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周质肽基脯氨酰异构酶在鼠伤寒沙门氏菌毒力中的作用。

Role of periplasmic peptidylprolyl isomerases in Salmonella enterica serovar Typhimurium virulence.

作者信息

Humphreys Sue, Rowley Gary, Stevenson Andrew, Kenyon William J, Spector Michael P, Roberts Mark

机构信息

Molecular Bacteriology Group, Institute of Comparative Medicine, Department of Veterinary Pathology, Glasgow University Veterinary School, Glasgow G61 1QH, United Kingdom.

出版信息

Infect Immun. 2003 Sep;71(9):5386-8. doi: 10.1128/IAI.71.9.5386-5388.2003.

Abstract

FkpA is a peptidylprolyl isomerase whose expression is regulated by the alternative sigma factor, sigma factor E (sigma(E)). In contrast to the results of a previous report, inactivation of fkpA was found to have only a minor effect on the ability of Salmonella enterica serovar Typhimurium to invade and survive within epithelial and macrophage cell lines and cause infection in mice. However, an effect of the fkpA mutation on serovar Typhimurium virulence was seen if the mutation was combined with mutations in surA or htrA, two other sigma(E)-regulated genes, which encode proteins involved in protein folding and/or degradation in the periplasm.

摘要

FkpA是一种肽基脯氨酰异构酶,其表达受替代σ因子E(σE)调控。与之前一份报告的结果相反,研究发现fkpA的失活对鼠伤寒沙门氏菌侵袭上皮细胞系和巨噬细胞系并在其中存活以及在小鼠体内引发感染的能力仅有轻微影响。然而,如果fkpA突变与surA或htrA(另外两个受σE调控的基因)的突变相结合,就会观察到fkpA突变对鼠伤寒沙门氏菌毒力的影响,surA和htrA编码参与周质中蛋白质折叠和/或降解的蛋白质。

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