Epidermal growth factor-induced contraction regulates paxillin phosphorylation to temporally separate traction generation from de-adhesion

dc.contributor.author Schneider, Ian
dc.contributor.author Hays, Cristen
dc.contributor.author Schneider, Ian
dc.contributor.author Waterman, Clare
dc.contributor.department Chemical and Biological Engineering
dc.date 2018-02-15T21:59:30.000
dc.date.accessioned 2020-06-30T01:08:32Z
dc.date.available 2020-06-30T01:08:32Z
dc.date.copyright Thu Jan 01 00:00:00 UTC 2009
dc.date.embargo 2015-03-03
dc.date.issued 2009-07-01
dc.description.abstract <p>Directed cell migration is mediated by cycles of protrusion, adhesion, traction generation on the extracellular matrix and retraction. However, how the events after protrusion are timed, and what dictates their temporal order is completely unknown. We used acute epidermal growth factor (EGF) stimulation of epidermal keratinocytes to initiate the cell migration cycle to study the mechanism of the timing of adhesion, traction generation, and de-adhesion. Using microscopic and biochemical assays, we surprisingly found that at ∼2 min after EGF stimulation protrusion, activation of myosin-II, traction generation, adhesion assembly, and paxillin phosphorylation occurred nearly simultaneously, followed by a 10-min delay during which paxillin became dephosphorylated before cell retraction. Inhibition of myosin-II blocked both the EGF-stimulated paxillin phosphorylation and cell retraction, and a paxillin phosphomimic blocked retraction. These results suggest that EGF-mediated activation of myosin-II acts as a mechanical signal to promote a cycle of paxillin phosphorylation/dephosphorylation that mediates a cycle of adhesion strengthening and weakening that delays cell retraction. Thus, we reveal for the first time a mechanism by which cells may temporally segregate protrusion, adhesion, and traction generation from retraction during EGF-stimulated cell migration.</p>
dc.description.comments <p>This is an article from <em>Molecular Biology of the Cell</em> 20 (2009): 3155, doi: <a href="http://dx.doi.org/10.1091/mbc.E09-03-0219" target="_blank">10.1091/mbc.E09-03-0219</a>. Posted with permission.</p>
dc.format.mimetype application/pdf
dc.identifier archive/lib.dr.iastate.edu/cbe_pubs/216/
dc.identifier.articleid 1219
dc.identifier.contextkey 6768363
dc.identifier.s3bucket isulib-bepress-aws-west
dc.identifier.submissionpath cbe_pubs/216
dc.identifier.uri https://dr.lib.iastate.edu/handle/20.500.12876/13309
dc.language.iso en
dc.source.bitstream archive/lib.dr.iastate.edu/cbe_pubs/216/2009_SchneiderIC_EpidermalGrowthFactor.pdf|||Fri Jan 14 22:38:17 UTC 2022
dc.source.uri 10.1091/mbc.E09-03-0219
dc.subject.disciplines Biological Engineering
dc.subject.disciplines Chemical Engineering
dc.subject.disciplines Genetics and Genomics
dc.subject.keywords cell biology
dc.subject.keywords The Scripps Research Institute
dc.subject.keywords Genetics Development and Cell Biology
dc.subject.keywords Laboratory of Cell and Tissue Morphodynamics
dc.subject.keywords National Heart Lung and Blood Institute
dc.subject.keywords epidermal growth factor
dc.subject.keywords myosin II
dc.subject.keywords cell adhesion
dc.subject.keywords cell migration
dc.subject.keywords fluorescence microscopy
dc.subject.keywords focal adhesion
dc.subject.keywords Epidermal Growth Factor
dc.subject.keywords Keratinocytes
dc.title Epidermal growth factor-induced contraction regulates paxillin phosphorylation to temporally separate traction generation from de-adhesion
dc.type article
dc.type.genre article
dspace.entity.type Publication
relation.isAuthorOfPublication 22eb24b7-a47b-44a4-bcf4-c83dd9d6b825
relation.isOrgUnitOfPublication 86545861-382c-4c15-8c52-eb8e9afe6b75
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