PspB and PspC of <i>Yersinia enterocolitica</i> are dual function proteins: regulators and effectors of the phage‐shock‐protein response

Maxson, Michelle E.; Darwin, Andrew J.

doi:10.1111/j.1365-2958.2006.05047.x

Cited by 48 publications

(134 citation statements)

References 31 publications

(84 reference statements)

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“…The only possible component of this system that has been identified in S. pneumoniae is the LiaR-controlled spr0810 gene. In Y. enterocolitica the product of the corresponding gene, PspC, functions both as a regulator of psp gene expression and as an effector that acts independently to support growth when the bacterium is subjected to extracytoplasmic stress (33). In contrast to the complex system regulated by HrcA, the Psp-like system in S. pneumoniae appears to consist of a single protein encoded on a monocistronic operon.…”

Section: Discussionmentioning

confidence: 98%

“…The Psp systems of E. coli and Y. enterocolitica have six proteins in common (PspABCD and PspFG) that are also present in many other Gram-negative bacteria. In these bacteria, the Psp system responds to extracytoplasmic stress and appears to play a role in maintaining cytoplasmic membrane integrity and/or the proton motive force (33). All but the spr0810 gene product, which shows a rather low level of homology to E. coli PspC, appear to be absent from the pneumococcal genome.…”

Section: Prediction Of the Liar Regulon In Pathogenic Strains Of Smentioning

confidence: 99%

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The Pneumococcal Cell Envelope Stress-Sensing System LiaFSR Is Activated by Murein Hydrolases and Lipid II-Interacting Antibiotics

et al. 2010

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In the Firmicutes, two-component regulatory systems of the LiaSR type sense and orchestrate the response to various agents that perturb cell envelope functions, in particular lipid II cycle inhibitors. In the current study, we found that the corresponding system in Streptococcus pneumoniae displays similar properties but, in addition, responds to cell envelope stress elicited by murein hydrolases. During competence for genetic transformation, pneumococci attack and lyse noncompetent siblings present in the same environment. This phenomenon, termed fratricide, increases the efficiency of horizontal gene transfer in vitro and is believed to stimulate gene exchange also under natural conditions. Lysis of noncompetent target cells is mediated by the putative murein hydrolase CbpD, the key effector of the fratricide mechanism, and the autolysins LytA and LytC. To avoid succumbing to their own lysins, competent attacker cells must possess a protective mechanism rendering them immune. The most important component of this mechanism is ComM, an integral membrane protein of unknown function that is expressed only in competent cells. Here, we show that a second layer of self-protection is provided by the pneumococcal LiaFSR system, which senses the damage inflicted to the cell wall by CbpD, LytA, and LytC. Two members of the LiaFSR regulon, spr0810 and PcpC (spr0351), were shown to contribute to the LiaFSR-coordinated protection against fratricide-induced self-lysis.

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Section: Discussionmentioning

confidence: 98%

Section: Prediction Of the Liar Regulon In Pathogenic Strains Of Smentioning

confidence: 99%

The Pneumococcal Cell Envelope Stress-Sensing System LiaFSR Is Activated by Murein Hydrolases and Lipid II-Interacting Antibiotics

et al. 2010

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“…Strains were grown under both non-Pspinducing (2YscC) and Psp-inducing (+YscC) conditions and b-galactosidase activities were determined (Table 2). YscC overproduction does not induce W(pspA-lacZ) expression as much as some other proteins (Maxson & Darwin, 2004, 2005, 2006. However, it does cause a severe growth defect in some psp null mutants (Darwin & Miller, 2001;Green & Darwin, 2004;Maxson & Darwin, 2006) and so its effect on pspA operon expression is probably physiologically significant.…”

Section: § Deletion Analysis Of the Pspa Control Regionmentioning

confidence: 99%

“…Apparently, the Y. enterocolitica Psp system must respond to a stress caused by mislocalization of the YscC secretin component of the type III secretion system (Darwin & Miller, 2001). Consequently, null mutations of some psp genes cause severe growth defects when yscC is overexpressed (Darwin & Miller, 2001;Green & Darwin, 2004;Maxson & Darwin, 2006).…”

Section: Introductionmentioning

confidence: 99%

Multiple promoters control expression of the Yersinia enterocolitica phage-shock-protein A (pspA) operon

