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Title: The horizontally-acquired response regulator SsrB drives a Salmonella lifestyle switch by relieving biofilm silencing
Authors: Desai S.K. 
Winardhi R.S.
Periasamy S.
Dykas M.M. 
Jie Y. 
Kenney L.J. 
Keywords: Article
atomic force microscopy
bacterial growth
bacterial strain
down regulation
fluorescence microscopy
gene silencing
molecular biology
protein expression
protein phosphorylation
protein purification
real time polymerase chain reaction
reverse transcription polymerase chain reaction
Salmonella enterica serovar Typhi
Salmonella enterica serovar Typhimurium
scanning electron microscopy
ssrB gene
Western blotting
gene expression regulation
genomic island
growth, development and aging
bacterial protein
SsrB protein, Salmonella typhimurium
transcription factor
Bacterial Proteins
Gene Expression Regulation, Bacterial
Genomic Islands
Salmonella typhimurium
Transcription Factors
Issue Date: 2016
Citation: Desai S.K., Winardhi R.S., Periasamy S., Dykas M.M., Jie Y., Kenney L.J. (2016). The horizontally-acquired response regulator SsrB drives a Salmonella lifestyle switch by relieving biofilm silencing. eLife 5 (42401) : e10747. ScholarBank@NUS Repository.
Abstract: A common strategy by which bacterial pathogens reside in humans is by shifting from a virulent lifestyle, (systemic infection), to a dormant carrier state. Two major serovars of Salmonella enterica, Typhi and Typhimurium, have evolved a two-component regulatory system to exist inside Salmonella-containing vacuoles in the macrophage, as well as to persist as asymptomatic biofilms in the gallbladder. Here we present evidence that SsrB, a transcriptional regulator encoded on the SPI-2 pathogenicity-island, determines the switch between these two lifestyles by controlling ancestral and horizontally-acquired genes. In the acidic macrophage vacuole, the kinase SsrA phosphorylates SsrB, and SsrB~P relieves silencing of virulence genes and activates their transcription. In the absence of SsrA, unphosphorylated SsrB directs transcription of factors required for biofilm formation specifically by activating csgD (agfD), the master biofilm regulator by disrupting the silenced, H-NS-bound promoter. Anti-silencing mechanisms thus control the switch between opposing lifestyles. © Desai et al.
Source Title: eLife
ISSN: 2050084X
DOI: 10.7554/eLife.10747
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