Effects Of Different Elicitors Treatments On Postharvest Blue Mold Decay In Sweet Cherry Fruit And The Possible Mechanisms

Sweet cherry(Prunus avium)is popular with consumers for its attractive red color,good flavor and high value of nutrients.The fruit is rich in carbohydrate,protein,vitamins,minerals and bioactive compounds such as anthocyanins,phenolics and carotenoids,which has high nutritional value and commercial value.Sweet cherry fruit matures and is commercially harvested in the hot early summer season.After harvest,the fruit has a high rate of respiratory metabolism.Meanwhile,the fruit is susceptible to mechanical injury and pathogenic attack due to its thin pericarp and juicy,so it has a short shelf-life under ambient temperature and adverse factors to storage and transportation.The fruit is susceptible to postharvest decay caused by several pathogenic fungi.Blue mold decay caused by P.expansum Link is one of the most important postharvest diseases of sweet cherries.Traditionally,control of postharvest diseases of fruits relies mainly on the application of synthetic fungicides.However,fungicide resistances of pathogens and public concern over chemical residues in food and environment have created interest in alternative approaches to disease control.In the storage and preservation methods of postharvest fruit and vegetable,heat treatment,a physical method,has been widely used to control fruit decay,delay ripening,and maintain quality,which has the advantage of safety,no pesticide residues and easy to operate.As a plant signaling molecule,methyl jasmonate(MeJA)plays an important role in plant growth and development,fruit ripening,and responses to environmental stress.As a non-protein amino acid,BABA has been shown to induce resistance response to protect numerous plants against various pathogens.The present study was designed to investigate the effect of hot air treatment,methyl jasmonate(MeJA)and ?-aminobutyric acid(BABA)on inhibiting blue mold decay caused by P.expansum in sweet cherry fruit(Prunus avium L.cv.Hongdeng),to evaluate the effect of defense-related enzymes activities,expression of defense-related genes and proteins,the effect of inhibitory in vitro and the possible mechanisms involved.The results were as follows:1.In order to determine the optimum condition of hot-air treatment enhanced disease resistance,the effect of hot-air treatment on inhibition efficiency of blue mould and quality in postharvest sweet cherry were investigated by response surface methodology(RSM).The harvested sweet cherry were treated in hot air at different temperatures(40?48?)for different treatment times(60?180 min),then inoculated with Penicillium expansum and stored at 20?for 5 days,lesion diameter,fruit firmness,content of ascorbic acid and TSS/TA were measured after storage.Four second-order quadratic equations were established,and the fitting degree were analyzed,the disease resistance and quality were also discussed through RSM.The results suggested that hot-air treatment temperature was 44?and the treatment time was 114 min.The optimum condition inhibited the blue mould in sweet cherry effectively and maintained the quality,which provided a theoretical foundation for application of hot-air treatment in sweet cherry fruit preservation.2.Effect of hot air(HA)treatment(44?,114 min)on reducing blue mold decay caused by Penicillium expansum in sweet cherry fruit was investigated.The results indicated that fruit treated with HA had significantly lower disease incidence and smaller lesion diameter than the control fruit did.HA treatment significantly enhanced activities of chitinase(CHI)and?-1,3-glucanase(GLU).The activities of polygalacturonase(PG)and pectinmethylesterase(PME)were significantly inhibited by HA treatment.Fruit treated with HA exhibited remarkably higher activities of superoxide dismutase(SOD),catalase(CAT),peroxidase(POD),and polyphenoloxidase(PPO)and lower activity of ascorbate peroxidase(APX)than control.Expression of defense related genes such as PaGLU,PaCAT,and PaNPRl-like was greatly induced in HA-treated fruit during storage,while the expression of expansins(EXP)was down-regulated by HA treatment.These results suggest that HA can effectively inhibit blue mold decay caused by P.expansum in harvested cherry fruit possibly by directly inducing disease resistance and delaying fruit tissue softening that helps to ward off the spread of pathogens.3.The effect of methyl jasmonate(MeJA)treatment on controlling blue mould decay caused by Penicillium expansum in sweet cherry fruit and the possible mechanisms were investigated.The results indicated that fruit treated with MeJA had significantly lower disease incidence and smaller lesion diameter than the control fruit did.The in vitro experiment showed that MeJA transiently inhibited spore germination and germ tube elongation of P.expansum.It is clear that MeJA triggers a priming mechanism in sweet cherry fruit,since only in fruit that had been pretreated with MeJA and then challenged with P.expansum was an enhanced capacity to augment defense responses observed.These augmented responses included enhanced activities of chitinase(CHI)and?-1,3-glucanase(GLU),and increased gene expression levels of catalase(CAT),calmodulin(CaM),GLU,phenylalanine ammonia-lyase(PAL),nonexpressor of pathogenesis-related genes 1(NPR1-like),and thaumatin-like(THAU).Moreover,MeJA inhibited the increase of activities of polygalacturonase(PG)and pectinmethylesterase(PME).MeJA treatment inhibited the increase of membrane permeability and MDA content and maintained the green color of stem and stem removal force.The results of two-dimensional polyacrylamide gel electrophoresis indicate that MeJA treatment enhance the expression of defense related protein and inhibit the basic metabolism of sweet cherry fruit.These results suggest that the efficacy of MeJA on controlling blue mould decay in sweet cherry fruit may be related to the transient direct inhibitory effect against the pathogens,suppressed activities of PG and PME,and the priming of defense responses.4.Fruit treated with 30mM BABA had significantly lower disease incidence and smaller lesion diameter than the control fruit did.The in vitro experiment showed that BABA significantly inhibited germ tube elongation of P.expansum spores,while no significant effect was observed in the germination of P.expansum spores.BABA treatment induced the increase of enzymes activities of GLU and CHI,enhanced the content of lignin and antioxidant activity.The effects of postharvest?-aminobutyric acid(BABA)treatment on fruit pectin degrading enzymes,cell wall constituents and microstructural alterations of pericarp in sweet cherry fruit were investigated.BABA significantly inhibited the increase of membrane permeability and the accumulation of malondialdehyde in cherries.The BABA-treated fruit exhibited significantly higher contents of water-soluble pectin,CDTA-soluble pectin,Na2CO3-soluble pectin,total pectin,cellulose and hemicellulose than the control during storage.Activities of pectin degrading enzymes including polygalacturonase and pectinmethylesterase were markedly reduced by BABA treatment.Observations by scanning electron microscopy showed BABA maintained smooth cuticle and integrated structure of subepidermal cell in sweet cherry.BABA-treated cherries had lower respiration rates and weight loss and higher levels of titratable acidity,ascorbic acid,fructose,glucose,sucrose,malic,citric and succinic acids compared with that in control fruit.BABA treatment inhibited the decrease of L*value of fruit pericarp.These results suggested that BABA enhanced the disease resistance of sweet cherry fruit,delayed the senescence of fruit and maintained the quality of fruit.