Fujian Key Laboratory on Conservation and Sustainable Utilization of Marine Biodiversity, Fuzhou Institute of Oceanography, College of Geography and Oceanography, Minjiang University, Fuzhou, 350108, China.
Department of Environmental Horticulture, Mid-Florida Research and Education Center, Institute of Food and Agricultural Sciences, University of Florida, Apopka, FL, United States.
Plant Physiol Biochem. 2024 Oct;215:108851. doi: 10.1016/j.plaphy.2024.108851. Epub 2024 Jun 16.
Grape ripe rot is one of the most important diseases caused by Colletotrichum spp. Chinese wild grape (Vitis davidii) is highly resistant to Colletotrichum viniferum infection. But mechanisms underlying the resistance remain largely unclear. In this study, transcriptomic and metabolomic responses of V. davidii to C. viniferum were studied before and after 1, 2, 4, and 6 days of inoculation. C. viniferum infection induced the expression of a large number of defense-related genes. KEGG analysis indicated that the differentially expressed genes (DEGs) were largely those involved in alpha-linolenic acid metabolism, flavonoid biosynthesis, phenylpropanoid biosynthesis, stilbenoid biosynthesis, and other defense-related metabolic pathways. Based on transcriptome data and experimental analysis, we found that jasmonic acid (JA) biosynthesis was closely related to V. davidii resistance to C. viniferum. In addition, many genes related to the synthesis of lignin and phytoalexin resveratrol are upregulated by pathogen infection, and metabolomic analysis showed that there was an increasing accumulation of resveratrol on day 6 of C. viniferum inoculation. Further analysis indicated that transcription factors, such as VdWRKY75 regulated the biosynthesis of lignin and stilbenes. A working model for V. davidii against C. viniferum infection was proposed. The infection of C. viniferum induced JA production, JA along with transcription factors regulated the biosynthesis of secondary metabolites, such as lignin and resveratrol that enhanced plant resistance to C. viniferum. This study elucidated molecular mechanisms underlying the resistance of Chinese wild V. davidii to C. viniferum which can provide a theoretical basis for grape disease resistance breeding.
葡萄成熟腐烂是由炭疽菌引起的最重要的病害之一。中国野生葡萄（Vitis davidii）对葡萄炭疽菌感染具有高度抗性。但抗性的机制在很大程度上仍不清楚。在这项研究中，研究了 V. davidii 在接种后 1、2、4 和 6 天对 C. viniferum 的转录组和代谢组反应。C. viniferum 感染诱导了大量防御相关基因的表达。KEGG 分析表明，差异表达基因（DEGs）主要涉及α-亚麻酸代谢、类黄酮生物合成、苯丙素生物合成、芪类生物合成和其他防御相关代谢途径。基于转录组数据和实验分析，我们发现茉莉酸（JA）生物合成与 V. davidii 对 C. viniferum 的抗性密切相关。此外，许多与木质素和植物抗毒素白藜芦醇合成有关的基因在病原体感染后上调，代谢组学分析表明，在接种 C. viniferum 后第 6 天，白藜芦醇的积累量增加。进一步分析表明，转录因子如 VdWRKY75 调节木质素和芪类的生物合成。提出了 V. davidii 对 C. viniferum 感染的作用模型。C. viniferum 的感染诱导 JA 的产生，JA 与转录因子一起调节木质素和白藜芦醇等次生代谢物的生物合成，从而增强植物对 C. viniferum 的抗性。本研究阐明了中国野生 V. davidii 对 C. viniferum 抗性的分子机制，可为葡萄抗病性育种提供理论依据。
