scholarly journals HIGH MUTABILITY IN MALE HYBRIDS OF DROSOPHILA MELANOGASTER

Genetics ◽  
1980 ◽  
Vol 96 (2) ◽  
pp. 479-490 ◽  
Author(s):  
Michael J Simmons ◽  
Nancy A Johnson ◽  
Thomas M Fahey ◽  
Sue M Nellett ◽  
John D Raymond

ABSTRACT The frequencies of sex-linked lethal mutations arising in hybrid male offspring from various crosses and in nonhybrid controls were determined. The hybrids were produced by crossing representative strains of the P-M system of hybrid dysgenesis in all possible combinations. Males from the cross of P males × M females had a mutation rate about 15 times higher than that of nonhybrid males from the P strain. Genetically identical males from the reciprocal cross had a mutation rate 3 to 4 times that of the nonhybrids. For crosses involving a Q strain, a significant increase in the mutation rate was detected in males produced by matings of Q males with M females. No increase was observed in genetically identical males from the reciprocal mating. Crosses between P and Q strains gave male hybrids with mutation rates not different from those of nonhybrids. Many of the lethals that occurred in hybrids from the cross of P males × M females appeared to be unstable; fewer lethals that arose in hybrids from the cross of Q males × M females were unstable. The relationship between P and Q strains is discussed with respect to a model of mutation induction in dysgenic hybrids.

2000 ◽  
Vol 76 (3) ◽  
pp. 323-326 ◽  
Author(s):  
JOSÉ FERNANDO VÁZQUEZ ◽  
TRINIDAD PÉREZ ◽  
JESÚS ALBORNOZ ◽  
ANA DOMÍNGUEZ

Microsatellite mutations were studied in a set of 175 mutation accumulation lines, all of them independently derived from a completely homozygous population of Drosophila melanogaster and maintained under strong inbreeding during 80 generations. We assayed 28 microsatellites and detected two mutations. One mutation consisted of a single addition of a dinucleotide repeat and the other was a deletion of five trinucleotide repeats. The average mutation rate was 5·1 × 10−6, in full agreement with previous estimates from two different sets of mutation accumulation lines.


1958 ◽  
Vol 11 (1) ◽  
pp. 85 ◽  
Author(s):  
BL Sheldon

The incidence of sex�linked recessive lethal mutations in Drosophila melano� gaster after heat shock treatment of both larvae and adult males is reported. There was no increase in the mutation rate after treatment of larvae and the results with adult males were not consistent. Treatment of the latter at 38�C caused an increase in mutation rate, due apparently to the large response of a few sensitive males. Treatment at 40�C caused no increase, and if one sensitive male was excluded, the mutation rate was significantly less than control. These results do not entirely support those of previous workers in the literature and possible reasons for this are discussed.


1966 ◽  
Vol 7 (1) ◽  
pp. 12-17 ◽  
Author(s):  
Mary F. Lyon ◽  
T. Morris

Previous measurements of specific locus mutation rates in mice had all involved the seven loci, a, b, c, d, p, s and se. An experiment was performed with the same mouse stock (C3H × 101) and the same radiation dose (600 rad) to spermatogonia as had been used previously, but employing a new group of six loci, a, bp, fz, In, pa and pe. The observed mutation rate, 5·0 × 10−8 per locus per rad, was significantly lower than that for the original seven loci, but was three to four times higher than the corresponding mutation rate in Drosophila melanogaster.


2016 ◽  
Author(s):  
Daniel A. Skelly ◽  
Paul M. Magwene ◽  
Brianna Meeks ◽  
Helen A. Murphy

AbstractNatural selection has the potential to act on all phenotypes, including genomic mutation rate. Classic evolutionary theory predicts that in asexual populations, mutator alleles, which cause high mutation rates, can fix due to linkage with beneficial mutations. This phenomenon has been demonstrated experimentally and may explain the frequency of mutators found in bacterial pathogens. In contrast, in sexual populations, recombination decouples mutator alleles from beneficial mutations, preventing mutator fixation. In the facultatively sexual yeastSaccharomyces cerevisiae, segregating alleles ofMLH1andPMS1have been shown to be incompatible, causing a high mutation rate when combined. These alleles had never been found together naturally, but were recently discovered in a cluster of clinical isolates. Here we report that the incompatible mutator allele combination only marginally elevates mutation rate in these clinical strains. Genomic and phylogenetic analyses provide no evidence of a historically elevated mutation rate. We conclude that the effect of the mutator alleles is dampened by background genetic modifiers. Thus, the relationship between mutation rate and microbial pathogenicity may be more complex than once thought. Our findings provide rare observational evidence that supports evolutionary theory suggesting that sexual organisms are unlikely to harbor alleles that increase their genomic mutation rate.


