Development Of Chilling Injury Research Articles

Multi-omics analysis of the effects of low-temperature storage on chilling injury of bitter gourd

Bitter gourd fruit are susceptible to chilling injury when stored at 4 °C. In this study, bitter gourds were stored at 20 °C to simulate normal ripening and senescence processes, and at 4 °C to induce chilling injury. Transcriptomic, metabolomic, and proteomic analyses were employed to investigate the molecular mechanisms of chilling injury development during low-temperature storage. The results showed that low-temperature storage induced the expression of genes related to proline metabolism (delta-1-pyrroline-5-carboxylate synthase-like, ornithine--oxo-acid transaminase, and proline dehydrogenase2, mitochondrial-like), antioxidants (glutathione peroxidase 2, superoxide dismutase, and L-ascorbate peroxidase 6), and membrane lipid metabolism. Additionally, low-temperature storage affected the ICE-CBF-COR pathway (calcium-binding protein CML15 and transcription factor ICE1). Correspondingly, free fatty acids (9,12,13-trihydroxy-10,15-octadecadienoic acid, 9-hydroperoxy-10E,12,15Z-octadecadienoic acid, γ-linolenic acid, α-linolenic acid*) and phospholipid metabolites LysoPC (18:4, 20:3, 19:1) and LysoPE (20:3, 20:3*, 20:2*) also accumulated during storage. Low-temperature storage increased POD and GPX activities. Overall, chilling injury in bitter gourd was associated with the induction of genes involved in proline metabolism, antioxidant activity, membrane lipid metabolism, cold perception mechanisms, and plant hormone signal transduction.

MaHsf24, a novel negative modulator, regulates cold tolerance in banana fruits by repressing the expression of HSPs and antioxidant enzyme genes

SummaryTranscriptional regulation mechanisms underlying chilling injury (CI) development have been widely investigated in model plants and cold‐sensitive fruits, such as banana (Musa acuminata). However, unlike the well‐known NAC and WRKY transcription factors (TFs), the function and deciphering mechanism of heat shock factors (HSFs) involving in cold response are still fragmented. Here, we showed that hot water treatment (HWT) alleviated CI in harvested banana fruits accomplishing with reduced reactive oxygen species (ROS) accumulation and increased antioxidant enzyme activities. A cold‐inducible but HWT‐inhibited HSF, MaHsf24, was identified. Using DNA affinity purification sequencing (DAP‐seq) combined with RNA‐seq analyses, we found three heat shock protein (HSP) genes (MaHSP23.6, MaHSP70‐1.1 and MaHSP70‐1.2) and three antioxidant enzyme genes (MaAPX1, MaMDAR4 and MaGSTZ1) were the potential targets of MaHsf24. Subsequent electrophoretic mobility shift assay (EMSA), chromatin immunoprecipitation coupled with quantitative PCR (ChIP‐qPCR) and dual‐luciferase reporter (DLR) analyses demonstrated that MaHsf24 repressed the transcription of these six targets via directly binding to their promoters. Moreover, stably overexpressing MaHsf24 in tomatoes increased cold sensitivity by suppressing the expressions of HSPs and antioxidant enzyme genes, while HWT could recover cold tolerance, maintaining higher levels of HSPs and antioxidant enzyme genes, and activities of antioxidant enzymes. In contrast, transiently silencing MaHsf24 by virus‐induced gene silencing (VIGS) in banana peels conferred cold resistance with the upregulation of MaHSPs and antioxidant enzyme genes. Collectively, our findings support the negative role of MaHsf24 in cold tolerance, and unravel a novel regulatory network controlling bananas CI occurrence, concerning MaHsf24‐exerted inhibition of MaHSPs and antioxidant enzyme genes.

