Chilling Injury In Peach Fruit Research Articles

PpCaM7 and PpCAMTA5 synergistically mitigate chilling-induced browning by suppressing reactive oxygen species synthesis in peach fruit

This study investigated the potential regulatory mechanisms influencing chilling injury in peach fruit under various storage temperatures (0 ℃ and 5 ℃) and calcium treatments (calcium chloride (CaCl2) and trifluoperazine (TFP)). The results showed that 0 ℃ storage and CaCl2 treatment activated the expression of PpCAMTA5, while repressed the expression of PpNAC25, PpPAO, PpRBOHA, PpRBOHC, and PpRBOHD, and reduced hydrogen peroxide (H2O2) content. This concerted regulation effectively suppressed chilling-induced browning in peach fruit during cold storage. However, the opposite effects were presented in TFP-treated fruit. Additionally, the interaction between PpCaM7 and PpCAMTA5 inhibited PpNAC25-mediated transcriptional activation of PpPAO, PpRBOHA, PpRBOHC, and PpRBOHD. Thus, these results suggested that the PpCaM7-PpCAMTA5 complex mitigates chilling injury in peach fruit via inhibiting reactive oxygen species (ROS) production.

Transcriptome analysis reveals that trehalose alleviates chilling injury of peach fruit by regulating ROS signaling pathway and enhancing antioxidant capacity

Peach fruit is prone to chilling injury (CI) during low-temperature storage, resulting in quality deterioration and economic losses. Our previous studies have found that exogenous trehalose treatment can alleviate the CI symptoms of peach by increasing sucrose accumulation. The purpose of this study was to explore the potential molecular mechanism of trehalose treatment in alleviating CI in postharvest peach fruit. Transcriptome analysis showed that trehalose induced gene expression in pathways of plant MAPK signaling, calcium signaling, and reactive oxygen species (ROS) signaling. Furthermore, molecular docking analysis indicated that PpCDPK24 may activate the ROS signaling pathway by phosphorylating PpRBOHE. Besides, PpWRKY40 mediates the activation of PpMAPKKK2-induced ROS signaling pathway by interacting with the PpRBOHE promoter. Accordingly, trehalose treatment significantly enhanced the activities of antioxidant-related enzymes such as superoxide dismutase (SOD), catalase (CAT), ascorbate peroxidase (APX), and gluathione reductase (GR), as well as the transcription levels AsA-GSH cycle related gene, which led to the reduction of H2O2 and malondialdehyde (MDA) content in peach during cold storage. In summary, our results suggest that the potential molecular mechanism of trehalose treatment is to enhance antioxidant capacity by activating CDPK-mediated Ca2 + −ROS signaling pathway and WRKY-mediated MAPK-WRKY-ROS signaling pathway, thereby reducing the CI in peach fruit.

Near-Freezing Temperature Storage Improves Peach Fruit Chilling Tolerance by Regulating the Antioxidant and Proline Metabolism

Chilling injury (CI) in peach fruit (Prunus persica cv. Yuhualu) is generally caused by long-time low temperature (5 °C or 0 °C) storage. However, peach fruit stored at near-freezing temperature (NFT in this research is −1 °C), defined as within 0.5 °C above the biological freezing point of biological tissue, does not exhibit CI symptoms. The effect of NFT on the CI, proline metabolism, and antioxidant capability of peach fruit during storage was studied and compared with 5 °C and 0 °C storage as controls. The results exhibit that NFT completely inhibited the occurrence of CI in peach fruit. NFT significantly (p < 0.05) enhanced the activities of superoxide dismutase, catalase, ascorbate peroxidase, and 1,1-diphenyl-2-picrylhydrazyl scavenging capacity. Moreover, the increase of malondialdehyde, ion leakage, and H2O2 accumulation were inhibited remarkably by NFT, and decreases in the contents of phenolics and ascorbic acid were slowed significantly in peach fruit stored at NFT (p < 0.05). Additionally, NFT storage enhanced proline accumulation by modulating the activity of proline metabolizing enzymes. In conclusion, the above results suggest that NFT storage can improve the chilling tolerance of peach fruit by regulating the antioxidant defense and proline metabolism, which might represent a potential novel method to store fruits and vegetables for longer storage times.

