Physiological biochemistry and multi-omics reveal the underlying mechanism of citral in controlling Colletotrichum scovillei in postharvest chili

Colletotrichum scovillei is the dominant pathogen in postharvest chili. Citral (CI) exhibits extensive inhibitory effects on pathogenic fungi, but the effect on C. scovillei is still unclear. This study suggested that CI inhibited C. scovillei mycelial growth with minimum inhibitory concentration (MIC) 0.30 mg/mL and spore germination at 44.79 +/- 1.40%. Physiological biochemistry studies demonstrated that CI destroyed spore cell wall and membrane integrity in a dose-dependent. Transcriptome and metabolome combined analysis suggested that MIC CI inhibited chitin synthesis by down-regulated the expression of five chitin synthetase genes (CHS1-1, CHS1-2, CHS1-3, CHS1-4, CHS1-5) and up-regulated the expression of four chitinase genes (CTS-1, CTS-2, CTS-3, CTS5), and also inhibited ergosterol synthesis by down-regulated the expression of ERG1, ERG3, ERG24-1, ERG24-2, ERG24-3 genes and up-regulated the expression of ERG4, ERG6-1, ERG6-2, ERG25-1, ERG26, ERG27 genes, resulting in the increase of substrate UDP-N-Acetylglucosamine (UDP-GlcNAc) content and the decrease of ergosterol content, respectively. Furthermore, CI fumigation induced resistance of chili against C. scovillei by increasing the activities of antioxidant enzymes (CAT, SOD, POD, APX), and the incidence of postharvest chili was significantly decreased by 30.61% and 32.14% in MIC and 2 x MIC CI treatment groups, respectively. This study provided technical support for CI application as chili postharvest preservative.