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A role for N‐WASP in invasin‐promoted internalisation
Author(s) -
McGee Karen,
Zettl Markus,
Way Michael,
Fällman Maria
Publication year - 2001
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(01)03139-8
Subject(s) - yersinia pseudotuberculosis , rac1 , cdc42 , phagosome , microbiology and biotechnology , phagocytosis , gtpase , yersinia , mutant , biology , small gtpase , src family kinase , ectopic expression , wiskott–aldrich syndrome protein , proto oncogene tyrosine protein kinase src , chemistry , kinase , signal transduction , cytoskeleton , actin cytoskeleton , bacteria , cell culture , gene , virulence , genetics , cell
Phagocytosis of Yersinia pseudotuberculosis occurs through interaction of the bacterial protein invasin with β1‐integrins. Here we report that N‐WASP plays a role in internalisation of an invasin‐expressing, avirulent strain of Y. pseudotuberculosis . Ectopic expression of N‐WASP mutants, which affect recruitment of the Arp2/3 complex to the phagosome, reduces uptake of Yersinia . In addition, expression of the Cdc42/Rac‐binding (CRIB) region of N‐WASP has an inhibitory effect on uptake. Using GFP‐tagged Rho GTPase mutants, we provide evidence that Rac1, but not Cdc42, is important for internalisation. Furthermore, activated Rac1 rescues Toxin B, CRIB and Src family kinase inhibitor PP2‐mediated impairment of uptake. Our observations indicate that invasin‐mediated phagocytosis occurs via a Src and WASP family‐dependent mechanism(s), involving the Arp2/3 complex and Rac, but does not require Cdc42.