Record Display for the EPA National Library Catalog


Main Title Hotspot Sites for Acridine-Induced Frameshift Mutations in Bacteriophage T4 Correspond to Sites of Action of the T4 Type II Topoisomerase.
Author Ripley, L. S. ; Dubins, J. S. ; deBoer, J. G. ; DeMarini, D. M. ; Bogerd, A. M. ;
CORP Author Health Effects Research Lab., Research Triangle Park, NC. Genetic Toxicology Div. ;New Jersey Medical School, Newark. ;National Inst. of Environmental Health Sciences, Research Triangle Park, NC. ;York Univ., Downsview (Ontario). Dept. of Biology. ;Duke Univ., Durham, NC.
Publisher c1988
Year Published 1988
Report Number EPA/600/J-88/362;
Stock Number PB89-237390
Additional Subjects Acridines ; Bacteriophages ; Mutations ; Genetics ; In vivo analysis ; In vitro analysis ; Reprints ; DNA damage ; Topoisomerase ; Mutagenicity tests ; Base sequence
Library Call Number Additional Info Location Last
NTIS  PB89-237390 Some EPA libraries have a fiche copy filed under the call number shown. 07/26/2022
Collation 18p
The type II topoisomerase of bacteriophage T4 is a central determinant of the frequency and specificity of acridine-induced frameshift mutations. Acridine-induced frameshift mutagenesis is specifically reduced in a mutant defective in topoisomerase activity. The ability of an acridine to promote topoisomerase-dependent cleavage at specific DNA sites in vitro is correlated to its ability to produce frameshift mutations at those sites in vivo. The specific phosphodiester bonds cleaved in vitro are precisely those at which frameshifts are most strongly promoted by acridines in vivo. The cospecificity of in vitro cleavage and in vivo mutation implicate acridine-induced, topoisomerase-mediated DNA cleavages as intermediates of acridine-induced mutagenesis in T4. (Copyright (c) 1988 Academic Press Limited.)