Regulation of
 osmC
 Gene Expression by the Two-Component System
 rcsB-rcsC
 in
 Escherichia coli

Davalos-Garcia, Marcela; Conter, Annie; Toesca, Isabelle; Gutierrez, Claude; Cam, Kaymeuang

doi:10.1128/jb.183.20.5870-5876.2001

Cited by 92 publications

(100 citation statements)

References 38 publications

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“…Like OmpRϳP, RcsBϳP represses flagellar synthesis directly (138,330). In addition, RcsBϳP activates both colanic acid biosynthesis (433) and at least one acetylϳP-responsive stress effector (osmC) (112). Several other acetylϳP-responsive genes are regulated by RcsC, the cognate HK of RcsB, suggesting that they might also be regulated by RcsB.…”

Section: Evidence In Vitromentioning

confidence: 99%

The Acetate Switch

Wolfe

2005

Microbiol Mol Biol Rev

1,080

1,274

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To succeed, many cells must alternate between life-styles that permit rapid growth in the presence of abundant nutrients and ones that enhance survival in the absence of those nutrients. One such change in life-style, the “acetate switch,” occurs as cells deplete their environment of acetate-producing carbon sources and begin to rely on their ability to scavenge for acetate. This review explains why, when, and how cells excrete or dissimilate acetate. The central components of the “switch” (phosphotransacetylase [PTA], acetate kinase [ACK], and AMP-forming acetyl coenzyme A synthetase [AMP-ACS]) and the behavior of cells that lack these components are introduced. Acetyl phosphate (acetyl∼P), the high-energy intermediate of acetate dissimilation, is discussed, and conditions that influence its intracellular concentration are described. Evidence is provided that acetyl∼P influences cellular processes from organelle biogenesis to cell cycle regulation and from biofilm development to pathogenesis. The merits of each mechanism proposed to explain the interaction of acetyl∼P with two-component signal transduction pathways are addressed. A short list of enzymes that generate acetyl∼P by PTA-ACKA-independent mechanisms is introduced and discussed briefly. Attention is then directed to the mechanisms used by cells to “flip the switch,” the induction and activation of the acetate-scavenging AMP-ACS. First, evidence is presented that nucleoid proteins orchestrate a progression of distinct nucleoprotein complexes to ensure proper transcription of its gene. Next, the way in which cells regulate AMP-ACS activity through reversible acetylation is described. Finally, the “acetate switch” as it exists in selected eubacteria, archaea, and eukaryotes, including humans, is described

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Section: Evidence In Vitromentioning

confidence: 99%

The Acetate Switch

Wolfe

2005

Microbiol Mol Biol Rev

1,080

1,274

View full text Add to dashboard Cite

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“…In addition to the cps genes and several other genes whose regulation by the Rcs system has been fairly thoroughly investigated (5,10,13,15,18,34), many genes were recently identified as putative Rcs regulon members (17,22,43). Some are positively and others are negatively regulated.…”

Section: Vol 186 2004mentioning

confidence: 99%

“…The rcsF gene product was reported to activate RcsB when overproduced (19), but its function in signal transduction was not clear until recently, when Hagiwara et al (22) showed its involvement in Rcs signaling in response to glucose and zinc at 20°C. The Rcs system was shown to affect the expression of tolQRA (10), rcsA (15), ftsAZ (5), osmC (13), rprA (34), and flhDC (18). Recent transcriptome analyses using DNA arrays identified many other genes that are under direct or indirect control of the Rcs system (17,22,43).…”

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confidence: 99%

Activation of the Rcs Signal Transduction System Is Responsible for the Thermosensitive Growth Defect of anEscherichia coliMutant Lacking Phosphatidylglycerol and Cardiolipin

et al. 2004

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The lethal effect of an Escherichia coli pgsA null mutation, which causes a complete lack of the major acidic phospholipids, phosphatidylglycerol and cardiolipin, is alleviated by a lack of the major outer membrane lipoprotein encoded by the lpp gene, but an lpp pgsA strain shows a thermosensitive growth defect. Using transposon mutagenesis, we found that this thermosensitivity was suppressed by disruption of the rcsC, rcsF, and yojN genes, which code for a sensor kinase, accessory positive factor, and phosphotransmitter, respectively, of the Rcs phosphorelay signal transduction system initially identified as regulating the capsular polysaccharide synthesis (cps) genes. Disruption of the rcsB gene coding for the response regulator of the system also suppressed the thermosensitivity, whereas disruption of cpsE did not. By monitoring the expression of a cpsB-lac fusion, we showed that the Rcs system is activated in the pgsA mutant and is reverted to a wild-type level by the rcs mutations. These results indicate that envelope stress due to an acidic phospholipid deficiency activates the Rcs phosphorelay system and thereby causes the thermosensitive growth defect independent of the activation of capsule synthesis.

