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在缺锌条件下,ZnuABC 介导的锌摄取缺失会影响尿路致病性大肠杆菌 CFT073 的毒力相关表型。

Absence of ZnuABC-mediated zinc uptake affects virulence-associated phenotypes of uropathogenic Escherichia coli CFT073 under Zn(II)-depleted conditions.

机构信息

Department of Chemistry and Biochemistry, Miami University, Oxford, OH 45056, USA.

出版信息

FEMS Microbiol Lett. 2009 Nov;300(1):36-41. doi: 10.1111/j.1574-6968.2009.01762.x. Epub 2009 Aug 19.

Abstract

In an effort to uncover the role of the high-affinity Zn(II) uptake system in uropathogenic Escherichia coli CFT073, we deleted the znuB gene, which encodes for the transmembrane component of the ZnuABC transporter system. The null mutant for znuB did not grow on minimal medium unless supplemented with excess Zn(II) (50 muM ZnCl(2)). In contrast, the E. coli K-12 DeltaznuB cell line grew well on minimal medium that was not supplemented with Zn(II). The DeltaznuB mutant was significantly deficient in the formation of biofilm under static conditions and also showed a substantially reduced migration front of swarm cells. Because motility and biofilm formation are important for E. coli CFT073 pathogenicity, we propose that the high-affinity Zn(II) uptake system may contribute to the virulence of this pathogen in the urinary tract.

摘要

为了揭示高亲和力 Zn(II)摄取系统在尿路致病性大肠杆菌 CFT073 中的作用,我们删除了编码 ZnuABC 转运系统跨膜成分的 znuB 基因。znuB 缺失突变体在缺乏 Zn(II)(50 μM ZnCl2)的基础培养基上无法生长。相比之下,大肠杆菌 K-12 DeltaznuB 细胞系在未补充 Zn(II)的基础培养基上生长良好。znuB 缺失突变体在静态条件下生物膜的形成显著减少, swarm 细胞的迁移前沿也显著减少。由于运动性和生物膜形成对大肠杆菌 CFT073 的致病性很重要,我们推测高亲和力 Zn(II)摄取系统可能有助于该病原体在泌尿道中的毒力。

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