DNA methylation at imprinting control regions (ICRs) is established in gametes in a sex-specific manner and has to be stably maintained during development and in somatic cells to ensure the correct monoallelic expression of imprinted genes. In addition to DNA methylation, the ICRs are marked by allele-specific histone modifications. Whether these marks are essential for maintenance of genomic imprinting is largely unclear. Here, we show that the histone H3 lysine 9 methylases G9a and GLP are required for stable maintenance of imprinted DNA methylation in embryonic stem cells; however, their catalytic activity and the G9a/GLP-dependent H3K9me2 mark are completely dispensable for imprinting maintenance despite the genome-wide loss of non-imprinted DNA methylation in H3K9me2-depleted cells. We provide additional evidence that the G9a/GLP complex protects imprinted DNA methylation by recruitment of de novo DNA methyltransferases, which antagonize TET dioxygenass-dependent erosion of DNA methylation at ICRs. Display omitted •ESCs lacking G9a and GLP display loss of DNA methylation from ICRs•The enzymatic activity of G9a/GLP is dispensable for imprinted DNA methylation•G9a/GLP stabilize imprinting by recruitment of de novo DNA methyltransferases to ICRs•Recruitment of DNMTs to ICRs antagonizes TET-dependent loss of DNA methylation Loss of allele-specific DNA methylation from imprinting control regions leads to unbalanced gene expression and disease. Here, Zhang et al. show that the KMT enzymes G9a and GLP stabilize imprinted DNA methylation in embryonic stem cells by recruitment of de novo DNA methyltransferase enzymes, which counteract TET dioxygenase-dependent demethylation pathways.