A novel DNA/RNA modifying enzyme catalyzing a previously unknown 5-carbamoyloxymethylcytosine modification has been discovered using a novel framework called Metagenomics Genome-Phenome Association.

Enzymes that remove amine groups from cytosine bases in DNA are likely involved in generating the clusters of mutations (kataegis) seen in breast cancer.

The repair of spontaneous DNA damage can introduce mutators that lead to further genetic changes, which could underlie evolutionary change, disease and aging.

Interbacterial interactions can promote mutagenesis, and possibly adaptation, when intoxicated cells survive exposure to type VI secretion-delivered DNA deaminase toxins.

Combining in vitro and in vivo assays demonstrates that the cytidine deaminase APOBEC3A can inhibit LINE-1 retrotransposition by deaminating transiently exposed single-strand DNA that arises during the process of LINE-1 integration.

Transcribed promoters are highly susceptible to mutation by cytidine deaminases, implicating stable exposure of single stranded DNA structures, rather than cofactors, in localising mutation during tumourigenesis and antibody maturation.

Accumulation of mutations in some cancers is correlated with an aberration of DNA repair and access of a DNA deaminase to normal genomic DNA.

Genomes take advantage of the gene-duplicating ability of retroelements to birth novel innate immune defense genes.

The antiviral and genomic DNA deaminase APOBEC3B is repressed in normal cells by PRC1.6/E2F6 and DREAM/E2F4 complexes and deregulation of this axis provides a unifying mechanism for overexpression in cancer.