Green mold, caused by Penicillium digitatum (P. digitatum), is a major cause of postharvest losses in citrus fruit. Although lignification is recognized as an important defense response, the epigenetic mechanisms controlling lignin biosynthesis during pathogen infection remain largely unknown. Here, we identify the citrus histone demethylase CsJMJ16 as a critical regulator of lignin-mediated defense. Transient overexpression of CsJMJ16 in citrus peel significantly enhanced resistance to P. digitatum, reducing lesion diameter by approximately 34 % at 3 days post-inoculations (dpi) and 17.6 % at 4 dpi compared to the control, accompanied by increased lignin deposition. Transcriptomic profiling revealed that CsJMJ16 activates multiple defense-associated pathways, including phenylpropanoid metabolism and cell-wall reinforcement. Biochemical assays demonstrated that CsJMJ16 specifically removes the repressive H3R2me2a mark. Consistent with this activity, ChIP-qPCR analysis showed decreased H3R2me2a enrichment at the promoters of key lignin biosynthetic genes (COMT, PAL, CCR, CSE, 4CL, and POD31), which was coupled with their transcriptional upregulation. Together, these findings establish CsJMJ16 as an epigenetic activator of lignin biosynthesis that strengthens citrus defense against fungal infection. This work provides new mechanistic insight into histone modification-regulated plant immunity and highlights CsJMJ16 as a promising target for improving citrus postharvest disease resistance.

Postharvest browning and senescence significantly reduce the commercial value of litchi, a nutritious tropical fruit. Although itaconate, a branched-chain metabolite of the tricarboxylic acid (TCA) cycle, is known as a food preservative, its effects on litchi fruit deterioration remain unclear. This study demonstrates that itaconate treatment effectively delays pericarp browning and suppresses respiratory rates in litchi fruit. The treatment enhanced the antioxidant capacity by boosting the activities of superoxide dismutase, catalase, and ascorbate peroxidase, while inhibiting peroxidase and polyphenol oxidase. Consequently, hydrogen peroxide, superoxide anions, and malondialdehyde accumulation decreased, whereas glutathione, ascorbic acid, total phenols, and anthocyanin levels increased. Furthermore, itaconate-maintained cellular energy homeostasis by elevating ATP content, energy charge, and the activity of key TCA cycle enzymes, succinate dehydrogenase and malate dehydrogenase. Transcriptomic and RT-qPCR analyses confirmed the upregulation of genes related to oxidative stress and energy metabolism (LcCAT, LcSOD, LcAPX1, LcF3H, LcUFGT, LcAtpB). Collectively, these findings indicate that itaconate mitigates browning and senescence in litchi fruit by improving redox balance and sustaining energy homeostasis.

The mycotoxigenic Fusarium proliferatum is a common fungus and contaminates plant hosts with mycotoxin, posing serious threats to human and animal health. The conserved activator protein-1 (AP1) transcription factor is found in filamentous fungi in response to oxidative stress. However, no information is available regarding its role in regulating growth and pathogenicity of F. proliferatum on plant hosts. In this study, we characterized FpAP1 in F. proliferatum sharing a conserved DNA-binding domain of YAP family and exhibiting transcriptional activation activity. FpAP1 deletion mutant (ΔFpap1) showed higher fumonisins content but was defective in virulence to banana fruit and Nicotiana benthamiana compared to wild type. Importantly, FpAP1 regulated tolerance to reactive oxygen species and fungicide stresses, revealing a connection between stress response and virulence of F. proliferatum. DNA affinity purification sequencing and transcriptome analysis identified 393 direct target genes of FpAP1-mediated regulation. Dual-luciferase report and electrophoretic mobility shift assay highlighted a new regulatory network of FpAP1 in regulating the expression of genes associated with a diverse range of F. proliferatum growth, stress response and virulence. Our findings uncovered the FpAP1-mediated regulatory network in controlling F. proliferatum growth and virulence, which offers promising targets for effective control of Fusarium diseases and mycotoxin contamination.

