Rac function is crucial for cell migration but is not required for spreading and focal adhesion formation.
Cast your vote
You can rate an item by clicking the amount of stars they wish to award to this item.
When enough users have cast their vote on this item, the average rating will also be shown.
Your vote was cast
Thank you for your feedback
Thank you for your feedback
Dimchev, Georgi A
Ladwein, Kathrin I
Margit Holleboom, J
Victor Small, J
Stradal, Theresia E B
MetadataShow full item record
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.
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.
AffiliationInstitute of Genetics, University of Bonn, Karlrobert-Kreiten Strasse 13, D-53115 Bonn, Germany.
JournalJournal of cell science
The following license files are associated with this item:
- Genetic deletion of Rac1 GTPase reveals its critical role in actin stress fiber formation and focal adhesion complex assembly.
- Authors: Guo F, Debidda M, Yang L, Williams DA, Zheng Y
- Issue date: 2006 Jul 7
- Rho, rac, and cdc42 GTPases regulate the assembly of multimolecular focal complexes associated with actin stress fibers, lamellipodia, and filopodia.
- Authors: Nobes CD, Hall A
- Issue date: 1995 Apr 7
- Cdc42 and Rac family GTPases regulate mode and speed but not direction of primary fibroblast migration during platelet-derived growth factor-dependent chemotaxis.
- Authors: Monypenny J, Zicha D, Higashida C, Oceguera-Yanez F, Narumiya S, Watanabe N
- Issue date: 2009 May
- The Small GTPase Rac1 Increases Cell Surface Stiffness and Enhances 3D Migration Into Extracellular Matrices.
- Authors: Kunschmann T, Puder S, Fischer T, Steffen A, Rottner K, Mierke CT
- Issue date: 2019 May 22
- Muscle costameric protein, Chisel/Smpx, associates with focal adhesion complexes and modulates cell spreading in vitro via a Rac1/p38 pathway.
- Authors: Schindeler A, Lavulo L, Harvey RP
- Issue date: 2005 Jul 15