Isolation and Characterization of Repair-Deficient Mutants of Drosophila melanogaster
Mutagen-sensitive mutants of Drosophila melanogaster are being utilized to determine the number and function of genes which control various aspects of DNA metabolism including replication, repair and recombination and to define the relationship of each of these functions to mutation production.
Nineteen loci which confer enhanced sensitivity to killing by methyl methanesulfonate have been detected on the X and second chromosomes. These loci can be grouped into five separate classes on the basis of cross-sensitivity to methyl methanesulfonate, x-ray, UV and nitrogen mustard. Some loci affect both somatic and meiotic functions, as assayed by mutagen sensitivity and recombination deficiency, while others affect only somatic functions.
Genetic methods have been employed to determine whether these mutants, which are able to survive in the absence of mutagen treatment, represent loci which have dispensable functions or leaky alleles of loci which have indispensable cellular functions. In several cases, both leaky and null alleles have been identified, indicating that at least some of these loci represent apparently dispensable cellular functions.
The mutagen sensitivity of doubly-mutant mus strains is being employed to assign mutants to common pathways for DNA repair in order to corroborate data obtained from biochemical studies and to explore whether a genetic ordering of metabolic steps in each repair pathway is possible. These data may be used in conjunction with the effects on the frequency and nature of mutations produced by various agents in each of the mutant strains to identify which of these pathways involve error-free or error-prone repair processes.
KeywordsNitrogen Mustard Mutagen Sensitivity Mutagen Treatment Methyl Methanesulfonate Mutation Production
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