Application of methyl jasmonate to control chilling tolerance of postharvest fruit and vegetables: a meta-analysis and eliciting metabolism review.

Chilling injury is one of the most significant limitations for low temperature storage of postharvest fruits and vegetables, causing quality deterioration and economic loss. Increasing studies indicated that methyl jasmonate (MeJA) is critical in regulating the postharvest fruit and vegetables chilling tolerance. Based on a meta-analysis, the review analyzed the action of exogenous MeJA application on the chilling index in postharvest fruit and vegetables and summarized MeJA's mechanisms for controlling postharvest chilling injury. The meta-analysis found that MeJA treatment remarkably inhibited postharvest fruit and vegetable chilling injury. Moreover, we concluded the following function mechanism of MeJA on postharvest fruit and vegetable chilling tolerance: (1) Enhancing membrane integrity and energy supply, (2) Increasing antioxidant activity, (3) Enhancing arginine pathway, (4) Enhancing sugar metabolism, (5) Regulating phenolic metabolism, (6) Activating CBF pathway, (7) Regulating HSP accumulation and expression, and (8) Crosstalk with phytohormone. Finally, we summarized the regulatory mechanisms of MeJA on postharvest fruit and vegetable biological processes at the transcriptional and post-translational levels.

Interaction of methionine sulfoxide reductase B5 with SlMYC2 stimulates the transcription of MeJA-mediated autophagy-related genes in tomato fruit.

Methyl jasmonate (MeJA) has been shown to induce autophagy in various plant stress responses and metabolic pathways. MYC2 is involved in MeJA-mediated postharvest fruit biological metabolism, but it is unclear how it affects MeJA-induced fruit autophagy. In this study, we noticed that silencing SlMYC2 significantly reduced the increase in autophagy-related genes (SlATGs) expression induced by MeJA. SlMYC2 could also bind to the promoters of several SlATGs, including SlATG13a, SlATG13b, SlATG18a, and SlATG18h, and activate their transcript levels. Moreover, SlMsrB5, a methionine sulfoxide reductase, could interact with SlMYC2. Methionine oxidation in SlMYC2 and mimicking sulfoxidation in SlMYC2 by mutation of methionine-542 to glutamine reduced the DNA-binding ability and transcriptional activity of SlMYC2, respectively. SlMsrB5 partially repaired oxidized SlMYC2 and restored its DNA-binding ability. On the other hand, silencing SlMsrB5 inhibited the transcript levels of SlMYC2-targeted genes (SlATG13a, SlATG13b, SlATG18a, and SlATG18h). Similarly, dual-luciferase reporter (DLR) analysis revealed that SlMsrB5-SlMYC2 interaction significantly increased the ability of SlMYC2-mediated transcriptional activation of SlATG13a, SlATG13b, SlATG18a, and SlATG18h. These findings demonstrate that SlMsrB5-mediated cyclic oxidation/reduction of methionine in SlMYC2 influences SlATGs expression. Collectively, these findings reveal the mechanism of SlMYC2 in SlATGs transcriptional regulation, providing insight into the mechanism of MeJA-mediated postharvest fruit quality regulation.

The Co-regulation of Ethylene Biosynthesis and Ascorbate-Glutathione Cycle by Methy Jasmonate Contributes to Aroma Formation of Tomato Fruit during Postharvest Ripening.

Currently, many fruits are always harvested at the early ripening stage to reduce postharvest losses followed by 1-methylcyclopropene (1-MCP) or ethephon treatment. However, harvesting at the early ripening stage adversely affects fruit quality, especially for the aroma. Methyl jasmonate (MeJA) treatment could induce the biosynthesis of bioactive compounds and maintain postharvest fruit quality. In the present work, the contributions of MeJA to tomato fruit quality during postharvest ripening were studied. The results showed that MeJA treatment significantly promoted the accumulation of volatile organic components (VOCs) by inducing the activities of enzymes related to lipoxygenase pathway and ethylene biosynthesis, whereas 1-MCP treatment largely inhibited the accumulation of VOCs by inhibiting activities of those enzymes. Although the application of ethephon also induced activities of the above enzymes in comparison with control, no significant differences were observed between the VOCs contents of the control and ethephon-treated fruit. Further study revealed that the ethephon treatment resulted in the enhancement of electrical conductivity and malondialdehyde content. Conversely, MeJA treatment inhibited the superoxide anion radical and hydrogen peroxide by regulating the ascorbate-glutathione cycle and further inhibited the enhancement of electrical conductivity and malondialdehyde content, which might be one of the most important reasons why the VOCs contents in fruit treated with ethephon were lower than those in MeJA-treated fruit. Thus, it is considered that MeJA treatment may be an effective and promising strategy to regulate postharvest tomato fruit quality, especially for the aroma, by regulating the ascorbate-glutathione cycle and ethylene biosynthesis.

The Synergism of 1-Methylcyclopropene and Ethephon Preserves Quality of "Laiyang" Pears With Recovery of Aroma Formation After Long-Term Cold Storage.