Modeling the relationship between postharvest storage conditions and grapefruit quality

The postharvest loss in quality of grapefruit during storage can be quantified by determining the change of the quality traits of grapefruit, including total soluble solids (TSS), titratable acidity (TA), TSS/TA, weight loss (WL), and the development of decay (DC) and chilling injury (CI). The objective of this study was, therefore, to develop models that encompass the relationship between both storage conditions and duration and the quality traits of grapefruit to predict the loss of grapefruit quality during storage. The models of TSS, TA and TSS/TA were developed with experimental data collected during the 2007–08 and 2008-09 growing seasons that were obtained from the literature. The models for WL, DC, and CI were developed with experimental data collected in Florida during the 2004–05 and 2005-06 growing seasons. The WL, DC and CI models were applied to determine storage life. The results indicated that there was a second-order polynomial relationship between storage duration and TSS and linear relationships between storage duration and TA and TSS/TA. A longer storage duration resulted in a higher TSS, a lower TA and a higher TSS/TA. There were linear relationships between storage duration and WL, thermal time above a threshold temperature of 0 °C and DC and thermal time below 10 °C and CI, with higher WL, DC and CI resulting from longer storage duration and larger number of thermal times. Model performance for simulating TSS, TA, TSS/TA for storage temperature between 2 °C and 11 °C was good. There is good performance for simulating WL for storage temperature between 4 °C and 12 °C, DC for storage temperature of 21.1 °C, and CI for storage temperature of 4.4 °C. Following model development, it was applied to determine the optimum storage life. Optimum storage condition was a storage temperature of 7.6 °C for approximately 20 d, resulting in less than 5 % of the stored fruits lost due to unacceptable quality based on predictions for WL, DC and CI.

The Role of MaWRKY70 in Regulating Lipoxygenase Gene Transcription during Chilling Injury Development in Banana Fruit.

Banana is a typical cold-sensitive fruit; it is prone to chilling injury (CI), resulting in a quality deterioration and commodity reduction. However, the molecular mechanism underlying CI development is unclear. In this study, cold storage (7 °C for 5 days) was used to induce CI symptoms in bananas. As compared with the control storage (22 °C for 5 days), cold storage increased the CI index and cell membrane permeability. Moreover, we found that the expression levels of the WRKY transcription factor MaWRKY70 were increased consistently with the progression of CI development. A subcellular localization assay revealed that MaWRKY70 was localized in the nucleus. Transcriptional activation analyses showed that MaWRKY70 processed a transactivation ability. Further, an electrophoretic mobility shift assay (EMSA) and dual-luciferase reporter (DLR) assays showed that MaWRKY70 was directly bound to the W-box motifs in the promoters of four lipoxygenase (LOX) genes associated with membrane lipid degradation and activated their transcription. Collectively, these findings demonstrate that MaWRKY70 activates the transcription of MaLOXs, thereby acting as a possible positive modulator of postharvest CI development in banana fruit.

Dissecting postharvest chilling injuries in pome and stone fruit through integrated omics.

Lowering the storage temperature is an effective method to extend the postharvest and shelf life of fruits. Nevertheless, this technique often leads to physiological disorders, commonly known as chilling injuries. Apples and pears are susceptible to chilling injuries, among which superficial scald is the most economically relevant. Superficial scald is due to necrotic lesions of the first layers of hypodermis manifested through skin browning. In peaches and nectarines, chilling injuries are characterized by internal symptoms, such as mealiness. Fruits with these aesthetic or compositional/structural defects are not suitable for fresh consumption. Genetic variation is a key factor in determining fruit susceptibility to chilling injuries; however, physiological, or technical aspects such as harvest maturity and storage conditions also play a role. Multi-omics approaches have been used to provide an integrated explanation of chilling injury development. Metabolomics in pome fruits specifically targets the identification of ethylene, phenols, lipids, and oxidation products. Genomics and transcriptomics have revealed interesting connections with metabolomic datasets, pinpointing specific genes linked to cold stress, wax synthesis, farnesene metabolism, and the metabolic pathways of ascorbate and glutathione. When applied to Prunus species, these cutting-edge approaches have uncovered that the development of mealiness symptoms is linked to ethylene signaling, cell wall synthesis, lipid metabolism, cold stress genes, and increased DNA methylation levels. Emphasizing the findings from multi-omics studies, this review reports how the integration of omics datasets can provide new insights into understanding of chilling injury development. This new information is essential for successfully creating more resilient fruit varieties and developing novel postharvest strategies.

