Svend K. Petersen-Mahrt

TL;DR: It is shown that expression of AID in Escherichia coli gives a mutator phenotype that yields nucleotide transitions at dC/dG in a context-dependent manner, which indicates that AID functions by deaminating dC residues in DNA.

TL;DR: It is shown thatAPOBEC1 and its homologs APOBEC3C and APOBec3G exhibit potent DNA mutator activity in an E. coli assay, revealing the existence of a family of potential active dC/dG mutators, with possible implications for cancer.

TL;DR: It is shown that Aid and Apobec1 are 5-methylcytosine deaminases resulting in a thymine base opposite a guanine, which can lead to C → T transition mutations in methylated DNA, or in conjunction with repair of the T:G mismatch, to demethylation.

TL;DR: It is found that although the family forms part of a larger superfamily of deaminases distributed throughout the biological world, the AID/APOBEC family itself is restricted to vertebrates with homologs of AID (a DNA deaminase that triggers antibody gene diversification) and of APOBEC2 (unknown function) identifiable in sequence databases from bony fish, birds, amphibians, and mammals.

TL;DR: The patterns of hypermutation in antibodies and retroviruses owe much to the intrinsic sequence preferences of the AID/APOBEC family of DNA deaminases: analogous biases might also contribute to the spectra of cancer-associated mutation.