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TIR催化的ADP-核糖基化反应产生植物免疫的信号分子
作者:小柯机器人 发布时间:2022/7/10 14:36:54

清华大学柴继杰等研究人员合作发现,TIR催化的ADP-核糖基化反应产生植物免疫的信号分子。相关论文于2022年7月7日在线发表在《科学》杂志上。

研究人员表示,植物病原体激活的免疫信号由核苷酸结合的富含亮氨酸的重复(NLR)受体发出,该受体具有N端Toll/白细胞介素-1受体(TIR)结构域,汇聚于Enhanced Disease Susceptibility 1 (EDS1)及其直接伙伴Phytoalexin Deficient 4(PAD4)或Senescence-Associated Gene 101(SAG101)。TIR编码的NAD酶产生信号分子,促进EDS1-PAD4和EDS1-SAG101与辅助NLR亚类的专有相互作用。

研究人员发现,含有TIR的蛋白质通过ADPR聚合酶样和NAD酶的活性催化二磷酸腺苷(ADP)-三磷酸腺苷(ATP)和ADP核糖(ADPR)的核糖基化,分别形成ADP-核糖基化ATP(ADPr-ATP)和ADPr-ADPR(di-ADPR)。ADPr-ATP或di-ADPR的特异性结合在体外和平面上促进EDS1-SAG101与辅助NLR N requirement gene 1A(NRG1A)的相互作用。这些数据揭示了TIR的一种酶活性,使EDS1-SAG101-NRG1免疫分支得到特异性激活。

附:英文原文

Title: TIR-catalyzed ADP-ribosylation reactions produce signaling molecules for plant immunity

Author: Aolin Jia, Shijia Huang, Wen Song, Junli Wang, Yonggang Meng, Yue Sun, Lina Xu, Henriette Laessle, Jan Jirschitzka, Jiao Hou, Tiantian Zhang, Wenquan Yu, Giuliana Hessler, Ertong Li, Shoucai Ma, Dongli Yu, Jan Gebauer, Ulrich Baumann, Xiaohui Liu, Zhifu Han, Junbiao Chang, Jane E. Parker, Jijie Chai

Issue&Volume: 2022-07-07

Abstract: Plant pathogen-activated immune signaling by nucleotide-binding leucine-rich repeat (NLR) receptors with an N-terminal Toll/Interleukin-1 receptor (TIR) domain converges on Enhanced Disease Susceptibility 1 (EDS1) and its direct partners Phytoalexin Deficient 4 (PAD4) or Senescence-Associated Gene 101 (SAG101). TIR-encoded NADases produce signaling molecules to promote exclusive EDS1-PAD4 and EDS1-SAG101 interactions with helper NLR sub-classes. Here we show that TIR-containing proteins catalyze adenosine diphosphate (ADP)-ribosylation of adenosine triphosphate (ATP) and ADP ribose (ADPR) via ADPR polymerase-like and NADase activity, forming ADP-ribosylated ATP (ADPr-ATP) and ADPr-ADPR (di-ADPR), respectively. Specific binding of ADPr-ATP or di-ADPR allosterically promotes EDS1-SAG101 interaction with helper NLR N requirement gene 1A (NRG1A) in vitro and in planta. Our data reveal an enzymatic activity of TIRs that enables specific activation of the EDS1-SAG101-NRG1 immunity branch.

DOI: abq8180

Source: https://www.science.org/doi/10.1126/science.abq8180

 

期刊信息
Science:《科学》,创刊于1880年。隶属于美国科学促进会,最新IF:41.037