Vernalization is a classic example of environmentally mediated epigenetic silencing. Central to vernalization is FLC, a floral repressor that antagonises the activation of all the genes required to switch the meristem to a floral fate. Vernalization quantitatively silences FLC, so relieving the repression on flowering.

Identification of Arabidopsis vrn mutants, defective in the cold-induced repression of FLC was facilitated through use of an FLC-luciferase fusion whose expression mimics the endogenous FLC gene to analyse regulators of the process. These mutants revealed that a conserved Polycomb Repressive Complex 2 (PRC2) chromatin -silencing mechanism mediates the epigenetic silencing of FLC.  There are at least two cold-induced steps in the mechanism, induction of the PHD protein VIN3 that forms part of a PHD-PRC2 complex and up-regulation of FLC antisense transcripts called COOLAIR. These components reduce FLC transcription and trigger epigenetic silencing in a cell-autonomous manner. This results in high H3K27me3 levels covering FLC that maintain the epigenetic stability of silencing through development. At embryogenesis, FLC expression is reset in a process involving an H3K27 demethylase.

We have developed a computational model of the vernalization process that has shown the quantitative nature of vernalization is due to an increasing proportion of cells switching off FLC (see Computational Modelling). We are also exploring the role of nuclear organization in FLC silencing and have found FLC loci physically cluster as they are epigenetically silenced, and COOLAIR forms 'clouds' over the FLC locus after cold exposure (see Nuclear Organization).