PDF(Pubmed)
Abstract：
Legionella pneumophila is a Gram-negative bacterium ubiquitously present in freshwater environments and causes a serious type of pneumonia called Legionnaires\' disease. During infections, L. pneumophila releases over 300 effector proteins into host cells through an Icm/Dot type IV secretion system to manipulate the host defense system for survival within the host. Notably, certain effector proteins mediate posttranslational modifications (PTMs), serving as useful approaches exploited by L. pneumophila to modify host proteins. Some effectors catalyze the addition of host protein PTMs, while others mediate the removal of PTMs from host proteins. In this review, we summarize L. pneumophila effector-mediated PTMs of host proteins, including phosphorylation, ubiquitination, glycosylation, AMPylation, phosphocholination, methylation, and ADP-ribosylation, as well as dephosphorylation, deubiquitination, deAMPylation, deADP-ribosylation, dephosphocholination, and delipidation. We describe their molecular mechanisms and biological functions in the regulation of bacterial growth and Legionella-containing vacuole biosynthesis and in the disruption of host immune and defense machinery.
摘要：
嗜肺军团菌是一种广泛存在于淡水环境中的革兰氏阴性细菌，可引起一种严重的肺炎，称为军团菌病。在感染期间,嗜肺乳杆菌通过Icm/DotIV型分泌系统将>300个效应蛋白释放到宿主细胞中以操纵宿主防御系统以在宿主内存活。值得注意的是,某些效应蛋白介导翻译后修饰（PTM），作为嗜肺乳杆菌修饰宿主蛋白的有用方法。一些效应子催化宿主蛋白PTM的添加，而其他人则介导宿主蛋白PTM的去除。在这次审查中,我们总结了嗜肺乳杆菌效应子介导的宿主蛋白PTM，包括磷酸化，泛素化，糖基化，AMPylation,磷酸胆化，甲基化,ADP-核糖基化,以及去磷酸化，去泛素化,脱AMPylation,去ADP-核糖基化，去磷酸胆化，和脱脂。我们描述了它们在调节细菌生长和含军团菌的液泡生物合成以及破坏宿主免疫和防御机制方面的分子机制和生物学功能。
