期刊
JOURNAL OF CELL BIOLOGY
卷 182, 期 4, 页码 741-752出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.200804131
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资金
- Canadian Institutes of Health Research (CIHR) [62890]
- [Burroughs Wellcome Fund]
Salmonella colonizes a vacuolar niche in host cells during infection. Maturation of the Salmonella containing vacuole (SCV) involves the formation of phosphatidylinositol 3-phosphate (PI(3) P) on its outer lea. et. SopB, a bacterial virulence factor with phosphoinositide phosphatase activity, was proposed to generate PI(3) P by dephosphorylating PI(3,4)P2, PI(3,5)P2, and PI(3,4,5)P3. Here, we examine the mechanism of PI(3)P formation during Salmonella infection. SopB is required to form PI(3,4) P2/PI(3,4,5)P3 at invasion ruffles and PI(3)P on nascent SCVs. However, we uncouple these events experimentally and reveal that SopB does not dephosphorylate PI(3,4)P2/PI(3,4,5)P3 to produce PI(3) P. Instead, the phosphatase activity of SopB is required for Rab5 recruitment to the SCV. Vps34, a PI3-kinase that associates with active Rab5, is responsible for PI(3) P formation on SCVs. Therefore, SopB mediates PI(3) P production on the SCV indirectly through recruitment of Rab5 and its effector Vps34. These findings reveal a link between phosphoinositide phosphatase activity and the recruitment of Rab5 to phagosomes.
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