Litchi, a popular tropical and subtropical fruit, is highly susceptible to pericarp browning after harvest, which affects its marketability. Riboflavin, a water-soluble B vitamin (VB2), is involved in various physiological processes in plants. This study investigated the effects of riboflavin on pericarp browning of harvested litchi fruit and explores the underlying mechanism. The results show that application of riboflavin effectively delayed pericarp browning, preserved fruit bright color, and maintained cell membrane integrity. Moreover, riboflavin treatment enhanced the activities of antioxidant enzymes such as SOD, GST, GR, and the contents of GSH and total phenol, while reducing the levels of GSSG, PPO, and POD over the storage period. Furthermore, transcriptome analysis and RT-qPCR revealed that riboflavin treatment inhibited the expression of phenolic metabolic genes (POD17 like, POD47, and PPO), and aquaporin genes (PIP2-4 like, PIP1-2, and TIP4-1), while upregulating the expression of glutathione metabolism gene GPX2, contributing to the delayed browning process. Overall, this study suggests that riboflavin delays litchi fruit browning via boosting antioxidant enzyme activity and inhibiting the enzymatic oxidation of phenolic compounds.

Plants of Salvia are frequently used for treatment infections of boils and sores in Traditional Chinese medicine, which might inhibit microbial. In this work, the chemical constituents of the effective fractions were analyzed using UPLC-Q-TOF-MS, and multivariate analysis and network pharmacology were used to predict potential antibacterial substances and their mechanism. Moreover, against methicillin-resistant Staphylococcus aureus (MRSA) effect and pathway of bioactive compounds were validated by experiments in vitro and in vivo. Two unreported anti-MRSA compounds, miltirone and przewaquinone A were proposed and then validated by serial experiments. They acted as bactericides and biofilm scavengers, respectively, and both targeted on the cell membrane, causing leakage of contents and affecting intracellular metabolism, leading to bacterial death without significant toxicity. Furthermore, miltirone ameliorated skin wound infection caused by MRSA in mice, roughly equal to vancomycin. The research supported the traditional use of Salvia plants, and presented two potent bactericidal agents for further investigation.

Leaf senescence of Chinese flowering cabbage after harvest is a key factor to cause quality deterioration. Both hydrogen peroxide (H2O2) and NAC (NAM/ATAF/CUC) transcription factors (TFs) were reported to be involved in leaf senescence, but the mechanism by which NAC TFs regulate H2O2-induced leaf senescence has not been fully elucidated. In this study, BrNAC046, a senescence-activated NAC TF was identified, whose expression was induced by exogenous 100 mM H2O2. BrNAC046 activated genes involved in chlorophyll catabolism (BrSGR2), programmed cell death (BrBFN1), and reactive oxygen species (ROS) production (BrRbohCL) by binding to their promoters. Interaction with radical-induced cell death1 (BrRCD1), a hub protein involved in ROS signaling, enhanced the BrNAC046's transcriptional activity. Overexpression of BrNAC046 accelerated senescence in tobacco and Arabidopsis. Our findings reveal that BrNAC046 induces H2O2-regulated leaf senescence by modulating chlorophyll degradation, ROS production, and cell death, providing new molecular insights into postharvest senescence of Chinese flowering cabbage.

Combined manganese (Mn) and iron (Fe) exposure is increasingly recognized as a risk factor for neurotoxicity, but the underlying mechanisms and potential interventions remain incompletely understood. Here, PC12 cells and Sprague-Dawley rats were used to investigate neuroinjury induced by combined Mn-Fe exposure and the potential protective effects of sodium para-aminosalicylate (PAS-Na). Cognitive performance was evaluated using the Morris water maze and Y-maze, whereas histopathological changes, regional Mn and Fe accumulation, oxidative-inflammatory injury, Wnt/β-catenin/GSK-3β-related proteins, Tau/Aβ-related alterations, and apoptosis were assessed in PC12 cells and in the hippocampus and cortex of rats. Combined Mn-Fe exposure induced marked neuroinjury, characterized by impaired spatial learning and memory, neuronal damage in the hippocampus and cortex, increased regional brain Mn and Fe burden, enhanced oxidative stress and neuroinflammation, Tau/Aβ-related abnormalities, apoptosis, and alterations in Wnt/β-catenin/GSK-3β-related protein expression. PAS-Na attenuated these alterations, with medium and high doses generally showing more consistent effects than the low dose. PAS-Na treatment was associated with reduced Mn and Fe accumulation in cognition-related brain regions, partial normalization of Wnt/β-catenin/GSK-3β-related protein expression, and attenuation of oxidative-inflammatory injury and neuropathological changes. These novel findings indicate that PAS-Na partially alleviates combined Mn-Fe-induced neuroinjury and is associated with reduced regional metal burden, oxidative-inflammatory injury, apoptosis, and changes in Wnt/β-catenin/GSK-3β-related signaling.

