Advances in Cell Wall Dynamics and Gene Expression in Postharvest Fruit Softening

Abstract

Postharvest fruit softening is a critical determinant of fruit shelf life, significantly influencing mechanical damage susceptibility, pathogen invasion, and consumer preference. Collectively, these factors lead to substantial losses in the fruit industry. The structural modifications of cell wall and cuticle during ripening primarily govern fruit softening. The objective of this review is to synthesize recent advances and provide a comprehensive analysis of the molecular mechanisms underlying this process. In this review, we provide a comprehensive analysis of cell wall composition and softening-associated cell wall remodeling proteins. We examine recent advances in manipulating single or multiple genes encoding cell wall-modifying proteins that influence fruit softening, and identify key transcription factors regulating the expression of these gene networks. This review synthesizes current understanding of the molecular mechanisms governing fruit ripening, providing a foundation for future research in postharvest biology.

1. Introduction

The transition of fruits from commercial harvest maturity to edible ripeness is referred to as the postharvest ripening process, which simultaneously constitutes their storage period. Fleshy fruits exhibit considerable variation in structure, development, and biochemical makeup across different species. Nevertheless, their postharvest ripening processes are highly coordinated and share many common characteristics. During postharvest ripening, fruits undergo a series of physiological and biochemical changes, that enhance their appeal and nutritional value for seed-dispersing animals, and in the case of cultivated species, for human consumers [1]. Key changes include the buildup of sugars, pigments, and flavor or aromatic compounds, along with a reduction in firmness [2].

The postharvest softening of fruits represents one of the most significant alterations during fruit storage. On one hand, fruit firmness directly affects sensory texture; on the other hand, it serves as an important indicator of fruit quality and market value [3]. Fruit softening is due in large part to the controlled breakdown and modification of cell wall polysaccharides and water loss [2,4]. These postharvest mechanisms are controlled by evolutionarily conserved and convergent regulatory networks involving transcription factors and hormones [5]. In this article, we consider recent advances in cell wall modification and cuticle biology that address controlling fruit softening and extending storage and shelf life, providing insights into the molecular mechanisms underlying fruit postharvest ripening.

2. The Process of Fruit Softening

As living biological systems, postharvest fruits maintain essential metabolic activities, with respiration serving as the predominant physiological process that critically influences both fruit quality attributes and storage performance [6]. Based on distinct respiratory patterns, fleshy fruits are categorized into two types: climacteric fruits (e.g., apples, bananas, and kiwifruits) and non-climacteric fruits (e.g., grapes, strawberries, and cherries). Fruits may be crisp like apples or very soft like peaches and berries, but they all soften when ripening [2]. The textural changes associated with fruit softening reflect composite effects of primary cell wall and middle lamella modifications (impacting structural stability and cellular adhesion) and decreasing turgor within cells [7,8].

In climacteric fruits, ethylene concentration remains extremely low during developmental stages while respiratory rate progressively declines. Upon entering the ripening phase, ethylene production gradually increases to reach its peak level, concomitant with the occurrence of respiratory climacteric [9]. Following the respiratory climacteric, both ethylene production and respiratory rate decline, accompanied by significant deterioration in fruit quality and storability. The accelerated respiratory activity rapidly depletes nutritional reserves, leading to quality degradation and progressive loss of edibility [10,11]. In non-climacteric fruits, relatively low levels of endogenous ethylene still participate in regulating the postharvest ripening, despite the absence of a respiratory climacteric [12] (Figure 1).

3. Cell Wall and Fruits Softening

3.1. Composition of the Cell Wall

The plant cell wall is a rigid, multilayered structure that provides mechanical support and gives the cell its shape and form (Figure 2A) [13]. Plant cell wall consists of the primary cell wall, secondary cell wall, and middle lamella [14]. The middle lamella forms a sticky pectin layer outside the primary wall, acting as nature’s glue that bonds plant cells together [15]. After the primary wall stops expanding, some cells deposit a thick, rigid secondary wall inside the primary wall structure, a phenomenon most pronounced in woody tissues [16]. The softening of fruits is primarily related to the modifications of the primary wall and middle lamella, affecting wall strength and intercellular adhesion [2].

