Temperature-sensitive mutations in Drosophila melanogaster. 8. Temperature-sensitive periods of the lethal and morphological phenotypes of selected combinations of notch-locus mutations

Temperature-shift experiments were performed on five Notch-locus genotypes with temperature-sensitive phenotypes. The results show that temperature-sensitive periods (TSPs) for lethality may occur at any developmental stage: (1) $\text{N}{}^{\mathrm{g11}}\text{N}{}^{\mathrm{g11}}$;Dp^51b7 having a short embryonic TSP for lethality, (2) $\text{Ax}{}^{16172}\text{N}{}^{\mathrm{?40}}$ having a second-instar TSP for lethality, and (3) $\text{N}{}^{\mathrm{?103}}\text{fa}{}^{\mathrm{no}}$ with a long, possibly polyphasic, TSP, beginning in the embryonic stage and ending in the pupal stage. On the other hand, TSPs for adult morphological phenotypes appear to be restricted to the third larval instar: (1) $\text{Ax}{}^{16172}\text{N}{}^{\mathrm{?40}}$ having third-instar TSPs for wing vein gapping and ocellar bristle loss, and (2) $\text{N}{}^{\mathrm{?103}}\text{spl}$ having third-instar TSPs for eye facet disarray, wing notching, bristle number variation, and fusion of tarsal segments. The significance of these results is discussed in terms of the role of the Notch locus in development.     

Temperature-sensitive mutations in Drosophila melanogaster. XI. Male sterile mutants of the Y chromosome

Eight temperature-sensitive (ts) male sterile mutations have been induced by ethyl methanesulfonate treatment of Y chromosomes derived from a selected temperature-resistant Amherst wild-type stock of Drosophila melanogaster. Males carrying such mutated Y chromosomes (Y^ts) are sterile when raised at 29°C but fertile when reared at 22°C. Complementation tests of the mutants with Y chromosome fragments, deletions, and inter se localized all eight to the long arm of the chromosome in four different complementation groups.When Y^ts-bearing males, reared to adulthood at 22°C, were subjected to a 48-hr regimen at 29°C and mated to fresh virgin females daily, a significant reduction in fertility resulted 5 days after initiation of 29°C treatments. This period of sterility was transient (48–72-hr duration) and corresponded to a temperature-sensitive period (TSP) of spermatogenesis during the primary spermatocyte stage. A more precise definition of the TSP utilized exposure of subadult males to 29°C at selected developmental periods during which only certain germ cell stages are present. Upon eclosion adult males were subjected to a similar schedule of consecutive matings of 12-hr duration in order to detect any delay in the appearance of fertility. Different ts males could be distinguished by the resultant pattern of sterility, and the TSP of different mutations thus localized to either primary spermatocyte or immediately post-meiotic stage.Associated with Y^ts-mediated sterility, spermiogenesis is defective at restrictive temperature as evidenced by the production of nonmotile sperm and a failure to transfer such sperm to the female during copulation. In addition, electron microscopy detected a variety of ultrastructural abnormalities, including defects of axoneme formation, irregularities of Nebenkern derivative development, and failures of separation from the syncitial state or mature cyst with subsequent degeneration.     

Temperature-sensitive autosomal dominant lethal mutations in Drosophila melanogaster induced by ethylmethane sulfonate

Cold- and heat-sensitive dominant autosome and recessive sex-linked lethals were scored using C(1)RM, y; vg bw; e ss tester stock. The frequencies of heat-sensitive mutations were 1.43, 0.30, 0.07% and of cold-sensitive ones were 0.39, 0.16 and 0.09% in the 1-st, 2-nd and 3-rd chromosomes, respectively. For the first time, dominant cold-sensitive lethals were obtained in chromosome 3. The data from genetic analysis point to the fact that penetrance of such mutations strongly depends on the genetic background. That may be the reason, why they were not obtained using some of the balancer-3 chromosomes. Also, "cryptic" dominant autosome mutants were found which were not conditional but only revealed in the F2 generation. Their possible origin as gonado-somatic mosaics is discussed.     

