Department of Biology, Center for Bionanotechnology and Environmental Research, Texas Southern University Houston, TX, USA ; Department of Environmental and Interdisciplinary Sciences, Texas Southern University Houston, TX, USA.
Front Cell Infect Microbiol. 2013 Nov 19;3:81. doi: 10.3389/fcimb.2013.00081. eCollection 2013.
Microbes are incessantly challenged by both biotic and abiotic stressors threatening their existence. Therefore, bacterial pathogens must possess mechanisms to successfully subvert host immune defenses as well as overcome the stress associated with host-cell encounters. To achieve this, bacterial pathogens typically experience a genetic re-programming whereby anti-host/stress factors become expressed and eventually translated into effector proteins. In that vein, the bacterial host-cell induced stress-response is similar to any other abiotic stress to which bacteria respond by up-regulating specific stress-responsive genes. Following the stress encounter, bacteria must degrade unnecessary stress responsive transcripts through RNA decay mechanisms. The three pathogenic yersiniae (Yersinia pestis, Y. pseudo-tuberculosis, and Y. enterocolitica) are all psychrotropic bacteria capable of growth at 4°C; however, cold growth is dependent on the presence of an exoribonuclease, polynucleotide phosphorylase (PNPase). PNPase has also been implicated as a virulence factor in several notable pathogens including the salmonellae, Helicobacter pylori, and the yersiniae [where it typically influences the type three secretion system (TTSS)]. Further, PNPase has been shown to associate with ribonuclease E (endoribonuclease), RhlB (RNA helicase), and enolase (glycolytic enzyme) in several Gram-negative bacteria forming a large, multi-protein complex known as the RNA degradosome. This review will highlight studies demonstrating the influence of PNPase on the virulence potentials and stress responses of various bacterial pathogens as well as focusing on the degradosome-dependent and -independent roles played by PNPase in yersiniae stress responses.
微生物不断受到生物和非生物胁迫因素的挑战，这些因素威胁着它们的生存。因此，细菌病原体必须拥有机制来成功颠覆宿主的免疫防御，以及克服与宿主细胞接触相关的压力。为了实现这一目标，细菌病原体通常会经历基因重编程，从而表达抗宿主/应激因子，并最终将其转化为效应蛋白。在这种情况下，细菌宿主细胞诱导的应激反应与细菌对任何其他非生物应激的反应相似，通过上调特定的应激响应基因来响应。在应激后，细菌必须通过 RNA 衰减机制降解不必要的应激响应转录本。三种致病性耶尔森菌（鼠疫耶尔森菌、假结核耶尔森菌和小肠结肠炎耶尔森菌）都是能够在 4°C 下生长的嗜冷细菌；然而，低温生长依赖于外切核酸酶多核苷酸磷酸化酶（PNPase）的存在。PNPase 也被认为是几种重要病原体的毒力因子，包括沙门氏菌、幽门螺杆菌和耶尔森菌[其中它通常影响 III 型分泌系统（TTSS）]。此外，PNPase 已被证明与核糖核酸酶 E（内切核酸酶）、RhlB（RNA 解旋酶）和烯醇酶（糖酵解酶）在几种革兰氏阴性细菌中结合，形成一个称为 RNA 降解酶体的大型多蛋白复合物。这篇综述将重点介绍研究表明 PNPase 对各种细菌病原体的毒力潜力和应激反应的影响，以及关注 PNPase 在耶尔森菌应激反应中依赖和不依赖降解酶体的作用。
