Comparison of the Induction of Specific Locus Mutations in Wild-Type and Repair-Deficient Strains of NeurosporaCrassa
A comparison of mutation induction between wild-type and excision repair-deficient strains has shown that, after treatment with four of the five mutagens tested, an enhanced recovery of induced mutants was found in the excision repair-deficient strains. In this sense we have confirmed for Neurospora Ames’ (1977) observations with Salmonella. Furthermore, genetic analysis of the mutants induced in Neurospora in both wild-type and excision repair-deficient strains has shown that in some cases the enhanced recovery of mutants can be attributed to the recovery of a spectrum of genetic alterations in the excision repair-deficient strains that is qualitatively different from that found in the wild-type strain. This qualitatively different spectrum appears to arise as a result of a preferential increase in frameshift mutations. Thus, it appears that in excision repair-deficient strains of Neurospora genetic lesions are processed differently than in wild-type strains both to give enhanced yield as well as a selective increase in frameshift mutations. In this regard, the apparent difference between Salmonella and Neurospora data with regard to the characterization of the genetic effects of chemical carcinogens is most likely attributed to a difference in the genetic background of the strains. The present data with Neurospora suggest that this difference not only results in an enhanced recovery of revertants in Salmonella strains carrying the uvrB mutation but also that a different spectrum of genetic damage was detected from that which would have been observed in the standard wild-type strain G46.
Observations from the present experiments with Neurospora have important implications not only for comparative mutagenesis, where the effects of the same mutagen are studied in different laboratory organisms, but also for risk estimation since the spectrum of genetic damage produced by a given agent may not be uniform in our genetically heterogeneous human population.
KeywordsEthyl Adduct Polypeptide Hydrochloride Histidine
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