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在Arabidopsis exo70B1突变物中,CAMTA3抑制器的破坏稳定触发了TIR域蛋白TN2介导的自身免疫

Na Liu^1,2, Xiyuan Jiang³, Guitao Zhong^1,4

¹State Key Laboratory of Ecological Control of Fujian-Taiwan Crop Pests, Key Laboratory of Ministry of Education for Genetics, Breeding and Multiple Utilization of Crops, Plant Immunity Center, Fujian Agriculture and Forestry University, Fuzhou 350002, China.

|February 3, 2024

概括

取决于的蛋白激酶 (CPK) 调节植物免疫力. 在Arabidopsis中,CPK5与TN2相互作用,触发免疫力和酸化CAMTA3,导致其降解和免疫激活.

科学领域:

植物分子生物学植物分子生物学
植物免疫信号传递.

背景情况:

取决于的蛋白激酶 (CPK) 对于将信号转化为植物免疫反应至关重要.
外囊子单元基因EXO70B1突变导致了依赖CPK5和TIR-NBS2 (TN2) 的自身免疫.
CPK5和TN2之间的相互作用稳定了CPK5的活动,但下游信号仍然不清楚.

研究的目的:

为了阐明由Arabidopsis thaliana中CPK5-TN2相互作用启动的下游信号通路.
研究CPK5在调节芽素结合转录激活剂3 (CAMTA3) 的作用.
为了发现负责EXO70B1介导自身免疫的信号模块.

主要方法:

研究了CPK5和TN2之间的蛋白质-蛋白质相互作用.
在各种突变背景 (cpk5, exo70B1) 中分析了CAMTA3的酸化和降解.
利用功能增益变体 (CAMTA3A855V) 来评估免疫表型的救援.

主要成果:

在exo70B1突变体中,CPK5和TN2之间的物理相互作用会触发免疫激活.
在S964处,CPK5直接化CAMTA3,促进其不稳定.
一种功能增强的CAMTA3变体抵抗CPK5诱导的降解,拯救了免疫力.
通过CPK5介导的免疫包括CAMTA3通过酸化和/或calmodulin调节的降解.
在camta3突变体中的自身免疫部分需要功能CPK5.5.

结论:

一个TN2-CPK5-CAMTA3信号模块调解了Arabidopsis中的EXO70B1诱导的自身免疫.
CPK5充当感应解码器,将其功能嵌入到电阻信号体中.
由CPK5驱动的CAMTA3降解是植物免疫的一个关键执行步骤.

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