The TCP transcription factors function diversely in plant growth, development and stress response. The flower bud dormancy was particularly important for the yield formation of fruit trees. However, there has been no in-depth study on the involvement of TCP genes in regulating flower bud dormancy in sweet cherry so far. In the present study, a total of 18 TCP genes were obtained based on the whole genome, which were divided into two subfamilies and three subclasses (PCF, CIN, CYC/TB1) by multiple sequence alignment and evolutionary analysis. Four TCP genes targeted by miR319 were identified in the degradome results. Tissue-specific expression of TCP gene was verified based on transcriptome data and qRT-PCR. The expression patterns of PavTCPs under cold treatment in dormant buds of two cold-requiring sweet cherry cultivars were analyzed, among which PavTCP17 was significantly positively correlated with the gene expressions of gibberellin (GA) degradation and abscisic acid (ABA) synthesis. The abundance of PavTCP17 gene expression was significantly reduced after low cold-requiring cultivars met its chilling demand. The qRT-PCR quantification also showed a decreasing trend of PavTCP17 expression level during blooming process. To further unravel the role of PavTCP17 gene in positively regulating floral bud dormancy, transgenic Arabidopsis overexpressed PavTCP17 was obtained by genetic transformation. Compared with the WT, the number of main branches and rosette leaves was significantly reduced in PavTCP17-overexpressing lines. Moreover, the outgrowth of lateral buds of the PavTCP17-overexpressing lines were remarkably inhibited, mirroring the formation of bud dormancy. Furthermore, PavTCP17 might directly bind to PavNCED3 promoter of sweet cherry, suggesting the implication of PavTCP17 in promoting ABA synthesis, which was essential for bud dormancy. Our study bettered the understanding of TCP gene functions and revealed the mechanism by which PavTCP17 positively regulates flower bud dormancy in sweet cherry.

TCP 转录因子在植物生长、发育和胁迫反应中具有多种功能。花芽休眠对果树产量的形成尤为重要。然而，目前还没有关于TCP基因参与调控甜樱桃花芽休眠的深入研究。本研究基于全基因组共获得18个TCP基因，通过多序列比对和进化分析分为2个亚家族和3个亚类（PCF、CIN、CYC/TB1）。在降解组结果中鉴定出 miR319 靶向的四个 TCP 基因。基于转录组数据和 qRT-PCR 验证了 TCP 基因的组织特异性表达。PavTCPs的表达模式分析了2个需冷甜樱桃品种休眠芽在冷处理下的变化，其中PavTCP17与赤霉素（GA）降解和脱落酸（ABA）合成基因表达呈显着正相关。PavTCP17基因表达的丰度在低冷需求品种满足其冷需求后显着降低。qRT-PCR 定量也显示PavTCP17表达水平在开花过程中呈下降趋势。为了进一步阐明PavTCP17基因在正调控花芽休眠中的作用，转基因拟南芥过表达PavTCP17是通过基因改造获得的。与 WT 相比， PavTCP17过表达株系的主枝和莲座叶数量显着减少。此外， PavTCP17过表达品系的侧芽生长受到显着抑制，反映了芽休眠的形成。此外，PavTCP17可能直接与甜樱桃的PavNCED3启动子结合，表明PavTCP17参与促进 ABA 合成，这对芽休眠至关重要。我们的研究加深了对 TCP 基因功能的理解，揭示了PavTCP17正调控甜樱桃花芽休眠的机制。