GENETIC HOMEOSTASIS IN DROSOPHILA MELANOGASTER

1969 ◽  
Vol 11 (2) ◽  
pp. 414-425 ◽  
Author(s):  
P. D. Walton
Keyword(s):  
Drosophila Melanogaster ◽  
Genetic Variation ◽  
Natural Selection ◽  
Genetic Variance ◽  
Additive Genetic Variance ◽  
The Other ◽  
Diallel Crosses ◽  
Additive Component ◽  
Selection For ◽  
Genetic Homeostasis

The literature provides three explanations of the way in which genetic homeostasis functions. An attempt was made to determine which of these was applicable to the changes which occurred when selection for geotaxis was relaxed in certain strains of Drosophila melonogaster. The strains, for which selection stopped, were divided into two parts and generations were advanced in two environments. One was the same as that in which selection had been made and the other was new. When selection was relaxed strains reverted to a mean geotactic score close to that of the populations from which they had been selected. This change was more rapid in the new environment. A series of diallel crosses compared strains for which selection was continued with those for which it was relaxed. An analysis of the components of genetic variation showed that the principle change that had taken place was in the additive component of genetic variation. It was concluded that genetic homeostasis resulted from the action of natural selection on additive genetic variance, a conclusion which is in agreement with one of the three current hypotheses.

scholarly journals Autosomal and X-Linked Additive Genetic Variation for Lifespan and Aging: Comparisons Within and Between the Sexes in Drosophila melanogaster

2016 ◽  
Vol 6 (12) ◽  
pp. 3903-3911 ◽  
Author(s):  
Robert M Griffin ◽  
Holger Schielzeth ◽  
Urban Friberg
Keyword(s):  
Drosophila Melanogaster ◽  
Genetic Variation ◽  
X Chromosome ◽  
Dosage Compensation ◽  
Genetic Variance ◽  
Additive Genetic Variance ◽  
Conclusive Evidence ◽  
Substitution Lines ◽  
Chromosome Substitution Lines ◽  
Sexually Antagonistic Selection

Abstract Theory makes several predictions concerning differences in genetic variation between the X chromosome and the autosomes due to male X hemizygosity. The X chromosome should: (i) typically show relatively less standing genetic variation than the autosomes, (ii) exhibit more variation in males compared to females because of dosage compensation, and (iii) potentially be enriched with sex-specific genetic variation. Here, we address each of these predictions for lifespan and aging in Drosophila melanogaster. To achieve unbiased estimates of X and autosomal additive genetic variance, we use 80 chromosome substitution lines; 40 for the X chromosome and 40 combining the two major autosomes, which we assay for sex-specific and cross-sex genetic (co)variation. We find significant X and autosomal additive genetic variance for both traits in both sexes (with reservation for X-linked variation of aging in females), but no conclusive evidence for depletion of X-linked variation (measured through females). Males display more X-linked variation for lifespan than females, but it is unclear if this is due to dosage compensation since also autosomal variation is larger in males. Finally, our results suggest that the X chromosome is enriched for sex-specific genetic variation in lifespan but results were less conclusive for aging overall. Collectively, these results suggest that the X chromosome has reduced capacity to respond to sexually concordant selection on lifespan from standing genetic variation, while its ability to respond to sexually antagonistic selection may be augmented.

Models of the evolution of dominance

1968 ◽  
Vol 171 (1022) ◽  
pp. 127-143 ◽  
Keyword(s):  
Mathematical Model ◽  
Genetic Variation ◽  
Natural Selection ◽  
Genetic Variance ◽  
Deleterious Mutation ◽  
The Other ◽  
Wild Type ◽  
Selective Forces ◽  
Mutant Homozygote ◽  
Selective Effects

