Abstract：
The marine antifungal peptide epinecidin-1 (EPI) have been shown to inhibit Botrytis cinerea growth, while the molecular mechanism have not been explored based on omics technology. This study aimed to investigate the molecular mechanism of EPI against B. cinerea by transcriptome technology. Our findings indicated that a total of 1671 differentially expressed genes (DEGs) were detected in the mycelium of B. cinerea treated with 12.5 μmol/L EPI for 3 h, including 773 up-regulated genes and 898 down-regulated genes. Cluster analysis showed that DEGs (including steroid biosynthesis, (unsaturated) fatty acid biosynthesis) related to cell membrane metabolism were significantly down-regulated, and almost all DEGs involved in DNA replication were significantly inhibited. In addition, it also induced the activation of stress-related pathways, such as the antioxidant system, ATP-binding cassette transporter (ABC) and MAPK signaling pathways, and interfered with the tricarboxylic acid (TCA) cycle and oxidative phosphorylation pathways related to mitochondrial function. The decrease of mitochondrial related enzyme activities (succinate dehydrogenase, malate dehydrogenase and adenosine triphosphatase), the decrease of mitochondrial membrane potential and the increase content of hydrogen peroxide further confirmed that EPI treatment may lead to mitochondrial dysfunction and oxidative stress. Based on this, we speculated that EPI may impede the growth of B. cinerea through its influence on gene expression, and may lead to mitochondrial dysfunction and oxidative stress.
摘要：
海洋抗真菌肽epinecidin-1（EPI）已被证明可以抑制灰霉病的生长，而分子机制尚未基于组学技术进行探索。本研究旨在通过转录组技术探讨EPI抗灰霉病的分子机制。我们的发现表明，在用12.5μmol/LEPI处理3h的灰霉病菌菌丝体中检测到总共1671个差异表达基因（DEGs），包括773个上调基因和898个下调基因。聚类分析表明，DEGs(包括类固醇生物合成，（不饱和）脂肪酸生物合成）与细胞膜代谢有关的显著下调，几乎所有参与DNA复制的DEGs都被显著抑制。此外,它还诱导了应激相关途径的激活，比如抗氧化系统，ATP结合盒转运蛋白（ABC）和MAPK信号通路，并干扰与线粒体功能相关的三羧酸（TCA）循环和氧化磷酸化途径。线粒体相关酶活性的降低（琥珀酸脱氢酶，苹果酸脱氢酶和腺苷三磷酸酶），线粒体膜电位的降低和过氧化氢含量的增加进一步证实了EPI治疗可能导致线粒体功能障碍和氧化应激。基于此,我们推测EPI可能通过其对基因表达的影响来阻碍灰霉病的生长，并可能导致线粒体功能障碍和氧化应激。
