Fruit ripening refers to the process by which fruits achieve the best edible quality through a series of physiological and biochemical changes at the end of growth. Ethylene has been shown to play an important role in fruit ripening. When the ethylene signaling pathway genes Gr and Never ripe (Nr) were mutated, the tomato fruit could not mature ^[4][29]. Studies have shown that system 2 ethylene mediated by ACC synthase (ACS1) is regulated by JA induction. JA regulates its signal sensing element MdMYC2 to bind directly to promoters of the ethylene biosynthesis gene MdACS1 and the ACC oxidase gene MdACO1 and enhances its transcription to promote ethylene biosynthesis in apple fruit. Interaction with MdERF3 and the MdACS1 inhibitor MdERF2 resulted in increased MdACS1 transcription ^[5][30]. Treatment of ‘French pear’ (Pyrus communis L.) with PDJ can enhance ACS1 and ACO1 expression levels to increase ethylene production and promote fruit ripening and can induce an increase in endogenous JA levels ^[6][31].

JAs’ content changes dynamically with the fruit ripening process, reaching a maximum value before fruit ripening and decreasing gradually. MeJA treatment can promote the development and maturity of strawberry fruit and participate in pigment metabolism, sugar metabolism, fruit softening, and hormone metabolism. The overexpression of FaAOC and FaAOS can accelerate the ripening of strawberry fruit. The endogenous JA content in strawberry fruit increased sharply from the small fruit stage to the white fruit stage but decreased after fruit maturity, reaching the lowest value at full maturity ^[7][32]. JA concentrations were higher in the early growth stages of apple flesh development, decreased with increasing days after flowering, and then increased for pericarp-free ripening. MeJA concentrations in apple flesh initially decreased and then generally increased during the harvest period. The concentrations of JA and MeJA in the pulp of sweet cherry were high during the early growth stages, then decreased towards harvest. PDJ treatment at 104 DAFB (preclimacteric stage) increased the endogenous abscisic acid concentration and anthocyanin concentration at 122 and 131 DAFB (maturation stages) in apples, and relatively high amounts of JA and MeJA are associated with young developing fruit ^[8][33].

Color is an important commodity quality for agricultural crops. Ripening coloration is the result of chlorophyll degradation and the formation or manifestation of carotenoids (yellow or orange) or anthocyanins (purple or red) ^[9][34]. It was found that JAs can promote chlorophyll degradation of broccoli (Brassica oleracea ssp. Italica) and cause postharvest yellowing quality deterioration. MeJA treatment resulted in increased AOC activity, increased endogenous JA levels, strongly reduced maximum quantum yield (Fv/Fm), fluorescence decay rate (Rfd), and total chlorophyll content, promoted phenanthrene oxidase (PAO) activity, and upregulated the expression of chlorophyll degradation genes ^[10][35]. MYC2/3/4, an important element of JA signaling, has been shown to directly regulate the chlorophyll metabolism regulatory genes NON-YELLOW COLORING 1, NON-YELLOWING 1, and PAO, triggering Chl breakdown during leaf aging ^[11][36]. JA, MeJA, and PDJ treatments enhanced fruit coloration in the early postharvest period of grape berries (“Pione”) ^[12][37]. In grape suspension culture cells, after addition of JA or light, anthocyan in biosynthesis was enhanced and cell growth was inhibited. The anthocyanins on day 7 after JA (0.02 mM) treatment increased 8.5-fold compared to the control culture ^[13][38]. It can be seen that JAs can play an important role in the coloring process of agricultural crops such as fruits by promoting chlorophyll degradation and anthocyanin synthesis.

JAs regulate fruit coloration via ethylene-dependent and independent of the ethylene pathways. Fan et al. (1998) found that exogenous JAs promote ethylene synthesis and fruit coloration in a concentration-dependent manner, and JA treatment stimulates ACC oxidase and ACC synthetase activities. During the onset of ripening in apple and tomato fruits, endogenous JA has a transition peak earlier than ethylene which, together with ethylene, drives the fruit’s early ripening process ^[14][39]. Moreover, studies have shown that JA might function independently of ethylene to promote lycopene biosynthesis in tomato fruit. The exogenous application of MeJA to Nr, the ethylene-insensitive mutant, significantly promoted lycopene accumulation and lycopene biosynthetic gene expression. The lycopene content was significantly reduced in spr2 and def1 fruit but increased in 35S::prosys fruits. MeJA treatment significantly enhanced fruit lycopene content and restored lycopene accumulation in mutant spr2 and def1 ^[15][40].

