IraL Is an RssB Anti-adaptor That Stabilizes RpoS during Logarithmic Phase Growth in Escherichia coli and
            <i>Shigella</i>

Hryckowian, Andrew J.; Battesti, Aurélia; Lemke, Justin J.; Meyer, Zachary C.; Welch, Rodney A.

doi:10.1128/mbio.01043-14

Cited by 23 publications

(16 citation statements)

References 31 publications

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“…(B) Representative flow cytometry analysis of spontaneous SOS induction showing the small cell subpopulation with spontaneous SOS-activating DNA damage, as described previously (82), in arbitrary fluorescence units. (C) The Δ gcvB MBR-deficient phenotype is suppressed by Δ rssB , a mutation that increases σ S protein levels by reducing σ S proteolytic degradation (97), and increases MBR as shown here and shown previously (39, 98). The results of a representative experiment are shown.…”

Section: Resultssupporting

confidence: 63%

“…3B and C). RssB is a protein chaperone that brings σ S to the ClpXP protease for degradation (97), such that its removal causes artificially high σ S levels (97). …”

Section: Resultsmentioning

confidence: 99%

“…We found that both the mutagenesis defect and the high spontaneous SOS response in Δ gcvB cells were reversed by deletion of rssB , which upregulates σ S by reducing ClpXP-mediated proteolytic degradation of σ S (97). Deletion of rssB increases the general stress response (97), and it also increases MBR (39). rssB deletion fully restored mutagenesis to Δ gcvB cells, elevated mutagenesis to the greater-than-wild-type levels seen in Δ rssB cells (Fig.…”

Section: Resultsmentioning

confidence: 99%

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The Small RNA GcvB Promotes Mutagenic Break Repair by Opposing the Membrane Stress Response

et al. 2016

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Microbes and human cells possess mechanisms of mutagenesis activated by stress responses. Stress-inducible mutagenesis mechanisms may provide important models for mutagenesis that drives host-pathogen interactions, antibiotic resistance, and possibly much of evolution generally. In Escherichia coli, repair of DNA double-strand breaks is switched to a mutagenic mode, using error-prone DNA polymerases, via the SOS DNA damage and general (σS) stress responses. We investigated small RNA (sRNA) clients of Hfq, an RNA chaperone that promotes mutagenic break repair (MBR), and found that GcvB promotes MBR by allowing a robust σS response, achieved via opposing the membrane stress (σE) response. Cells that lack gcvB were MBR deficient and displayed reduced σS-dependent transcription but not reduced σS protein levels. The defects in MBR and σS-dependent transcription in ΔgcvB cells were alleviated by artificially increasing σS levels, implying that GcvB promotes mutagenesis by allowing a normal σS response. ΔgcvB cells were highly induced for the σE response, and blocking σE response induction restored both mutagenesis and σS-promoted transcription. We suggest that GcvB may promote the σS response and mutagenesis indirectly, by promoting membrane integrity, which keeps σE levels lower. At high levels, σE might outcompete σS for binding RNA polymerase and so reduce the σS response and mutagenesis. The data show the delicate balance of stress response modulation of mutagenesis.IMPORTANCE Mutagenesis mechanisms upregulated by stress responses promote de novo antibiotic resistance and cross-resistance in bacteria, antifungal drug resistance in yeasts, and genome instability in cancer cells under hypoxic stress. This paper describes the role of a small RNA (sRNA) in promoting a stress-inducible-mutagenesis mechanism, mutagenic DNA break repair in Escherichia coli. The roles of many sRNAs in E. coli remain unknown. This study shows that ΔgcvB cells, which lack the GcvB sRNA, display a hyperactivated membrane stress response and reduced general stress response, possibly because of sigma factor competition for RNA polymerase. This results in a mutagenic break repair defect. The data illuminate a function of GcvB sRNA in opposing the membrane stress response, and thus indirectly upregulating mutagenesis.

