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柠檬锌指蛋白ClSUP通过与ClDOF3.4相互作用诱导活性氧积累并抑制柑橘黄脉明病毒感染。

Lemon zinc finger protein ClSUP induces accumulation of reactive oxygen species and inhibits citrus yellow vein-clearing virus infection via interactions with ClDOF3.4.

作者信息

Liao Ping, Zeng Ting, Chen Yuan, Ding Dong-Dong, Zhou Chang-Yong, Zhou Yan

机构信息

Integrative Science Center of Germplasm Creation in Western China (CHONGQING) Science City, Citrus Research Institute, Southwest University/ National Citrus Engineering and Technology Research Center, Citrus Research Institute, Southwest University, Chongqing, 400712, P.R. China.

出版信息

J Exp Bot. 2024 Dec 4;75(22):7300-7316. doi: 10.1093/jxb/erae361.

DOI:10.1093/jxb/erae361
PMID:39185708
Abstract

Citrus yellow vein-clearing virus (Potexvirus citriflavivenae; CYVCV) is an increasing threat to citrus cultivation. Notably, the role of zinc finger proteins (ZFPs) in mediating viral resistance in citrus plants is unclear. In this study, we demonstrated that ZFPs ClSUP and ClDOF3.4 enhanced citrus defense responses against CYVCV in Eureka lemon (Citrus limon 'Eureka'). ClSUP interacted with the coat protein (CP) of CYVCV to reduce CP accumulation and inhibited its silencing suppressor function. Overexpression of CISUP triggered reactive oxygen species (ROS) and salicylic acid (SA) pathways, and enhanced resistance to CYVCV infection. In contrast, ClSUP silencing resulted in increased CP accumulation and down-regulated ROS and SA-related genes. ClDOF3.4 interacted with ClSUP to facilitate its interactions with CP. Furthermore, ClDOF3.4 synergistically regulated the accumulation of ROS and SA with ClSUP and accelerated down-regulation of CP accumulation. Transgenic plants co-expressing ClSUP and ClDOF3.4 significantly decreased the CYVCV. These findings provide a new reference for understanding the interaction mechanism between the host and CYVCV.

摘要

柑橘黄脉明脉病毒(马铃薯X病毒属柑橘黄脉明脉病毒;CYVCV)对柑橘种植的威胁日益增大。值得注意的是,锌指蛋白(ZFPs)在介导柑橘类植物抗病毒抗性中的作用尚不清楚。在本研究中,我们证明了锌指蛋白ClSUP和ClDOF3.4增强了尤力克柠檬(Citrus limon 'Eureka')对CYVCV的防御反应。ClSUP与CYVCV的外壳蛋白(CP)相互作用,以减少CP积累并抑制其沉默抑制子功能。CISUP的过表达触发了活性氧(ROS)和水杨酸(SA)途径,并增强了对CYVCV感染的抗性。相反,ClSUP沉默导致CP积累增加,并下调了ROS和SA相关基因。ClDOF3.4与ClSUP相互作用,以促进其与CP的相互作用。此外,ClDOF3.4与ClSUP协同调节ROS和SA的积累,并加速CP积累的下调。共表达ClSUP和ClDOF3.4的转基因植物显著降低了CYVCV。这些发现为理解宿主与CYVCV之间的相互作用机制提供了新的参考。