Abstract

Leaf senescence is a critically regulated developmental process that determines crop yield and quality. MYB and NAC transcription factors (TFs) are central regulators within this network, yet the crosstalk between these TF families and their connection to the gibberellin (GA) pathway remain poorly understood. This study revealed that overexpression ofDIV1, a MYB-like TF, leads to significantly reduced chlorophyll content and precocious leaf senescence. Based on the public transcriptome profiling ofDIV1-overexpression leaves, 37 senescence-associated differentially expressed genes (DEGs), including the highly upregulatedNAC59andNAC92, were identified. Molecular assays confirmed that DIV1 directly binds to the promoters ofNAC59andNAC92and activates their transcription. Meanwhile, yeast two-hybrid and split-luciferase assays demonstrated that DIV1 physically interacts with the GA biosynthetic enzymeent-kaurene oxidase (KO1) both in vitro and in vivo. The promoted senescence phenotype in DIV1-overexpression lines was rescued by treatment with paclobutrazol (PAC), a GA biosynthesis inhibitor. In summary, our findings reveal a dual mechanism whereby DIV1 integrates the GA pathway and NAC-mediated transcription to regulate leaf senescence. This work provides new insights into the coordination between MYB and NAC TFs during hormone-mediated senescence.