HISTONE DEACETYLASE 9 Functions with Polycomb Silencing to Repress FLOWERING LOCUS C Expression1

Abstract

Histone deacetylase, Polycomb repressive complex, and epigenome readers through a cis-element mediate histone deacetylation and methylation to repress FLOWERING LOCUS C in rapid-cycling accessions. Polycomb repressive complex 2 (PRC2) catalyzes repressive histone 3 Lys-27 trimethylation (H3K27me3) to mediate genome-wide transcriptional repression in plants and animals. PRC2 controls various developmental processes in plants and plays a critical role in the developmental transition to flowering. FLOWERING LOCUS C (FLC), first identified in Arabidopsis (Arabidopsis thaliana), is a potent floral repressor in crucifers and some other plants that is subjected to complex regulation. Here, we show that HISTONE DEACETYLASE 9 (HDA9)-mediated H3K27 deacetylation is required for PRC2-mediated H3K27me3 in Arabidopsis. We further demonstrate that through physical association with the epigenome readers VP1/ABI3-LIKE 1 (VAL1) and VAL2, which recognize a cis-regulatory element at the FLC locus, HDA9 and PRC2 function in concert to mediate H3K27 deacetylation and subsequent trimethylation at this residue. This leads to FLC repression in the rapid-cycling Arabidopsis accessions. Our study uncovers roles for HDA9 in PRC2-mediated H3K27me3, FLC repression, and flowering-time regulation.