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
|
Holdings |
Library |
Call Number |
Additional Info |
Location |
Last Modified |
Checkout Status |
NTIS |
PB89-237390 |
Some EPA libraries have a fiche copy filed under the call number shown. |
|
07/26/2022 |
|
Collation |
18p |
Abstract |
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.) |