The primary wall contains strong and rigid cellulose microfibrils embedded in a hydrated matrix made of polysaccharides classified as pectins and hemicelluloses [17,18]. Cellulose is made of many parallel β1,4-D-glucan chains (Figure 2A). These chains are made by cellulose synthase complexes in the cell membrane, then form stiff microfibrils outside the membrane. The cellulose synthase enzyme has two main parts: a glucose-adding site inside the cell and a tube that moves the growing chain outside. It takes glucose from UDP-glucose inside the cell and adds it to the chain’s growing end [19].

Xyloglucan, the primary hemicellulose in primary walls (with minor arabinoxylan content), possesses a β1,4-linked glucan backbone (like cellulose) with xylose residues linked to three glucose residues per tetrameric repeat (Figure 2C). Xylose residues can be decorated with diverse sugar groups including galactose and fucose in varying patterns. Branched sugar groups create spatial hindrance that inhibits dense packing of xyloglucan polymers while maintaining their cellulose adhesion capacity [20].

Homogalacturonan (HGA), the predominant structural component of pectin, possesses a α1,4-linked D-galacturonic acid backbone (Figure 2C). During biosynthesis in Golgi apparatus, the majority of homogalacturonan residues undergo carboxyl group methylation [21]. The methyl esters can be partially eliminated by pectin methylesterase (PME), which makes HGA susceptible to depolymerization by endo-polygalacturonase (PG) and pectate lyase (PL) [22,23]. Processive de-esterification by PME also generates linear segments of six or more residues that sometimes form calcium-mediated ionic crosslinks with neighboring chains, thereby stiffening the pectic matrix [24,25]. Rhamnogalacturonan-I (RG-I), another important pectin component, consists of a linear chain with alternating rhamnose and galacturonic acid molecules (Figure 2C). The RG-I polymer often carries multiple oligosaccharide side chains and can form covalent bonds with both homogalacturonan and glycoproteins [26]. These structural features enable RG-I to participate in middle lamella adhesion and influence various cell wall characteristics [27].

Beyond the classical tethered network and pectic hydrogel models, a wall model was recently developed [14]. Cellulose microfibers join together through different physical links to form tight bundles and an interwoven network, where direct fiber-to-fiber junctions are strongest [28,29,30]. Xyloglucans adopt various conformations, and they bound to cellulose surfaces in extended or coiled forms or get caught inside cellulose bundles. They can also link multiple cellulose fibers like ropes [14]. Pectins assemble into a hydrogel matrix encapsulating cellulose and xyloglucan [31]. Xyloglucan and pectins may regulate wall mechanics by controlling cellulose’s assembly into a load-bearing nanostructure [30]. The matrix polysaccharides are flexible and have unique traits, molecular connections, dynamic changes, and structural functions, and the matrix also contains trace amounts of structurally diverse proteins and proteoglycans with diverse proposed functions [32].

Figure 2. (A). The model of the growing cell wall [14]. Cellulose microfibrils establish lateral connections, creating bundles and an integrated framework. Xyloglucans associate with cellulose surfaces in extended or folded conformations or are enclosed within cellulose aggregates. Pectins generate a gel-like matrix that encompasses cellulose and xyloglucan. (B). Transmission electron micrographs of TCJ (left) and ML (right) [33]. The ML between adjacent cells is rich in de-esterified homogalacturonan (HGA). PCW, primary cell wall. ML, middle lamella. TCJ, tricellular junctions. The bar (left) indicates 5 μm, and the bar (right) indicates 1 μm. (C). Schematic diagrams of molecular structures of several dominant cell wall polysaccharides [14]. (i) Xyloglucans. (ii) Homogalacturonan. (iii) Rhamnogalacturonan-I.

Figure 2. (A). The model of the growing cell wall [14]. Cellulose microfibrils establish lateral connections, creating bundles and an integrated framework. Xyloglucans associate with cellulose surfaces in extended or folded conformations or are enclosed within cellulose aggregates. Pectins generate a gel-like matrix that encompasses cellulose and xyloglucan. (B). Transmission electron micrographs of TCJ (left) and ML (right) [33]. The ML between adjacent cells is rich in de-esterified homogalacturonan (HGA). PCW, primary cell wall. ML, middle lamella. TCJ, tricellular junctions. The bar (left) indicates 5 μm, and the bar (right) indicates 1 μm. (C). Schematic diagrams of molecular structures of several dominant cell wall polysaccharides [14]. (i) Xyloglucans. (ii) Homogalacturonan. (iii) Rhamnogalacturonan-I.

