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Nucleic Acids Research, 1991, Vol. 19, No. 18 5065-5072
© 1991

MOLECULAR BIOLOGY

Aphidicolin-induced topological and recombinational events in simian virus 40

Robert M. Snapka1,2,*, Cha-Gyun Shin2, Paskasari a. Permana2 and John Strayer1

1Department of Radiology Columbus, OH 43210, USA 2Department of Medical Microbiology and Immunology, The Ohia State University Columbus, OH 43210, USA

*To whom correspondence should be addressed

Received March 20, 1991. Accepted August 16, 1991.

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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