Ferrières Lionel, Thompson Aoife, Clarke David J
Molecular Microbiology Laboratory, Department of Biology and Biochemistry, University of Bath, Bath BA2 7AY, UK.
Department of Microbiology and Alimentary Pharmabiotic Centre, University College Cork, Ireland.
Microbiology (Reading). 2009 Nov;155(Pt 11):3544-3553. doi: 10.1099/mic.0.032722-0. Epub 2009 Aug 20.
The Rcs phosphorelay is composed of RcsC, RcsD and the response regulator RcsB, and this signalling pathway has been implicated in virulence and biofilm formation in many enteric bacteria. It was previously shown that a mutation in rcsC resulted in defective biofilm formation in Escherichia coli [Ferrières, L. & Clarke, D. J. (2003) Mol Microbiol 50, 1665-1682]. To identify the molecular mechanisms underlying the observed biofilm defect we carried out a screen looking for suppressor mutants that restored biofilm formation in the rcsC mutant background. One of the mutants was identified to be in rprA, a gene encoding a small RNA molecule that is involved in the post-transcriptional control of the alternative sigma factor, sigma(S). The expression of rprA is regulated by the Rcs phosphorelay, and there are elevated sigma(S) levels present in the rcsC mutant due to the overexpression of rprA in this background. Using different approaches, we have established that the increase in sigma(S) levels is responsible for the biofilm defect. Therefore, the Rcs phosphorelay is involved in maintaining appropriate levels of sigma(S) during biofilm formation in E. coli.
Rcs磷酸化信号转导途径由RcsC、RcsD和应答调节因子RcsB组成,该信号通路与许多肠道细菌的毒力和生物膜形成有关。先前的研究表明,rcsC基因突变会导致大肠杆菌生物膜形成缺陷[Ferrières, L. & Clarke, D. J. (2003) Mol Microbiol 50, 1665 - 1682]。为了确定观察到的生物膜缺陷背后的分子机制,我们进行了一项筛选,寻找能在rcsC突变体背景下恢复生物膜形成的抑制突变体。其中一个突变体被鉴定为位于rprA基因中,该基因编码一种小RNA分子,参与替代σ因子σ(S)的转录后调控。rprA的表达受Rcs磷酸化信号转导途径调控,在rcsC突变体中,由于rprA在此背景下的过表达,σ(S)水平升高。通过不同的方法,我们确定了σ(S)水平的升高是生物膜缺陷的原因。因此,Rcs磷酸化信号转导途径在大肠杆菌生物膜形成过程中参与维持σ(S)的适当水平。