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SnRK1α1介导的RBOH1磷酸化调控活性氧以增强番茄对低氮的耐受性。

SnRK1α1-mediated RBOH1 phosphorylation regulates reactive oxygen species to enhance tolerance to low nitrogen in tomato.

作者信息

Zheng Xuelian, Yang Hongfei, Zou Jinping, Jin Weiduo, Qi Zhenyu, Yang Ping, Yu Jingquan, Zhou Jie

机构信息

Department of Horticulture, Zhejiang Key Laboratory of Horticultural Crop Quality Improvement, Zijingang Campus, Zhejiang University, Hangzhou 310058, China.

Key Laboratory of Horticultural Plants Growth, Development and Quality Improvement, Ministry of Agriculture and Rural Affairs of China, Hangzhou 310058, China.

出版信息

Plant Cell. 2024 Dec 23;37(1). doi: 10.1093/plcell/koae321.

DOI:10.1093/plcell/koae321
PMID:39667074
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11684077/
Abstract

Nitrogen is essential for plant growth and development. SNF1-related protein kinase 1 (SnRK1) is an evolutionarily conserved protein kinase pivotal for regulating plant responses to nutrient deficiency. Here, we discovered that the expression and activity of the SnRK1 α-catalytic subunit (SnRK1α1) increased in response to low-nitrogen stress. SnRK1α1 overexpression enhanced seedling tolerance, nitrate uptake capacity, apoplastic reactive oxygen species (ROS) accumulation, and NADPH oxidase activity in tomato (Solanum lycopersicum L.) under low-nitrogen stress compared to wild type plants, while snrk1α1 mutants exhibited the opposite phenotypes. Mutation of the NADPH oxidase gene Respiratory burst oxidase homolog 1 (RBOH1) suppressed numerous nitrate uptake and metabolism genes during low-nitrogen stress. rboh1 mutants displayed lower NADPH oxidase activity, apoplastic ROS production, and seedling tolerance to low nitrogen. Silencing RBOH1 expression also compromised SnRK1α1-mediated seedling tolerance to low-nitrogen stress. SnRK1α1 interacts with and activates RBOH1 through phosphorylation of three N-terminal serine residues, leading to increased apoplastic ROS production and enhanced tolerance to low nitrogen conditions. Furthermore, RBOH1-dependent ROS oxidatively modified the transcription factor TGA4 at residue Cys-334, which increased NRT1.1 and NRT2.1 expression under low-nitrogen stress. These findings reveal a SnRK1α1-mediated signaling pathway and highlight the essential role of RBOH1-dependent ROS production in enhancing plant tolerance to low nitrogen.

摘要

氮对于植物的生长和发育至关重要。蔗糖非发酵-1-相关蛋白激酶1(SnRK1)是一种在进化上保守的蛋白激酶,对调节植物对营养缺乏的反应起着关键作用。在此,我们发现SnRK1α催化亚基(SnRK1α1)的表达和活性会响应低氮胁迫而增加。与野生型植株相比,在低氮胁迫下,SnRK1α1过表达增强了番茄(Solanum lycopersicum L.)幼苗的耐受性、硝酸盐吸收能力、质外体活性氧(ROS)积累以及NADPH氧化酶活性,而snrk1α1突变体则表现出相反的表型。NADPH氧化酶基因呼吸爆发氧化酶同源物1(RBOH1)的突变在低氮胁迫期间抑制了许多硝酸盐吸收和代谢基因。rboh1突变体表现出较低的NADPH氧化酶活性、质外体ROS产生以及幼苗对低氮的耐受性。沉默RBOH1表达也损害了SnRK1α1介导的幼苗对低氮胁迫的耐受性。SnRK1α1通过磷酸化三个N端丝氨酸残基与RBOH1相互作用并激活RBOH1,导致质外体ROS产生增加以及对低氮条件的耐受性增强。此外,RBOH1依赖的ROS在Cys-334残基处对转录因子TGA4进行氧化修饰,这在低氮胁迫下增加了NRT1.1和NRT2.1的表达。这些发现揭示了一条SnRK1α1介导的信号通路,并突出了RBOH1依赖的ROS产生在增强植物对低氮耐受性中的重要作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/972a/11684077/aee52628aac9/koae321f9.jpg
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