LHP1 promotes axillary bud dormancy by epigenetically repressing TIE1 in Arabidopsis

Axillary bud dormancy is tightly regulated to control shoot branching through an intricate gene regulatory network (GRN). While epigenetic regulation of gene expression plays a key role in modulating GRNs underlying numerous developmental and physiological processes, its contribution to axillary bud dormancy remains largely unexplored. Here, we investigate the role of the plant polycomb repressive complex 1 (PRC1) component LIKE HETEROCHROMATIN PROTEIN 1 (LHP1) in lateral shoot branching. Arabidopsis thaliana lhp1 mutants exhibited increased axillary branching, whereas plants overexpressing LHP1 displayed reduced branching compared to wild-type plants. Consistently, the analysis of a transcriptional reporter revealed promoter activity within axillary bud tissues, further indicating that LHP1 plays a role in branch outgrowth repression. Notably, we found that LHP1 directly controls the TCP INTERACTOR CONTAINING EAR MOTIF PROTEIN 1 (TIE1) locus on axillary buds. TIE1 promotes axillary branch development by inhibiting the activity of the master regulator of bud dormancy BRANCHED1 (BRC1). Constitutive expression of TIE1 rescued the reduced-branching phenotype of 35S::LHP1-GFP plants. Moreover, BRC1 direct-target loci are induced when LHP1 is overexpressed and severely repressed when TIE1 is artificially expressed avoiding LHP1 control, further indicating that LHP1 acts upstream of TIE1 to induce bud dormancy. Altogether, these results reveal an epigenetic mechanism by which PRC1-mediated repression limits axillary branch development in Arabidopsis.