Antifungal mechanism of (E)-2-hexenal against Botrytis cinerea growth revealed by transcriptome analysis

Abstract

Gray mold caused by Botrytis cinerea, a necrotrophic plant pathogen, is one of the most damaging diseases of tomato, resulting in both pre- and post-harvest losses. (E)-2-Hexenal dose-dependently inhibited the mycelial growth of B. cinerea, and caused distortion of mycelia and loss of the cytoplasm content, thus altering the morphology of B. cinerea hyphae. To understand molecular processes in response to (E)-2-hexenal, transcriptome sequencing was carried out using RNA-Seq technology. RNA-Seq results revealed that a total of 3,893 genes were differentially expressed in B. cinerea samples treated with (E)-2-hexenal fumigation. Among these genes, 1,949 were upregulated and 1,944 were downregulated. Moreover, further analysis results showed 2,113 unigenes were mapped onto 259 pathways in Kyoto Encyclopedia of Genes and Genomes (KEGG). Moreover, (E)-2-hexenal stress affected the expression of genes involved in the pathways of cell wall, cell membrane, and energy metabolism. KEGG pathway analysis showed that the terpenoid backbone biosynthesis and steroid biosynthesis were the most enriched in ergosterol biosynthetic process transcriptome data. Particularly, (E)-2-hexenal fumigation had influenced ergosterol biosynthetic gene expression levels (e.g., ERG1, ERG3, ERG4, ERG7, ERG12, ERG13, ERG24, ERG25, ERG26, and ERG27), which were in good agreement with the experimental measurement results, and the ergosterol content decreased. Collectively, the results of this study increase our current understanding of (E)-2-hexenal inhibition mechanisms in B. cinerea and provide relevant information on postharvest shelf life extension and preservation of fruits and vegetables.