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First published online May 24, 2006
doi: 10.1242/10.1242/jcs.02926

Journal of Cell Science 119, 2269-2281 (2006)
Published by The Company of Biologists 2006
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Research Article

Myosin light chain kinase plays a role in the regulation of epithelial cell survival

Laureen E. Connell1,2 and David M. Helfman1,3,*

1 Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA
2 Department of Molecular and Cellular Biology, SUNY Stony Brook, Stony Brook, NY 11794, USA
3 Department of Cell Biology and Anatomy, Sylvester Comprehensive Cancer Center, University of Miami, Miller School of Medicine, 1550 NW 10 Avenue M-877, Miami, FL 33136, USA

* Author for correspondence (e-mail: dhelfman{at}med.miami.edu)

Accepted 14 December 2005

Myosin II activation is essential for stress fiber and focal adhesion formation, and is implicated in integrin-mediated signaling events. In this study we investigated the role of acto-myosin contractility, and its main regulators, i.e. myosin light chain kinase (MLCK) and Rho-kinase (ROCK) in cell survival in normal and Ras-transformed MCF-10A epithelial cells. Treatment of cells with pharmacological inhibitors of MLCK (ML-7 and ML-9), or expression of dominant-negative MLCK, led to apoptosis in normal and transformed MCF-10A cells. By contrast, treatment of cells with a ROCK inhibitor (Y-27632) did not induce apoptosis in these cells. Apoptosis following inhibition of myosin II activation by MLCK is probably meditated through the death receptor pathway because expression of dominant-negative FADD blocked apoptosis. The apoptosis observed after MLCK inhibition is rescued by pre-treatment of cells with integrin-activating antibodies. In addition, this rescue of apoptosis is dependent on FAK activity, suggesting the participation of an integrin-dependent signaling pathway. These studies demonstrate a newly discovered role for MLCK in the generation of pro-survival signals in both untransformed and transformed epithelial cells and supports previous work suggesting distinct cellular roles for Rho-kinase- and MLCK-dependent regulation of myosin II.

Key words: Acto-myosin contractility, MLCK, ROCK, Apoptosis




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