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Dev Cell. 2012 Mar 13;22(3):530-43. doi: 10.1016/j.devcel.2011.12.026.

ADF/cofilin regulates actomyosin assembly through competitive inhibition of myosin II binding to F-actin.

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  • 1Department of Biochemistry and Molecular Biology, Colorado State University, Fort Collins, CO 80523, USA. owiggan@colostate.edu

Abstract

The contractile actin cortex is important for diverse fundamental cell processes, but little is known about how the assembly of F-actin and myosin II motors is regulated. We report that depletion of actin depolymerizing factor (ADF)/cofilin proteins in human cells causes increased contractile cortical actomyosin assembly. Remarkably, our data reveal that the major cellular defects resulting from ADF/cofilin depletion, including cortical F-actin accumulation, were largely due to excessive myosin II activity. We identify that ADF/cofilins from unicellular organisms to humans share a conserved activity to inhibit myosin II binding to F-actin, indicating a mechanistic rationale for our cellular results. Our study establishes an essential requirement for ADF/cofilin proteins in the control of normal cortical contractility and in processes such as mitotic karyokinesis. We propose that ADF/cofilin proteins are necessary for controlling actomyosin assembly and intracellular contractile force generation, a function of equal physiological importance to their established roles in mediating F-actin turnover.

Copyright © 2012 Elsevier Inc. All rights reserved.

PMID:
22421043
[PubMed - indexed for MEDLINE]
PMCID:
PMC3306597
Free PMC Article
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