%0 Journal Article %1 Zhou20131690 %A Zhou*, Xiaohui %A Gewurz*, Benjamin E. %A Ritchie, Jennifer M. %A Takasaki, Kaoru %A Greenfeld, Hannah %A Kieff, Elliott %A Davis, Brigid M. %A Waldor, Matthew K. %D 2013 %J Cell Reports %K myown %N 5 %P 1690 - 1702 %R http://dx.doi.org/10.1016/j.celrep.2013.03.039 %T A Vibrio parahaemolyticus \T3SS\ Effector Mediates Pathogenesis by Independently Enabling Intestinal Colonization and Inhibiting \TAK1\ Activation %U http://www.sciencedirect.com/science/article/pii/S2211124713001630 %V 3 %X Summary Vibrio parahaemolyticus type \III\ secretion system 2 (T3SS2) is essential for the organism’s virulence, but the effectors required for intestinal colonization and induction of diarrhea by this pathogen have not been identified. Here, we identify a type \III\ secretion system (T3SS2)-secreted effector, VopZ, that is essential for V. parahaemolyticus pathogenicity. VopZ plays distinct, genetically separable roles in enabling intestinal colonization and diarrheagenesis. Truncation of VopZ prevents V. parahaemolyticus colonization, whereas deletion of VopZ amino acids 38–62 abrogates V. parahaemolyticus-induced diarrhea and intestinal pathology but does not impair colonization. VopZ inhibits activation of the kinase \TAK1\ and thereby prevents the activation of \MAPK\ and NF-κB signaling pathways, which lie downstream. In contrast, the VopZ internal deletion mutant cannot counter the activation of pathways regulated by TAK1. Collectively, our findings suggest that VopZ’s inhibition of \TAK1\ is critical for V. parahaemolyticus to induce diarrhea and intestinal pathology.

@article{Zhou20131690, abstract = {Summary Vibrio parahaemolyticus type \{III\} secretion system 2 (T3SS2) is essential for the organism’s virulence, but the effectors required for intestinal colonization and induction of diarrhea by this pathogen have not been identified. Here, we identify a type \{III\} secretion system (T3SS2)-secreted effector, VopZ, that is essential for V. parahaemolyticus pathogenicity. VopZ plays distinct, genetically separable roles in enabling intestinal colonization and diarrheagenesis. Truncation of VopZ prevents V. parahaemolyticus colonization, whereas deletion of VopZ amino acids 38–62 abrogates V. parahaemolyticus-induced diarrhea and intestinal pathology but does not impair colonization. VopZ inhibits activation of the kinase \{TAK1\} and thereby prevents the activation of \{MAPK\} and NF-κB signaling pathways, which lie downstream. In contrast, the VopZ internal deletion mutant cannot counter the activation of pathways regulated by TAK1. Collectively, our findings suggest that VopZ’s inhibition of \{TAK1\} is critical for V. parahaemolyticus to induce diarrhea and intestinal pathology. }, added-at = {2016-11-29T17:00:08.000+0100}, author = {Zhou*, Xiaohui and Gewurz*, Benjamin E. and Ritchie, Jennifer M. and Takasaki, Kaoru and Greenfeld, Hannah and Kieff, Elliott and Davis, Brigid M. and Waldor, Matthew K.}, biburl = {https://www.bibsonomy.org/bibtex/241beb52b1990bd453dabb1faeae736a2/bgewurz}, doi = {http://dx.doi.org/10.1016/j.celrep.2013.03.039}, interhash = {6dc1922aa1f27f1a9fff4c16c41859b7}, intrahash = {41beb52b1990bd453dabb1faeae736a2}, issn = {2211-1247}, journal = {Cell Reports }, keywords = {myown}, number = 5, pages = {1690 - 1702}, timestamp = {2017-05-10T21:00:22.000+0200}, title = {A Vibrio parahaemolyticus \{T3SS\} Effector Mediates Pathogenesis by Independently Enabling Intestinal Colonization and Inhibiting \{TAK1\} Activation }, url = {http://www.sciencedirect.com/science/article/pii/S2211124713001630}, volume = 3, year = 2013 }