Metabolism and transcriptional regulation in chilling injury development of nectarine fruit during postharvest cold storage

Peach fruit is susceptible to chilling injury during postharvest long-term cold storage, but the understanding of metabolic and transcriptional reaction of nectarine cultivar fruit to cold storage remains incomplete. In this study, nectarine fruit was used for a low temperature treatment, which gradually leading to the deterioration of fruit quality. Comparative metabolome and transcriptome analyses were performed to comprehensively understand the metabolic and transcriptional changes occurring during cold storage in nectarine fruit. The result showed that numerous primary and secondary metabolites exhibited increased levels following the low-temperature treatment. And there were 3400 differentially expressed genes continuously regulated by cold storage, which were mostly enriched in metabolic and secondary metabolite biosynthesis pathways. The combined pathways enrichment of differential metabolites and genes were primarily centered on secondary metabolite biosynthesis. Correspondingly, a strong correlation was observed between changes in secondary metabolites and the expression of key enzymes including 4-coumarate CoA ligase (4CL), hydroxycinnamoyl-CoA shikimate/quinate hydroxycinnamoyl transferase (HCT), flavonol synthase (FLS), dihydroflavonol reductase (DFR), and UDP-glycose flavonoid glycosyltransferase (UFGT), which were involved in flavonoids biosynthesis. Additionally, several fruit quality characteristics (carotenoids, cell wall components, antioxidant enzymes) and stress related signaling genes were markedly affected by cold storage. These findings offer new insights into the networks governing metabolic and transcriptional regulation during nectarine fruit cold storage.

Azacytidine shows potential in controlling the chilling injury of banana peel during cold storage

Banana suffers from chilling injury at low temperatures, which significantly challenges industrial banana quality control worldwide without a widely-accepted solution, to date. In this study, 5-azacytidine (5-azaC), a common DNA methylation inhibitor (DNA methylation is a conserved modification that regulates physiological processes), was used to treat banana fingers with subsequent storage at 7 °C for 9 days, which can be a novel strategy for controlling banana peel chilling injury and quality deterioration. In most sampling days, 5-azaC treatment significantly increased lightness value (L*), hue angle, and firmness while significantly decreased the browning index. Surprisingly, the chilling injury index was persistently declined by 5-azaC up to 26.8 % (p < 0.05). 5-azaC also reduced electrolyte leakage and levels of malondialdehyde and reactive oxygen species, indicating the control of chilling injury development. Further results showed that 5-azaC-inhibited DNA methylation contributed to banana chilling injury control by modulating the redox system and energy homeostasis. Collectively, this study offered new insights into fruit chilling injury development and control, as well as inspired potential strategies for postharvest quality control.

Melatonin: A biomolecule for mitigating postharvest chilling injury in fruits and vegetables

AbstractThe best strategy to extend the shelf life of fresh horticultural produce is to keep it at a low temperature. However, storing fruits and vegetables at a temperature lower than their recommended storage temperature and above the freezing point for a prolonged time leads to the development of chilling injury (CI). Melatonin (MT) being a versatile biological signal has been reported to possess antioxidant properties that aid in mediating stress response and extending the postharvest storage life of horticultural crops. Among CI‐induced mechanisms, MT substantially reduces oxidative stress by elevating the reactive oxygen species scavenging and triggering the phenol accumulation in association with 2, 2‐diphenyl‐1 picryl hydrazyl scavenging activity. Besides, MT increases intracellular energy by maintaining a proper ratio of unsaturated to saturated fatty acid and improving cellular fluidity. Additionally, MT regulates arginine metabolism by maintaining the γ‐aminobutyric acid synthesis. Furthermore, MT encodes the mitogen‐activated protein kinases, and calcium‐dependent protein kinases cascade and acclimate to cold stress by activating C‐repeat binding factors and helps in maintaining postharvest quality. This review reports the recent progress of MT‐induced physiological, biochemical, and molecular mechanisms for enhancing chilling tolerance, which can elevate the marketability and earnings from postharvest horticultural crops.

