文献类型： 外文期刊
作者： Chang, Ming 1 ; Zhao, Jinping 3 ; Chen, Huan 1 ; Li, Guangyong 4 ; Chen, Jian 1 ; Li, Min 2 ; Palmer, Ian A. 2 ; Song, Ju 1 ;
作者机构： 1.Jiangsu Acad Agr Sci, Inst Plant Protect, Minist Sci & Technol, Jiangsu Key Lab Food Qual & Safety,State Key Lab, Nanjing 210014, Jiangsu, Peoples R China
2.Univ South Carolina, Dept Biol Sci, Columbia, SC 29208 USA
3.Texas A&M Univ Syst, Texas A&M AgriLife Res Ctr Dallas, Dallas, TX 75252 USA
4.Univ Nebraska, Ctr Plant Sci Innovat, Lincoln, NE 68588 USA
5.Univ Nebraska, Dept Plant Pathol, Lincoln, NE 68588 USA
6.Texas A&M Univ, Dept Plant Pathol & Microbiol, College Stn, TX 77843 USA
关键词： PBS3; EDS1; NPR3; NPR4; the 26S proteasome; PAMP-triggered immunity
期刊名称：MOLECULAR PLANT （ 影响因子：13.164； 五年影响因子：16.357 ）
ISSN： 1674-2052
年卷期： 2019 年 12 卷 5 期
页码：
收录情况： SCI
摘要： Plant immunity is controlled by both positive regulators such as PBS3 and EDS1 and negative regulators such as NPR3 and NPR4. However, the relationships among these important immune regulators remain elusive. In this study, we found that PBS3 interacts with EDS1 in both the cytoplasm and the nucleus, and is required for EDS1 protein accumulation. NPR3 and NPR4, which function as salicylic acid receptors and adaptors of Cullin3-based E3 ligase, interact with and mediate the degradation of EDS1 via the 26S proteasome. We further discovered that PBS3 inhibits the polyubiquitination and subsequent degradation of EDS1 by reducing the association of EDS1 with the Cullin3 adaptors NPR3 and NPR4. Furthermore, we showed that PBS3 and EDS1 also contribute to PAMP-triggered immunity in addition to effector-triggered immunity. Collectively, our study reveals a novel mechanism by which plants fine-tune defense responses by inhibiting the degradation of a positive player in plant immunity.
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