Hwang C K, Svarovskaia E S, Pathak V K
HIV Drug Resistance Program, National Cancer Institute, Frederick, MD 21702, USA.
Proc Natl Acad Sci U S A. 2001 Oct 9;98(21):12209-14. doi: 10.1073/pnas.221289898. Epub 2001 Oct 2.
We recently proposed a dynamic copy-choice model for retroviral recombination in which a steady state between the rates of polymerization and RNA degradation determines the frequency of reverse transcriptase (RT) template switching. The relative contributions of polymerase-dependent and polymerase-independent RNase H activities during reverse transcription and template switching in vivo have not been determined. We developed an in vivo trans-complementation assay in which direct repeat deletion through template switching reconstitutes a functional green fluorescent protein gene in a retroviral vector. Complementation in trans between murine leukemia virus Gag-Pol proteins lacking polymerase and RNase H activities restored viral replication. Because only polymerase-independent RNase H activity is present in this cell line, the relative roles of polymerase-dependent and -independent RNase H activities in template switching could be determined. We also analyzed double mutants possessing polymerase and RNase H mutations that increased and decreased template switching, respectively. The double mutants exhibited low template switching frequency, indicating that the RNase H mutations were dominant. Trans-complementation of the double mutants with polymerase-independent RNase H did not restore the high template switching frequency, indicating that polymerase-dependent RNase H activity was essential for the increased frequency of template switching. Additionally, trans-complementation of RNase H mutants in the presence and absence of hydroxyurea, which slows the rate of reverse transcription, showed that hydroxyurea increased template switching only when polymerase-dependent RNase H activity was present. This is, to our knowledge, the first demonstration of polymerase-dependent RNase H activity in vivo. These results provide strong evidence for a dynamic association between the rates of DNA polymerization and polymerase-dependent RNase H activity, which determines the frequency of in vivo template switching.
我们最近提出了一种用于逆转录病毒重组的动态复制选择模型,其中聚合速率与RNA降解速率之间的稳态决定了逆转录酶(RT)模板转换的频率。在体内逆转录和模板转换过程中,聚合酶依赖性和非聚合酶依赖性核糖核酸酶H(RNase H)活性的相对贡献尚未确定。我们开发了一种体内反式互补测定法,其中通过模板转换进行的直接重复缺失可在逆转录病毒载体中重建功能性绿色荧光蛋白基因。缺乏聚合酶和RNase H活性的鼠白血病病毒Gag-Pol蛋白之间的反式互补恢复了病毒复制。由于该细胞系中仅存在非聚合酶依赖性RNase H活性,因此可以确定聚合酶依赖性和非聚合酶依赖性RNase H活性在模板转换中的相对作用。我们还分析了分别具有增加和降低模板转换的聚合酶和RNase H突变的双突变体。双突变体表现出低模板转换频率,表明RNase H突变占主导。用非聚合酶依赖性RNase H对双突变体进行反式互补不能恢复高模板转换频率,表明聚合酶依赖性RNase H活性对于增加模板转换频率至关重要。此外,在存在和不存在羟基脲(其减慢逆转录速率)的情况下对RNase H突变体进行反式互补表明,仅当存在聚合酶依赖性RNase H活性时,羟基脲才会增加模板转换。据我们所知,这是体内聚合酶依赖性RNase H活性的首次证明。这些结果为DNA聚合速率与聚合酶依赖性RNase H活性之间的动态关联提供了有力证据,该关联决定了体内模板转换的频率。