Transcriptomic and metabolomic analysis reveal the role of 5-aminolevulinic acid hydrochloride in suppressing postharvest decay development in sweet cherry

Abstract

The development of fungal rots is one of the main limitations of the storage and marketing of sweet cherry fruit. Sweet cherry (Prunus avium L.) var ‘Xiangquan No.1’ fruit were treated with 1 g L⁻¹ 5-aminolevulinic acid (5-ALA) hydrochloride and stored at 20 °C for 12 d. Results showed that fruit treated with 5-ALA hydrochloride had significantly lowered postharvest decay. Transcriptomic and metabolomic analysis indicated that 1031 differentially accumulated metabolites (DAMs) and 6903 differentially expressed genes (DEGs) were detected between 5-ALA hydrochloride treatment and the control at 6 d. A weighted gene co-correlation network analysis was employed to evaluate the gene regulatory network of DEGs. The DEGs and DAMs were co-enriched in the phenylpropanoid biosynthesis and flavonoid biosynthesis pathways. Moreover, the 5-ALA hydrochloride treatment improved disease resistance of the fruit by activating genes related to salicylic acid signal transduction and down-regulation of the metabolite gibberellin in sweet cherry fruit. The multiple transcription factors, including NAC50, MYB62, LEP and WRKY40 were also activated by 5-ALA hydrochloride treatment. These results provided new ideas for research on the postharvest management and maintenance of sweet cherry fruit during storage.