The rare red Phyllanthus emblica L. fruit, with its distinctive appeal and potential nutritional profile, holds promise as an ideal material for both fresh consumption and plant-derived health food sector. Limited knowledge is available on the metabolic and molecular mechanism underlying this red phenotype. In this study, metabolic and transcriptome profiles of emblica fruits from four cultivars ranging from green to red color were analyzed. 726 differential accumulated metabolites (DAMs) were annotated with 72 critical metabolites for fruit reddening, which were primarily enriched in phenylpropanoid metabolism and flavonoid/anthocyanins biosynthesis pathways. Anthocyanin-targeted metabolome revealed that delphinidin 3-O-glucoside, cyanidin 3-O-glucoside and procyanidin B1 were key accumulated pigment substrates explaining fruit red coloration. WGCNA (Weighted Gene Co-Expression Network Analysis) identified PeCHS1, PeF3H1, PeDFR and PeLAR1 as hub genes responsible for diverse emblica fruit coloration among different cultivars. In addition, transient overexpression of PeCHS1, PeF3H1, PeDFR and PeLAR1 respectively in emblica fruits confirmed their roles in red coloration. Overall, our findings shed light on the metabolic basis and regulatory mechanism underlying the diverse emblica fruit coloration.

Flavonoid biosynthesis is crucial for pigmentation and quality formation in ripening pineapple fruit; however, its transcriptional regulation remains poorly understood. Here, we identify AcBBX6 as a key positive regulator. We demonstrate that AcBBX6 activates the transcription of flavonoid pathway genes (AcCHI2, AcF3'5'H2, AcF3H, AcFLS2, AcPAL1, AcLAR, AcGST1) by binding to their G-box elements in the promoters. Furthermore, the interaction of AcBBX6 and AcHY5 synergistically enhances the activation of flavonoid biosynthesis. Intriguingly, AcHY5 also interacts with AcBBX4, forming a ternary AcBBX6-AcBBX4-AcHY5 complex with stronger activation than any individual component, but its activity did not exceed that of the binary complexes. Silencing of AcBBX6 or AcBBX4 led to reduced flavonoid accumulation, whereas overexpression enhanced it. Coordinated manipulation of all three factors produced the most pronounced phenotypic effects on flavonoid content. Collectively, our results define the AcBBXs-AcHY5 complex as a core transcriptional module governing flavonoid biosynthesis during pineapple fruit ripening.

INTRODUCTION:Significant progress has been made in uncovering the role of DNA methylation in the development and ripening of fruit. However, whether DNA methylation is involved in litchi fruit ripening and in the corresponding mechanisms remain unknown. OBJECTIVES:The goal of this study was to explore the role of DNA methylation in the ripening, senescence, and the regulatory mechanism of litchi as well as to provide new perspectives for controlling litchi pericarp browning after harvest. METHODS:Here, single-base resolution maps of the DNA methylome during litchi fruit ripening and senescence was generated using whole genome bisulfite sequencing (WGBS). Association analysis of WGBS and RNA-sequencing was performed to reveal the potential regulatory effects of different regional methylation sites on gene expression in litchi in different fruit ripening and postharvest stages. A DNA methylation inhibitor, 5-azacytidine, treatment was also conducted. Meanwhile, the LcDML1 silencing mutant (TRV-LcDML1) was obtained using virus-induced gene silencing to confirm the regulatory role of LcDML1 in litchi ripening. RESULTS:Results showed that about 55%, 34%, and 11% of CG, CHG and CHH sites were methylated, respectively. Genome-wide DNA methylation increased during litchi fruit ripening and exhibited a regulatory role in gene expression during ripening but had limited influence during senescence. Furthermore, WGBS and RNA-sequencing analysis indicated that LcDML1 contributed to changes in genome-wide DNA methylation during litchi maturation. A 5-azacytidine treatment inhibited anthocyanin synthesis in litchi pericarp. In addition, LcDML1 silencing induced early coloration of litchi pericarp and upregulation of anthocyanin synthesis-related genes but downregulation of potential negative regulator of anthocyanin synthesis genes (NRAs). McrBC-PCR and dual-luciferase reporter assay suggested methylation regulation of NRAs promoters regulated the maturation and coloration of litchi fruit. CONCLUSION:LcDML1 is an important factor modulating the change of genome-wide DNA methylation as well as anthocyanin synthesis and participates in regulating litchi fruit ripening.

