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Abstracts 1999 Environmental Mutagen Society Meeting March 27–April 1, 1999 Washington, D.C. James Felton, Chair

Book ID
101265406
Publisher
John Wiley and Sons
Year
1999
Tongue
English
Weight
226 KB
Volume
33
Category
Article
ISSN
0893-6692

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✦ Synopsis

Previous work showed that the DNA double-strand cleaving agents bleomycin and neocarzinostatin were more mutagenic in plateau-phase than in log-phase cells. To determine whether topoisomerase II poisons that produce double-strand breaks by trapping of cleavable complexes would likewise induce mutations specific to plateau-phase cells, aprt mutations induced by amsacrine (m-AMSA) in both log-phase and plateau-phase CHO cells were analyzed. Much higher levels of mutagenesis were achievable in plateau-than in log-phase cells, but the spectra of mutations were similar, and included small deletions, insertions and duplications, base substitutions, and a few large-scale deletions or rearrangements. About 6% of the log-phase mutants and 17% of the plateau-phase mutants were +1 frameshifts, and all but one of these were targeted to potential free 3' termini of cleavable complexes, as determined by mapping of cleavage sites in DNA treated with topoisomerase II plus amsacrine in vitro. Thus, these insertions may arise from templated extension of the exposed 3' terminus by a DNA polymerase, followed by resealing of the strand, as shown previously for acridine-induced frameshifts in T4 phage. Among the small nontandem deletion mutations, the deleted segments tended to encompass prominent sites of cleavable complex formation, suggesting that they may have arisen by end-joining repair of frank double-strand breaks resulting from disruption of drug-stabilized cleavable complexes.

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