Brown Nat F, Finlay B Brett
Department of Microbiology and Immunology; University of Melbourne; Melbourne, VIC Australia.
Mob Genet Elements. 2011 Jul;1(2):118-121. doi: 10.4161/mge.1.2.16733. Epub 2011 Jul 1.
A major virulence mechanism used by pathogenic Gram-negative bacteria is the delivery of effector proteins from the bacterial cytoplasm into host cells by type III secretion. Typically, genes encoding type III secretion systems (T3SS) and effectors have been horizontally acquired by the bacteria that employ them. In proteobacteria, and especially Salmonella, and attaching and effacing (A/E) pathogens, the genetic structure of these systems presents as a large locus encoding a T3SS with a small number of effectors, plus numerous small unlinked loci encoding additional individual effectors. We discuss the generation of novel effectors, and the evolution of G+C content following acquisition. We also consider the currently held view that each locus has been acquired individually, as well as propose an alternative where recombination may have redistributed and broken up clusters of effectors. It is clear that the evolution of this virulence strategy is highly complex and challenging to analyze.
致病性革兰氏阴性菌使用的一种主要毒力机制是通过III型分泌将效应蛋白从细菌细胞质传递到宿主细胞中。通常，编码III型分泌系统（T3SS）和效应蛋白的基因是由使用它们的细菌通过水平基因转移获得的。在变形菌中，尤其是沙门氏菌以及黏附性和蚀损性（A/E）病原体中，这些系统的遗传结构表现为一个大型基因座，编码一个带有少量效应蛋白的T3SS，再加上许多编码其他单个效应蛋白的小型不连锁基因座。我们讨论了新效应蛋白的产生以及获得后G+C含量的演变。我们还考虑了目前的观点，即每个基因座都是单独获得的，并提出了一种替代观点，即重组可能重新分布并打散了效应蛋白簇。显然，这种毒力策略的进化非常复杂，难以分析。
