Role of insertion elements and yycFG in the development of decreased susceptibility to vancomycin in Staphylococcus aureus

Jansen, Andrea; Türck, Michael; Szekat, Christiane; Nagel, Michael; Clever, I.; Bierbaum, Gabriele

doi:10.1016/j.ijmm.2007.02.002

Cited by 98 publications

(101 citation statements)

References 42 publications

(56 reference statements)

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“…In other closely related streptococci, studies involving VicRK orthologs have clearly established a role in adapting to osmotic stress (26,27), oxidative stress (11,48), antibiotic stress (16,27), and high temperature (27). Hence, it is possible that the VicR/Kmediated stress responses observed in various bacteria are caused by defective cell walls.…”

Section: Resultsmentioning

confidence: 99%

Regulation of Bacteriocin Production and Cell Death by the VicRK Signaling System in Streptococcus mutans

et al. 2012

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The VicRK two-component signaling system modulates biofilm formation, genetic competence, and stress tolerance in Streptococcus mutans. We show here that the VicRK modulates bacteriocin production and cell viability, in part by direct modulation of competence-stimulating peptide (CSP) production in S. mutans. Global transcriptome and real-time transcriptional analysis of the VicK-deficient mutant (SmuvicK) revealed significant modulation of several bacteriocin-related loci, including nlmAB, nlmC, and nlmD (P < 0.001), suggesting a role for the VicRK in producing mutacins IV, V, and VI. Bacteriocin overlay assays revealed an altered ability of the vic mutants to kill related species. Since a well-conserved VicR binding site (TGTWAH-N 5 -TGTWAH) was identified within the comC coding region, we confirmed VicR binding to this sequence using DNA footprinting. Overexpression of the vic operon caused growth-phase-dependent repression of comC, comDE, and comX. In the vic mutants, transcription of nlmC/cipB encoding mutacin V, previously linked to CSP-dependent cell lysis, as well as expression of its putative immunity factor encoded by immB, were significantly affected relative to the wild type (P < 0.05). In contrast to previous reports that proposed a hyper-resistant phenotype for the VicK mutant in cell viability, the release of extracellular genomic DNA was significantly enhanced in SmuvicK (P < 0.05), likely as a result of increased autolysis compared with the parent. The drastic influence of VicRK on cell viability was also demonstrated using vic mutant biofilms. Taken together, we have identified a novel regulatory link between the VicRK and ComDE systems to modulate bacteriocin production and cell viability of S. mutans.

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Section: Resultsmentioning

confidence: 99%

Regulation of Bacteriocin Production and Cell Death by the VicRK Signaling System in Streptococcus mutans

et al. 2012

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“…In addition to the roles of VicRK and STK-STP in bacterial responses to environmental stresses and host immune challenges, these systems also affect bacterial susceptibility to different classes of antibiotics. Accumulated mutations in vicRK and STK-encoding genes were detected among Staphylococcus strains resistant to vancomycin and daptomycin that target the cell wall and membrane, respectively [152–154]. Also, STK protein PknB (also called Stk1) appears to activate a transcriptional regulator of the antibiotic efflux pump NorA [146].…”

Section: Interactions Of Vicrk Tcs With Other Regulatory Systemsmentioning

confidence: 99%

Two-component signal transduction systems in oral bacteria

Mattos-Graner

Duncan²

2017

Journal of Oral Microbiology

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We present an overview of how members of the oral microbiota respond to their environment by regulating gene expression through two-component signal transduction systems (TCSs) to support conditions compatible with homeostasis in oral biofilms or drive the equilibrium toward dysbiosis in response to environmental changes. Using studies on the sub-gingival Gram-negative anaerobe Porphyromonas gingivalis and Gram-positive streptococci as examples, we focus on the molecular mechanisms involved in activation of TCS and species specificities of TCS regulons.

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“…VISA-type mutants have now been identified in every one of the major epidemic clones of MRSA (4,28,30,36,(47)(48)(49)(50)(51)(52)(53). Cross-infection with VISA isolates has been described only in two reports, one from a French and another from an Italian hospital in which "epidemic" VISA strains appeared and spread in the hospital environment (54,55).…”

Section: Introductionmentioning

confidence: 99%