Nonmuscle myosin IIA-dependent force inhibits cell spreading and drives F-actin flow

Yunfei Cai, Nicolas Biais, Gregory Giannone, Monica Tanase, Guoying Jiang, Jake M. Hofman, Chris H. Wiggins, Pascal Silberzan, Axel Buguin, Benoit Ladoux, Michael P. Sheetz

Research output: Contribution to journalArticle

209 Scopus citations

Abstract

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 ∼60% of traction force on fibronectin-coated surfaces is contributed by NMM-IIA and ∼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.

Original languageEnglish (US)
Pages (from-to)3907-3920
Number of pages14
JournalBiophysical journal
Volume91
Issue number10
DOIs
StatePublished - Nov 2006

ASJC Scopus subject areas

  • Biophysics

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