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Review

The Role of 1-methylcyclopropylene (1-MCP) and Salicylic Acid (SA) in Induced Resistance of Postharvest Fruits

by
Xiangzhi Meng
1,
Jiazhen Fang
1,
Maorun Fu
1,
Wenxiao Jiao
1,
Pengfei Ren
2 and
Xiaoying Yang
1,*
1
School of Food Science and Engineering, Qilu University of Technology (Shandong Academy of Sciences), Jinan 250353, China
2
Key Laboratory of Wastes Matrix Utilization, Ministry of Agriculture, Shandong Academy of Agricultural Sciences, Jinan 250100, China
*
Author to whom correspondence should be addressed.
Horticulturae 2023, 9(1), 108; https://doi.org/10.3390/horticulturae9010108
Submission received: 10 November 2022 / Revised: 2 January 2023 / Accepted: 10 January 2023 / Published: 13 January 2023
(This article belongs to the Section Postharvest Biology, Quality, Safety, and Technology)
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Abstract

:
Postharvest diseases cause huge postharvest losses of horticultural fresh produce. Cooling and synthetic fungicide are used as traditional postharvest preservation technology. Recently, induced resistance has been thought to be an optional and perhaps alternative preservation technology. 1-methylcyclopropylene (1-MCP) and salicylic acid (SA) are two more common chemical agents used mostly as a preservative for harvested fruit in order to achieve better quality and better taste. Many reports have also proven that 1-MCP and SA could induce postharvest fruit resistance. The purpose of this review is to summarize the role of 1-MCP and SA in postharvest fruit resistance, including the effect of 1-MCP and SA on the induced resistance as well as its involved mechanism; the effects of 1-MCP and SA on firmness, phenolic metabolism, membrane lipid metabolism, and reactive oxygen species in fruit after harvest; and the effects of 1-MCP and SA on disease resistance-related defense enzymes, proteins, signaling synthesis, and signaling pathways as well as the combined effect of 1-MCP and SA on the induced resistance and its mechanism. Meanwhile, we prospect for the future direction of increasing postharvest fruit resistance by 1-MCP and SA in more depth.

1. Introduction

Although the harvested fruit loses the supply of water and nutrients from the mother, it maintains life activities using its own stored nutrients. During postharvest storage, transport, and sale, a series of biochemical reactions occur, the metabolism changes from synthesis to hydrolysis, and the susceptibility to pathogens increase. Pathogens infecting fruits before or after harvest can cause postharvest decay during storage, transport, and marketing, and the occurrence and development of diseases depends on both fruit physiological characteristics and storage environmental conditions after harvest [1]. It was reported that 10 to 30% of fresh fruit in developed countries rotted after harvest, and 30 to 50% in developing countries decayed due to lacking storage technique [2]. Citrus, for example, is the world’s largest fruit industry. Citrus postharvest diseases are mainly caused by fungi. The rot rate was 10% to 30% and even up to 50%, causing serious economic losses in China [3].
Fungicides are widely used for fruit disease control. Currently, there is growing consumer concern about fungicide residues in fruit and the emergence of fungicide-resistant strains. It is necessary to explore effective and harmless fungicides or treatments that can induce resistance. With the treatment of biotic or abiotic elicitors, postharvest fruits can be indued with a natural resistance to pathogenic microorganism through activation of their own defense system, effectively resisting and killing pathogenic microorganisms, which is called postharvest induced resistance. The induced resistance is characterized by persistence and broad-spectrum to green mold, blue mold, gray mold, anthracnose, and several fugal diseases, conferring resistance to many kinds of pathogen infection without leading to the appearance of resistant strains, indicating a potential application perspective in the control and prevention of postharvest disease in fruit [4]. Treatment with yeast, heat, UV, 1-methylcyclopropylene (1-MCP), ethylene, and aminobutyric acid has been widely used to induce resistance in postharvest fruit.
1-MCP is an ethylene competitive inhibitor that can irreversibly occupy the ethylene binding receptor and therefore delay fruit senescence. For its efficiency, simplicity to operate, low cost, and good economic benefits, 1-MCP has been used widely in fruit storage. It can be used as a preservative alone or mixed with other preservatives or treatments, such as heat treatment, ClO2, salicylic acid (SA), jasmonic acid (JA), etc., to achieve the preservation effect. However, some literature also reported that 1-MCP could induce fruit resistance, for example, in apple, fragrant pear, strawberry, peach, and persimmon [5,6]. Therefore, in addition, 1-MCP can be used as an abiotic elicitor to induce resistance and prevent postharvest disease in fruits after harvest.
SA is a common, simple phenolic compound in plants. It can not only produce antagonistic substances with many pathogenic microorganisms such as bacteria, fungi, and viruses but also act as a plant growth regulator to improve the resistance of crops to adverse environmental factors and promote photosynthesis. SA has important influence on plant disease resistance as well as on fruit maturity, horticultural produce preservation, and seed germination [7]. SA is an endogenous signaling molecule to activate the system-acquired disease resistance (SAR) and enhance plant defense and protection mechanisms [8]. It has been reported that exogenous SA has the potential to significantly improve harvest fruit resistance [9].
This review focuses on the role of 1-MCP and SA in the induction of postharvest fruit resistance, including their effects on reactive oxygen metabolism, phenolic metabolism, defense enzymes and proteins, resistance-related hormone synthesis and the signal transduction pathway, and their combined use in the control of postharvest diseases of fruits. This study sheds important light on the role of 1-MCP and SA in postharvest fruits resistance and facilitates the development of new and safer strategies for elevating postharvest fruit resistance against pathogenic microorganism. The outlook for further application of 1-MCP and SA on postharvest storage of fruit is also presented in this study.

2. The Role of 1-MCP in Induced Resistance of Postharvest Fruits

2.1. Effect of 1-MCP on Induced Resistance and Its Involved Mechanism

As shown in Table 1, some certain concentrations of 1-MCP can improve fruit disease resistance and, ultimately, disease performance. Li et al. showed that treatment with 1-MCP at a concentration of 5 μL/L effectively inhibited postharvest blue mold caused by Penicillium expansum in apple fruit [10]. Further, 1 μL/L 1-MCP significantly reduced the incidence of apple gray mold and inhibited the expansion of disease spots compared with the control [11], and 1 μL/L 1-MCP treatment could also reduce the disease of blue mold, gray mold, and anthracnose in golden delicious apples [12]. Jiang et al. showed that the main disease of “Everest” strawberry was fruit rot caused by a natural infection of the roots in strawberry, and treatment with 1 μL/L 1-MCP reduced disease occurrence [13], while 5 μL/L 1-MCP could effectively inhibit the increase of spot diameter, significantly reduce the disease incidence, and enhance the disease resistance to Penicillium digitatum in citrus fruit [14]. Additionally, 1 mg/L 1-MCP treatment could also prevent and control postharvest fruit diseases such as in peach and jujube [15,16]. In this way, 1-MCP can induce resistance to blue mold (Penicillium expansum), gray mold (Botrytis cinerea), anthracnose (anthracnosis), and other diseases in apple, strawberry, kumquat, peach, jujube, and other fruits. 1-MCP at 1 μL/L for 24 h is generally the best choice for treatment.
The current mechanism of resistance of 1-MCP-induced fruits includes maintaining firmness and delaying senescence to maintain natural resistance, which inhibits the increase in conductivity and malondialdehyde content, reduces the accumulation of reactive oxygen species (ROS), impairs phenolic metabolism, and increases the activity of certain key antioxidant enzymes and the induction of higher defense-related enzymatic activity such as chitinase and β-1, 3-glucanase.

2.2. Effect of 1-MCP on Reactive Oxygen Metabolism

Reactive oxygen species generally refer to some oxygen metabolites and their derivatives that contain oxygen atoms but have more active chemical reactivity than oxygen [25], such as superoxide anion radicals (O2−), hydroxyl radicals (OH), hydrogen peroxide (H2O2), lipid peroxides (ROO−), and singlet oxygen (1O2). Among them, superoxide anions, hydroxyl radicals, and hydrogen peroxide exert their main effects on plant physiological activities. Producing reactive oxygen species is the inherent biological feature in plants. The concentration of reactive oxygen species is quite low under normal physiological conditions: not enough to damage the plant because plants have formed a perfect defense system of removing reactive oxygen species in the process of long-term evolution, which has caused the production and clearance of reactive oxygen species to be kept at a dynamic equilibrium, and the reactive oxygen species will not accumulate. Once the plant is stressed, however, the metabolism of oxygen in the plant changes, the production of reactive oxygen species is accelerated, and the function of the scavenging system is diminished, leading to the accumulation of reactive oxygen species in the body, causing damage to the structure and function of the plant cell and even resulting in death; i.e., the plant is damaged by reactive oxygen species. The antioxidant removal system can transfer or eliminate free radicals and oxidative intermediates, and it is important in the ripening and aging of fruit [26]. Reactive oxygen species can also transmit signals to the disease-infected plants, thus activating the plant defense system and obtaining resistance to pathogens in time.
The excessive accumulation of reactive oxygen species was eliminated by controlling the activity of superoxide dismutase (SOD) and catalase (CAT) so that the reactive oxygen species in fruit was in a dynamic equilibrium, which is the mechanism of 1-MCP in scavenging reactive oxygen species. SOD is widely found in aerobic prokaryotes and eukaryotes and is also the first antioxidant enzyme to function in a reactive oxygen species scavenger system. SOD makes superoxide anion radicals in order to generate hydrogen peroxide and molecular oxygen, which play an important role in the protection of cells from oxidative damage. High SOD activity and lower values of ion leakage were detected in apricots treated with 1 MCP, indicating that 1 MCP reduced ethylene production, enhanced antioxidant capacity, and improved disease resistance [27]. SOD and CAT activity as well as higher levels of ascorbate were significantly increased by 1-MCP treatment, which enhanced the antioxidant capacity and improved the disease resistance in “Conference” pear fruit [28]. 1-MCP treatment significantly enhanced SOD activity, effectively extended fruit storage time, and increased disease resistance and antioxidant capacity in “Hayward” and “Zihong” kiwifruit [29]. Xia et al. found that by treating red-fleshed kiwifruit with 1-MCP (0.8 μL/L), fruit decay mainly caused by Phomopsis sp. was effectively reduced, increased SOD and CAT activity was found to improve the antioxidant capacity of the fruit, and phenolic compound contents and defense-related enzyme activity was elevated [30]. Shi et al. found that 1-MCP had a significant effect on non-climacteric fruit as well. They treated strawberries with 1-MCP, which increased the activity of a variety of antioxidant enzymes such as SOD and increased the protein content, which helped to lower the toxicity of the reactive oxygen species generated during catabolic activity, improving strawberry quality and increasing strawberry disease resistance [31]. Zhang et al. found that 1-MCP did indeed limit the development of the blue rot lesion diameter, causing significant reductions in the incidence of natural rot and increases in SOD activity in jujube fruits, which suggests that 1-MCP-induced resistance in jujube fruit was associated with increased enzymes involved in scavenging reactive oxygen species [16].

