Can dominance genetic variance be ignored in evolutionary quantitative genetic analyses of wild populations?

Abstract Standard genetic analyses assume that reciprocal heterozygotes are, on average, phenotypically identical. If a locus is subject to genomic imprinting, however, this assumption does not hold. We incorporate imprinting into the standard quantitative-genetic model for two alleles at a single locus, deriving expressions for the additive and dominance components of genetic variance, as well as measures of resemblance among relatives. We show that, in contrast to the case with Mendelian expression, the additive and dominance deviations are correlated. In principle, this correlation allows imprinting to be detected solely on the basis of different measures of familial resemblances, but in practice, the standard error of the estimate is likely to be too large for a test to have much statistical power. The effects of genomic imprinting will need to be incorporated into quantitative-genetic models of many traits, for example, those concerned with mammalian birthweight.

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Towards evolutionary agroecology

INTERdisciplina ◽

10.22201/ceiich.24485705e.2018.14.63380 ◽

2018 ◽

Vol 6 (14) ◽

pp. 51 ◽

Cited By ~ 1

Author(s):

Kristin L. Mercer

Keyword(s):

Social Dynamics ◽

Agricultural Systems ◽

Short Term ◽

Ecological Processes ◽

Genetic Analyses ◽

Holistic Perspective ◽

Evolutionary Study ◽

Quantitative Genetic ◽

Field Evolution

Agroecology derives much of its strength from interactions between disciplines that produce a holistic perspective on agricultural systems and issues. Although ongoing integration of social dynamics into agroecology has strengthened the field, evolution and genetics have not been embraced to the same degree, despite the fact that they have been are discussed in some common agroecology texts. I argue that the field of agroecology could extend its reach and depth by embracing the evolutionary study of agroecosystems. Areas of evolutionary inquiry with relevance to agriculture focus on long or short term processes, encompass a range of scales, incorporate molecular or quantitative genetic analyses, and explore ecological processes to differing degrees.

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Genetic and environmental architecture of conscientiousness in adolescence

Scientific Reports ◽

10.1038/s41598-021-82781-5 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Yusuke Takahashi ◽

Anqing Zheng ◽

Shinji Yamagata ◽

Juko Ando

Keyword(s):

Individual Differences ◽

Effortful Control ◽

Genetic Variance ◽

Genetic Factors ◽

Common Factor ◽

Genetic Correlations ◽

Self Control ◽

Genetic Analyses ◽

Environmental Correlations ◽

Per Se

AbstractUsing a genetically informative design (about 2000 twin pairs), we investigated the phenotypic and genetic and environmental architecture of a broad construct of conscientiousness (including conscientiousness per se, effortful control, self-control, and grit). These four different measures were substantially correlated; the coefficients ranged from 0.74 (0.72–0.76) to 0.79 (0.76–0.80). Univariate genetic analyses revealed that individual differences in conscientiousness measures were moderately attributable to additive genetic factors, to an extent ranging from 62 (58–65) to 64% (61–67%); we obtained no evidence that shared environmental influences were observed. Multivariate genetic analyses showed that for the four measures used to assess conscientiousness, genetic correlations were stronger than the corresponding non-shared environmental correlations, and that a latent common factor accounted for over 84% of the genetic variance. Our findings suggest that individual differences in the four measures of conscientiousness are not distinguishable at both the phenotypic and behavioural genetic levels, and that the overlap was substantially attributable to genetic factors.

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Phenotypic plasticity of labile traits in the wild

Current Zoology ◽

10.1093/czoolo/59.4.485 ◽

2013 ◽

Vol 59 (4) ◽

pp. 485-505 ◽

Cited By ~ 37

Author(s):

Jon E. Brommer

Keyword(s):