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Section: Resultssupporting

confidence: 63%

“…3B and C). RssB is a protein chaperone that brings σ S to the ClpXP protease for degradation (97), such that its removal causes artificially high σ S levels (97). …”

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

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The Small RNA GcvB Promotes Mutagenic Break Repair by Opposing the Membrane Stress Response

et al. 2016

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“…For example, naturally occurring strains can differ in the amount of RpoS they produce during exponential phase (12) or stationary phase (13). All studies that have measured RpoS levels in naturally occurring strains of E. coli have detected variations (13)(14)(15)(16)(17), though the extent and cause of the variations in RpoS between strains is still a matter of some controversy (16,17).…”

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confidence: 99%

Genome-Wide Transcriptional Response to Varying RpoS Levels in Escherichia coli K-12

et al. 2017

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The alternative sigma factor RpoS is a central regulator of many stress responses in Escherichia coli. The level of functional RpoS differs depending on the stress. The effect of these differing concentrations of RpoS on global transcriptional responses remains unclear. We investigated the effect of RpoS concentration on the transcriptome during stationary phase in rich media. We found that 23% of genes in the E. coli genome are regulated by RpoS, and we identified many RpoS-transcribed genes and promoters. We observed three distinct classes of response to RpoS by genes in the regulon: genes whose expression changes linearly with increasing RpoS level, genes whose expression changes dramatically with the production of only a little RpoS ("sensitive" genes), and genes whose expression changes very little with the production of a little RpoS ("insensitive"). We show that sequences outside the core promoter region determine whether an RpoS-regulated gene is sensitive or insensitive. Moreover, we show that sensitive and insensitive genes are enriched for specific functional classes and that the sensitivity of a gene to RpoS corresponds to the timing of induction as cells enter stationary phase. Thus, promoter sensitivity to RpoS is a mechanism to coordinate specific cellular processes with growth phase and may also contribute to the diversity of stress responses directed by RpoS. IMPORTANCEThe sigma factor RpoS is a global regulator that controls the response to many stresses in Escherichia coli. Different stresses result in different levels of RpoS production, but the consequences of this variation are unknown. We describe how changing the level of RpoS does not influence all RpoS-regulated genes equally. The cause of this variation is likely the action of transcription factors that bind the promoters of the genes. We show that the sensitivity of a gene to RpoS levels explains the timing of expression as cells enter stationary phase and that genes with different RpoS sensitivities are enriched for specific functional groups. Thus, promoter sensitivity to RpoS is a mechanism that coordinates specific cellular processes in response to stresses. KEYWORDS RpoS, promoters, S , stress response, transcriptional regulation, transcriptome G enome-wide measurements of RNA levels have revolutionized our understanding of how cells organize their patterns of transcription. These studies have given us snapshots of how patterns of gene expression change in response to changes in the external environment. They have also allowed us to define the regulons controlled by specific transcription factors (TFs). A major weakness of the vast majority of these

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“…These proteins interact with RssB and prevent the degradation of S , leading thus to S accumulation in the cell. Surprisingly, except for enterobacteria, the post-translational regulation of S is unknown in other Gram-negative bacteria (21)(22)(23).…”

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confidence: 99%

The General Stress Response σS Is Regulated by a Partner Switch in the Gram-negative Bacterium Shewanella oneidensis

Bouillet¹,

Genest²,

Jourlin-Castelli³

et al. 2016

Journal of Biological Chemistry

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Edited by Thomas SöllnerHere, we show that a partner-switching system of the aquatic Proteobacterium Shewanella oneidensis regulates post-translationally S (also called RpoS), the general stress response sigma factor. Genes SO2118 and SO2119 encode CrsA and CrsR, respectively. CrsR is a three-domain protein comprising a receiver, a phosphatase, and a kinase/anti-sigma domains, and CrsA is an anti-sigma antagonist. In vitro, CrsR sequesters S and possesses kinase and phosphatase activities toward CrsA. In turn, dephosphorylated CrsA binds the anti-sigma domain of CrsR to allow the release of S . This study reveals a novel pathway that post-translationally regulates the general stress response sigma factor differently than what was described for other proteobacteria like Escherichia coli. We argue that this pathway allows probably a rapid bacterial adaptation.

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IraL Is an RssB Anti-adaptor That Stabilizes RpoS during Logarithmic Phase Growth in Escherichia coli and Shigella

Cited by 23 publications

References 31 publications

The Small RNA GcvB Promotes Mutagenic Break Repair by Opposing the Membrane Stress Response

The Small RNA GcvB Promotes Mutagenic Break Repair by Opposing the Membrane Stress Response

Genome-Wide Transcriptional Response to Varying RpoS Levels in Escherichia coli K-12

The General Stress Response σS Is Regulated by a Partner Switch in the Gram-negative Bacterium Shewanella oneidensis

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