title: dpr and sod in Streptococcus mutans are involved in coexistence with S. sanguinis, and PerR is associated with resistance to H2O2.
abstract: Large numbers of bacteria coexist in the oral cavity. Streptococcus sanguinis, one of the major bacteria in dental plaque, produces hydrogen peroxide (H(2)O(2)), which interferes with the growth of other bacteria. Streptococcus mutans, a cariogenic bacterium, can coexist with S. sanguinis in dental plaque, but to do so, it needs a means of detoxifying the H(2)O(2) produced by S. sanguinis. In this study, we investigated the association of three oxidative stress factors, Dpr, superoxide dismutase (SOD), and AhpCF, with the resistance of S. sanguinis to H(2)O(2). The knockout of dpr and sod significantly increased susceptibility to H(2)O(2), while the knockout of ahpCF had no apparent effect on susceptibility. In particular, dpr inactivation resulted in hypersensitivity to H(2)O(2). Next, we sought to identify the factor(s) involved in the regulation of these oxidative stress genes and found that PerR negatively regulated dpr expression. The knockout of perR caused increased dpr expression levels, resulting in low-level susceptibility to H(2)O(2) compared with the wild type. Furthermore, we evaluated the roles of perR, dpr, and sod when S. mutans was cocultured with S. sanguinis. Culturing of the dpr or sod mutant with S. sanguinis showed a significant decrease in the S. mutans population ratio compared with the wild type, while the perR mutant increased the ratio. Our results suggest that dpr and sod in S. mutans are involved in coexistence with S. sanguinis, and PerR is associated with resistance to H(2)O(2) in regulating the expression of Dpr.
authors.affiliation: Department of Oral Microbiology,Kagoshima University Graduate School of Medical and Dental Sciences,Kagoshima, Japan.
authors.forename: Kei
authors.initials: K
authors.lastname: Fujishima
authors.forename: Miki
authors.initials: M
authors.lastname: Kawada-Matsuo
authors.forename: Yuichi
authors.initials: Y
authors.lastname: Oogai
authors.forename: Masayuki
authors.initials: M
authors.lastname: Tokuda
authors.forename: Mitsuo
authors.initials: M
authors.lastname: Torii
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Komatsuzawa
mesh_terms: D001426:Bacterial Proteins / Q000235:genetics / Q000378:metabolism*; D004268:DNA-Binding Proteins / Q000235:genetics / Q000378:metabolism*; D024881:Drug Resistance, Bacterial; D055786:Gene Knockout Techniques; D006861:Hydrogen Peroxide / Q000378:metabolism* / Q000633:toxicity; D053858:Metabolic Networks and Pathways; D056265:Microbial Interactions; D008954:Models, Biological; D018384:Oxidative Stress; D012097:Repressor Proteins / Q000378:metabolism*; D013295:Streptococcus mutans / Q000187:drug effects / Q000201:enzymology / Q000235:genetics / Q000254:growth & development* / Q000502:physiology; D013298:Streptococcus sanguis / Q000254:growth & development* / Q000378:metabolism; D013482:Superoxide Dismutase / Q000235:genetics / Q000378:metabolism*
chemical_list: D001426:Bacterial Proteins; D004268:DNA-Binding Proteins; C414750:Dpr protein, Streptococcus; D012097:Repressor Proteins; C122138:peroxide repressor proteins; D006861:Hydrogen Peroxide; C095500:SodA protein, Bacteria; D013482:Superoxide Dismutase