BRANCHED1 acts as a rheostat of Nuclear Factor Y-dependent epigenetic regulation in axillary bud development

Abstract

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. However, the gene regulatory networks governed by BRC1 and the mechanisms underlying its regulation remain poorly understood. Here, we identify a cluster of transcription factor-encoding genes that are dynamically responsive to multiple branching pathways, inversely correlated in expression with BRC1 levels, and functionally enriched in pathways related to floral organ development (FOD) and shoot system morphogenesis. Mechanistically, the heterotrimeric Nuclear Factor Y (NF-Y) complex is required for transcriptional activation of representative FOD genes, 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 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. Shoot branching plasticity is largely regulated by BRC1. The authors show that BRC1 acts as a dose-dependent rheostat, modulating NF-Y-mediated chromatin looping and H3K27me3 demethylation at floral organ development genes to fine-tune axillary bud activity.