Chromatin contains different epigenetic marks, including histone-tail modifications and DNA methylation. These marks have varying effects on the expression state of a gene at different points in development and life. However, there is evidence that these modifications do not act independently, and that interaction between epigenetic marks is necessary for proper cell function. Our previous study showed mutual antagonism between two epigenetic marks, histone 3 lysine 27 trimethylation (H3K27me3) and DNA methylation (DNAme), upstream of the Rasgrf1 gene in mouse embryonic stem (ES) cells. H3K27me3 is deposited on chromatin by Polycomb Repressive Complex 2 (PRC2), and was shown to both restrict and be restricted by the placement of DNAme at this locus. Here, I look at the methylation profiles of DNA from wild type mouse ES cells and ES cells with a mutation in Eed of the PRC2 complex that results in a global loss of H3K27me3 to determine if this mutual antagonism occurs genome-wide. Using a combination of a Methyl DNA Immunopreciptiation microarray and sodium bisulfite sequencing, I show that H3K27me3 does indeed influence DNAme at numerous promoters in the embryonic mouse genome. Instead of seeing a consistent increase in DNAme after loss of H3K27me3 however, I found that only some of these promoters showed DNAme enrichment, while others showed depletion in DNAme. Additionally, several genes were shown to have both DNAme enrichment and depletion in the same promoter. My findings suggest that mutual antagonism is not observed consistently genome wide, and that more complexity exists regarding the interaction between these two marks.