The combined effect of aroma components can objectively reflect the flavor characteristics and ripeness of agricultural crops such as different fruits. The aroma components of agricultural crops include esters (strawberries, apples, grapes), aldehydes and alcohols (peaches, watermelons, tomatoes), lactones (peaches, coconut, tomatoes), terpenes (nectarines, grapes, oranges), phenols and ethers (bananas, citrus, strawberries), and some sulfur-containing substances. MeJA treatment can increase the content of flavor substances such as 1-butanol, isoamyl acetate, furfural, 2-methyl butanoic acid, hexanoic acid, octyl butanoate, decyl acetate, jasmolactone, R- and S-furaneol, and dodecylacetatein strawberries ^[16][41]. The synthesis of several volatile compounds that are considered positive contributors to grape aroma was improved by MeJA application. MeJA treatment improved p-cymene, methyl jasmonate, and hexanal synthesis, and degraded 2-hexen-1-ol acetate, (Z)-3-hexen-1-ol, and n-hexanol, but the effect of MeJA foliar application on grape volatile content was mainly dependent on vintage ^[17][42]. MeJA may be useful in preventing the decline in ester biosynthesis caused by cold storage. MeJA up-regulated the expression of key genes (PuAAT, PuADH3, PuADH5, PuADH9, PuLOX1, and PuLOX3) in the LOX pathway and transcription factors (PuMYB21-like, PuMYB108-like, PuWRKY61, PuWRKY72 and PuWRKY31) in cold storage ‘Nanguo’ pears, while it increased volatile esters and unsaturated fatty acids ^[18][43]. In addition, MeJA treatment increased the concentration of fatty acids and total aromatic volatiles, monoterpenes, sesquiterpenes, aromatic compounds, isoprene, alcohols, and esters in mango pulp and decreased the yield of n-tetradecane ^[19][44]. It is worth noting that MeJA treatment significantly promoted the accumulation of volatile organic compounds (VOCs) by inducing the activity of enzymes related to the lipoxygenase pathway and ethylene biosynthesis in tomato fruit, while 1-MCP treatment greatly inhibited the accumulation of VOCs by inhibiting the activity of these enzymes, indicating that MeJA regulated fruit aroma metabolism and the ethylene signaling pathway ^[20][45].

Exogenous stimuli such as MeJA affect source–sink changes in aroma biosynthesis and catabolism in tea leaves. Exogenous application of MeJA can induce significant changes in tea volatile components, particularly geraniol, linalool, and its oxides, as well as key aroma precursors such as α-linolenic acid, geranyl diphosphate, farnesyl diphosphate, geranyl diphosphate, and phenylalanine. Moreover, the transcriptome analysis showed increased expression of genes in the α-linolenic acid degradation pathway, which produced massive amounts of JA and quickly activated the holistic JA pathway in tea leaves, while the terpenoid backbone biosynthesis pathway was also significantly affected after MeJA treatment ^[21][22][46,47]. MeJA, as an effective inducer, can induce gene expression in the signal transduction and secondary metabolism of wild chrysanthemum, regulate the biosynthesis pathway of flavor volatiles, and improve aroma quality by promoting flavor volatiles ^[23][48].

Aging is the final stage of the whole process of development and growth of plants. It is a sort of ordered self-disintegration process regulated by genetic factors. With the initiation of leaf senescence, the degradation and extinction of various organelles (chloroplasts, mitochondria, etc.) in senescent leaf cells proceed in an orderly manner. A large number of senescence-associated genes (SAGs) are expressed in the leaf senescence regulatory network, and SAGs encode proteins that have various physiological functions.