3.2. Cell Wall Remodeling Proteins

Many cell wall remodeling proteins (CWRPs) are secreted into the apoplast to modify these wall polysaccharides during postharvest ripening. These include the hemicellulose-modifying expansin (EXP), endo-1,4-β-glucanase (EGase), and the xyloglucan endo-transglycosylase/hydrolase (XTH), and the pectin-modifying enzymes PL, PG, PME, rhamnogalacturonan lyase (RGL), β-galactosidase (BGAL), and α-arabinofuranosidase (AFase) [34]. The corresponding HGA and xyloglucan breakdown, HGA demethylesterification, and RG-I side-chain removal reduce intercellular adhesion [2]. The influence of these enzymatic activities on wall properties is determined by their temporal expression patterns, quantitative activity levels, and the species-specific wall composition. The composition of the cell wall is species dependent. The structural and compositional diversity of microalgal cell walls has been systematically cataloged [35]. Poaceae species exhibit a distinctive capacity to synthesize (1,3;1,4)-β-glucans with mid-range ratios of cellotriosyl to cellotetraosyl units, which may explain the widespread occurrence of these polysaccharides across the family [36]. Variations in cell wall architectural properties among different switchgrass (Panicum virgatum) genotypes directly affect their accessibility to hydrolytic enzymes [37]. Ripening-related PG1 was specifically detected in fast-softening ‘Royal Gala’ but absent in ‘Scifresh’, confirming its cultivar-dependent expression and pivotal role in apple texture determination [38,39]. Goulao et al. systematically profiled the enzymatic activity patterns of cell wall-modifying enzymes throughout both growth and ripening phases. Their comprehensive analysis revealed that while distinct enzyme isoforms may mediate specific developmental processes, the overall coordination of fruit growth and ripening appears to be governed by members of the same families of cell wall-modifying enzymes [40].

3.3. Modulators Involved in the CWRPs-Mediated Regulatory Network of Fruit Softening

Efforts to directly modify genes encoding homogalacturonan-depolymerizing enzymes have proven effective in fruit softening regulation. The slow-softening ‘Scifresh’ variety exhibited diminished endo-polygalacturonase and pectin methylesterase activity in early development phases, correlating with enhanced cellular cohesion and delayed softening kinetics [41]. Manipulation of these individual genes triggers cascading effects on fruit ripening and softening [23]. MdPG1, an endo-polygalacturonase gene, functions as a key marker for fruit softening in apples. While tomato ripening-related SlPG2a is induced exclusively by very low ethylene concentrations, apple MdPG1 expression responds not only to ethylene but also to extended cold temperatures during postharvest storage in the absence of ethylene [42,43]. Moreover, MdPG1 expression remained minimal in firmness-retaining cultivars following extended cold storage, regardless of ethylene synthesis [44]. In short-shelf-life ‘Golden Delicious’, MdPG1 expression in the cortex increased rapidly during ripening [45]. Up-regulation of MdPG1 enhances pectin hydrolysis in the middle lamella, elevating water-soluble pectin levels and accelerating postharvest softening in apples [23]. Down-regulation of MdPG1 reduced pectin solubilization, pectin depolymerization, and fruit softening [46]. MdEIL2 and MdCBF2 directly control the expression of MdPG1, working together to regulate ethylene-induced apple fruit softening during cold storage [43]. MADS-box transcription factors also play important roles in fruit softening regulation. MdMADS6, MdMADS8, and MdMADS9 directly regulate MdPG1 transcription in apples [47]. Ethylene-induced MdPUB24 mediates the ubiquitination and subsequent degradation of MdNAC72. Moreover, ethylene stimulates MdMAPK3 to phosphorylate MdNAC72, further diminishing its inhibitory effect on MdPG1 expression. These coordinated mechanisms ultimately accelerate fruit softening in postharvest storage [3]. The MdZFP3 assembles with co-repressor MdTPL4 and chromatin modifier MdHDA19 to form a repression complex that epigenetically silences cell wall degradation genes (MdPG1, MdPL5, Mdβ-Gal9, Mdα-AFase2, MdXET1, and MdEXP8). Additionally, E3 ubiquitin ligase MdEAEL1 targets MdZFP3 for ubiquitin-mediated degradation, resulting in disassembly of the repression complex [5]. The 8 bp deletion in the MdERF3 promoter abolished MdDOF5.3 binding, leading to down-regulation of MdERF3. This loss of repression enhanced the expression of MdPGLR3, MdPME2, and MdACO4, ultimately impairing fruit firmness and crispness retention. Similarly, a 3 bp deletion in the MdERF118 promoter attenuated MdRAVL1 binding, suppressing MdERF118 expression. Consequently, MdPGLR3 and MdACO4 were up-regulated, further contributing to fruit softening [48]. MdPL5 promoted fruit softening in apples and tomatoes. MdNAC1-L acted as a transcriptional activator that positively regulates fruit ripening and softening through promoting the expression of cell wall degradation genes MdPL5 and MdPG1, and ethylene biosynthesis genes MdACS1 and MdACO1 [49].

