Journal
JOURNAL OF CELL BIOLOGY
Volume 176, Issue 5, Pages 573-580Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.200612043
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Funding
- NIGMS NIH HHS [R37 GM023244, R01 GM023244, GM23244] Funding Source: Medline
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We have used isoform-specifc 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.
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