The Arabidopsis E3 ubiquitin ligase PUB4 regulates BIK1 and is targeted by a bacterial type-III effector

Yu, Gang, Derkacheva, Maria, Rufian, Jose S., Brillada, Carla, Kowarschik, Kathrin, Jiang, Shushu, Derbyshire, Paul, Ma, Miaomiao, Defalco, Thomas A., Morcillo, Rafael J. L., Stransfeld, Lena, Wei, Yali, Zhou, Jian‐Min, Menke, Frank L. H. ORCID:, Trujillo, Marco, Zipfel, Cyril and Macho, Alberto P. (2022) The Arabidopsis E3 ubiquitin ligase PUB4 regulates BIK1 and is targeted by a bacterial type-III effector. The EMBO Journal, 41 (23). ISSN 0261-4189

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Plant immunity is tightly controlled by a complex and dynamic regulatory network, which ensures optimal activation upon detection of potential pathogens. Accordingly, each component of this network is a potential target for manipulation by pathogens. Here, we report that RipAC, a type III-secreted effector from the bacterial pathogen Ralstonia solanacearum, targets the plant E3 ubiquitin ligase PUB4 to inhibit pattern-triggered immunity (PTI). PUB4 plays a positive role in PTI by regulating the homeostasis of the central immune kinase BIK1. Before PAMP perception, PUB4 promotes the degradation of non-activated BIK1, while after PAMP perception, PUB4 contributes to the accumulation of activated BIK1. RipAC leads to BIK1 degradation, which correlates with its PTI-inhibitory activity. RipAC causes a reduction in pathogen-associated molecular pattern (PAMP)-induced PUB4 accumulation and phosphorylation. Our results shed light on the role played by PUB4 in immune regulation, and illustrate an indirect targeting of the immune signalling hub BIK1 by a bacterial effector.

Item Type: Article
Additional Information: Funding Information: This project has received funding from the Strategic Priority Research Program of the Chinese Academy of Sciences (grant XDB27040204 to APM), the National Natural Science Foundation of China (grant 31571973 to APM), the Chinese 1000 Talents Program (to APM), the Shanghai Center for Plant Stress Biology (to APM), the China Postdoctoral Science Foundation (fellowship 2016M600339 to GY), the President's International Fellowship Initiative (PIFI) (fellowships 2018PB0057 and 2020PB0088 to JSR), the European Union's Horizon 2020 research and innovation programme under the Marie Skłodowska-Curie grant agreement No. 753641 (to MD), the Gatsby Charitable Foundation (to CZ), the European Research Council under the Grant Agreement No. 309858 (grant “PHOSPHinnATE” to CZ), the University of Zürich (to CZ), and the Swiss National Science Foundation (grant 31003A_182625) (to CZ). SJ was supported by a post-doctoral fellowship from the European Molecular Biology Organization (EMBO-LTF #225-2015). TAD was supported by a post-doctoral fellowship from the Natural Sciences and Engineering Council of Canada (fellowship PDF-532561-2019). This work also received funding from the Alexander von Humboldt Foundation (Humboldt Research Fellowship for Experienced Researchers for CB), the Boeringer Ingelheim Foundation (to KK) and the Deutsche Forschungsgemeinschaft-Heisenberg Program (to MT).
Uncontrolled Keywords: bik1,pamp-triggered immunity,pub4,ralstonia solanacearum,phosphorylation,neuroscience(all),molecular biology,biochemistry, genetics and molecular biology(all),immunology and microbiology(all) ,/dk/atira/pure/subjectarea/asjc/2800
Faculty \ School: Faculty of Science > The Sainsbury Laboratory
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Depositing User: LivePure Connector
Date Deposited: 20 Mar 2023 14:52
Last Modified: 20 Mar 2023 14:52
DOI: 10.15252/embj.2020107257

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