HGA depolymerization serves as a key driver of fruit softening in both crisp and soft fruit, though the relative contributions of PG- versus PL-mediated degradation pathways vary significantly across species [50]. In strawberry, silencing either the PL gene FaPLC or the PG genes FaPG1 and FaPG2 significantly inhibited fruit softening [51,52,53]. Overexpression of grapevine VvPL11 in tomato significantly elevated ethylene production and reduced fruit firmness, accompanied by decreased propectin content and increased water-soluble pectin accumulation [54]. VIGS-mediated silencing of PpPG21 and PpPG22 in peach fruit substantially decreased PG activity and preserved firmness during postharvest storage [55]. Down-regulation of SlPL expression increased cellulose and hemicellulose content while decreasing water-soluble pectin, leading to enhanced intercellular adhesion, substantial reduction in fruit softening, and improved resistance to biotic stress in tomato [56]. PpERF/ABR1 up-regulates PpPG expression to promote peach fruit softening [57]. The ethylene-down-regulated transcription factor SlERF.F12 associates with SlTPL2 via its C-terminal EAR motif and recruits histone deacetylases SlHDA1/3 into a tripartite complex. This complex reduces histone acetylation at the promoter regions of cell wall disassembly-related genes including SlPG2a and SlPL, thereby repressing their expression and consequently delaying fruit softening [58].

The cell wall loosening and swelling induced by EXP may promote further wall modification by increasing substrate accessibility for other enzymes, including PG and PL [2]. Tomato SlPG2a affects pectin metabolism but contributes little to softening when inhibited [59]. Co-suppression of both SlPG2a and SlEXP1 results in substantially increased tomato fruit firmness relative to individual suppression of either gene [60]. Suppression of SlEXP1 in tomato significantly elevated fruits firmness throughout ripening. This suppression markedly inhibited late-stage polyuronide depolymerization while having minimal effect on the degradation of hemicelluloses [61]. Apple MdEXLB1-overexpressing transgenic tomato lines exhibited multiple phenotypic alterations, including reduced plant height, accelerated reproductive development, and advanced fruit maturation, and overall faster ripening progression [62]. MdEXP7 is also linked with fruit softening [63]. In banana (Musa acuminata), the zinc finger transcription factors MaC2H2-1 and MaC2H2-2 up-regulate the expression of cell wall-modifying genes, including MaEXP-A2, MaEXP-A8, and MaSUR14, thereby accelerating postharvest ripening and softening [64]. SlLOB1 activates SlEXP1 and SlPL expression, and its repression delays fruit softening and extends shelf life [65]. Silencing of MdBBX25 accelerated fruit softening in apple by increasing ethylene synthesis and elevating the expression of cell wall-related genes, including MdPG, MdCEL, and MdEXPA8 [66].

The XTH plays crucial roles throughout fruit development. XTH activity peaked in both apple and kiwifruit fruits within two weeks of post-anthesis, then declined sharply before rebounding during fruit expansion. In apples, activity peaked at harvest then declined postharvest, while kiwifruit core tissue showed similar patterns but continued increasing until ripening. Outer pericarp XTH increased only during postharvest ripening [67]. Persimmon DkXTH8 overexpression induces cellular fragility, and enhances membrane leakage and oxidative damage, while promoting premature leaf aging and fruit texture softening in transgenic plants [68]. In strawberry, transient overexpression of FvXTH9 or FvXTH6 promoted ripening and softening [69]. The knock-out of SlXTH5 in tomato resulted in slightly firmer fruit pericarp [70]. Overexpression of MdXTHB in ‘Golden Delicious’ and ‘Fuji’ apples resulted in accelerated softening and an earlier ethylene production peak [71]. Overexpression of MdXTH2 and MdXTH10 in tomato fruits increased the expression of ethylene-related genes (ACS2 and ACO1) and cell wall-modifying enzymes (XTHs, PG2A, Cel2, and TBG4) [72]. Ethylene-repressed MdWRKY31 interacts with ethylene-induced MdNAC7, relieving MdWRKY31-mediated transcriptional repression of MdXTH2. This molecular interplay promotes fruit softening through loosening the cell wall and facilitating catabolic activities within the cellulose–xyloglucan matrix [73].

