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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.


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.

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