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The Xanthomonas effector XopK harbours E3 ubiquitin‐ligase activity that is required for virulence
Author(s) -
Qin Jun,
Zhou Xiaogang,
Sun Lifan,
Wang Kailun,
Yang Fan,
Liao Haicheng,
Rong Wei,
Yin Junjie,
Chen Huamin,
Chen Xuewei,
Zhang Jie
Publication year - 2018
Publication title -
new phytologist
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.742
H-Index - 244
eISSN - 1469-8137
pISSN - 0028-646X
DOI - 10.1111/nph.15287
Subject(s) - xanthomonas oryzae , xanthomonas oryzae pv. oryzae , virulence , effector , biology , xanthomonas , type three secretion system , microbiology and biotechnology , ubiquitin ligase , pathogen , ubiquitin , genetics , bacteria , gene
SummaryXanthomonas 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 (Os SERK 2), resulting in its degradation. Accordingly, mutation of a putative ubiquitin‐conjugation enzyme (E2) binding site abolished XopK‐induced degradation of Os SERK 2 and compromised XopK‐dependent virulence. As crucial immune regulators associated with a multitude of immune receptors, SERK s 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.