JAs promote senescence in leaves, petals, and other agricultural crop tissues. JA can trigger Chl breakdown during leaf senescence in broccoli ^[9][34]. The application of exogenous ethylene and JA can significantly accelerate rose petal senescence by mediating the high expression of the signaling receptor RhMYB108 (R2R3-MYB transcription factor), which regulates RhNAC053, RhNACO92, and RhSAG113 genes ^[24][49]. MdZAT10 expression was induced by MeJA, which enhanced the transcriptional activity of MdABI5 for MdNYC1 and MdNYE1. MdABI5, an important positive regulator of leaf senescence, significantly accelerated JA-induced senescence in apple leaves. However, a negative feedback pathway also exists for JA-induced leaf senescence, with the JA-responsive protein MdBT2 interacting directly with MdZAT10 and reducing its stability through ubiquitination and degradation, thus delaying MdZAT10-mediated leaf senescence ^[25][50].

Secondary metabolism plays an important role in the growth and development of agricultural crops and their resistance to stresses. JAs can induce the synthesis of secondary metabolites such as terpenoids, alkaloids, phenylpropanoids, and flavonoids.

Terpenoids are widely distributed in fruit, flower, leaf, root, and stem tissues and are important components of cell membranes, electron transport carriers, and phytochemicals. In grape cell suspensions, the peak accumulation of sesquiterpenes occurred 72 h after MeJA addition. MeJA-induced sesquiterpenes are synthesized via the MVA pathway, and the induction effect is strictly dependent on cell density in the cell suspension exciton addition ^[26][51]. Spraying JAs on lemon leaves significantly increased the content of two phenolic monoterpenoids, namely thymol and carvol ^[27][52].

MeJA treatment increased rosmarinic acid synthesis in Mentha × Piperita suspension culture cells, which was almost 1.5 times higher than the control sample ^[28][53]. In flask and bioreactor cultures, 10 mg L⁻¹ JA significantly increased the ginsenoside content. Total ginsenoside and protopanaxadiol ginsenosides increased more than fivefold after 7 days of JA treatment ^[29][54]. In marigold-isolated trichome root culture tissues, JA treatment increased both the accumulation of oleanolic acid saponins in hairy root tissue (up to 20-fold) and, in particular, the secretion of these compounds into the medium (up to 113-fold), while inhibiting sterol biosynthesis and accumulation (by about 60%), with some alterations to their profile ^[30][55].

JA mediates the R2R3-MYB transcription factor SlMYB14 to participate in the regulation of flavonoid biosynthesis and maintain the dynamic balance of plant active oxygen species. The overexpression of SlMYB14 in tomatoes leads to increased flavonoid accumulation, and tomato SlMYB14 acts downstream of SlMYC2 in the JA signaling pathway ^[31][56]. MeJA treatment of Salvia miltiorrhiza hairy roots suppressed SmKFB5 expression while inducing SmPAL1 and SmPAL3 transcription and enhanced phenolic acid biosynthesis through transcriptional and post-translational regulatory mechanisms ^[32][57]). JA treatment can remove SmJAZ8 inhibition on SmMYB97 and its downstream regulatory genes PAL1, TAT1, CPS1, and KSL1. SmMYB97 overexpression upregulates genes related to these processes and increases phenolic acid and tanshinone biosynthesis ^[33][58].

In addition, MeJA treatment of broccoli increased the accumulation of indolyl and aromatic glucosinolates (GSs) in floret tissues ^[34][59]. Two sets of WRKY transcription factors (TFs), NnWRKY70a and NnWRKY70b, positively regulated the biosynthesis of BIA in lotus. Both NnWRKY70s were sensitive to JA, and their expression profiles were highly correlated with BIA concentration and BIA pathway gene expression ^[35][60].

Reduction–oxidation (redox) signaling has been perceived as a balance between low levels of reactive oxygen species (ROS), acting as signals to trigger signaling pathways involved in developmental processes and plant responses to environmental fluctuations, and high levels of ROS, causing oxidative cellular damage. ROS produced in the plant cell can be scavenged or processed by highly efficient antioxidant systems that are composed of antioxidants and antioxidant enzymes ^[36][61].

