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Transformation‐based gene silencing and functional characterization of an ISC effector reveal how a powdery mildew fungus disturbs salicylic acid biosynthesis and immune response in the plant

白粉病 生物 效应器 烟草 水杨酸 拟南芥 拟南芥 寄主(生物学) 转化(遗传学) 植物对草食的防御 转基因作物 微生物学 植物 细胞生物学 转基因 基因 生物化学 遗传学 突变体
作者
Jinyao Yin,Xiao Li,Longying Dong,Xuehuan Zhu,Yalong Chen,Wenyuan Zhao,Yuhan Liu,Jiaxin Shan,Wenbo Liu,Chunhua Lin,Weiguo Miao
出处
期刊:Molecular Plant Pathology [Wiley]
卷期号:25 (11): e70030-e70030 被引量:2
标识
DOI:10.1111/mpp.70030
摘要

Abstract Obligate biotrophic powdery mildew fungi infect a wide range of economically important plants. These fungi often deliver effector proteins into the host tissues to suppress plant immunity and sustain infection. The phytohormone salicylic acid (SA) is one of the most important signals that activate plant immunity against pathogens. However, how powdery mildew effectors interact with host SA signalling is poorly understood. Isochorismatase (ISC) effectors from two other filamentous pathogens have been found to inhibit host SA biosynthesis by hydrolysing isochorismate, the main SA precursor in the plant cytosol. Here, we identified an ISC effector, named EqIsc1, from the rubber tree powdery mildew fungus Erysiphe quercicola . In ISC enzyme assays, EqIsc1 displayed ISC activity by transferring isochorismate to 2,3‐dihydro‐2,3‐dihydroxybenzoate in vitro and in transgenic Nicotiana benthamiana plants. In EqIsc1‐expressing transgenic Arabidopsis thaliana , SA biosynthesis and SA‐mediated immune response were significantly inhibited. In addition, we developed an electroporation‐mediated transformation method for the genetic manipulation of E. quercicola . Inoculation of rubber tree leaves with EqIsc1 ‐silenced E. quercicola strain induced SA‐mediated immunity. We also detected the translocation of EqIsc1 into the plant cytosol during the interaction between E. quercicola and its host. Taken together, our results suggest that a powdery mildew effector functions as an ISC enzyme to hydrolyse isochorismate in the host cytosol, altering the SA biosynthesis and immune response.
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