Phenotypic analysis of Yersinia pseudotuberculosis 32777 response regulator mutants: New insights into two-component system regulon plasticity in bacteria

Flamez, Claire; Ricard, Isabelle; Arafah, Sonia; Simonet, Michel; Marceau, Michaël

doi:10.1016/j.ijmm.2007.05.005

Cited by 51 publications

(42 citation statements)

References 46 publications

(38 reference statements)

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“…2). The findings are in accordance with results of earlier studies on phoP mutant of Y. pseudotuberculosis and Y. pestis (Oyston et al 2000;Flamez et al 2008). We then determined the in vivo lethal dose 50 of both strains after intravenous inoculation in mice.…”

Section: Resultssupporting

confidence: 90%

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Th1-type immune response to infection by pYV-cured phoP-phoQ null mutant of Yersinia pseudotuberculosis is defective in mouse model

Kumar

Balakrishna

Agarwal

et al. 2008

Antonie van Leeuwenhoek

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The PhoP-PhoQ two-component system of Yersinia pseudotuberculosis, a Gram-negative enteric pathogen which causes a variety of gastrointestinal and extraintestinal infections in humans, has been shown to be necessary for virulence. A phoP-phoQ null mutant of a strain of Y. pseudotuberculosis cured of its native plasmid pYV was obtained and studied for generation of immune response in mouse model following intravenous inoculation. The phoP-phoQ null mutant elicited much weaker IgG antibody response to whole cell sonicated (WCS) antigen, in particular that of IgG2a isotype. Interferon-gamma levels were also significantly reduced in cultured splenocytes of mice immunized with phoP-phoQ null mutant. The null mutant was found to be about 72-fold less virulent than the parent isogenic strain of Y. pseudotuberculosis. Average counts in spleen of mice inoculated with the null mutant were observed to reduce by at least four logs when compared with the counts in the spleen of mice inoculated with parent isogenic strain. We can thus suggest that the Th1-type immune response of the phoP-phoQ null mutant of Y. pseudotuberculosis is diminished in mice.

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Section: Resultssupporting

confidence: 90%

“…The survival of strains 1A and DPQ1A was determined under stress of high hydrogen peroxide and salt concentrations (Flamez et al 2008). Briefly, cultures grown overnight at 28°C were centrifuged and pelleted.…”

Section: Stress Response Assaysmentioning

confidence: 99%

Th1-type immune response to infection by pYV-cured phoP-phoQ null mutant of Yersinia pseudotuberculosis is defective in mouse model

Kumar

Balakrishna

Agarwal

et al. 2008

Antonie van Leeuwenhoek

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“…Together with its sibling ncRNA GlmZ, they regulate expression of the glucosamine-6-phosphate synthase GlmS. Transcription of glmY is activated from a σ 54 -dependent promoter and controlled by the GlrR/GlrK twocomponent system, which plays a role in virulence (88,89).…”

Section: Growth In Lymphatic Tissues Alters the Abundance Of Conservedmentioning

confidence: 99%

Tissue dual RNA-seq allows fast discovery of infection-specific functions and riboregulators shaping host–pathogen transcriptomes

Nuss

Beckstette

Пименова

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

136

117

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Pathogenic bacteria need to rapidly adjust their virulence and fitness program to prevent eradication by the host. So far, underlying adaptation processes that drive pathogenesis have mostly been studied in vitro, neglecting the true complexity of host-induced stimuli acting on the invading pathogen. In this study, we developed an unbiased experimental approach that allows simultaneous monitoring of genome-wide infection-linked transcriptional alterations of the host and colonizing extracellular pathogens. Using this tool for Yersinia pseudotuberculosis-infected lymphatic tissues, we revealed numerous alterations of host transcripts associated with inflammatory and acute-phase responses, coagulative activities, and transition metal ion sequestration, highlighting that the immune response is dominated by infiltrating neutrophils and elicits a mixed T H 17/T H 1 response. In consequence, the pathogen's response is mainly directed to prevent phagocytic attacks. Yersinia up-regulates the gene and expression dose of the antiphagocytic type III secretion system (T3SS) and induces functions counteracting neutrophil-induced ion deprivation, radical stress, and nutritional restraints. Several conserved bacterial riboregulators were identified that impacted this response. The strongest influence on virulence was found for the loss of the carbon storage regulator (Csr) system, which is shown to be essential for the up-regulation of the T3SS on host cell contact. In summary, our established approach provides a powerful tool for the discovery of infection-specific stimuli, induced host and pathogen responses, and underlying regulatory processes.tissue dual RNA-seq | host-pathogen interaction | host-adapted metabolism | noncoding RNAs | Yersinia

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“…In Salmonella , GlrK is required for an undisturbed expression of virulence genes and glrK mutants are impaired in invasion of epithelial cells, survival within macrophages, and in vivo colonization of liver and spleen in mice 75 . In Yersinia pseudotuberculosis , glrR mutants are significantly less virulent than the wild-type as assessed in a mouse model 76 . In enterohemorrhagic E. coli (EHEC), the orthologs of GlrK/GlrR are named QseE/QseF for quorum-sensing regulators E and F. Together, with the second TCS QseB/QseC, QseE/QseF controls virulence functions presumably in response to autoinducer-3 (AI-3), which is a quorum-sensing signal produced by the intestinal microbiota, and to host signals epinephrine/norepinephrine.…”

Section: A Second Function For Glmy and Glmz In Interaction With Hostmentioning

confidence: 99%

Ménage à trois

Göpel

Khan

Görke³

2014

RNA Biology

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In Escherichia coli, small RNAs GlmY and GlmZ feedback control synthesis of glucosamine-6-phosphate (GlcN6P) synthase GlmS, a key enzyme required for synthesis of the cell envelope. Both small RNAs are highly similar, but only GlmZ is able to activate the glmS mRNA by base-pairing. Abundance of GlmZ is controlled at the level of decay by RNase adaptor protein RapZ. RapZ binds and targets GlmZ to degradation by RNase E via protein–protein interaction. GlmY activates glmS indirectly by protecting GlmZ from degradation. Upon GlcN6P depletion, GlmY accumulates and sequesters RapZ in an RNA mimicry mechanism, thus acting as an anti-adaptor. As a result, this regulatory circuit adjusts synthesis of GlmS to the level of its enzymatic product, thereby mediating GlcN6P homeostasis. The interplay of RNase adaptor proteins and anti-adaptors provides an elegant means how globally acting RNases can be re-programmed to cleave a specific transcript in response to a cognate stimulus.

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Phenotypic analysis of Yersinia pseudotuberculosis 32777 response regulator mutants: New insights into two-component system regulon plasticity in bacteria

Cited by 51 publications

References 46 publications

Th1-type immune response to infection by pYV-cured phoP-phoQ null mutant of Yersinia pseudotuberculosis is defective in mouse model

Th1-type immune response to infection by pYV-cured phoP-phoQ null mutant of Yersinia pseudotuberculosis is defective in mouse model

Tissue dual RNA-seq allows fast discovery of infection-specific functions and riboregulators shaping host–pathogen transcriptomes

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