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M M Green

Publications and source records attributed to M M Green.

At least 73 records · Page 4Linked to original sources
PubMed1982

Genetic instability in Drosophila melanogaster: deletion induction by insertion sequences.

Females of Drosophila melanogaster heteroallelic or homoallelic for X chromosome giant (gt) mutants generate deletions involving the wild-type alleles at two X chromosome gene loci: yellow body color (y) and white eye color (w). The deletions, bidirectional in the case of y and with fixed endpoint in the case of w, are associated with particular X chromosomes. Distinctive insertion sequences, located proximal to the target loci, are presumed to generate the deletions.

Animals↗
PubMed1981

mus(3)312D1, A mutagen sensitive mutant with profound effects on female meiosis in Drosophila melanogaster.

The third chromosome, mutagen sensitive mutant mus(3)312D1 impairs the meiotic process in females by increasing the frequency of first division nondisjunction and decreasing the frequency of meiotic crossing over. These genetic properties connote 312 to be defective in DNA replication and/or repair intimately associated with the crossing over exchange process. The mutant maps to the left arm of chromosome III between ru and h, and represents a new genetic site for a meiotic mutant.

Animals↗
PubMed1981

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.

Animals↗
PubMed1979

Genetic instability in Drosophila melanogaster: tandem duplications as monitors of intrastrand exchange.

Two tandem duplications of the X chromosome associated with the white eye color locus are described. In heterozygous females both revert to a nonduplicated chromosome without detectable meiotic recombination. Clustering of revertants suggests the reversion event occurs in the germ line prior to meiosis. Similarly in males one duplication also reverts with clustering implying a premeiotic event. Revertant X chromosomes derived from males are either nonduplicated or deleted. Intrastrand exchange can account for some but not all revertants recovered.

Animals↗
PubMed1979

Genetic identification of dominant overproducing mutations: the Beadex gene.

A model system for the identification of presumptive overproducing mutations from among visible dominant mutations in D. melanogaster is described. An overproducing mutation is expected if a dominant mutation is readily reverted by gene deletion and if gene deletions suppress the expression of the original dominant mutation in flies heterozygous for the deletion. The Beadex (1:59.4) mutations are shown to satisfy these requirements, since a Bx dominant mutations is reverted by induced deletion [Df(Bx)/+) is wild type], and is also suppressed in trans by such a deletion [(Bx/Df)Bx) is wild type]. In addition, all 13 mutations recovered as Bx reversions or suppressors were associated with recessive held up (hdp) mutations allelic inter se, but not allelic to any known hdp gene. One such hdp mutations does not function as an independent dominant suppressor of Bx, is not always associated with Bx deletion, and in the latter situation is readily separable from Bx. We suggest that it functions as a Bx deletion, and may therefore represent the structural gene which is cis-regulated by the overproducing Bx mutations.

Chromosome Mapping↗
PubMed1979

Sensitivity of drosophila mutants to chemical carcinogens.

7 single-mutant and five double-mutant strains of Drosophila melanogaster were tested for their relative sensitivity to the chemical carcinogens: 1-acetylaminofluorene, benzo(alpha)pyrene, N-methyl-N'-nitro-N-nitrosoguanidine, 4-nitro quinoline-1-oxide and aflatoxin B1. Among the single mutants, mei-9a, mei-41D5 and mus(1)104D1 are hypersensitive to all 5 chemicals, whereas mus(1)107D1 is hypersensitive only to 4-nitroquinoline-1-oxide and is slightly sensitive to benzo(alpha)pyrene. The mei-9a mei-41D5 double-mutant is the most sensitive of 5 tested double-mutants which carry the mei-9a allele. When treated with 0.025 mM benzo(alpha)pyrene this double-mutant produces significantly more sex-linked recessive lethals and dominant lethals than does the control. Analysis of double-mutants reveals that the mei-9+ product functions in a different repair pathway of methyl methanesulfonate-induced damage than do the normal products of the mus(1)103, mus(1)104 and mus(1)107 loci. Our findings suggest that the sensitivity of Drosophila repair-deficient mutants could be exploited in screening for potential mutagens and carcinogens.

4-Nitroquinoline-1-oxide↗
PubMed1979

Mutagen-sensitive mutants in Drosophila melanogaster: effects on 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.

Animals↗
PubMed1979

Genetic instability in Drosophila melanogaster: the induction of specific chromosome 2 deletions by MR elements.

We describe the spontaneous induction of deletions by MR elements at the l(2)gl, net, pr and cn loci. The frequent induction of l(2)gl deletions mimics the high frequency of l(2)gl alleles found in wild populations of D. melanogaster. We suggest that these and other data that we present militate for the conclusion that, in the wild, autonomous MR elements occur and function as mutators. We contend that MR elements are not simply the by-products of hybridization between wild and laboratory strains.

Alleles↗
PubMed1977

Genetic instability in Drosophila melanogaster: putative multiple insertion mutants at the singed bristle locus.

A series of eleven independent mutants at the X chromosome singed bristle (sn) locus of Drosophila melanogaster is described. All mutants descend from flies caught in the wild and bred in the laboratory. On the basis of their inordinately high spontaneous mutation frequency, ten of the mutants are classified as putative insertion mutants. Reversions to wild type occur at frequencies of 10(-4)-10(-3). Some reversions appear to be losses of the inserted element, others appear (by analogy with prokaryotes) to be changes in the orientation of the inserted elements. Consistent with the insertion hypothesis, some sn mutants generate what are interpreted to be deletions at the sn locus. In their mutational properties, the sn mutants are analogous to insertion sequence (IS) elements and bacteriophage Mu of Escherichia coli, but the precise nature of the insertion remains unknown.

Alleles↗
PubMed1977

Genetic instability in Drosophila melanogaster: De novo induction of putative insertion mutations.

The capacity of a so-called male recombination (MR) chromosome in Drosophila melanogaster to generate mutations at 14 X-chromosome loci specifying visible phenotypes was investigated. Appreciable increases in mutation were found at three loci y, sn, and ras. Tests of represnetative mutants generated at each locus establish all to be putative insertion mutants, as judged by their spontaneous mutability. These facts suggest that insertion mutation production may be a general function of MR chromosomes. The relationship of the MR chromosomes to established insertion elements (IS and Mu) is discussed.

Journal Article↗