scholarly journals MUTATION RATE AND DOMINANCE OF GENES AFFECTING VIABILITY IN DROSOPHILA MELANOGASTER

Genetics ◽  
1972 ◽  
Vol 72 (2) ◽  
pp. 335-355
Author(s):  
Terumi Mukai ◽  
Sadao I Chigusa ◽  
L E Mettler ◽  
James F Crow
Keyword(s):  
Drosophila Melanogaster ◽  
Mutation Rate ◽  
Genetic Variance ◽  
Genetic Load ◽  
Spontaneous Mutations ◽  
Average Effect ◽  
Lethal Mutations ◽  
Nearly Neutral Mutations ◽  
The Individual ◽  
Neutral Mutations

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.

scholarly journals The Effect of Temperature on the Mutation Rate in Drosophila Melanogaster

1958 ◽  
Vol 11 (1) ◽  
pp. 85 ◽  
Author(s):  
BL Sheldon
Keyword(s):  
Drosophila Melanogaster ◽  
Mutation Rate ◽  
Shock Treatment ◽  
Effect Of Temperature ◽  
Adult Males ◽  
Heat Shock Treatment ◽  
Recessive Lethal ◽  
Lethal Mutations ◽  
Consistent Treatment ◽  
Large Response

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.

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
Keyword(s):  
Drosophila Melanogaster ◽  
Mutation Rate ◽  
Reciprocal Cross ◽  
Mutation Rates ◽  
Mutation Induction ◽  
Hybrid Male ◽  
Lethal Mutations ◽  
The Cross ◽  
The Relationship ◽  
Reciprocal Mating

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.

scholarly journals Transient mutators: a semiquantitative analysis of the influence of translation and transcription errors on mutation rates.

Genetics ◽  
1991 ◽  
Vol 129 (3) ◽  
pp. 957-962 ◽  
Author(s):  
J Ninio
Keyword(s):  
Steady State ◽  
Synonymous Codon ◽  
Experimental Manipulation ◽  
Mutation Rates ◽  
Wild Type ◽  
Lethal Mutations ◽  
Nearly Neutral Mutations ◽  
Neutral Mutations ◽  
Translation Errors ◽  
State Composition

Abstract A population of bacteria growing in a nonlimiting medium includes mutator bacteria and transient mutators defined as wild-type bacteria which, due to occasional transcription or translation errors, display a mutator phenotype. A semiquantitative theoretical analysis of the steady-state composition of an Escherichia coli population suggests that true strong genotypic mutators produce about 3 x 10(-3) of the single mutations arising in the population, while transient mutators produce at least 10% of the single mutations and more than 95% of the simultaneous double mutations. Numbers of mismatch repair proteins inherited by the offspring, proportions of lethal mutations and mortality rates are among the main parameters that influence the steady-state composition of the population. These results have implications for the experimental manipulation of mutation rates and the evolutionary fixation of frequent but nearly neutral mutations (e.g., synonymous codon substitutions).

scholarly journals MUTATIONAL ANALYSIS OF THE REGION SURROUNDING THE 93D HEAT SHOCK LOCUS OF DROSOPHILA MELANOGASTER

Genetics ◽  
1984 ◽  
Vol 106 (2) ◽  
pp. 249-265
Author(s):  
Jym Mohler ◽  
Mary Lou Pardue
Keyword(s):  
Drosophila Melanogaster ◽  
Heat Shock ◽  
Mutational Analysis ◽  
Point Mutations ◽  
Γ Irradiation ◽  
Lethal Mutations ◽  
Complementation Groups ◽  
In Trans ◽  
Shock Locus ◽  
Shock Proteins

ABSTRACT The region containing subdivisions 93C, 93D and 93E on chromosome 3 of Drosophila melanogaster has been screened for visible and lethal mutations. Treatment with three mutagens, γ irradiation, ethyl methanesulfonate and diepoxybutane, has produced mutations that fall into 20 complementation groups, including the previously identified ebony locus. No point mutations affecting the heat shock locus in 93D were detected; however, a pair of deficiencies that overlap in the region of this locus was isolated. Flies heterozygous in trans for this pair of deficiencies are capable of producing all of the major heat shock puffs (except 93D) and the major heat shock proteins. In addition, these flies show recovery of normal protein synthesis following a heat shock.

scholarly journals Linkage disequilibrium and genetic variances under mutation-selection balance.

