Yu pan nwm12/8/2023 Our own genomes reveal the remarkable effects of retrotransposition, as about 45% of our genomic DNA results directly from this process ( Lander et al. ![]() Mobile genetic elements have been in conflict with host genomes for over a billion years. Ratio of non-synonymous to synonymous changes SIV, Phylogenetic analysis by maximum likelihood R:S, ![]() Number of substitutions per synonymous site LTR, Number of substitutions per non-synonymous site Ks, This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.Ĭompeting interests: The authors have declared that no conflicts of interest exist.Īpolipoprotein B–editing catalytic polypeptide G-to-A, Received: ApAccepted: JPublished: July 20, 2004Ĭopyright: © 2004 Sawyer et al. PLoS Biol 2(9):Īcademic Editor: Paul Harvey, University of Oxford Despite being only recently discovered, editing of RNA and DNA may thus represent an ancient form of host defense in primate genomes.Ĭitation: Sawyer SL, Emerman M, Malik HS (2004) Ancient Adaptive Evolution of the Primate Antiviral DNA-Editing Enzyme APOBEC3G. Furthermore, five additional APOBEC genes in the human genome appear to be engaged in similar genetic conflicts, displaying some of the highest signals for positive selection in the human genome. Unexpectedly, this selection appears more ancient than, and is likely only partially caused by, modern lentiviruses. We show that the APOBEC3G gene has been subject to strong positive selection throughout the history of primate evolution. This kind of conflict leads to rapid fixation of mutations that alter amino acids at the protein–protein interface, referred to as positive selection. The HIV-encoded virion infectivity factor (Vif) protein targets APOBEC3G for destruction, setting up a genetic conflict between the APOBEC3G and Vif genes. A recently discovered novel primate defense against retroviral infection involves a single-stranded DNA-editing enzyme, APOBEC3G, that causes hypermutation of HIV. Host genomes have adopted several strategies to curb the proliferation of transposable elements and viruses.
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