Charbonneau S, Gendron D, Samson E, Bourgaux-Ramoisy D, Bourgaux P
Department of Microbiology and Infectious Diseases, The Medical School, Sherbrooke, Québec, J1H 5N4, Canada.
Virology. 2000 Dec 5;278(1):122-32. doi: 10.1006/viro.2000.0654.
We have previously observed that a polyoma-mouse chimeric DNA molecule (RmI) in which the murine DNA insert is flanked by directly repeated viral sequences is effectively converted into unit-length polyoma DNA upon transfection of permissive mouse cells. This intramolecular recombination event appears to be dependent on VmP1, a protein encoded by RmI which includes the 328 N-terminal amino acids of polyoma VP1, and nine amino acids of murine origin carrying the C-terminus of the protein. We report here that introducing mutations into the VP2/VP3 coding sequence reduces the ability of RmI to generate polyoma DNA, even though the same mutations seem to exert little or no effect on the ability of polyoma DNA to either replicate or accumulate inside transfected cells. A mutation affecting VP2 alone being as effective as one that affects both VP2 and VP3, VP2 appears to be playing a critical role in recombination.
我们之前观察到，一种多瘤病毒-小鼠嵌合DNA分子（RmI），其中小鼠DNA插入片段两侧是直接重复的病毒序列，在转染允许性小鼠细胞后能有效地转化为单位长度的多瘤病毒DNA。这种分子内重组事件似乎依赖于VmP1，它是由RmI编码的一种蛋白质，包含多瘤病毒VP1的328个N端氨基酸以及携带该蛋白质C端的9个源自小鼠的氨基酸。我们在此报告，将突变引入VP2/VP3编码序列会降低RmI产生多瘤病毒DNA的能力，尽管相同的突变似乎对多瘤病毒DNA在转染细胞内复制或积累的能力几乎没有影响。单独影响VP2的突变与同时影响VP2和VP3的突变效果相同，VP2似乎在重组中起着关键作用。
