Microtubule depolymerization induces traction force increase through two distinct pathways.

Abstract:

:Traction forces increase after microtubule depolymerization; however, the signaling mechanisms underlying this, in particular the dependence upon myosin II, remain unclear. We investigated the mechanism of traction force increase after nocodazole-induced microtubule depolymerization by applying traction force microscopy to cells cultured on micropatterned polyacrylamide hydrogels to obtain samples of homogeneous shape and size. Control cells and cells treated with a focal adhesion kinase (FAK) inhibitor showed similar increases in traction forces, indicating that the response is independent of FAK. Surprisingly, pharmacological inhibition of myosin II did not prevent the increase of residual traction forces upon nocodazole treatment. This increase was abolished upon pharmacological inhibition of FAK. These results suggest two distinct pathways for the regulation of traction forces. First, microtubule depolymerization activates a myosin-II-dependent mechanism through a FAK-independent pathway. Second, microtubule depolymerization also enhances traction forces through a myosin-II-independent, FAK-regulated pathway. Traction forces are therefore regulated by a complex network of complementary signals and force-generating mechanisms.

journal_name

J Cell Sci

journal_title

Journal of cell science

authors

Rape A,Guo WH,Wang YL

doi

10.1242/jcs.090563

subject

Has Abstract

pub_date

2011-12-15 00:00:00

pages

4233-40

issue

Pt 24

eissn

0021-9533

issn

1477-9137

pii

jcs.090563

journal_volume

124

pub_type

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