Cotton 4‐coumarate‐CoA ligase 3 enhanced plant resistance to Verticillium dahliae by promoting jasmonic acid signaling‐mediated vascular lignification and metabolic flux

大丽花黄萎病 生物 生物化学 肉桂酸 茉莉酸 茉莉酸 植保素 化学 水杨酸 植物 拟南芥 突变体 基因 白藜芦醇
作者
Muna Alariqi,Mohamed Ramadan,Qiongqiong Wang,Ziyi Yang,Hui Xi,Xiaoqin Nie,Amani Mohedein Mohammed Ahmed,Qiansi Chen,Wang Yan-yin,Longfu Zhu,Xianlong Zhang,Shuangxia Jin
出处
期刊:Plant Journal [Wiley]
卷期号:115 (1): 190-204 被引量:9
标识
DOI:10.1111/tpj.16223
摘要

Lignins and their antimicrobial-related polymers cooperatively enhance plant resistance to pathogens. Several isoforms of 4-coumarate-coenzyme A ligases (4CLs) have been identified as indispensable enzymes involved in lignin and flavonoid biosynthetic pathways. However, their roles in plant-pathogen interaction are still poorly understood. This study uncovers the role of Gh4CL3 in cotton resistance to the vascular pathogen Verticillium dahliae. The cotton 4CL3-CRISPR/Cas9 mutant (CR4cl) exhibited high susceptibility to V. dahliae. This susceptibility was most probably due to the reduction in the total lignin content and the biosynthesis of several phenolic metabolites, e.g., rutin, catechin, scopoletin glucoside, and chlorogenic acid, along with jasmonic acid (JA) attenuation. These changes were coupled with a significant reduction in 4CL activity toward p-coumaric acid substrate, and it is likely that recombinant Gh4CL3 could specifically catalyze p-coumaric acid to form p-coumaroyl-coenzyme A. Thus, overexpression of Gh4CL3 (OE4CL) showed increasing 4CL activity that augmented phenolic precursors, cinnamic, p-coumaric, and sinapic acids, channeling into lignin and flavonoid biosyntheses and enhanced resistance to V. dahliae. Besides, Gh4CL3 overexpression activated JA signaling that instantly stimulated lignin deposition and metabolic flux in response to pathogen, which all established an efficient plant defense response system, and inhibited V. dahliae mycelium growth. Our results propose that Gh4CL3 acts as a positive regulator for cotton resistance against V. dahliae by promoting JA signaling-mediated enhanced cell wall rigidity and metabolic flux.
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