Physiological and Molecular Basis of Delayed Bud Dormancy Release by Exogenous Ethylene Treatment in Blueberry

Global warming leads to premature dormancy release and untimely flowering in southern highbush blueberry during winter, resulting in chilling injury and yield losses. However, effective strategies to delay flowering by modulating dormancy progression without compromising fruit quality remain lacking. This study demonstrated through field trials that spraying 1 mg/mL ethephon (ETH) during the early endodormancy stage effectively delayed dormancy release and reduced the bud break rate of spring shoots by approximately 33.92% relative to the control, with no adverse effects on fruit quality. The treatment also reduces sucrose content in floral buds, a change potentially associated with dormancy maintenance. To explore the molecular basis of this process, we examined two ethylene-responsive transcription factors, VcERF112 and VcERF115, previously identified in our laboratory. Their expression was rapidly upregulated following ETH treatment. Heterologous expression of either gene in Arabidopsis delayed both seed germination and flowering, suggesting a conserved growth-suppressive function. Dual-luciferase reporter assays confirmed that VcERF112 and VcERF115 bind to the T2 region (−2310 to −1595 bp) of the VcBRC1 (VcBRANCHED1) promoter and enhance its expression. In contrast, sucrose treatment suppressed VcBRC1 expression. Collectively, these results propose that ethylene may sustain bud dormancy through a coordinated mechanism that operates independently of the classic abscisic acid (ABA)/gibberellins (GA) balance, a relationship not addressed in this study. This mechanism involves the induction of VcERF112/115 to activate VcBRC1, coupled with the reduction in sucrose levels to alleviate its repressive effect on VcBRC1. These findings provide new molecular insights into the ethylene-mediated regulatory network underlying bud dormancy in blueberry.