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A single-locus quantitative genetic model incorporating DNA methylation.

We describe a single-locus quantitative genetic model that incorporates effects due to DNA methylation. Extending Fisher's decomposition of the genotypic value, we distinguish two quantities to predict an individual's phenotypic or genetic values: the "basic genetic value" and the "expressed genetic value". We show how these quantities relate to the concept of breeding value and derive their corresponding formulas, along with those for phenotypic variance and covariance between relatives. The resulting parameters are influenced by several factors, including the population distribution of DNA methylation levels, the functional relationship between methylation and phenotype, the magnitudes of genetic and methylation effects, and allele frequencies. We show that under the conditions modeled, the presence of DNA methylation does not bias estimated breeding values.

DNA Methylation

Quantitative genetic study on sexual difference in emigration behavior of Drosophila melanogaster in a natural population.

A quantitative genetic analysis was conducted on emigration response behavior using 140 second chromosome lines of Drosophila melanogaster. Fourteen sets of 5 x 5 partial diallel cross experiments were made in the parental generation. The emigration activity per batch of 50 male and 50 female F1 progeny was scored with Sakai's population system. Sexual difference did not appear in the emigration activity in these experiments. A significant genotype x sex x set interaction was detected. The genetic variance components of emigration activity differed between sexes: In males, additive genetic variance of emigration activity was 0.0497 +/- 0.0092 and dominance variance, 0.0018 +/- 0.0046; in females, additive, 0.0373 +/- 0.0076 and dominance, 0.0169 +/- 0.0044. Additive genetic correlation between sexes for the emigration activity was 0.685 +/- 0.150, deviating significantly from unity. These results suggested that the genes affecting emigration activity would operate differently between sexes of D. melanogaster in natural populations.

Animals

Dissecting fluctuating selection: A unified population and quantitative genetics framework.

One of the longstanding debates in evolutionary biology is the effect of fluctuating selection on genetic changes in populations. However, the extent to which these periodic forces influence organisms at both genomic and phenotypic levels remains unclear. Despite the compelling evidence of fluctuating selection from recent studies, there is a disconnect between empirical and theoretical findings concerning the underlying mechanisms due to the limited evidence regarding the scale and processes that generate genome-wide oscillations. This study aims to elucidate how both genetic factors (e.g. heritability, number of causative loci) and ecological factors (e.g. season length, the difference in the phenotypic optima between seasons, population size dynamics) drive fluctuating selection and to identify the parameters that produce consistent oscillatory patterns. We developed a modeling framework integrating quantitative and population genetics to simulate a population under various selection regimes. We applied spectral analysis to detect periodicity, indicating cyclical selective environments. Our simulations highlight the conditions sustaining oscillations in allele frequencies over time. Spectral analysis successfully identifies the periodic patterns from allele frequency trajectories, even under highly complex selection regimes. Not only does our study clarify the conditions that yield oscillatory behaviors, but these parameters can also potentially be estimated in natural populations, providing a possibility of empirically testing these models.

Fluctuating selection

Dissecting fluctuating selection: A unified population and quantitative genetics framework.

One of the longstanding debates in evolutionary biology is the effect of fluctuating selection on genetic changes in populations. However, the extent to which these periodic forces influence organisms at both genomic and phenotypic levels remains unclear. Despite the compelling evidence of fluctuating selection from recent studies, there is a disconnect between empirical and theoretical findings concerning the underlying mechanisms due to the limited evidence regarding the scale and processes that generate genome-wide oscillations. This study aims to elucidate how both genetic factors (e.g. heritability, number of causative loci) and ecological factors (e.g. season length, the difference in the phenotypic optima between seasons, population size dynamics) drive fluctuating selection and to identify the parameters that produce consistent oscillatory patterns. We developed a modeling framework integrating quantitative and population genetics to simulate a population under various selection regimes. We applied spectral analysis to detect periodicity, indicating cyclical selective environments. Our simulations highlight the conditions sustaining oscillations in allele frequencies over time. Spectral analysis successfully identifies the periodic patterns from allele frequency trajectories, even under highly complex selection regimes. Not only does our study clarify the conditions that yield oscillatory behaviors, but these parameters can also potentially be estimated in natural populations, providing a possibility of empirically testing these models.

