Bud endodormancy in perennial plants is a sophisticated system that adapts to seasonal climatic changes. Growth-promoting signals such as low temperature and gibberellins (GAs) are crucial for facilitating budbreak following endodormancy release (EDR). However, the regulatory mechanisms underlying GA-mediated budbreak in tree peony (Paeonia suffruticosa) remain unclear. In tree peony, the expression of PsmiR159b among three differentially expressed miR159 members was inhibited with the prolonged chilling, and overexpression of PsMIR159b delayed budbreak, whereas silencing PsmiR159b promoted budbreak after dormancy. PsMYB65, a downstream transcription factor in the GA pathway, was induced by prolonged chilling and exogenous GA₃ treatments. PsMYB65 was identified as a target of PsmiR159b, and promoted budbreak in tree peony. RNA-seq of PsMYB65-slienced buds revealed significant enrichment in the GO terms regulation of ‘cell cycle’ and ‘DNA replication’ among differentially expressed genes. Yeast one-hybrid and electrophoretic mobility shift assays demonstrated that PsMYB65 directly bound to the promoter of the type-D cyclin gene PsCYCD3;1. Dual-luciferase reporter assay indicated that PsMYB65 positively regulate PsCYCD3;1 expression, suggesting that miR159b-PsMYB65 module contributes to budbreak by influencing the cell cycle. Our findings revealed that the PsmiR159b-PsMYB65 module functioned in budbreak after dormancy by regulating cell proliferation, providing valuable insights into the endodormancy release regulation mechanism.

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