2.3. Effect of 1-MCP on Phenolic Metabolism

Phenolic metabolism forms an integral part of secondary metabolism and has an important role in plant defense responses. Phenolic bacteriostat, mainly biosynthesized by benzene propane metabolic pathway, including simple phenolic acids, flavonoids, benzene propane, and polyphenol, is closely related to plant disease resistance. PPO (polyphenol oxidase), POD (peroxidase), and PAL (phenylalanine ammonialyase) are the enzymes involved in the metabolism of phenolic compounds in plants, and they play an important role in the induced disease resistance of fruits.
The mechanism of 1-MCP on phenolic metabolism is to effectively accumulate PAL, PPO, lignin, total phenol, and other disease-resistant substances in pulp through the influence of phenylpropane pathway in fruit, thus improving the postharvest resistance of fruit. PAL is the key enzyme involved in the metabolic pathways of benzene propane, which is involved in the biosynthesis of phenols, flavonoids, phytoalexins, lignins, and other chemical resistance compounds. The activity level of PAL is often regarded as a biochemical index of plant disease resistance. 1-MCP treatment increased PAL, POD, SOD, and CAT in jujube fruit, which enhanced resistance. This suggests that enhanced fruit resistance was associated with increased activity of phenylalanine ammonialyase. Combined 1-MCP and ClO2 treatment improved PAL activity, with dual physiological and antibacterial effects, and effectively improved the resistance of strawberries [21].
Polyphenol oxidase is a key enzyme in the phenolic metabolism pathway, which is involved in enzymatic browning as well as in the biodefense reactions in fruits. PPO mainly oxidizes phenols into highly toxic material, directly limiting or poisoning the invasive pathogenic microorganism. Peroxidase is mainly involved in the generation of lignin and phytoalexin and can also remove H2O2 and O2− from tissue cells to avoid their excessive accumulation in cells. Zhang et al. found that immersion of mature avocado in aqueous solution with 1-MCP significantly retarded the accumulation of total soluble phenolics, flavonoids, and total antioxidant capacity [32]. 1-MCP treatment inhibited postharvest rot of “Anxi” persimmons, delayed the synthesis of phenolic substances, increased PPO enzyme activity, and increased the strength of the postharvest fruit [20].

2.4. Effect of 1-MCP on Disease Resistance-Related Defense Enzymes and Proteins

Plants respond to attacks by pathogens by producing a wide range of pathogenesis related (PR) proteins [33,34]. The first family of these proteins (PR-1) was identified in the early 1980s [35]. Since then, a crowd of reports have documented similar PR-1 proteins originating from numerous species of monocot and dicot plants [36,37,38,39,40]. Transgenic expression in plants confirmed the defensive function of some PR-1 proteins [41,42,43,44,45]. These PR proteins have now been classified into 17 different families [46], including β-1,3-glucanases (PR-2), chitinases (PR-3, -4, -8, and -11), osmotins with proteins similar to proteins (PR-5), defensins (PR-12), thionins (PR-13), lipid-transfer proteins (PR-14), etc. It is well-established that signaling compounds such as abscisic acid (ABA), ethylene, jasmonic acid (JA), salicylic acid (SA), mechanical wounding, UV light exposure, osmotic stress, and microbial infection are involved in the regulation of PR expression [47,48,49,50,51]. PR proteins have been shown to be closely related to systemic acquired resistance (SAR) and systemic induced resistance (ISR) [52].
1-MCP can improve fruit resistance to pathogens by inducing a wide range of pathogenesis-related (PR) proteins in fruit. Chitinase (CHI) acts on the fungal cell wall to degrade its chitin, to destroy the cytoskeleton of the fungus, and to achieve antifungal effect [53]. After fungal infection, rice was treated with 1-MCP, and the rice’s chitinase activity increased; the germination, growth, and reproduction of fungal spores was inhibited; and the rice’s resistance was enhanced [54]. Using a transcriptome study, Li et al. found that 1-MCP alleviated the overall transcriptome changes after refrigeration in cactus pear fruit [17]. Functional classifier analysis revealed that the most significant effect of 1-MCP was to avoid the large-scale downregulation of transcripts belonging to the stress, RNA and transcription, signaling, and cellular classes. In addition, exposure to 1-MCP significantly reduced the levels of phytase and chlorophyll enzyme transcripts as well as increased chitinase transcript levels, thereby providing molecular evidence for its observed effects in delaying pericarp staining and increasing resistance to pathogens. β-1,3-glucanases (GLU) belong to the PR-2 class and play an important role in disease resistance in plants [55]. β-1,3-Dextran is an important structural component of the fungal cell wall, exposed on the surface of many fungal hyphal tips and capable of being directly attacked by β-1,3-glucanase [56]. β-1,3-glucanase is often expressed in concert with chitinase in plant defense responses, thus enhancing plant disease resistance [57]. Cao et al. found that 1-MCP treatment significantly reduced the rot incidence of loquat fruit by significantly inhibiting the accumulation of superoxide radicals and hydrogen peroxide, inducing higher activity of chitinase and β-1,3-glucanase and maintaining natural resistance by delaying senescence [19]. Treatment with 1-MCP inhibited fruit decomposition in postharvest “Anxi” persimmon likely because 1-MCP promoted disease resistance by increasing the activity of chitinase and β-1,3-glucanase and by retaining higher amounts of substances related to disease resistance. 1-MCP + PL treatment also induced an increase in PAL activity and increased intracellular lignin and total phenolic content, which is conducive to the formation of structural barriers with indirect resistance to pathogens. The disease index of the 1-MCP + PL-treated fruit was significantly lower than control. The 1-MCP treatment alleviated the occurrence of disease during fruit storage and reduced postharvest decay loss in melo fruit [58]. Lin et al. found that treatment with paper leaf 1-MCP effectively reduced disease index in the carambola fruit; produced increased CHI, GLU, PAL, PPO, and POD activity; and maintained a high total phenolic content. [18].
PR1 is a marker gene of SAR. The molecular mechanism of the SA-regulating PR1 gene in response to pathogenic microorganism infection has been widely studied in model plants. Studies in Arabidopsis showed that the nonexpressor of pathogenesis-related gene-1 (NPR1), as a key contributor to SA signaling, interacts with TGACG motif-binding transcription factor (TGA) transcription factors, activating SA response elements in the promoter of PR1 [59]. Later, the researchers successively confirmed the prevalence of PR1 in plants and its role in the defense process in the plant leaves. Niki et al. found that overexpression of AtPR1 in Arabidopsis enhanced resistance to downy mildew [60]. Li et al. found that expression of VvPR1 in response to tobacco wildfire infection and PsPR1 expression increased within 24 h [61]. To our knowledge, there was no report on induced expression of PR1 by 1-MCP treatment in postharvest fruits. However, in soft spring wheat (Triticum aestivum L.), 1-MCP induced disease resistance to leaf spots (Septoria nodorum Berk.) by increasing zeatin, hydrogen peroxide, and accumulation of gene transcripts (PR-1 and PR-2). All of the defense responses studied were suppressed, and pathogen development was more concentrated in control and ethylene-treated wheat. Cytokinins were localized to the mesophyll cells and cell walls of wheat leaves treated with 1-MCP. The cell walls of ET-treated leaves were devoid of zeatin, and the hormone was concentrated in the developing hyphae of the pathogen. These findings make it possible to hypothesize that wheat resistance is controlled by an antagonistic interplay of salicylic acid and ethylene signaling pathways with cytokinin participation [62].

2.5. Effect of 1-MCP on Fruit Firmness

Texture softening mostly occurs in the process of fruit ripening, which makes the fruit flavor quality and taste reach its best state but makes the fruit more susceptible to microbial infection and physical damage [63]. 1-MCP improves fruit resistance to pathogens by inhibiting the degradation of cell walls. It was shown that 1-MCP could inhibit the enzyme activity related to softening in the ripening process (exo-polygalacturonase, pectin methylesterase, β-galactosidase, and α-L-arabinofuranosidase), thus inhibiting the degradation of cell wall and delaying fruit softening in apple fruits [64]. Lohani et al. determined the activity changes of pectinesterase (PE), polygalacturonase (PG), and cellulase (Cx) in banana fruits during storage and found that 1-MCP was able to effectively inhibit the effect of ethylene on cell wall hydrolase as well as reduce fruit softening. The addition of 1-MCP could significantly reduce the rate of starch conversion in harvested apple; inhibit degradation of pectin, cellulose, and hemicellulose; and retard softening [65]. 1-MCP could significantly reduce the conversion rate of starch in harvested apple; inhibit the degradation of pectin, cellulose, and hemicellulose, and delay softening [66]. 1-MCP treatment could delay the peak emergence of amylase and PE activity in kiwi fruit, inhibit the degradation of starch and pectin, significantly maintain fruit firmness, and delay softening and aging [67]. Ethylene induced the expression of the PG gene DkPG1 in persimmon fruit, while 1-MCP treatment suppressed gene expression of DkPG1, reduced the PG enzyme activity, and maintained a high pulp firmness [68]. It is possible that 1-MCP may effectively inhibit the activity of softening-related enzymes such as PE and PG and delay the process of softening after ripening in “Santa Rosa” plum fruit [69].

