Chilling Tolerance Of Banana Fruit Research Articles

Banana ERF transcription factor MaERF110 is involved in ethylene-induced chilling tolerance by regulating ROS accumulation

Banana fruit is susceptive to chilling injury (CI), resulting in quality deterioration. Although ethylene treatment alleviates banana CI symptom, the underlying mechanism remains largely unknown. Here, as compared with control banana fruit, ethrel (an ethylene-releasing compound) treatment maintained lower levels of CI index and relative electrolytic leakage, lower contents of malondialdehyde (MDA) and reactive oxygen species (ROS) in cold-stored fruit and inhibited the expressions of ROS-synthesis genes, including MaRbohB, MaRbohE, and MaRbohJ. A potential upstream regulator of MaRbohE was identified by Yeast one-hybrid assay and named as MaERF110. Ethrel repressed MaERF110 expression during cold storage, and MaERF110 protein was localized in the nucleus with transcriptional activation activity. Gel mobility shift assay and dual-luciferase reporter assay displayed that MaERF110 bound to GCC-box in the promoters of MaRbohB, MaRbohE, and MaRbohJ and activated their expressions. Thus, the results expand our understandings of ethylene-improved chilling tolerance in banana fruit during cold storage.

Melatonin maintained higher contents of unsaturated fatty acid and cell membrane structure integrity in banana peel and alleviated postharvest chilling injury

Exogenous melatonin confers the chilling tolerance of banana fruit by promoting reactive oxygen species (ROS) scavenging system and inducing the unsaturated fatty acid synthesis. The results showed that melatonin treatment increased the contents of phospholipids, promoted the ROS scavenging enzyme, and restrained the activities of lipoxygenase (LOX), and thus reduced the lipid peroxidation of banana peel. In addition, melatonin treatment increased the flavonoids and proline contents, which was conducive to antioxidant capacity. Interestingly, the enhanced antioxidant capacity is conducive to the stability of unsaturated fatty acids and reduce the enzymatic browning reaction. Moreover, melatonin treatment induced the expression of omega-3/6 fatty acid desaturase and triggered the fatty acid metabolism activity, by which maintained higher contents of unsaturated fatty acid in banana peel. Moreover, melatonin treatment stimulated the accumulation of fatty acids in banana peel, and was involved in alleviating fruit chilling injury.

Brassinolide alleviated chilling injury of banana fruit by regulating unsaturated fatty acids and phenolic compounds

The effects of brassinolide (BL) on alleviating the occurrence of chilling injury (CI) of banana fruit were investigated. The present results showed that BL effectively decreased the CI index, enhanced the proline accumulation, reduced the malondialdehyde production, and accelerated starch degradation. Meanwhile, it also enhanced the activities of antioxidative enzymes and contents of the phenolic compounds, and decreased the reactive oxygen species accumulation. Higher integrity of plasma membrane was observed in the epidermal tissues and higher levels of unsaturated fatty acids were detected in the membrane, indicated that BL enhanced membrane lipid fluidity and maintained the cell membrane integrity of banana fruit. In conclusion, BL treatment is a potential method in enhancing chilling tolerance of banana fruit under low temperature storage or cold chain circulation.

Banana MaABI5 is involved in ABA-induced cold tolerance through interaction with a RING E3 ubiquitin ligase, MaC3HC4-1

Abstract Abscisic acid (ABA) is a phytohormone essential for the adaptation of plants to environmental stresses, and transcription factor abscisic acid-insensitive 5 (ABI5) is a key regulator of ABA signaling and response. Although exogenous application of ABA is effective in retarding chilling injury (CI) symptoms of banana fruit, the possible roles of ABI5 in ABA-induced chilling tolerance in banana fruit remain largely unknown. In this study, ABA treatment significantly induced chilling tolerance in banana fruit, as indicated by the changes in the CI index, peel color, and relative electrolyte leakage. Moreover, MaABI5, a gene encoding banana ABI5, was induced by ABA treatment during low-temperature storage. Importantly, through yeast two-hybrid (Y2H) screening, MaABI5 was found to interact with MaC3HC4-1, a C3HC4-type RING finger E3 ubiquitin ligase. Expression of MaC3HC4-1 was downregulated by ABA application. Furthermore, MaC3HC4-1 possessed intrinsic ubiquitin ligase activity in vitro. The predicted MaABI5–MaC3HC4-1 network will help decipher the possible role of ABA in the cold stress signaling pathway of banana fruit.