Melatonin mobilizes the metabolism of sugars, ascorbic acid and amino acids to cope with chilling injury in postharvest pear fruit

Chilling injury manifesting as internal browning is an irreversible physiological disorder in cold-stored ‘Yali’ pear fruit, which seriously restricts postharvest handling and commercialization of pear fruit. This study investigated the impact of melatonin (MN) treatment on chilling injury and the metabolism of sugars, ascorbic acid (AsA), proline, and γ-aminobutyric acid (GABA) during chilling injury development in ‘Yali’ pears. The findings revealed that MN-treated pear fruit exhibited considerably improved tolerance to chilling stress compared with untreated control fruit. MN application augmented proline accumulation, likely owing to increased activities and transcriptional concentrations of Δ1-pyrroline-5-carboxylate synthase and ornithine-δ-aminotransferase as well as diminished activity and transcriptional level of proline dehydrogenase. MN immersion increased enzyme activities and gene expression related to the GABA shunt pathway, leading to increased GABA concentrations in cold-stored pear fruit. Furthermore, MN treatment elevated AsA concentrations in the fruit, exerting protective effects against cell membrane damage and mitigating oxidative stress damage caused by chilling. Compared with the control group, MN-treated fruit exhibited reduced neutral invertase enzyme activity and gene expression. Additionally, MN treatment increased both sucrose-phosphate synthase and sucrose synthase activities and gene expression in pear fruit. These observations indicated that the enhanced chilling tolerance of ‘Yali’ pear fruit following MN treatment may be associated with the regulation of proline, GABA, AsA, and soluble sugars metabolism.

Methyl salicylate-improved mitochondrial stability obstructed cell death activation in preventing visible chilling injury in sweet basil under cold storage

Mitochondrial stability plays an important part in compelling plant senescence and physiological disorders. The research aimed to investigate the role of mitochondrial reactive oxygen species (ROS) and oxidative damage in mediated cell death and chilling in sweet basil and to investigate the role of methyl salicylate (MeSA) immersion in retarding chilling injury development via activation of antioxidant defense systems to protect mitochondria-induced deterioration. Sweet basils were subjected to a 5-min immersion in 1 mM MeSA and stored at 6 °C for 8 d. In the control group, evident symptoms of chilling injury were observed on day 4, coinciding with a substantial accumulation of mitochondrial ROS and reduction in mitochondrial stability, particularly evident in cytochrome c dissipation. Concurrently, an increase in caspase-like enzyme activities, known to drive cell death, was observed following exposure to low temperatures. In contrast, chilling injury was mitigated in the MeSA-treated leaves. The MeSA treatment significantly enhanced the overall antioxidant capacity of the mitochondria and improved mitochondrial stability, thereby preventing the activation of caspase-like enzymes. Consequently, this treatment preserved membrane integrity and suppressed cell death activation, ultimately leading to a delay in the appearance of cold damage during storage.

The role of respiratory metabolism in chilling injury development of Chinese olive fruit during cold storage

Chilling injury (CI) and browning occurrence are pivotal issues during the cold storage of postharvest Chinese olive fruit. This study evaluates the effects of non-chilling temperature (8 °C) and chilling temperature (2 °C) on CI development, browning occurrence, and respiratory metabolism in postharvest Chinese olives. Compared to storage at 8 °C, storage at 2 °C significantly induced CI, accompanied by higher indices of CI and browning, as well as a higher fruit respiratory rate. Storage at 2 °C increased the activities of phosphohexose isomerase (PGI), succinate dehydrogenase (SDH), ascorbic acid oxidase (AAO), and cytochrome C oxidase (CCO) by 55.1%, 11.1%, 26.4%, and 98.8%, respectively, on day 120. On the other hand, storage at 2 °C reduced the activities of NAD kinase (NADK), 6-phosphogluconate dehydrogenase (6-PGDH) + glucose-6-phosphate dehydrogenase (G-6-PDH) by 95.6% and 6.6%, respectively, on day 120. The contents of nicotinamide adenine dinucleotide (NAD) and its reduced form of NAD (NADH) increased by 10.0% and 22.8%, respectively, in fruit stored at 2 °C on day 120. Conversely, the contents of nicotinamide adenine dinucleotide phosphate (NADP) and its reduced form (NADPH) decreased by 58.3% and 64.4%, respectively, in fruit stored 2 °C on day 120. These findings indicate that CI development and browning occurrence in Chinese olives induced by storage at 2 °C were associated with a higher respiratory rate, increased activities of PGI, SDH, AAO, and CCO, higher contents of NAD(H), reduced activities of 6-PGDH + G-6-PDH, and lower contents of NADP(H).

Transcriptomic analysis in tomato fruit reveals divergences in genes involved in cold stress response and fruit ripening.

