Hogan A, Faust E A
Mol Cell Biol. 1984 Oct;4(10):2239-42. doi: 10.1128/mcb.4.10.2239-2242.1984.
Previous work (E. A. Faust and D. C. Ward, J. Virol. 32:276-292, 1979) revealed a remarkably high rate of spontaneous deletion in viral DNA during lytic infection of cultured murine cells with minute virus of mice (MVM), an autonomous parvovirus. In the present study, we have isolated plasmid and phage recombinants containing MVM DNA inserts bearing deletions and we have determined the DNA sequence spanning three deletion junctions. The deletions, which average 3 kilobases in length, occur between pairs of perfectly homologous 4- to 10-base-pair direct repeats, such that one copy of the repeated sequence is lost, whereas the other remains behind at the deletion junction. When compared, the three sets of direct repeats exhibit no apparent sequence homology and have an A + T content of between 50 and 80%. These results indicate that 4- to 10-base-pair homologies mediate spontaneous deletion formation in the MVM genome and highlight parvoviruses as novel model systems for studies of this ubiquitous pathway of genetic variation.
先前的研究工作(E. A. 福斯特和D. C. 沃德,《病毒学杂志》32:276 - 292,1979年)表明,在用小鼠微小病毒(MVM,一种自主细小病毒)对培养的鼠细胞进行裂解感染期间,病毒DNA中自发缺失的发生率极高。在本研究中,我们分离出了含有带有缺失的MVM DNA插入片段的质粒和噬菌体重组体,并确定了跨越三个缺失连接点的DNA序列。这些缺失的平均长度为3千碱基,发生在成对的完全同源的4至10个碱基对的直接重复序列之间,结果是重复序列的一个拷贝丢失,而另一个则保留在缺失连接点处。经比较,这三组直接重复序列没有明显的序列同源性,A + T含量在50%至80%之间。这些结果表明,4至10个碱基对的同源性介导了MVM基因组中自发缺失的形成,并突出了细小病毒作为研究这种普遍存在的遗传变异途径的新型模型系统。