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研究揭示TIR催化的小分子在植物免疫中的识别和受体机制
作者:小柯机器人 发布时间:2022/7/10 14:37:50

清华大学柴继杰等研究人员合作揭示TIR催化的小分子在植物免疫中的识别和受体机制。该项研究成果于2022年7月7日在线发表在《科学》杂志上。

据研究人员介绍,具有N端Toll/白细胞介素-1受体(TIR)结构域的植物核苷酸结合的富含白细胞重复的(NLR)受体感知病原体效应物,使TIR编码的NAD酶活性用于免疫信号传递。TIR-NLR信号传导需要辅助NLR N requirement gene 1(NRG1)和Activated Disease Resistance 1(ADR1),以及Enhanced Disease Susceptibility 1(EDS1),该基因与它的每个旁系同源物Phytoalexin Deficient 4(PAD4)和Senescence-Associated Gene101(SAG101)形成一个异质二聚体。

研究人员发现,含有TIR的蛋白在体外和植物体中催化2'-(5′'-磷酰)-5′-腺苷单/二-磷酸(pRib-AMP/ADP)的产生。生物化学和结构数据表明,EDS1-PAD4是pRib-AMP/ADP的受体复合物,它易购地促进EDS1-PAD4与ADR1-L1的相互作用,但不是NRG1A。这项研究发现,TIR催化的pRib-AMP/ADP是通过EDS1-PAD4的TIR信号传递中的一个缺失环节,并可能是植物免疫的第二信使。

附:英文原文

Author: Shijia Huang, Aolin Jia, Wen Song, Giuliana Hessler, Yonggang Meng, Yue Sun, Lina Xu, Henriette Laessle, Jan Jirschitzka, Shoucai Ma, Yu Xiao, Dongli Yu, Jiao Hou, Ruiqi Liu, Huanhuan Sun, Xiaohui Liu, Zhifu Han, Junbiao Chang, Jane E. Parker, Jijie Chai

Issue&Volume: 2022-07-07

Abstract: Plant nucleotide-binding leucine-rich repeat-containing (NLR) receptors with an N-terminal Toll/interleukin-1 receptor (TIR) domain sense pathogen effectors to enable TIR-encoded NADase activity for immune signaling. TIR-NLR signaling requires helper NLRs N requirement gene 1 (NRG1) and Activated Disease Resistance 1 (ADR1), and Enhanced Disease Susceptibility 1 (EDS1) that forms a heterodimer with each of its paralogs Phytoalexin Deficient 4 (PAD4) and Senescence-Associated Gene101 (SAG101). Here, we show that TIR-containing proteins catalyze production of 2'-(5′'-phosphoribosyl)-5′-adenosine mono-/di-phosphate (pRib-AMP/ADP) in vitro and in planta. Biochemical and structural data demonstrate that EDS1-PAD4 is a receptor complex for pRib-AMP/ADP, which allosterically promote EDS1-PAD4 interaction with ADR1-L1 but not NRG1A. Our study identifies TIR-catalyzed pRib-AMP/ADP as a missing link in TIR signaling via EDS1-PAD4 and as likely second messengers for plant immunity.

DOI: abq3297

Source: https://www.science.org/doi/10.1126/science.abq3297

 

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