M.M. Green

Mutagen-sensitive mutants in Drosophila melanogaster: Effects of premutational damage

Drosophila melanogaster males from a Basc stock were mutagenized with either X-rays, ethyl methanesulfonate (EMS), or nitrogen mustard (HN2). Groups of identically treated males were crossed to different types of female. Sex-linked recessive lethals were scored as a genetic end point. The females used were homozygous for X-chromosomal mutations (mus(1)101D1, mus(1)104D1, mei-9 or mei-41D5) which lead to defective DNA repair and which increase the mutagen sensitivity of larvae. Females from a white stock with normal DNA repair capacities served as controls. The premutational lesions induced in mature sperm are only processed after insemination by the maternal enzyme systems present in the oocytes. Differences in the efficiency of the processing of lesions can lead to maternal effects on the frequency of mutations recovered from mutagenized sperm. It was found that, with the exception of mus(1)104D1, all mutants analysed significantly modify the mutation fixation of one or more types of premutational lesions. The most drastic effect is found with the mus(1)101D1 stock in which HN2-induced DNA cross-links do not lead to sex-linked recessive lethals. It is assumed that mus(1)101D1 is defective in an early step of DNA cross-link repair. Our first set of data clearly demonstrates that the study of maternal effects in Drosophila is an efficient tool to analyse the in vivo function of repair mutations on chemically induced mutagenesis.

Genetic analysis of X-linked mutagen-sensitive mutants of Drosophila melanogaster

Mutants at 2 new loci which control mutagen-sensitivity are described. Mutants of both foci are female-sterile and are hypersensitive to killing by MMS; neither increases the frequency of sex-linked recessive lethals. A screen of previously described female-sterile and meiotic mutants has revealed that a number of these are also sensitive to mutagens. In addition, several new mutants have been identified on the basis of sensitivity to either HN2 or MMS. An analysis of complementation data suggests that all of the X-linked genes controlling sensitivity to MMS may now have been identified. Among the new mei-41 alleles are mutants which show very little meiotic nondisjunction or loss. Cytogenetic mapping of previously known mutants is also described. The mutants mus(1)104D1 and mei-41D5 are located in the region 14B13+/- -14D1,2 on the polytene chromosome map, and they map very close to each other genetically. Cytogenetically mus(1)101D1 is between salivary chromosome bands 12A6,7 and 12D3, mus(1)103D1 is between bands 12A1,2 and 12A6,7 and mus(1)109A1 is in section 8F3--9A2.

The genetics of a mutator gene in Drosophila melanogaster

Abstract The genetic properties of an apparently new mutator gene in Drosophila melanogaster are described. The mutator gene causes the recessive, sex-linked mutant gene, yellow -2 ( y 2 ), to revert to wild-type at an inordinately high rate (about 1 2500 y 2 genes). At a somewhat lower frequency it induces partial reversions of y 2 as well as mutations to a phenotypically more extreme allele. The mutator is not locus-specific causing the recessive, sex-linked mutant forked -3 N to revert frequently to wild-type and white-apricot to mutate to a phenotypically white-eyed allele. Linkage analysis has localized the mutator to map position 57 on chromosome 3 as a probable allele of c 3 G . The mutator functions only in females, is partially dominant and appears to be incapable of reverting or mutating mutations it causes. The possible mechanism of mutator action is conjectured in the light of current knowledge on the mechanism of action of bacterial and bacteriophage mutator genes.

The mutagenic effects of diepoxybutane in wild-type and mutagen-sensitive mutants of Drosophila melanogaster

Genetic tests reported here demonstrate that among the DEB-induced mutants on 2 X-chromosome loci, viz. y and w, at a minimum, one-third are chromosome deletions. Among 11 MMS-sensitive mutants tested, 9 are also somatically sensitive to DEB. In addition direct genetic tests established that the capacity to repair DEB damage induced in sperm is impaired in females homozygous for 2 mutagen-sensitive mutants. By inference the same is also the case in females homozygous for 3 other mutagen-sensitive mutants.

The cytogenetics of mutator gene-induced X-linked lethals in Drosophila melanogaster ☆

Abstract A third chromosome mutator gene effectively increases the spontaneous frequency of sex-linked recessive lethals in females but not in females of Drosophila melanogaster . Approximately half the mutator-induced mutants occur as clusters of the same mutant implying a premeiotic origin. An appreciable number of the mutator-induced lethals are associated with comparatively long deficiencies of several salivary gland chromosome bands. The possible modes of mutator gene action are conjectured.