
ROS‐inhibitory activity of YopE is required for full virulence of Yersinia in mice
Author(s) -
Songsungthong Warangkhana,
Higgins Mary C.,
Rolán Hortensia G.,
Murphy Julia L.,
Mecsas Joan
Publication year - 2010
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1111/j.1462-5822.2010.01448.x
Subject(s) - yersinia pseudotuberculosis , biology , effector , yersinia , microbiology and biotechnology , rac1 , rhoa , virulence , gtpase , rac gtp binding proteins , mutant , bacteria , gene , signal transduction , genetics
Summary YopE, a type III secreted effector of Yersinia , is a GTPase Activating Protein for Rac1 and RhoA whose catalytic activity is critical for virulence. We found that YopE also inhibited reactive oxygen species (ROS) production and inactivated Rac2. How YopE distinguishes among its targets and which specific targets are critical for Yersinia survival in different tissues are unknown. A screen identifying YopE mutants in Yersinia pseudotuberculosis that interact with different Rho GTPases showed that YopE residues at positions 102, 106, 109 and 156 discern among switch I and II regions of Rac1, Rac2 and RhoA. Two mutants, which expressed YopE alleles with different antiphagocytic, ROS‐inhibitory and cell‐rounding activities, YptbL109A and YptbESptP, were studied in animal infections. Inhibition of both phagocytosis and ROS production were required for splenic colonization, whereas fewer YopE activities were required for Peyer's patch colonization. This study shows that Y. pseudotuberculosis encounters multiple host defences in different tissues and uses distinct YopE activities to disable them.