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Nucleic Acids Research, 1983, Vol. 11, No. 23 8485-8494
© 1983

MOLECULAR BIOLOGY

Daunomycin inhibits the B <- Z transition in poly d(G-C)

Jonathan B. Chaires

Department of Biochemistry, University of Mississippi Medical Center 2500 North State Street, Jackson, MS 39216, USA

Received August 22, 1983. Revised October 18, 1983. Accepted October 18, 1983.

The cancer drug daunomycin is an effective inhibitor of the B <- Z transition in poly d(G-C) in 4 M NaCl. Both the rate and extent of the B <- Z transition are decreased by the drug, as judged by equilibrium and kinetic studies. Daunomycin can, under some conditions, convert Z form DNA back to B form. Drug binding to poly d(G-C) in 4 M NaCl is slow and highly cooperative, consistent with a role for daunomycin as an allosteric effector on the B <- Z equilibrium. Since daunomycin binds preferentially to alternating purine-pyrimidine sequences, which are the very sequences capable of undergoing the B <- Z transition, these effects may be an important part of the mechanism by which the drug inhibits transcription and replication.


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