Genetics ◽  
1989 ◽  
Vol 121 (4) ◽  
pp. 857-860 ◽  
Author(s):  
A Hastings
Keyword(s):  
Linkage Disequilibrium ◽  
Mutation Rate ◽  
Genetic Variance ◽  
Harmonic Mean ◽  
Recombination Rates ◽  
Genetic Variances ◽  
Locus Selection

Abstract I determine the contribution of linkage disequilibrium to genetic variances using results for two loci and for induced or marginal systems. The analysis allows epistasis and dominance, but assumes that mutation is weak relative to selection. The linkage disequilibrium component of genetic variance is shown to be unimportant for unlinked loci if the gametic mutation rate divided by the harmonic mean of the pairwise recombination rates is much less than one. For tightly linked loci, linkage disequilibrium is unimportant if the gametic mutation rate divided by the (induced) per locus selection is much less than one.

scholarly journals GENETIC LOAD IN NATURAL POPULATIONS: IS IT COMPATIBLE WITH THE HYPOTHESIS THAT MANY POLYMORPHISMS ARE MAINTAINED BY NATURAL SELECTION?

Genetics ◽  
1974 ◽  
Vol 77 (3) ◽  
pp. 569-589
Author(s):  
Martin L Tracey ◽  
Francisco J Ayala
Keyword(s):  
Drosophila Melanogaster ◽  
Natural Selection ◽  
Natural Population ◽  
Natural Populations ◽  
Genetic Load ◽  
Structural Genes ◽  
Invertebrate Species ◽  
Average Proportion ◽  
Mean Fitness ◽  
The Mean

ABSTRACT Recent studies of genetically controlled enzyme variation lead to an estimation that at least 30 to 60% of the structural genes are polymorphic in natural populations of many vertebrate and invertebrate species. Some authors have argued that a substantial proportion of these polymorphisms cannot be maintained by natural selection because this would result in an unbearable genetic load. If many polymorphisms are maintained by heterotic natural selection, individuals with much greater than average proportion of homozygous loci should have very low fitness. We have measured in Drosophila melanogaster the fitness of flies homozygous for a complete chromosome relative to normal wild flies. A total of 37 chromosomes from a natural population have been tested using 92 experimental populations. The mean fitness of homozygous flies is 0.12 for second chromosomes, and 0.13 for third chromosomes. These estimates are compatible with the hypothesis that many (more than one thousand) loci are maintained by heterotic selection in natural populations of D. melanogaster.

scholarly journals THE INTERCELLULAR DISTRIBUTION OF MUTATIONS INDUCED IN OOCYTES OF DROSOPHILA MELANOGASTER BY CHEMICAL AND PHYSICAL MUTAGENS

Genetics ◽  
1979 ◽  
Vol 92 (1) ◽  
pp. 151-160
Author(s):  
H Traut
Keyword(s):  
Drosophila Melanogaster ◽  
Mitomycin C ◽  
Mutation Frequency ◽  
Lethal Mutation ◽  
X Rays ◽  
Mutagenic Treatment ◽  
X Chromosomes ◽  
Recessive Lethal ◽  
Lethal Mutations ◽  
X Irradiation

