Shoot branching exhibits significant plasticity and is largely regulated by BRANCHED1 (BRC1), a key integrator of endogenous and environmental cues that acts locally to control axillary bud development. Despite its central role, the gene regulatory networks governed by BRC1 and the mechanisms underlying its regulation remain poorly understood. This study identified a cluster of transcription factor-encoding genes (C4 genes) that are dynamically responsive to multiple branching pathways (e.g., decapitation and strigolactone signalling), inversely correlated in expression with BRC1 levels, and functionally enriched in pathways related to floral organ development (FOD) and shoot system morphogenesis. Mechanistically, we demonstrate that the heterotrimeric Nuclear Factor Y (NF-Y) complex is required for transcriptional activation of representative C4 genes (e.g., the FOD genes FRUITFULL and CAULIFLOWER), functioning through chromatin looping and H3K27me3 demethylation to establish active chromatin states at target loci. In contrast, BRC1 inhibits NF-Y complex assembly and its epigenetic regulatory effects in a dose-dependent, decapitation-responsive manner, thereby enabling tunable FOD gene expression and plastic bud development. These findings position BRC1 as a molecular rheostat of NF-Y-dependent epigenetic regulation, providing mechanistic insights into the dynamic control of axillary bud development.