The SseC translocon component in Salmonella enterica serovar Typhimurium is chaperoned by SscAReportar como inadecuado

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BMC Microbiology

, 13:221

Microbe-host interactions and microbial pathogenicity


BackgroundSalmonella 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.

ResultsHere 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.

ConclusionsThis work completes the characterization of the chaperone complement within SPI-2 and identifies SscA as the chaperone for the SseC translocon.

KeywordsSalmonella Pathogenesis Chaperone Translocon T3SS AbbreviationsSPISalmonella pathogenicity Island

T3SSType 3 secretion system

S. TyphimuriumSalmonella enterica serovar Typhimurium

TPRTetratricopeptide repeat

CICompetitive index.

Electronic supplementary materialThe online version of this article doi:10.1186-1471-2180-13-221 contains supplementary material, which is available to authorized users.

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Autor: Colin A Cooper - David T Mulder - Sarah E Allison - Ana Victoria C Pilar - Brian K Coombes


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