2.6. Effect of 1-MCP on Increasing Fruit Disease

In some studies, 1-MCP was reported to be able to reduce postharvest fruit strength and promote disease occurrence. For example, treatment with 1-MCP reduced resistance in Japanese prickly pear, with more severe symptoms of black spots [70]. Porat et al. found that 1-MCP increased rot caused by penicillium in “Shamouti” oranges because ethylene inhibited mold growth, while 1-MCP inhibited ethylene [23]. Janisiewicz et al. found that 1-MCP treatment increased the severity of bitter rot and blue molds, reducing disease resistance of “Golden Delicious” apples [71]. It was shown that although 1-MCP treatment delayed fruit ripening, it also changed the component of the fruit, which increased tissue morbidity [21]. Sun et al. found that after storage for 120 days, the rot rate of 1-MCP-treated fruit was significantly higher than control and increased with the treatment concentration. This indicates that 1-MCP may reduce the resistance of Dangshan pear to Penicillium and increase the disease [22]. Jiang et al. found that the effect of 1-MCP treatment on strawberry fruit was related to the treatment dose: low doses of 1-MCP treatment inhibited rot, while high doses of 1-MCP treatment promoted fruit rot occurrence [13]. Similarly, the 0.5 μL/L 1-MCP-treated group in “Emerald” pear reduced the fruit decay rate, and the fruit decay rate (mainly fungal diseases) in the 1.0 μL/L-treated group was higher than that of control group and the 0.5 μL/L-treated group. The results showed that the high concentration of (1.0 μL/L) 1-MCP treatment aggravated the occurrence of fruit fungal disease in “Emerald” pear [72].
Taken together, 1-MCP can enhance fruit resistance or reduce fruit resistance, which depends on different fruit species and treatment concentration. The reason for reducing resistance is that in some fruits, ethylene participates in fruit defense reaction induced by fungi or bacteria, and if 1-MCP combines with the ethylene receptor, ethylene cannot participate in the fruit defense reaction, eventually leading to more serious disease. Therefore, when inducing resistance with 1-MCP, we should pay attention to determine the effect of 1-MCP on disease resistance in different fruit species and varieties and optimize the concentration of 1-MCP.

3. The Role of SA in Induced Resistance of Postharvest Fruits

3.1. Effect of SA on Induced Resistance and Its Involved Mechanism

Salicylic acid (SA) is an endogenous phenolic substance with low content in higher plants. As an intracellular signaling molecule, SA can regulate important metabolic processes in plants, such as inducing flowering, affecting sex differentiation, and regulating photoperiod [73]. SA plays a role in the plant resistance response to both biotic and abiotic stresses. Exogenous SA can induce resistance to fungi, bacteria, and viruses in a variety of plants, including tobacco, cucumber, tomato, potato, pea, wheat, rice, and Arabidopsis, which has been identified as a chemical inducer of systemic acquired resistance [74]. For example, Mandal et al. found that exogenous application of 200 μM salicylate by root feeding and leaf spray induced resistance to Fusarium oxysporum in tomato [75]. Exogenous SA significantly inhibited the expansion of Penicillium expansum during room-temperature and low-temperature storage, reduced the weight loss rate, maintained total soluble solid and titrate acid content, and enhanced preservation effect in apple fruit [76]. SA could not only produce allergic reactions (hypersensitive, HR) and systemic acquired resistance (SAR) in plants but also activate a series of important components of defense response signal transduction process after pathogen infection [77]. Different concentrations of SA induced disease resistance. Apple (Malus domestica) fruits were treated with 2.5 mmol/L SA and were then soaked and inoculated with penicillium fungi (Penicillium expansum), which could effectively inhibit the occurrence of blue mold [76,78]. Further, 3 mmol/L SA treatment reduced the occurrence of citrus (Citrus reticulata) fruit disease to some extent; when the SA concentration was higher than 6 mmol/L, the growth of citrus blue mold (Penicillium digitatum) and green mold (Penicillium italicum) was completely inhibited [79,80]. SA at a concentration of 2 mmol/L or higher could significantly inhibit Alternaria-induced postharvest rot and trigger defense-related mechanisms (such as enhancement of phenlypropanoid metabolism and stimulation of Chitinase and β-1,3-glucanase) in jujube fruit [81] (Table 2). Treatment with SA can enhance the production of multiple defense response mechanisms, including various reactive oxygen species, metabolism of phenols, metabolism of membrane lipid, defense-reaction-related enzymes, and pathogenesis-related (PR) protein, thus improving fruit disease resistance.

3.2. Effect of SA on Reactive Oxygen Metabolism

Superoxide dismutase (SOD) and catalase (CAT) are two enzymes closely related to reactive oxygen species metabolism. SA can improve the activity of the fruit superoxide dismutase (SOD), reduce the rate of production of the superoxide anion, and reduce the damage caused to the fruit. SODs act as the first line of defense to scavenge the superoxide free radicals present in fruits so that SOD activity and superoxide free radical content reach a certain balance. When the fruit is susceptible to disease, the superoxide radical content in the fruit increases, and the SOD activity also increases at this time, achieving the effect of scavenging free radicals. In addition, SOD is related to the synthesis of lignin and antiviral substance, which could enhance the resistance of fruits to various pathogenic microorganisms. CAT plays an important role in plant defense, stress response, and the control of the redox balance of cells. The main function of CAT is to catalyze the decomposition of H2O2 in the fruit into H2O and O2 and remove the hydrogen peroxide in the body so as to protect the fruit from the poisoning of H2O2. Similarly, ascorbate peroxidase (APX), mainly existing in the chloroplast, is the key enzyme for scavenging H2O2 in the chloroplast. After SA treatment, the activity of SOD, CAT, and APX enzymes was improved, and the excess reactive oxygen species were eliminated, so the reactive oxygen species in the fruit were in balance, and the resistance of the fruit to pathogens was enhanced. Gao et al. found that 0.2 mmol/L salicylic acid solution effectively improved the SOD enzyme activity and induced enhanced resistance to ring rot disease [94]. SA treatment improved the activity of SOD, POD, CAT, and APX in Murraya paniculata fruit; slowed down the production rate of superoxide anion (O2−); and reduced the cell membrane permeability [94]. Likewise, 0.01 g/L SA improved the activity of SOD and CAT while reducing the content of malondialdehyde (MDA) in chestnut [95]. Similarly, SA treatment increased the activity of SOD, POD, CAT, and APX and reduced the production rate of O2 and MDA content in sugar apple fruit [85]. However, some studies have also shown that SA treatment could inhibit CAT activity in fruits and vegetables and increase H2O2 content [96,97,98,99,100]. Treatment of 0.3 mmol/L SA significantly induced the increase of superoxide anion and H2O2 content in peach fruit, increased the activity of SOD, and enhanced the resistance of apple fruit to Penicillium expansum [91]. Zhu et al. found that exogenous SA treatment induced H2O2 accumulation in citrus, showing that H2O2 as an important messenger molecule could induce enhanced cell wall resistance and induce the biosynthesis of plant disease resistance-related substances and the expression of defense-related genes [101].

3.3. Effects of SA on Membrane Lipid Metabolism

In addition, SA treatment may also alter the membrane lipid permeability of harvested fruit, resulting in improved disease resistance of the fruit. Compared with the control fruit, SA treatment reduced fruit disease index and pericarp cell membrane permeability in P. longanae-inoculated longans [102]. Furthermore, treatment with SA decreased activities of phospholipase D (PLD), phospholipase C (PLC), lipase, and lipoxygenase (LOX); lowered the content of saturated fatty acids (SFAs), phosphatidic acid (PA), and diacylglycerol (DAG); but suppressed the reductions in phosphatidylcholine (PC), phosphatidylinositol (PI), unsaturated fatty acids (USFAs), the ratio of USFAs to SFAs (U/S), and the index of unsaturated fatty acids (IUSFA) in the pericarp of P. longanae-inoculated longans. Together, these data demonstrated that SA treatment was able to retain the integrity of membrane structures, enhance fruit disease resistance to P. longanae, and thus suppress disease development in P. longanae-inoculated longans during storage.

3.4. Effect of SA on Phenolic Metabolism

Similar to the mechanism of 1-MCP-induced resistance, salicylic acid can improve disease resistance by changing the phenolic metabolism inside the fruit. Three enzymes are closely related to phenolic metabolism, including POD, PPO, and PAL. Zeng et al. found that the activity of PAL, POD, and PPO was significantly enhanced after soaking mango fruits in SA [86]. Compared with control, PPO activity during the whole storage period (16 d) increased, PAL activity increased by 5 times at 4 d, and the resistance of mango fruit to anthrax was enhanced. After inducing tomato plants with SA, THE PAL, CAT, POD, and PPO activity in tomato leaves showed a trend of rising firstly and then decreasing and then was significantly higher than control, and the resistance of tomato to powdery mildew was improved [103]. SA treatment of tomatoes inoculated with gray mold pathogens could induce an increase in the MDA content, increase ascorbate levels and POD and PPO enzyme activity, and improve disease resistance of carambola [88]. An optimal concentration of 1.5 mM SA was used to treat chickpea, and the treated fruits showed higher induction of POD and PPO activity in addition to higher phenolics, H2O2, and protein accumulation, which ultimately induced plant defense [104]. Three citrus species, including “Kinnow”, “Meyer” lemon, and “Mosambi”, treated with salicylic and jasmonic acid, were infected with green mold (Penicillium digitatum) and blue mold (P. italicum). The activity of PPO and POD was proportional to the concentration of salicylic and jasmonic acid applied, the development of both mildew was inhibited, and the resistance of the three citrus fruits was improved [92]. It has also been found that SA combined with ultrasound treatment could improve PAL, POD, CHI, and GLU activities in mango pulp tissue; promote total phenol accumulation; and effectively inhibit mango postharvest anthrax [87]. Treatment of apricot fruits with SA spray before harvest could significantly reduce the incidence of fruit blackspot. The activity of phenylpropane metabolism key enzymes is increased, thus enhancing the resistance of apricot fruit to postharvest blackspot [82].