ABSTRACT When females of Drosophila melanogaster are treated with chemical or physical mutagens, not only in one but also in both of the two homologous X chromosomes of a given oocyte, a recessive sex-linked lethal mutation may be induced. A method is described that discriminates between such "single" and "double mutations." A theory is developed to show how a comparison between the expected and the observed frequency of double mutations yields an indication of the intercellular distribution (random or nonrandom) of recessive lethal mutations induced by mutagenic agents in oocytes and, consequently, of the distribution (homogeneous or nonhomogeneous) of those agents.—Three agents were tested: FUdR (12.5, 50.0 and 81.0,μg/ml), mitomycin C (130.0 μg/ml) and X rays (2000 R, 150 kV). After FUdR feeding, no increase in the mutation frequency usually observed in D. melanogaster without mutagenic treatment was obtained (u=0.13%, namely three single mutations among 2332 chromosomes tested). After mitomycin C feeding, 104. single and three double mutations were obtained. All of the 50 mutations observed after X irradiation were single mutations. The results obtained in the mitomycin C and radiation experiments favor the assumption of a random intercellular distribution of recessive lethal mutations induced by these two agents in oocytes of D. melanogaster. Reasons are discussed why for other types of mutagenic agents nonrandom distributions may be observed with our technique.

scholarly journals SITE-SPECIFIC INSTABILITY IN DROSOPHILA MELANOGASTER: EVIDENCE FOR TRANSPOSITION OF DESTABILIZING ELEMENT

Genetics ◽  
1982 ◽  
Vol 101 (3-4) ◽  
pp. 461-476
Author(s):  
Todd R Laverty ◽  
J K Lim
Keyword(s):  
Drosophila Melanogaster ◽  
X Chromosome ◽  
Lethal Mutation ◽  
Chromosome Rearrangements ◽  
Chromosome Break ◽  
Secondary Mutation ◽  
X Chromosomes ◽  
Site Specific ◽  
Normal Sequence ◽  
Lethal Mutations

ABSTRACT In this study, we show that at least one lethal mutation at the 3F-4A region of the X chromosome can generate an array of chromosome rearrangements, all with one chromosome break in the 3F-4A region. The mutation at 3F-4A (secondary mutation) was detected in an X chromosome carrying a reverse mutation of an unstable lethal mutation, which was mapped in the 6F1-2 doublet (primary mutation). The primary lethal mutation at 6F1-2 had occurred in an unstable chromosome (Uc) described previously (Lim 1979). Prior to reversion, the 6F1-2 mutation had generated an array of chromosome rearrangements, all having one break in the 6F1-2 doublet (Lim 1979, 1980). In the X chromosomes carrying the 3F-4A secondary lethal mutation the 6F1-2 doublet was normal and stable, as was the 3F-4A region in the X chromosome carrying the primary lethal mutation. The disappearance of the instability having a set of genetic properties at one region (6F1-2) accompanied by its appearance elsewhere in the chromosome (3F-4A) implies that a transposition of the destabilizing element took place. The mutant at 3F-4A and other secondary mutants exhibited all but one (reinversion of an inversion to the normal sequence) of the eight properties of the primary lethal mutations. These observations support the view that a transposable destabilizing element is responsible for the hypermutability observed in the unstable chromosome and its derivaties.

A NOTE ON KIDWELL'S CHROMOSOMAL ANALYSIS OF EGG PRODUCTION AND CHAETA NUMBER IN DROSOPHILA MELANOGASTER

1970 ◽  
Vol 12 (2) ◽  
pp. 356-358 ◽  
Author(s):  
P. Glaser ◽  
J. F. Kldwell
Keyword(s):  
Drosophila Melanogaster ◽  
Egg Production ◽  
Genetic Variance ◽  
Chromosomal Analysis ◽  
Epistatic Variance

An earlier paper (Kidwell, J.F., 1969, Can. J. Genet. Cytol 11: 547-557) has described partitioning of the genetic variance of egg production and chaeta number in Drosophila melanogaster, assuming equal frequencies of all chromosomes. Kidwell's data were analyzed again, and the new analyses were based on several panmictic populations with varying frequencies for each genotype. The importances of the several portions of the genetic variance were estimated for each population; several cases are presented. In most cases the ranges were substantial, especially those of the dominance and four-factor epistatic variances. The results of the present study generally support Kidwell's previous conclusions and suggest that epistatic variance should not routinely be assumed negligible.

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