A "Laiyang" pear is a climacteric fruit with a special taste and nutritional value but is prone to a post-harvest aroma compound loss and a loss in fruit quality. In this study, pears were pretreated with 0.5 µl L-1 1-methylcyclopropene (1-MCP) at 20°C for 12 h and then stored at 0 ± 1°C for 150 days to evaluate the influence of 1-MCP on fruit quality and the changes in components of volatile aromas. In addition, pears were further treated with 2 mmol L-1 ethephon. The effects of ethephon on the recovery of aroma production were investigated during the 150 day storage at 0 ± 1°C and the subsequent 7 day shelf life at 20 ± 1°C. Treatment with 1-MCP inhibited firmness loss, increased electrical conductivity, reduced respiration and ethylene production rates as well as the contents of soluble solids, and maintained the storage quality of the fruits. However, 1-MCP treatment inhibited the emission of volatile aromas in pear fruits by decreasing the activities of various enzymes, such as lipoxygenase (LOX), hydroperoxide lyase (HPL), alcohol dehydrogenase (ADH), pyruvate carboxylase (PDC), and alcohol acetyltransferase (AAT). During the shelf-life, activities of the above mentioned enzymes were significantly enhanced, and a higher content of volatile aromas were found in fruits treated with 1-MCP + ethephon, while other qualities were not compromised. These results showed that 1-MCP treatment could effectively maintain the quality of the "Laiyang" pear during cold storage, and the additional application of ethephon on fruits during shelf-life may be a promising way to restore volatile aromas in pear fruits after long-term storage.

SlARG2 contributes to MeJA-induced defense responses to Botrytis cinerea in tomato fruit.

BACKGROUND: Arginase plays key roles in methyl jasmonate (MeJA)-mediated quality maintenance in vegetables and fruits. MeJA treatment induced the Arginase 2 (SlARG2) expression, which is one of the most important encoding genes of arginase. In addition, the treatment with MeJA induced resistance to pathogenic infection in many plants. However, the functions of SlARG2 in MeJA-induced defense to Botrytis cinerea are unclear. In our work, control and SlARG2-silenced tomato fruits (Solanum lycopersicum) were treated with 0.05 mmoL L-1 MeJA before storage to assay the roles of SlARG2 in MeJA-induced defense responses to Botrytis cinerea. RESULTS: Our results indicated that MeJA treatment induced both pathogenesis-related gene expression (PR1, PR2a, PR2b and PR3b), and the activity of defense-related enzymes, as well as upregulated arginine metabolism. Compared to control fruits, the treatment with MeJA also induced the activity of arginase, arginine decarboxylase (ADC) and ornithine aminotransferase (OAT), and expression of SlARG2, SlADC, ornithine decarboxylase (SlODC) and SlOAT, and consequently increased the accumulation of arginine, proline, glutamate, putrescine and spermine. However, the induction effects by MeJA were significantly reduced in fruits in which SlARG2 was silenced and severe disease symptoms were observed. CONCLUSION: MeJA fumigation could inhibit disease development by inducing pathogenesis-related gene expression (PR1, PR2a, PR2b and PR3b) and defense-related enzymes activity, as well as upregulated arginine metabolism. In addition, SlARG2 silencing could inhibit the functions of MeJA in inducing the accumulation of the above substances. Overall, our study provided strong evidence that SlARG2 was essential for MeJA-induced tomato fruit defense responses to Botrytis cinerea. © 2020 Society of Chemical Industry.

CRISPR/Cas9-Mediated SlMYC2 Mutagenesis Adverse to Tomato Plant Growth and MeJA-Induced Fruit Resistance to Botrytis cinerea.

Methyl jasmonate (MeJA), a natural phytohormone, played a critical role not only in plant growth but also in plant defense response to biotic and abiotic stresses. MYC2, a basic helix-loop-helix transcription factor, is a master regulator in MeJA signaling pathway. In the present work, slmyc2 mutants were generated by the clustered regularly interspaced short palindromic repeats and associated Cas9 protein (CRISPR/Cas9) system to investigate the role of SlMYC2 in tomato plant growth and fruit disease resistance induced by exogenous MeJA. The results showed that slmyc2 mutants possessed a higher number of flowers and a lower fruit setting rate in comparison with wild-type plants. In addition, the fruit shape of slmyc2 mutant was prolate, while the control fruits were oblate. Knockout of SlMYC2 significantly decreased the activities of disease defensive and antioxidant enzymes, as well as the expression levels of pathogen-related (PR) genes (SlPR-1 and SlPR-STH2) and the key genes related to jasmonic acid (JA) biosynthesis and signaling pathway including allene oxide cyclase (SlAOC), lipoxygenase D (SlLOXD), SlMYC2, and coronatine insensitive 1 (SlCOI1), and consequently aggravated the disease symptoms. By contrast, the disease symptoms were largely reduced in MeJA-treated fruit that possessed higher activities of these enzymes and expression levels of genes. However, the induction effects of MeJA on fruit disease resistance and these enzymes' activities and genes' expressions were significantly attenuated by knockout of SlMYC2. Therefore, the results indicated that SlMYC2 played positive regulatory roles not only in the growth of tomato plants but also in MeJA-induced disease resistance and the antioxidant process in tomato fruits.

