Table 1.

Examples of alterations to chromatin that cause redistribution of H3K27me

Organism	Normal H3K27me distribution	Perturbation	H3K27me redistribution
A. thaliana	Promoters and gene bodies[77]	Loss of MET1 (DNA methyltransferase)	Some normal H3K27me regions lost and replaced by H3K9me and DNA-me H3K27me gained at constitutive heterochromatin and CG hypomethylated transposons [42]
C. neoformans	Sub-telomeres	Loss of Ccc1 (chromodomain protein in PRC2 complex)	H3K27me3 lost at telomeres H3K27me3 gained at centromeres [15]
N. crassa	Sub-telomeres and interspersed genic regions	Loss of DIM-2 (DNA methyltransferase) Loss of DIM-5 (H3K9 methyltransferase) or HP1	Normal H3K27me2/3 H3K27me lost or reduced at normal regions and gained at centromeres and other regions normally bound by HP1 [38,40]
C. elegans	Alternating H3K27me3 and H3K36me3 domains on autosomes	Loss of MES-4 (H3K36 methyltransferase)	H3K27me3 reduced at some normally methylated genes H3K27me3 gained at genes that lost H3K36me3 [60]
M. musculus (mesenchymal progenitor cells)	Promoters and gene bodies	H3.3K36M or depletion of Nsd1/2 and Setd2 (H3K36 methyltransferases)	H3K27me3 retained at normal target genes H3K27me3 gained at intergenic regions that lost H3K36me2/3 [61]
M. musculus (neural stem cells)	Promoters and gene bodies	DNMT3a KO (DNA methyltransferase)	H3K27me3 retained at normal targets H3K27me3 gained at genes that are DNA-me depleted and down- regulated [46]
M. musculus (embryonic fibroblasts)	Promoters and gene bodies	DNMT1n/n (DNA methyltransferase hypomorph)	H3K27me lost from normally methylated promoters H3K27me gained at CpGs that normally have high levels of DNA-me [44]