Mutation of a nucleotide-binding leucine-rich repeat immune receptor-type protein disrupts immunity to bacterial blight.
Mutation of a nucleotide-binding leucine-rich repeat immune receptor-type protein disrupts immunity to bacterial blight.
复制标题
富含亮氨酸的核苷酸结合重复免疫受体型蛋白的突变会破坏对白叶枯病的免疫力。
DOI：
10.1104/pp.19.00686
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发表时间：
2019
期刊：
影响因子：
7.4
通讯作者：
Chu Chengcai
中科院分区：
文献类型：
--
作者：
Tang Jiuyou;Wang Yi Qin;Yin Wenchao;Dong Guojun;Sun Kai;Teng Zhengfeng;Wu Xujiang;Wang Shimei;Qian Yangwen;Pan Xuebiao;Qian Qian;Chu Chengcai
大多数植物抗性蛋白属于核苷酸结合域和富含亮氨酸重复序列（NLR）家族。在没有特定病原体的情况下，NLR以自身抑制状态存在，而NLR中的功能获得性突变通常引起自身免疫。在这里，我们表明，功能获得性突变，弱防御（wed），这导致了一个典型的NLR在水稻（水稻）的核苷酸结合结构域的Phe-到-Leu取代，导致增强的敏感性，以黄单胞菌。水稻中水杨酸（SA）的意外积累，沿着PR 1非表达子（NPR 1）的下调，暗示了SA生物合成的反馈调节回路的潜在存在。上位性分析表明，SA积累和NLR相关组分RAR 1，OsRac 1和PhyB与这些表型相关。有趣的是，除了模式触发的免疫之外，由不同抗性蛋白（包括Xa 3/Xa 26、Xa 4和Xa 21）赋予的效应物触发的免疫也在一定程度上受到wed的干扰，这表明各种防御系统存在共同的调节机制。因此，对它们的鉴定提供了一个独特的系统，用于对由不同类型的免疫受体激活的共享免疫信号传导途径进行遗传解剖。
Most characterized plant resistance proteins belong to the nucleotide-binding domain and Leu-rich repeat-containing (NLR) family. NLRs are present in an auto-inhibited state in the absence of specific pathogens, while gain-of-function mutations in NLRs usually cause autoimmunity. Here, we show that a gain-of-function mutation,weaker defense(wed), which caused a Phe-to-Leu substitution in the nucleotide-binding domain of a typical NLR in rice (Oryza sativa), led to enhanced susceptibility toXanthomonas oryzaepv.Oryzae. The unexpected accumulation of salicylic acid (SA), along with downregulation ofNONEXPRESSOR OF PR1(NPR1), inwedindicates the potential presence of a feedback regulation loop of SA biosynthesis in rice. Epistasis analyses illustrated that SA accumulation and the NLR-associated components RAR1, OsRac1, and PhyB are dispensable for thewedphenotypes. Intriguingly, besides pattern-triggered immunity, effector-triggered immunity conferred by different resistance proteins, including Xa3/Xa26, Xa4, and Xa21, was also disturbed bywedto a certain extent, indicating the existence of shared regulatory mechanisms for various defense systems. The identification ofwedtherefore provides a unique system for genetic dissection of shared immune signaling pathways activated by different types of immune receptors.