GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE331nnn/GSE331299/primaryOK200GenomicsArabidopsis thalianaGenome binding/occupancy profiling by high throughput sequencing Methylation profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE331299GEOGSEfalseDNA methylation either antagonizes or promotes Polycomb recruitment at transposable elements in ArabidopsisTransposable elements (TEs) are usually silenced by DNA methylation and H3K9me2, but in the absence of DNA methylation they can instead acquire the Polycomb-associated mark H3K27me3. Here, we initially set out to test whether DNA methylation and H3K27me3 compete during TE silencing establishment in Arabidopsis. Although we observe this competition at one newly inserted transgenic TE, we unexpectedly find that H3K27me3 deposition at another neo-inserted TE requires the de novo methyltransferase DRM2, revealing that DNA methylation can also promote Polycomb recruitment. Genome-wide H3K27me3 profiling in drm2, met1, and rdd mutants shows that DNA methylation either antagonizes or promotes H3K27me3 in a locus-specific manner, and that DNA demethylation also shapes H3K27me3 levels in vegetative tissues. Targeted methylation experiments demonstrate that DNA methylation directly influences PcG recruitment, and analyses using a drm2 catalytic mutant further confirm that this effect depends on DNA methylation itself rather than on DNA the methylation machinery. Overall, our work reveals an unexpected, cooperative crosstalk between DNA methylation and Polycomb pathways that maintains genome and epigenome integrity in eukaryotes.2026/05/22GSE331299GSM9743469GSM9743479GSM9743468GSM9743474GSM9743473GSM9743472GSM9743482GSM9743471GSM9743467GSM9743478GSM9743477GSM9743466GSM9743476GSM9743465GSM9743475GSM9743470GSM9743481GSM974348028290331299Arabidopsis thaliana