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Cell adaptive response to extracellular matrix density is controlled by ICAP-1-dependent beta1-integrin affinity.

Abstract : Cell migration is an integrated process requiring the continuous coordinated assembly and disassembly of adhesion structures. How cells orchestrate adhesion turnover is only partially understood. We provide evidence for a novel mechanistic insight into focal adhesion (FA) dynamics by demonstrating that integrin cytoplasmic domain-associated protein 1 (ICAP-1) slows down FA assembly. Live cell imaging, which was performed in both Icap-1-deficient mouse embryonic fibroblasts and cells expressing active beta(1) integrin, shows that the integrin high affinity state favored by talin is antagonistically controlled by ICAP-1. This affinity switch results in modulation in the speed of FA assembly and, consequently, of cell spreading and migration. Unexpectedly, the ICAP-1-dependent decrease in integrin affinity allows cell sensing of matrix surface density, suggesting that integrin conformational changes are important in mechanotransduction. Our results clarify the function of ICAP-1 in cell adhesion and highlight the central role it plays in the cell's integrated response to the extracellular microenvironment.
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https://www.hal.inserm.fr/inserm-00263537
Contributor : Marc Block <>
Submitted on : Wednesday, March 12, 2008 - 1:34:10 PM
Last modification on : Tuesday, September 1, 2020 - 4:00:03 PM
Long-term archiving on: : Friday, May 21, 2010 - 12:22:16 AM

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Angélique Millon-Frémillon, Daniel Bouvard, Alexei Grichine, Sandra Manet-Dupé, Marc Block, et al.. Cell adaptive response to extracellular matrix density is controlled by ICAP-1-dependent beta1-integrin affinity.. Journal of Cell Biology, Rockefeller University Press, 2008, 180 (2), pp.427-41. ⟨10.1083/jcb.200707142⟩. ⟨inserm-00263537⟩

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