There are three essentially different models to explain how dominance might gradually evolve by natural selection. In Fisher’s model, the wild-type evolves dominance in response to the occurrence of deleterious mutation s: genetic variations in the expression of the mutant heterozygote will be selected to raise its fitness an d produce dominance or over-dominance. The rate of this selection is slow and depends on what the fitness of the heterozygote will be at its optimum. In Parsons & Bodmer’s model, the fitness of an advantageous mutant hetero ¬ zygote is raised up to or above that of the mutant homozygote while the mutation is spreading through a population. Whether dominance or over-dominance is reached depends on the heterozygote’s genetic variance and optimum fitness. In both these models, the variations in the mutant heterozygote must be caused by modifiers with more or less neutral selective effects on other characters. Fisher’s theoretical arguments on the origin of genetic variation and Lewontin & Hub by ’s experiments show that such modifiers may exist. In Sheppard’s model, dominance evolves in a polymorphism maintained by disruptive or frequencydependent selection. If two different alleles produce two different mimetic forms, the hetero ¬ zygote and one of the homozygotes will be selected to give the optimum phenotype of one of the mimics and the other homozygote will be selected to give the optimum phenotype of the other one. In this model, the mimic which is the last to appear by mutation evolves dominance. Other small selective forces acting on the modifiers do not stop the evolution of dominance. Sheppard’s model should therefore be true in nature whether the modifiers are subject to other selective forces or not. A mathematical model demonstrated that a rare mimic would not evolve dominance if the modifier was maintained in the population by other selective forces producing a heterozygous advantage of more than 1%. Thus it follows from Clarke & S heppard’s discovery of certain rare mimics of Papilio dardanus that this is the greatest possible heterozygous advantage that can be acting on the modifiers.

scholarly journals The limits to artificial selection for body weight in the mouse II. The Genetic Nature of the Limits

1966 ◽  
Vol 8 (3) ◽  
pp. 361-375 ◽  
Author(s):  
R. C. Roberts
Keyword(s):  
Body Weight ◽  
Natural Selection ◽  
Artificial Selection ◽  
Sharp Increase ◽  
Genetic Variance ◽  
Additive Genetic Variance ◽  
Base Population ◽  
Relaxed Selection ◽  
Genetic Nature ◽  
Selection For

1. The effects of long-continued selection for body weight in two lines of mice, one large and one small, are described.2. The large line showed a sharp increase in weight after remaining at an apparent limit for twenty generations. A rare combinational event is suggested as the most likely explanation.3. Reversed and relaxed selection from the large line at the limit failed to yield any response. This indicates that effectively, the additive genetic variance in this line had been exhausted.4. In contrast, the small line at the limit regressed slightly towards the base population when selection was relaxed. Reversed selection yielded a ready response until a new limit was apparently reached. Loci affecting body weight in this line had therefore not been fixed by selection.5. Natural selection, operating on viability between conception and the time when the selection was made, appears to explain best the lack of fixation in the small line.6. Attention is drawn to the necessity of more experimental work to elucidate the genetic nature of the limits to artificial selection.

scholarly journals SELECTION FOR BLOOD PRESSURE LEVELS IN MICE

Genetics ◽  
1974 ◽  
Vol 76 (3) ◽  
pp. 537-549
Author(s):  
Gunther Schlager
Keyword(s):  
Blood Pressure ◽  
Systolic Blood Pressure ◽  
Genetic Variance ◽  
Additive Genetic Variance ◽  
Population Bottleneck ◽  
Control Line ◽  
Selected Lines ◽  
High Line ◽  
Selection For ◽  
Random Control

ABSTRACT Response to two-way selection for systolic blood pressure was immediate and continuous for about eight generations. In the twelfth generation, the High males differed from the Low males by 38 mmHG; the females differed by 39 mmHg. There was little overlap between the two lines and they were statistically significant from each other and from the Random control line. There appeared to be no more additive genetic variance in the eleventh and twelfth generations. Causes for the cessation of response are explored. This is probably due to a combination of natural selection acting to reduce litter sizes in the Low line, a higher incidence of sudden deaths in the High line, and loss of favorable alleles as both selection lines went through a population bottleneck in the ninth generation.—In the eleventh generation, the selected lines were used to produce F1, F2, and backcross generations. A genetic analysis yielded significant additive and dominance components in the inheritance of systolic blood pressure.

scholarly journals How does parental environment influence the potential for adaptation to global change?

