Laifeng Lu

Niacin contents vary significantly among fresh-cut potato cultivars with different browning sensitivities, whereas its role as a browning inhibitor for fresh-cut produce has not been previously reported. In this study, potato slices were soaked in distilled water (control) or 1% food-grade niacin solution for 5 min, then stored at 4 ± 1 °C for 8 days with sampling every 2 days for physiological and molecular analyses. In particular, the optimal niacin (1%) treatment showed higher brightness and lower color change than the control. The activities of polyphenol oxidase (PPO), peroxidase (POD), and phenylalanine ammonia lyase (PAL), and phenol content were reduced. Higher activities of superoxide dismutase (SOD) and catalase (CAT), and greater glutathione accumulation, were observed following niacin treatment. Meanwhile, lower levels of malondialdehyde and reactive oxygen species (ROS), and lower nicotinamide adenine dinucleotide phosphate oxidase (NOX) activity, indicated lower oxidant damage. The contents of NADP and NAD, and activities of nicotinamide adenine dinucleotide kinase (NADK) and glucose-6-phosphate dehydrogenase (G6PDH) were improved. Furthermore, the gene expression patterns of StRBOH, StPPO, and StG6PDH also supported the hypothesis that niacin regulates pyridine nucleotide and ROS homeostasis.

Postharvest decay, primarily occurring after ripening, leads to substantial losses. Ripening increases tomato susceptibility to Botrytis cinerea, linked to desensitization of jasmonate (JA) biosynthesis and defense signaling. During ripening, key JA biosynthesis genes such as allene oxide synthase (AOS) and 12-oxophytodienoate reductase 3 (OPR3) were downregulated in response to wounding or fungal challenges. The Slmyc2 mutants with impaired JA responses showed heightened pathogen sensitivity. Conversely, EIN3-Like sleil1 mutants exhibited elevated SlMYC2 levels, which increased expression of JA biosynthesis genes such as lipoxygenase D (LOXD), OPR3, AOS, and allene oxide cyclase (AOC) alongside defense genes including proteinase inhibitor PI-6, PI-27, polyphenol oxidase, and pathogenesis-related proteins, thereby enhancing resistance. Treatment with DNA methyltransferase inhibitor 5-azacytidine increased JA content, suggesting epigenetic regulation of JA-mediated defense. Collectively, intensified ethylene signaling during ripening, mediated by SlEIL1, suppressed JA-dependent responses against B. cinerea, highlighting ethylene-JA antagonism as a key driver of postharvest decay.

Postharvest decay, primarily caused by pathogenic fungi in ripening fruits and fresh vegetables, poses a challenge to agricultural sustainability and results in significant economic losses. The regulation of the fruit ripening by DNA methylation has been well demonstrated, while defense response of fruit underlying epigenetic regulation against postharvest decay remains uncertain. In the present study, treatment of tomato fruits with the DNA methyltransferase inhibitor 5-Azacytidine (5-Aza) notably decreased their susceptibility to gray mold. Following 5-Aza treatment, we observed a substantial increase in activities of chitinase (CHI) and glucanase (GLU) in tomato fruits, as well as an increase in the expression of the dicer-like SlDCL2 gene family. Suppression of SlDCL2c through double-stranded RNA-induced RNA interference (RNAi) resulted in a decrease in the expression of chitinases CHI3, CHI9, Class V chitinase, and endochitinase 4 by 71%, 29%, 55%, 64%, as well as glucanases Cel1, Cel2, and GluB by 19%, 93%, and 87%, respectively. This was accompanied by decreased activities of resistance-related enzymes, including CHI and GLU. The expression levels of genes phenylalanine ammonia-lyase PAL2, peroxidase POD 12, POD P7, CCR1, CYP84A2, and COMT in phenylpropanoid biosynthesis pathway also decreased by 33%, 53%, 18%, 50%, 30%, and 24% in SlDCL2c-RNAi fruit, resulting in decreased activities of PAL and POD. Consequently, the lesion diameter of gray mold in SlDCL2c-RNAi fruit increased by 55% compared to the control group. Overall, the present study indicated that DNA methyltransferase inhibitor 5-Aza reduces susceptibility of tomato fruit to gray mold through regulation of DCL2c-mediated inducible defense response.

Fresh walnuts (Juglans regia L.) are challenging to store due to their high water content and delicate green appearance. It has been reported that sodium nitroprusside (SNP, a nitric oxide donor) can promote stress tolerance. However, whether SNP affects the postharvest quality of fresh walnuts remains unknown. This research showed that appropriate SNP treatment contributed to walnut preservation; in particular, 0.5 mmol/L SNP treatment resulted in a better appearance and less decay (59.7%). Compared with the control, this treatment not only increased the levels of proteases related to fresh walnut disease (chitinase and β-1,3-glucanase) but also increased the overall antioxidant level and reduced oxidant damage. Moreover, respiratory metabolism and ethylene release were greatly suppressed (9.5%), and the overall sensory evaluation did not reveal any adverse effects associated with a lower acid or peroxide content. Thus, it was inferred that the optimal SNP dose activated disease-related enzymes, mediated the physiological metabolism rate, regulated the ROS-redox balance and therefore reduced decay and maintained the walnut quality. This is the first report of SNP (NO) application for the preservation of fresh walnuts and may provide information to facilitate practical application of this potential innovation.