Bitter pit is one of the most common physiological disorders for pome fruit, causing significant annual losses. Despite over a century of research, the exact causes of bitter pit are still not fully understood. Bitter pit symptoms manifest from cellular breakdown under the peel, causing necrotic and corky lesions generally concentrated at the calyx end of the fruit. These lesions are commonly darkened, dry, and spongy with a bitter taste ( Figure 1 ). Bitter pit symptoms may appear on the tree or after harvest during the first month or two of storage (Serban et al., 2019). Since the identification of bitter pit as a disorder in the 1920s, numerous efforts have been made to explain the underlying physiological reasons behind its development. However, most of the publications have focused on describing the agronomic factors contributing to increased bitter pit incidence.

Traditionally, bitter pit has been most often associated with low calcium (Ca) content in the fruit (Smock and Van Doren, 1937; Van Stuivenberg and Pouwer, 1950; Yamazaki et al., 1968; Ferguson et al., 1979). Ca is taken up by the tips of actively growing roots and is transported through xylem tissue to transpiring tissues above ground including leaves and fruit (de Freitas and Mitcham, 2012; Miqueloto et al., 2014; Kalcsits et al., 2017). Uptake and transport of Ca are through the transpiration stream, and unlike many other nutrients, Ca is not phloem mobile and cannot be easily translocated from one organ to another when demands change (de Freitas and Mitcham, 2012). Ca deficiency can be due to low Ca availability or water stress, which results in low transpiration rates since Ca cannot be mobilized from older tissues and redistributed via phloem (Thomas and Adarsh, 2020). Therefore, localized Ca deficiencies like bitter pit commonly appear on the furthest ends of an organ to the xylem supply (Miqueloto et al., 2014). However, bitter pit is a complex process that involves not only the total input of Ca into the fruit but also a proper Ca²⁺ homeostasis at the cellular level, affecting different cellular fractions present in the plant (free Ca²⁺, pectates, phosphates, carbonates, and oxalates) and bitter pit development (de Freitas et al., 2010). The proportion of Ca pectate in cell walls is associated with the susceptibility of tissue to fungal and bacterial infections (Thomas and Adarsh, 2020), and together with Ca²⁺ accumulation into storage organelles, both fractions may have an important role in the bitter pit development as shown by de Freitas et al. (2010). Additionally, Ca can act as a secondary messenger for several metabolic processes (Xu et al., 2022), and its cytosolic levels must be precisely controlled since variation can trigger diverse metabolic responses and even lead the cell to death (Tang and Luan, 2017; Paiva, 2019). There is a clear relationship between the status of Ca²⁺ homeostasis inside cells and bitter pit. However, as we will present later, the mechanisms underlying bitter pit development still remain unclear.

The uptake and distribution of Ca in apples are interconnected with other nutrients, and an imbalance can also lead to the appearance of Ca disorders (Ludders, 1979; Ferguson and Watkins, 1983; Hopfinger et al., 1984; Pavičić and Miljcović, 1991; Amarante et al., 2013). Since many nutrients are phloem mobile, Ca relative to other nutrients is an important indicator of bitter pit risk (Ferguson and Watkins, 1983). However, additional factors have been identified that also contribute to its development, like variation in auxin concentration (Griffith et al., 2022; Huang et al., 2023), high concentration of gibberellins (Saure, 2005), changes in xylem functionality (Miqueloto et al., 2014), or physiological responses to abiotic stress (Mao et al., 2021). All these factors have been implicated in bitter pit development, but the relationships among them are still not well defined. In fact, most of these additional factors also contribute to fruit Ca content; hence, Ca deficiencies could possibly be parallel phenomena rather than direct causes of bitter pit in some cases.