Exploring the Effects of Different 1-MCP Concentration Treatment on Chilling Injury of Postharvest Peach Fruit

Peach (Prunus persica (L.) Batsch) fruit are susceptible to chilling injury that is often manifested as browning of the internal flesh. As the ethylene antagonist, 1-methylcyclopropene (1-MCP) is an important contributor to resist chilling stress during peach (Prunus persica (L.) Batsch) storage at low temperatures, but the molecular mechanism of it is still elusive. The study examined in detail the effects of two concentrations (1 and 2 μL·L−1) of 1-MCP on alleviating chilling injury (CI) of postharvest peach fruit stored at 4 ± 0.5°C. The results showed that although all treatments relieved CI, treatment with 1 μL·L−1 more effectively alleviated CI symptoms of postharvest peach fruit than 2 μL·L−1. The internal browning (IB) and weight loss were significantly inhibited by 1 μL·L−1 1-MCP. Lower concentration of 1-MCP maintained normal softening by decreasing the gene expression of expansin (Exp) 1,3, polygalacturonase (PG) 3, and pectate lyase (PLY) 1, 2, 3 and increased the content of soluble sugar during the whole storage period. Meanwhile, the activities of polygalacturonase, pectinmethylesterase (PME), and endo-1,4-β-glucanase (EGase) were reduced by lower concentration of 1-MCP. Our results demonstrate that 1-MCP inhibited CI by suppressing the degradation of cell wall. This study provides a theoretical basis for revealing that 1-MCP alleviates chilling injury in peach fruit.

IAA regulated levels of endogenous phytohormones in relation to chilling tolerance in cold-stored peaches after harvest

The effects of indoleacetic acid (IAA) treatment on chilling injury and endogenous phytohormones in peach fruit were studied. The results showed that IAA treatment decreased chilling injury index of cold-stored peaches, effectively maintaining fruit firmness and reducing the electrical conductivity level. IAA treatment upregulated the expression of IAA biosynthetic gene PpMES and signaling pathway gene PpSAUR, but reduced the transcript abundance of IAA degradative genes PpDAO, PpGH3, and PpIAMT, leading to endogenous IAA accumulation in treated peaches. Meanwhile, after IAA treatment, contents of melatonin and γ-aminobutyric acid (GABA) were also increased which was associated with the upregulation of their anabolic genes and downregulation in GABA catabolic genes. In addition, the levels of abscisic acid (ABA) and gibberellin (GA) were reduced in treated peaches due to its modification in the transcript levels of ABA and GA metabolic genes. Collectively, IAA could alleviate the symptoms of chilling injury in peach fruit via regulating contents of endogenous phytohomones such as IAA, melatonin, GABA and GA.

The polygalacturonase-inhibiting protein PpPGIP1, positively regulates vacuolar invertase activity via a protein-protein interaction with PpVIN2 in peach fruit

The vacuolar invertase (VIN) gene PpVIN2 is induced at chilling temperatures, and plays an important role in sucrose metabolism in peach fruit during cold storage. Using a dual membrane yeast two-hybrid system, we found 22 proteins interacted with PpVIN2. Of these, PpPGIP1 (polygalacturonase-inhibiting protein) is a leucine-rich repeat glycoprotein and sensitives to chilling temperature (5 °C), based on the expression level of which increased significantly accompanied with the chilling injury. Colocalization of PpPGIP1 and PpVIN2 was demonstrated by confocal microscopy and their interaction between was demonstrated by bimolecular fluorescence complementation (BiFC). Transient overexpression of PpPGIP1 in peach fruit increased VIN activity significantly. Transient virus-induced gene silencing of PpPGIP1 decreased VIN activity significantly, which led to decreases sucrose decomposition. PpPGIP1 recombinant protein was successfully expressed by constructing pMAL-c6T-PpPGIP1, and PpPGIP1 increased the VIN activity in vitro. Taken together, PpPGIP1 positively regulates VIN activity via an interaction with PpVIN2; this interaction results in accelerated sucrose decomposition in peaches under chilling temperature. These findings provide a new perspective for understanding the new function of PpPGIP1 related with the rapid decomposition of sucrose and the occurrence of chilling injury in peach fruit during cold storage.