Fluctuating selection

Quantitative genetically nonequivalent reciprocal crosses in cultivated plants.

Quantitative expressions of character difference between reciprocal crosses have been studied by different researchers in a number of plant species, such as Epilobium, Zea mays, Oryza sativa, Hordeum sativum, Triticum aestivum, Trifolium hybridum, Linum usitatissimum, Nicotiana rustica, and others. In all cases it was found that the nonequivalence of reciprocal crosses manifested itself beginning with the F1 generation, with the exception of some flax crosses in which reciprocals differed beginning with the F2 generation. The nonequivalence of reciprocal crosses usually manifested itself in the inequality of their F1 and/or F2 or backcross means; however, there were instances in which their means were the same but the variances were different. Both matroclinous and patroclinous inheritances were reported in plants. Because of the casual complexity of reciprocal differences the experimental results often lack a simple explanation.

Cell Nucleus

The nature of quantitative genetic variation in Drosophila. III. Mechanism of dosage compensation for sex-linked abdominal bristle polygenes.

Seventeen lines, each homozygous for a different X chromosome but all with a common autosomal genetic blackground, were constructed and assayed for abdominal bristle number to determine whether dosage compensation operates for sex-linked genes affecting this character. --The regression coefficient of male mean on female mean using a logarithmic scale was 0.90 +/- 0.13 and the genetic regression coefficient 0.92, neither differing significantly from unity. The genetic components of variance in males and females were also very similar (0.000234 or 0.000228, respectively). These results indicate that dosage compensation is complete (or nearly so) for sex-linked genes affecting this character. The bristle scores of females did not differ in reciprocal crosses between these lines, thus dosage compensation does not operate by paternal X inactivation. --The question of an adequate scale for abdominal bristle number had to be examined during the study. A logarithmic scale appeared to be adequate for both genotypic and environmental differences.

Animals

Some models of genetic selection.

This paper begins with a description of the classical theory of viability selection in which probabilities that individuals of various genotypes survive are in proportions that do not change with time and are independent of population structure. Salient features of viability selection with one and two loci are reviewed. This theory is intimately connected with the usual theory of mass selection in quantitative genetics. It is well known that the mean of the relative viabilities does not necessarily increase if there is viability selection at more than one locus. It also turns out that if there is selection for fecundity with one locus, the mean fecundity may steadily decrease or oscillate rather than increase. This and the fact that a Hardy-Weinberg structure may no longer exist at any stage of life may have a bearing on predicting progress from artificial selection on reproductive characters. Classical viability selection theory does not completely describe natural selection. Other possibilities are discussed. Among these is the density and frequency dependent selection induced when the population lives in a limited habitat. Implications in quantitative genetics are discussed.

Alleles

Drosophila with postponed aging as a model for aging research.

Species of the genus Drosophila, commonly known as "fruitflies," are good model systems for research in aging. Drosophila are extremely well-known genetically, developmentally, and otherwise. They are also genetically analogous to mammalian species in most important respects. Previous work with Drosophila has been hampered by inbreeding depression, but more recent work using selection has created Drosophila with postponed aging that is inherited normally. Genetic transformation has also increased Drosophila life spans in some cases. Several biologic approaches have been applied to the analysis of genetically postponed aging in Drosophila: quantitative genetics, organismal physiology, and protein electrophoresis. Ultimately, these different approaches will be integrated into an overall analysis of aging in Drosophila, one that could be valuable for research with other taxa as well.

Aging

Genetic studies in outpatients: plasma cholesterol in family and twin studies.

Quantitative genetic studies have much potential in partitioning the causes of variation of quantitative traits such as risk factors for atherosclerosis. Only if specific causes of variation are identified can specific therapy be developed to modify risks. There have been extensive family studies of plasma cholesterol which reveal that the level of plasma cholesterol is correlated in family members. However, except for the relatively rare familial hypercholesterolemia the evidence is not convincing that correlations of relatives are due to genetic rather than environmental factors. Early twin studies were interpreted as supporting the hypothesis that levels of plasma cholesterol were strongly influenced by genetic factors. However a recent large study of twins cast doubt upon this hypothesis by finding no significant genetic variance of plasma cholesterol after correcting for differences in total variance of monozygotic and dizygotic twins.

Arteriosclerosis