The results showed that MeJA treatment could increase the antioxidant enzymes SOD, POD, CAT, and APX, increase the free-radical-scavenging rate of DPPH, reduce MDA content, and increase the shelf life of strawberries. It can also delay fruit softening and increase sugar content ^[37][62]. Foliar spraying with MJ was effective in alleviating the deleterious effects of NaCl-induced salinity stress. Spraying 0.05 and 0.1 mM MeJA on leaves significantly reduced ion leakage and malondialdehyde and hydrogen peroxide production under saline conditions but increased photosynthetic pigments, soluble carbohydrates, proline, total phenols, and flavonoids ^[38][63]. MeJA (0.05 mM) treatment up-regulated the expression of antioxidant enzyme genes (PavPOD, PavPPO, PavSOD, and PavCAT) and key genes related to JA biosynthesis and signal transduction pathways (PavLOX, PavAOS, PavOPR3, and PavMYC2) and enhanced antioxidant enzyme and disease-resistance enzyme activities (catalase, peroxidase, superoxide dismutase, polyphenol oxidase, phenylalanine ammonia-lyase, chitinase, β-1,3-glucanase) to reduce the decay rate of Alternaria alternata in post-harvest sweet cherry ^[39][64]. JAs are capable of enhancing date palm root resistance to Foa (Fusarium oxysporum f. sp. albedinis) infection through the activation of defense-related enzymes such as PPO and POX ^[40][65].

In addition, JAs also functions in regulating the antioxidants of fruit. Impaired JA perception (MT-jai) led to an increase in the total tocopherol level in mature fruits and enhanced antioxidant capacity ^[41][66]. The reason for the contradiction with the antioxidant-promoting effect of JA is related to the seeds. Tocopherols are abundant in tomato seeds, while homozygous MT-jai fruits are seedless; the lack of seeds might contribute to the increased levels of tocopherols in the pericarp of these fruits.

The JA signal pathway is the main way for plants to resist insect pests. Low concentrations of JAs induced the synthesis of polyphenol oxidase, protease inhibitor, lipoxygenase, and peroxidase in tomato leaves in a dose-dependent manner. Exogenous JA sprayed on farm plants increased the levels of polyphenol oxidase and protease inhibitors, which can stimulate plant resistance against insects in the field ^[42][67]. The JA signaling pathway strongly influences midgut protein content in phytophagous insects and supports the hypothesis that amino acids in the insect digestive tract are catabolized by host enzymes and play a role in plant resistance to herbivores ^[43][68]. However, the treatment of plants with exogenous applications of JA presumably activates the natural defensive response of plants and thus enhances resistance to attack. For example, treatment of tomatoes with JA at concentrations of 10 mM or 1 mM resulted in fewer but larger fruits, longer ripening times, and delayed fruit setting, indicating that JA-induced defenses caused losses in tomato plant and fruit growth and development ^[44][69]. Similar to ethylene, the above findings suggest JAs also have a dual role in defense regulation at the development stage, which resulted in a delay in fruit development, as well as fruit ripening promotion during the ripening stage.

In terms of pathogen infection, JA treatment or the JA signal pathway in strawberry provides the fruit with resistance against gray mold, and JA positively regulates its biosynthetic pathway genes LOS, AOS, and OPR and signaling pathway genes COI1 and JMT. The SlMYC2 gene plays a key regulatory role in MeJA-induced disease resistance in agricultural crops. Knockout of SlMYC2 significantly decreased defensive and antioxidant enzyme activities, as well as PR gene expression levels (SlPR-1 and SlPR-STH2) and key genes related to JA biosynthesis and its signaling pathway, which aggravated the disease symptoms ^[45][70]. MeJA mediates terpene synthesis of strawberry fruit against B. cinerea infection. In strawberry fruit, MeJA induces FaTPS1 expression through FaMYC2 and rapidly increases the content of sesquiterpenoids such as daulene D, which improves strawberry resistance against B. cinerea infection ^[46][71]. The bHLH transcription factor gene SlJIG, which participates in JA-induced terpene biosynthesis, is the direct target of MYC2, forms a MYC2-SlJIG module, and functions in terpene biosynthesis and resistance against the cotton bollworm and B. cinerea. SlJIG knockout plants generated by gene editing had a lower terpene content than the wild type due to the lower expression of TERPENE SYNTHASE genes ^[47][72].

