Force generated by actomyosin contraction builds bridges between adhesive contacts

Olivier M Rossier, Nils Gauthier, Nicolas Biais, Wynn Vonnegut, Marc-Antoine Fardin, Philip Avigan, Evan R Heller, Anurag Mathur, Saba Ghassemi, Michael S Koeckert, James C Hone, Michael P Sheetz
EMBO J. 2010-02-11; 29(6): 1055-1068
DOI: 10.1038/emboj.2010.2

Lire sur PubMed

1. EMBO J. 2010 Mar 17;29(6):1055-68. doi: 10.1038/emboj.2010.2. Epub 2010 Feb 11.

Force generated by actomyosin contraction builds bridges between adhesive

Rossier OM(1), Gauthier N, Biais N, Vonnegut W, Fardin MA, Avigan P, Heller ER,
Mathur A, Ghassemi S, Koeckert MS, Hone JC, Sheetz MP.

Author information:
(1)Department of Biological Sciences, Columbia University, New York, NY, USA.

Extracellular matrices in vivo are heterogeneous structures containing gaps that
cells bridge with an actomyosin network. To understand the basis of bridging, we
plated cells on surfaces patterned with fibronectin (FN)-coated stripes separated
by non-adhesive regions. Bridges developed large tensions where concave cell
edges were anchored to FN by adhesion sites. Actomyosin complexes assembled near
those sites (both actin and myosin filaments) and moved towards the centre of the
non-adhesive regions in a treadmilling network. Inhibition of myosin-II (MII) or
Rho-kinase collapsed bridges, whereas extension continued over adhesive areas.
Inhibition of actin polymerization (latrunculin-A, jasplakinolide) also collapsed
the actomyosin network. We suggest that MII has distinct functions at different
bridge regions: (1) at the concave edges of bridges, MIIA force stimulates actin
filament assembly at adhesions and (2) in the body of bridges, myosin cross-links
actin filaments and stimulates actomyosin network healing when breaks occur. Both
activities ensure turnover of actin networks needed to maintain stable bridges
from one adhesive region to another.

DOI: 10.1038/emboj.2010.2
PMCID: PMC2845274
PMID: 20150894 [Indexed for MEDLINE]

Auteurs Bordeaux Neurocampus