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肠炎沙门氏菌血清型 Typhimurium 的 QseB 反应调节剂在缺乏 QseC 传感器激酶的情况下负调控细菌的运动性和猪的定植。

The Salmonella enterica serovar Typhimurium QseB response regulator negatively regulates bacterial motility and swine colonization in the absence of the QseC sensor kinase.

机构信息

Agroecosystems Management Research Unit, USDA, ARS, National Laboratory for Agriculture and the Environment, Ames, IA 50011, USA.

出版信息

Microb Pathog. 2010 Jun;48(6):214-9. doi: 10.1016/j.micpath.2010.03.005. Epub 2010 Mar 19.

DOI:10.1016/j.micpath.2010.03.005
PMID:20227482
Abstract

Salmonella enterica serovar Typhimurium (S. Typhimurium) responds to the catecholamine, norepinephrine by increasing bacterial growth and enhancing motility. In this study, iron with or without the siderophore, ferrioxamine E also enhanced bacterial motility. Iron-enhanced motility was growth-rate dependent, while norepinephrine-enhanced motility was growth-rate independent. The outer membrane catecholate receptors, IroN, FepA and CirA (required for norepinephrine-enhanced growth) were not required for norepinephrine-enhanced motility, nor was ExbD of the energy-transducing TonB-ExbB-ExbD ferri-siderophore uptake system. Examination of the QseBC two-component system revealed that qseB and qseBC mutants have motility phenotypes similar to wild-type S. Typhimurium, while motility of the qseC mutant was significantly decreased (P<0.01). Each mutant of the QseBC system, as well as mutants of qseE and pmrA, responded to norepinephrine with increased motility, suggesting that other genes are involved in norepinephrine-enhanced motility of S. Typhimurium. In the swine host, fecal shedding of the qseBC mutant was similar to wild-type S. Typhimurium, whereas fecal shedding of the qseC mutant was significantly decreased (P<0.01). Our data indicate that, in a qseC mutant, the QseB response regulator decreases motility and swine colonization; inactivation of the qseBC operon restores these bacterial phenotypes, classifying QseB as a negative regulator of bacterial motility and swine colonization.

摘要

鼠伤寒沙门氏菌(S. Typhimurium)通过增加细菌生长和增强运动性来响应儿茶酚胺去甲肾上腺素。在这项研究中,铁(无论是否带有铁载体)也增强了细菌的运动性。铁增强的运动性依赖于生长速率,而去甲肾上腺素增强的运动性则不依赖于生长速率。外膜儿茶酚受体 IroN、FepA 和 CirA(增强去甲肾上腺素增强生长所需)不参与去甲肾上腺素增强的运动性,能量传递 TonB-ExbB-ExbD 亚铁载体摄取系统的 ExbD 也不参与。对 QseBC 双组分系统的检查表明,qseB 和 qseBC 突变体具有与野生型鼠伤寒沙门氏菌相似的运动表型,而 qseC 突变体的运动性显著降低(P<0.01)。QseBC 系统的每个突变体,以及 qseE 和 pmrA 的突变体,对去甲肾上腺素的反应是运动性增加,这表明其他基因参与了鼠伤寒沙门氏菌去甲肾上腺素增强的运动性。在猪宿主中,qseBC 突变体的粪便脱落与野生型鼠伤寒沙门氏菌相似,而 qseC 突变体的粪便脱落显著降低(P<0.01)。我们的数据表明,在 qseC 突变体中,QseB 反应调节剂降低了运动性和猪定植;qseBC 操纵子的失活恢复了这些细菌表型,将 QseB 归类为细菌运动性和猪定植的负调节剂。

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