Elevated levels of σ
            S inhibit biofilm formation in Escherichia coli: a role for the Rcs phosphorelay

Ferrières, Lionel; Thompson, A.; Clarke, David J.

doi:10.1099/mic.0.032722-0

Cited by 24 publications

(22 citation statements)

References 51 publications

(58 reference statements)

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“…The RcsB phosphorylation shift mediated by the dual kinase/ phosphatase activity of RcsC was also proposed previously to be a key feature of the regulation of biofilm formation in E. coli (12). However, the Rcs-dependent regulation of biofilm development in E. coli differs from that of S. Typhimurium, as the mutation of RcsB alone in E. coli has no effect on biofilm formation, while null and point mutations that impede RcsC activity result in a negative phenotype.…”

Section: Discussionmentioning

confidence: 64%

“…This situation seems to be exactly the opposite of that found for Salmonella. One possible explanation for this is that the inactivation of rcsC might result in the accumulation of phosphorylated RcsB in E. coli (12), whereas the same mutation might result in the accumulation of unphosphorylated RcsB in S. Typhimurium. We can envision at least two different mechanisms that could lead to this different outcome: first, the phosphatase activity of RcsC could prevail over the kinase activity in E. coli, while the opposite balance would take place in S. Typhimurium.…”

Section: Discussionmentioning

confidence: 99%

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Salmonella Biofilm Development Depends on the Phosphorylation Status of RcsB

et al. 2012

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The Rcs phosphorelay pathway is a complex signaling pathway involved in the regulation of many cell surface structures in enteric bacteria. In response to environmental stimuli, the sensor histidine kinase (RcsC) autophosphorylates and then transfers the phosphate through intermediary steps to the response regulator (RcsB), which, once phosphorylated, regulates gene expression. Here, we show that Salmonella biofilm development depends on the phosphorylation status of RcsB. Thus, unphosphorylated RcsB, hitherto assumed to be inactive, is essential to activate the expression of the biofilm matrix compounds. The prevention of RcsB phosphorylation either by the disruption of the phosphorelay at the RcsC or RcsD level or by the production of a nonphosphorylatable RcsB allele induces biofilm development. On the contrary, the phosphorylation of RcsB by the constitutive activation of the Rcs pathway inhibits biofilm development, an effect that can be counteracted by the introduction of a nonphosphorylatable RcsB allele. The inhibition of biofilm development by phosphorylated RcsB is due to the repression of CsgD expression, through a mechanism dependent on the accumulation of the small noncoding RNA RprA. Our results indicate that unphosphorylated RcsB plays an active role for integrating environmental signals and, more broadly, that RcsB phosphorylation acts as a key switch between planktonic and sessile life-styles in Salmonella enterica serovar Typhimurium.

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Section: Discussionmentioning

confidence: 64%

Section: Discussionmentioning

confidence: 99%

Salmonella Biofilm Development Depends on the Phosphorylation Status of RcsB

et al. 2012

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“…A, compare lane 10 to lane 6 and lane 15 to lane 11). This is consistent with work suggesting that RpoS can repress biofilm formation in cells assayed in LB media (Ferrieres et al ., ).…”

Section: Resultsmentioning

confidence: 97%

Alternative pathways for Escherichia coli biofilm formation revealed by sRNA overproduction

Parker

Cureoglu

Lay

et al. 2017

Molecular Microbiology

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Small regulatory RNAs have major roles in many regulatory circuits in Escherichia coli and other bacteria, including the transition from planktonic to biofilm growth. We tested Hfq-dependent sRNAs in E. coli for their ability, when overproduced, to inhibit or stimulate biofilm formation, in two different growth media. We identify two mutually exclusive pathways for biofilm formation. In LB, PgaA, encoding an adhesion export protein, played a critical role; biofilm was independent of the general stress factor RpoS or CsgD, regulator of curli and other biofilm genes. The PgaA-dependent pathway was stimulated upon overproduction of DsrA, via negative regulation of H-NS, or of GadY, likely by titration of CsrA. In YESCA (Yeast Extract Casamino acids) media, biofilm was dependent upon RpoS and CsgD, but independent of PgaA; RpoS appears to indirectly negatively regulate the PgaA-dependent pathway in YESCA medium. Deletions of most sRNAs had very little effect on biofilm, although deletion of hfq, encoding an RNA chaperone, was defective in both LB and YESCA. Deletion of ArcZ, a small RNA activator of RpoS, decreased biofilm in YESCA; only a portion of this defect could be bypassed by overproduction of RpoS. Overall, sRNAs highlight different pathways to biofilm formation.

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“…However, the genes in the Rcs regulon and the observation that the system is induced by solid surfaces suggest that the Rcs phosphorelay may be important during the development of biofilms, when motility needs to be shut down and capsule accumulates. RpoS is needed for biofilm maturation, and too much or too little RpoS interferes with biofilm development (40). It is attractive to suggest that RprA activation of rpoS translation helps to ensure properly timed expression of RpoS during biofilm maturation.…”

Section: Specific Stresses and The Role Of Srnasmentioning

confidence: 99%

The RpoS-Mediated General Stress Response inEscherichia coli

Battesti

Majdalani

Gottesman

2011

Annu. Rev. Microbiol.

778

903

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Under conditions of nutrient deprivation or stress, or as cells enter stationary phase, Escherichia coli and related bacteria increase the accumulation of RpoS, a specialized sigma factor. RpoS-dependent gene expression leads to general stress resistance of cells. During rapid growth, RpoS translation is inhibited and any RpoS protein that is synthesized is rapidly degraded. The complex transition from exponential growth to stationary phase has been partially dissected by analyzing the induction of RpoS after specific stress treatments. Different stress conditions lead to induction of specific sRNAs that stimulate RpoS translation or to induction of small-protein antiadaptors that stabilize the protein. Recent progress has led to a better, but still far from complete, understanding of how stresses lead to RpoS induction and what RpoS-dependent genes help the cell deal with the stress.

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Elevated levels of σ S inhibit biofilm formation in Escherichia coli: a role for the Rcs phosphorelay

Cited by 24 publications

References 51 publications

Salmonella Biofilm Development Depends on the Phosphorylation Status of RcsB

Salmonella Biofilm Development Depends on the Phosphorylation Status of RcsB

Alternative pathways for Escherichia coli biofilm formation revealed by sRNA overproduction

The RpoS-Mediated General Stress Response inEscherichia coli

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