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RING 指泛素 E3 连接酶 TaPIR1 靶向 TaHRP1 进行降解,以抑制叶绿体功能。

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

机构信息

State Key Laboratory of Crop Gene Exploration and Utilization in Southwest China, Sichuan Agricultural University, Chengdu, China.

Triticeae Research Institute, Sichuan Agricultural University, Chengdu, China.

出版信息

Nat Commun. 2024 Aug 12;15(1):6905. doi: 10.1038/s41467-024-51249-1.

DOI:10.1038/s41467-024-51249-1
PMID:39134523
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11319775/
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 K and K 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.

摘要

叶绿体是光合作用和抵御微生物病原体的关键角色。然而,在植物免疫中,控制与光合作用相关的核基因(PhANGs)表达的精确和及时的调控机制在很大程度上仍然未知。在这里,我们报告 TaPIR1,一种 Pst 诱导的 RING-finger E3 泛素连接酶,通过特异性与 TaHRP1 相互作用来负调控 Pst 抗性,TaHRP1 是一种非典型转录因子组氨酸丰富蛋白。TaPIR1 泛素化 TaHRP1 的赖氨酸残基 K 和 K 以调节其稳定性。TaHRP1 直接结合到 PhANGs 启动子内的 TaHRP1 结合位点元件上,通过 TaHRP1 的组氨酸丰富域激活它们的转录。PhANGs 的表达诱导叶绿体衍生的 ROS 的产生。尽管敲除 TaHRP1 会降低 Pst 抗性,但 TaHRP1 的过表达有助于光合作用和叶绿体衍生的 ROS 产生,并提高抗病性。TaPIR1 的表达抑制了 TaHRP1 的下游激活和 TaHRP1 在叶绿体中诱导的 ROS 积累。总的来说,我们表明 TaPIR1 介导的 TaHRP1 泛素化和降解改变了 PhANGs 的表达,从而破坏了叶绿体的功能,从而增加了植物对 Pst 的易感性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf14/11319775/63cf3e0caaf9/41467_2024_51249_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf14/11319775/aa4c0359994b/41467_2024_51249_Fig1_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf14/11319775/c50239c62365/41467_2024_51249_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf14/11319775/0e7af073528b/41467_2024_51249_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf14/11319775/63cf3e0caaf9/41467_2024_51249_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf14/11319775/aa4c0359994b/41467_2024_51249_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf14/11319775/760e085a5b10/41467_2024_51249_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf14/11319775/3e87889214be/41467_2024_51249_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf14/11319775/e9fe6ed5f0c6/41467_2024_51249_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf14/11319775/c50239c62365/41467_2024_51249_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf14/11319775/0e7af073528b/41467_2024_51249_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf14/11319775/63cf3e0caaf9/41467_2024_51249_Fig7_HTML.jpg

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