Lewis Claire, Skovierova Henrieta, Rowley Gary, Rezuchova Bronislava, Homerova Dagmar, Stevenson Andrew, Sherry Aileen, Kormanec Jan, Roberts Mark
Institute of Comparative Medicine, Faculty of Veterinary Medicine, University of Glasgow, Bearsden Road, Glasgow G61 1QH, UK.
Institute of Molecular Biology, Slovak Academy of Science, Dubravska cesta 21, 845 51 Bratislava, Slovak Republik.
Microbiology (Reading). 2008 Mar;154(Pt 3):979-988. doi: 10.1099/mic.0.2007/011999-0.
SmpA is a small outer-membrane lipoprotein that is a component of the essential YaeT outer-membrane protein assembly complex. In Salmonella enterica serovar Typhimurium (S. Typhimurium), expression of the smpA gene was shown to be directed by two promoters, smpAp1 and smpAp2. The more distal promoter, smpAp1, is dependent upon the extracytoplasmic stress response sigma factor sigma(E). An smpA null mutant was constructed in S. Typhimurium SL1344 and was shown to be more sensitive than its wild-type parent to growth at high temperature and in the presence of sodium cholate, SDS plus EDTA, and the hydrophobic antibiotic rifampicin. The lack of SmpA in S. Typhimurium elicits a sigma(E)-dependent stress response. These findings are indicative of altered outer-membrane integrity in the smpA mutant, probably due to a defect in outer-membrane protein biogenesis. SmpA was not important for entry or survival within murine macrophages; however, the S. Typhimurium smpA mutant was attenuated in mice by both the oral and parenteral routes of infection, and SmpA appeared to be most important for the growth of S. Typhimurium at systemic sites.
SmpA是一种小的外膜脂蛋白，是必需的YaeT外膜蛋白组装复合物的一个组成部分。在鼠伤寒沙门氏菌（鼠伤寒沙门菌）中，smpA基因的表达由两个启动子smpAp1和smpAp2指导。距离更远的启动子smpAp1依赖于胞外应激反应σ因子σ(E)。在鼠伤寒沙门菌SL1344中构建了一个smpA缺失突变体，结果显示该突变体比其野生型亲本在高温下以及在胆酸钠、SDS加EDTA和疏水性抗生素利福平存在的情况下对生长更为敏感。鼠伤寒沙门菌中SmpA的缺失引发了一种依赖于σ(E)的应激反应。这些发现表明smpA突变体中外膜完整性发生了改变，可能是由于外膜蛋白生物合成存在缺陷。SmpA对在鼠巨噬细胞内的进入或存活并不重要；然而，鼠伤寒沙门菌smpA突变体通过口服和非肠道感染途径在小鼠体内的毒力减弱，并且SmpA似乎对鼠伤寒沙门菌在全身部位的生长最为重要。
