Wen Li

Proanthocyanidins (PAs) display antioxidant properties and can partially delay pericarp browning in postharvested litchi (Litchi chinensis Sonn.) fruits. In this study, litchi fruit was treated with 3 g/L PA and then stored at 25 °C for 10 days. Differential metabolites and differentially expressed genes were comprehensively analyzed in litchi pericarp across four stages of browning progression. A total of 630 metabolites were identified through untargeted metabolomic analysis, with 237 of them being annotated in the kyoto encyclopedia of genes and genomes (KEGG) database. The abundance of flavonoids (kaempferol), six types of anthocyanins, cyanidins, (−)-epicatechin, and (+)-catechin in the PA biosynthetic pathway was notably reduced in PA-treated pericarp compared to that of the control fruit. Transcriptomic analysis also revealed that five genes in the phenylpropanoid biosynthesis pathways and seven genes of phenoloxidase were significantly downregulated. In addition, correlation analysis revealed significant positive correlations between the browning index and genes like LcFLS (flavonol synthase), LcANS (anthocyanidin synthase), LcUFGT (UDP-glucose:anthocyanidin 3-O-glucosyltransferase), LcPPO (polyphenol oxidase), and LcLAC7 (laccase), and a significant negative correlation with PAs and (−)-epicatechin. In conclusion, PA treatment can efficiently delay pericarp browning, mainly by reducing brown substrate accumulation and oxidation, and decreasing PA oxidation and polymerization. This study delves into the regulatory mechanisms through which PA delays litchi pericarp browning.

Anthocyanin accumulation is regulated by specific genes during fruit ripening. Currently, peel coloration of mango fruit in response to exogenous ethylene and the underlying molecular mechanism remain largely unknown. The role of MiMYB8 on suppressing peel coloration in postharvest ‘Guifei’ mango was investigated by physiology detection, RNA-seq, qRT-PCR, bioinformatics analysis, yeast one-hybrid, dual-luciferase reporter assay, and transient overexpression. Results showed that compared with the control, low concentration of exogenous ethylene (ETH, 500 mg·L⁻¹) significantly promoted peel coloration of mango fruit (cv. Guifei). However, a higher concentration of ETH (1000 mg·L⁻¹) suppressed color transformation, which is associated with higher chlorophyll content, lower a* value, anthocyanin content, and phenylalanine ammonia-lyase (PAL) activity of mango fruit. M. indica myeloblastosis8 MiMYB8 and MiPAL1 were differentially expressed during storage. MiMYB8 was highly similar to those found in other plant species related to anthocyanin biosynthesis and was located in the nucleus. MiMYB8 suppressed the transcription of MiPAL1 by binding directly to its promoter. Transient overexpression of MiMYB8 in tobacco leaves and mango fruit inhibited anthocyanin accumulation by decreasing PAL activity and down-regulating the gene expression. Our observations suggest that MiMYB8 may act as repressor of anthocyanin synthesis by negatively modulating the MiPAL gene during ripening of mango fruit, which provides us with a theoretical basis for the scientific use of exogenous ethylene in practice.

Inappropriate low temperatures can induce harmful effects on post-harvest papaya fruit, a phenomenon known as "chilling injury." This study aims to elucidate the role of CpCOR1, a gene encoding a cold-regulated protein, in the manifestation of low temperature-induced chilling injury in papaya fruit. Our results demonstrate that cold shock treatment (CST, 2 ℃ ice-water for 0.5 h) significantly reduced the chilling injury index (CII), concurrently preserving the cell microstructure and mitigating the increase in cell membrane permeability during both 5 ℃ and 25 ℃ storage. Transcriptome analysis and qRT-PCR revealed a substantial up-regulation of the CpCOR1 gene in CST papaya fruit compared to the control fruit. Furthermore, bioinformatics and phylogenetic tree analysis identified CpCOR1 as a basic hydrophobic protein with a coding sequence of 606 bp and an amino acid sequence of 201 aa, classifying it under the COR413 subgroup. Sub-cellular localization assays confirmed that CpCOR1 is primarily localized to the cell membrane. Moreover, overexpression of CpCOR1 in tobacco leaves and papaya fruit significantly alleviated chilling injury symptoms, suppressed yellowing, reduced malondialdehyde (MDA) accumulation, and maintained higher activities of antioxidant enzymes, including catalase (CAT) and ascorbate peroxidase (APX), compared to the control group. In summary, our findings suggest that cold shock treatment is an effective strategy to retard the onset of low-temperature damage, with CpCOR1 playing a pivotal role in enhancing cold resistance and delaying ripening by activating antioxidant activity in papaya fruit.