Intrinsic restriction activity by AID/APOBEC family of enzymes against the mobility of retroelements.

A large portion of the mammalian genome is derived from ancient transposable elements. Retroelements, transported by an intracellular copy-and-paste process involving an RNA intermediate (retrotransposition), constitute a majority of these mobile genetic elements. Endogenous retroviruses are LTR-type retroelements accounting for around 8% of human or murine genomic DNA. Non-LTR members are present in extremely high copy numbers; with LINE-1 contributing to nearly 40% of human and murine genomes. These LINE-1 elements modify mammalian genomes not only through insertions, but also by indirect replication of nonautonomous retrotransposons such as SINEs. As expected, cellular machineries of vertebrate's innate immunity have evolved to support a balance between retroelement insertions that cause deleterious gene disruptions and those that confer beneficial genetic diversity. The ability of APOBEC3 cytidine deaminases targeting DNA to restrict a broad number of retroviruses and retro-elements is now well established. More recently, the RNA editing family member APOBEC1, a protein involved in lipid transport, has also been shown to be involved in keeping mobile elements under control. This review discusses current understanding of the mechanism of action of the AID/APOBEC family, and their role in controlling the retrotransposition of endogenous retroelements.