Cold shock treatment enhances cold tolerance in peach fruit through modulating PpbZIP9 and PpVIP1-mediated respiratory metabolism

Peach fruit are susceptible to chilling injury after prolonged cold storage. Cold shock (CS) treatment can mitigate the chilling injury of peach fruit, but the molecular mechanism remains obscure. In this study, peaches were immersed in ice water at 0 °C for 10 min then stored at 5.0 ± 1.0 °C for 35 d. The results showed that CS treatment reduced the browning index and relative electrical conductivity of peach fruit under chilling stress. Respiration rate, NADH, NADPH contents, enzyme activities and gene expressions of HXK, PGI, NADP-ICDH, NADP-ME, G6PDH, 6PGDH and NADK were higher in the treated fruit during cold storage. The expression levels of PpbZIP9 and PpVIP1 were down-regulated by CS treatment. Moreover, PpbZIP9 repressed the expressions of PpNADP-ME and PpNADK1. PpVIP1 acted as the transcriptional repressor of PpNADP-ICDH and PpNADK1. Overall, the findings indicated that PpbZIP9 and PpVIP1 were involved in CS treatment-induced cold tolerance of peach fruit via respiratory metabolism.

Transcriptome Co-Expression Network Analysis of Peach Fruit with Different Sugar Concentrations Reveals Key Regulators in Sugar Metabolism Involved in Cold Tolerance.

Peach fruits are known to be highly susceptible to chilling injury (CI) during low-temperature storage, which has been linked to the level of sugar concentration in the fruit. In order to better understand the relationship between sugar metabolism and CI, we conducted a study examining the concentration of sucrose, fructose, and glucose in peach fruit with different sugar concentrations and examined their relationship with CI. Through transcriptome sequencing, we screened the functional genes and transcription factors (TFs) involved in the sugar metabolism pathway that may cause CI in peach fruit. Our results identified five key functional genes (PpSS, PpINV, PpMGAM, PpFRK, and PpHXK) and eight TFs (PpMYB1/3, PpMYB-related1, PpWRKY4, PpbZIP1/2/3, and PpbHLH2) that are associated with sugar metabolism and CI development. The analysis of co-expression network mapping and binding site prediction identified the most likely associations between these TFs and functional genes. This study provides insights into the metabolic and molecular mechanisms regulating sugar changes in peach fruit with different sugar concentrations and presents potential targets for breeding high-sugar and cold-tolerant peach varieties.

A New Regulatory Network Controls Chilling Injury in Peach Fruit by γ-Aminobutyric Acid.

The control of chilling injury in peach fruit by a new regulator network, that exogenous γ-aminobutyric acid (GABA) regulates the metabolisms of polyamines (PAs), the GABA shunt, and proline, is still unclear. This study found that GABA induced an increase in the expression of PpADC and PpODC and a decrease in the expression of PpPAO expression, resulting in the accumulation of PAs. There was also an increase in the expression of PpGAD, which improved GABA content, and an increase in the expression of PpP5CS and PpOAT, which improved proline content. The correlation analysis showed that an increase in PpADC/PpP5CS expression was closely associated with the accumulation of putrescine and that the synergistic increase in the expression of PpODC and PpGAD/PpP5CS/PpOAT was closely related to the accumulation of spermine, proline, and GABA induced by GABA. Importantly, arginine and PpADC played a key role in putrescine accumulation, whereas ornithine and PpODC/PpOAT played a crucial role in the synergistic accumulation of spermine, proline, and GABA induced by GABA. This study provides new information on GABA-induced cold tolerance in peach fruit.

ERF transcription factor PpRAP2.12 activates PpVIN2 expression in peach fruit and reduces tolerance to cold stress

The vacuolar invertase gene PpVIN2 negatively regulates cold resistance in peach fruit by promoting sucrose degradation. However, the regulatory mechanisms that control PpVIN2 transcription are not yet understood. In this study, we identified an ethylene-responsive transcription factor (ERF) in a yeast one-hybrid library screen using the PpVIN2 promoter (PpVIN2pro) as bait. ERF PpRAP2.12 directly binds to the ACCGAC cis-element in the PpVIN2pro region, resulting in enhanced promoter activity. In peach fruit, transient overexpression of PpRAP2.12 increases PpVIN2 expression and vacuolar invertase (VIN) activity and decreases sucrose levels. Ectopic expression of PpRAP2.12 in tobacco reduces tolerance to cold stress, resulting in a lower survival rate, higher NtVIN expression and VIN enzymatic activity, and elevated production of reactive oxygen species. Together, these findings suggest that PpRAP2.12 binds to PpVIN2pro and positively regulates its activity to promote sucrose degradation. PpRAP2.12 thus functions as a negative regulator of plant defenses against chilling stress, and may provide a target for mitigating chilling injury in peach fruit.

