedLine Citation:
PMID:  22496418     Owner:  NLM     Status:  MEDLINE    
Cell-cell contact formation following cadherin engagement requires actomyosin contraction along the periphery of cell-cell contact. The molecular mechanisms that regulate myosin activation during this process are not clear. In this paper, we show that two polarity proteins, partitioning defective 3 homologue (Par3) and mammalian homologues of Drosophila Lethal (2) Giant Larvae (Lgl1/2), antagonize each other in modulating myosin II activation during cell-cell contact formation in Madin-Darby canine kidney cells. While overexpression of Lgl1/2 or depletion of endogenous Par3 leads to enhanced myosin II activation, knockdown of Lgl1/2 does the opposite. Intriguingly, altering the counteraction between Par3 and Lgl1/2 induces cell-cell internalization during early cell-cell contact formation, which involves active invasion of the lateral cell-cell contact underneath the apical-junctional complexes and requires activation of the Rho-Rho-associated, coiled-coil containing protein kinase (ROCK)-myosin pathway. This is followed by predominantly nonapoptotic cell-in-cell death of the internalized cells and frequent aneuploidy of the host cells. Such effects are reminiscent of entosis, a recently described process observed when mammary gland epithelial cells were cultured in suspension. We propose that entosis could occur without matrix detachment and that overactivation of myosin or unbalanced myosin activation between contacting cells may be the driving force for entosis in epithelial cells.
Qingwen Wan; Jing Liu; Zhen Zheng; Huabin Zhu; Xiaogang Chu; Zheng Dong; Shuang Huang; Quansheng Du
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2012-04-11
Journal Detail:
Title:  Molecular biology of the cell     Volume:  23     ISSN:  1939-4586     ISO Abbreviation:  Mol. Biol. Cell     Publication Date:  2012 Jun 
Date Detail:
Created Date:  2012-05-31     Completed Date:  2012-09-24     Revised Date:  2013-06-26    
Medline Journal Info:
Nlm Unique ID:  9201390     Medline TA:  Mol Biol Cell     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2076-91     Citation Subset:  IM    
Institute of Molecular Medicine and Genetics, Medical College of Georgia, Georgia Health Sciences University, Augusta, GA 30912, USA.
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MeSH Terms
Cell Communication*
Cell Line
Enzyme Activation
Extracellular Matrix / metabolism*,  ultrastructure
Gene Knockdown Techniques
HEK293 Cells
Intercellular Junctions / metabolism,  ultrastructure
Membrane Proteins / antagonists & inhibitors*,  metabolism
Myosin Light Chains / metabolism
Myosin Type II / metabolism*
Signal Transduction
Tumor Suppressor Proteins / antagonists & inhibitors*,  metabolism
rho GTP-Binding Proteins / metabolism
rho-Associated Kinases / metabolism
Grant Support
Reg. No./Substance:
0/Membrane Proteins; 0/Myosin Light Chains; 0/Tumor Suppressor Proteins; EC Kinases; EC 3.6.1.-/Myosin Type II; EC GTP-Binding Proteins

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