Cold storage is widely used to extend the postharvest life of most horticultural crops, including tomatoes, but this practice triggers cold stress and leads to the development of undesirable chilling injury (CI) symptoms. The underlying mechanisms of cold stress response and CI development in fruits remain unclear as they are often intermingled with fruit ripening changes. To gain insight into cold responses in fruits, we examined the effect of the potent ethylene signaling inhibitor 1-methylcyclopropene (1-MCP) on fruit ripening, CI occurrence and gene expression in mature green tomatoes during storage at 20°C and 5°C. 1-MCP treatments effectively inhibited ethylene production and peel color changes during storage at 20°C. Storage at 5°C also inhibited both ethylene production and peel color change; during rewarming at 20°C, 1-MCP treatments inhibited peel color change but failed to inhibit ethylene production. Furthermore, fruits stored at 5°C for 14 d developed CI symptoms (surface pitting and decay) during the rewarming period at 20°C regardless of 1-MCP treatment. Subsequent RNA-Seq analysis revealed that cold stress triggers a large-scale transcriptomic adjustment, as noticeably more genes were differentially expressed at 5°C (8,406) than at 20°C (4,814). More importantly, we have found some important divergences among genes involved in fruit ripening (up- or down-regulated at 20°C; inhibited by 1-MCP treatment) and those involved in cold stress (up- or down-regulated at 5°C; unaffected by 1-MCP treatment). Transcriptomic adjustments unique to cold stress response were associated with ribosome biogenesis, NcRNA metabolism, DNA methylation, chromatin formation/remodeling, and alternative splicing events. These data should foster further research into cold stress response mechanisms in fruits with the ultimate aim of improving tolerance to low temperature and reduction of CI symptoms during cold storage.

Elevated level of chilling tolerance in cucumber fruit was obtained by β-aminobutyric acid via the regulation of antioxidative response and metabolism of energy, proline and unsaturated fatty acid

• BABA treatment enhances the chilling tolerance in cucumber fruit. • BABA application improved the antioxidant capacity of harvested cucumber fruit. • BABA-treated fruit exhibited higher level of energy status. • BABA promoted proline accumulation and maintained higher level of UFA contents. This experimental study was conducted to investigate the effects of β-aminobutyric acid (BABA) on chilling injury in cold-stored cucumber fruit. Results showed that BABA decreased the development of chilling injury in cucumber fruit. BABA-treated fruit exhibited elevated antioxidant ability, indicated by high activities of superoxide dismutase (SOD) and catalase (CAT) and low levels of hydrogen peroxide and superoxide anion. BABA treatment maintained a high level of energy status by promoting the activities and genes expression of H + -ATPase, Ca 2+ -ATPase, succinate dehydrogenase (SDH) and cytochrome C oxidase (CCO). Increased enzymes activities and genes expression of Δ 1 -pyrroline-5-carboxylate synthase (PCS) and ornithine-δ-aminotransferase (OAT) and depressed enzyme activity and gene expression of proline dehydrogenase (PDH) in BABA-treated cucumber collectively promoted the accumulation of proline. Furthermore, BABA treatment delayed the decreasing trend of unsaturated fatty acid content in cucumber. Thus, BABA is effective in enhancing chilling tolerance in cucumber fruit possibly by improving the antioxidant ability and adjusting the metabolism of energy, proline and unsaturated fatty acids.

Effect of exogenous melatonin in fruit postharvest, crosstalk with hormones, and defense mechanism for oxidative stress management

AbstractDerived from tryptophan, melatonin (MT; N‐acetyl‐5‐methoxytryptamine) is a ubiquitous indoleamine that is widely distributed in species ranging from microorganisms to mammals. It has been associated to play vital roles in the human body like cardiac rhythms, immunological enhancement, and antioxidant activity. In plants, it is a pleiotropic molecule with multiple roles, as it not only performs extensive functions like delaying senescence, growth and development regulation, exerting antioxidant effects, and facilitating adaption of plants to certain biotic and abiotic stress responses but also provides resistance to chilling injury and disease development. This paper reviews the latest progress in the multiple roles of MT in fruits, summarizes the pathways for its biosynthesis, and presents the relation of MT with plant hormones, like auxin, cytokinin, ethylene, gibberellins, abscisic acid, jasmonic, and salicylic acid, and highlights the effect of postharvest application of MT on physiology and quality of fruits, action mechanisms, and safety regulations of MT. Recent trends focus on using alternatives that are safe for postharvest produce and do not have major side effects. MT is a better alternative to hazardous chemicals being commercially used in the postharvest management of fruits and providing future directions for its utilization.

