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dc.contributor.authorSteffen, Anika
dc.contributor.authorLadwein, Markus
dc.contributor.authorDimchev, Georgi A
dc.contributor.authorHein, Anke
dc.contributor.authorSchwenkmezger, Lisa
dc.contributor.authorArens, Stefan
dc.contributor.authorLadwein, Kathrin I
dc.contributor.authorMargit Holleboom, J
dc.contributor.authorSchur, Florian
dc.contributor.authorVictor Small, J
dc.contributor.authorSchwarz, Janett
dc.contributor.authorGerhard, Ralf
dc.contributor.authorFaix, Jan
dc.contributor.authorStradal, Theresia E B
dc.contributor.authorBrakebusch, Cord
dc.contributor.authorRottner, Klemens
dc.date.accessioned2013-12-03T15:16:23Z
dc.date.available2013-12-03T15:16:23Z
dc.date.issued2013-10-15
dc.identifier.citationRac function is crucial for cell migration but is not required for spreading and focal adhesion formation. 2013, 126 (Pt 20):4572-88 J. Cell. Sci.en
dc.identifier.issn1477-9137
dc.identifier.pmid23902686
dc.identifier.doi10.1242/jcs.118232
dc.identifier.urihttp://hdl.handle.net/10033/306170
dc.description.abstractCell migration is commonly accompanied by protrusion of membrane ruffles and lamellipodia. In two-dimensional migration, protrusion of these thin sheets of cytoplasm is considered relevant to both exploration of new space and initiation of nascent adhesion to the substratum. Lamellipodium formation can be potently stimulated by Rho GTPases of the Rac subfamily, but also by RhoG or Cdc42. Here we describe viable fibroblast cell lines genetically deficient for Rac1 that lack detectable levels of Rac2 and Rac3. Rac-deficient cells were devoid of apparent lamellipodia, but these structures were restored by expression of either Rac subfamily member, but not by Cdc42 or RhoG. Cells deficient in Rac showed strong reduction in wound closure and random cell migration and a notable loss of sensitivity to a chemotactic gradient. Despite these defects, Rac-deficient cells were able to spread, formed filopodia and established focal adhesions. Spreading in these cells was achieved by the extension of filopodia followed by the advancement of cytoplasmic veils between them. The number and size of focal adhesions as well as their intensity were largely unaffected by genetic removal of Rac1. However, Rac deficiency increased the mobility of different components in focal adhesions, potentially explaining how Rac - although not essential - can contribute to focal adhesion assembly. Together, our data demonstrate that Rac signaling is essential for lamellipodium protrusion and for efficient cell migration, but not for spreading or filopodium formation. Our findings also suggest that Rac GTPases are crucial to the establishment or maintenance of polarity in chemotactic migration.
dc.language.isoenen
dc.rightsArchived with thanks to Journal of cell scienceen
dc.titleRac function is crucial for cell migration but is not required for spreading and focal adhesion formation.en
dc.typeArticleen
dc.contributor.departmentInstitute of Genetics, University of Bonn, Karlrobert-Kreiten Strasse 13, D-53115 Bonn, Germany.en
dc.identifier.journalJournal of cell scienceen
refterms.dateFOA2018-06-12T22:37:38Z
html.description.abstractCell migration is commonly accompanied by protrusion of membrane ruffles and lamellipodia. In two-dimensional migration, protrusion of these thin sheets of cytoplasm is considered relevant to both exploration of new space and initiation of nascent adhesion to the substratum. Lamellipodium formation can be potently stimulated by Rho GTPases of the Rac subfamily, but also by RhoG or Cdc42. Here we describe viable fibroblast cell lines genetically deficient for Rac1 that lack detectable levels of Rac2 and Rac3. Rac-deficient cells were devoid of apparent lamellipodia, but these structures were restored by expression of either Rac subfamily member, but not by Cdc42 or RhoG. Cells deficient in Rac showed strong reduction in wound closure and random cell migration and a notable loss of sensitivity to a chemotactic gradient. Despite these defects, Rac-deficient cells were able to spread, formed filopodia and established focal adhesions. Spreading in these cells was achieved by the extension of filopodia followed by the advancement of cytoplasmic veils between them. The number and size of focal adhesions as well as their intensity were largely unaffected by genetic removal of Rac1. However, Rac deficiency increased the mobility of different components in focal adhesions, potentially explaining how Rac - although not essential - can contribute to focal adhesion assembly. Together, our data demonstrate that Rac signaling is essential for lamellipodium protrusion and for efficient cell migration, but not for spreading or filopodium formation. Our findings also suggest that Rac GTPases are crucial to the establishment or maintenance of polarity in chemotactic migration.


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