The abstract is read at the publisher; the summary is JClub's.
6S RNA in Yersinia pseudotuberculosis during mouse cecal lumen-to-lymphoid tissue invasion tunes virulence and immune-visible surface traits, with its absence causing T3SS overexpression and delayed colonization.
- Why it matters: In vivo transcriptional reprogramming during tissue invasion is poorly defined because most work relies on in vitro culture, leaving infection-linked regulatory roles uncertain.
- What they did: The study used in vivo RNA-seq to recover near-complete transcriptomes from bacteria in the mouse cecal lumen and associated lymphoid tissue, then tested the infection phenotype of 6S RNA loss.
- The result: Tissue-localized bacteria induced the type III secretion system and shifted toward alternative sigma factor regulons, with 6S RNA most strongly induced; 6S RNA absence increased T3SS, elevated TLR-activating envelope component display and proinflammatory mediator expression, reduced tissue phenotypic heterogeneity, and delayed colonization.
The findingWhy it mattersWhat they didThe result
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