An effector of Erysiphe necator translocates to chloroplasts and plasma membrane to suppress host immunity in grapevine.
An effector of Erysiphe necator translocates to chloroplasts and plasma membrane to suppress host immunity in grapevine.
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DOI：
10.1093/hr/uhad163
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发表时间：
2023-09
影响因子：
8.7
通讯作者：
中科院分区：
文献类型：
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白粉病（Erysiphe necator）是一种阻碍葡萄园葡萄树生长的常见病原体。线虫基因组中编码了一系列候选分泌效应蛋白（CSEP），但目前尚不清楚 CSEP 在线虫感染过程中发挥什么作用。在本研究中，我们鉴定了E. necator的分泌效应子CSEP080，其位于植物叶绿体和质膜中。瞬时表达 CSEP080 促进植物光合作用并抑制 INF1 诱导的烟叶细胞死亡。我们发现CSEP080是E. necator致病性的必要效应子，它与葡萄叶绿体蛋白VviB6f（细胞色素b6-f复合铁硫亚基）相互作用，影响植物光合作用。瞬时沉默 VviB6f 增加了植物过氧化氢的产生，以及植物对白粉病的抵抗力。此外，CSEP080 操纵 VviPE（果胶酯酶）来促进果胶降解。我们的结果证明了线虫效应子易位到宿主叶绿体和质膜的分子机制，通过靶向叶绿体蛋白 VviB6f 抑制过氧化氢积累并操纵 VviPE 促进果胶降解，从而抑制葡萄免疫系统。
The powdery mildew (Erysiphe necator) is a prevalent pathogen hampering grapevine growth in the vineyard. An arsenal of candidate secreted effector proteins (CSEPs) was encoded in the E. necator genome, but it is largely unclear what role CSEPs plays during the E. necator infection. In the present study, we identified a secreted effector CSEP080 of E. necator, which was located in plant chloroplasts and plasma membrane. Transient expressing CSEP080 promotes plant photosynthesis and inhibits INF1-induced cell death in tobacco leaves. We found that CSEP080 was a necessary effector for the E. necator pathogenicity, which interacted with grapevine chloroplast protein VviB6f (cytochrome b6-f complex iron–sulfur subunit), affecting plant photosynthesis. Transient silencing VviB6f increased the plant hydrogen peroxide production, and the plant resistance to powdery mildew. In addition, CSEP080 manipulated the VviPE (pectinesterase) to promote pectin degradation. Our results demonstrated the molecular mechanisms that an effector of E. necator translocates to host chloroplasts and plasma membrane, which suppresses with the grapevine immunity system by targeting the chloroplast protein VviB6f to suppress hydrogen peroxide accumulation and manipulating VviPE to promote pectin degradation.
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