State Key Laboratory of Plant Genomics, Institute of Microbiology, Chinese Academy of Sciences, Beijing, 100101, China.
State Key Laboratory of Hybrid Rice, Key Laboratory of Major Crop Diseases and Collaborative Innovation Center for Hybrid Rice in Yangtze River Basin, Rice Research Institute, Sichuan Agricultural University at Wenjiang, Chengdu, Sichuan, 611130, China.
New Phytol. 2018 Oct;220(1):219-231. doi: 10.1111/nph.15287. Epub 2018 Jun 27.
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.
稻黄单胞菌引起的水稻细菌性条斑病是由稻黄单胞菌 pv. 稻引起的。虽然稻黄单胞菌 pv. 稻的 III 型分泌系统对毒力是必需的，但该系统传递的非转录激活因子样（non-TAL）效应子的生化活性和毒力机制在很大程度上是未知的。在这里，我们通过筛选有助于稻黄单胞菌 pv. 稻毒力的非 TAL 效应子，揭示了黄单胞菌外蛋白 K（XopK）在上游的丝裂原激活蛋白激酶级联反应中抑制病原体相关分子模式触发的免疫。具体来说，XopK 与水稻体细胞胚性受体激酶 2（OsSERK2）相互作用，并直接泛素化 OsSERK2，导致其降解。因此，一个假定的泛素结合酶（E2）结合位点的突变消除了 XopK 诱导的 OsSERK2 降解，并损害了 XopK 依赖性毒力。作为与多种免疫受体相关的重要免疫调节剂，SERKs 已被证明通过不同的机制被假单胞菌效应子扰乱。我们的研究揭示了一种通过泛素化实现的 SERK 活性的独特扰动机制，该机制由黄单胞菌非 TAL 效应子介导。