A better knowledge of the factors that stimulate bitter pit development will help refine research hypotheses and develop more effective control strategies. The present article aims to review the relevant available research literature identifying different proposed physiological mechanisms that contribute to the development of bitter pit. We focused on the role of mineral nutrition, plant growth regulators, and other factors in the development of this disorder ( Figure 2 ), providing a comprehensive overview of the state of the art in bitter pit research and highlighting the key challenges and opportunities for future research to understand the factors that influence in bitter pit occurrence and management strategies to prevent or mitigate the impact of bitter pit on apple production.

Auxins are key phytohormones contributing to plant growth and development through their impact on cellular elasticity and, subsequently, cell growth and elongation. There have been many studies that have delineated the controlling pathways for auxin perception, signaling, and its contribution to Ca transport (Benjamins and Scheres, 2008). Auxin regulates the mobilization of photoassimilates in source tissues (mainly leaves) and elevates the translocation of carbohydrates toward sink organs (e.g., roots and fruits, respectively) (Balasubramanian et al., 2023). The relationship between auxins and bitter pit may be related to the link between Ca absorption in plant tissue and polar auxin transport, where tissues that are low in auxins have poor absorption of Ca. Polar auxin transport is the regulated transport of auxins in plants, and among its functions, the most important is the ability to coordinate signaling controlling plant development (Balasubramanian et al., 2023). Many studies indicate that Ca-mediated processes may be involved in modulating auxin response and polar auxin transport (Li et al., 2019). Indeed, Stahly and Benson (1970) and Oberly (1973) observed in ‘Golden Delicius’ and ‘Northern Spy’ apples, respectively, lower accumulation of Ca in the fruit and higher bitter pit incidence when spraying triiodobenzoic acid (TIBA), a known inhibitor of polar auxin transport ( Table 1 ). Parallel patterns in polar basipetal auxin transport and Ca transport have been observed for multiple fruit species including tomato, kiwifruit, and apple (Stahly and Benson, 1970; Banuelos et al., 1987; Sorce et al., 2011).

Indole-3-acetic acid (IAA) is the most common naturally occurring auxin. IAA is produced in seeds, in the apical meristems of shoots, stems, and roots from transamination and decarboxylation reactions of tryptophan (Griffith and Einhorn, 2023; Luckwill, 1953; Van der Krieken et al., 1993). Hertel (1983) and Banuelos et al. (1987) related the appearance of bitter pit to the low auxin concentrations in fruit. Hertel (1983) suggested that IAA transport can preferentially stimulate the release of Ca from vacuoles or cell walls to the cytoplasm, increasing cytoplasmic Ca concentrations. This increase of cytoplasmic Ca would be associated with stimulation of synthesis or renewal of cell wall material and, consequently, with a reduction of the degradation and risk of bitter pit. Banuelos et al. (1987) reported that endogenous IAA controls Ca transport mechanisms, independent from transpiration flow, by increasing sink strength in those specific tissues. Additionally, intercellular Ca mobilization across very short distances occurs through the auxin pump mechanism. According to Banuelos et al. (1987), lower auxin content could limit Ca transport through these two pathways, contributing to bitter pit development in apple fruit.

Exogenous auxin applications were proposed to reduce bitter pit but with irregular results ( Table 1 ). Van Stuivenberg and Pouwer (1950) hypothesized that auxin concentrations must exceed a specific threshold to overcome B deficiencies and prevent the development of cork spot and bitter pit (Griffith and Einhorn, 2023). Indeed, they suggested that disorder incidence could be controlled by spraying the trees with IAA at the end of June or in the first half of July (northern hemisphere) during the cell expansion phase of fruit growth. However, another study where the IAA was supplemented by the synthetic auxin 1-naphthaleneacetic acid (NAA) reported increased bitter pit incidence in NAA-treated trees (Mulder, 1951 cited by Griffith and Einhorn, 2023). Cline (2019) also obtained different responses to pre-harvest NAA applications depending on the number of applications ( Table 1 ). According to these results, the relationship between auxins and bitter pit incidence may vary depending on several factors, such as differences in growing conditions, weather, and soil (Cline, 2019; Griffith and Einhorn, 2023).

