Pathak V K, Temin H M
McArdle Laboratory for Cancer Research, University of Wisconsin, Madison 53706.
Proc Natl Acad Sci U S A. 1990 Aug;87(16):6024-8. doi: 10.1073/pnas.87.16.6024.
In the preceding paper we described an experiment that determined the in vivo forward mutation rate in a single replication cycle for spleen necrosis virus. In addition to substitutions, frameshifts, and hypermutations, the mutated proviruses contained two classes of deletions. One class of deletions contained short direct repeats at the deletion junctions. Another class of deletions had short stretches of sequences inserted at the deletion junctions. In this report, we describe the deletion mutations, and we present models for their generation. Detailed analysis of two deletions with insertions indicates that these mutations occurred as a result of template switching during plus-strand DNA synthesis. The analysis also indicates that fragments of viral RNA generated by the viral RNase H endonuclease are used as templates and contribute to the sequences inserted at the deletion junctions.
在之前的论文中,我们描述了一项实验,该实验确定了脾坏死病毒在单个复制周期中的体内正向突变率。除了替换、移码和超突变外,突变的前病毒还包含两类缺失。一类缺失在缺失连接处含有短的直接重复序列。另一类缺失在缺失连接处插入了短的序列片段。在本报告中,我们描述了缺失突变,并提出了它们产生的模型。对两个带有插入的缺失的详细分析表明,这些突变是在正链DNA合成过程中模板切换的结果。分析还表明,由病毒RNase H核酸内切酶产生的病毒RNA片段被用作模板,并对插入到缺失连接处的序列有贡献。