Salmonella exploits host Rho GTPase signalling pathways through the phosphatase activity of SopB |
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| Authors: | Dorothy Truong Kirsten C Boddy Veronica Canadien Danielle Brabant Gregory D Fairn Vanessa M D'Costa Etienne Coyaud Brian Raught Dolores Pérez‐Sala Wei Sun Park Won Do Heo Sergio Grinstein John H Brumell |
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| Institution: | 1. Cell Biology Program, Hospital for Sick Children, Toronto, ON, Canada;2. Department of Molecular Genetics, University of Toronto, Toronto, ON, Canada;3. Institute of Medical Science, University of Toronto, Toronto, ON, Canada;4. Keenan Research Centre for Biomedical Science, St. Michael's Hospital, Toronto, ON, Canada;5. Princess Margaret Cancer Centre, University Health Network, Toronto, Ontario, Canada;6. Department of Medical Biophysics, University of Toronto, Toronto, Ontario, Canada;7. Department of Structural and Chemical Biology, Centro de Investigaciones Biológicas, Consejo Superior de Investigaciones Científicas, Madrid, Spain;8. Department of Biological Sciences, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, Republic of Korea;9. Center for Cognition and Sociality, Institute of Basic Science (IBS), Daejeon, Republic of Korea;10. Department of Biochemistry, University of Toronto, Toronto, ON, Canada;11. Sickkids IBD Centre, Hospital for Sick Children, Toronto, ON, Canada |
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| Abstract: | Salmonella uses Type 3 secretion systems (T3SSs) to deliver virulence factors, called effectors, into host cells during infection. The T3SS effectors promote invasion into host cells and the generation of a replicative niche. SopB is a T3SS effector that plays an important role in Salmonella pathogenesis through its lipid phosphatase activity. Here, we show that SopB mediates the recruitment of Rho GTPases (RhoB, RhoD, RhoH, and RhoJ) to bacterial invasion sites. RhoJ contributes to Salmonella invasion, and RhoB and RhoH play an important role in Akt activation. R‐Ras1 also contributes to SopB‐dependent Akt activation by promoting the localised production of PI(3,4)P2/PI(3,4,5)P3. Our studies reveal new signalling factors involved in SopB‐dependent Salmonella infection. |
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