Overall, it appears evident that auxins may affect bitter pit development in apples. However, the exact mechanisms underlying the relationship between auxins and bitter pit in apples are not fully understood. In addition to the connection between Ca absorption and polar auxin transport, auxins could also contribute to xylem disruption (Jacobs, 1952; Johnsson et al., 2019). It is widely known that Ca is translocated from the root system to the shoot and fruits via the xylem; hence, some authors have worked on the role of auxins in the differentiation and timing of xylem development and its relationship with the bitter pit (Griffith et al., 2022).

Xylem functionality has been associated with bitter pit (Griffith and Einhorn, 2023). Since Ca movement from roots to above-ground tissues follows the transpiration stream, xylem connectivity and continued flow into developing fruit are important for Ca accumulation to occur (Hocking et al., 2016). Xylem vessel functionality naturally decreases during fruit growth and development (Dražeta et al., 2004; Miqueloto et al., 2014). This xylem function decays relatively early in the season and mirrors the decline in Ca import (Wilkinson, 1968; Jones et al., 1983; Lang, 1990; Casero et al., 2017).

Dražeta et al. (2004) suggested that decreases in xylem functionality are naturally programmed to reduce diurnal apoplastic backflow of solutes from fruit to the tree during late fruit development. The direction of xylem movement can reverse course during diurnal cycles in apples such that flow is negative into the fruit during the day and positive at night (Lang, 1990; Lang and Volz, 1998). Hence, xylem dysfunction may be a response to minimize the outflow of xylem sap from the fruit but may also come at the expense of reducing the import of xylem‐borne minerals, such as Ca, to the fruit. According to Dražeta et al. (2004), xylem dysfunction begins earlier in the season for apple cultivars that are more susceptible to bitter pit. Other studies have also investigated the relationship between xylem vessel disruption and bitter pit in apples (Amarante et al., 2012; Miqueloto et al., 2014; Angmo et al., 2022). According to Song et al. (2018), xylem conductivity is also determined by xylem anatomic features in the pedicel, which is the site where xylem functionality is lost. All these studies found that fruit with bitter pit had a higher incidence of disrupted xylem vessels compared to fruit without bitter pit. This has led to the hypothesis that xylem disruption could affect Ca uptake and, consequently, trigger bitter pit occurrence as a result of a Ca deficiency in the fruit.

There are two competing theories on the cause of losses to xylem functionality in fruit: 1) mechanical damage to xylem vessels creating permanent losses to functionality and 2) a shift from xylem water transport to phloem water transport from carbohydrate loading into fruit leading to reversible changes in xylem functionality (Dražeta et al., 2004). Losses in xylem functionality may be associated with an increase in the number and/or elongation of parenchyma cells, which compresses xylem vessels without affecting the functionality of phloem vessels. This would cause a decline in Ca import flow to the fruit but would not affect K, Mg, and N flow, resulting in higher susceptibility to bitter pit (Lang and Ryan, 1994; Amarante et al., 2013; Miqueloto et al., 2014). Miqueloto et al. (2018) investigated the mechanisms that regulate fruit Ca content and susceptibility to bitter pit in two cultivars with low or high susceptibility to bitter pit (‘Fuji’ and ‘Catarina’, respectively). They found that losses to xylem functionality, reductions in lenticel pore area, and increases in pectin methylesterase (PME) activity in the peel tissue may all contribute to reductions in fruit Ca content at the distal portions of the fruit and increase bitter pit incidence. The disruptions in the xylem vessels may also further affect the transport of water and other nutrients from the root system. When xylem functionality decreases, water and nutrient transport must occur through the phloem. These changes to transport dynamics may affect the fruit gas exchange and lenticel functionality. Water transport and lenticel functionality are critical for gas exchange and regulating fruit temperature (Venturas et al., 2017). Hence, xylem vessel degradation could increase the risk of hypoxia and temperature stress, stimulating cell death in affected tissues and, consequently, the bitter pit symptoms. Hypoxia and temperature stress promote the increase of reactive oxygen species (ROS), leading to oxidative stress (Pucciariello and Perata, 2017), which is implicated in different physiological disorders suffered by various horticultural crops related to Ca deficiency (Saure, 2014).

