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在拟南芥中,RIN13介导的抗病性依赖于SNC1-EDS1/PAD4信号通路。

RIN13-mediated disease resistance depends on the SNC1-EDS1/PAD4 signaling pathway in Arabidopsis.

作者信息

Liu Xiaoxiao, Liu Hui, He Jingjing, Zhang Siyuan, Han Hui, Wang Zhangying, Liu Wen-Cheng, Liang Yun-Kuan, Gao Zhiyong

机构信息

State Key Laboratory of Hybrid Rice, Key Laboratory for Research and Utilization of Heterosis in Indica Rice of Ministry of Agriculture, College of Life Sciences, Wuhan University, Wuhan, China.

State Key Laboratory of Cotton Biology, State Key Laboratory of Crop Stress Adaptation and Improvement, School of Life Sciences, Henan University, Kaifeng, China.

出版信息

J Exp Bot. 2020 Dec 31;71(22):7393-7404. doi: 10.1093/jxb/eraa433.

DOI:10.1093/jxb/eraa433
PMID:32937656
Abstract

Plants have evolved an innate immune system to protect themselves from pathogen invasion with the help of intracellular nucleotide-binding leucine-rich repeat (NLR) receptors, though the mechanisms remain largely undefined. RIN13 (RPM1-interacting protein 13) was previously reported to enhance disease resistance, and suppress RPM1 (a CNL-type NLR)-mediated hypersensitive response in Arabidopsis via an as yet unknown mechanism. Here, we show that RIN13 is a nuclear-localized protein, and functions therein. Overexpression of RIN13 leads to autoimmunity with high accumulation of salicylic acid (SA), constitutive expression of pathogenesis-related genes, enhanced resistance to a virulent pathogen, and dwarfism. In addition, genetic and transcriptome analyses show that SA-dependent and SA-independent pathways are both required for RIN13-mediated disease resistance, with the EDS1/PAD4 complex as an integration point. RIN13-induced dwarfism was rescued completely by either the pad4-1 or the eds1-2 mutant but partially by snc1-r1, a mutant of the TNL gene SNC1, suggesting the involvement of EDS1/PAD4 and SNC1 in RIN13 functioning. Furthermore, transient expression assays indicated that RIN13 promotes the nuclear accumulation of PAD4. Collectively, our study uncovered a signaling pathway whereby SNC1 and EDS1/PAD4 act together to modulate RIN13-triggered plant defense responses.

摘要

植物已经进化出一种先天免疫系统,借助细胞内核苷酸结合富含亮氨酸重复序列(NLR)受体来保护自身免受病原体入侵,尽管其机制在很大程度上仍不明确。RIN13(RPM1相互作用蛋白13)先前被报道可增强抗病性,并通过一种未知机制抑制拟南芥中RPM1(一种CNL型NLR)介导的超敏反应。在这里,我们表明RIN13是一种定位于细胞核的蛋白,并在细胞核中发挥作用。RIN13的过表达导致自身免疫,伴有水杨酸(SA)的高积累、病程相关基因的组成型表达、对强毒病原体抗性增强以及植株矮化。此外,遗传和转录组分析表明,SA依赖和SA非依赖途径对于RIN13介导的抗病性都是必需的,EDS1/PAD4复合物作为一个整合点。RIN13诱导的矮化完全被pad4 - 1或eds1 - 2突变体挽救,但部分被TNL基因SNC1的突变体snc1 - r1挽救,这表明EDS1/PAD4和SNC1参与了RIN13的功能。此外,瞬时表达分析表明RIN13促进PAD4的核积累。总的来说,我们的研究揭示了一条信号通路,即SNC1和EDS1/PAD4共同作用来调节RIN13触发的植物防御反应。

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RIN13-mediated disease resistance depends on the SNC1-EDS1/PAD4 signaling pathway in Arabidopsis.在拟南芥中,RIN13介导的抗病性依赖于SNC1-EDS1/PAD4信号通路。
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