3.5. Effect of SA on Disease Resistance-Related Signaling Synthesis and Signaling Pathways

The SA-mediated disease resistance signaling pathway contains many genes. At present, most studies in postharvest fruits have found that the expression of PR-1, PR-2 (encoding chitinase), and PR-4 (encoding β-1,3 glucanase) are directly related with resistance, but more in-depth research is still relatively rare. Earlier studies in rice found that OsBWMK1 localized in the nucleus mediated PR gene expression by activating the OsEREBP1 transcription factor [105]. It was also found that OsBWMK1 phosphorylates OsWRKY33, a WRKY transcription factor with WRKY domain (the amino acid motif WRKYGQK). The DNA binding activity of OsWRKY33 with W-box element (TTGACCA) of several PR gene promoters was enhanced. [106]. In postharvest banana fruit, SA and methyl jasmonate (MeJA) treatments significantly increased the content of endogenous SA and JA and resulted in higher expression levels of MaWRKYs, MaPR1-1, MaPR2, MaPR10c, MaCHI3, MaCHI4, and MaCHIL1. Yeast one-hybrid analysis showed that MaWRKYs could bind to the promoters of four SA and MeJA-inducible PR genes, i.e., MaPR1-1, MaPR2, MaPR10c, and MaCHIL1. This indicated that SA and MeJA treatment activated the banana PRs and WRKYs genes as well as the WRKY TFs bound to the PR promoter to induce resistance to anthracnose [85]. It was also found that MaNAC1, MaNAC2, and MaNAC5 were up-regulated after Colletotrichum musae infection and were also significantly enhanced by SA and MeJA treatment in banana fruit. MaNAC5 cooperates with MaWRKY1 and MaWRKY2 to induce the expression of several PR genes [84]. Treatment of peach fruits infected with Rhizopus stolonifer with β-aminobutyric acid (BABA) significantly increased peach fruit resistance. This was an integrated defense response including an H2O2 burst, ABA accumulation, and callose deposition. Yeast two-hybrid, luciferase complementation imaging, and co-immunoprecipitation assays showed that MADS2 was an interacting partner with NPR1. MAPK1 also participated in post-translational modification of MADS2 for signal amplification. MADS2 mediated SA-dependent NPR1 activation to positively regulate BABA-elicited defense in peach [107]. These are relatively new discoveries in recent years, extending our understanding of transcriptional regulation associated with induction of pathogen resistance in economic fruit crops.

3.6. Effect of SA on Disease Resistance-Related Defense Enzymes and Proteins

Most reports found that the enzymes related to fruit resistance are basically chitinase and β-1,3 glucanase. Treatment with SA improved the activity of chitinase and β-1,3 glucanase, induced pathogenesis-related proteins, and enhanced resistance in eggplant [108]. The combination of SA and chitosan increased chitinase and β-1,3 glucanase activities, effectively activating disease resistance to green mold in grapefruit [93]. SA and chitosan treatment of grape fruit also effectively enhanced the activity of chitinase and β-1,3 glucanase, improving the resistance of grape fruit to gray mildew [109]. Treatment with SA and ultrasound effectively inhibited Penicillium-induced caries, enhancing the activity of defense enzymes such as chitinase and β-1,3 glucanase, as well as increasing disease resistance in peach fruit [83].
The relationship between PR-1 and SA has been mentioned in the above paragraph. Many reports suggested that SA treatment could affect PR gene expression and induce fruit resistance. For example, SA significantly reduced the occurrence of anthrax; increased endogenous SA accumulation; increased MaPR1-1, MaPR2, and MaPR10c gene expression; and enhanced the resistance in banana fruit [110]. Treatment of tomato with SA and Ca2+ caused a significant increase in the expression of PR gene, resulting in increased resistance to Penicillium and gray leaf spot [111,112]. SA and JA jointly increased the transcription levels of PR-1, PR-6, and genes encoding isoperoxidase (M21334) and increased the resistance to advanced blight in potato (Sorokan et al. 2014). SA induced expression of five PR genes, including PR-1, PR-2 (β-1,3 glucanase), PR-4(chitinase), PR-5, and PR-8, and enhanced resistance to leaf spot caused by Glomerella cingulata in apple [89].

4. 1-MCP and SA Synergistically Reduced the Fruit Disease

Since both 1-MCP and SA can increase the resistance effect of harvested fruit and reduce the occurrence of disease, can their combined treatment affect the resistance of harvested fruit? A 5 mM SA and 1-MCP compound treatment decreased the rate of ethylene production and incidence of flesh browning, increased texture attributes and reduced the red color of the skin, and enhanced the resistance in postharvest “Laetitia” plum fruits. Compound treatment with 1-MCP and SA in “Campbell early” table grapes increased both firmness and titratable acidity compared to control and single treatment and effectively alleviated stem browning and berry rot during the 16-day storage period of 19 °C [113]. Xu et al. found that combined 1-MCP and SA treatment inhibited the rate of respiration, ethylene production, decay incidence, MDA content, soluble sugars, and soluble solids content. The combination treatment also delayed the sweetness and color changes compared to the untreated bananas, effectively increased the activity of SOD and CAT, and inhibited the increase in POD activity in banana [114]. The compound treatment enhanced the disease resistance of bananas and reduced the occurrence of disease better than 1-MCP or SA alone. SA combined with 1-MCP treatment could effectively inhibit the occurrence of decay rate and weight loss rate in plums during storage; maintain good fruit firmness, total soluble solid, titrable acid, and ascorbic acid (VC) content; inhibit the increase of malondialdehyde and H2O2 content; improve the activity of peroxidase, superoxide dismutase, and catalase; and reduce O2− production rate [115].
Although the compound treatment of 1-MCP and SA is better than single treatment in some fruits, the internal mechanism is still not very clear. The above-mentioned papers gave explanations for fruit firmness, phenols, resistance-related enzymes, and so on. In plants, there are primarily two types of induced resistance: systemic acquired resistance (SAR) and systemic induced resistance (ISR), which mostly interact antagonistically. In our opinion, after compound treatment, 1-MCP competes for ethylene binding sites; the ISR pathway is inhibited, its antagonism to SAR is alleviated, and the SAR pathway is further induced by SA, both reaching a certain equilibrium point perhaps coupled with the increase of endogenous SA. This approach strongly induces the synthesis of disease resistance-related protein PR and enhances the signal expression of the defense response, jointly improving the fruit resistance. On the other hand, it was also found that SA treatment inhibited ethylene production by reducing ACC synthase (ACS) and ACC oxidase (ACO) activities [116]. This indicates that 1-MCP and SA together reduce the content of ethylene after compound treatment. In brief, salicylic-acid-, ethylene-, and jasmonic-acid-mediated fruit disease resistance signals interact. 1-MCP combined with SA is better than a single treatment, possibly due to the synergy between 1-MCP and SA in the induction of disease resistance. 1-MCP inhibits ethylene signaling, while ethylene and SA are antagonistic in disease resistance signaling, and compound treatment reduces ethylene content, reversely inducing SA production, enhancing SAR resistance pathway response, and ultimately improving fruit disease resistance. However, the mechanism of which we speculate still needs to be verified experimentally.

5. Conclusions and Prospect

Postharvest fungal diseases in fruit have received increased attention from researchers in different fields, mainly including horticulture, plant protection, and food science. Synthetic fungicides, which have discernable health or environmental risks, are still the main method used for the control of decay incidence in today’s fruit warehouses. Although many non-chemical treatments, primarily including biological control agents, natural compounds, UV, ultrasound, irradiation, hot water and electrolyzed water treatment, and salts, have been used for the control of fungal diseases in fruits after harvest, these diseases still lead to enormous economic losses worldwide every year. In recent years, more chemicals have been used to improve the resistance of various harvested fruits and reduce the occurrence of disease. Induced resistance helps fruits maintain the energy level to respond to the attack of different fungi. Induced resistance is also considered to be a sustainable strategy to deal with the rigorous food safety standards. Increasing evidence shows that the use of safe and healthy chemical treatment is crucial for the development of new and safer strategies to continuously manage postharvest fruit decay. 1-MCP and SA are effective, safe, and harmless, so the role of 1-MCP and SA in induced resistance of postharvest fruits are reviewed, including the synergetic resistance between 1-MCP and SA, reactive oxygen metabolism, membrane lipid metabolism, phenolic metabolism, disease resistance-related defense enzymes and proteins, and genes related to signaling synthesis and signaling pathways (Figure 1).
Transcriptional regulation mechanisms are very important as the basis for 1-MCP and SA to indirectly or directly affect disease resistance in postharvest fruits. 1-MCP induced fruit resistance by affecting the ethylene signal transduction and ISR pathway, and SA induced fruit resistance through the SAR resistance pathway. However, the mechanism of induced resistance in postharvest fruits is basically the study of physiological defense response-related mechanisms and disease resistance-related proteins at present. How is the ISR pathway regulated by 1-MCP in order to induced resistance? Since there is report about the induction of the expression of PR1 by 1-MCP [58], and PR1 is a marker gene of SAR, does 1-MCP treatment regulate the SAR pathway? The crosstalk model between the ISR and SAR pathways in postharvest fruits is still unknown. We should pay much attention to the molecular mechanism of induced resistance by using 1-MCP and SA treatment, especially starting with the ISR and SAR pathways.
Fruits with 1-MCP or SA treatment alone show increased resistance to pathogen infection, and recent studies provide new insights into improving self-resistance by the treatment of 1-MCP in combination with SA. We should apply this compound treatment technology to preserve a wider variety of fruits and especially to improve the resistance of fruits. The preservation technique in combination with 1-MCP and SA may be a promising approach to extend shelf life. In order to explore the mechanism of the synergistic effect of 1-MCP and SA in fruit resistance, the transcriptional regulation mechanism should particularly be further studied, and new target genes for inducing resistance should be found, which will provide theoretical guidance for molecular breeding and postharvest processing.

Author Contributions

X.M. and J.F., conceptualization, investigation, and writing—original draft; W.J. and M.F., conceptualization, writing—review and editing, project administration, and funding acquisition; P.R. and X.Y., writing—review and editing, project administration, supervision, and funding acquisition. All authors have read and agreed to the published version of the manuscript.

Funding

This work was based upon research funded by natural science foundation of Shandong province (Project No. ZR2022MC123), national natural science foundation of China (Project No. 31701973), China Agriculture Research System-20 (CARS-20), and major innovation pilot project of integration of science, education and industry of Qilu University of Technology (Shandong Academy of Science) (No. 2022JBZ01-08).

Data Availability Statement

No new data were created or analyzed in this study. Data sharing is not applicable to this article.

Conflicts of Interest

The authors declare that they have no conflict of interest to this paper. We declare that we do not have any financial interests or personal relationships that represent a conflict of interest in connection with the paper submitted.