JAs’ regulation of disease resistance involves the epigenetic regulatory mechanism. AGO4-dependent miRNAs play a central role in modulating JA biogenesis and signaling during hemibiotrophic fungal infections. The silence of AGO4 strongly altered the miRNA accumulation dynamics. IrAGO4 plants accumulated lower levels of JAs and fewer transcripts of JA biosynthesis genes. Treating irAGO4 plants with JA, MeJA, or cis-(+)-12-oxo-phytodienoic acid restored the WT susceptibility level ^[48][27]. LncRNA4504 may play a vital role in MeJA-induced tomato disease resistance, possibly by promoting the accumulation of total phenols and total flavonoids, enhancing defense enzyme activities, and upregulating JA signal pathway genes’ expression. MeJA treatment also promoted transcripts of genes related to JA biosynthesis (SlLOXD, SlAOS, and SlAOC) and its signal transduction (SlMYC2 and SlCOI1), along with increased endogenous JA content. However, lncRNA4504 silencing almost counteracted the effects of MeJA on the above indexes, leading to higher disease incidence and lesion diameter in the lncRNA4504-silenced+MeJA group than those in the MeJA group ^[49][73].

Expression of LeARG2, encoding arginase, and arginase activity are important for components of the JA-activated plant defense response. Trauma- and JA-induced LeARG2 expression was not observed in tomato jar1 mutants, indicating that this response is strictly dependent on the intact JA signaling pathway ^[50][74]. Tomato plants require activation of the JA biosynthetic pathway in response to injury or (pro)-systemin to generate distant signals, and their recognition in distal leaves is dependent on JA signaling, suggesting that JA or a related compound derived from the octadecane pathway may act as a transmissible wound signal ^[51][75].

Temperature is an important factor affecting the quality and shelf life of fruits and vegetables in post-harvest storage. Cold damage to fruits and vegetables refers to damage to tissues in cold storage above the freezing point due to internal structural damage to cells and resulting physiological dysfunction, as an adverse response to low-temperature stress. Cold damage leads to surface sinking, wrinkling, fruit-surface browning, flesh browning, and other symptoms in agricultural crops. Ripening bananas, mangoes, peaches, and other fruits lose part of their aroma components with the occurrence of cold damage. In addition, cold damage to fruits and vegetables weakens their ability to resist pathogenic bacteria and increases susceptibility to pathogenic bacteria infestation, leading to rapid decay and odor production, seriously affecting the commercial value ^[52][76].

MeJA can alleviate the losses related to cold damage in various fruit varieties by inhibiting the expression of PpPAL1, PpPPO1, and PpPOD1/2 and increasing the content of phosphatidylcholine, phosphatidylethanolamine, and phosphatidylglycerol ^[53][77]. The JA signaling pathway contributed to the mitigation of chilling injury (CI) in peaches during cold storage. Treatment with 10 M MeJA can delay the decrease in unsaturated fatty acids and increase in saturated fatty acids, improve the unsaturation of fatty acids in the cell membrane, and maintain a higher α-linolenic acid concentration and higher LOX, AOS, and AOC activities. The accumulation of JA and JA-Ile enhanced the JA signaling pathway and alleviated the CI index of solute and hard peach cultivars ^[54][78]. JA plays an important role in reducing seed browning caused by low temperature in pepper fruits. When treated with 0.05 mM MeJA, seed browning was highly inhibited, and endogenous JA production was increased through the early activation of JA synthesis genes ^[55][79].

The mechanism of JAs inhibiting the occurrence of cold damage in peaches currently includes the following two types. First, JA reduces the tolerance of peaches to cold damage and CI based on the regulation of fatty acids in phospholipids. Exogenous MeJA inhibits the expression of PpPAL1, PpPPO1, PpPOD1/2, and PpFAD8.1, increasing the expression and JA content of PpLOX3.1, PpMYC2.2, and PpCBF3 ^[53][77].

MeJA treatment markedly induced SlMYC2 expression; increased proline content, lycopene content, and antioxidant enzyme activities, including superoxide dismutase, peroxidase, catalase, and ascorbate peroxidase; inhibited electrical conductivity and malondialdehyde content; and effectively reduced CI incidence and the CI index. However, these effects of MeJA treatment were partially counteracted in SlMYC2-silenced tomato fruit, and the CI incidence and CI index of SlMYC2-silenced fruit increased ^[56][80]. Secondly, JAs improve the cold resistance of peach fruits by increasing the amount of ethylene and soluble sugar content. JA treatment reduces the severity of internal browning of peach pulp and does not inhibit fruit softening during the 35-day storage period ^[57][81].