The SseC translocon component in Salmonella enterica serovar Typhimurium is chaperoned by SscA.

Abstract:

BACKGROUND:Salmonella enterica is a causative agent of foodborne gastroenteritis and the systemic disease known as typhoid fever. This bacterium uses two type three secretion systems (T3SSs) to translocate protein effectors into host cells to manipulate cellular function. Salmonella pathogenicity island (SPI)-2 encodes a T3SS required for intracellular survival of the pathogen. Genes in SPI-2 include apparatus components, secreted effectors and chaperones that bind to secreted cargo to coordinate their release from the bacterial cell. Although the effector repertoire secreted by the SPI-2 T3SS is large, only three virulence-associated chaperones have been characterized. RESULTS:Here we report that SscA is the chaperone for the SseC translocon component. We show that SscA and SseC interact in bacterial cells and that deletion of sscA results in a loss of SseC secretion, which compromises intracellular replication and leads to a loss of competitive fitness in mice. CONCLUSIONS:This work completes the characterization of the chaperone complement within SPI-2 and identifies SscA as the chaperone for the SseC translocon.

journal_name

BMC Microbiol

journal_title

BMC microbiology

authors

Cooper CA,Mulder DT,Allison SE,Pilar AV,Coombes BK

doi

10.1186/1471-2180-13-221

subject

Has Abstract

pub_date

2013-10-04 00:00:00

pages

221

issn

1471-2180

pii

1471-2180-13-221

journal_volume

13

pub_type

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