Nitric oxide is involved in melatonin-induced cold tolerance in postharvest litchi fruit

Previous studies indicate that melatonin, as an important bioactive molecule, appreciably improves cold tolerance in postharvest litchi fruit. However, whether other signaling molecules are involved in melatonin-induced cold tolerance in litchi fruit has not been clarified. In this study, the effect of the interplay between melatonin and nitric oxide (NO) on chilling stress tolerance in relation to redox homeostasis in litchi fruit was investigated. In the first experiment, exogenous applications of melatonin and sodium nitroprusside (SNP) showed similar efficacy in decelerating the development of chilling injury (CI), as indicated by lower CI index and higher retention of pericarp redness in litchi fruit during refrigeration, whereas the opposite effect was found with NO scavenger 2-(4-carboxyphenyl)− 4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO). The ameliorating effect of melatonin on CI was evidently impaired under cotreatment with melatonin and cPTIO (melatonin + cPTIO). In the second experiment, the biochemical response of litchi fruit to melatonin and melatonin + cPTIO during cold storage was analyzed. The results exhibited that melatonin triggered NO accumulation by activating nitrate reductase (NR) and nitric oxide synthase (NOS) in refrigerated litchi fruit. Melatonin-induced NO accumulation was reduced under treatment with melatonin + cPTIO, but this combined treatment did not affect the NR and NOS activities when compared to melatonin alone. Reactive oxygen species (ROS) in melatonin-treated fruit were markedly quenched by activating antioxidant enzymes and increasing antioxidant metabolite contents, thus alleviating membrane lipid peroxidation and maintaining membrane integrity. Melatonin also led to increased expression of oxidized protein repair-related genes, including LcMsrA1, LcMsrA2, LcMsrB1, LcMsB2, LcTrx2 and LcNTR1. Moreover, an enhanced level of protein S-nitrosylation was observed in fruit upon melatonin treatment. However, the above physiological effect associated with improved fruit cold tolerance afforded by melatonin was partially counteracted by cPTIO. The results suggest that endogenous NO could mediate melatonin-induced cold tolerance in litchi fruit via regulation of redox status.

Aroma volatiles as predictors of chilling injury development during peach (Prunus persica (L) Batsch) cold storage and subsequent shelf-life

As peaches ripen and deteriorate quickly, cold storage is used to extend their marketability. However, peach cold storage is limited by the development of physiological disorders, such as chilling injury (CI), that express during subsequent shelf-life. The aim of this research was three-fold: first, to determine CI incidence in the melting flesh ‘Red Haven’ peach stored at different temperatures throughout postharvest; secondly, to characterize and compare differences among these fruit with regards to ethylene production rates, physicochemical properties, flesh texture, and aroma volatile profiles; and thirdly, to assess correlations among CI incidence and all the evaluated features, and identify potential key aroma volatile compounds that could predict early stage peach CI development during storage. Fruit were harvested at optimal maturity and stored at 0 °C, 5 °C, and 20 °C for up to 30 d. Evaluations were conducted at harvest (0) and after 1, 3, 5, 15, and 30 d of storage, with and without 3 d shelf-life period. Fruit stored at 5 °C were sensitive to CI displaying impaired capacity for ethylene production, and alterations in fruit textural properties, including reduced expressible juice contents and failure to soften. Chilling-injured fruit decreased accumulation of fruity note lactones, esters and terpenoids (i.e., linalool), and increased production of aldehydes and alcohols, as compared to sound fruit. Furthermore, multivariate regression identified thirteen potential key volatiles that could predict peach CI. These volatiles could be used as markers to discriminate chilling-injured from sound fruit at early stages of development of the disorder, optimizing cold storage and fruit handling practices, while decreasing loss and waste.

