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鼠伤寒沙门氏菌中双精氨酸转运系统的缺失导致感染期间的定植缺陷。

Abrogation of the twin arginine transport system in Salmonella enterica serovar Typhimurium leads to colonization defects during infection.

机构信息

Department of Microbial and Molecular Pathogenesis, College of Medicine, Texas A & M University System Health Science Center, College Station, Texas, United States of America.

出版信息

PLoS One. 2011 Jan 26;6(1):e15800. doi: 10.1371/journal.pone.0015800.

DOI:10.1371/journal.pone.0015800
PMID:21298091
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3027627/
Abstract

TatC (STM3975) is a highly conserved component of the Twin Arginine Transport (Tat) systems that is required for transport of folded proteins across the inner membrane in gram-negative bacteria. We previously identified a ΔtatC mutant as defective in competitive infections with wild type ATCC14028 during systemic infection of Salmonella-susceptible BALB/c mice. Here we confirm these results and show that the ΔtatC mutant is internalized poorly by cultured J774-A.1 mouse macrophages a phenotype that may be related to the systemic infection defect. This mutant is also defective for short-term intestinal and systemic colonization after oral infection of BALB/c mice and is shed in reduced numbers in feces from orally infected Salmonella-resistant (CBA/J) mice. We show that the ΔtatC mutant is highly sensitive to bile acids perhaps resulting in the defect in intestinal infection that we observe. Finally, the ΔtatC mutant has an unusual combination of motility phenotypes in Salmonella; it is severely defective for swimming motility but is able to swarm well. The ΔtatC mutant has a lower amount of flagellin on the bacterial surface during swimming motility but normal levels under swarming conditions.

摘要

TatC(STM3975)是 Twin Arginine Transport(Tat)系统中高度保守的成分,对于革兰氏阴性细菌中折叠蛋白穿过内膜的运输是必需的。我们之前发现ΔtatC 突变体在全身性沙门氏菌易感 BALB/c 小鼠感染中与野生型 ATCC14028 的竞争感染中存在缺陷。在这里,我们证实了这些结果,并表明ΔtatC 突变体在培养的 J774-A.1 小鼠巨噬细胞中内化不良-一种表型可能与全身性感染缺陷有关。该突变体在经口感染 BALB/c 小鼠后的短期肠道和全身定植中也存在缺陷,并且在经口感染的沙门氏菌抗性(CBA/J)小鼠的粪便中脱落的数量减少。我们表明,ΔtatC 突变体对胆汁酸高度敏感,这可能导致我们观察到的肠道感染缺陷。最后,ΔtatC 突变体在沙门氏菌中具有不寻常的运动表型组合;它在游泳运动中严重缺陷,但在群集运动中表现良好。在游泳运动中,ΔtatC 突变体在细菌表面的鞭毛蛋白数量较少,但在群集条件下正常。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1f9/3027627/ad1f2145acb0/pone.0015800.g007.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1f9/3027627/b4fcbd9b7124/pone.0015800.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1f9/3027627/f43fbcb47dc3/pone.0015800.g003.jpg
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