The composition and relative abundance of auxins within fruit tissue could have a significant role in xylem disruption during fruit growth (Miqueloto et al., 2014). Saure (2005), and more recently Griffith and Einhorn (2023), proposed that the correlative relationships between bitter pit and nutrient concentrations within fruit tissues may be merely consequences of hormonal imbalances, especially notably auxins, gibberellins, and abscisic acid, that facilitate xylem dysfunction and, consequently, lead to imbalances in nutrient supplies to fruit. Griffith et al. (2022) hypothesized that strategies that limit mechanical xylem vessel damage may help to improve Ca transport to fruit and, consequently, prevent the development of bitter pit ( Table 1 ). They tested this working hypothesis and observed that three successive applications of 20 ppm IAA at 30 days, 45 days, and 60 days after full bloom slowed the development of xylem dysfunction and decreased bitter pit incidence in ‘Honeycrisp’ apples by 65%.

Saure (1996) hypothesized that an increase of gibberellins in fruit may be an underlying cause for bitter pit. This theory was based on the observation that sound fruit without bitter pit symptoms can sometimes have extremely low Ca fruit concentrations. Following this, cell permeability could increase with increasing gibberellins and with it the risk of dehydration and cellular degradation. Conforming to this hypothesis, Ca could play a secondary role where apples with a high Ca content have more stable membranes that resist degradation. Elevated concentrations of gibberellins in fruit could also have consequences on xylem formation. Gradual reductions in auxin concentration and a concurrent increase in the concentration of active gibberellins may constitute a signal for cells to transition from an expansive phase to a maturation one or disruption of xylem (Immanen et al., 2016; Johnsson et al., 2019). Therefore, high levels of gibberellins in fruit may accelerate xylem dysfunction and, consequently, contribute to the development of bitter pit through mechanisms described earlier.

Furthermore, gibberellins play a key role in the stimulation of fruit and shoot growth. Vigorous growth often coincides with high levels of physiologically active gibberellins in the tissues (Saure, 2005). Rapid fruit and shoot growth correlate positively with bitter pit susceptibility through changes in Ca distribution to fruit and diluting Ca as fruit growth increases. Therefore, high gibberellin content during periods of vigorous growth could have both direct and indirect effects that stimulate the development of bitter pit (Saure, 2005). Supporting this hypothesis, Greene (1991), Silveira et al. (2012), and do Amarante et al. (2020) reported a reduction in bitter pit when trees were treated with gibberellin synthesis inhibitors ( Table 1 ). Greene (1991) reported that ‘Gardiner Delicious’ apple trees treated with paclobutrazol had lower vegetative vigor, higher Ca fruit content, and lower bitter pit incidence. Silveira et al. (2012) observed either a reduction or an increase in bitter pit in ‘Catarina’ and ‘Fuji’ apple trees when prohexadione-Ca and gibberellin GA₃ were applied, respectively. do Amarante et al. (2020) also reported that ‘Braeburn’ apple trees treated with GA_{4 + 7} showed a higher incidence of bitter pit in fruit than trees treated with prohexadione-Ca. These three studies demonstrate the negative effects that gibberellins can have on bitter pit. However, Serban and Kalcsits (2018) and Donahue et al. (2018) did not observe changes in fruit Ca concentrations or bitter pit incidences by applying GA₃ or prohexadione-Ca after full bloom in young ‘Honeycrisp’ apple trees. These results highlight a need for further studies to identify the factors explaining the relationship between gibberellins and bitter pit.

