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复制起点的缺失会损害多瘤病毒DNA转化细胞以及形成串联插入的能力。

Deletion of the origin of replication impairs the ability of polyomavirus DNA to transform cells and to form tandem insertions.

作者信息

Dailey L, Pellegrini S, Basilico C

出版信息

J Virol. 1984 Mar;49(3):984-7. doi: 10.1128/JVI.49.3.984-987.1984.

Abstract

We examined the transforming properties of polyomavirus DNA molecules which can produce a functional large T-antigen but which are cis defective for viral DNA replication. The inability of these molecules to replicate results from the deletion of sequences comprising the viral replication origin. We found that even in the presence of a functional large T-antigen, transformation of rat cells by these viral DNAs was greatly reduced when compared with replication-competent parental DNA, and cells transformed by origin-minus mutants generally contained the integrated viral DNA in a nontandem arrangement. Therefore, polyomavirus large T-antigen promotes the establishment of transformation and tandem integration by interacting with the viral origin of DNA replication. This indicates that viral DNA synthesis is directly involved in these processes.

摘要

我们研究了多瘤病毒DNA分子的转化特性,这些分子能够产生功能性大T抗原,但在病毒DNA复制方面存在顺式缺陷。这些分子无法复制是由于包含病毒复制起点的序列缺失所致。我们发现,即使存在功能性大T抗原,与具有复制能力的亲本DNA相比,这些病毒DNA对大鼠细胞的转化能力也大大降低,并且由缺失复制起点的突变体转化的细胞中,整合的病毒DNA通常呈非串联排列。因此,多瘤病毒大T抗原通过与病毒DNA复制起点相互作用,促进转化的建立和串联整合。这表明病毒DNA合成直接参与了这些过程。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be07/255561/b7d1b47b7352/jvirol00138-0360-a.jpg

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