In vivo mapping of DNA topoisomerase II-specific cleavage sites on SV40 chromatin.
In vivo mapping of DNA topoisomerase II-specific cleavage sites on SV40 chromatin.
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SV40 染色质上 DNA 拓扑异构酶 II 特异性切割位点的体内作图。
DOI：
10.1016/0092-8674(85)90067-4
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发表时间：
1985
期刊：
影响因子：
64.5
通讯作者：
Liu,LF
中科院分区：
文献类型：
--
作者：
Yang,L;Rowe,TC;Nelson,EM;Liu,LF
The antitumor drug, m-AMSA (4’-(9-acridinylamino)-methanesulfon-m-anisidide), is known to interfere with the breakage-reunion reaction of mammalian DNA topoisomerase II by blocking the enzyme-DNA complex in its putative cleavable state. Treatment of SV40 virus infected monkey cells with m-AMSA resulted in both single-and double-stranded breaks on SV40 viral chromatin. These strand breaks are unusual because they are covalently associated with protein. Immunoprecipitation results suggest that the covalently linked protein is DNA topoisomerase II. These results are consistent with the proposal that the drug action in vivo involves the stabilization of a cleavable complex between topoisomerase II and DNA in chromatin. Mapping of these double-stranded breaks on SV40 viral DNA revealed multiple topoisomerase II cleavage sites. A major topoisomerase II cleavage site was preferentially induced during late infection and was mapped in the DNAase I hypersensitive region of SV40 chromatin.
