Langlois Marc-André, Beale Rupert C L, Conticello Silvestro G, Neuberger Michael S
Medical Research Council Laboratory of Molecular Biology, Division of Protein and Nucleic Acid Chemistry Hills Road, Cambridge CB2 2QH, UK.
Nucleic Acids Res. 2005 Apr 4;33(6):1913-23. doi: 10.1093/nar/gki343. Print 2005.
Human APOBEC3F and APOBEC3G are double-domained deaminases that can catalyze dC-->dU deamination in HIV-1 and MLV retroviral DNA replication intermediates, targeting T-C or C-C dinucleotides, respectively. HIV-1 antagonizes their action through its vif gene product, which has been shown (at least in the case of APOBEC3G) to interact with the N-terminal domain of the deaminase, triggering its degradation. Here, we compare APOBEC3F and APOBEC3G to APOBEC3C, a single-domained deaminase that can also act on both HIV-1 and MLV. We find that whereas APOBEC3C contains all the information necessary for both Vif-binding and cytidine deaminase activity in a single domain, it is the C-terminal domain of APOBEC3F and APOBEC3G that confer their target site specificity for cytidine deamination. We have exploited the fact that APOBEC3C, whilst highly homologous to the C-terminal domain of APOBEC3F, exhibits a distinct target site specificity (preferring Y-C dinucleotides) in order to identify residues in APOBEC3F that might affect its target site specificity. We find that this specificity can be altered by single amino acid substitutions at several distinct positions, suggesting that the strong dependence of APOBEC3-mediated deoxycytidine deamination on the 5'-flanking nucleotide is sensitive to relatively subtle changes in the APOBEC3 structure. The approach has allowed the isolation of APOBEC3 DNA mutators that exhibit novel target site preferences.
人类载脂蛋白B mRNA编辑酶催化多肽样蛋白3F(APOBEC3F)和载脂蛋白B mRNA编辑酶催化多肽样蛋白3G(APOBEC3G)是双结构域脱氨酶,它们可在HIV-1和莫洛尼氏鼠白血病病毒(MLV)逆转录病毒DNA复制中间体中催化胞嘧啶(dC)向尿嘧啶(dU)的脱氨基作用,分别靶向T-C或C-C二核苷酸。HIV-1通过其病毒感染性因子(vif)基因产物拮抗它们的作用,该产物已被证明(至少在APOBEC3G的情况下)与脱氨酶的N端结构域相互作用,触发其降解。在此,我们将APOBEC3F和APOBEC3G与APOBEC3C进行比较,APOBEC3C是一种单结构域脱氨酶,也可作用于HIV-1和MLV。我们发现,虽然APOBEC3C在单个结构域中包含Vif结合和胞苷脱氨酶活性所需的所有信息,但赋予APOBEC3F和APOBEC3G胞苷脱氨基作用靶点特异性的是其C端结构域。我们利用了APOBEC3C与APOBEC3F的C端结构域高度同源这一事实,但其表现出不同的靶点特异性(偏好Y-C二核苷酸),以鉴定APOBEC3F中可能影响其靶点特异性的残基。我们发现,在几个不同位置的单个氨基酸替换可改变这种特异性,这表明APOBEC3介导的脱氧胞苷脱氨基作用对5'侧翼核苷酸的强烈依赖性对APOBEC3结构中相对细微的变化敏感。该方法已分离出表现出新靶点偏好的APOBEC DNA诱变剂。