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“…The Rcs phosphorelay has been implicated in the synthesis of virulence factors in Pcc and other plant-pathogenic bacteria and also in human pathogens (Hinchliffe et al, 2008;Mouslim et al, 2004;Wang et al, 2009Wang et al, , 2007. RcsB activates the biosynthesis of capsular exopolysaccharides, transcription of the cell division gene, ftsZ, transcription of a cell envelope protein, osmC, and transcription of RprA RNA to increase expression of the stationary-phase sigma factor, RpoS, in E. coli (Carballes et al, 1999;Davalos-Garcia et al, 2001;Gervais et al, 1992;Gottesman et al, 1985;Majdalani et al, 2002). Francez-Charlot et al (2003) demonstrated that the Rcs phosphorelay system represses motility through the direct binding of RcsB to the promoter of flhDC in E. coli.…”

Section: Introductionmentioning

confidence: 99%

A role for the Rcs phosphorelay in regulating expression of plant cell wall degrading enzymes in Pectobacterium carotovorum subsp. carotovorum

et al. 2010

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The Rcs phosphorelay is a signal transduction system that influences the virulence phenotype of several pathogenic bacteria. In the plant pathogen Pectobacterium carotovorum subsp. carotovorum (Pcc) the response regulator of the Rcs phosphorelay, RcsB, represses expression of plant cell wall degrading enzymes (PCWDE) and motility. The focus of this study was to identify genes directly regulated by the binding of RcsB that also regulate expression of PCWDE genes in Pcc. RcsB-binding sites within the regulatory regions of the flhDC operon and the rprA and rsmB genes were identified using DNase I protection assays, while in vivo studies using flhDC : : gusA, rsmB : : gusA and rprA : : gusA gene fusions revealed gene regulation. These experiments demonstrated that the operon flhDC, a flagellar master regulator, was repressed by RcsB, and transcription of rprA was activated by RcsB. Regulation of the rsmB promoter by RcsB is more complicated. Our results show that RcsB represses rsmB expression mainly through modulating flhDC transcription. Neverthless, direct binding of RcsB on the rsmB promoter region is possible in certain conditions. Using an rprA-negative mutant, it was further demonstrated that RprA RNA is not essential for regulating expression of PCWDE under the conditions tested, whereas overexpression of rprA increased protease expression in wild-type cells. Stationary-phase sigma factor, RpoS, is the only known target gene for RprA RNA in Escherichia coli; however, in Pcc the effect of RprA RNA was found to be rpoS-independent. Overall, our results show that the Rcs phosphorelay negatively affects expression of PCWDE by inhibiting expression of flhDC and rsmB. INTRODUCTIONThe phytopathogenicity of Pectobacterium carotovorum subsp. carotovorum (Pcc) is largely due its capacity to synthesize and secrete plant cell wall degrading enzymes (PCWDE), including pectinases, cellulases and protease Marits et al., 1999; Mäe et al., 1995;Pirhonen et al., 1991). Survival of infecting Pcc largely depends on production of PCWDE for the transition from latent infection to disease state. A number of global and specific regulatory genes contribute to expression of PCWDE in Pcc (Burr et al., 2006;Chatterjee et al., 1995;Cui et al., 1995Cui et al., , 1999Cui et al., , 2001Cui et al., , 2005Eriksson et al., 1998;Flego et al., 2000;Harris et al., 1998; Hyytiäinen et al., 2003;Liu et al., 1998Liu et al., , 1999 Sjöblom et al., 2006). The posttranscriptional Rsm system plays a key role in regulating the expression of PCWDE Cui et al., 1995;Liu et al., 1998).The Rsm system consists of two regulators in Pcc: a small protein, RsmA, and RsmB RNA. RsmA is a post-transcriptional global regulator that is thought to bind mRNAs of PCWDE genes and affect their stability, whereas RsmB RNA binds multiple molecules of RsmA, thereby neutralizing its effect (Liu et al., 1998). Recently, the Rsm system was shown to be dependent on expression of a global regulator of flagellar genes, FlhDC. FlhDC activates the expression of PCWDE in Pcc strain 7...

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Regulation of osmC Gene Expression by the Two-Component System rcsB-rcsC in Escherichia coli

Cited by 92 publications

References 38 publications

The Acetate Switch

The Acetate Switch

Activation of the Rcs Signal Transduction System Is Responsible for the Thermosensitive Growth Defect of anEscherichia coliMutant Lacking Phosphatidylglycerol and Cardiolipin

A role for the Rcs phosphorelay in regulating expression of plant cell wall degrading enzymes in Pectobacterium carotovorum subsp. carotovorum

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