Fruit cell wall galactosyl levels show a correlation with tissue firmness [74]. Transient silencing of PpBGAL10 or PpBGAL16 in peach inhibited ethylene production and subsequent PpPG expression, leading to delayed fruit ripening and softening [75]. Overexpression of β-galactosidase DkGAL1 induced earlier ethylene evolution, which subsequently promoted pigmentation shift and textural softening [76]. Silencing β-galactosidase 4 reduces fruit softening in tomato [77]. Suppression of FaβGal4 elevates cell wall galactose content and decreases fruit softening in strawberry [78]. Ethylene-induced MdAP2-like promotes fruit softening by activating Mdβ-GAL18 expression, which increases β-galactosidase activity and free galactose levels in apple fruits [79]. Ethylene-induced MdZF-HD11 also positively regulates the expression of Mdβ-GAL18 to promote the postharvest softening in apple [7]. α-AFase catalytic activity also shows a persistent positive association with fruit hardness, which grew with a lengthened storage time. MdAF3 expression is increased in fruits harvested from plants persistently exhibiting mealiness characteristics and elevated α-AFase activity [80]. MdDof43 activates Mdβ-Gal2 and Mdα-AF3 transcription, enhancing cell wall degradation and accelerating fruit softening [81], and the αAFase, β-Gal, and PG can complement each other in pectin degradation, thereby reducing cell adhesion and promoting fruit softening [82]. The key factor in apple anthocyanin regulation, MdbHLH3, also enhances the αAFase, β-Gal, and PG activities during postharvest storage [82].

Hormones play a crucial role in regulating fruit softening. In addition to ethylene as mentioned above, abscisic acid (ABA) and gibberellins (GAs) are also involved in this process. Abscisic acid accelerates postharvest softening of blueberry fruit by enhancing cell wall metabolism [83]. Gibberellins are involved in fruit ripening and softening by mediating multiple hormonal signals [84]. Interestingly, a newly identified macromolecule, class 1 non-symbiotic hemoglobin (MdHb1), promoted fruit softening through mediating the depolymerization of protopectin to water-soluble pectin. Two metabolites, D-galacturonic acid and D-glucuronic acid, suppress the transcription of MdHb1 through the MdMYB2/MdNAC14/MdNTL9-MdHb1 regulatory module, thereby delaying fruit softening in apple [85].

Certainly, the role of hormones in regulating the ripening/softening of climacteric and non-climacteric fruits exhibits significant differences. In climacteric fruits, ethylene and ABA interact to coordinately regulate these processes, whereas in non-climacteric fruits, ripening/softening are predominantly controlled by ABA in an ethylene-independent manner, as extensively reviewed by Kou et al., making the investigation of these regulatory differences a highly promising research direction [86].

4. Water Loss

Postharvest water loss from the entire fruit considerably accelerates softening [87]. Mature fruit generally lack functional stomata, which turn into lenticels covered by periderm tissue [23,88]. Composed of a matrix of the polyester cutin impregnated with various waxes or phenolics, the fruit cuticle serves as nature’s waterproof coating that minimizes dehydration [89]. A reduction in cellular turgor pressure, resulting from solute and water movements between the apoplast and symplast, further contributes to fruit softening [2,90].

Epidermal wax disruption treatments significantly increased postharvest weight loss in peach, plum, and citrus [91,92,93]. Moreover, blueberries subjected to epidermal wax disruption treatments exhibited rapid cell wall degradation postharvest, leading to a significant decline in fruit firmness. In contrast, berries with intact natural wax coatings maintained extended shelf life [94]. The thicker cuticle and higher wax content in citrus fruits also reduce pathogen invasion and decrease fruit maceration [95].

