Hutchison K W, Copeland N G, Jenkins N A
Mol Cell Biol. 1984 Dec;4(12):2899-904. doi: 10.1128/mcb.4.12.2899-2904.1984.
The unstable dilute-coat-color mutation (d) of DBA/2J mice has been shown to be the result of integration of an ecotropic murine leukemia virus within the mouse genome. Molecular cloning and restriction enzyme analysis of the dilute allele and the viral preintegration site (+ allele), as well as two independent dilute revertants (d+2J and d+Ha), suggested that reversion is due to virus excision occurring by homologous recombination involving the viral long terminal repeats. The DNA sequence has now been determined for the cell-virus junctions of the provirus associated with the d mutation, for the viral preintegration site, and for the two revertant sites. These data (i) indicate that the d mutation was caused by a normal virus integration, (ii) confirm that virus excision occurs by precise homologous recombination, as exactly one long terminal repeat is present in each revertant site, and (iii) suggest that the virus induced the d mutation by integration into a noncoding sequence.
DBA/2J小鼠的不稳定稀释毛色突变（d）已被证明是嗜亲性鼠白血病病毒整合到小鼠基因组中的结果。对稀释等位基因、病毒整合前位点（+等位基因）以及两个独立的稀释回复突变体（d+2J和d+Ha）进行分子克隆和限制性酶切分析表明，回复突变是由于病毒通过涉及病毒长末端重复序列的同源重组而切除所致。现已确定了与d突变相关的前病毒的细胞-病毒连接点、病毒整合前位点以及两个回复突变位点的DNA序列。这些数据（i）表明d突变是由正常病毒整合引起的，（ii）证实病毒切除是通过精确的同源重组发生的，因为每个回复突变位点恰好存在一个长末端重复序列，（iii）表明病毒通过整合到非编码序列中诱导了d突变。