Litchi downy blight is a postharvest disease caused by Peronophythora litchii, causing yield loss and postharvest deterioration. The role of native plant peptides in fruit responses to fungal infections has seldom been reported. Here, we identified LcprePIP1 encoding a precursor of pathogen-associated molecular pattern (PAMP)-induced secreted peptide (LcPIP1) and characterized gene expression during P. litchii infection. Synthetic LcPIP1 application improved litchi fruit resistance to P. litchii by enhancing ATP, anthocyanin, and lignin accumulation as well as defense response. Furthermore, LcPIP1 treatment enhanced immunity responses by increasing cytosolic Ca2+ as well as reactive oxygen species accumulation and triggering mitogen-activated protein kinase signaling. We highlighted the crucial role of LcWRKY34 in LcPIP1-induced disease resistance by activating the LcprePIP1 expression. Transcriptomic and metabolomic analyses found that LcPIP1 regulated defense-related gene expression and metabolite accumulation. Overall, for the first time, our findings provided novel insights into the vital role of LcPIP1 in eliciting fruit defense responses.

Longan (Dimocarpus longan) as an important subtropical fruit exhibit a high nutritional and commercial value. Postharvest longan fruit undergo a rapid senescence, as characterized with endocarp browning. In this study, melatonin was applied to longan fruit to examine the mediated-browning during storage at 25 degrees C. Application of 0.1 mM melatonin significantly delayed endocarp browning, reduced respiration rate and the contents of H2O2 and malondialdehyde (MDA), and increased the activities of superoxide dismutase (SOD) and peroxidase (POD) at the early stage and catalase (CAT) activity throughout the storage period in longan fruit. Furthermore, two NAC famliy transcription factors, NAC083 and ATAF1, were used to investigate the endocarp browning of longan fruit during storage. The expression levels of both NAC083 and ATAF1 were upregulated in longan pericarp. Exogenous melatonin induced significantly the NAC083 expression in the pericarp at the early storage stage. Furthermore, DNA affinity purification and sequencing (DAP-seq), electrophoretic mobility shift assay (EMSA), dual-luciferase reporter (DLR), and stable transformation of longan root assay collectively confirmed that NAC083 can bind to the promoter region of respiratory burst oxidase homolog D-3 (RbohD-3), a key gene in ROS metabolic pathway, and then inhibit its transcription. This study provides new insights into the involvement of the NAC083-RbohD-3 module in the reactive oxygen species (ROS)-mediated endocarp browning of longan fruit during storage.

Banana fruit is susceptible to chilling injury (CI) under low-temperature stress, leading to quality deterioration. Although alpha-ketoglutarate (AKG) has been extensively studied for its role in cellular homeostasis, its effects on postharvest fruit and preservation mechanisms remain unclear. This study demonstrates that AKG treatment alleviates CI in banana fruit by preserving phenolic compounds, ascorbic acid (AsA) and glutathione (GSH) content while enhancing antioxidant enzyme activity-including catalase (CAT), superoxide dismutase (SOD), peroxidase (POD) and ascorbate peroxidase (APX). Concurrently, AKG maintained lower H2O2 and O2 center dot- levels. Furthermore, AKG sustained the activity of key tricarboxylic acid (TCA) cycle enzymes (succinate dehydrogenase (SDH), alpha-ketoglutarate dehydrogenase (alpha-KGDH) and malate dehydrogenase (MDH), promoting higher ATP levels and energy charge (EC). Transcriptome analysis revealed that AKG modulates genes associated with oxidoreductase activity, small molecule transport, glycosyltransferase function, mitochondrial energy metabolism and antioxidant pathways. RT-qPCR validation confirmed significant upregulation of key cold-responsive genes (MaAOX1a, MaRbohH, MaHSP22, MaPLD1, MaPAL and MaMYB4). Collectively, these findings suggest that AKG alleviates CI in banana fruit by simultaneously improving redox homeostasis and preserving mitochondrial energy metabolism.

Histone methylation is an important epigenetic mechanism that regulates plant development and stress responses, but its role in postharvest fruit chilling injury remains unknown. Here, we identified a cold-inducible SET domain protein, MaSET40, in banana (Musa acuminata) and found that it functions as a trimethylation of histone H3 lysine 36 (H3K36me3) methyltransferase. Transient overexpression of MaSET40 in banana fruit peel accelerated chilling injury, whereas virus-induced silencing of MaSET40 alleviated cold-induced peel damage. Transcriptome profiling revealed that MaSET40 activates genes involved in reactive oxygen species (ROS) accumulation and membrane lipid degradation, including MaPPO1, MaPPO3, MaRBOHB, Malipase, MaPLA2, and MaLOX3.1. Chromatin immunoprecipitation followed by quantitative PCR (ChIP-qPCR) further showed that MaSET40 increased H3K36me3 enrichment at these gene loci, accompanied by higher transcript levels. These results reveal an H3K36me3-mediated epigenetic mechanism that promotes chilling injury in postharvest banana fruit and identify MaSET40 as a potential target for improving cold tolerance in tropical fruits.

