Abscisic acid promotes sweet cherry fruit cracking dependent on cell wall disassembly.

Fruit cracking is a devastating physiological disorder in fleshy fruits, severely affects the commercial value, however, the molecular mechanisms coordinating these processes remain poorly understood. In this study, we integrated physiological, imaging, and transcriptomic analyses to elucidate the regulatory network underlying cherry fruit cracking. We initially surveyed 11 sweet cherry cultivars grown in an orchard, and identified 6 cultivars, including 'Lijing', 'Samba' and 'Pisuntian' as cracking-resistant varieties. Magnetic resonance imaging revealed rapid internal water accumulation during immersion, commencing after 6 h. Furthermore, our results demonstrated that exogenous abscisic acid (ABA) treatment significantly induced fruit cracking and upregulated the expression of several key cell wall-modifying genes, including PavPG30, PavPL11, and PavEXP15, indicating that ABA functions as a master regulator of cell wall remodeling. Transcriptome profiling identified candidate transcription factors, such as PavERF113-like, PavWRKY37, and PavMYB34, which were highly upregulated in cracking fruits compared with non-cracking fruits, potentially serving as mediators between ABA signaling and cell wall related gene activation. Together, our study highlights cell wall integrity and ABA accumulation as key determinants of cherry cracking susceptibility and offers the potential strategies for variety selection and molecular targets for cherry breeders to reduce fruit cracking.