The Xanthomonas effector XopK harbours E3 ubiquitin-ligase activity that is required for virulence
The Xanthomonas effector XopK harbours E3 ubiquitin-ligase activity that is required for virulence
复制标题
黄单胞菌效应子 XopK 具有毒力所需的 E3 泛素连接酶活性
DOI：
10.1111/nph.15287
复制
发表时间：
2018-10-01
期刊：
影响因子：
9.4
通讯作者：
Zhang, Jie
中科院分区：
文献类型：
--
作者：
Qin, Jun;Zhou, Xiaogang;Zhang, Jie
水稻白水稻白叶枯病的病原菌是稻瘟病菌。而X.由于X. tagpv是致病性的关键因子，因此该系统所传递的非转录激活因子样（non-TAL）效应子的生物化学活性和致病机制在很大程度上是未知的。黄单胞菌外蛋白K（XanthomonasouterproteinK，XopK）抑制了丝裂原活化蛋白激酶级联反应上游的病原相关分子模式触发的免疫，并与水稻体细胞胚胎发生受体激酶2（OsSERK 2）相互作用，直接泛素化，导致OsSERK 2降解。因此，突变泛素结合酶（ubiquitin-conjugation enzyme，E2）结合位点可以抑制XopK诱导的OsSERK 2降解，降低XopK依赖的毒力。我们的研究揭示了一个独特的干扰机制，通过泛素化实现的黄单胞菌非TAL效应的SERK活性。
Xanthomonas oryzae pv. oryzae is the causative agent of rice bacterial leaf blight. While the type III secretion system of X.oryzae pv. oryzae is essential for virulence, the biochemical activities and virulence mechanisms of non-transcription activator-like (non-TAL) effectors delivered by this system are largely unknown.Here, by screening for non-TAL effectors that contribute to X.oryzae pv. oryzae virulence, we revealed that Xanthomonas outer protein K (XopK) inhibits pathogen-associated molecular pattern-triggered immunity upstream of mitogen-activated protein kinase cascades.Specifically, XopK interacted with and directly ubiquitinated rice somatic embryogenic receptor kinase 2 (OsSERK2), resulting in its degradation. Accordingly, mutation of a putative ubiquitin-conjugation enzyme (E2) binding site abolished XopK-induced degradation of OsSERK2 and compromised XopK-dependent virulence.As crucial immune regulators associated with a multitude of immune receptors, SERKs have been shown to be perturbed by Pseudomonas effectors via different mechanisms. Our study revealed a distinct perturbation mechanism of SERK activity via ubiquitination achieved by Xanthomonas non-TAL effector.