Verticillium dahliae secretory effector PevD1 induces leaf senescence by promoting ORE1-mediated ethylene biosynthesis.

Verticillium dahliae secretory effector PevD1 induces leaf senescence by promoting ORE1-mediated ethylene biosynthesis.
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大丽黄萎病分泌效应子 PevD1 通过促进 ORE1 介导的乙烯生物合成来诱导叶片衰老。

DOI:
10.1016/j.molp.2021.07.014
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发表时间:
2021-07
期刊:
影响因子:
27.5
通讯作者:
Guo Hongwei
Guo Hongwei
中科院分区:
生物学1区
文献类型:
--
作者:
Zhang Yi;Gao Yuhan;Wang Hou-Ling;Kan Chengcheng;Li Ze;Yang Xiufen;Yin Weilun;Xia Xinli;Nam Hong Gil;Li Zhonghai;Guo Hongwei

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叶片衰老是叶片发育的最后阶段,受许多内部和环境信号的影响。然而,生物胁迫,如病原菌感染如何调节叶片衰老仍不清楚。在本研究中,我们发现,由土传维管真菌大丽轮枝菌(Verticillium dahliae)引起的叶片早衰抑制作用可被来自大丽轮枝菌1(V.dahliae1)的一种名为PevD 1的蛋白激发子破坏。组成型或诱导型PevD 1过表达可加速紫茎泽兰叶片衰老。有趣的是,衰老相关的NAC转录因子ORE 1被PevD 1靶向。PevD 1可以通过破坏ORE 1蛋白与RING型泛素E3连接酶NLA的相互作用而与ORE 1蛋白相互作用并稳定ORE 1蛋白。ORE 1的突变抑制了PevD 1过表达引起的叶片早衰,而ORE 1或PevD 1的过表达则导致乙烯产生增加,从而导致叶片衰老。我们发现ORE 1直接结合ACS 6的启动子并促进其表达,从而介导PevD 1诱导的乙烯生物合成。在ORE 1过表达植物中,ACS功能的丧失可以抑制大丽轮枝菌诱导的叶片衰老。此外,我们发现PevD 1还与陆地棉ORE 1(Gossypium hirsutum ORE 1,GhORE 1)相互作用,并且病毒诱导的GhORE 1基因沉默能够延缓大丽轮枝菌引发的棉花叶片衰老,这表明PevD 1在植物中可能具有保守的机制。综上所述,这些结果表明,大丽轮枝菌通过分泌效应子PevD 1来操纵ORE 1-ACS 6级联反应诱导叶片衰老,为生物胁迫诱导的植物衰老提供了新的见解。
Leaf senescence, the final stage of leaf development, is influenced by numerous internal and environmental signals. However, how biotic stresses such as pathogen infection regulate leaf senescence remains largely unclear. In this study, we found that the premature leaf senescence inArabidopsiscaused by the soil-borne vascular fungusVerticillium dahliaewas impaired by disruption of a protein elicitor fromV. dahliae1 named PevD1. Constitutive or inducible overexpression ofPevD1acceleratedArabidopsisleaf senescence. Interestingly, a senescence-associated NAC transcription factor, ORE1, was targeted by PevD1. PevD1 could interact with and stabilize ORE1 protein by disrupting its interaction with the RING-type ubiquitin E3 ligase NLA. Mutation ofORE1suppressed the premature senescence caused by overexpressingPevD1, whereas overexpression ofORE1orPevD1led to enhanced ethylene production and thereby leaf senescence. We showed that ORE1 directly binds the promoter ofACS6and promotes its expression for mediating PevD1-induced ethylene biosynthesis. Loss-of-function ofACSscould suppressV. dahliae–induced leaf senescence inORE1-overexpressing plants. Furthermore, we found thatPevD1 also interacts withGossypium hirsutumORE1 (GhORE1) and that virus-induced gene silencing ofGhORE1delaysV. dahliae–triggered leaf senescence in cotton, indicating a possibly conserved mechanism in plants. Taken together, these results suggest thatV. dahliaeinduces leaf senescence by secreting the effector PevD1 to manipulate the ORE1-ACS6 cascade, providing new insights into biotic stress-induced senescence in plants.
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