Journal
EMBO JOURNAL
Volume 20, Issue 19, Pages 5373-5382Publisher
WILEY
DOI: 10.1093/emboj/20.19.5373
Keywords
actin; pore; type III secretion; Yersinia; YopE
Categories
Funding
- NIAID NIH HHS [R01 AI043389, R56 AI043389, AI 43389] Funding Source: Medline
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The bacterial pathogen Yersinia pseudotuberculosis uses type III secretion machinery to translocate Yop effector proteins through host cell plasma membranes. A current model suggests that a type III translocation channel is inserted into the plasma membrane, and if Yops are not present to fill the channel, the channel will form a pore. We examined the possibility that Yops act within the host cell to prevent pore formation. Yop(-) mutants of Y. pseudotuberculosis were assayed for pore-forming activity in HeLa cells. A YopE(-) mutant exhibited high levels of pore-forming activity. The GTPase-downregulating function of YopE was required to prevent pore formation. YopE(+) bacteria had increased pore-forming activity when HeLa cells expressed activated Rho GTPases. Pore formation by YopE- bacteria required actin polymerization. F-actin was concentrated at sites of contact between HeLa cells and YopE- bacteria. The data suggest that localized actin polymerization, triggered by the type III machinery, results in pore formation in cells infected with YopE- bacteria. Thus, translocated YopE inhibits actin polymerization to prevent membane damage to cells infected with wild-type bacteria.
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