References

  1. Belay, Z.A.; Caleb, O.J. Role of integrated omics in unravelling fruit stress and defence responses during postharvest: A review. Food Chem. Mol. Sci. 2022, 5, 100118. [Google Scholar] [CrossRef] [PubMed]
  2. Chan, Z.; Tian, S. Interaction of antagonistic yeasts against postharvest pathogens of apple fruit and possible mode of action. Postharvest Biol. Technol. 2005, 36, 215–223. [Google Scholar] [CrossRef]
  3. Cai, X.; Xu, Z.; Li, X.; Wang, D.; Ren, X.; Kong, Q. Underlying mechanism of menthol on controlling postharvest citrus sour rot caused by Geotrichum citri-aurantii. Postharvest Biol. Technol. 2023, 196, 112160. [Google Scholar] [CrossRef]
  4. Cao, Z.; Zhou, D.; Ge, X.; Luo, Y.; Su, J. The role of essential oils in maintaining the postharvest quality and preservation of peach and other fruits. J. Food Biochem. 2022, 46, e14513. [Google Scholar] [CrossRef] [PubMed]
  5. Du, M.; Jia, X.; Li, J.; Li, X.; Jiang, J.; Li, H.; Zheng, Y.; Liu, Z.; Zhang, X.; Fan, J. Regulation effects of 1-MCP combined with flow microcirculation of sterilizing medium on peach shelf quality. Sci. Hortic. 2020, 260, 108867. [Google Scholar] [CrossRef]
  6. Testempasis, S.; Tanou, G.; Minas, I.; Samiotaki, M.; Molassiotis, A.; Karaoglanidis, G. Unraveling Interactions of the Necrotrophic Fungal Species Botrytis cinerea with 1-Methylcyclopropene or Ozone-Treated Apple Fruit Using Proteomic Analysis. Front. Recent Dev. Plant Sci. 2021, 12, 644255. [Google Scholar] [CrossRef]
  7. Palmer, I.A.; Shang, Z.; Fu, Z.Q. Salicylic acid-mediated plant defense: Recent developments, missing links, and future outlook. Front. Cell Dev. Biol. 2017, 12, 258–270. [Google Scholar] [CrossRef]
  8. Li, S.; Huan, C.; Liu, Y.; Zheng, X.; Bi, Y. Melatonin induces improved protection against Botrytis cinerea in cherry tomato fruit by activating salicylic acid signaling pathway. Sci. Hortic. 2022, 304, 111299. [Google Scholar] [CrossRef]
  9. Zhang, H.; Liu, F.; Wang, J.; Yang, Q.; Wang, P.; Zhao, H.; Wang, J.; Wang, C.; Xu, X. Salicylic acid inhibits the postharvest decay of goji berry (Lycium barbarum L.) by modulating the antioxidant system and phenylpropanoid metabolites. Postharvest Biol. Technol. 2021, 178, 111558. [Google Scholar] [CrossRef]
  10. Li, J.; Lei, H.; Song, H.; Lai, T.; Xu, X.; Shi, X. 1-methylcyclopropene (1-MCP) suppressed postharvest blue mold of apple fruit by inhibiting the growth of Penicillium expansum. Postharvest Biol. Technol. 2017, 125, 59–64. [Google Scholar] [CrossRef]
  11. Zhou, X.; Tang, Y.; Shi, Y.; Zhou, H. Mechanism of 1-MCP treatment in induced resistance to gray mold of apples during low-temperature storage. Food Sci. 2016, 37, 254–260. [Google Scholar] [CrossRef]
  12. Saftner, R.A.; Abbott, J.A.; Conway, W.S.; Barden, C.L. Effects of 1-Methylcyclopropene and Heat Treatments on Ripening and Postharvest Decay in ‘Golden Delicious’ Apples. J. Am. Soc. Hortic. Sci. 2003, 128, 120–127. [Google Scholar] [CrossRef] [Green Version]
  13. Jiang, Y.; Joyce, D.C.; Terry, L.A. 1-Methylcyclopropene treatment affects strawberry fruit decay. Postharvest Biol. Technol. 2001, 23, 227–232. [Google Scholar] [CrossRef]
  14. Wang, Z.; Yuan, G.; Pu, H.; Shan, S.; Zhang, Z.; Song, H.; Xu, X. 1-Methylcyclopropene suppressed the growth of Penicillium digitatum and inhibited the green mould in citrus fruit. J. Phytopathol. 2021, 169, 83–90. [Google Scholar] [CrossRef]
  15. Liu, H.; Jiang, W.; Zhou, L.; Wang, B.; Luo, Y. The effects of 1-methylcyclopropene on peach fruit (Prunus persica L. cv. Jiubao) ripening and disease resistance. Int. J. Food Sci. Technol. 2005, 40, 1–7. [Google Scholar] [CrossRef]
  16. Zhang, Z.; Tian, S.; Zhu, Z.; Xu, Y.; Qin, G. Effects of 1-methylcyclopropene(1-MCP) on ripening and resistance of jujube (Zizyphus jujuba cv. Huping) fruit against postharvest disease. LWT Food Sci and Technol. 2012, 45, 13–19. [Google Scholar] [CrossRef]
  17. Li, L.; Kashash, Y.; Goldenberg, L.; Sabag, A.; Doron-Faigenboim, A.; Porat, R. Effects of 1-methylcyclopropene on postharvest storage performance and the transcriptome of cactus pear fruit. Int. J. Food Sci. Technol. 2017, 52, 1801–1809. [Google Scholar] [CrossRef]
  18. Lin, Y.; Sun, J.; Chen, Y.; Lin, Y.; Jiang, X.; Lin, H. Inhibition of postharvest disease and induction of defence-related enzymes by paper containing 1-methlcyclopropene(1-MCP) in averrhoa carambola fruit. Chin. J. Trop. Crops. 2016, 37, 1172–1176. [Google Scholar]
  19. Cao, S.; Zheng, Y. Effect of 1-methylcyclopropene on anthracnose rot caused by Colletotrichum acutatum and disease resistance in loquat fruit. J. Sci. Food Agric. 2010, 90, 2289–2294. [Google Scholar] [CrossRef]
  20. Zeng, L.; Shi, L.; Lin, H.; Lin, Y.; Lin, Y.; Wang, H. Paper-containing 1-methylcyclopropene treatment suppresses fruit decay of fresh Anxi persimmons by enhancing disease resistance. Food Qual. Saf. 2021, 5, fyab007. [Google Scholar] [CrossRef]
  21. Hofman, P.J.; Jobin-Décor, M.; Meiburg, G.F.; Macnish, A.J.; Joyce, D.C. Ripening and quality responses of avocado, custard apple, mango and papaya fruit to 1-methylcyclopropene. Aust. J. Exp. Agric. 2001, 41, 567–572. [Google Scholar] [CrossRef]
  22. Sun, X.; Wang, W.; Li, Z.; Wang, Z.; Zhang, Z. Effects of 1-MCP on cold storage of dangshangsuii pears. Storage Process 2001, 6, 14–17. [Google Scholar] [CrossRef]
  23. Porat, R.; Weiss, B.; Cohen, L.; Daus, A.; Goren, R.; Droby, S. Effects of ethylene and 1-methylcyclopropene on the postharvest qualities of ‘Shamouti’ oranges. Postharvest Biol. Technol. 1999, 15, 155–163. [Google Scholar] [CrossRef]
  24. Chai, J.; Wang, Y.; Liu, Y.; Yong, K.; Liu, Z. 1-MCP extends the shelf life of ready-to-eat ‘Hayward’ and ‘Qihong’ kiwifruit stored at room temperature. Sci. Hortic. 2021, 289, 110437. [Google Scholar] [CrossRef]
  25. Mansoor, S.; Wani, O.A.; Lone, J.K.; Manhas, S.; Kour, N.; Alam, P.; Ahmad, A.; Ahmad, P. Reactive Oxygen Species in Plants: From Source to Sink. Antioxidants 2022, 11, 225. [Google Scholar] [CrossRef]
  26. Jones, A.M. Surprising Signals in Plant Cells. Science 1994, 263, 183–184. [Google Scholar] [CrossRef]
  27. Egea, I.; Flores, F.B.; Martínez-Madrid, M.C.; Romojaro, F.; Sánchez-Bel, P. 1-Methylcyclopropene affects the antioxidant system of apricots (Prunus armeniaca L. cv. Búlida) during storage at low temperature. J. Sci. Food Agric. 2010, 90, 549–555. [Google Scholar] [CrossRef]
  28. Chiriboga, M.-A.; Bordonaba, J.G.; Schotsmans, W.C.; Larrigaudière, C.; Recasens, I. Antioxidant potential of ‘Conference’ pears during cold storage and shelf life in response to 1-methylcyclopropene. LWT-Food Sci. Technol. 2013, 51, 170–176. [Google Scholar] [CrossRef]
  29. Xia, Y.; Zhuo, R.; Li, B.; Tian, S. Effects of 1-methylcyclopropene on disease resistance of red-fleshed kiwifruit during long-term cold storage and the possible mechanisms. N. Z. J. Crop. Hortic. 2020, 49, 182–195. [Google Scholar] [CrossRef]
  30. Shi, L.; Shen, L.; Yu, M.; Ouyang, L.; Fan, B.; Sheng, J. Effects of 1-methylcyclopropene treatment on the shelf-life quality of strawberry cv. Jingnong 1st. Acta Hortic. 2008, 768, 311–315. [Google Scholar] [CrossRef]
  31. Yang, X.; Zhang, X.; Fu, M.; Chen, Q.; Muzammil, J.M. Chlorine dioxide fumigation generated by a solid releasing agent enhanced the efficiency of 1-MCP treatment on the storage quality of strawberry. J. Food Sci. Technol. 2018, 55, 2003–2010. [Google Scholar] [CrossRef] [PubMed]
  32. Zhang, Z.; Huber, D.J.; Rao, J. Antioxidant systems of ripening avocado (Persea americana Mill.) fruit following treatment at the preclimacteric stage with aqueous 1-methylcyclopropene. Postharvest Biol. Technol. 2013, 76, 58–64. [Google Scholar] [CrossRef]
  33. Raji, M.R.; Lotfi, M.; Tohidfar, M.; Ramshini, H.; Sahebani, N.; Aalifar, M.; Baratian, M.; Mercati, F.; De Michele, R.; Carimi, F. Multiple fungal diseases resistance induction in Cucumis melo through co-transformation of different pathogenesis related (PR) protein genes. Sci. Hortic. 2022, 297, 110924. [Google Scholar] [CrossRef]
