4.5 Article

Control of effector export by the Pseudomonas aeruginosa type III secretion proteins PcrG and PcrV

期刊

MOLECULAR MICROBIOLOGY
卷 75, 期 4, 页码 924-941

出版社

WILEY
DOI: 10.1111/j.1365-2958.2009.07027.x

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资金

  1. Case Western Reserve University
  2. University Hospitals of Cleveland [P30 CA43703]
  3. National Institutes of Health [T32 HL083823]
  4. American Cancer Society [RSG-09-198-01-MPC]
  5. Cystic Fibrosis Foundation [R447-CR07]

向作者/读者索取更多资源

P>Pseudomonas aeruginosa uses a type III secretion system to inject protein effectors into a targeted host cell. Effector secretion is triggered by host cell contact. How effector secretion is prevented prior to cell contact is not well understood. In all secretion systems studied to date, the needle tip protein is required for controlling effector secretion, but the mechanism by which needle tip proteins control effector secretion is unclear. Here we present data that the P. aeruginosa needle tip protein, PcrV, controls effector secretion by assembling into a functional needle tip complex. PcrV likely does not simply obstruct the secretion channel because the pore-forming translocator proteins can still be secreted while effector secretion is repressed. This finding suggests that PcrV controls effector secretion by affecting the conformation of the apparatus, shifting it from the default, effector secretion 'on' conformation, to the effector secretion 'off' conformation. We also present evidence that PcrG, which can bind to PcrV and is also involved in controlling effector export, is cytoplasmic and that the interaction between PcrG and PcrV is not required for effector secretion control by either protein. Taken together, these data allow us to propose a working model for control of effector secretion by PcrG and PcrV.

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