A Csr-type regulatory system, including small non-coding RNAs, regulates the global virulence regulator RovA of Yersinia pseudotuberculosis through RovM.

TitleA Csr-type regulatory system, including small non-coding RNAs, regulates the global virulence regulator RovA of Yersinia pseudotuberculosis through RovM.
Publication TypeJournal Article
Year of Publication2008
AuthorsHeroven, AK, Böhme, K, Rohde, M, Dersch, P
JournalMol Microbiol
Volume68
Issue5
Pagination1179-95
Date Published2008 Jun
ISSN1365-2958
KeywordsBacterial Proteins, Gene Expression Regulation, Bacterial, Genes, Regulator, RNA, Bacterial, RNA-Binding Proteins, RNA, Untranslated, Transcription Factors, Virulence, Yersinia pseudotuberculosis
Abstract

The MarR-type regulator RovA controls expression of virulence genes of Yersinia pseudotuberculosis in response to environmental signals. Using a genetic strategy to discover components that influence rovA expression, we identified new regulatory factors with homology to components of the carbon storage regulator system (Csr). We showed that overexpression of a CsrB- or a CsrC-type RNA activates rovA, whereas a CsrA-like protein represses RovA synthesis. We further demonstrate that influence of the Csr system on rovA is indirect and occurs through control of the LysR regulator RovM, which inhibits rovA transcription. The CsrA protein had also a major influence on the motility of Yersinia, which was independent of RovM. The CsrB and CsrC RNAs are differentially expressed in Yersinia. CsrC is highly induced in complex but not in minimal media, indicating that medium-dependent rovM expression is mediated through CsrC. CsrB synthesis is generally very low. However, overexpression of the response regulator UvrY was found to activate CsrB production, which in turn represses CsrC synthesis independent of the growth medium. In summary, the post-transcriptional Csr-type components were shown to be key regulators in the co-ordinated environmental control of physiological processes and virulence factors, which are crucial for the initiation of Yersinia infections.

DOI10.1111/j.1365-2958.2008.06218.x
Alternate JournalMol. Microbiol.