Aphidicolin-induced topological and recombinational events in simian virus 40 (original) (raw)
Journal Article
,
1
Department of Radiology
Columbus, OH 43210, USA
2
Department of Medical Microbiology and Immunology, The Ohia State University
Columbus, OH 43210, USA
*To whom correspondence should be addressed
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,
2
Department of Medical Microbiology and Immunology, The Ohia State University
Columbus, OH 43210, USA
Search for other works by this author on:
,
2
Department of Medical Microbiology and Immunology, The Ohia State University
Columbus, OH 43210, USA
Search for other works by this author on:
1
Department of Radiology
Columbus, OH 43210, USA
Search for other works by this author on:
Published:
25 September 1991
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Robert M. Snapka, Cha-Gyun Shin, Paskasari a. Permana, John Strayer, Aphidicolin-induced topological and recombinational events in simian virus 40, Nucleic Acids Research, Volume 19, Issue 18, 25 September 1991, Pages 5065–5072, https://doi.org/10.1093/nar/19.18.5065
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Abstract
Highly compacted (40S) SV40 DNA replication Intermediates formed in vivo during aphldlcolin exposure and immediately broke down in two stages. In the rapid initial stage, single strand DNA breaks caused loss of superhelicity in the 40S replication intermediates. This DNA breakage was accompanied by the formation of strong, permanent protein-DNA crosslinks which reached a maximum as nicking of the aberrant DNA replication Intermediates was completed. These protein-associated DNA strand breaks were not repaired. In the slower second stage of breakdown, the aberrant DNA replication intermediates remained nicked and strongly associated with protein as they underwent DNA replication fork breakage and recombinational changes to produce high molecular weight forms.
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© 1991 Oxford University Press
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