Antioxidant enzyme activities and exogenous ascorbic acid treatment of ‘Williams’ banana during long-term cold storage stress

Abstract The effect of exogenous ascorbic acid (AA) application on chilling injury (CI) of banana fruit ‘Williams’ (Giant Cavendish AAA sub-group) harvested at the mature green stage. The investigation aimed to increase chilling tolerance of banana fruits under cold storage temperature. The experiment was carried throughout growth two seasons 2014 and 2015. Fruits were immersed in 0, 3, 6, and 9 mM ascorbic acid (AA) for 15 min at cold temperature. Thereafter, fruits were stored at cold temperature (6 ± 1 °C with 90% RH) for 27days. The results pointed out that the immersing banana fruits at 9 mM of AA were most effective in reducing chilling injury incidences in fruit peel. Also, the treatment reduced increases in cell membrane dysfunction at to lipid peroxidation (MDA) and protein oxidation (PCG) accumulation consequently, decreases ion leakage. Moreover, immersing in AA at 9 mM minimized superoxide anion (O2 −) and H2O2 production. Also, it increased significantly antioxidant enzyme activities during cold storage stress of ascorbate peroxidase (APX; CE: 1.11.1.11), peroxidase (POD; EC: 1.11.1.7), catalase (CAT; EC:1.11.1.6), and superoxide dismutase (SOD; EC: 1.15.1.1) so, less chilling injury symptoms on fruit peel which it reflects on fruit appearing compared to control fruit and other AA treatments. These results pointed out that the AA treatments at 9 mM might increase chilling tolerance of banana fruit by increasing antioxidant enzyme activities. Consequently, decrease/alleviate O2 − and H2O2 generation during cold storage stress. Thus, exogenous AA treatment at 9 mM could be a useful application to reduce/delay/alleviate CI in banana fruit during cold storage.

Enhanced chilling tolerance of banana fruit treated with malic acid prior to low-temperature storage

The effects of postharvest malic acid (MA) treatment on alleviating the occurrence of chilling injury (CI) symptoms in banana (Musa spp., AAA group, cv. Brazil) fruit under 6°C were evaluated. Application of 80mM MA alleviated CI symptoms (surface browning), delayed the decrease in chlorophyll fluorescence (Fv/Fm) and chlorophyll content. The activities of peroxidase (POD) and polyphenol oxidase (PPO) were also suppressed by MA. Furthermore, compared with the control group, fruit that were treated with MA showed lower levels of reactive oxygen species, but higher antioxidant activities. The results suggest that the application of MA, as an organic acid, exhibited the potential for alleviating chilling injury symptoms of banana fruit by reducing skin browning and inducing antioxidant activities under low temperature.

Effect of nitric oxide on energy metabolism in postharvest banana fruit in response to chilling stress

Effects of postharvest nitric oxide (NO) treatment on energy metabolism and chilling injury in cold-stored banana fruit were investigated. Banana fruit were treated with 0.05mM NO donor sodium nitroprusside, and then stored at 7°C for up to twenty days. NO treatment apparently inhibited the development of chilling injury. The contents of adenosine triphosphate (ATP) and energy charge in the NO-treated fruit were significantly higher than control fruit. Meanwhile, the activities of enzymes involved in energy metabolism, including H+-ATPase, Ca2+-ATPase, succinic dehydrogenase and cytochrome C oxidase were markedly enhanced by NO treatment. In addition, notably elevated activities of fructokinase, glucokinase, glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase were observed in NO-treated banana fruit. These results indicated that NO could enhance chilling tolerance of banana fruit through maintaining high levels of energy status and inducing enzyme activities involved in energy metabolism during cold storage.