Transcriptional repression of MaRBOHs by MaHsf26 is associated with heat shock-alleviated chilling injury in banana fruit

Both heat shock factors (Hsfs) and reactive oxygen species (ROS) are widely perceived to be involved in chilling stress response. However, the particular mechanism of Hsfs mediated-ROS metabolism related to chilling stress remains largely unknown, especially during chilling injury development of postharvest economically cold-sensitive fruit such as banana. In this study, we found that heat shock treatment (HST) could effectively alleviate postharvest banana chilling injury and reduce ROS accumulation during storage. The expression levels of several respiratory burst oxidase homolog (RBOH) genes, encoding ROS-producing enzymes, increased consistently with the progression, whereas were inhibited upon HST. Significantly, we identified an Hsfs MaHsf26, which exhibited a opposite expression pattern as that of MaRBOHs, as the putative binding protein of MaRBOHB-like1, MaRBOHE-like and MaRBOHF-like promoters using yeast one-hybrid (Y1H) screening analysis. Further electrophoretic mobility shift assay (EMSA) and dual luciferase reporter (DLR) analysis displayed MaHsf26 suppressed the transcriptions of MaRBOHB-like1, MaRBOHE-like and MaRBOHF-like through binding to the heat shock elements (HSE) in their promoters, respectively. In general, our results suggested that MaHsf26 plays as a transcriptional repressor of ROS generation by suppressing the transcriptions of MaRBOHs and thereby involving in the HST-mitigated chilling injury in postharvest banana fruit.

Effect of storage temperature on development of chilling injury and its transcriptome analysis in ‘Fuyu’ persimmon fruit with or without 1-MCP treatment

Effect of storage temperature on development of chilling injury and its transcriptome analysis in ‘Fuyu’ persimmon fruit with or without 1-MCP treatment

Antioxidative Responses to Pre-Storage Hot Water Treatment of Red Sweet Pepper (Capsicum annuum L.) Fruit during Cold Storage.

The effects of hot water treatments on antioxidant responses in red sweet pepper (Capsicum annuum L.) fruit during cold storage were investigated. Red sweet pepper fruits were treated with hot water at 55 °C for 1 (HWT-1 min), 3 (HWT-3 min), and 5 min (HWT-5 min) and stored at 10 °C for 4 weeks. The results indicated that HWT-1 min fruit showed less development of chilling injury (CI), electrolyte leakage, and weight loss. Excessive hot water treatment (3 and 5 min) caused cellular damage. Moreover, HWT-1 min slowed the production of hydrogen peroxide and malondialdehyde and promoted the ascorbate and glutathione contents for the duration of cold storage as compared to HWT-3 min, HWT-5 min, and control. HWT-1 min enhanced the ascorbate-glutathione cycle associated with ascorbate peroxidase, monodehydroascorbate reductase, dehydroascorbate reductase, and glutathione reductase, but it was less effective in simulating catalase activity. Thus, HWT-1 min could induce CI tolerance in red sweet pepper fruit by activating the ascorbate-glutathione cycle via the increased activity of related enzymes and the enhanced antioxidant level.

Nitric oxide alleviates chilling injury by regulating the metabolism of lipid and cell wall in cold-storage peach fruit

Peach fruit are prone to development of chilling injury during cold storage at around 0–7 °C. Nitric oxide (NO) has been proven to alleviate chilling injury, but the mechanism was still unclear. In this study, peach fruit were immersed in a NO donor (sodium nitroprusside, SNP) solution for 10 min, then stored at 0 °C. The SNP alleviated chilling injury, including decreasing the internal browning index, malondialdehyde content, electrolyte leakage, and lipoxygenase activity, and maintaining firmness. Furthermore, SNP maintenance of fruit firmness was associated with reduction of xyloglucan endotransglycosylase/hydrolase family member gene expression and decrease of cell wall hydrolase activity, especially the activities of polygalacturonase, xyloglucan endoglycosyl transferase, cellulase, and β-galactosidase. Meanwhile, SNP regulated the lipid metabolism by up-regulating the expression of genes encoding glycerol-3-phosphate acyltransferase, ketoacy-ACP synthase, phosphatidylinositol bisphosphate and long-chain acyl-CoA. Thus, the results of this study indicate that SNP alleviates chilling injury of post-harvest peach fruit by regulating cell wall and lipid metabolism.