adaptive evolution of mus apobec3 includes retroviral insertion and positive selection at two clusters of residues flanking the substrate groove自适应进化的亩apobec3包括逆转录病毒插入和积极的选择残留在底物槽侧面的两个集群.pdfVIP
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adaptive evolution of mus apobec3 includes retroviral insertion and positive selection at two clusters of residues flanking the substrate groove自适应进化的亩apobec3包括逆转录病毒插入和积极的选择残留在底物槽侧面的两个集群
Adaptive Evolution of Mus Apobec3 Includes Retroviral
Insertion and Positive Selection at Two Clusters of
Residues Flanking the Substrate Groove
1. 2. 2. 1 1
Bradley Sanville , Michael A. Dolan , Kurt Wollenberg , Yuhe Yan , Carrie Martin , Man Lung
1 1 1 1
Yeung , Klaus Strebel , Alicia Buckler-White , Christine A. Kozak *
1 Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland, United States of America, 2 Bioinformatics and
Computational Biosciences Branch, Office of Cyber Infrastructure and Computational Biology, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland,
United States of America
Abstract
Mouse APOBEC3 (mA3) is a cytidine deaminase with antiviral activity. mA3 is linked to the Rfv3 virus resistance factor, a gene
responsible for recovery from infection by Friend murine leukemia virus, and mA3 allelic variants differ in their ability to
restrict mouse mammary tumor virus. We sequenced mA3 genes from 38 inbred strains and wild mouse species, and
compared the mouse sequence and predicted structure with human APOBEC3G (hA3G). An inserted sequence was
identified in the virus restrictive C57BL strain allele that disrupts a splice donor site. This insertion represents the long
terminal repeat of the xenotropic mouse gammaretrovirus, and was acquired in Eurasian mice that harbor xenotropic
retrovirus. This viral regulatory sequence does not alter splicing but is associated with elevated mA3 expression levels in
spleens of laboratory and wild-d
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