Coordinately repressible arginine deiminase system inStreptococcus sanguis

Ferro, Keith J.; Bender, Gary R.; Marquis, Robert E.

doi:10.1007/bf01567287

Cited by 34 publications

(30 citation statements)

References 9 publications

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“…Many known bacterial strains rely on arginolysis to produce ammonia in conjunction with the production of ATP (reviewed in Abdelal, 1979;Cunin et al, 1986 The ADS is inducible in the presence of arginine and catabolite repressible in the presence of glucose, in most bacteria, including S. sanguis (Ferro et al, 1983). Results from studies with a baro-tolerant mutant strain of Streptococcusfaecium (now Enterococcusfaecium) have indicated that the strain was able to degrade both glucose and arginine, suggesting that the catabolite repression had been damaged in the mutants (Campbell et al, 1985 Marquis, 1988), at levels known to cause severe membrane damage (Marquis et al, 1973).…”

Section: (C) Regulation Of the S Mutans F-atpase Operonmentioning

confidence: 99%

Genetics of Acid Adaptation in Oral Streptococci

Quivey

Kuhnert

Hähn

2001

Critical Reviews in Oral Biology & Medicine

115

107

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A growing body of information has provided insights into the mechanisms by which the oral streptococci maintain their niches in the human mouth. In at least one case, Streptococcus mutans, the organism apparently uses a panel of proteins to survive in acidic conditions while it promotes the formation of dental caries. Oral streptococci, which are not as inherently resistant to acidification, use protective schemes to ameliorate acidic plaque pH values. Existing information clearly shows that while the streptococci are highly related, very different strategies have evolved for them to take advantage of their particular location in the oral cavity. The picture that emerges is that the acid-adaptive regulatory mechanisms of the oral streptococci differ markedly from those used by Gram-negative bacteria. What future research must determine is the extent and complexity of the acid-adaptive systems in these organisms and how they permit the organisms to maintain themselves in the face of a low-pH environment and the microbial competition present in their respective niches.

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Section: (C) Regulation Of the S Mutans F-atpase Operonmentioning

confidence: 99%

Genetics of Acid Adaptation in Oral Streptococci

Quivey

Kuhnert

Hähn

2001

Critical Reviews in Oral Biology & Medicine

115

107

View full text Add to dashboard Cite

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“…In addition, ornithine is produced which can be decarboxylated, particularly at low pH, leading to a rise in pH. Supplementation of carbohydrates with arginine when pulsed to arginolytic bacteria (e.g., S. sanguis) resulted in a higher terminal pH (Ferro et al, 1983), while arginine as either the free amino acid or as part of a short peptide can stimulate the gcowth of streptococci associated with sound enamel, such as S. sanguis and members of the "S. milleri" group (Rogers etal, 1987a;Rogers, 1990). These findings have prompted attempts to manipulate the composition of the plaque microflora by augmentation of endogenous levels of base-generating compounds with pulses of arginine or urea.…”

Section: Prevention Of Low Phmentioning

confidence: 99%

Physiological Approaches to the Control of Oral Biofilms

1997

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Evidence that physiological strategies may be potential routes for oral biofilm control has come from (i) observations of the variations in the intra-oral distribution of members of the resident oral microflora, (ii) changes in plaque composition in health and disease, and (iii) data from laboratory model systems. Key physiological factors that were identified as significant in modulating the microflora included the local pH, redox potential (Eh), and nutrient availability. Increases in mutans streptococci and lactobacilli occur at sites with caries; growth of these species is selectively enhanced at low pH. In contrast, periodontal diseases are associated with plaque accumulation, followed by an inflammatory host response. The increases in Gram-negative, proteolytic, and obligately anaerobic bacteria reflect a low redox potential and a change in nutrient status due to the increased flow of gingival crevicular fluid (GCF). Consequently, physiological strategies for oral biofilm control should focus on reducing the frequency of low pH in plaque by (i) inhibiting acid production, (ii) using sugar substitutes, and (iii) promoting alkali generation from arginine or urea supplements. Similarly, strategies to make the pocket environment less favorable to periodontopathogens include (i) anti-inflammatory agents to reduce the flow of (and hence nutrient supply by) GCF, (ii) bacterial protease inhibitors, and (iii) redox agents to raise the Ehh locally. Most laboratory and clinical findings support the concept of physiological control. However, some data suggest that the ordered structure and metabolically interactive organization of mature dental plaque could generate a community with a high level of homeostasis that is relatively resistant to deliberate external manipulation.

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“…In contrast, the ADS of oral streptococci, including S. gordonii, Streptococcus sanguis, and Streptococcus rattus, appears to be a primary defense against killing by acidification (2). In these organisms, which lack a respiratory chain, the ADS is subject to carbon catabolite repression (CCR) and arginine acts as an induction signal to further increase expression (8)(9)(10)14).…”

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confidence: 99%

Characterization of cis- Acting Sites Controlling Arginine Deiminase Gene Expression in Streptococcus gordonii

2006

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The arginine deiminase system (ADS) is responsible for the production of ornithine, CO 2 , ammonia, and ATP from arginine. The ADS of the oral bacterium Streptococcus gordonii plays major roles in physiologic homeostasis, acid tolerance, and oral biofilm ecology. To further our understanding of the transcriptional regulation of the ADS (arc) operon, the binding of the ArcR transcriptional activator, which governs expression of the ADS in response to arginine, was investigated by DNase I protection and gel mobility shift assays. An ArcR binding sequence was found that was 27 bp in length and had little sequence similarity to binding sites of other arginine metabolism regulators. The presence of arginine at physiologically relevant concentrations enhanced the binding of ArcR to its target. Using cat fusions, various deletion and substitution mutations within the putative ArcR footprint were shown to cause dramatic reductions in expression from the arcA promoter in vivo, confirming that the 27-bp sequence is required for optimal expression and induction of the ADS by arginine. Mutation of two putative catabolite response elements (CREs) within the arc promoter region showed that both CREs contribute to catabolite repression. A thorough understanding of the regulation of the ADS in S. gordonii and related organisms is needed to develop ways to exploit arginine catabolism for the control of oral diseases. Identification of the ArcR and CcpA binding sites lays the foundation for a more complete understanding of the complex interactions of multiple regulatory proteins with elements in the arc promoter region.

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Coordinately repressible arginine deiminase system inStreptococcus sanguis

Cited by 34 publications

References 9 publications

Genetics of Acid Adaptation in Oral Streptococci

Genetics of Acid Adaptation in Oral Streptococci

Physiological Approaches to the Control of Oral Biofilms

Characterization of cis- Acting Sites Controlling Arginine Deiminase Gene Expression in Streptococcus gordonii

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