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ETI 依赖性受体样激酶 1 通过稳定拟南芥中 NLR 所需的细胞死亡 4 来正向调控效应子触发的免疫。

The ETI-dependent receptor-like kinase 1 positively regulates effector-triggered immunity by stabilizing NLR-required for cell death 4 in Nicotiana benthamiana.

机构信息

Department of Plant Pathology, Nanjing Agricultural University, Nanjing, Jiangsu, 210095, China.

The Key Laboratory of Plant Immunity, Nanjing Agricultural University, Nanjing, Jiangsu, 210095, China.

出版信息

New Phytol. 2024 Apr;242(2):576-591. doi: 10.1111/nph.19596. Epub 2024 Feb 16.

Abstract

Leucine-rich repeat receptor-like kinases (LRR-RLKs) comprise the largest class of membrane-localized receptor-like kinases in plants. Leucine-rich repeat receptor-like kinases are key immune sectors contributing to pattern-triggered immunity (PTI), but whether LRR-RLK mediates effector-triggered immunity (ETI) in plants remains unclear. In this study, we evaluated the function of LRR-RLKs in regulating ETI by using a virus-induced gene silencing (VIGS)-based reverse genetic screening assay, and identified a LRR-RLK named ETI-dependent receptor-like kinase 1 (EDK1) required for ETI triggered by the avirulence effector AVRblb2 secreted by Phytophthora infestans and its cognate receptor Rpi-blb2. Silencing or knockout of EDK1 compromised immunity mediated by Rpi-blb2 and the cell death triggered by recognition of AVRblb2. NLR-required for cell death 4 (NRC4), a signaling component acts downstream of Rpi-blb2, was identified that interacts with EDK1 using the LC-MS analysis and the interaction was further evaluated by co-immunoprecipitation. EDK1 promotes protein accumulation of NRC4 in a kinase-dependent manner and positively regulates resistance to P. infestans in Nicotiana benthamiana. Our study revealed that EDK1 positively regulates plant ETI through modulating accumulation of the NLR signaling component NRC4, representing a new regulatory role of the membrane-localized LRR-RLKs in plant immunity.

摘要

富含亮氨酸重复受体样激酶(LRR-RLKs)构成了植物中最大的一类定位于膜的受体样激酶。富含亮氨酸重复受体样激酶是参与模式触发免疫(PTI)的关键免疫区,但 LRR-RLK 是否介导植物中的效应子触发免疫(ETI)尚不清楚。在这项研究中,我们通过基于病毒诱导的基因沉默(VIGS)的反向遗传筛选测定来评估 LRR-RLK 调节 ETI 的功能,并鉴定了一种称为 ETI 依赖的受体样激酶 1(EDK1)的 LRR-RLK,该激酶对于由 Phytophthora infestans 分泌的无毒效应子 AVRblb2 和其同源受体 Rpi-blb2 触发的 ETI 是必需的。EDK1 的沉默或敲除会损害由 Rpi-blb2 介导的免疫和由 AVRblb2 识别触发的细胞死亡。鉴定了 NLR-需要细胞死亡 4(NRC4),它是一种信号成分,位于 Rpi-blb2 的下游,使用 LC-MS 分析鉴定了与 EDK1 相互作用的信号成分,并通过共免疫沉淀进一步评估了相互作用。EDK1 以激酶依赖性方式促进 NRC4 的蛋白积累,并正向调节 Nicotiana benthamiana 对 P. infestans 的抗性。我们的研究表明,EDK1 通过调节 NLR 信号成分 NRC4 的积累正向调节植物 ETI,这代表了膜定位的 LRR-RLKs 在植物免疫中的一个新的调节作用。

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