Abiotic stress refers to the negative impact of non-living factors on plants and includes drought-, heat-, or soil-based nutrient deficiencies. An increase in intracellular Ca²⁺ concentrations is a common event in most stress-induced signal transduction pathways (Xu et al., 2022). Ca²⁺ is an important second messenger for understanding plant–abiotic stimulus interactions (Van Zelm et al., 2020). However, when apple trees experience soil-based abiotic stress, root activity and Ca uptake from the soil may decline, leading to deficiencies in the fruit (Fallahi, 2012). For example, nutrient accumulation in the biomass of woody plants can decrease under drought conditions as transpiration declines, particularly for those that depend on transpiration such as Ca, Mg, Fe, and S (Sardans et al., 2008). This can be related to several factors including a decrease in soil moisture that reduces soil mass flow and diffusion of nutrients, a decrease in root growth, and a decrease in photosynthetic capacity, sap flow, and transpiration (Sardans et al., 2008). These factors have a cascading effect on plant growth affecting overall nutrient demand and changing nutrient balance within the tree.

Abscisic acid (ABA) is a critical hormone regulating plant response to abiotic stress. ABA is synthesized in response to various environmental stresses (Finkelstein et al., 2002), including drought (Zhang et al., 2019), high salinity (Wang et al., 2022), extreme temperatures (Yang et al., 2011), and other factors that can disrupt normal plant growth and development. One of the primary functions of ABA is to regulate stomatal closure, which helps to reduce water loss from the plant during times of drought or high temperatures. Overall, ABA helps plants tolerate abiotic stresses by regulating water use, enhancing stress tolerance, and activating stress-responsive genes and pathways. The role of ABA on bitter pit incidence identified in the literature has attributed its effect on leaf stomatal closure and reducing transpiration to the distribution of Ca to fruit and leaves (Falchi et al., 2017). ABA was reported to reduce blossom end-rot in tomato and is a disorder analogous to bitter pit in apple (de Freitas et al., 2011). For a study using ‘Super Chief’ apple cultivar, Falchi et al. (2017) revealed that four foliar sprays with ABA during the season (starting from 66 days after full bloom) can be effective in apple bitter pit prevention via a preferential supply of Ca²⁺ to fruit. They hypothesized that bitter pit reduction could be associated with the increased Ca²⁺ concentration in the apoplast and a coordinated regulation of specific Ca²⁺-related genes.

Saure (2014) implicated abiotic stress as a cause of physiological disorders suffered by various horticultural crops related to Ca deficiency. According to this author, Ca deficiencies observed when disorders such as bitter pit are present could be the result of stress and not the cause of the disorder. Supporting this hypothesis, stress increases the production of ROS associated with lipid peroxidation and an increase in the leakiness of membranes, leading to rapid vacuolation of parenchyma cells and the loss of ions, including water-soluble apoplastic Ca²⁺. Prior to Wińska-Krysiak and Łata (2010); Saure (2014) investigated the relationship between the development of bitter pit and the activity of the enzyme lipoxygenase (LOX), an enzyme involved in fruit respiration. They concluded that apple cultivars with higher LOX activity are more stressed and more susceptible to bitter pit. Supporting this, Krawitzky et al. (2016) identified several types of proteins related to the responses to oxidative stress induced in fruit affected by bitter pit. Pathogenesis-related proteins are expressed in biological systems as a defense response to abiotic stress (Pühringer et al., 2000). These proteins may be synthesized in response to several stress factors during bitter pit development and may be expressed even before external symptoms are visible in the skin tissues (Krawitzky et al., 2016).