Life History ◽

Phenotypic Plasticity ◽

Statistical Approach ◽

Scale Up ◽

Population Level ◽

Wild Populations ◽

Quantitative Genetic ◽

In The Wild ◽

The Individual ◽

Quantitative Genetic Parameters

Abstract Individual-based studies allow quantification of phenotypic plasticity in behavioural, life-history and other labile traits. The study of phenotypic plasticity in the wild can shed new light on the ultimate objectives (1) whether plasticity itself can evolve or is constrained by its genetic architecture, and (2) whether plasticity is associated to other traits, including fitness (selection). I describe the main statistical approach for how repeated records of individuals and a description of the environment (E) allow quantification of variation in plasticity across individuals (IxE) and genotypes (GxE) in wild populations. Based on a literature review of life-history and behavioural studies on plasticity in the wild, I discuss the present state of the two objectives listed above. Few studies have quantified GxE of labile traits in wild populations, and it is likely that power to detect statistically significant GxE is lacking. Apart from the issue of whether it is heritable, plasticity tends to correlate with average trait expression (not fully supported by the few genetic estimates available) and may thus be evolutionary constrained in this way. Individual-specific estimates of plasticity tend to be related to other traits of the individual (including fitness), but these analyses may be anti-conservative because they predominantly concern stats-on-stats. Despite the increased interest in plasticity in wild populations, the putative lack of power to detect GxE in such populations hinders achieving general insights. I discuss possible steps to invigorate the field by moving away from simply testing for presence of GxE to analyses that ‘scale up’ to population level processes and by the development of new behavioural theory to identify quantitative genetic parameters which can be estimated.

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Quantitative genetic variance in experimental fly populations evolving with or without environmental heterogeneity

Evolution ◽

10.1111/evo.12771 ◽

2015 ◽

Vol 69 (10) ◽

pp. 2735-2746 ◽

Cited By ~ 17

Author(s):

Yuheng Huang ◽

John R. Stinchcombe ◽

Aneil F. Agrawal

Keyword(s):

Genetic Variance ◽

Environmental Heterogeneity ◽

Quantitative Genetic

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The distribution of allelic effects under mutation and selection

Genetics Research ◽

10.1017/s0016672300025350 ◽

1990 ◽

Vol 55 (2) ◽

pp. 111-117 ◽

Cited By ~ 16

Author(s):

Steven A. Frank ◽

Montgomery Slatkin

Keyword(s):

Assortative Mating ◽

Genetic Variance ◽

Price Equation ◽

Genetic Character ◽

Quantitative Genetic ◽

Mutation And Selection

SummaryThe Price (1970, 1972) equation is applied to the problem of describing the changes in the moments of allelic effects caused by selection, mutation and recombination at loci governing a quantitative genetic character. For comparable assumptions the resulting equations are the same as those obtained by different means by Barton & Turelli (1987; Turelli & Barton, 1989). The Price equation provides a natural framework within which to examine certain kinds of non-additive allelic effects, recombination and assortative mating. The use of the Price equation is illustrated by finding the equilibrium genetic variance under multiplicative dominance and epistasis and under assortative mating at an additive locus. The limitations of the use of recursion equations for the moments of allelic effects are also discussed.

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Quantitative genetics and the evolution of ontogeny: I. Ontogenetic changes in quantitative genetic variance components in randombred mice

Genetics Research ◽

10.1017/s0016672300021492 ◽

1983 ◽

Vol 42 (1) ◽

pp. 65-75 ◽

Cited By ~ 33

Author(s):

James M. Cheverud ◽

Larry J. Leamy ◽

William R. Atchley ◽

J. J. Rutledge

Keyword(s):

Maternal Effects ◽

Environmental Effects ◽

Variance Components ◽

Genetic Variance ◽

Tail Length ◽

Head Length ◽

Ontogenetic Changes ◽

Trunk Length ◽

Quantitative Genetic ◽

Significant Difference

SUMMARYWe report the results of an ontogenetic analysis of quantitative genetic variance components with two replicates drawn from the randombred ICR strain of mice. A total of 432 mice from 108 full-sib families raised in a cross-fostering design were used to estimate direct effects heritability, maternal effects, and environmental effects for weight, head length, trunk length, trunk circumference, and tail length at 17, 24, 31, 38, 45, 52, 59, and 66 days of age. There was no significant difference in heritability between the replicates. Heritabilities either stayed more or less constant with age at about 0·30 (weight, trunk length, trunk circumference) or increased slightly with age (head length, tail length). Maternal effects decreased with age from a maximum of about 0·50 at weaning to about 0·15 at age 66 when growth was nearly complete. Environmental effects increased in relative importance during ontogeny.

