Coevolution analysis suggests that a DNA methylation-related role for the nucleosome remodeling ATPase HELLS and its activator CDCA7 was broadly inherited from the last eukaryotic common ancestor.

Mouse and tissue culture studies reveal that adipose DNA methyltransferase 3a mediates insulin resistance, partially through repressing the expression of FGF21.

Dnmt3a and Dnmt3b are dispensable for epidermal homeostasis but act as potent tumor suppressors regarding skin squamous tumorigenesis.

Ectopic expression of Dnmt3b leads to wide-spread CpG island hypermethylation that is largely defined by chromatin state and has some distinct features when compared to the cancer methylome.

DNA methylation deposition is dependent on the presence of H3K4me3 and H3K36me3 histone marks.

The maintenance methyltransferase Dnmt1 and the de novo methyltransferase Dnmt3b cooperate to maintain DNA methylation and genomic stability in the adult intestinal epithelium.

Correction of the DNA methyltransferase 3B gene in ICF1 syndrome fails to rescue the abnormal DNA hypomethylation at subtelomeric regions due to accompanied epigenetic abnormalities in these regions.

A new role is identified for GLI1 in modulating the inflammatory response of macrophages and the overaction of osteoclasts in collagen-induced arthritis by collaboratively regulating DNMT1 and DNMT3a.

Normal adipogenesis requires de novo DNA methyltransferase 3A (DNMT3A) for proper differentiation and suppression of an age-associated pathogenic inflammatory program.

Loss of Dnmt3a in excitatory neurons disrupts synaptic morphology and behavior, and triggers the expansion of H3K27me3 binding, suggestive of increased polycomb repression.