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A novel effector CfEC92 of Colletotrichum fructicola contributes to glomerella leaf spot virulence by suppressing plant defences at the early infection phase.
Molecular Plant Pathology ( IF 4.8 ) Pub Date : 2020-04-22 , DOI: 10.1111/mpp.12940 Shengping Shang 1 , Bo Wang 1 , Song Zhang 1 , Guangli Liu 1 , Xiaofei Liang 1 , Rong Zhang 1 , Mark L Gleason 2 , Guangyu Sun 1
Molecular Plant Pathology ( IF 4.8 ) Pub Date : 2020-04-22 , DOI: 10.1111/mpp.12940 Shengping Shang 1 , Bo Wang 1 , Song Zhang 1 , Guangli Liu 1 , Xiaofei Liang 1 , Rong Zhang 1 , Mark L Gleason 2 , Guangyu Sun 1
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The ascomycete fungus Colletotrichum fructicola causes diseases on a broad range of plant species. On susceptible cultivars of apple, it induces severe early defoliation and fruit spots, named glomerella leaf spot (GLS), but the mechanisms of pathogenicity have remained elusive. Phytopathogens exhibit small secreted effectors to advance host infection by manipulating host immune reactions. We report the identification and characterization of CfEC92, an effector required for C. fructicola virulence. CfEC92 is a Colletotrichum‐specific small secreted protein that suppresses BAX‐triggered cell death in Nicotiana benthamiana. Accumulation of the gene transcript was barely detectable in conidia or vegetative hyphae, but was highly up‐regulated in appressoria formed during early apple leaf infection. Gene deletion mutants were not affected in vegetative growth, appressorium formation, or appressorium‐mediated cellophane penetration. However, the mutants were significantly reduced in virulence toward apple leaves and fruits. Microscopic examination indicated that infection by the deletion mutants elicited elevated deposition of papillae at the penetration sites, and formation of infection vesicles and primary hyphae was retarded. Signal peptide activity, subcellular localization, and cell death‐suppressive activity (without signal peptide) assays suggest that CfEC92 could be secreted and perform virulence functions inside plant cells. RNA sequencing and quantitative reverse transcription PCR results confirmed that the deletion mutants triggered elevated host defence reactions. Our results strongly support the interpretation that CfEC92 contributes to C. fructicola virulence as a plant immunity suppressor at the early infection phase.
中文翻译：
果炭疽菌 (Colletotrichum fructicola) 的一种新型效应子 CfEC92 通过在感染早期抑制植物防御来增强肾小球叶斑病的毒力。
子囊菌Colletotrichum fructicola会引起多种植物疾病。在苹果的易感品种上，它会引起严重的早期落叶和果斑，称为肾小球叶斑病（GLS），但致病机制仍不清楚。植物病原体表现出小型分泌效应子，通过操纵宿主免疫反应来促进宿主感染。我们报告了 CfEC92 的鉴定和表征，CfEC92 是C. fructicola毒力所需的效应子。CfEC92 是一种炭疽菌特异性小分泌蛋白，可抑制本塞姆氏烟草中 BAX 触发的细胞死亡。该基因转录物的积累在分生孢子或营养菌丝中几乎检测不到，但在早期苹果叶感染期间形成的附着胞中高度上调。基因缺失突变体的营养生长、附着胞形成或附着胞介导的玻璃纸渗透不受影响。然而，突变体对苹果叶和果实的毒力显着降低。显微镜检查表明，缺失突变体的感染引起了渗透位点乳头沉积的增加，并且感染囊泡和初级菌丝的形成被延迟。信号肽活性、亚细胞定位和细胞死亡抑制活性（无信号肽）测定表明 CfEC92 可以在植物细胞内分泌并发挥毒力功能。RNA测序和定量逆转录PCR结果证实，缺失突变体引发了宿主防御反应的升高。我们的结果强烈支持这样的解释：CfEC92作为早期感染阶段的植物免疫抑制剂，有助于C. fructicola毒力。
更新日期：2020-04-22
中文翻译：
果炭疽菌 (Colletotrichum fructicola) 的一种新型效应子 CfEC92 通过在感染早期抑制植物防御来增强肾小球叶斑病的毒力。
子囊菌Colletotrichum fructicola会引起多种植物疾病。在苹果的易感品种上，它会引起严重的早期落叶和果斑，称为肾小球叶斑病（GLS），但致病机制仍不清楚。植物病原体表现出小型分泌效应子，通过操纵宿主免疫反应来促进宿主感染。我们报告了 CfEC92 的鉴定和表征，CfEC92 是C. fructicola毒力所需的效应子。CfEC92 是一种炭疽菌特异性小分泌蛋白，可抑制本塞姆氏烟草中 BAX 触发的细胞死亡。该基因转录物的积累在分生孢子或营养菌丝中几乎检测不到，但在早期苹果叶感染期间形成的附着胞中高度上调。基因缺失突变体的营养生长、附着胞形成或附着胞介导的玻璃纸渗透不受影响。然而，突变体对苹果叶和果实的毒力显着降低。显微镜检查表明，缺失突变体的感染引起了渗透位点乳头沉积的增加，并且感染囊泡和初级菌丝的形成被延迟。信号肽活性、亚细胞定位和细胞死亡抑制活性（无信号肽）测定表明 CfEC92 可以在植物细胞内分泌并发挥毒力功能。RNA测序和定量逆转录PCR结果证实，缺失突变体引发了宿主防御反应的升高。我们的结果强烈支持这样的解释：CfEC92作为早期感染阶段的植物免疫抑制剂，有助于C. fructicola毒力。
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