Abiotic stress does not always stimulate bitter pit development. Reid and Kalcsits (2020) reported that bitter pit incidence was lower for trees that were exposed to water limitations in a semi-arid environment. Strong reductions in stem water potential were observed, and bitter pit was the lowest in trees where abiotic stress was imposed during the summer when water demand was the greatest. In this case, water limitations were used to limit fruit expansion and increase fruit density, which reduced Ca dilution often observed in these cases (Kalcsits et al., 2020). Therefore, the timing of the abiotic stress is important. If it occurs at a point in development where Ca development is high and uptake is reduced, then the results would be expected to be negative. If stressful conditions reduce fruit growth or vigor, then it may improve the distribution and reduce dilution of Ca that regularly occurs during the season in susceptible cultivars (Casero et al., 2017). Nevertheless, there is a need for further research to separate the conflicting factors associated with abiotic stress on root activity, overall tree physiology, and fruit biochemistry to better understand environmental factors that contribute to bitter pit development.

Bitter pit development is a complex process influenced by multiple factors in addition to those indicated here, including cultivar (Ferguson and Watkins, 1989), rootstock (Lordan et al., 2019), irrigation (Reid and Kalcsits, 2020), fruit maturity (Prange et al., 2011), and storage conditions (Watkins et al., 2004). Horticultural management affecting crop load and vegetative vigor can also have strong effects on bitter pit development (Serra et al., 2016). However, the direct connections between these management strategies and planting decisions still need to be more closely studied to identify optimum combinations that lead to the consistent production of fruit with lower bitter pit incidence (Baugher et al., 2017). The effect of other classes of hormones and plant growth regulators such as cytokinins, ethylene, jasmonates, and salicylic acid also suggest the potential for bitter pit mitigation; however, their link to bitter pit is not yet clear (Griffith and Einhorn, 2023).

Another hypothesis, suggested by Steenkamp et al. (1983), is the mechanisms of metabolization of toxic substances generated during photosynthesis, such as oxalic acid and citric acid (Steenkamp et al., 1983). Plants do not have mechanisms to extrude these toxic compounds and instead can metabolize them through the formation of insoluble salts with Ca²⁺. When the Ca content in the cell would not be enough to metabolize these acids, cell death would occur, resulting in bitter pit symptoms. From this perspective, we suggest that the disruptions in xylem vessels may also affect the photosynthesis and mechanisms that eliminate the toxic substances and/or Ca availability to metabolize the acids; however, this hypothesis has yet to be thoroughly tested. Steenkamp et al. (1983) observed high oxalate and citrate concentrations in bitter pit areas, and by vacuum infiltration, they identified deterioration of the middle lamella of fruit cells, similar to those observed in naturally occurring pits. From these results, Val et al. (2006) used ammonium oxalate cortical injections to trigger like-bitter pit symptoms and study the polypeptide pattern in symptomatic and asymptomatic fruits. Finally, they found the novel 18-kDa protein both in natural bitter pit spots and in chemically induced corky lesions. They suggested that the novel protein may be an inhibitor of pectin methylesterase, a small heat-stress protein. More recently, Zupan et al. (2013) found that higher levels of many phenolics, including chlorogenic acid and catechin, were observed in peel and cortex with bitter pit symptoms, and higher levels of hydroxycinnamates and flavonols were found in the peel immediately above bitter pit symptoms; in contrast, flavonols and anthocyanins were higher in healthy peel (Zupan et al., 2013). These metabolic profile changes could be linked to sun stress (McTavish et al., 2020). Indeed, the bagging of apples provides protection from high-intensity sunlight, and bagging apples alters metabolic profile, which helps prevent bitter pit-like symptoms (Sharma et al., 2014; Sheick et al., 2023).

