ArticleMolecular microbiology2009
The TviA auxiliary protein renders the Salmonella enterica serotype Typhi RcsB regulon responsive to changes in osmolarity.
Article in Molecular microbiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 89 citations in OpenAlex.
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- Host restriction, pathogenesis and chronic carriage of typhoidal Salmonella.FEMS microbiology reviews · 2021Review
- A Salmonella Typhi RNA thermosensor regulates virulence factors and innate immune evasion in response to host temperature.PLoS pathogens · 2021Article
- New Roles for Two-Component System Response Regulators ofMicroorganisms · 2020Article
- The YrbE phospholipid transporter ofGut microbes · 2020Article
- Molecular Mechanisms ofInfection and drug resistance · 2020Review
- Persistent Infection and Long-Term Carriage of Typhoidal and Nontyphoidal Salmonellae.Clinical microbiology reviews · 2019Review
- Evolution of Salmonella within Hosts.Trends in microbiology · 2018Review
- Why Is Eradicating Typhoid Fever So Challenging: Implications for Vaccine and Therapeutic Design.Vaccines · 2018Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 3 countries.
Funding
Abstract
In response to osmolarity, Salmonella enterica serotype Typhi (S. Typhi) regulates genes required for Vi capsular antigen expression oppositely to those required for motility and invasion. Previous studies suggest that osmoregulation of motility, invasion and capsule expression is mediated through the RcsC/RcsD/RcsB phosphorelay system. Here we performed gene expression profiling and functional studies to determine the role of TviA, an auxiliary protein of the RcsB response regulator, in controlling virulence gene expression in S. Typhi. TviA repressed expression of genes encoding flagella and the invasion-associated type III secretion system (T3SS-1) through repression of the flagellar regulators flhDC and fliZ, resulting in reduced invasion, reduced motility and reduced expression of FliC. Both RcsB and TviA repressed expression of flhDC, but only TviA altered flhDC expression in response to osmolarity. Introduction of tviA into S. enterica serotype Typhimurium rendered flhDC transcription sensitive to changes in osmolarity. These data suggest that the auxiliary TviA protein integrates a new regulatory input into the RcsB regulon of S. Typhi, thereby altering expression of genes encoding flagella, the Vi antigen and T3SS-1 in response to osmolarity.
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