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首页> 外文期刊>Journal of bacteriology >Increased Oxidative Stress Tolerance of a Spontaneously Occurring perR Gene Mutation in Streptococcus mutans UA159
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Increased Oxidative Stress Tolerance of a Spontaneously Occurring perR Gene Mutation in Streptococcus mutans UA159

机译:增加氧化胁迫耐受性钙质钙质突变体中的钙化胁迫耐受性钙质突变体Mutans UA159

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摘要

The ability of bacteria, such as the dental pathogen Streptococcus mutans, to coordinate a response against damage-inducing oxidants is a critical aspect of their pathogenicity. The oxidative stress regulator SpxA1 has been demonstrated to be a major player in the ability of S. mutans to withstand both disulfide and peroxide stresses. While studying spontaneously occurring variants of an S. mutans Δ spxA1 strain, we serendipitously discovered that our S. mutans UA159 host strain bore a single-nucleotide deletion within the coding region of perR , resulting in a premature truncation of the encoded protein. PerR is a metal-dependent transcriptional repressor that senses and responds to peroxide stress such that loss of PerR activity results in activation of oxidative stress responses. To determine the impact of loss of PerR regulation, we obtained a UA159 isolate bearing an intact perR copy and created a clean perR deletion mutant. Our findings indicate that loss of PerR activity results in a strain that is primed to tolerate oxidative stresses in the laboratory setting. Interestingly, RNA deep sequencing (RNA-Seq) and targeted transcriptional expression analyses reveal that PerR offers a minor contribution to the ability of S. mutans to orchestrate a transcriptional response to peroxide stress. Furthermore, we detected loss-of-function perR mutations in two other commonly used laboratory strains of S. mutans, suggesting that this may be not be an uncommon occurrence. This report serves as a cautionary tale regarding the so-called domestication of laboratory strains and advocates for the implementation of more stringent strain authentication practices. IMPORTANCE A resident of the human oral biofilm, Streptococcus mutans is one of the major bacterial pathogens associated with dental caries. This report highlights a spontaneously occurring mutation within the laboratory strain S. mutans UA159 found in the coding region of perR , a gene encoding a transcriptional repressor associated with peroxide tolerance. Though perR mutant strains of S. mutans showed a distinct growth advantage and enhanced tolerance toward H_(2)O_(2), a Δ perR deletion strain showed a small number of differentially expressed genes compared to the parent strain, suggesting few direct regulatory targets. In addition to characterizing the role of PerR in S. mutans, our findings serve as a warning to laboratory researchers regarding bacterial adaptation to in vitro growth conditions.
机译:细菌(例如牙科病原体链球菌)的能力,以协调抗伤害氧化剂的反应是其致病性的关键方面。已经证明了氧化应激调节器SPXA1是S.Ulans以承受二硫化物和过氧化物应力的能力的主要参与者。在研究S.umantaδSpxa1菌株的自发性发生变体的同时,我们偶然发现了我们的S.UA159宿主菌株在PERR的编码区域内进行单核苷酸缺失,导致编码蛋白质过早截短。 PERR是一种金属依赖性转录阻遏物,其感测并响应过氧化物应激,使得钙磷酸盐活性的丧失导致氧化应激反应的活化。为了确定损失彼得规则的影响,我们获得了一个UA159隔离载有完整的Perr复制并创建了清洁的Perr删除突变体。我们的研究结果表明,钙活性的丧失导致菌株引发,以耐受实验室环境中的氧化应力。有趣的是,RNA深度测序(RNA-SEQ)和靶向转录表达分析表明,珀尔对S. mutans协调对过氧化物应激的转录反应的能力提供了微小的贡献。此外,我们检测到常用实验室菌株中的两种常用实验室菌株中的函数损失突变,表明这可能不是罕见的发生。本报告担任关于实验室队伍的所谓驯化的警告故事,并倡导实施更严格的应变认证实践。人口腔生物膜的重要性,链球菌的居民是与龋齿相关的主要细菌病原体之一。该报告突出显示在Perr编码区域中的实验室菌株S.uA159中的自发发生的突变,该基因编码了与过氧化物耐受相关的转录压缩机。虽然S. mutAns的Perr突变体菌株表现出明显的生长优势和对H_(2)O_(2)的增强的耐受性,与亲本菌株相比,δPERR缺失菌株显示少量的差异表达基因,表明少数直接监管目标。除了表征彼得·普拉斯的角色,我们的研究结果还是对实验室研究人员的警告,关于细菌适应体外生长条件。

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