Postharvest preservation treatments can alter epidermal wax composition, thereby influencing fruit storability. A 1-MCP treatment significantly inhibited the decline of cuticular wax content in apple fruit, while concurrently delaying the reduction in fruit firmness and loss of nutritional compounds [96,97]. Ethylene treatment induced increased cuticular wax accumulation in citrus fruit, concomitant with structural modifications of wax morphology and reduced incidence of brown spot disease [98]. The distinctive morphological structures and biological functions of cuticular wax play critical roles in the application of fruits postharvest preservation technologies. Various wax coating applications enhance marketability and extend storage duration in commercial fruits such as citrus and apples [89,98,99].

A correlation was observed between alterations in the cell wall architecture and dehydration processes during fruit softening. Peel cell walls of MdPG1-overexpressing fruits exhibited thinner with reduced cell wall content, along with increased water-soluble pectin. The outer cell layers became disorganized, with cells separating widely and large air spaces below the epidermis, resulting in increased water loss in apples [23,46]. Overexpression of MdPG1 also reduces fruit skin fracture force, leading to cuticular microcracking and ultimately full-scale fruit cracking [23,100]. Down-regulation of SlPL expression in tomato induced tighter cellular packing and decreased transpirational water loss [56]. Moreover, specific genetic loci regulate fruit water loss without significantly altering cuticular architecture. Following harvest, SlLOB1-silenced fruit exhibited diminished tissue collapse and markedly decreased water loss, while cuticle thickness remained unchanged [65]. Overexpression of SlFSR significantly reduced the shelf life and increased water loss in stored fruits by promoting the expression of cell wall genes, including SlPG, SlPL, and SlEXP1 [101]. Increased skin cracking may result from altered cell wall structure, caused by β-galactosidase TBG6 silencing, increased SlEXP1/SlPG2a expression, or heterologous VvPL1 pectate lyase overexpression in tomato, which impair the cuticle’s barrier function, allowing water vapor to penetrate the skin [102,103,104,105]. Overexpression of the myo-inositol monophosphate gene SlIMP3 enhanced wall thickening and decreased fruit softening, as well as water loss [106]. To facilitate the interpretation of the review data, we have summarized the main genes/enzymes involved in fruit softening in Supplementary Table S1.

5. Conclusions and Prospects

Pectin depolymerization, primarily facilitated by PG or PL, is a well-established key driver of fruit softening in many species (Figure 3, Supplementary Table S1). Significant progress has been made in understanding that the loss of primary cell wall integrity, intercellular adhesion, turgor pressure, and water content collectively shape the final fruit texture. This knowledge has been beneficially applied to distinguish the phenotypic outcomes of softening: for instance, firm fruits retain robust cell walls and high turgor, while weakened adhesion promotes mealiness. Beyond canonical enzymes, the exploration of various other cell wall-modifying proteins has expanded our understanding of texture regulation, although their mechanisms remain an active area of research.

Building on this foundation, recent studies have begun to characterize the roles of expansion (EXPs) and xyloglucan endotransglucosylase/hydrolases (XTHs) in fruit softening, moving beyond their well-defined functions in seed germination or herbaceous species [107,108]. These investigations represent a promising shift towards elucidating how diverse enzymatic activities coordinate in the complex process of cell wall remodeling (Figure 3, Supplementary Table S1). Furthermore, the recognition that softening is influenced by environmental signals (temperature, humidity, and light) has opened a new frontier: a major forthcoming challenge and opportunity lies in deciphering the molecular links between these environmental signals and the cell wall-modifying pathways [109].

The development of CRISPR/Cas9 technology has been a transformative change, enabling precise multiplexed gene editing to improve fruit quality traits—such as simultaneously enhancing water retention and reducing cell wall disassembly. This strategy offers a superior alternative to RNAi silencing, as it can generate a spectrum of natural partial-loss-of-function mutations without unintended side effects, presenting significant potential for biotechnological cultivar improvement. Concurrently, traditional breeding enhanced by GWAS and QTL mapping continues to be a pivotal and successful approach for quality improvement and gene discovery. Recently, we developed a new cultivar ‘Yuguan’ with high wax content and prolonged shelf life [110], which provides an excellent model for future research. While CRISPR/Cas9 is a powerful tool for fruit quality improvement, the elimination of transgenes remains a significant challenge in vegetatively propagated crops. Alternatively, manipulating upstream master transcription factors that regulate gene networks offers a more straightforward and commercially viable strategy. Looking forward, strategic perspectives for both research and application should prioritize these two avenues. These data-driven perspectives, grounded in contemporary technological advances, chart a clear course for developing the next generation of fruit cultivars with optimized postharvest quality.