Genetics ◽  
1972 ◽  
Vol 72 (2) ◽  
pp. 335-355
Author(s):  
Terumi Mukai ◽  
Sadao I Chigusa ◽  
L E Mettler ◽  
James F Crow

ABSTRACT Spontaneous mutations were allowed to accumulate in a second chromosome that was transmitted only through heterozygous males for 40 generations. At 10-generation intervals the chromosomes were assayed for homozygous effects of the accumulated mutants. From the regression of homozygous viability on the number of generations of mutant accumulation and from the increase in genetic variance between replicate chromosomes it is possible to estimate the mutation rate and average effect of the individual mutants. Lethal mutations arose at a rate of 0.0060 per chromosome per generation. The mutants having small effects on viability are estimated to arise with a frequency at least 10 times as high as lethals, more likely 20 times as high, and possibly many more times as high if there is a large class of very nearly neutral mutations.—The dominance of such mutants was measured for chromosomes extracted from a natural population. This was determined from the regression of heterozygous viability on that of the sum of the two constituent homozygotes. The average dominance for minor viability genes in an equilibrium population was estimated to be 0.21. This is lower than the value for new mutants, as expected since those with the greatest heterozygous effect are most quickly eliminated from the population. That these mutants have a disproportionately large heterozygous effect on total fitness (as well as on the viability component thereof) is shown by the low ratio of the genetic load in equilibrium homozygotes to that of new mutant homozygotes.


Genetics ◽  
1993 ◽  
Vol 133 (2) ◽  
pp. 299-305 ◽  
Author(s):  
K Sawamura ◽  
T Taira ◽  
T K Watanabe

Abstract Hybrid females from Drosophila simulans females x Drosophila melanogaster males die as embryos while hybrid males from the reciprocal cross die as late larvae. The other two classes are sterile adults. Letting C, X, and Y designate egg cytoplasm, X, and Y chromosomes, respectively, and subscripts m and s stand for melanogaster and simulans, CmXmYs males are lethal in the larval stage and are rescued by the previously reported genes, Lhr (Lethal hybrid rescue) in simulans or Hmr (Hybrid male rescue) in melanogaster. We report here another rescue gene located on the second chromosome of simulans, mhr (maternal hybrid rescue) that, when present in the mother, rescues CsXmXs females from embryonic lethality. It has been postulated that the hybrids not carrying the Xs like CmXmYs males are larval lethal and that the hybrids carrying both the Cs and the Xm like CsXmXs females are embryonic lethal. According to these postulates CsXmYs males (obtained by mating attached-X simulans females to melanogaster males) should be doubly lethal, at both embryo and larval stages. When both rescuing genes are present, Hmr in the father and mhr in the mother, males of this genotype are fully viable, as predicted.


Genetics ◽  
1973 ◽  
Vol 75 (1) ◽  
pp. 133-153
Author(s):  
Margaret Gale Kidwell ◽  
J F Kidwell ◽  
M Nei

ABSTRACT A spontaneous lethal mutation rate approximately twenty to thirty times greater than normal has been discovered in second and third chromosomes derived from an irradiated isogenic line and paired with marked inversion chromosomes. Mutations resulting in reductions of viability of varying magnitude short of complete lethality apparently also occur at a very high rate in the third but not in the second chromosome. The pattern of accumulation of lethal mutations over several generations and viability frequency distributions within generations have been studied in a number of independent experiments. High mutation rate occurs in heterozygous isogenic-derived second and third chromosomes, either together or apart, irrespective of the genetic constitution of nonhomologous chromosomes. High mutation rates were not observed using the same methods with chromosomes of an inbred line from a different source. The possible mechanisms responsible for these results are discussed.


Genetics ◽  
1993 ◽  
Vol 133 (2) ◽  
pp. 307-313 ◽  
Author(s):  
K Sawamura ◽  
M T Yamamoto ◽  
T K Watanabe

Abstract Hybrid females from Drosophila simulans females x Drosophila melanogaster males die as embryos while hybrid males from the reciprocal cross die as larvae. We have recovered a mutation in melanogaster that rescues the former hybrid females. It was located on the X chromosome at a position close to the centromere, and it was a zygotically acting gene, in contrast with mhr (maternal hybrid rescue) in simulans that rescues the same hybrids maternally. We named it Zhr (Zygotic hybrid rescue). The gene also rescues hybrid females from embryonic lethals in crosses of Drosophila mauritiana females x D. melanogaster males and of Drosophila sechellia females x D. melanogaster males. Independence of the hybrid embryonic lethality and the hybrid larval lethality suggested in a companion study was confirmed by employing two rescue genes, Zhr and Hmr (Hybrid male rescue), in doubly lethal hybrids. A model is proposed to explain the genetic mechanisms of hybrid lethalities as well as the evolutionary pathways.


Genetics ◽  
1973 ◽  
Vol 75 (4) ◽  
pp. 643-649
Author(s):  
Barton E Slatko ◽  
Yuichiro Hiraizumi

ABSTRACT One group of the second chromosome lines isolated from a southern Texas population of Drosophila melanogaster, which has been known to show relatively high frequencies of male recombinations, was found to increase the frequency of sex-linked recessive lethal mutations from a control frequency of 0.18% to 1.63%. The second group, which showed a very much reduced frequency of male recombinations, was found to cause a slight increase to 0.48%, although it was not statistically significant. The first group was also tested for the recessive lethal mutation frequency in the second chromosome; the frequency increased from a control frequency of 0.28% to 2.82%. Mapping of a portion of the sex-linked lethals indicated a distribution along the entire X chromosome, although there was a tendency of clustering towards the tip of the X chromosome. One sex-linked lethal line so far tested was found to be associated with an inversion (approximate breakpoints, 14A–18A). It was suggested that the element causing male recombination might be similar to the hi mutator gene studied earlier by Ives (1950).


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