Bacterial phenotypes mediated bymviAand their relationship to the mouse virulence ofSalmonella typhimurium

Swords, W. Edward; Giddings, Angela M.; Benjamin, William H.

doi:10.1006/mpat.1996.0117

Cited by 8 publications

(9 citation statements)

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“…Although 40 to 50 genes have been shown elsewhere to be required for Salmonella pathogenesis (30), our selection procedure produced only a very small subset of virulence proteins. To determine whether additional regulators were involved in the attenuation of the bacterial growth rate within fibroblasts, we tested mutants affected in the following regulatory proteins: (i) RpoE, an alternative sigma factor (38); (ii) SpiR (SsrA) and SpiA, a regulator and a type III structural protein, respectively, both encoded in SPI-2 (34, 51); (iii) OmpR, a transcriptional regulator controlling outer membrane protein content (43); (iv) Dam, a DNA-adenine methylase required for systemic disease (23,33); (v) the global regulators Crp, RelA, and Lrp (18); (vi) OxyR and SoxRS, related to oxidative stress (13, 67); (vii) MviA, a regulator required for eliciting systemic disease in mice (66); and (viii) Fnr, which controls switching to anaerobic metabolism. Unlike the mutations in the phoP, phoQ, slyA, rpoS, spvR, and igaA genes, none of the other virulence-related mutations resulted in an I pro value higher than that of the wt (Table 4).…”

Section: Resultsmentioning

confidence: 99%

Salmonella enterica Serovar Typhimurium Response Involved in Attenuation of Pathogen Intracellular Proliferation

et al. 2001

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Salmonella enterica serovar Typhimurium proliferates within cultured epithelial and macrophage cells. Intracellular bacterial proliferation is, however, restricted within normal fibroblast cells. To characterize this phenomenon in detail, we investigated the possibility that the pathogen itself might contribute to attenuating the intracellular growth rate. S. enterica serovar Typhimurium mutants were selected in normal rat kidney fibroblasts displaying an increased intracellular proliferation rate. These mutants harbored loss-of-function mutations in the virulence-related regulatory genes phoQ, rpoS, slyA, and spvR. Lack of a functional PhoP-PhoQ system caused the most dramatic change in the intracellular growth rate. phoP-and phoQ-null mutants exhibited an intracellular growth rate 20-to 30-fold higher than that of the wild-type strain. This result showed that the PhoP-PhoQ system exerts a master regulatory function for preventing bacterial overgrowth within fibroblasts. In addition, an overgrowing clone was isolated harboring a mutation in a previously unknown serovar Typhimurium open reading frame, named igaA for intracellular growth attenuator. Mutations in other serovar Typhimurium virulence genes, such as ompR, dam, crp, cya, mviA, spiR (ssrA), spiA, and rpoE, did not result in pathogen intracellular overgrowth. Nonetheless, lack of either SpiA or the alternate sigma factor RpoE led to a substantial decrease in intracellular bacterial viability. These results prove for the first time that specific serovar Typhimurium virulence regulators are involved in a response designed to attenuate the intracellular growth rate within a nonphagocytic host cell. This growth-attenuating response is accompanied by functions that ensure the viability of intracellular bacteria.

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Section: Resultsmentioning

confidence: 99%

Salmonella enterica Serovar Typhimurium Response Involved in Attenuation of Pathogen Intracellular Proliferation

et al. 2001

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“…Mutations that block S degradation lead to inappropriate expression of S -dependent genes during exponential growth (Muffler et al 1996a) and to decreased virulence in Salmonella and Erwinia (Swords et al 1997;Andersson et al 1999).…”

Section: Discussionmentioning

confidence: 99%

The RssB response regulator directly targets ς^S for degradation by ClpXP

Zhou¹,

Gottesman²,

Hoskins³

et al. 2001

Genes Dev.

270

277

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“…A null mutation in mviA (for mouse virulence gene A [7]) leads to avirulence in mice in almost all the S. enterica serovar Typhimurium strains examined (77). The exception is LT2, a strain that was originally described as virulent for mice in 1948 (53).…”

Section: Resultsmentioning

confidence: 99%

“…One of the most interesting phenotypes of Salmonella mviA mutants is avirulence in mice (77). The prevalent view is that this virulence defect is caused by increased levels of RpoS (77,85).…”

Section: Resultsmentioning

confidence: 99%

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Regulation ofigaAand the Rcs System by the MviA Response Regulator inSalmonella enterica

2009

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IgaA is a membrane protein that prevents overactivation of the Rcs regulatory system in enteric bacteria. Here we provide evidence that igaA is the first gene in a 70 -dependent operon of Salmonella enterica serovar Typhimurium that also includes yrfG, yrfH, and yrfI. We also show that the Lon protease and the MviA response regulator participate in regulation of the igaA operon. Our results indicate that MviA regulates igaA transcription in an RpoS-dependent manner, but the results also suggest that MviA may regulate RcsB activation in an RpoS-and IgaA-independent manner.

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Bacterial phenotypes mediated bymviAand their relationship to the mouse virulence ofSalmonella typhimurium

Cited by 8 publications

References 28 publications

Salmonella enterica Serovar Typhimurium Response Involved in Attenuation of Pathogen Intracellular Proliferation

Salmonella enterica Serovar Typhimurium Response Involved in Attenuation of Pathogen Intracellular Proliferation

The RssB response regulator directly targets ς^S for degradation by ClpXP

Regulation ofigaAand the Rcs System by the MviA Response Regulator inSalmonella enterica

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Bacterial phenotypes mediated bymviAand their relationship to the mouse virulence ofSalmonella typhimurium

Cited by 8 publications

References 28 publications

Salmonella enterica Serovar Typhimurium Response Involved in Attenuation of Pathogen Intracellular Proliferation

Salmonella enterica Serovar Typhimurium Response Involved in Attenuation of Pathogen Intracellular Proliferation

The RssB response regulator directly targets ςS for degradation by ClpXP

Regulation ofigaAand the Rcs System by the MviA Response Regulator inSalmonella enterica

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The RssB response regulator directly targets ς^S for degradation by ClpXP