2018 ◽  
Vol 285 (1886) ◽  
pp. 20181374 ◽  
Author(s):  
Evatt Chirgwin ◽  
Dustin J. Marshall ◽  
Carla M. Sgrò ◽  
Keyne Monro
Keyword(s):  
Genetic Variation ◽  
Global Change ◽  
Adaptive Capacity ◽  
Genetic Variance ◽  
Life Stage ◽  
Additive Genetic Variance ◽  
Parental Exposure ◽  
Future Warming ◽  
The Mean ◽  
Negative Impacts

Parental environments are regularly shown to alter the mean fitness of offspring, but their impacts on the genetic variation for fitness, which predicts adaptive capacity and is also measured on offspring, are unclear. Consequently, how parental environments mediate adaptation to environmental stressors, like those accompanying global change, is largely unknown. Here, using an ecologically important marine tubeworm in a quantitative-genetic breeding design, we tested how parental exposure to projected ocean warming alters the mean survival, and genetic variation for survival, of offspring during their most vulnerable life stage under current and projected temperatures. Offspring survival was higher when parent and offspring temperatures matched. Across offspring temperatures, parental exposure to warming altered the distribution of additive genetic variance for survival, making it covary across current and projected temperatures in a way that may aid adaptation to future warming. Parental exposure to warming also amplified nonadditive genetic variance for survival, suggesting that compatibilities between parental genomes may grow increasingly important under future warming. Our study shows that parental environments potentially have broader-ranging effects on adaptive capacity than currently appreciated, not only mitigating the negative impacts of global change but also reshaping the raw fuel for evolutionary responses to it.

scholarly journals Estimation of Genetic Variance in Fitness, and Inference of Adaptation, When Fitness Follows a Log-Normal Distribution

2019 ◽  
Vol 110 (4) ◽  
pp. 383-395 ◽  
Author(s):  
Timothée Bonnet ◽  
Michael B Morrissey ◽  
Loeske E B Kruuk
Keyword(s):  
Natural Selection ◽  
Animal Models ◽  
Normal Distribution ◽  
Genetic Variance ◽  
Additive Genetic Variance ◽  
Relative Fitness ◽  
Parameter Estimates ◽  
Log Normal ◽  
Change In Mean ◽  
Log Normal Distribution

AbstractAdditive genetic variance in relative fitness (σA2(w)) is arguably the most important evolutionary parameter in a population because, by Fisher’s fundamental theorem of natural selection (FTNS; Fisher RA. 1930. The genetical theory of natural selection. 1st ed. Oxford: Clarendon Press), it represents the rate of adaptive evolution. However, to date, there are few estimates of σA2(w) in natural populations. Moreover, most of the available estimates rely on Gaussian assumptions inappropriate for fitness data, with unclear consequences. “Generalized linear animal models” (GLAMs) tend to be more appropriate for fitness data, but they estimate parameters on a transformed (“latent”) scale that is not directly interpretable for inferences on the data scale. Here we exploit the latest theoretical developments to clarify how best to estimate quantitative genetic parameters for fitness. Specifically, we use computer simulations to confirm a recently developed analog of the FTNS in the case when expected fitness follows a log-normal distribution. In this situation, the additive genetic variance in absolute fitness on the latent log-scale (σA2(l)) equals (σA2(w)) on the data scale, which is the rate of adaptation within a generation. However, due to inheritance distortion, the change in mean relative fitness between generations exceeds σA2(l) and equals (exp⁡(σA2(l))−1). We illustrate why the heritability of fitness is generally low and is not a good measure of the rate of adaptation. Finally, we explore how well the relevant parameters can be estimated by animal models, comparing Gaussian models with Poisson GLAMs. Our results illustrate 1) the correspondence between quantitative genetics and population dynamics encapsulated in the FTNS and its log-normal-analog and 2) the appropriate interpretation of GLAM parameter estimates.

scholarly journals Effects of stress combinations on the expression of additive genetic variation for fecundity in Drosophila melanogaster

1998 ◽  
Vol 72 (1) ◽  
pp. 13-18 ◽  
Author(s):  
CARLA M. SGRÒ ◽  
ARY A. HOFFMANN
Keyword(s):  
Drosophila Melanogaster ◽  
Genetic Variance ◽  
Cold Shock ◽  
Additive Genetic Variance ◽  
Combined Stress ◽  
Heritable Variation ◽  
Environmental Variance ◽  
Apparent Increase ◽  
Nutrition Environment ◽  
Stress Combinations

To test whether stressful conditions altered levels of heritable variation in fecundity in Drosophila melanogaster, parent–offspring comparisons were undertaken across three generations for flies reared in a combined stress (ethanol, cold shock, low nutrition) environment or a control environment. The stressful conditions did not directly influence fecundity but did lead to a reduced fecundity in the offspring generations, perhaps reflecting cross-generation maternal effects. Both the heritability and evolvability estimates were higher in the combined stress treatment, reflecting an apparent increase in the additive genetic variance under stress. In contrast, there were no consistent changes in the environmental variance across environments.

