How to silence a gene? Insights from a cold-induced epigenetic switch

Abstract

The Polycomb repressive complex 2 (PRC2) mediates epigenetic silencing of target genes in animals and plants by catalyzing the trimethylation of lysine 27 of histone 3 as a hallmark of gene repression. In Arabidopsis, PRC2 and its accessory proteins VIN3 and VRN5 of the VEL protein family are required for the cold-induced silencing of the floral repressor gene FLC. To understand the mechanistic basis of this, we combined protein characterization assays with functional analysis in vivo. We demonstrate that the VEL proteins interact via head-to-tail VEL polymerization domains, required to physically connect VIN3 with VRN5-PRC2. VIN3 VEL polymerization also involves higher order nuclear VIN3 assemblies in vivo, promotes strong chromatin association and efficient H3K27me3 nucleation. In contrast, the VRN5 VEL domain is not required for FLC silencing and is unable to functionally replace VIN3 VEL in vivo. Our work therefore defines the distinct roles of VEL proteins in conferring cold-induced silencing on FLC and extends our understanding of the principles that initiate epigenetic silencing.