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首页> 外文期刊>Applied Microbiology >PerR-Regulated Manganese Ion Uptake Contributes to Oxidative Stress Defense in an Oral Streptococcus
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PerR-Regulated Manganese Ion Uptake Contributes to Oxidative Stress Defense in an Oral Streptococcus

机译：PerR调节的锰离子摄取有助于口腔链球菌的氧化应激防御。

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Metal homeostasis plays a critical role in antioxidative stress. Streptococcus oligofermentans , an oral commensal facultative anaerobe lacking catalase activity, produces and tolerates abundant H_(2)O_(2), whereas Dpr (an Fe~(2+)-chelating protein)-dependent H_(2)O_(2) protection does not confer such high tolerance. Here, we report that inactivation of perR , a peroxide-responsive repressor that regulates zinc and iron homeostasis in Gram-positive bacteria, increased the survival of H_(2)O_(2)-pulsed S. oligofermentans 32-fold and elevated cellular manganese 4.5-fold. perR complementation recovered the wild-type phenotype. When grown in 0.1 to 0.25 mM MnCl_(2), S. oligofermentans increased survival after H_(2)O_(2) stress 2.5- to 23-fold, and even greater survival was found for the perR mutant, indicating that PerR is involved in Mn~(2+)-mediated H_(2)O_(2) resistance in S. oligofermentans . Mutation of mntA could not be obtained in brain heart infusion (BHI) broth (containing ～0.4 μM Mn~(2+)) unless it was supplemented with ≥2.5 μM MnCl_(2) and caused 82 to 95% reduction of the cellular Mn~(2+) level, while mntABC overexpression increased cellular Mn~(2+) 2.1- to 4.5-fold. Thus, MntABC was identified as a high-affinity Mn~(2+) transporter in S. oligofermentans. mntA mutation reduced the survival of H_(2)O_(2)-pulsed S. oligofermentans 5.7-fold, while mntABC overexpression enhanced H_(2)O_(2)-challenged survival 12-fold, indicating that MntABC-mediated Mn~(2+) uptake is pivotal to antioxidative stress in S. oligofermentans. perR mutation or H_(2)O_(2) pulsing upregulated mntABC , while H_(2)O_(2)-induced upregulation diminished in the perR mutant. This suggests that perR represses mntABC expression but H_(2)O_(2) can release the suppression. In conclusion, this work demonstrates that PerR regulates manganese homeostasis in S. oligofermentans , which is critical to H_(2)O_(2) stress defenses and may be distributed across all oral streptococci lacking catalase.
机译：金属稳态在抗氧化应激中起关键作用。寡链链球菌，一种缺乏过氧化氢酶活性的口服共性厌氧菌，产生并耐受大量的H_（2）O_（2），而依赖Dpr（Fe〜（2 +）-螯合蛋白）的H_（2）O_（2）保护没有赋予如此高的容忍度。在这里，我们报告说，perR的失活，一种过氧化物反应性阻遏物，调节革兰氏阳性细菌中的锌和铁稳态，增加了H_（2）O_（2）脉冲的S. oligofermentans的存活率是32倍且细胞锰含量升高。 4.5倍perR互补恢复了野生型的表型。当在0.1至0.25 mM MnCl_（2）中生长时，寡聚链霉菌在H_（2）O_（2）胁迫2.5至23倍后提高了存活率，并且发现perR突变体的存活率更高，表明PerR参与其中寡聚链霉菌中Mn〜（2+）介导的H_（2）O_（2）抗性除非添加≥2.5μMMnCl_（2）并导致细胞Mn减少82％至95％，否则在脑心浸液（BHI）肉汤（含〜0.4μMMn〜（2+））中无法获得mntA突变。 〜（2+）水平，而mntABC过表达使细胞Mn〜（2+）增加2.1-至4.5倍。因此，MntABC被确定为低聚链球菌中​​的高亲和力Mn〜（2+）转运蛋白。 mntA突变使H_（2）O_（2）脉冲寡聚链霉菌的存活降低了5.7倍，而mntABC过表达使H_（2）O_（2）激发的存活提高了12倍，表明MntABC介导的Mn〜（ 2+）的摄取对于寡聚链霉菌中的抗氧化应激至关重要。 perR突变或H_（2）O_（2）刺激mntABC上调，而H_（2）O_（2）诱导的上调在perR突变体中减弱。这表明perR抑制mntABC表达，但H_（2）O_（2）可以释放抑制作用。总之，这项工作表明PerR调节寡聚链球菌中​​的锰稳态，这对H_（2）O_（2）压力防御至关重要，并且可能分布在所有缺乏过氧化氢酶的口腔链球菌中。

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