Abstract
Polycomb-mediated epigenetic silencing is central to correct growth and development in higher eukaryotes. The evolutionarily conserved Polycomb repressive complex 2 (PRC2) transcriptionally silences target genes through a mechanism requiring the histone modification H3K27me3. However, we still do not fully understand what defines Polycomb targets, how their expression state is switched from epigenetically ON to OFF and how silencing is subsequently maintained through many cell divisions. An excellent system in which to dissect the sequence of events underlying an epigenetic switch is the Arabidopsis FLC locus. Exposure to cold temperatures progressively induces a PRC2-dependent switch in an increasing proportion of cells, through a mechanism that is driven by the local chromatin environment. Temporally distinct phases of this silencing mechanism have been identified. First, the locus is transcriptionally silenced in a process involving cold-induced antisense transcripts; second, nucleation at the first exon/intron boundary of a Polycomb complex containing cold-induced accessory proteins induces a metastable epigenetically silenced state; third, a Polycomb complex with a distinct composition spreads across the locus in a process requiring DNA replication to deliver long-term epigenetic silencing. Detailed understanding from this system is likely to provide mechanistic insights important for epigenetic silencing in eukaryotes generally.
Highlights
The Polycomb silencing mechanism was originally identified using molecular genetic approaches in Drosophila
Distinct complexes of Polycomb proteins, known as Polycomb repressive complex 2 (PRC2) and Polycomb repressive complex 1 (PRC1), were shown to impart a cis-acting transcriptional silencing to the local chromatin [1,2,3,4,5,6]
Upon return to warm temperatures, H3K27me3 spreads from the nucleation region to cover the FLC locus and this spreading is required for the long-term stability of the epigenetic silencing (Figure 1c) [9,20]
Summary
The Polycomb silencing mechanism was originally identified using molecular genetic approaches in Drosophila. The long timescale over which the FLC silencing occurs has enabled its distinct phases to be elaborated: first, transcription is down-regulated, and to other Polycomb targets, this involves non-coding transcripts. Once the transcription is down-regulated, there is a switch to epigenetic silencing mediated by PRC2 and accessory proteins, independently of DNA methylation [16,17,18,19].
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