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Fruit cracking or splitting is a severe physiological disease that significantly affects appearance and quality, compromising the commodity value of fruit and causing substantial economic losses to the producers of several fleshy fruit crops. The growth-promoting plant hormone gibberellins (GAs) and growth-inhibiting abscisic acid (ABA) antagonistically regulate numerous processes throughout the plant life cycle. The homeostasis of GA and ABA plays a significant role in the normal growth and development of fruits, and the imbalance of them may lead to the occurrence of cracking or splitting during the process of fruit growth, development, ripening and postharvest storage. The pathways of GA and ABA metabolism and signaling have been studied widely, and the major components are well characterized, including the genes encoding major biosynthesis and catabolism enzymes and the key signaling components. Nevertheless, our knowledge of the mechanisms of GA and ABA governing fruit cracking is not comprehensive enough. In this review, we summarize the advances in understanding the effects of endogenous GAs and ABA contents in fruits and exogenous GAs and ABA treatments on fruit cracking, and we endeavor to provide some genetic cues on the function of GAs and ABA responsible for fruit cracking modulation. The progress in understanding the molecular bases underlying the actions of GAs and ABA in fruit cracking coordination control will facilitate breeding strategies of cracking-resistant ideotypes of fruits, and also carry great theoretical significance in guiding the establishment of integrated prevention and control measures in fruit cracking.
Zhang et al. (Sun,) studied this question.