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Quantitative genetic variability maintained by mutation-stabilizing selection balance: sampling variation and response to subsequent directional selection

Genetics Research ◽

10.1017/s0016672300028366 ◽

1989 ◽

Vol 54 (1) ◽

pp. 45-58 ◽

Cited By ~ 17

Author(s):

Peter D. Keightley ◽

William G. Hill

Keyword(s):

Genetic Variance ◽

Directional Selection ◽

Quantitative Character ◽

Stabilizing Selection ◽

Effective Population ◽

Selection Responses ◽

Quantitative Genetic ◽

Before And After ◽

Cage Population ◽

Selection Of

SummaryA model of genetic variation of a quantitative character subject to the simultaneous effects of mutation, selection and drift is investigated. Predictions are obtained for the variance of the genetic variance among independent lines at equilibrium with stabilizing selection. These indicate that the coefficient of variation of the genetic variance among lines is relatively insensitive to the strength of stabilizing selection on the character. The effects on the genetic variance of a change of mode of selection from stabilizing to directional selection are investigated. This is intended to model directional selection of a character in a sample of individuals from a natural or long-established cage population. The pattern of change of variance from directional selection is strongly influenced by the strengths of selection at individual loci in relation to effective population size before and after the change of regime. Patterns of change of variance and selection responses from Monte Carlo simulation are compared to selection responses observed in experiments. These indicate that changes in variance with directional selection are not very different from those due to drift alone in the experiments, and do not necessarily give information on the presence of stabilizing selection or its strength.

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No Support for a Genetic Basis of Mandible Crossing Direction in Crossbills (Loxia SPP)

The Auk ◽

10.1093/auk/122.4.1123 ◽

2005 ◽

Vol 122 (4) ◽

pp. 1123-1129 ◽

Cited By ~ 1

Author(s):

Pim Edelaar ◽

Erik Postma ◽

Peter Knops ◽

Ron Phillips

Keyword(s):

Genetic Basis ◽

Vertical Plane ◽

Statistical Techniques ◽

Wild Populations ◽

Quantitative Genetic ◽

Males And Females ◽

Few Data ◽

Lower Mandible ◽

Significant Support ◽

Rule Out

AbstractUnusual among birds, the bill tips in crossbills (Loxia spp.) overlap in the vertical plane, with the tip of the lower mandible to either the left or right of the tip of the upper mandible when viewed from above. Patterns observed in wild populations and experimental foraging data suggest that a 1:1 ratio of left- to right-crossing individuals is maintained by frequency-dependent natural selection in some populations, and that genetic drift causes deviation from a 1:1 ratio in other populations. Both processes require a genetic basis for this remarkable polymorphism, yet few data are available that address whether, and how, mandible crossing direction is heritable. To test for a genetic basis of this trait (single or quantitative, autosomal or sex-linked), we analyzed resemblance in mandible crossing direction between related captive-bred individuals of several crossbill taxa with standard statistical techniques as well as modern animal model methodology. Surprisingly, we did not find statistically significant support for a genetic basis of mandible crossing direction. Comparisons of the ratio of left- to right-crossing males and females in wild populations also did not support a sex-linked quantitative genetic basis. We conclude that mandible crossing direction may have uncharacteristically low heritability, but we cannot rule out that it is nongenetically determined.La Dirección de Cruzamiento de la Mandíbula en las Especies de Loxia no Presenta Base Genética

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Genetic Susceptibility of Myocardial Infarction

Twin Research and Human Genetics ◽

10.1375/twin.10.6.848 ◽

2007 ◽

Vol 10 (6) ◽

pp. 848-852 ◽

Cited By ~ 12

Author(s):

Slobodan Zdravkovic ◽

Andreas Wienke ◽

Nancy L. Pedersen ◽

Ulf de Faire

Keyword(s):

Myocardial Infarction ◽

Acute Myocardial Infarction ◽

Genetic Factors ◽

First Episode ◽

Phenotypic Variance ◽

Genetic Analyses ◽

Quantitative Genetic ◽

Equal Variance ◽

First Occurrence ◽

Mz Twins

AbstractThe aim of this study was to determine the influence of genetic factors on the first episode of acute myocardial infarction. Probandwise concordances, tetrachoric correlations and quantitative genetic analyses of liability were applied to data drawn from the Swedish Twin Registry and the Swedish Acute Myocardial Infarction Register. All same-sexed twin pairs born between 1886 and 1958 who were alive in 1987 were included in the analyses. Our results show that concordance rates for acute myocardial infarction in monozygotic (MZ) twins were similar across sexes (among males .26 and females .27). For dizygotic (DZ) twins the concordances were .20 for males and .16 for females, yielding a greater MZ–DZ concordance differential for females than males. Tetrachoric correlations were greater for MZ than DZ twins for both sexes (.49 for male MZ and .34 for male DZ-twins and .56 and .35 for female MZ and DZ twins respectively). Quantitative genetic analyses of liability resulted in equal variance components for males and females (.36) but significantly different thresholds (prevalences). In conclusion, liability to first occurrence of acute myocardial infarction is moderately influenced by genetic variants in both sexes. The familial influence on phenotypic variance is exclusively explained by additive genetic factors.

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