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E3泛素连接酶OsRFI2通过靶向抗坏血酸过氧化物酶OsAPX8促进其降解来调控水稻的耐盐性。

E3 Ubiquitin Ligase OsRFI2 Regulates Salinity Tolerance by Targeting Ascorbate Peroxidase OsAPX8 for its Degradation in Rice.

作者信息

Zhao Wenjing, Wen Junli, Zhao Juan, Liu Linlin, Wang Mei, Huang Menghan, Fang Chaowei, Liu Qingpo

机构信息

College of Advanced Agricultural Sciences, Zhejiang A&F University, Lin'an Hangzhou, 311300, P. R. China.

Institute of Horticulture, Zhejiang Academy of Agricultural Sciences, Hangzhou, 310021, P. R. China.

出版信息

Rice (N Y). 2025 Mar 10;18(1):12. doi: 10.1186/s12284-025-00763-x.

DOI:10.1186/s12284-025-00763-x
PMID:40059282
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11891124/
Abstract

Salinity is a major abiotic stress that adversely affects rice growth and production. However, the detailed regulatory mechanisms of salt stress response in rice remain largely unexplored. In this study, we established that the RING-type E3 ubiquitin ligase OsRFI2 plays a negative role in salt tolerance in rice. Knockout mutants of OsRFI2 (Osrfi2) exhibited high tolerance, whereas OsRFI2-overexpressed transgenic lines (OE-OsRFI2) were more sensitive to salt stress. OsRFI2 that has E3 ligase activity interacts with ascorbate peroxidase OsAPX8 in chloroplast, and catalyzes its ubiquitination and degradation through the 26 S proteasome pathway. The Osapx8 mutants, like OE-OsRFI2 lines, showed high sensitivity to high salt concentrations, accumulating greater amounts of MDA, HO and O, which lead to compromised cell permeability and ROS accumulation. Thus, the OsRFI2-OsAPX8 module adds novel clues for better understanding the regulatory mechanism of salt stress response in rice.

摘要

盐度是一种主要的非生物胁迫,对水稻生长和产量产生不利影响。然而,水稻中盐胁迫响应的详细调控机制在很大程度上仍未被探索。在本研究中,我们确定了环状E3泛素连接酶OsRFI2在水稻耐盐性中起负作用。OsRFI2的敲除突变体(Osrfi2)表现出高耐受性,而OsRFI2过表达转基因系(OE-OsRFI2)对盐胁迫更敏感。具有E3连接酶活性的OsRFI2在叶绿体中与抗坏血酸过氧化物酶OsAPX8相互作用,并通过26S蛋白酶体途径催化其泛素化和降解。Osapx8突变体与OE-OsRFI2系一样,对高盐浓度表现出高敏感性,积累了更多的丙二醛、过氧化氢和超氧阴离子,这导致细胞通透性受损和活性氧积累。因此,OsRFI2-OsAPX8模块为更好地理解水稻盐胁迫响应的调控机制提供了新线索。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/117e/11891124/d1a7e900c0ae/12284_2025_763_Fig7_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/117e/11891124/d654bdffb056/12284_2025_763_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/117e/11891124/6873a6dcd8a3/12284_2025_763_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/117e/11891124/d1a7e900c0ae/12284_2025_763_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/117e/11891124/60403bba383f/12284_2025_763_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/117e/11891124/f3e58ef24460/12284_2025_763_Fig2_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/117e/11891124/d654bdffb056/12284_2025_763_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/117e/11891124/6873a6dcd8a3/12284_2025_763_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/117e/11891124/d1a7e900c0ae/12284_2025_763_Fig7_HTML.jpg

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本文引用的文献

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Suppression of OsSAUR2 gene expression immobilizes soil arsenic bioavailability by modulating root exudation and rhizosphere microbial assembly in rice.
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