The RING-finger ubiquitin E3 ligase TaPIR1 targets TaHRP1 for degradation to suppress chloroplast function

Rongrong Zhang, Yu Wu, Xiangru Qu, Wenjuan Yang, Qin Wu, Lin Huang, Qiantao Jiang, Jian Ma, Yazhou Zhang, Pengfei Qi, Guoyue Chen, Yunfeng Jiang, Youliang Zheng, Xiaojie Wang (), Yuming Wei () and Qiang Xu ()
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Rongrong Zhang: Sichuan Agricultural University
Yu Wu: Sichuan Agricultural University
Xiangru Qu: Sichuan Agricultural University
Wenjuan Yang: Sichuan Agricultural University
Qin Wu: Sichuan Agricultural University
Lin Huang: Sichuan Agricultural University
Qiantao Jiang: Sichuan Agricultural University
Jian Ma: Sichuan Agricultural University
Yazhou Zhang: Sichuan Agricultural University
Pengfei Qi: Sichuan Agricultural University
Guoyue Chen: Sichuan Agricultural University
Yunfeng Jiang: Sichuan Agricultural University
Youliang Zheng: Sichuan Agricultural University
Xiaojie Wang: Northwest A&F University
Yuming Wei: Sichuan Agricultural University
Qiang Xu: Sichuan Agricultural University

Nature Communications, 2024, vol. 15, issue 1, 1-17

Abstract: Abstract Chloroplasts are key players in photosynthesis and immunity against microbial pathogens. However, the precise and timely regulatory mechanisms governing the control of photosynthesis-associated nuclear genes (PhANGs) expression in plant immunity remain largely unknown. Here we report that TaPIR1, a Pst-induced RING-finger E3 ubiquitin ligase, negatively regulates Pst resistance by specifically interacting with TaHRP1, an atypical transcription factor histidine-rich protein. TaPIR1 ubiquitinates the lysine residues K131 and K136 in TaHRP1 to regulate its stability. TaHRP1 directly binds to the TaHRP1-binding site elements within the PhANGs promoter to activate their transcription via the histidine-rich domain of TaHRP1. PhANGs expression induces the production of chloroplast-derived ROS. Although knocking out TaHRP1 reduces Pst resistance, TaHRP1 overexpression contributes to photosynthesis, and chloroplast-derived ROS production, and improves disease resistance. TaPIR1 expression inhibits the downstream activation of TaHRP1 and TaHRP1-induced ROS accumulation in chloroplasts. Overall, we show that the TaPIR1-mediated ubiquitination and degradation of TaHRP1 alters PhANGs expression to disrupt chloroplast function, thereby increasing plant susceptibility to Pst.

Date: 2024
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DOI: 10.1038/s41467-024-51249-1

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