Laboratory of Biotechnology, Chulabhorn Research Institute, Lak Si, Bangkok 10210, Thailand.
J Bacteriol. 2010 Apr;192(8):2093-101. doi: 10.1128/JB.01510-09. Epub 2010 Feb 5.
ohrR encodes an organic hydroperoxide sensor and a transcriptional repressor that regulates organic hydroperoxide-inducible expression of a thiol peroxidase gene, ohr, and itself. OhrR binds directly to the operators and represses transcription of these genes. Exposure to an organic hydroperoxide leads to oxidation of OhrR and to subsequent structural changes that result in the loss of the repressor's ability to bind to the operators that allow expression of the target genes. Differential induction of ohrR and ohr by tert-butyl hydroperoxide suggests that factors such as the repressor's dissociation constants for different operators and the chemical nature of the inducer contribute to OhrR-dependent organic hydroperoxide-inducible gene expression. ohrR and ohr mutants show increased and decreased resistance to organic hydroproxides, respectively, compared to a parental strain. Moreover, the ohrR mutant had a reduced-virulence phenotype in the Pseudomonas aeruginosa-Caenorhabditis elegans pathogenicity model.
ohrR 编码一种有机过氧化物传感器和一种转录阻遏物,该阻遏物调节有机过氧化物诱导的硫氧还蛋白过氧化物酶基因 oh 和自身的表达。OhR 直接结合到操纵子上,抑制这些基因的转录。暴露于有机过氧化物会导致 OhR 氧化,随后发生结构变化,导致阻遏物丧失与允许靶基因表达的操纵子结合的能力。叔丁基过氧化物对 ohrR 和 ohr 的差异诱导表明,阻遏物对不同操纵子的解离常数和诱导剂的化学性质等因素有助于 OhR 依赖的有机过氧化物诱导的基因表达。与亲本菌株相比,ohrR 和 ohr 突变体对有机过氧化物的抗性分别增加和降低。此外,ohrR 突变体在铜绿假单胞菌-秀丽隐杆线虫致病性模型中表现出降低的毒力表型。