Nonmuscle myosin IIA-dependent force inhibits cell spreading and drives F-actin flow.
Biophysical Journal. 2006-11-01; 91(10): 3907-3920
DOI: 10.1529/biophysj.106.084806
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1. Biophys J. 2006 Nov 15;91(10):3907-20. Epub 2006 Aug 18.
Nonmuscle myosin IIA-dependent force inhibits cell spreading and drives F-actin
flow.
Cai Y(1), Biais N, Giannone G, Tanase M, Jiang G, Hofman JM, Wiggins CH,
Silberzan P, Buguin A, Ladoux B, Sheetz MP.
Author information:
(1)Department of Biological Sciences, Columbia University, New York, New York,
USA.
Nonmuscle myosin IIA (NMM-IIA) is involved in the formation of focal adhesions
and neurite retraction. However, the role of NMM-IIA in these functions remains
largely unknown. Using RNA interference as a tool to decrease NMM-IIA expression,
we have found that NMM-IIA is the major myosin involved in traction force
generation and retrograde F-actin flow in mouse embryonic fibroblast cells.
Quantitative analyses revealed that approximately 60% of traction force on
fibronectin-coated surfaces is contributed by NMM-IIA and approximately 30% by
NMM-IIB. The retrograde F-actin flow decreased dramatically in NMM-IIA-depleted
cells, but seemed unaffected by NMM-IIB deletion. In addition, we found that
depletion of NMM-IIA caused cells to spread at a higher rate and to a greater
area on fibronectin substrates during the early spreading period, whereas
deletion of NMM-IIB appeared to have no effect on spreading. The distribution of
NMM-IIA was concentrated on the dorsal surface and approached the ventral surface
in the periphery, whereas NMM-IIB was primarily concentrated around the nucleus
and to a lesser extent at the ventral surface in cell periphery. Our results
suggest that NMM-IIA is involved in generating a coherent cytoplasmic contractile
force from one side of the cell to the other through the cross-linking and the
contraction of dorsal actin filaments.
DOI: 10.1529/biophysj.106.084806
PMCID: PMC1630492
PMID: 16920834 [Indexed for MEDLINE]