Molecular characterization of a cold-responsive RING-H2 finger gene from banana fruit and its interaction with MaMYC2a

Many reports indicate that RING finger proteins play key roles in regulating plant defense responses against abiotic and biotic stresses, but few have thus far been investigated in economic fruit, such as bananas. In this study, a RING finger gene, designated MaRING1, was isolated and characterized from banana fruit. MaRING1 belonged to the ATL RING-H2 finger protein family, and localized preferentially to the nucleus. Gene expression profiles revealed that MaRING1 was cold-responsive and induced by methyl jasmonate (MeJA) treatment during cold storage. Moreover, yeast two-hybrid (Y2H) and bimolecular fluorescence complementation (BiFC) assays showed that MaRING1 physically interacted with MaMYC2a, a transcription factor (TF) related to MeJA-induced chilling tolerance of banana fruit. Taken together, our results suggest that MaRING1 might functionally coordinate with MaMYC2a in response to cold stress of banana fruit, expanding our understanding of the possible involvement of RING finger proteins in the regulatory network of MeJA-induced chilling tolerance.

Impact of postharvest nitric oxide treatment on antioxidant enzymes and related genes in banana fruit in response to chilling tolerance

Banana fruits harvested at the mature green stage were treated with 60μLL−1 nitric oxide (NO) for 3h at 22°C, and then stored at 7±1°C with 90% RH for 15 days. The results showed that the application of NO at 60μLL−1 was most effective in reducing chilling injury in banana fruit. The treatment reduced increases in electrolyte leakage and malondialdehyde content, and delayed increases in both superoxide anion (O2−) production rate and H2O2 content. Fruit treated with NO exhibited higher activities of superoxide dismutase (SOD), catalase (CAT), peroxidase (POD), and ascorbate peroxidase (APX), and significantly higher expression of MaSOD, MaCAT, MaPOD and MaAPX genes than control fruit during storage. These results indicate that NO treatment might enhance chilling tolerance of banana fruit via improving the activities of antioxidant enzymes and inducing the expression of antioxidant-related genes.

Induction of jasmonate signalling regulators MaMYC2s and their physical interactions with MaICE1 in methyl jasmonate‐induced chilling tolerance in banana fruit

MYC2, a basic helix-loop-helix (bHLH) transcription factor, is a key regulator in the activation of jasmonate (JA) response. However, the molecular details of MYC2 involving in methyl jasmonate (MeJA)-induced chilling tolerance of fruit remain largely unclear. In the present work, two MYC2 genes, MaMYC2a and MaMYC2b, and one homolog of the inducer of the C-repeat-binding factor (CBF) gene, MaICE1 were isolated and characterized from banana fruit. MaMYC2s and MaICE1 were found to be all localized in the nucleus. In addition, the proline-rich domain (PRD) and the acidic domain (AD) in the N-terminus were important for the transcriptional activation of MaMYC2 in yeast cells. Unlike MaICE1's constitutive expression, MaMYC2a and MaMYC2b were induced rapidly following MeJA treatment during cold storage. Moreover, protein-protein interaction analysis confirmed that MaMYC2s interacted with MaICE1. The expression of ICE-CBF cold-responsive pathway genes including MaCBF1, MaCBF2, MaCOR1, MaKIN2, MaRD2 and MaRD5 was also significantly induced by MeJA. Taken together, our work provides strong evidence that MaMYC2 is involved in MeJA-induced chilling tolerance in banana fruit through physically interacting and likely functionally coordinating with MaICE1, revealing a novel mechanism for ICE1 in response to cold stress as well as during development of induced chilling tolerance.