  34. Van Loon, L.C.; Van Strien, E.A. The families of pathogenesis-related proteins, their activities, and comparative analysis of PR-1 type proteins. Physiol. Mol. Plant Pathol. 1999, 55, 85–97. [Google Scholar] [CrossRef]
  35. van Loon, L.C.; Rep, M.; Pieterse, C.M.J. Significance of Inducible Defense-related Proteins in Infected Plants. Annu. Rev. Phytopathol. 2006, 44, 135–162. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  36. Antoniw, J.F.; Ritter, C.E.; Pierpoint, W.S.; Loon, L.V.C. Comparison of Three Pathogenesis-related Proteins from Plants of Two Cultivars of Tobacco Infected with TMV. J. Gen. Virol. 1980, 47, 79–87. [Google Scholar] [CrossRef]
  37. Ohshima, M.; Matsuoka, M.; Yamamoto, N.; Tanaka, Y.; Kano-Murakami, Y.; Ozeki, Y.; Kato, A.; Harada, N.; Ohashi, Y. Nucleotide sequence of the PR-1 gene of Nicotiana tabacum. FEBS Lett. 1987, 225, 243–246. [Google Scholar] [CrossRef] [Green Version]
  38. Tornero, P.; Gadea, J.; Conejero, V.; Vera, P. Two PR-1 Genes from Tomato Are Differentially Regulated and Reveal a Novel Mode of Expression for a Pathogenesis-Related Gene During the Hypersensitive Response and Development. Mol. Plant-Microbe Interactions 1997, 10, 624–634. [Google Scholar] [CrossRef] [Green Version]
  39. Maleck, K.; Levine, A.M.; Eulgem, T.; Morgan, A.; Schmid, J.; Lawton, K.A.; Dangl, J.L.; Dietrich, R.A. The transcriptome of Arabidopsis thaliana during systemic acquired resistance. Nat. Genet. 2000, 26, 403–410. [Google Scholar] [CrossRef]
  40. Liu, Q.; Xue, Q. Computational identification of novel PR-1-type genes in Oryza sativa. J. Genet. Genom. 2006, 85, 193–198. [Google Scholar] [CrossRef]
  41. Joshi, V.; Joshi, N.; Vyas, A.; Jadhav, S.K. 25—Pathogenesis-Related Proteins: Role in Plant Defense. In Biocontrol Agents and Secondary Metabolites, 1st ed.; Woodhead Publishing: Sawston, UK; Cambridge, MA, USA, 2021; p. 573. [Google Scholar]
  42. Mitsuhara, I.; Iwai, T.; Seo, S.; Yanagawa, Y.; Kawahigasi, H.; Hirose, S.; Ohkawa, Y.; Ohashi, Y. Characteristic expression of twelve rice PR1 family genes in response to pathogen infection, wounding, and defense-related signal compounds (121/180). Mol. Genet. Genom. Genom. 2008, 279, 415–427. [Google Scholar] [CrossRef]
  43. Wang, Y.; Tan, L.-X.; Xu, Z.-Q.; Jiao, Y.-X.; Zhu, D.-X.; Yang, Y.-S.; Wei, J.-F.; Sun, J.-L.; Tian, M. Identification and characterization of natural PR-1 protein as major allergen from Humulus japonicus pollen. Mol. Immunol. 2023, 153, 170–180. [Google Scholar] [CrossRef]
  44. Alexander, D.C.; Goodman, R.M.; Gut-Rella, M.; Glascock, C.B.; Weymann, K.; Friedrich, L.; Maddox, D.W.; Ahl-Goy, P.; Luntz, T.L.; Ward, E.R. Increased tolerance to two oomycete pathogens in transgenic tobacco expressing pathogenesis-related protein 1a. Proc. Natl. Acad. Sci. USA 1993, 90, 7327–7331. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  45. Niderman, T.; Genetet, I.; Bruyere, T.B.L.; Gees, R.; Stintzi, A.; Legrand, M.; Fritig, B.; Mosinger, E. Pathogenesis-Related PR-1 Proteins Are Antifungal (Isolation and Characterization of Three 14-Kilodalton Proteins of Tomato and of a Basic PR-1 of Tobacco with Inhibitory Activity against Phytophthora infestans). Plant Physiol. 1995, 108, 17–27. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  46. Hong, J.K.; Hwang, B.K. Induction of enhanced disease resistance and oxidative stress tolerance by overexpression of pepper basic PR-1 gene in Arabidopsis. Physiol. Plant. 2005, 124, 267–277. [Google Scholar] [CrossRef]
  47. Dabravolski, S.A.; Frenkel, Z. Diversity and evolution of pathogenesis-related proteins family 4 beyond plant kingdom. Plant Gene 2021, 26, 100279. [Google Scholar] [CrossRef]
  48. Rabari, A.; Ruparelia, J.; Jha, C.K.; Sayyed, R.Z.; Mitra, D.; Priyadarshini, A.; Senapati, A.; Panneerselvam, P.; Mohapatra, P.K.D. Articulating beneficial rhizobacteria mediated plant defenses through induced systemic resistance. Pedosphere 2022. [Google Scholar] [CrossRef]
  49. Ali, S.; Ganai, B.A.; Kamili, A.N.; Bhat, A.A.; Mir, Z.A.; Bhat, J.A.; Tyagi, A.; Islam, S.T.; Mushtaq, M.; Yadav, P.; et al. Pathogenesis-related proteins and peptides as promising tools for engineering plants with multiple stress tolerance. Microbiol. Res. 2018, 212–213, 29–37. [Google Scholar] [CrossRef]
  50. Menezes, S.P.; Silva, E.M.D.A.; Lima, E.M.; de Sousa, A.O.; Andrade, B.S.; Lemos, L.S.L.; Gramacho, K.P.; Gesteira, A.D.S.; Pirovani, C.P.; Micheli, F. The pathogenesis-related protein PR-4b from Theobroma cacao presents RNase activity, Ca2+ and Mg2+ dependent-DNase activity and antifungal action on Moniliophthora perniciosa. BMC Plant Biol. 2014, 14, 161. [Google Scholar] [CrossRef] [Green Version]
  51. Sinha, M.; Singh, R.P.; Kushwaha, G.S.; Iqbal, N.; Singh, A.; Kaushik, S.; Kaur, P.; Sharma, S.; Singh, T.P. Current Overview of Allergens of Plant Pathogenesis Related Protein Families. Sci. World J. 2014, 2014, 1–19. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  52. Loake, G.J.; Grant, M. Salicylic acid in plant defence—The players and protagonists. Curr. Opin. Plant Biol. 2007, 10, 466–472. [Google Scholar] [CrossRef]
  53. Appu, M.; Ramalingam, P.; Sathiyanarayanan, A.; Huang, J. An overview of plant defense-related enzymes responses to biotic stresses. Plant Gene 2021, 27, 100302. [Google Scholar] [CrossRef]
  54. Vaghela, B.; Vashi, R.; Rajput, K.; Joshi, R. Plant chitinases and their role in plant defense: A comprehensive review. Enzym. Microb. Technol. 2022, 159, 110055. [Google Scholar] [CrossRef]
  55. Anusuya, S.; Sathiyabama, M. Identification of defence proteins from the seed exudates of Cicer arietinum L. and its effect on the growth of Fusarium oxysporumf. sp. ciceri. Arch. Phytopathol. 2014, 47, 1611–1620. [Google Scholar] [CrossRef]
  56. Zhou, J.; Chen, J.; Li, Z.; Ye, X.; Dong, W.; Jiang, M.; Huang, Y.; Cui, Z. Enzymatic properties of a multi-specific β-(1,3)-glucanase from Corallococcus sp. EGB and its potential antifungal applications. Protein Expr. Purif. 2019, 164, 105481. [Google Scholar] [CrossRef]
  57. Liu, L.; Fu, Y. Chitinase and its role in plant disease resistance. Mod Agric. 2003, 5, 5–7. [Google Scholar] [CrossRef]
  58. de Sousa, A.E.D.; Lopes, M.M.D.A.; Moreira, A.D.R.; Macedo, J.J.N.; Moura, C.F.H.; de Aragão, F.A.S.; Zocolo, G.; de Miranda, M.R.A.; Silva, E.D.O. Induction of postharvest resistance in melon using pulsed light as abiotic stressor. Sci. Hortic. 2019, 246, 921. [Google Scholar] [CrossRef]
  59. Kim, Y.; Youn, J.; Roh, J.; Kim, J.; Kim, S.; Kim, T. Brassinosteroids enhance salicylic acid-mediated immune responses by in-hibiting BIN2 phosphorylation of clade I TGA transcription factors in Arabidopsis. Mol. Plant. 2022, 15, 991. [Google Scholar] [CrossRef]
  60. Niki, T.; Mitsuhara, I.; Seo, S.; Ohtsubo, N.; Ohashi, Y. Antagonistic Effect of Salicylic Acid and Jasmonic Acid on the Expression of Pathogenesis-Related (PR) Protein Genes in Wounded Mature Tobacco Leaves. Plant Cell Physiol. 1998, 39, 500–507. [Google Scholar] [CrossRef]
  61. Li, Z.T.; Dhekney, S.A.; Gray, D.J. PR-1 gene family of grapevine: A uniquely duplicated PR-1 gene from a Vitis interspecific hybrid confers high level resistance to bacterial disease in transgenic tobacco. Plant Cell Rep. 2010, 30, 1–11. [Google Scholar] [CrossRef]
  62. Veselova, S.V.; Burkhanova, G.F.; Nuzhnaya, T.V.; Maksimov, I.V. Roles of ethylene and cytokinins in development of defense responses in Triticum aestivum plants infected with Septoria nodorum. Russ. J. Plant Physiol. 2016, 63, 609–619. [Google Scholar] [CrossRef]
  63. Dou, J.-F.; Kou, X.-H.; Wu, C.-E.; Fan, G.-J.; Li, T.-T.; Li, X.-J.; Zhou, D.-D.; Yan, Z.-C.; Zhu, J.-P. Recent advances and development of postharvest management research for fresh jujube fruit: A review. Sci. Hortic. 2023, 310, 111769. [Google Scholar] [CrossRef]
  64. Win, N.M.; Yoo, J.; Naing, A.H.; Kwon, J.-G.; Kang, I.-K. 1-Methylcyclopropene (1-MCP) treatment delays modification of cell wall pectin and fruit softening in “Hwangok” and “Picnic” apples during cold storage. Postharvest Biol. Technol. 2021, 180, 111599. [Google Scholar] [CrossRef]
