A viral protein hijacks the key effector of transcriptional gene silencing, Su(var)3-9, to evade host plant surveillance.

The H3K4 methyltransferase Setd1b is intrinsically required for hematopoietic stem and progenitor cell homeostasis and regulates lineage specification in mice.

Methylation of a key transcription factor gene by a de novo DNA methyltransferase assures the maintenance of hematopoietic stem cell fate.

The innate immune DNA sensor IFI16 is in association with H3K9 methyltransferases SUV39H1 and GLP under physiological conditions in the nucleus which facilitates the epigenetic silencing of foreign viral DNA.

SARS-CoV-2 infection reduces the intracellular levels of a human tRNA modification enzyme and alters host tRNA modification profiles.

Transient interactions between NleE and PMSD10 suppress PSMD10 interaction with ATG7 to attenuate host autophagosome formation.

Evolutionary innovation and turnover in the IFIT1 antiviral gene family has led to diverse repertoires of antiviral specificity across mammals.

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

Clr4, a highly conserved SUV39 histone methyltransferase, requires its SET domain to sense histone H3K14 ubiquitination in order to maintain heterochromatin and H3K9 methylation.

Structured RNA elements bind to the human methyltransferase like-3 (METTL3)-METTL14 enzyme complex with high affinity and restrict the formation of N⁶-deoxymethyladenosine in DNA.