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.
We initiated the investigation of the molecular mechanism of vernalization by identifying Arabidopsis vrn mutants (Chandler et al 1996), defective in the cold-induced repression of FLC. We use an FLC-luciferase (Mylne et al 2005) fusion whose expression mimics the endogenous FLC gene to analyse regulators of the process.
Molecular analysis then revealed a conserved Polycomb Repressive Complex 2 (PRC2 Gendall et al 2001) chromatin (Bastow et al 2004)-silencing mechanism mediated the epigenetic silencing of FLC. FLC transcription is down regulated in the early phase of cold exposure and this is associated with increased abundance of FLC antisense (Swiezewski et al 2009) transcripts. Independently, the PHD (Greb et al 2007) protein VIN3 accumulates in the cold and forms a PHD-PRC2 (De Lucia et al 2008) that nucleates (Angel et al 2011) H3K27me3 silencing at a specific site within FLC. Upon transfer back to warm there is a switch of epigenetic states associated with spreading of the PHD-PRC2 along the length of the gene and a concomitant sharp increase in H3K27me3. These high H3K27me3 levels are required for the epigenetic stability of silencing through development until embryogenesis, when FLC expression is reset (Sheldon et al 2008).
We have a large European Research Council funded grant to develop a computational model of the vernalization process (see Computational Modelling). We are also setting up to explore the role of nuclear organization in FLC silencing and investigate the molecular basis of resetting.
This work involves Jie Song, Qianwen Sun, Hongchun Yang, Tibor Csorba, Andrew Angel, Scott Berry, Danling Zhu and Pedro Crevillen