The effect of pathogens on selection against deleterious mutations in Drosophila melanogaster

In natural populations, fitness is reduced by both deleterious mutations and parasites. Few studies have examined interactions between these two factors, particularly at the level of individual genes. We examined how the presence of a bacterial pathogen, Pseudomonas aeruginosa, affected the selection against each of eight deleterious mutations in Drosophila melanogaster. We found that mutations tended to become more deleterious in the presence of disease. This increase in the average selection was primarily due to three genes with the remainder showing little evidence of change.     

Dietary stress does not strengthen selection against single deleterious mutations in Drosophila melanogaster

Stress is generally thought to increase the strength of selection, although empirical results are mixed and general conclusions are difficult because data are limited. Here we compare the fitness effects of nine independent recessive mutations in Drosophila melanogaster in a high- and low-dietary-stress environment, estimating the strength of selection on these mutations arising from both a competitive measure of male reproductive success and productivity (female fecundity and the subsequent survival to adulthood of her offspring). The effect of stress on male reproductive success has not been addressed previously for individual loci and is of particular interest with respect to the alignment of natural and sexual selection. Our results do not support the hypothesis that stress increases the efficacy of selection arising from either fitness component. Results concerning the alignment of natural and sexual selection were mixed, although data are limited. In the low-stress environment, selection on mating success and productivity were concordant for five of nine mutations (four out of four when restricted to those with significant or near-significant productivity effects), whereas in the high-stress environment, selection aligned for seven of nine mutations (two out of two when restricted to those having significant productivity effects). General conclusions as to the effects of stress on the strength of selection and the alignment of natural and sexual selection await data from additional mutations, fitness components and stressors.     

Sexual selection is ineffectual or inhibits the purging of deleterious mutations in Drosophila melanogaster

The effects of sexual selection on population mean fitness are unclear and a subject of debate. Recent models propose that, because reproductive success may be condition dependent, much of the genome may be a target of sexual selection. Under this scenario, mutations that reduce health, and thus nonsexual fitness, may also be deleterious with respect to reproductive success, meaning that sexual selection may contribute to the purging of deleterious alleles. We tested this hypothesis directly by subjecting replicate Drosophila melanogaster populations to two treatments that altered the opportunity for sexual selection and then tracked changes in the frequency of six separate deleterious alleles with recessive and visible phenotypic effects. While natural selection acted to decrease the frequency of all six mutations, the addition of sexual selection did not aid in the purging of any of them, and for three of them appears to have hampered it. Courtship and mating have harmful effects in this species and mate choice assays showed that males directed more courtship and mating behavior toward wild-type over mutant females, providing a likely explanation for sexual selection's cost. Whether this cost extends to other mutations (e.g., those lacking visible phenotypic effects) is an important topic for future research.     

A model system for analyzing somatic mutations in Drosophila melanogaster

Presently there are no good assays for comparing somatic mutation frequencies and spectra between different vertebrate and invertebrate organisms. Here we describe a new lacZ mutation reporter system in D. melanogaster, which complements existing systems in the mouse. The results obtained with the new model indicate two-to threefold higher frequencies of spontaneous mutations than in the mouse, with most of the mutations characterized as large genome rearrangements.     

Genetic instability in Drosophila melanogaster. Evidence for insertion mutations

Summary An X chromosome in Drosophila melanogaster is described which is mutationally unstable. Mutational events were identified through phenotypic changes associated with a tandem duplication of the X chromosome in which the white locus is present in duplicate. The left segment of the tandem duplication was marked with the mutant w ^sp, the right segment with mutant w ^17G. Some of the phenotypic changes were identified as deletions involving the w ^17G marked segment of the duplication. Other phenotypic changes involved the left segment in which phenotypically w ^sp mutated to w. Experimental evidence is presented which attributes these latter mutations to insertions of foreign DNA into the w locus equivalent to the insertion mutations of E. coli.