Expression of three sHSP genes involved in heat pretreatment‐induced chilling tolerance in banana fruit

Banana fruit is highly susceptible to chilling injury. In previous research it was shown that heat pretreatment of banana fruit at 38 °C for 3 days before storage at a chilling temperature of 8 °C for 12 days prevented increases in visible chilling injury index, electrolyte leakage and malondialdehyde content and also decreases in lightness and chroma, indicating that heat pretreatment could effectively alleviate chilling injury of banana fruit. However, little is known about the role of small heat shock proteins (sHSPs) in postharvest chilling tolerance of banana fruit. In the present study, three cytosolic sHSP expression profiles in peel and pulp tissues of banana fruit during heat pretreatment and subsequent chilled storage (8 °C) were investigated in relation to heat pretreatment-induced chilling tolerance. Three full-length cDNAs of cytosolic sHSP genes, including two class I sHSP (CI sHSP) and one class II sHSP (CII sHSP) cDNAs, named Ma-CI sHSP1, Ma-CI sHSP2 and Ma-CII sHSP3 respectively, were isolated and characterised from harvested banana fruit. Accumulation of Ma-CI sHSP1 mRNA transcripts in peel and pulp tissues and Ma-CII sHSP3 mRNA transcripts in peel tissue increased during heat pretreatment. Expression of all three Ma-sHSP genes in peel and pulp tissues was induced during subsequent chilled storage. Furthermore, Ma-CI sHSP1 and Ma-CII sHSP3 mRNA transcripts in pulp tissue and Ma-CI sHSP2 mRNA transcripts in peel and pulp tissues were obviously enhanced by heat pretreatment at days 6 and 9 of subsequent chilled storage. These results suggested that heat pretreatment enhanced the expression of Ma-sHSPs, which might be involved in heat pretreatment-induced chilling tolerance of banana fruit.

Role of phenylalanine ammonia‐lyase in heat pretreatment‐induced chilling tolerance in banana fruit

Increasing evidence suggests that phenylalanine ammonia-lyase (PAL, EC 4.3.1.5) is associated with low temperature stress in plant tissues. Banana fruit are highly susceptible to chilling injury. However, little is known about the role of PAL (i.e. gene expression, protein level and activity) in fruit chilling. In this work, the involvement of PAL induced by heat treatment (38 degrees C for 3 days) prior to storage (8 degrees C) in chilling tolerance was investigated. The PAL inhibitor 2-aminoindan-2-phosphonic acid (AIP) was also used to further study the role of PAL in the chilling tolerance. The results showed that mRNA transcripts (MaPAL1 and MaPAL2) and PAL protein levels increased during storage at chilling temperature. Heat treatment prior to storage alleviated chilling injury and enhanced PAL activity, protein amount and MaPAL1 and MaPAL2 transcript levels. The increases in parameters of PAL upon heat pretreatment were all inhibited by AIP treatment, which resulted in aggravation of chilling injury. Thus, these findings indicate that the induction of PAL by heat pretreatment was regulated at both the transcriptional and the translational levels and that PAL may play a role in heat pretreatment-induced chilling tolerance of banana fruit.

Cloning and expression analysis of phenylalanine ammonia-lyase in relation to chilling tolerance in harvested banana fruit

Bananas are highly susceptible to chilling injury (CI) and phenylalanine ammonia-lyase (PAL), as a key enzyme involved in plant phenylpropanoid metabolism, has been associated with low temperature stress in plant tissues. However, little is known about the role of PAL (including PAL activity, gene and protein expression) in postharvest chilling tolerance of banana fruit. Two partial cDNAs sequences ( MaPAL1 and MaPAL2) with about 760 bp were cloned from banana pulp by RT-PCR. Western and northern hybridizations were used to investigate expression of PAL protein and PAL genes in fruit stored for 10 days at 7 °C (chilling temperature) and then transferred to 22 °C (room temperature). The effects of propylene (a functional ethylene analog) on their expression in relation to CI were also examined. Northern and western blot analyses revealed that mRNA transcripts of MaPAL1 and MaPAL2 and PAL protein levels in banana fruit during storage increased, reaching a peak at about day 8, and finally decreased at chilling temperature. Prior to low temperature storage, pretreatment with propylene could alleviate CI and enhance PAL activity, protein amount and mRNA transcripts of MaPAL1 and MaPAL2. Moreover, changes in PAL activity, protein amount and accumulation of MaPAL1 and MaPAL2 exhibited almost the same patterns. The results suggest that the induction of PAL in banana fruit during low temperature storage is regulated at transcriptional and translational levels, and is related to reduction in CI symptoms.