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

A lysine-to-methionine mutation in histone H3 dominantly blocks histone H3K9 methylation by trapping its methyltransferase.

Origin recognition complex-associated (ORCA) is crucial for the stability of the Histone H3 lysine 9 methyltransferase megacomplex, which is essential for heterochromatin organization.

Elucidating the molecular mechanism by which the Hippo signaling effector Yorkie (Yki) functions as a transcriptional coactivator in growth control reveals the importance of a histone-modifying enzyme for this process.

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

Repression of gene expression by the histone methyltransferase G9a is guided by two zinc finger proteins that can recognize consensus sequences in DNA.

SUV39H1 histone methyltransferase directly binds chromosome associated RNA to promote constitutive heterochromatin formation.

Nucleosomes and linker histones block eukaryotic cytosine methylation.

In Caenorhabditis elegans histone methylation (H3K9me3) controls the synthesis of heritable small RNAs in a gene-specific manner and thus enables 'flagging' of newly-acquired genes.

Histone-lysine N-methyltransferase SETD3 (NP_115609.2) was identified as the actin-specific histidine N-methyltransferase, an enzyme catalyzing the extremely well-conserved methylation of H73 in β-actin.