Maxson

Darwin

2006

Microbiology

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The widely conserved phage-shock-protein A (pspA) operon encodes an extracytoplasmic stress response system that is essential for virulence in Yersinia enterocolitica, and has been linked to other important phenotypes in Escherichia coli, Salmonella enterica and Shigella flexneri. Regulation of pspA operon expression is mediated through a promoter upstream of pspA that depends on sigma factor RpoN (σ 54) and the enhancer binding protein PspF. PspA, PspB and PspC, encoded within the pspA operon, also regulate expression by participating in a putative signal transduction pathway that probably serves to modulate PspF activity. All of this suggests that appropriate expression of the pspA operon is critical. Previous genetic analysis of the Y. enterocolitica pspA operon suggested that an additional level of complexity might be mediated by PspF/RpoN-independent expression of some psp genes. Here, an rpoN null mutation and interposon analysis were used to confirm that PspF/RpoN-independent gene expression does originate within the psp locus. Molecular genetic approaches were used to systematically analyse the two large non-coding regions within the psp locus. Primer extension, control region deletion and site-directed mutagenesis experiments led to the identification of RpoN-independent promoters both upstream and downstream of pspA. The precise location of the PspF/RpoN-dependent promoter upstream of pspA was also determined. The discovery of these RpoN-independent promoters reveals yet another level of transcriptional complexity for the Y. enterocolitica pspA operon that may function to allow low-level constitutive expression of psp genes and/or additional regulation under some conditions.

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“…Although the precise details of how the psp response leads to protection against elevated pH and other stresses are not entirely clear, it has been suggested that PspA plays a role in maintenance of proton motive force (15). A complex network of interactions between PspA and other Psp members (PspF, PspB, and PspC) is thought to regulate PspA activity (1,9,19). We propose that 6S RNA regulation of pspF places an upper limit on the extent of the psp response when nutrients are limiting in stationary phase.…”

mentioning

confidence: 99%

6S RNA Regulation of pspF Transcription Leads to Altered Cell Survival at High pH

Trotochaud

Wassarman

2006

J Bacteriol

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6S RNA is a highly abundant small RNA that regulates transcription through direct interaction with RNA polymerase. Here we show that 6S RNA directly inhibits transcription of pspF, which subsequently leads to inhibition of pspABCDE and pspG expression. Cells without 6S RNA are able to survive at elevated pH better than wild-type cells due to loss of 6S RNA-regulation of pspF. This 6S RNA-dependent phenotype is eliminated in pspF-null cells, indicating that 6S RNA effects are conferred through PspF. Similar growth phenotypes are seen when PspF levels are increased in a 6S RNA-independent manner, signifying that changes to pspF expression are sufficient. Changes in survival at elevated pH most likely result from altered expression of pspABCDE and/or pspG, both of which require PspF for transcription and are indirectly regulated by 6S RNA. 6S RNA provides another layer of regulation in response to high pH during stationary phase. We propose that the normal role of 6S RNA at elevated pH is to limit the extent of the psp response under conditions of nutrient deprivation, perhaps facilitating appropriate allocation of diminishing resources.6S RNA is a noncoding small RNA conserved in many bacteria (4,30,35). 6S RNA function remained a mystery for several decades until the discovery that this RNA makes specific interactions with RNA polymerase (RNAP) (32). Bacterial RNAP is a multisubunit enzyme consisting of a catalytically active core enzyme (␣ 2 , ␤, ␤Ј, ) that requires an additional specificity subunit () to form the holoenzyme (E) required for transcription initiation. 6S RNA forms stable, specific complexes with the housekeeping holoenzyme of RNAP (i.e., E 70 in Escherichia coli and E A in Bacillus subtilis) but does not interact with other holoenzymes, the core enzyme, or free subunits (30). E. coli 6S RNA makes direct contact with the 70 subunit within this 6S RNA-E 70 complex (32), suggesting that RNA binding specificity may be mediated through the 70 subunit in a manner analogous to that of DNA binding specificity. The 6S RNA is primarily double-stranded, with a large single-stranded region in the center. This highly conserved secondary structure is essential for the ability of 6S RNA to form stable complexes with E 70 (30). These data have suggested models in which 6S RNA functions as a direct competitor for promoter DNA interactions with RNAP (4,30,31,32).6S RNA interactions with E 70 result in altered transcription at specific promoters, either directly at several 70 -dependent promoters or indirectly at several S -dependent promoters (29). Observed transcriptional changes are greatest during late-stationary phase (Ն18 h of growth), a time when 6S RNA levels are maximal. Intriguingly, not all 70 -dependent promoters are sensitive to 6S RNA, even though most E 70 is complexed with 6S RNA during this time frame (29,32). Several promoters directly regulated by 6S RNA contain an extended Ϫ10 element, which is defined by a conserved TGN sequence immediately upstream of the Ϫ10 sequence element. Promoters with e...

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PspB and PspC of Yersinia enterocolitica are dual function proteins: regulators and effectors of the phage‐shock‐protein response

Cited by 48 publications

References 31 publications

The Pneumococcal Cell Envelope Stress-Sensing System LiaFSR Is Activated by Murein Hydrolases and Lipid II-Interacting Antibiotics

The Pneumococcal Cell Envelope Stress-Sensing System LiaFSR Is Activated by Murein Hydrolases and Lipid II-Interacting Antibiotics

Multiple promoters control expression of the Yersinia enterocolitica phage-shock-protein A (pspA) operon

6S RNA Regulation of pspF Transcription Leads to Altered Cell Survival at High pH

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