Gene Regulation in <i>S. mutans</i>

Smith, Evan G.; Spatafora, Grace A.

doi:10.1177/0022034511415415

Cited by 119 publications

(76 citation statements)

References 75 publications

(116 reference statements)

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“…For example, the TCS ScnKR, likely involved in the regulation of bacteriocin production, is absent is a sub-set of S. mutans strains [23]. Molecular studies of several of these TCSs in particular S. mutans strains were previously reviewed [24]. Evolutionary analyses of TCSs indicate that bacterial lineages might acquire novel TCSs by gene duplication and lateral gene transfer under specific selective pressures.…”

Section: Bacterial Signal Transduction 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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Section: Bacterial Signal Transduction Systemsmentioning

confidence: 99%

Two-component signal transduction systems in oral bacteria

Mattos-Graner

Duncan²

2017

Journal of Oral Microbiology

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“…In contrast, S. mutans is an extracellular pathogen that is an important agent of dental caries (26). Its pathogenesis depends both on its ability to produce acid to cause the demineralization of dentin at the tooth surface and to its ability to adapt to the extreme-low-pH environment that its metabolism of carbohydrates generates (27). Whether the ADI-mediated catabolism of citrulline can also contribute to the pathogenesis of diseases caused by L. monocytogenes, S. mutans, or other acid-adapting pathogens remains to be determined.…”

Section: Figmentioning

confidence: 99%

Citrulline Protects Streptococcus pyogenes from Acid Stress Using the Arginine Deiminase Pathway and the F₁F_o-ATPase

Cusumano

Caparon

2015

J. Bacteriol.

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A common stress encountered by both pathogenic and environmental bacteria is exposure to a low-pH environment, which can inhibit cell growth and lead to cell death. One major defense mechanism against this stress is the arginine deiminase (ADI) pathway, which catabolizes arginine to generate two ammonia molecules and one molecule of ATP. While this pathway typically relies on the utilization of arginine, citrulline has also been shown to enter into the pathway and contribute to protection against acid stress. In the pathogenic bacterium Streptococcus pyogenes, the utilization of citrulline has been demonstrated to contribute to pathogenesis in a murine model of soft tissue infection, although the mechanism underlying its role in infection is unknown. To gain insight into this question, we analyzed a panel of mutants defective in different steps in the ADI pathway to dissect how arginine and citrulline protect S. pyogenes in a low-pH environment. While protection provided by arginine utilization occurred through the buffering of the extracellular environment, citrulline catabolism protection was pH independent, requiring the generation of ATP via the ADI pathway and a functional F 1 F o -ATP synthase. This work demonstrates that arginine and citrulline catabolism protect against acid stress through distinct mechanisms and have unique contributions to virulence during an infection. A daptation to environmental acidification presents a significant challenge to microorganisms, including both pathogenic and environmental bacterial species (1). Due to the near ubiquitous nature of this stress, elucidation of adaptive strategies and their associated molecular mechanisms has broad implications for our understanding of both bacterial physiology and virulence. One of the most widely used bacterial mechanisms for protection against acid stress involves the catabolism of arginine via the arginine deiminase (ADI) pathway (2-4). However, each of the various components of this pathway can be adapted in several different ways to promote survival in acidic environments. Therefore, the challenge becomes understanding how the ADI pathway has been adapted in an individual bacterial species. IMPORTANCE An important aspect of bacterial pathogenesis is the utilization of host-derived nutrients during an infection for growth and virulence. Previously published work from our lab identified a unique role for citrulline catabolism inIn the Gram-positive pathogen Streptococcus pyogenes (group A streptococcus), it has recently been shown that the ADI pathway metabolite citrulline makes an unexpected arginine-independent contribution to both colonization and virulence (5). This human pathogen is responsible for a large number of diseases that range in severity and invasiveness (6). Common, noninvasive soft tissue infections include bacterial pharyngitis and impetigo, in addition to the less common but invasive and often life-threatening necrotizing fasciitis and immune-pathological syndromes like rheumatic fever (6). It was recently ...

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“…Regulatory systems are involved in enhancing the ecological fitness and cariogenic virulence of S. mutans [7]. The VicRKX and LiaFSR two-component signal transduction systems (TCSTS) have been reported as the master regulatory system involved in expression of GTFs, biofilm formation and environment stress tolerance in S. mutans [8,9].…”

Section: Introductionmentioning

confidence: 99%

Antimicrobial peptide GH12 suppresses cariogenic virulence factors of Streptococcus mutans

Wang

Jiang

et al. 2018

Journal of Oral Microbiology

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Cariogenic virulence factors of Streptococcus mutans include acidogenicity, aciduricity, and extracellular polysaccharides (EPS) synthesis. The de novo designed antimicrobial peptide GH12 has shown bactericidal effects on S. mutans, but its interaction with virulence and regulatory systems of S. mutans remains to be elucidated. The objectives were to investigate the effects of GH12 on virulence factors of S. mutans, and further explore the function mechanisms at enzymatic and transcriptional levels. To avoid decrease in bacterial viability, we limited GH12 to subinhibitory levels. We evaluated effects of GH12 on acidogenicity of S. mutans by pH drop, lactic acid measurement and lactate dehydrogenase (LDH) assay, on aciduricity through survival rate at pH 5.0 and F1F0-ATPase assay, and on EPS synthesis using quantitative measurement, morphology observation, vertical distribution analyses and biomass calculation. Afterwards, we conducted quantitative real-time PCR to acquire the expression profile of related genes. GH12 at 1/2 MIC (4 mg/L) inhibited acid production, survival rate, EPS synthesis, and biofilm formation. The enzymatic activity of LDH and F1F0-ATPase was inhibited, and ldh, gtfBCD, vicR, liaR, and comDE genes were significantly downregulated. In conclusion, GH12 inhibited virulence factors of S. mutans, through reducing the activity of related enzymes, downregulating virulence genes, and inactivating specific regulatory systems.

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Gene Regulation in S. mutans

Cited by 119 publications

References 75 publications

Two-component signal transduction systems in oral bacteria

Two-component signal transduction systems in oral bacteria

Citrulline Protects Streptococcus pyogenes from Acid Stress Using the Arginine Deiminase Pathway and the F₁F_o-ATPase

Antimicrobial peptide GH12 suppresses cariogenic virulence factors of Streptococcus mutans

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Gene Regulation in S. mutans

Cited by 119 publications

References 75 publications

Two-component signal transduction systems in oral bacteria

Two-component signal transduction systems in oral bacteria

Citrulline Protects Streptococcus pyogenes from Acid Stress Using the Arginine Deiminase Pathway and the F1Fo-ATPase

Antimicrobial peptide GH12 suppresses cariogenic virulence factors of Streptococcus mutans

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Citrulline Protects Streptococcus pyogenes from Acid Stress Using the Arginine Deiminase Pathway and the F₁F_o-ATPase