  65. Lohani, S.; Trivedi, P.K.; Nath, P. Changes in activities of cell wall hydrolases during ethylene-induced ripening in banana: Effect of 1-MCP, ABA, and IAA. Postharvest Biol. Technol. 2004, 31, 119–126. [Google Scholar] [CrossRef]
  66. Wei, J.; Zhu, X.; Yuan, J.; Liu, C. Effects of 1-MCP on fruit’s starch and the components of cell-wall material during post-harvest of gala apples. Acta Agric. Boreali-Sin. 2008, 1, 121–124. [Google Scholar] [CrossRef]
  67. Fu, Y.; Chen, M.; Liu, K.; Chen, J. Effects of the second treatment with 1-MCP on post-harvest physiological and bio-chemical characteristics of kiwifruit. J. Fruit Sci. 2007, 1, 43–48. [Google Scholar] [CrossRef]
  68. Jiang, N.; Rao, J.; Fu, R. PG enzyme activity and the expression of the gene DkPG1 in the recovered softening of persimmon fruit. Hort. J. 2010, 9, 1507–1512. [Google Scholar]
  69. Sharma, S.; Sharma, R.R.; Pal, R.K.; Paul, V.; Dahuja, A. 1-Methylcyclopropene influences biochemical attributes and fruit softening enzymes of ‘Santa Rosa’ Japanese plum (Prunus salicina Lindl.). J. Plant Biochem. Biotechnol. 2011, 21, 295–299. [Google Scholar] [CrossRef]
  70. Itai, A.; Igori, T.; Fujita, N.; Egusa, M.; Kodama, M.; Murayama, H. Ethylene Analoge and 1-Methylcyclopropene Enhance Black Spot Disease Development in Pyrus pyrifolia Nakai. HortScience 2012, 47, 228–231. [Google Scholar] [CrossRef]
  71. Janisiewicz, W.J.; Leverentz, B.; Conway, W.S.; Saftner, R.A.; Reed, A.; Camp, M.J. Control of bitter rot and blue mold of apples by integrating heat and antagonist treatments on 1-MCP treated fruit stored under controlled atmosphere conditions. Postharvest Biol. Technol. 2003, 29, 129–143. [Google Scholar] [CrossRef]
  72. Wang, Z.; Wang, W.; Dong, W.; Ding, D.; Jia, X.; Zhang, Z. Research of 1-MCP treatment effects on fresh-keeping of ‘Lubaoshi’ pear. Storage Process 2007, 6, 9–12. [Google Scholar] [CrossRef]
  73. Endo, J.-I.; Takahashi, W.; Ikegami, T.; Beppu, T.; Tanaka, O. Induction of Flowering by Inducers of Systemic Acquired Resistance in the Lemna Plant. Biosci. Biotechnol. Biochem. 2009, 73, 183–185. [Google Scholar] [CrossRef]
  74. Blanco-Herrera, F.; Salinas, P.; Cecchini, N.M.; Jordana, X.; Van Hummelen, P.; Alvarez, M.E.; Holuigue, L. Early genomic responses to salicylic acid in Arabidopsis. Plant Mol. Biol. 2009, 70, 79–102. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  75. Mandal, S.; Mallick, N.; Mitra, A. Salicylic acid-induced resistance to Fusarium oxysporum f. sp. lycopersici in tomato. Plant Physiol. Biochem. 2009, 47, 642–649. [Google Scholar] [CrossRef]
  76. Da Rocha Neto, A.C.; Luiz, C.; Maraschin, M.; Di Piero, R.M. Efficacy of salicylic acid to reduce Penicillium expansum inoculum and preserve apple fruits. Int. J. Food Microbiol. 2016, 221, 54–60. [Google Scholar] [CrossRef] [PubMed]
  77. Zeier, J. Metabolic regulation of systemic acquired resistance. Curr. Opin. Plant Biol. 2021, 62, 102050. [Google Scholar] [CrossRef]
  78. Da Rocha Neto, A.C.; Maraschin, M.; Di Piero, R.M. Antifungal activity of salicylic acid against Penicillium expansum and its possible mechanisms of action. Int. J. Food Microbiol. 2015, 215, 64–70. [Google Scholar] [CrossRef]
  79. Iqbal, Z.; Singh, Z.; Khangura, R.K.; Ahmad, S. Management of citrus blue and green moulds through application of organic elicitors. Australas. Plant Pathol. 2011, 41, 69–77. [Google Scholar] [CrossRef]
  80. Panahirad, S.; Zaare-Nahandi, F.; Safaralizadeh, R.; Alizadeh-Salteh, S. Postharvest Control of Rhizopus stolonifer in Peach (Prunus persica L. Batsch) Fruits Using Salicylic Acid. J. Food Saf. 2012, 32, 502–507. [Google Scholar] [CrossRef]
  81. Cao, J.; Yan, J.; Zhao, Y.; Jiang, W. Effects of postharvest salicylic acid dipping on Alternaria rot and disease resistance of jujube fruit during storage. J. Sci. Food Agric. 2013, 93, 3252–3258. [Google Scholar] [CrossRef]
  82. Yatin, Z. Induction of disease resistance and phenylpropanoid metabolism in apricot fruits by pre-harvest salicylic acid treatment. J. Food Sci. 2015, 36, 216–220. [Google Scholar] [CrossRef]
  83. Yang, Z.; Cao, S.; Cai, Y.; Zheng, Y. Combination of salicylic acid and ultrasound to control postharvest blue mold caused by Penicillium expansum in peach fruit. Innov. Food Sci. Emerg. Technol. 2011, 12, 310–314. [Google Scholar] [CrossRef]
  84. Shan, W.; Chen, J.-Y.; Kuang, J.-F.; Lu, W.-J. Banana fruit NAC transcription factor MaNAC5 cooperates with MaWRKYs to enhance the expression of pathogenesis-related genes against Colletotrichum musae. Mol. Plant Pathol. 2016, 17, 330–338. [Google Scholar] [CrossRef] [PubMed]
  85. Tang, Y.; Kuang, J.-F.; Wang, F.-Y.; Chen, L.; Hong, K.-Q.; Xiao, Y.-Y.; Xie, H.; Lu, W.-J.; Chen, J.-Y. Molecular characterization of PR and WRKY genes during SA- and MeJA-induced resistance against Colletotrichum musae in banana fruit. Postharvest Biol. Technol. 2013, 79, 62–68. [Google Scholar] [CrossRef]
  86. Zeng, K.; Cao, J.; Jiang, W. Enhancing disease resistance in harvested mango (Mangifera indica L. cv. ‘Matisu’) fruit by salicylic acid. J. Sci. Food Agric. 2006, 86, 694–698. [Google Scholar] [CrossRef]
  87. He, J.; Ren, Y.; Chen, C.; Liu, J.; Liu, H.; Pei, Y. Defense Responses of Salicylic Acid in Mango Fruit Against Postharvest Anthracnose, Caused by Colletotrichum gloeosporioides and its Possible Mechanism. J. Food Saf. 2017, 37, e12294. [Google Scholar] [CrossRef]
  88. Mustafa, M.A.; Ali, A.; Seymour, G.B.; Tucker, G.A. The role of the ubiquitous phenolic compound ’salicylic acid’ in chilling tolerance of carambola. Acta Hortic. 2015, 1079, 679–683. [Google Scholar] [CrossRef]
  89. Zhang, Y.; Shi, X.; Li, B.; Zhang, Q.; Liang, W.; Wang, C. Salicylic acid confers enhanced resistance to Glomerella leaf spot in apple. Plant Physiol. Biochem. 2016, 106, 64–72. [Google Scholar] [CrossRef] [PubMed]
  90. Yao, H.; Tian, S. Effects of pre- and post-harvest application of salicylic acid or methyl jasmonate on inducing disease resistance of sweet cherry fruit in storage. Postharvest Biol. Technol. 2005, 35, 253–262. [Google Scholar] [CrossRef]
  91. Wang, Y.; Chen, J.; Bian, W.; Yang, X.; Ye, L.; He, S.; Song, X. Control Efficacy of Salicylic Acid Microcapsules against Postharvest Blue Mold in Apple Fruit. Molecules 2022, 27, 8108. [Google Scholar] [CrossRef]
  92. Moosa, A.; Sahi, S.T.; Khan, S.A.; Malik, A.U. Salicylic acid and jasmonic acid can suppress green and blue moulds of citrus fruit and induce the activity of polyphenol oxidase and peroxidase. Folia Hortic. 2019, 31, 195–204. [Google Scholar] [CrossRef] [Green Version]
  93. Shi, Z.; Wang, F.; Lu, Y.; Deng, J. Combination of chitosan and salicylic acid to control postharvest green mold caused by Penicillium digitatum in grapefruit fruit. Sci. Hortic. 2018, 233, 54–60. [Google Scholar] [CrossRef]
  94. Gao, L.; Zhang, Y. Effects of salicylic acid on the expression of SOD, PPO isozymes and NPR1 in pear. Hortic. Plant J. 2013, 40, 41–48. [Google Scholar] [CrossRef]
  95. Zhao, X.; Zhao, Y.; Wang, H.; Song, P. Effect of salicylic acid on quality and physiological character of postharvest pear (Pyrus pyrifolia cv. xingshui) fruit. Hubei Agric. Sci. 2009, 48, 1165–1167. [Google Scholar] [CrossRef]
  96. Zhu, F.; Chen, J.; Xiao, X.; Zhang, M.; Yun, Z.; Zeng, Y.; Xu, J.; Cheng, Y.; Deng, X. Salicylic acid treatment reduces the rot of postharvest citrus fruit by inducing the accumulation of H2O2, primary metabolites and lipophilic polymethoxylated flavones. Food Chem. 2016, 207, 68–74. [Google Scholar] [CrossRef]
  97. Mo, Y.; Gong, D.; Liang, G.; Han, R.; Xie, J.; Li, W. Enhanced preservation effects of sugar apple fruits by salicylic acid treatment during post-harvest storage. J. Sci. Food Agric. 2008, 88, 2693–2699. [Google Scholar] [CrossRef]
  98. Cao, J.; Zeng, K.; Jiang, W. Enhancement of Postharvest Disease Resistance in Ya Li Pear (Pyrus bretschneideri) Fruit by Salicylic Acid Sprays on the Trees during Fruit Growth. Eur. J. Plant Pathol. 2005, 114, 363–370. [Google Scholar] [CrossRef]
