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首页> 外文期刊>Infection and immunity >PafR, a Novel Transcription Regulator, Is Important for Pathogenesis in Uropathogenic Escherichia coli
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PafR, a Novel Transcription Regulator, Is Important for Pathogenesis in Uropathogenic Escherichia coli

机译：PafR，一种新型的转录调节剂，对致病性大肠杆菌的发病机制很重要

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The metV genomic island in the chromosome of uropathogenic Escherichia coli (UPEC) encodes a putative transcription factor and a sugar permease of the phosphotransferase system (PTS), which are predicted to compose a Bgl-like sensory system. The presence of these two genes, hereby termed pafR and pafP, respectively, has been previously shown to correlate with isolates causing clinical syndromes. We show here that deletion of both genes impairs the ability of the resulting mutant to infect the CBA/J mouse model of ascending urinary tract infection compared to that of the parent strain, CFT073. Expressing the two genes in trans in the two-gene knockout mutant complemented full virulence. Deletion of either gene individually generated the same phenotype as the double knockout, indicating that both pafR and pafP are important to pathogenesis. We screened numerous environmental conditions but failed to detect expression from the promoter that precedes the paf genes in vitro, suggesting that they are in vivo induced (ivi). Although PafR is shown here to be capable of functioning as a transcriptional antiterminator, its targets in the UPEC genome are not known. Using microarray analysis, we have shown that expression of PafR from a heterologous promoter in CFT073 affects expression of genes related to bacterial virulence, biofilm formation, and metabolism. Expression of PafR also inhibits biofilm formation and motility. Taken together, our results suggest that the paf genes are implicated in pathogenesis and that PafR controls virulence genes, in particular biofilm formation genes.
机译：尿路致病性大肠埃希氏大肠杆菌（UPEC）染色体中的 metV 基因组岛编码一个假定的转录因子和磷酸转移酶系统（PTS）的糖通透酶，据推测它们构成了类似Bgl的感觉系统。先前已证明这两个基因分别称为 pafR 和 pafP 的存在与引起临床综合征的分离株相关。我们在此处显示，与亲本菌株CFT073相比，两个基因的缺失均会损害所得突变体感染升尿路感染的CBA / J小鼠模型的能力。在两个基因敲除突变体的 trans 中表达两个基因补充了全部毒力。任一基因的缺失均会产生与双重敲除相同的表型，表明 pafR 和 pafP 对发病机理均很重要。我们筛选了许多环境条件，但未能检测到 paf 基因 之前的启动子中的启动子表达，表明它们是体内诱导的（ ivi）。尽管此处显示PafR能够充当转录抗终止剂，但其在UPEC基因组中的靶标尚不清楚。使用微阵列分析，我们已经表明，CFT073中来自异源启动子的PafR的表达会影响与细菌毒力，生物膜形成和代谢有关的基因的表达。 PafR的表达还抑制生物膜的形成和运动。两者合计，我们的结果表明， paf 基因与发病有关，并且PafR控制毒力基因，特别是生物膜形成基因。

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