Not surprisingly, bitter pit is under some degree of genetic control in fruit. Apple breeders and geneticists have tried to understand the relationship between genetic variability and bitter pit occurrence to generate bitter pit-resistant cultivars (Volz et al., 2006; Buti et al., 2018; Mao et al., 2021). Volz et al. (2006) identified a genetic component to bitter pit incidence, and this effect was present irrespective of the use of several cropping factors, average fruit weight, or even fruit mineral concentrations. For any one seedling, the family had the largest effect on bitter pit incidence followed by site and Ca content in fruit, while the harvest date had the smallest effect. Although Ca concentration also showed a strong genetic component, no relationship was found between genetic effects related to bitter pit incidence and Ca concentration. However, fruit Ca concentration is usually an important predictor of within-family variation in pit incidence. These results suggest that fruit Ca concentration may be useful as an indirect indicator index for bitter pit within, but not among families (Volz et al., 2006). More recently, Buti et al. (2018) obtained two candidate genes (MDP0000263725 and MDP0000300083) for the control of bitter pit symptom expression between susceptible and non-susceptible genotypes in the population. The authors hypothesized the ability of the fruit to regulate cell turgor and increase cell wall elasticity during fruit development in the reduction of bitter pit symptoms. Contrariwise, an inability to respond in this way to cell expansion during fruit development could lead to a higher incidence of bitter pit symptom expression in bitter pit-susceptible lines.

Apple rootstocks have different influences and effects on the nutrition and vigor of the canopy, which have been implicated in the physiology of bitter pit (Lordan et al., 2019). Donahue et al. (2021) concluded that apple rootstocks have an influence on the nutritional status of the tree canopy, which is implicated in the physiology of bitter pit and, therefore, its occurrence. Islam et al. (2022) demonstrated that rootstock selection significantly affects bitter pit incidence and can also modulate cell wall structure and Ca²⁺ homeostasis by affecting pectin de-esterification rate and pectin methylesterase activity in fruit skin and flesh tissues. This situation in the cell walls increases Ca²⁺ in the binding sites and reduces Ca²⁺ in the apoplast and could cause cell membrane breakdown. Hence, they suggested that bitter pit sensitivity could be attributed to high pectin methylesterase enzyme activity and increased pectin de-esterification rate.

Trees with different levels of crop load can show different levels of bitter pit incidence (Serra et al., 2016) possibly caused by differences in fruit growth, maturation rate, or hormone synthesis. Fruit size and maturation are important factors affecting bitter pit incidence, which, at the same time, are also influenced by crop load and irrigation. According to de Freitas and Mitcham (2012), cultivars with higher fruit senescence and ethylene production at harvest had fruit with lower Ca content and, consequently, more bitter pit. Irrigation management can also affect tree vigor and fruit growth rates. For example, Reid and Kalcsits (2020) concluded that reducing irrigation at critical phases of fruit expansion can reduce bitter pit incidence.

Despite bitter pit being exhaustively investigated for more than a century, the mechanisms involved in its development are still not clearly known. This is most likely due to the interrelatedness of responses that have been previously observed. However, in the past decade, significant progress has been made in understanding the biochemical changes associated with bitter pit, key factors regulating its development, and management strategies that reduce it. Even so, there is no single management option to control bitter pit, just as there is no single cause for its development. Indeed, a precise management option for bitter pit control should consider multiple factors such as cultivar, rootstock, training system, climate/meteorology, and soil, as well as the economic implications. Ca clearly corresponds to bitter pit occurrence, but the cause of localized deficiencies is minimally corrected through improved Ca fertilization. The different theories that suggest causes of bitter pit in the literature are not necessarily contradictory even though they can be inconsistent most likely due to complex interactions at whole plant and cellular scales. These theories are often complementary, and all of them share, in a direct way, Ca nutrition as a common response. However, it is not clear whether it is a consequence or an underlying cause. Emerging evidence from this review suggests that Ca deficiencies should be seen as a symptom related to complex processes and not viewed simply as a diagnosis of bitter pit risk. Nevertheless, given the strong relationship between Ca content and balance with other nutrients in fruit and bitter pit within cultivars, it still retains value as one of the most reliable predictors of bitter pit occurrence.

ET: Conceptualization, Investigation, Writing – original draft, Writing – review & editing. LK: Investigation, Writing – review & editing. LG: Investigation, Writing – review & editing.