Sensor NLR immune proteins activate oligomerization of their NRC helpers in response to plant pathogens.

Sensor NLR immune proteins activate oligomerization of their NRC helpers in response to plant pathogens.
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DOI:
10.15252/embj.2022111519
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发表时间:
2023-03-01
期刊:
The EMBO journal
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其他
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核苷酸结合域富含亮氨酸重复序列(NLR)免疫受体是植物和后生动物先天免疫的重要组成部分,可以作为单个单位或成对或网络发挥作用。活化后,NLR形成称为抵抗体或炎性体的多蛋白复合物。虽然后生动物配对NLR,如NAIP/NLRC 4,在激活时形成杂合物,但支持植物配对NLR激活的分子机制,特别是它们是否在抗性体杂合物中缔合,是未知的。在植物中,细胞死亡所需的NLR(NRC)免疫受体网络由多个抗性蛋白传感器和下游助手组成,赋予对不同植物病原体的免疫力。在这里,我们表明病原体效应物激活NLR蛋白Rx(赋予病毒抗性)和Bs 2(赋予细菌抗性)导致其辅助NLR NRC 2的寡聚化。活化的Rx不寡聚化或与NRC 2寡聚体形成稳定的复合物,并保持在细胞质中。相比之下,活化的NRC 2寡聚体积聚在膜相关斑点中。我们提出了NRC免疫受体网络中NLR的激活和释放模型。这表明与哺乳动物配对NLR相比,有一种独特的激活模型。在感染后,植物NRC 2和NRC 4在质膜中形成抗性体复合物,其排除其活化的NRC依赖性传感器。
Nucleotide‐binding domain leucine‐rich repeat (NLR) immune receptors are important components of plant and metazoan innate immunity that can function as individual units or as pairs or networks. Upon activation, NLRs form multiprotein complexes termed resistosomes or inflammasomes. Although metazoan paired NLRs, such as NAIP/NLRC4, form hetero‐complexes upon activation, the molecular mechanisms underpinning activation of plant paired NLRs, especially whether they associate in resistosome hetero‐complexes, is unknown. In asterid plant species, the NLR required for cell death (NRC) immune receptor network is composed of multiple resistance protein sensors and downstream helpers that confer immunity against diverse plant pathogens. Here, we show that pathogen effector‐activation of the NLR proteins Rx (confers virus resistance), and Bs2 (confers bacterial resistance) leads to oligomerization of their helper NLR, NRC2. Activated Rx does not oligomerize or enter into a stable complex with the NRC2 oligomer and remains cytoplasmic. In contrast, activated NRC2 oligomers accumulate in membrane‐associated puncta. We propose an activation‐and‐release model for NLRs in the NRC immune receptor network. This points to a distinct activation model compared with mammalian paired NLRs. Upon infection, plant NRC2 and NRC4 form resistosome complexes in the plasma membrane which exclude their activated NRC‐dependent sensors.