  99. Huang, R.-H.; Liu, J.-H.; Lu, Y.-M.; Xia, R.-X. Effect of salicylic acid on the antioxidant system in the pulp of ‘Cara cara’ navel orange (Citrus sinensis L. Osbeck) at different storage temperatures. Postharvest Biol. Technol. 2008, 47, 168–175. [Google Scholar] [CrossRef]
  100. Mora-Herrera, M.E.; López-Delgado, H.A.; Castillo-Morales, A.; Foyer, C.H. Salicylic acid and H2O2 function by independent pathways in the induction of freezing tolerance in potato. Physiol. Plant. 2005, 125, 430–440. [Google Scholar] [CrossRef]
  101. Chen, Z.; Ricigliano, J.W.; Klessig, D.F. Purification and characterization of a soluble salicylic acid-binding protein from tobacco. Proc. Natl. Acad. Sci. USA 1993, 90, 9533–9537. [Google Scholar] [CrossRef] [Green Version]
  102. Zhang, F.; Wang, Y.; Liu, X.; Guo, X.; Wang, G.; Li, L. Effect of pre-harvest salicylic acid spray treatment on fruit quality and antioxidant capacity of raspberry during post-harvest storge. J. Food Sci. 2010, 31, 308–312. [Google Scholar]
  103. Chen, Y.; Sun, J.; Lin, H.; Lin, M.; Lin, Y.; Wang, H.; Hung, Y.-C. Salicylic acid treatment suppresses Phomopsis longanae Chi-induced disease development of postharvest longan fruit by modulating membrane lipid metabolism. Postharvest Biol. Technol. 2020, 164, 111168. [Google Scholar] [CrossRef]
  104. Hong, X.; Hou, X.; Zheng, Y.; Zhang, X. Induction effect of salicylic acid on resistance to powdery mildew of Jiulixiang. For. Pro. Des. 2013, 1, 125–127. [Google Scholar] [CrossRef]
  105. War, A.R.; Paulraj, M.G.; War, M.Y.; Ignacimuthu, S. Role of salicylic acid in induction of plant defense system in chickpea (Cicer arietinum L.). Plant Signal. Behav. 2011, 6, 1787–1792. [Google Scholar] [CrossRef] [Green Version]
  106. Cheong, Y.H.; Moon, B.C.; Kim, J.K.; Kim, C.Y.; Kim, M.C.; Kim, I.H.; Park, C.Y.; Kim, J.C.; Park, B.O.; Koo, S.C.; et al. BWMK1, a Rice Mitogen-Activated Protein Kinase, Locates in the Nucleus and Mediates Pathogenesis-Related Gene Expression by Activation of a Transcription Factor1. Plant Cell Physiol. 2003, 132, 1961–1972. [Google Scholar] [CrossRef] [Green Version]
  107. Koo, S.C.; Moon, B.C.; Kim, J.K.; Kim, C.Y.; Sung, S.J.; Kim, M.C.; Cho, M.J.; Cheong, Y.H. OsBWMK1 mediates SA-dependent defense responses by activating the transcription factor OsWRKY33. Biochem. Biophys. Res. Commun. 2009, 387, 365–370. [Google Scholar] [CrossRef]
  108. Li, C.; Lei, C.; Wang, K.; Tan, M.; Xu, F.; Wang, J.; Zheng, Y. MADS2 regulates priming defence in postharvest peach through combined salicylic acid and abscisic acid signaling. J. Exp. Bot. 2022, 73, 3787–3806. [Google Scholar] [CrossRef]
  109. Mahesh, H.M.; Murali, M.; Pal, M.A.C.; Melvin, P.; Sharada, M. Salicylic acid seed priming instigates defense mechanism by inducing PR-Proteins in Solanum melongena L. upon infection with Verticillium dahliae Kleb. Plant Physiol. Biochem. 2017, 117, 12–23. [Google Scholar] [CrossRef]
  110. Shen, Y.; Yang, H. Effect of preharvest chitosan-g-salicylic acid treatment on postharvest table grape quality, shelf life, and resistance to Botrytis cinerea -induced spoilage. Sci. Hortic. 2017, 224, 367–373. [Google Scholar] [CrossRef]
  111. Zhang, X.C.; Ren, A.; Zhang, P.; Yang, H.H.; Zhao, T.T.; Xu, X.Y.; Jiang, J.B.; Li, J.F. Identification of salicylic acid conferred resistance genes against gray leaf spot disease in tomato. Int. J. Agric. Biol. 2020, 23, 109–116. [Google Scholar] [CrossRef]
  112. Li, L.; Zou, Y. Induction of disease resistance by salicylic acid and calcium ion against Botrytis cinerea in tomato (Lycopersicon esculentum). Emir. J. Food Agric. 2017, 29, 78. [Google Scholar] [CrossRef] [Green Version]
  113. Kim, S.-J.; Noh, S.-I.; Choi, C.; Lim, B.-S.; Ahn, Y.-J.; Chun, J.-P. Effects of Salicylic Acid and 1-Methylcyclopropene on Physiological Disorders and Berry Quality in ‘Campbell Early’ Table Grapes. Prot. Hortic. Plant Fact. 2019, 28, 218–224. [Google Scholar] [CrossRef]
  114. Xu, F.; Liu, Y.; Xu, J.; Fu, L. Influence of 1-methylcyclopropene (1-MCP) combined with salicylic acid (SA) treatment on the postharvest physiology and quality of bananas. J. Food Process. Preserv. 2019, 43, 13880. [Google Scholar] [CrossRef]
  115. Luo, D.; Zhai, G.; Cao, S.; Zhu, T.; Chen, R.; Xiao, Q.; Zhang, D.; Ba, L. Effect of preharvest salicylic acid combined with postharvest 1-MCP treatment on quality and antioxidant ablity of plum fruit during storage. Science 2022, 43, 327–333. [Google Scholar] [CrossRef]
  116. Li, Y.; He, H.; Hou, Y.Y.; Kelimu, A.; Wu, F.; Zhao, Y.; Shi, L.; Zhu, X. Salicylic acid treatment delays apricot (Prunus armeniaca L.) fruit softening by inhibiting ethylene biosynthesis and cell wall degradation. Sci. Hortic. 2022, 300, 111061. [Google Scholar] [CrossRef]
Horticulturae 09 00108 g001 550
Figure 1. The induced resistance of 1-MCP and SA in postharvest fruits.
Figure 1. The induced resistance of 1-MCP and SA in postharvest fruits.
Horticulturae 09 00108 g001
Table
Table 1. Studies on the induced resistance effect of 1-MCP treatment on different types of fungus in postharvest fruits.
Table 1. Studies on the induced resistance effect of 1-MCP treatment on different types of fungus in postharvest fruits.
FruitsTreatment ConcentrationFungiReference
“Fuji” apple1 μL/LBotrytis cinerea[6]
“Everest” strawberry1 μL/LBotrytis cinerea[13]
Jujube1 μL/LBotrytis cinerea[16]
“Golden Delicious” apple0.3 μL/LColletotrichum acutatum[12]
Cactus pear1 μL/LColletotrichum gloeosporioides[17]
Carambola0.6 μL/LColletotrichum gloeosporioides[18]
Loquat50 nL/LColletotrichum gloeosporioides[19]
“Anxi” persimmon1.35 μL/LGloeosporium kaki[20]
“Dangshan” pear1 μL/LPenicillium digitatum[21]
“Emerald” pear1 μL/LPenicillium digitatum[22]
Citrus5 μL/LPenicillium digitatum[14]
“Fuji” apple5 μL/LPenicillium expansum[10]
“Golden Delicious” apple0.3 μL/LPenicillium expansum[23]
Peach0.6 μL/LPenicillium expansum[15]
“Hongyang” kiwifruit0.8 μL/LPhomopsis sp. [24]
Table
Table 2. Studies on the induced resistance effect of SA treatment to different type of fungus in postharvest fruits.
Table 2. Studies on the induced resistance effect of SA treatment to different type of fungus in postharvest fruits.
FruitsTreatment ConcentrationFungiReference
Apricot1 mmol/LAlternaria alternata[82]
Jujube2 mmol/LAlternaria alternata[81]
Tomato2 mmol/LBotrytis cinerea[83]
Banana2 mmol/L
2 mmol/L		Colletotrichum musae
Colletotrichum gloeosporioides		[84]
[85]
Mango1 mmol/L
5 mmol/L		Colletotrichum gloeosporioides
Colletotrichum gloeosporioides		[86]
[87]
Carambola1 mmol/LColletotrichum gloeosporioides[88]
Tomato200 μmol/LFusarium oxysporum[76]
Apple0.2 mmol/LGlomerella cingulata[89]
Cherry2 mmol/LMonilinia fructicola[90]
Apple0.3 mmol/LPenicillium expansum[91]
Peach0.05 mmol/LPenicillium expansum[83]
Citrus2.5 mmol/LPenicillium expansum[92]
Apple2.5 mmol/LPenicillium digitatum[76,78]
Citrus3 mmol/LPenicillium digitatum[79]
Grapefruit2 mmol/LPenicillium digitatum[93]
Pear0.2 mmol/LPhysalospora piricola[94]
Peach5 mmol/LRhizopus stolonifer[80]
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Meng, X.; Fang, J.; Fu, M.; Jiao, W.; Ren, P.; Yang, X. The Role of 1-methylcyclopropylene (1-MCP) and Salicylic Acid (SA) in Induced Resistance of Postharvest Fruits. Horticulturae 2023, 9, 108. https://doi.org/10.3390/horticulturae9010108

AMA Style

Meng X, Fang J, Fu M, Jiao W, Ren P, Yang X. The Role of 1-methylcyclopropylene (1-MCP) and Salicylic Acid (SA) in Induced Resistance of Postharvest Fruits. Horticulturae. 2023; 9(1):108. https://doi.org/10.3390/horticulturae9010108

Chicago/Turabian Style

Meng, Xiangzhi, Jiazhen Fang, Maorun Fu, Wenxiao Jiao, Pengfei Ren, and Xiaoying Yang. 2023. "The Role of 1-methylcyclopropylene (1-MCP) and Salicylic Acid (SA) in Induced Resistance of Postharvest Fruits" Horticulturae 9, no. 1: 108. https://doi.org/10.3390/horticulturae9010108

APA Style

Meng, X., Fang, J., Fu, M., Jiao, W., Ren, P., & Yang, X. (2023). The Role of 1-methylcyclopropylene (1-MCP) and Salicylic Acid (SA) in Induced Resistance of Postharvest Fruits. Horticulturae, 9(1), 108. https://doi.org/10.3390/horticulturae9010108

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