Non-thermal effects of microwave irradiation alleviates postharvest chilling injury of peach fruit by retarding phenolic accumulation and enhancing membrane stability

Postharvest chilling injury (CI) of fruit, including peaches, is a huge challenge to horticultural product preservation. Microwave irradiation can be used as a physiological regulator due to the thermal effects; however, its non-thermal effects on the CI of postharvest fruit remain unclear. Thus, the physiological attributes and metabolisms involving phenolics, fatty acids, and sugars were compared between ‘Zhongtao No.9’ peaches treated with microwave irradiation at 45.5 W for different durations and control. Microwave treatment especially at 45.5 W for 7 min without inducing thermal effects could significantly inhibit internal browning caused by CI, concomitant with reduced total phenolic content. Moreover, the maintenance of membrane stability was indicated by a boosted double bond index, which may be attributed to the inhibition of membrane lipid degradation, and sucrose accumulation. In summary, the non-thermal effects of microwave irradiation contribute to CI alleviation through restraining phenolic content and maintaining membrane stability in peach fruit.

Identification of COR413 Gene Family in Peach and Its Expression in Low Temperature and LTC Treatment at Postharvest

Peach were susceptible to chilling injury during low temperature (0 o C) storage at postharvest, and LTC (Low temperature conditioning) treatment could reduce chilling injury such as of H 2 O 2  production and fruit browning. In order to study the function of peach COR413  in the regulation of postharvest chilling injury in peach ‘Beijing No. 9’, four COR413 gene family members were identified based on the peach genome database, namely  PpCOR1 ~ PpCOR4 . Phylogenetic analysis showed that the four PpCORs could be clustered into two subfamilies. PpCOR1 ~ PpCOR3  belonged to the first subfamily, and most of the members in this subfamily were located in plasma membrane. PpCOR4  belongs to the second subfamily, and its members are mainly located in thylakoid membrane. The cis-acting elements analysis of PpCORs  promoter showed that PpCOR3  contained abundant abiotic stress responsive and hormone responsive elements such as jasmonate and abscisic acid. The results of gene expression showed that PpCOR3 was induced by low temperature while LTC treatment could repress the induction of PpCOR3  by low temperature. Interestingly, the expression of PpCOR3  was positively correlated with the change of H 2 O 2  content in peach, which indicated that PpCOR 3 was involved in the regulation of postharvest chilling injury in peach fruit. This result provides a theoretical basis for the study of postharvest storage and quality maintenance of peach fruit as well as the breeding of cold resistant peach varieties.

γ-Aminobutyric acid treatment induced chilling tolerance in postharvest peach fruit by upregulating ascorbic acid and glutathione contents at the molecular level.

Peach fruit was treated with 5 mM γ-aminobutyric acid (GABA) to further investigate the mechanism by which GABA induced chilling tolerance. Here, we found that GABA not only inhibited the occurrence of chilling injury in peach fruit during cold storage but also maintained fruit quality. Most of the ascorbic acid (AsA) and glutathione (GSH) biosynthetic genes were up-regulated by GABA treatment, and their levels were increased accordingly, thus reducing chilling damage in treated peaches. Meanwhile, the increased transcript of genes in the AsA-GSH cycle by GABA treatment was also related to the induced tolerance against chilling. GABA treatment also increased the expression levels of several candidate ERF transcription factors involved in AsA and GSH biosynthesis. In conclusion, our study found that GABA reduced chilling injury in peach fruit during cold storage due to the higher AsA and GSH contents by positively regulating their modifying genes and candidate transcription factors.

Characterization and expression analysis of basic leucine zipper (bZIP) transcription factors responsive to chilling injury in peach fruit.

