Premium
Relationship between benzo(a)pyrene‐DNA adducts and somatic mutation and recombination in drosophila melanogaster
Author(s) -
Zordan M.,
Osti M.,
Pavanello S.,
Costa R.,
Levis A. G.
Publication year - 1994
Publication title -
environmental and molecular mutagenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1
H-Index - 87
eISSN - 1098-2280
pISSN - 0893-6692
DOI - 10.1002/em.2850230304
Subject(s) - mitotic crossover , mutagenesis , drosophila melanogaster , mutagen , dna , mutation , somatic cell , genetics , biology , carcinogen , microbiology and biotechnology , mutant , germline mutation , dna repair , dna damage , homologous recombination , gene
The evaluation of the relationship between the dose to DNA of a mutagen/carcinogen and in vivo somatic cell mutagenesis may provide information on the mechanisms leading to induced mutational events. This can be achieved, for example, by coupling test systems that permit the detection of somatic mutation and recombination on the basis of phenotypic changes in cuticular structures of Drosophila melanogaster , with methods for the quantitation of carcinogen‐DNA adducts such as the 32 P‐postlabeling technique. In this article, we evaluate the quantitative relationship between BaP‐DNA adduct formation, determined by 32 P‐postlabeling, and the induction of mutant cells in the wing marker version of the somatic mutation and recombination test (SMART) in Drosophila melanogaster. The total single clones in the trans‐heterozygous mwh/flr 3 flies show a linear relationship with the BaP‐DNA adduct levels, suggesting a single hit mechanism for the genetic damage giving rise to this type of clones. In contrast, the twin clones (which are of recombinational origin) display a linear‐quadratic relationship with the adduct levels, suggesting that multiple hits may be involved in generating these clones. The total single clones in the mwh /TM3, Ser flies (in which mitotic recombination is suppressed) show a logarithmic relationship with the adduct levels. The discussion of these data in terms of the pathways that may be involved in the repair of the BaP‐DNA adducts leads to the suggestion that in Drosophila melanogaster the repair of Bap metabolite‐DNA adducts in somatic cells may proceed, in large part, via post‐replicative recombinational repair. © 1994 Wiley‐Liss, Inc.