INTEGRATION OF SIMIAN VIRUS-40 INTO CELLULAR DNA OCCURS AT OR NEAR TOPOISOMERASE-II CLEAVAGE HOT-SPOTS INDUCED BY VM-26 (TENIPOSIDE)

被引：36

作者：

BODLEY, AL ^{[1
]}

HUANG, HC ^{[1
]}

YU, CA ^{[1
]}

LIU, LF ^{[1
]}

机构：

[1] UMDNJ,ROBERT WOOD JOHNSON MED SCH,DEPT PHARMACOL,675 HOES LANE,PISCATAWAY,NJ 08854

来源：

MOLECULAR AND CELLULAR BIOLOGY | 1993年 / 13卷 / 10期

关键词：

D O I：

10.1128/MCB.13.10.6190

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Inhibition of DNA topoisomerase II in simian virus 40 (SV40)-infected BSC-1 cells with a topoisomerase II poison, VM-26 (teniposide), resulted in rapid conversion of a population of the SV40 DNA into a high-molecular-weight form. Characterization of this high-molecular-weight form of SV40 DNA suggests that it is linear, double stranded, and a recombinant with SV40 DNA sequences covalently joined to cellular DNA. The majority of the integrants contain fewer than two tandem copies of SV40 DNA. Neither DNA-damaging agents, such as mitomycin and UV, nor the topoisomerase I inhibitor camptothecin induced detectable integration in this system. In addition, the recombination junctions within the SV40 portion of the integrants correlate with VM-26-induced, topoisomerase II cleavage hot spots on SV40 DNA. These results suggest a direct and specific role for topoisomerase II and possibly the enzyme-inhibitor-DNA ternary cleavable complex in integration. The propensity of poisoned topoisomerase II to induce viral integration also suggests a role for topoisomerase II in a pathway of chromosomal DNA rearrangements.

引用

页码：6190 / 6200

页数：11

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