疫病疫霉菌
茉莉酸
效应器
植物免疫
植物
免疫
生物
生物合成
疫霉菌
细胞生物学
免疫学
生物化学
免疫系统
枯萎病
基因
拟南芥
突变体
作者
Hongyang Wang,Di Zhao,Wei Ji,Yumeng Xiong,Shengnan Chen,Jing Liu,Liu Zeng,Juan Du,Canhui Li
标识
DOI:10.1016/j.scienta.2024.113122
摘要
P. infestans, the causative agent of the most destructive potato disease, significantly diminishes crop yields. The pathogen's RXLR effector, PiAVR3b, dampens pattern-triggered immunity (PTI) and mitigates cell necrosis caused by other effectors, thus playing a pivotal role in P. infestans infection. The mechanism by which PiAVR3b undermines plant defenses, however, has remained obscure. Our research establishes that PiAVR3b's transient expression promotes P. infestans colonization in Nicotiana benthamiana and that PiAVR3b-transgenic potato lines show reduced PTI to flg22 and heightened susceptibility to P. infestans. Transcriptomic analysis indicate that PiAVR3b expression downregulates genes associated with phenylpropanoid, monoterpenoid biosynthesis, and phenylalanine, alpha-linolenic acid metabolism, leading to a substantial reduction in jasmonic acid (JA) synthesis. Moreover, application of methyl jasmonate (MeJA) on both wild-type and transgenic lines bolsters resistance to P. infestans and activates JA signaling pathways. Our findings reveal that PiAVR3b is a virulence factor that compromises JA-mediated defense, thus facilitating P. infestans invasion.
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