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The V‐antigen of Yersinia is surface exposed before target cell contact and involved in virulence protein translocation
Author(s) -
Pettersson Jonas,
Holmström Anna,
Hill Jim,
Leary Sophie,
FrithzLindsten Elisabet,
Von EulerMatell Anne,
Carlsson Eva,
Titball Richard,
Forsberg Åke,
WolfWatz Hans
Publication year - 1999
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1046/j.1365-2958.1999.01408.x
Subject(s) - biology , secretion , yersinia , effector , yersinia pestis , virulence , yersinia enterocolitica , chromosomal translocation , microbiology and biotechnology , cytosol , immunity , bacteria , immune system , genetics , biochemistry , gene , enzyme
Type III‐mediated translocation of Yop effectors is an essential virulence mechanism of pathogenic Yersinia LcrV is the only protein secreted by the type III secretion system that induces protective immunity. LcrV also plays a significant role in the regulation of Yop expression and secretion. The role of LcrV in the virulence process has, however, remained elusive on account of its pleiotropic effects. Here, we show that anti‐LcrV antibodies can block the delivery of Yop effectors into the target cell cytosol. This argues strongly for a critical role of LcrV in the Yop translocation process. Additional evidence supporting this role was obtained by genetic analysis. LcrV was found to be present on the bacterial surface before the establishment of bacteria target cell contact. These findings suggest that LcrV serves an important role in the initiation of the translocation process and provides one possible explanation for the mechanism of LcrV‐induced protective immunity.