Intrinsic restriction activity by apolipoprotein B mRNA editing enzyme APOBEC1 against the mobility of autonomous retrotransposons

摘要: The ability of mammalian cytidine deaminases encoded by the APOBEC3 (A3) genes to restrict a broad number endogenous retroelements and exogenous retroviruses, including murine leukemia virus human immunodeficiency (HIV)-1, is now well established. RNA editing family member apolipoprotein B (apo B)-editing catalytic subunit 1 (APOBEC1; A1) from variety species, protein involved in lipid transport which mediates C-U deamination mRNA for apo B, has also been shown modify range but its activity against remains unclear. Here, we show cell culture-based retrotransposition assays that A1 proteins multiple species can reduce mobility infectivity potential LINE-1 (long interspersed nucleotide sequence-1, L1) long-terminal repeats (LTRs) retrotransposons (or retroviruses), such as intracisternal A-particle (IAP) MusD sequences. anti-L1 was mainly mediated deamination-independent mechanism, not affected subcellular localization proteins. In contrast, inhibition LTR-retrotransposons appeared require deaminase Thus, AID/APOBEC A1s employ mechanisms regulate autonomous several species.