Prenylated stilbenoids are valuable nutraceutical candidates found in dietary plants. Compared to their nonprenylated counterparts, they often exhibit enhanced bioactivities, which are attributed to the increased lipophilicity conferred by the prenyl groups, facilitating their partitioning into cell membranes and interaction with lipid-associated targets. This review systematically examines prenylated stilbenoid biosynthesis via three core aspects: the structural diversity and structure-activity relationships of prenylated stilbenoids, focusing on how prenyl chain length, linkage, and substitution position modulate bioactivities; catalytic mechanisms and regioselectivity of prenyltransferases that transfer from prenyl donors to stilbenoid backbones; and metabolic engineering strategies for microbial heterologous production, emphasizing precursor flux optimization, enzyme and host engineering such as peroxisomal compartmentalization, and strain mating. Finally, we outline key challenges─poor prenyltransferase expression, precursor competition, and product cytotoxicity─and discuss future AI-guided enzyme engineering and autonomous dynamic control systems, providing a roadmap for the sustainable industrial production of these high-value nutraceuticals.

Chilling injury (CI) affects greatly postharvest quality of banana fruit during storage at < 13 degrees C. Apyrases (APYs) as a class of nucleoside triphosphate diphosphohydrolases (NTPDases) play a crucial role in regulating energy levels under various stress conditions. The potential effects of MaAPY2 on CI in banana fruit stored for 6 d at 6 degrees C involved in the regulation of antioxidant ability and energy status were investigated. Ultrastructural observation revealed more severe mitochondrial structures in the transient overexpressed MaAPY2 (OE-MaAPY2) fruit. Furthermore, enhanced generation of reactive oxygen species, in association with the accelerated CI symptoms in the OE-MaAPY2 fruit under cold stress condition was observed, with low activities of antioxidant enzymes, including superoxide dismutase, catalase, and peroxidase, accompanied by a high activity of polyphenol oxidase. Transcriptomic analysis was performed to uncover the variations of transcriptional levels in banana fruit during CI development. Overall, these results implied that MaAPY2 to serve as a negative modulator could reinforce CI symptom in banana fruit by triggering oxidative stress and damaging mitochondrial integrity, which provided new insights on the regulatory CI mechanism of banana fruit during low-temperature storage.

Chilling injury (CI) poses a significant postharvest challenge for tropical fruits, such as banana (Musa acuminata). This study demonstrated that arachidonic acid (ARA) applied at 10 μM effectively enhanced chilling tolerance in banana fruit stored at 6 °C for 6 d. ARA treatment reduced the CI index from 3.44 to 2.73, curtailed respiratory activity, alleviated H₂O₂ and malondialdehyde (MDA) contents, while increased the catalase and peroxidase activities by 150 and 180%, respectively. Transcriptomic and metabolomic analyses identified 4194 differentially expressed genes and 1434 differentially accumulated metabolites, highlighting enrichment in jasmonate signaling, phenylpropanoid biosynthesis, and glutathione metabolism. Key metabolites, including jasmonic acid, phlorizin, and 4-hydroxycinnamic acid, were significantly upregulated. ARA treatment maintained energy levels by increasing ATP content by 1.3-fold. These findings elucidated that ARA alleviates chilling injury in banana fruit by enhancing antioxidant capacity, membrane stabilization and metabolic reprogramming through the coordinated transcriptomic and metabolomic reorganizations.

