Mutation induction by difunctional alkylating agents in Neurospora crassa.
The genetic characterization of ad-3 mutants of Neurospora crassa induced by two carcinogenic difunctional akylating agents, 1,2,4,5-diepoxypentane (DEP) and 1,2,7,8-diepoxyoctane (DEO), has shown that point mutations at the ad-3B locus have similar complementation patterns. In addition to the induction of point mutations, DEP induces a low frequency (7.5%) of multilocus deletions, whereas DEO induces an extremely high frequency (42.0%). The distribution of the different classes of ad-3 mutants and the frequency of multilocus deletion mutants among DEP-induced mutants are not significantly different from those induced by the monofunctional alkylating agents EI, EMS and ICR-177 at comparable forward-mutation frequencies. Moreover, the frequencies of DEP-induced ad-3B mutants showing allelic completion or having nonpolarized complementation patterns are similar to those of ad-3B mutants induced by monofunctional agents. It is suggested, therefore, that the mechanism of mutation-induction by DEP in N. crassa is similar to that of monofunctional alkylating agents. Mutation-induction by DEO probably results both from the mechanism of action of monofunctional alkylating agents and from inter-strand cross-linkage of the DNA molecular by the two functional epoxy groups.
D000225:Adenine / Q000378:metabolism*; D000473:Alkanes / Q000494:pharmacology*; D000477:Alkylating Agents / Q000494:pharmacology*; D002073:Butanes / Q000494:pharmacology; D002273:Carcinogens; D002467:Cell Nucleus; D004852:Epoxy Compounds / Q000494:pharmacology*; D004988:Ethers, Cyclic / Q000494:pharmacology*; D005816:Genetic Complementation Test; D005838:Genotype; D009154:Mutation; D009491:Neurospora / Q000378:metabolism*; D009492:Neurospora crassa / Q000166:cytology / Q000378:metabolism*; D010641:Phenotype
D000473:Alkanes; D000477:Alkylating Agents; D002073:Butanes; D002273:Carcinogens; D004852:Epoxy Compounds; D004988:Ethers, Cyclic; D000225:Adenine