4/ We propose that the non-enzymatic functions of EZH1-PRC2 and canonical PRC1 complexes play a critical role in maintaining long-term repression of Polycomb target genes in non-dividing cells.

3/ Our data shows that in quiescent cells (non-dividing), there’s a shift to less enzymatically active PRC1 (the canonical CBX containing forms) and PRC2 (containing EZH1). These changes appear to be evolutionarily conserved. 🧬

2/ We discovered that non-dividing cells are refractory to PRC2 inhibitors, meaning H3K27me2/3 are not reduced and gene expression is unchanged. This indicates that replicative dilution, not active H3K27 demethylation, is the main mechanism for H3K27me2/3 reduction upon inhibition of PRC2🔬