Litchi fruit are highly susceptible to browning during ambient storage, which results in a marked reduction in commercial value. This study investigated the regulatory effects and underlying mechanisms of alpha-ketoglutaric acid (AKG) on postharvest browning and senescence in litchi fruit. AKG treatment significantly reduced the browning index, delayed pigment degradation, and preserved cell membrane integrity. Moreover, AKG treatment alleviated the accumulation of reactive oxygen species (ROS) and enhanced antioxidant capacity. In parallel, AKG elevated the activities of key enzymes involved in the tricarboxylic acid (TCA) cycle, maintained high ATP levels and energy charge, and thereby provided sufficient energy to support ROS scavenging and cellular repair processes. Consequently, AKG synergistically improved both antioxidant capacity and energy metabolism. Transcriptomic analysis further revealed that AKG modulated the expression of genes associated with oxidoreductase activity, transmembrane transporter function, glycosyltransferase activity, and organic acid trans-membrane transporter activity. Specifically, AKG downregulated genes involved in browning and lignin synthesis (LcGOLS2, Lc4CL3, LcLAC14), ethylene signaling regulators (LcEIN4, LcERF4, LcERS1), and senescence regulators (LcNAC083, LcNAC090, LcNAC100, LcWRKY75, LcMYB73), while upregulating stress-responsive genes (LcTIFY9, LcbZIP44 and LcbHLH123). Collectively, these findings demonstrate that AKG delays postharvest browning and senescence in litchi by modulating ROS metabolism, enhancing TCA cycle-mediated energy production, and suppressing the expression of senescence-related genes.

Chilling injury (CI) occurs with banana fruit during < 13 degrees C storage, resulting in great economic losses. Low-concentration hydrogen peroxide (H2O2) can act as a signaling molecule under various stress conditions, and involve in defense responses. However, the perception and transduction of H2O2 signal in banana fruit under chilling temperature remains unclear. In this study, 0.01 mM H2O2 was used to treat banana fruit stored at 6 +/- 1 degrees C. The role of H2O2 receptors in regulating cold damage was investigated. Results indicated that H2O2 treatment significantly reduced CI index, respiration rate, electrolyte leakage, malondialdehyde content, and Reactive oxygen species levels (H2O2 and superoxide anion), along with enhancing activities of antioxidant enzymes, including catalase, superoxide dismutase and peroxidase. Transcriptomic analysis identified nine H2O2 receptor candidates MaHPCA1s, with MaHPCA1-1 and MaHPCA1-3 involved in cold response. qPCR data validated the reliability of transcriptome data. Transient overexpression of MaHPCA1-1/-3 (OE-MaHPCA1-1/-3) in banana fruit alleviated CI symptoms and upregulated the expression of calcium ion (Ca & sup2;(+)) signaling pathway genes, whereas silencing of MaHPCA1-1/-3 led to contrasting results. Ca & sup2;(+) inhibitor treatment on OE-MaHPCA1-1/-3 fruit and Ca & sup2;(+) treatment on MaHPCA1-1/-3-silenced fruit co-confirmed that MaHPCA1-1 and MaHPCA1-3 might enhance chilling tolerance by interacting with Ca & sup2;(+) signaling pathway. These results indicated that MaHPCA1-1 and MaHPCA1-3 acted as positive regulators in alleviating chilling process of banana fruit by cooperating with Ca & sup2;(+) signaling.

Litchi fruit is highly susceptible to rapid postharvest deterioration, primarily manifested as pericarp browning and senescence, which severely compromise its commercial value. Meclofenamic acid sodium (MA), an arylacetic acid-type nonsteroidal anti-inflammatory drug with recognized antioxidant properties, presents a potential intervention strategy, yet its efficacy and mechanistic role in postharvest litchi preservation remain unexplored. In this study, we demonstrate that postharvest MA treatment significantly delayed pericarp browning, maintained visual quality, suppressed respiration rate, and extended marketability. At the physiological and biochemical levels, MA application effectively attenuated oxidative stress, as evidenced by reduced accumulation of reactive oxygen species (superoxide anion and hydrogen peroxide) and lipid peroxidation product (malondialdehyde), alongside elevated pools of non-enzymatic antioxidants (glutathione, ascorbic acid, total phenols, and anthocyanins). Furthermore, MA enhanced the activities of key antioxidant enzymes (superoxide dismutase, catalase, and ascorbate peroxidase) while inhibiting the activities of browning-related enzymes (peroxidase and polyphenol oxidase). To sustain cellular energy homeostasis, MA treatment elevated ATP content and energy charge by activating succinate dehydrogenase and malate dehydrogenase. Transcriptomic and RT-qPCR analyses corroborated these findings, showing upregulation of genes involved in flavonoid/anthocyanin biosynthesis, oxidative stress response, and energy metabolism. Importantly, MA treatment mitigated the storage-induced decline in global N6-methyladenosine (m6A) methylation and increased m6A modification levels in specific senescence-related transcripts. Collectively, our results indicate that MA delays litchi senescence and browning through an integrated mechanism involving the modulation of oxidative stress, maintenance of energy homeostasis, and regulation of m6A modifications.