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首页> 外文期刊>Infection and immunity >Involvement of Mismatch Repair in the Reciprocal Control of Motility and Adherence of Uropathogenic Escherichia coli
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Involvement of Mismatch Repair in the Reciprocal Control of Motility and Adherence of Uropathogenic Escherichia coli

机译：错配修复参与相互控制运动性和致病性大肠埃希菌的粘附

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Type 1 fimbriae and flagella, two surface organelles critical for colonization of the urinary tract by uropathogenic Escherichia coli (UPEC), mediate opposing virulence objectives. Type 1 fimbriae facilitate adhesion to mucosal cells and promote bacterial persistence in the urinary tract, while flagella propel bacteria through urine and along mucous layers during ascension to the upper urinary tract. Using a transposon screen of the E. coli CFT073 fim locked-ON (L-ON) mutant, a construct that constitutively expresses type 1 fimbriae and represses motility, we identified six mutants that exhibited a partial restoration of motility. Among these six mutated genes was mutS, which encodes a component of the methyl-directed mismatch repair (MMR) system. When complemented with mutS in trans, motility was again repressed. To determine whether the MMR system, in general, is involved in this reciprocal control, we characterized the effects of gene deletions of other MMR components on UPEC motility. Isogenic deletions of mutS, mutH, and mutL were constructed in both wild-type CFT073 and fim L-ON backgrounds. All MMR mutants showed an increase in motility in the wild-type background, and ΔmutH and ΔmutS mutations increased motility in the fim L-ON background. Cochallenge of the wild-type strain with an MMR-defective strain showed a subtle but significant competitive advantage in the bladder and spleen for the MMR mutant using the murine model of ascending urinary tract infection after 48 h. Our findings demonstrate that the MMR system generally affects the reciprocal regulation of motility and adherence and thus could contribute to UPEC pathogenesis during urinary tract infections.
机译：1型菌毛和鞭毛是尿道致病性大肠杆菌（UPEC）对尿道定殖的关键两个表面细胞器，介导了相反的毒力目标。 1型菌毛有助于粘膜细胞的粘附并促进细菌在尿道中的持久性，而鞭毛则在升至上尿道的过程中通过尿液和粘液层推动细菌。使用转座子筛选大肠杆菌CFT073 fim锁定ON（L-ON）突变体，该构建体组成型表达1型菌毛并抑制运动，我们确定了六个突变体，它们表现出部分运动性。在这六个突变基因中，有mutS，它编码了甲基定向错配修复（MMR）系统的一个组成部分。当与反式的mutS互补时，运动性再次受到抑制。为了确定一般而言，MMR系统是否参与这种相互控制，我们表征了其他MMR成分的基因缺失对UPEC运动性的影响。在野生型CFT073和fim L-ON背景中均构建了mutS，mutH和mutL的同基因缺失。所有MMR突变体在野生型背景中均显示出运动性增强，而ΔmutH和ΔmutS突变在fim L-ON背景中均显示出运动性。使用升尿路感染的鼠模型在48 h后，野生型菌株与MMR缺陷型菌株的共刺激表现为MMR突变体在膀胱和脾脏中具有微妙但显着的竞争优势。我们的研究结果表明，MMR系统通常会影响运动性和依从性的相互调节，因此可能在尿路感染期间促成UPEC发病机理。

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