SlMYC2 are required for methyl jasmonate-induced tomato fruit resistance to Botrytis cinerea.

The mechanism of SlMYC2, involved in methyl jasmonate (MJ)-induced tomato fruit resistance to pathogens, was investigated. The data indicated that MJ treatment enhanced the accumulation of total phenolics and flavonoids, as well as individual phenolic acids and flavonoids, which might be caused by the increased phenylalanine ammonia-lyase and polyphenol oxidase activities, induced pathogenesis-related gene (PR) expression, ß-1,3-glucanase and chitinase activities, as well as α-tomatine, by inducing GLYCOALKALOID METABOLISM gene expression. These effects, induced by MJ, partly contributed to tomato fruit resistance to Botrytis cinerea. Nevertheless, the induction effects of MJ were almost counteracted by silence of SlMYC2, and the disease incidence and lesion diameter in MJ + SlMYC2-silenced fruit were higher than those in MJ-treated fruit. These observations are the first evidence that SlMYC2 plays vital roles in MJ-induced fruit resistance to Botrytis cinerea, possibly by regulating defence enzyme activities, SlPRs expression, α-tomatine, special phenolic acids and flavonoid compounds.

SlMYC2 Involved in Methyl Jasmonate-Induced Tomato Fruit Chilling Tolerance.

MYC2, a basic helix-loop-helix transcription factor, is a master regulator in Jasmonic acid (JA) signaling pathway. However, the functions of SlMYC2 in methyl jasmonate (MeJA)-mediated fruit chilling tolerance are far from being clearly understood. Thus, in the present work, we constructed SlMYC2-silenced tomato fruit by virus-induced gene silencing (VIGS) and investigated the function of SlMYC2 in MeJA-induced tomato fruit chilling tolerance. The results showed that MeJA treatment markedly induced the SlMYC2 expression; increased proline content, lycopene content, and antioxidant enzyme activities, including superoxide dismutase, peroxidase, catalase, and ascorbate peroxidase; inhibited the increase of electrical conductivity and malondialdehyde content; and effectively reduced the chilling injury (CI) incidence and CI index. However, these effects of MeJA treatment were partially counteracted in SlMYC2-silenced tomato fruit, and the CI incidence and CI index in ( SlMYC2-silenced + MeJA)-treated fruit were higher than those in MeJA-treated fruit. Our results indicated that SlMYC2 might be involved in MeJA-induced chilling tolerance, possibly by ameliorating the antioxidant enzyme system of fruit and increasing proline and lycopene levels.

Effect of methyl salicylate in combination with 1-methylcyclopropene on postharvest quality and decay caused by Botrytis cinerea in tomato fruit.

BACKGROUND: Postharvest diseases result in major losses in fruits. Tomato is susceptible to postharvest rot caused by Botrytis cinerea and is regarded as a good model system to study postharvest disease and quality deterioration in fruit. To develop a safe and effective technique to alleviate disease and maintain fruit quality, the effects of methyl salicylate (MeSA) and 1-methylcyclopropene (1-MCP) either separately or combined on quality and gray mold caused by B. cinerea in tomato fruit were investigated. RESULTS: The results showed that application of MeSA (0.05 mmol L-1 ) delayed fruit ripening and reduced gray mold. Compared with MeSA treatment, 1-MCP (0.5 µL L-1 ) effectively delayed fruit ripening. Further, MeSA combined with 1-MCP treatment was more effective in inhibiting fungal decay during storage than MeSA treatment alone. The combined treatment not only enhanced pathogenesis-related protein 1 (PR1) expression, activities of defense enzymes and total phenolic content but also inhibited the increase in electrical conductivity and malondialdehyde content. The combined treatment was also more effective in retaining firmness, color change and titratable acidity content than MeSA treatment alone. CONCLUSION: MeSA combined with 1-MCP treatment was a useful technique to maintain quality and alleviate gray mold in postharvest tomato fruit during storage. © 2018 Society of Chemical Industry.

Synergistic Effects of l-Arginine and Methyl Salicylate on Alleviating Postharvest Disease Caused by Botrysis cinerea in Tomato Fruit.

The effects of l-arginine (Arg, 1 mM) and/or methyl salicylate (MeSA, 0.05 mM) treatment on gray mold caused by Botrytis cinerea in tomato fruit were studied. Results indicated that Arg or MeSA alleviated the incidence and severity of fruit disease caused by B. cinerea, and that both Arg and MeSA (Arg + MeSA) further inhibited the development of fruit decay. Treatment with Arg + MeSA not only enhanced the activities of superoxide dismutase, catalase, and peroxidase but also promoted the expression levels of pathogenesis-related protein 1 gene and the activities of defense-related enzymes of phenylalanine ammonia-lyase, polyphenol oxidase, ß-1,3-glucanase, and chitinase during most of the storage periods, which were associated with lower disease incidence and disease index. In addition, the combined treatment elevated the levels of total phenolics, polyamines, especially putrescine, and nitric oxide. These observations suggest that treatment of fruit with Arg + MeSA is an effective and promising way to alleviate postharvest decays on a commercial scale.