A unique arabinose 5-phosphate isomerase found within a genomic island associated with the uropathogenicity of Escherichia coli CFT073.
A unique arabinose 5-phosphate isomerase found within a genomic island associated with the uropathogenicity of Escherichia coli CFT073.
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在基因组岛中发现的一种独特的阿拉伯糖 5-磷酸异构酶，与大肠杆菌 CFT073 的尿路致病性相关。
DOI：
10.1128/jb.00033-11
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发表时间：
2011
影响因子：
3.2
通讯作者：
Woodard,RonaldW
中科院分区：
文献类型：
--
作者：
Mosberg,JoshuaA;Yep,Alejandra;Meredith,TimothyC;Smith,Sara;Wang,Pan-Fen;Holler,TodP;Mobley,HarryLT;Woodard,RonaldW
先前的研究表明，从大肠杆菌 CFT073 的基因组岛 PAI-metV 中删除基因 c3405 至 c3410，会导致菌株在小鼠经尿道 cochallenge 后无法与野生型 CFT073 竞争，并且缺乏独立定植小鼠肾脏的能力。我们对 c3405 至 c3410 的分析表明，这些基因构成操纵子，在未知碳水化合物的内化和利用中发挥作用。该操纵子在大肠杆菌 K-12 中未发现，但存在于少数致病性大肠杆菌和博伊迪志贺氏菌菌株中。其中一个基因 c3406 编码的蛋白质与阿拉伯糖 5-磷酸异构酶的糖异构酶结构域具有显着同源性，但缺乏大肠杆菌其他阿拉伯糖 5-磷酸异构酶中发现的串联胱硫醚 β-合酶结构域。我们制备了重组c3406蛋白，发现其具有阿拉伯糖5-磷酸异构酶活性，并详细表征了该活性。我们还构建了大肠杆菌 CFT073 的 c3406 缺失突变体，并证明该缺失突变体仍然能够在小鼠经尿道 cochallenge 中与野生型 CFT073 竞争，并且可以在小鼠肾脏中定殖。这些结果证明 c3406 的存在对于致病表型并不是必需的。
Previous studies showed that deletion of genes c3405 to c3410 from PAI-metV, a genomic island from Escherichia coli CFT073, results in a strain that fails to compete with wild-type CFT073 after a transurethral cochallenge in mice and is deficient in the ability to independently colonize the mouse kidney. Our analysis of c3405 to c3410 suggests that these genes constitute an operon with a role in the internalization and utilization of an unknown carbohydrate. This operon is not found in E. coli K-12 but is present in a small number of pathogenic E. coli and Shigella boydii strains. One of the genes, c3406, encodes a protein with significant homology to the sugar isomerase domain of arabinose 5-phosphate isomerases but lacking the tandem cystathionine beta-synthase domains found in the other arabinose 5-phosphate isomerases of E. coli. We prepared recombinant c3406 protein, found it to possess arabinose 5-phosphate isomerase activity, and characterized this activity in detail. We also constructed a c3406 deletion mutant of E. coli CFT073 and demonstrated that this deletion mutant was still able to compete with wild-type CFT073 in a transurethral cochallenge in mice and could colonize the mouse kidney. These results demonstrate that the presence of c3406 is not essential for a pathogenic phenotype.