Ding D, Jones M D, Leigh-Brown A, Griffin B E
EMBO J. 1982;1(4):461-6. doi: 10.1002/j.1460-2075.1982.tb01191.x.
An unusual non-defective mutant of polyoma virus with an anomalously large genome, designated din-21, has been isolated. The viral chromosome lacks 49 base pairs of the putative control region between the origin of replication and the initiation codon for the early proteins, the T-antigens. In their stead , 95 base pairs, with limited homology to the deleted sequence and apparently of mouse origin, have been inserted. The primary sequence of the insert DNA has been determined and some of the biological properties of the mutant examined. It transforms rat-1 cells slightly better than wild-type virus and grows slightly less well in lytically infected mouse cells. It does not interfere with the growth of wild-type polyoma virus. The properties of this mutant suggest that it is a natural isolate of mouse cells. The mutant was presumably generated by reciprocal recombination between polyoma DNA and mouse host DNA. This could be associated with the integration of a viral DNA sequence into the host chromosome during the viral replicative cycle.
已分离出一种不寻常的多瘤病毒非缺陷型突变体,其基因组异常大,命名为din - 21。病毒染色体在复制起点和早期蛋白(T抗原)起始密码子之间的假定控制区域缺少49个碱基对。取而代之的是插入了95个碱基对,与缺失序列有有限的同源性,且显然源自小鼠。已确定插入DNA的一级序列,并检测了该突变体的一些生物学特性。它转化大鼠 - 1细胞的能力略优于野生型病毒,在溶细胞感染的小鼠细胞中生长略差。它不干扰野生型多瘤病毒的生长。该突变体的特性表明它是小鼠细胞的天然分离株。该突变体可能是由多瘤病毒DNA与小鼠宿主DNA之间的相互重组产生的。这可能与病毒复制周期中病毒DNA序列整合到宿主染色体中有关。