期刊
MOLECULAR MICROBIOLOGY
卷 74, 期 1, 页码 175-193出版社
WILEY
DOI: 10.1111/j.1365-2958.2009.06859.x
关键词
-
资金
- Division of Microbiology and Infectious Disease
- NIAID
- NIH
- DHHS
- Faculty of Medicine, Chiang Mai University, Thailand
- University of California, Davis, CA, USA
- Public Health Service Grant [AI040124, AI044170, AI076246, AI079173]
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI044170, R01AI076246, R29AI040124, R01AI040124, R21AI079173] Funding Source: NIH RePORTER
P>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.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据