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在稻瘟病菌侵染过程中,E3 连接酶 IPI7 通过非水解性 K29 泛素化对 IPA1 转录激活活性的精细调控。

Fine-tuning of IPA1 transactivation activity by E3 ligase IPI7-mediated non-proteolytic K29-ubiquitination during Magnaporthe oryzae infection.

机构信息

State Key Laboratory of Crop Gene Exploration and Utilization in Southwest China, Sichuan Agricultural University at Wenjiang, Chengdu, 611130, Sichuan, China.

Key Laboratory of Seed Innovation, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, 100101, Beijing, China.

出版信息

Nat Commun. 2024 Sep 1;15(1):7608. doi: 10.1038/s41467-024-51962-x.

DOI:10.1038/s41467-024-51962-x
PMID:39218986
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11366762/
Abstract

The Ideal Plant Architecture 1 (IPA1) transcription factor promotes rice yield and immunity through phosphorylation at its amino acid residue Ser163 as a switch. Although phosphorylated IPA1 mimic, IPA1(S163D), directly targets the promoter of immune response gene WRKY45, it cannot activate its expression. Here, we identified a co-activator of IPA1(S163D), a RING-finger E3 ligase IPA1 interactor 7 (IPI7), which fine-tunes the transcriptional activity of IPA1 to timely promote plant immunity and simultaneously maintain growth for yield. IPI7 interacts with IPA1 and promotes K29-polyubiquitination of IPA1 in vitro and in vivo. However, the stability of IPA1 protein is not affected by IPI7-mediated ubiquitination. The IPI7-promoted K29-polyubiquitination of IPA1 is induced by Magnaporthe oryzae infection and required for phosphorylated IPA1 to transactivate WRKY45 expression for immune response but not for plain IPA1 to transactivate DENSE AND ERECT PANICLES 1 (DEP1) expression for panicle development. IPI7 knockout impairs IPA1-mediated immunity but not yield. Our study reveals that plants utilize non-proteolytic K29-ubiquitination as a response to pathogen infection to fine-tune IPA1 transactivation activity for promoting immunity.

摘要

理想株型 1(IPA1)转录因子通过其丝氨酸残基 Ser163 的磷酸化作为开关促进水稻产量和免疫力。虽然磷酸化 IPA1 模拟物 IPA1(S163D) 可以直接靶向免疫反应基因 WRKY45 的启动子,但它不能激活其表达。在这里,我们鉴定了 IPA1(S163D)的共激活因子,即 RING 指 E3 连接酶 IPA1 相互作用蛋白 7(IPI7),它可以微调 IPA1 的转录活性,及时促进植物免疫,同时保持生长以提高产量。IPI7 与 IPA1 相互作用,并在体外和体内促进 IPA1 的 K29 多聚泛素化。然而,IPA1 蛋白的稳定性不受 IPI7 介导的泛素化影响。IPI7 促进的 IPA1 的 K29 多聚泛素化是由稻瘟病菌感染诱导的,对于磷酸化 IPA1 转激活 WRKY45 表达以响应免疫是必需的,但对于普通 IPA1 转激活 DENSE AND ERECT PANICLES 1(DEP1)表达以促进穗发育则不是必需的。IPI7 敲除会损害 IPA1 介导的免疫,但不会影响产量。我们的研究揭示了植物利用非蛋白水解的 K29 泛素化作为对病原体感染的反应,以微调 IPA1 的转激活活性,从而促进免疫。

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