Peach (Prunus persica L.) is prone to chilling injury as exhibited by inhibition of the ethylene production, failure in softening, and the manifestation of internal browning. The basic leucine zipper (bZIP) transcription factors play an essential role in regulatory networks that control many processes associated with physiological, abiotic and biotic stress responses in fruits. Formerly, the underlying molecular and regulatory mechanism of (bZIP) transcription factors responsive to chilling injury in peach fruit is still elusive. In the current experiment, the solute peach 'Zhongyou Peach No. 13' was used as the test material and cold storage at low temperature (4°C). It was found that long-term low-temperature storage induced the production of ethylene, the hardness of the pulp decreased, and the low temperature also induced ABA accumulation. The changes of ABA and ethylene in peach fruits during low-temperature storage were clarified. Since the bZIP transcription factor is involved in the regulation of downstream pathways of ABA signals, 47 peach bZIP transcription factor family genes were identified through bioinformatics analysis. Further based on RT-qPCR analysis, 18 PpbZIP genes were discovered to be expressed in refrigerated peach fruits. Among them, the expression of PpbZIP23 and PpbZIP25 was significantly reduced during the refrigeration process, the promoter analysis of these genes found that this region contains the MYC/MYB/ABRES binding element, but not the DRES/CBFS element, indicating that the expression may be regulated by the ABA-dependent cold induction pathway, thereby responding to chilling injury in peach fruit. Over investigation will provide new insights for further postharvest protocols related to molecular changes during cold storage and will prove a better cope for chilling injury.

Genome-wide identification of the CDPK gene family reveals the CDPK-RBOH pathway potential involved in improving chilling tolerance in peach fruit

Calcium-dependent protein kinase (CDPK), as an essential calcium receptor, plays a major role in the perception and decoding of intracellular calcium signaling in plant development and stress responses. Here, the CDPK gene family was analyzed at the genome-wide level in peach. This study identified 17 PpCDPK gene members from the peach genome, and systematically investigated phylogenetic relationships, conserved motifs, exon-intron structures, chromosome distribution, and cis-acting elements of each PpCDPK gene using bioinformatics. Furthermore, the expression levels of most PpCDPK genes were significantly changed under the CaCl2, EBR, GB, cold shock, hot water treatments, and various temperatures in the cold storage of peach fruits. RNA-seq data showed that PpCDPK2, PpCDPK7, PpCDPK10, and PpCDPK13 were related to postharvest chilling stress in peach. The interaction network of PpCDPK7 protein showed that the interaction between PpCDPK7 and PpRBOH may be the intersectional point of Ca2+ and ROS signal transmission during cold storage of peach fruits. These systematic analyses are helpful to further characterize the regulation of PpCDPKs and CDPK-RBOH mediated signal cascades in postharvest chilling injury in peach fruit.

NMR revealed that trehalose enhances sucrose accumulation and alleviates chilling injury in peach fruit

• Trehalose alleviates the effects of chilling injury in peach fruit • NMR reveals higher sucrose content in trehalose treated peaches • Trehalose treatment decreases expression of SnRK1, promoting the accumulation of sucrose • Trehalose improves the cold tolerance of peach by affecting sucrose levels Nuclear magnetic resonance (NMR) was applied to identify the metabolic differences in trehalose-treated and -untreated peach fruit during storage at 5°C in this study. Forty-one metabolites were identified using NMR; trehalose-treated peaches had higher sucrose, proline, and choline content, and lower glucose, fructose and gluconic acid content. These metabolic changes were accompanied by lower levels of chilling injury (CI). Trehalose-treated fruit had lower levels PpSnRK1 expression, resulting in lower sucrose decomposition and higher sucrose synthesis. We suggest that accumulated sucrose in trehalose-treated peaches is associated with the decrease in expression of PpSnRK1 and increases in the expression and activity of the sucrose phosphate synthase (SPS). This probably results in the improvement of chilling resistance in peach fruit.

Exogenous 24-epibrassinolide alleviates chilling injury in peach fruit through modulating PpGATA12-mediated sucrose and energy metabolisms

24-Epibrassinolide (EBR) may act as a modulator for chilling injury in peach fruit during cold storage. In this study, we screened a EBR-induced GATA-type zinc finger protein PpGATA12. The objective of this study was to investigate the potential roles of EBR treatment and transcriptional regulation of PpGATA12 in regulating chilling resistance of peaches. In the current study, we found that EBR treatment promoted the activities and transcriptions of energy and sucrose metabolism-related enzymes, maintained higher ATP content and energy status, improved the accumulation of sucrose and hexose. Furthermore, molecular biology assays suggested that PpGATA12 up-regulated transcriptions of sucrose metabolism-related genes including PpSS and PpNI, and energy metabolism-related genes including PpCCO, PpSDH and PpH+-ATPase. These results provided a new insight that the enhancement of chilling resistance in peach fruit by EBR treatment might be closely related to the regulatory role of PpGATA12 on sucrose and energy metabolisms.

