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A correction to this article has been published: Vicente-Manzanares et al., J. Cell Biol. 176 (7) 1073
Published online February 20, 2007
doi:10.1083/jcb.200612043
The Journal of Cell Biology, Vol. 176, No. 5, 573-580
The Rockefeller University Press, 0021-9525 $30.00
© 2007 Vicente-Manzanares et al.
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Regulation of protrusion, adhesion dynamics, and polarity by myosins IIA and IIB in migrating cells



Miguel Vicente-Manzanares, Jessica Zareno, Leanna Whitmore, Colin K. Choi, and Alan F. Horwitz

Department of Cell Biology, University of Virginia, Charlottesville, VA 22908

Correspondence to Miguel Vicente-Manzanares: mv2f{at}virginia.edu

We have used isoform-specific RNA interference knockdowns to investigate the roles of myosin IIA (MIIA) and MIIB in the component processes that drive cell migration. Both isoforms reside outside of protrusions and act at a distance to regulate cell protrusion, signaling, and maturation of nascent adhesions. MIIA also controls the dynamics and size of adhesions in central regions of the cell and contributes to retraction and adhesion disassembly at the rear. In contrast, MIIB establishes front–back polarity and centrosome, Golgi, and nuclear orientation. Using ATPase- and contraction-deficient mutants of both MIIA and MIIB, we show a role for MIIB-dependent actin cross-linking in establishing front–back polarity. From these studies, MII emerges as a master regulator and integrator of cell migration. It mediates each of the major component processes that drive migration, e.g., polarization, protrusion, adhesion assembly and turnover, polarity, signaling, and tail retraction, and it integrates spatially separated processes.

Abbreviations used in this paper: MHC, myosin heavy chain; MII, myosin II; MLC, myosin light chain.


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