Bud endodormancy represents an ecological adaptation mechanism in perennial deciduous fruit trees to endure winter cold conditions. Sucrose serves a crucial role in bud endodormancy as both an energy metabolizer and signaling molecule. Sugars Will Eventually be Exported Transporters (SWEETs) function as sugar-efflux transporters that respond to environmental stimuli and contribute to plant growth and development. While SWEET gene families have been identified in various plant species for sugar transport regulation, their mechanism in regulating peach bud endodormancy remains undefined. In this study, we identified 15 SWEET genes in peach. The nomenclature was established through homologous alignment with the Arabidopsis SWEET gene family, resulting in four distinct clades through phylogenetic analysis. Covariance correlation analysis revealed 6 and 12 collinear SWEET genes in peach and Arabidopsis, respectively, forming 13 collinear gene pairs. Real-time quantitative polymerase chain reaction (RT-qPCR) analysis demonstrated significantly elevated expression of PpSWEET6 during peach bud endodormancy release, correlating positively with sucrose content. Transient overexpression of PpSWEET6 enhanced peach bud endodormancy release, while overexpressing PpSWEET6 in Arabidopsis enhanced seed germination and flowering. Y2H and luciferase complementation imaging (LCI) assays confirmed PpSWEET6 interacted with PpABF2. Additionally, dual luciferase reporter (DLR) assays showed that PpSWEET6 significantly decreased the activation of PpDAM6 (key dormancy-inducing gene) through PpABF2, thereby modulating peach bud endodormancy release. These findings advance our understanding of SWEET genes in peach bud endodormancy regulation.

Although it is well established that nitrogen (N) deficiency induces leaf senescence, the molecular mechanism of N deficiency-induced leaf senescence remains largely unknown. Here, we show that an abscisic acid (ABA)-responsive NAC transcription factor (TF) is involved in N deficiency-induced leaf senescence. The overexpression of MdNAC4 led to increased ABA levels in apple calli by directly activating the transcription of the ABA biosynthesis gene MdNCED2. In addition, MdNAC4 overexpression promoted N deficiency-induced leaf senescence. Further investigation showed that MdNAC4 directly bound the promoter of the senescence-associated gene (SAG) MdSAG39 and upregulated its expression. Interestingly, the function of MdNAC4 in promoting N deficiency-induced leaf senescence was enhanced in the presence of ABA. Furthermore, we identified an interaction between the ABA receptor protein MdPYL4 and the MdNAC4 protein. Moreover, MdPYL4 showed a function similar to that of MdNAC4 in ABA-mediated N deficiency-induced leaf senescence. These findings suggest that ABA plays a central role in N deficiency-induced leaf senescence and that MdPYL4 interacts with MdNAC4 to enhance the response of the latter to N deficiency, thus promoting N deficiency-induced leaf senescence. In conclusion, our results provide new insight into how MdNAC4 regulates N deficiency-induced leaf senescence.