Quantitative inheritance studies in sugar-cane. I. Estimation of variance components

1971 ◽  
Vol 22 (1) ◽  
pp. 93 ◽  
Author(s):  
DM Hogarth
Keyword(s):  
Factorial Design ◽  
Variance Components ◽  
Genetic Variance ◽  
Additive Genetic Variance ◽  
The Other ◽  
Quantitative Inheritance ◽  
Genetic Determination ◽  
Nested Design ◽  
Dominance Genetic Variance ◽  
Estimation Of Variance

Two experiments in quantitative genetics were conducted, one based on a nested design in lattice squares and the other on a factorial design in a balanced lattice. Lattice designs were found to be suitable for genetic experiments if a large number of crosses was involved, but posed some problems in partitioning the sum of squares for treatments. The factorial design was considered preferable to the nested design, although neither design permitted estimation of epistatic variances which, therefore, were assumed to be negligible. Additive genetic variance was found to be more important than dominance genetic variance for most characters. However, most estimates of genetic variance lacked precision in spite of the use of large, precise experiments, which illustrated the difficulty in obtaining estimates of variance components with adequate precision. The validity of assumptions made for these analyses is discussed. The effect of competition was studied and estimates of heritability and degree of genetic determination were determined.

scholarly journals The limits to artificial selection for body weight in the mouse: IV. Sources of new genetic variance—irradiation and outcrossing

1967 ◽  
Vol 9 (1) ◽  
pp. 87-98 ◽  
Author(s):  
R. C. Roberts
Keyword(s):  
Body Weight ◽  
Artificial Selection ◽  
Genetic Variance ◽  
Additive Genetic Variance ◽  
Negative Results ◽  
Selection For ◽  
The Cross

1. Two methods are examined of introducing new genetic variance into a line of mice selected for high 6-week weight which, at its limit, displayed no additive genetic variance.2. The first method—irradiation—gave largely negative results. Any further gain under selection that was achieved could not be clearly distinguished from a possible environmental trend.3. The second method—outcrossing to an unselected strain and then selecting from the cross—resulted in a clear gain over the original limit, but nine generations were required even to recover the original limit.4. Various methods of transcending selection limits are evaluated in terms of their application to livestock improvement.

scholarly journals Variance component analysis for viability in an isolated population of Drosophila melanogaster

1983 ◽  
Vol 42 (2) ◽  
pp. 207-217 ◽  
Author(s):  
Hidenori Tachida ◽  
Muneo Matsuda ◽  
Shin-Ichi Kusakabe ◽  
Terumi Mukai
Keyword(s):  
Drosophila Melanogaster ◽  
Genetic Variance ◽  
Balancing Selection ◽  
Additive Genetic Variance ◽  
Diallel Cross ◽  
Variance Component Analysis ◽  
Logarithmic Scale ◽  
Dominance Variance ◽  
Diversifying Selection ◽  
Partial Diallel

SUMMARYUsing the 602 second chromosome lines extracted from the Ishigakijima population of Drosophila melanogaster in Japan, partial diallel cross experiments (Design II of Comstock & Robinson, 1952) were carried out, and the additive genetic variance and the dominance variance of viability were estimated. The estimated value of the additive genetic variance is 0·01754±0·00608, and the dominance variance 0·00151±0·00114, using a logarithmic scale. Since the value of the additive genetic variance is much larger than expected under mutation–selection balance although the dominance variance is compatible with it, we speculate that in the Ishigakijima population some type of balancing selection must be operating to maintain the genetic variability with respect to viability at a minority of loci. As candidates for such selection, overdominance, frequency-dependent selection, and diversifying selection are considered, and it is suggested that diversifying selection is the most probable candidate for increasing the additive genetic variance.

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