Hydrogen sulfide alleviates chilling injury in peach fruit by maintaining cell structure integrity via regulating endogenous H2S, antioxidant and cell wall metabolisms

Effects of hydrogen sulfide (H2S) on chilling injury (CI), H2S, antioxidant and cell-wall metabolisms of refrigerated peaches treated with H2S and hypotaurine (HT, H2S scavenger) were investigated in present study. Results revealed that H2S treatment enhanced endogenous H2S content, which was associated with increased related H2S synthase enzymes activities, while HT showed the opposite results. Moreover, H2S treatment induced the accumulation of ascorbic acid, glutathione and the enhancement of antioxidant enzymes activities compared to control and HT, contributing to lower hydrogen peroxide content and superoxide radical production. Furthermore, H2S suppressed the increase of cell-wall degradation enzymes accompanied by higher levels of water-insoluble pectin, 24% KOH-soluble hemicellulose and cellulose, while HT accelerated these components degradation. Therefore, results indicated that H2S mitigated CI of refrigerated peaches by regulating H2S, antioxidant and cell-wall metabolisms, maintaining higher H2S and antioxidants contents, suppressing cell-wall degradation, thereby contributing to redox homeostasis maintenance and cell structure integrity.

Methyl jasmonate treatment regulates α-linolenic acid metabolism and jasmonate acid signaling pathway to improve chilling tolerance in both stony hard and melting flesh peaches

Peach are susceptible to chilling injury (CI) when stored at a low temperature and the postharvest application of methyl jasmonate (MeJA) is well known to alleviate CI in peach fruit. However, the optimal dose for the treatment of MeJA is still debated in peaches and the underlying mechanism remains largely unknown. In this study, we screened the optimal concentration of MeJA treatment in stony hard and melting flesh peaches, then investigated the involvement of α-linolenic acid metabolism and jasmonate acid (JA) signaling pathway in the MeJA-induced chilling tolerance. The results showed that 10 mol L−1 was the broad-spectrum concentration of MeJA treatment for CI alleviation in the two peach cultivars. Also, MeJA treatment improved the degree of fatty acid unsaturation in cell membrane by delaying the decrease in unsaturated fatty acids (USFAs) and the increase in saturated fatty acids (SFAs), resulting in the activation of α-linolenic acid metabolism. Correspondingly, it maintained a higher concentration of α-linolenic acid and higher activities of lipoxygenase (LOX), allene oxide synthase (AOS) and allene oxide cyclase (AOC). It also induced the expressions of PpLOX, PpAOS, PpAOC, PpACOX and PpFadA in peaches during the end of the cold storage at 5 °C and the shelf-life at 20 ℃. Meanwhile, the increased α-linolenic acid metabolism in MeJA treated fruit led to accumulations in JA and jasmonic acid isoleucine (JA-Ile), which boosted the JA signaling pathway by up-regulating the expressions of PpCOI1, PpJAZ and PpMYC2. Thus, it was suggested that MeJA treatment activated α-linolenic acid metabolism and JA signaling pathway might be contributing to alleviating CI in peaches during cold storage.

Membrane lipid metabolism influences chilling injury during cold storage of peach fruit

Peach fruit is prone to chilling injury (CI) during long-term low temperature (LT) storage, and develops protective mechanisms against LT stress. This study revealed that 4 °C storage induced the occurrence of CI in peach fruit by promoting the expression of membrane lipid metabolism genes and phosphatidic acid (PA) accumulation, and stimulated a protective mechanism for peach fruit against LT by increasing diacylglycerol (DAG), triacylglycerol (TAG) and several phosphatidylcholine (PC) components in the later storage stage. In contrast, 0 °C delayed the occurrence of CI in peach fruit by delaying the degradation of phospholipids, upregulation of fatty acid desaturase (FAD) and the process of fatty acid unsaturation, and maintaining higher levels of PC and PE. Results from this study provide new information on the mechanism of CI in peach fruit, and lay the foundation for the transcriptional regulation mechanism of CI and cold tolerance in peach fruit mediated by membrane lipid metabolism.