Gram-negative bacterial pathogens rely on the type III secretion system to inject virulence proteins into host cells. These type III secreted "effector" proteins directly manipulate cellular processes to cause disease. Although the effector repertoires in different bacterial species are highly variable, the Yersinia outer protein J (YopJ) effector family is unique in that its members are produced by diverse animal and plant pathogens as well as a nonpathogenic microsymbiont. All YopJ family effectors share a conserved catalytic triad that is identical to that of the C55 family of cysteine proteases. However, an accumulating body of evidence demonstrates that many YopJ effectors modify their target proteins in hosts by acetylating specific serine, threonine, and/or lysine residues. This unique acetyltransferase activity allows the YopJ family effectors to affect the function and/or stability of their targets, thereby dampening innate immunity. Here, we summarize the current understanding of this prevalent and evolutionarily conserved type III effector family by describing their enzymatic activities and virulence functions in animals and plants. In particular, the molecular mechanisms by which representative YopJ family effectors subvert host immunity through posttranslational modification of their target proteins are discussed.

中文翻译：

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YopJ家庭效应器通过独特的乙酰转移酶活性促进细菌感染。

革兰氏阴性细菌病原体依靠III型分泌系统将毒力蛋白注入宿主细胞。这些III型分泌的“效应子”蛋白直接操纵细胞过程导致疾病。尽管不同细菌物种中的效应子库变化很大，但耶尔森氏菌外蛋白J（YopJ）效应子家族的独特之处在于其成员由多种动植物病原体以及非致病性微共生体产生。所有的YopJ家族效应子都具有一个保守的催化三联体，该催化三联体与C55家族的半胱氨酸蛋白酶相同。然而，越来越多的证据表明，许多YopJ效应子通过乙酰化特定的丝氨酸，苏氨酸和/或赖氨酸残基来修饰宿主中的靶蛋白。这种独特的乙酰转移酶活性可使YopJ家族效应子影响其靶标的功能和/或稳定性，从而减弱先天免疫力。在这里，我们通过描述它们在动物和植物中的酶促活性和毒力功能，总结了对这一普遍存在且进化上保守的III型效应子家族的当前理解。特别是，讨论了代表性的YopJ家族效应子通过其靶蛋白的翻译后修饰来破坏宿主免疫力的分子机制。通过描述它们在动植物中的酶促活性和毒力功能，我们总结了对这一普遍存在且进化上保守的III型效应子家族的当前理解。特别是，讨论了代表性的YopJ家族效应子通过其靶蛋白的翻译后修饰来破坏宿主免疫力的分子机制。通过描述它们在动植物中的酶促活性和毒力功能，我们总结了对这一普遍存在且进化上保守的III型效应子家族的当前理解。特别是，讨论了代表性的YopJ家族效应子通过其靶蛋白的翻译后修饰来破坏宿主免疫力的分子机制。