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PMID: 12169593 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.

Salmonella type III secretion-associated protein InvE controls translocation of effector proteins into host cells.

Journal of bacteriology ·Vol. 184 ·No. 17 ·2002-09-00 ·Pages 4699-708

Kubori T, Galán JE

Abstract

Salmonella enterica encodes a type III secretion system (TTSS) within a pathogenicity island located at centisome 63 (SPI-1), which is essential for its pathogenicity. This system mediates the transfer of a battery of bacterial proteins into the host cell with the capacity to modulate cellular functions. The transfer process is dependent on the function of protein translocases SipB, SipC, and SipD. We report here that Salmonella protein InvE, which is also encoded within SPI-1, is essential for the translocation of bacterial proteins into host cells. An S. enterica serovar Typhimurium mutant carrying a loss-of-function mutation in invE shows reduced secretion of SipB, SipC, and SipD while exhibiting increased secretion of other TTSS effector proteins. We also demonstrate that InvE interacts with a protein complex formed by SipB, SipC, and their cognate chaperone, SicA. We propose that InvE controls protein translocation by regulating the function of the Sip protein translocases.

MeSH Terms
Bacterial Proteins/physiology Biological Transport Salmonella typhimurium/metabolism
Chemicals
Bacterial Proteins
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Kubori Tomoko
Section of Microbial Pathogenesis, Yale School of Medicine, New Haven, CT 06536, USA.
Galán Jorge E
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Article Info
Journal
Journal of bacteriology
Abbr.
J Bacteriol
ISSN
0021-9193
Published
2002-09-00
Pages
4699-708
Language
English
Region
United States
NLM ID
2985120R
PMCID
PMC135284
Subset
IM
Grants
NIAID NIH HHS · R01 AI030492 · United States
NIAID NIH HHS · R37 AI030492 · United States
NIAID NIH HHS · AI 30492 · United States
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