Please use this identifier to cite or link to this item: https://doi.org/10.1073/pnas.1117814109
DC FieldValue
dc.titleCell crawling mediates collective cell migration to close undamaged epithelial gaps
dc.contributor.authorAnon, E.
dc.contributor.authorSerra-Picamal, X.
dc.contributor.authorHersen, P.
dc.contributor.authorGauthier, N.C.
dc.contributor.authorSheetz, M.P.
dc.contributor.authorTrepat, X.
dc.contributor.authorLadoux, B.
dc.date.accessioned2014-10-27T08:23:23Z
dc.date.available2014-10-27T08:23:23Z
dc.date.issued2012-07-03
dc.identifier.citationAnon, E., Serra-Picamal, X., Hersen, P., Gauthier, N.C., Sheetz, M.P., Trepat, X., Ladoux, B. (2012-07-03). Cell crawling mediates collective cell migration to close undamaged epithelial gaps. Proceedings of the National Academy of Sciences of the United States of America 109 (27) : 10891-10896. ScholarBank@NUS Repository. https://doi.org/10.1073/pnas.1117814109
dc.identifier.issn00278424
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/100221
dc.description.abstractFundamental biological processes such as morphogenesis and wound healing involve the closure of epithelial gaps. Epithelial gap closure is commonly attributed either to the purse-string contraction of an intercellular actomyosin cable or to active cell migration, but the relative contribution of these two mechanisms remains unknown. Here we present a model experiment to systematically study epithelial closure in the absence of cell injury. We developed a pillar stencil approach to create well-defined gaps in terms of size and shape within an epithelial cell monolayer. Upon pillar removal, cells actively respond to the newly accessible free space by extending lamellipodia and migrating into the gap. The decrease of gap area over time is strikingly linear and shows two different regimes depending on the size of the gap. In large gaps, closure is dominated by lamellipodium-mediated cell migration. By contrast, closure of gaps smaller than 20 μm was affected by cell density and progressed independently of Rac, myosin light chain kinase, and Rho kinase, suggesting a passive physical mechanism. By changing the shape of the gap, we observed that low-curvature areas favored the appearance of lamellipodia, promoting faster closure. Altogether, our results reveal that the closure of epithelial gaps in the absence of cell injury is governed by the collective migration of cells through the activation of lamellipodium protrusion.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1073/pnas.1117814109
dc.sourceScopus
dc.subjectEpithelial cell migration
dc.subjectMadin-Darby canine kidney cells
dc.subjectMicrofabrication
dc.subjectWound model assay
dc.typeArticle
dc.contributor.departmentBIOLOGICAL SCIENCES
dc.description.doi10.1073/pnas.1117814109
dc.description.sourcetitleProceedings of the National Academy of Sciences of the United States of America
dc.description.volume109
dc.description.issue27
dc.description.page10891-10896
dc.description.codenPNASA
dc.identifier.isiut000306641100040
Appears in Collections:Staff Publications

Show simple item record
Files in This Item:
There are no files associated with this item.

SCOPUSTM   
Citations

110
checked on Mar 30, 2020

WEB OF SCIENCETM
Citations

102
checked on Mar 30, 2020

Page view(s)

80
checked on Mar 28, 2020

Google ScholarTM

Check

Altmetric


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.