Quantitative genetic variation in the skeleton of the mouse. I. Variation between inbred strains.
Explore the source record for details and available documents.
Animals↗
SEARCH · PubMed Health
Results for “quantitative genetic variation”
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Quantitative genetic variation for oviposition preference with respect to phenylthiocarbamide in Drosophila melanogaster.
Seven isogenic strains of Drosophila melanogaster were assayed for oviposition preference on food with phenylthiocarbamide (PTC) versus plain food. There was significant variation among strains for the percentage of eggs oviposited on each medium, ranging from 70 +/- 4% (SE) preference for plain food to no significant preference. Reciprocal hybrid, backcross, and F2 generations derived from two extreme parent strains revealed significant additive and nonadditive genetic variation but no evidence of maternal, paternal, or sex-chromosome effects.
Animals↗
Unequal crossing over at the rRNA locus as a source of quantitative genetic variation.
Explore the source record for details and available documents.
Animals↗
The nature of quantitative genetic variation in drosophila. II. Average dominance of abdominal bristle polygenes.
Explore the source record for details and available documents.
Abdomen↗
Quantitative genetic variation of enzyme activities in natural populations of Drosophila melanogaster.
The genetic component of variation of enzyme activity in natural populations of Drosophila melanogaster was investigated by using two sets of chromosome substitution lines. The constitution of a line of each type is: i(1)/i(1);+(2)/ +(2);i(3)/i(3) and i(1)/i(1);i(2)/ i(2);+(3)/+(3), where i refers to a chromosome from a highly inbred line and + refers to a chromosome from a natural population. The + but not the i chromosomes vary within a set of lines. By use of a randomized block design to test and estimate components of variance, 50 of the second- and 50 of the third- chromosome substitution lines have been screened for variation in the activity levels of seven enzymes. Six of the seven enzymes show a significant genetic component in at least one set of lines, and five of the seven enzymes show activity variations attributable to factors that are not linked to the structural gene. These unlinked activity modifiers identify possible regulatory elements. Analyses of covariance show that most of the genetic variation of enzyme activities cannot be accounted for by genetic variation of live weight or protein content. These results and the lack of strong correlations between the genetic effects on the activities of different enzymes indicate that the effects are mainly specific for individual enzymes.
Journal Article↗
Evolution and maintenance of quantitative genetic variation by mutations.
The genotypic variance within, sigma 2w, and between, sigma 2b, random mating populations and rates and times for convergence to equilibrium values from different founder populations are formulated for an additive genetic model with an arbitrary number of alleles k, number of loci m, population size N, and mutation rate u, with unequal mutation rates for alleles. As a base of reference, the additive variance sigma 2a in an infinite equilibrium population is used. sigma 2a increases as k increases and decreases with variation in the mutation rates. Both transitional and equilibrium values of the variance within populations could be expressed as sigma 2w = (1 - theta)sigma 2a, where theta is the coancestry with mutations of individuals within populations. Thus, rates of convergence and evolutionary times are a function of those for theta, which involves both N and u. When the founder population is fixed, very long times are required to obtain a perceptible increase in sigma 2w and equilibrium values of sigma 2w are very small when 4Nu less than or equal to 10(-1). The variance between populations can be expressed as sigma 2b = 2 theta sigma 2a when the founder population is an infinite equilibrium population, and as sigma 2b = 2(theta - alpha)sigma 2a when the founder population is fixed, where alpha is a function only of u. In this latter case, rates of divergence, while affected by both N and u, are dominated by u and asymptotically a function of u only. With u = 10(-5), very long times (10(3) generations) are required for any perceptible divergence, even for N = 1-10. At equilibrium, most of the variance is between small populations and within very large populations. Migration increases the variance within populations and decreases the variance between populations.
Alleles↗
Quantitative genetic variation in body size of mice from new mutations.
To measure the amount of new genetic variation in 6-week weight of mice arising each generation from mutation, selection lines derived from an initially inbred strain were maintained for 25 generations. An analysis using an animal model with restricted maximum likelihood was applied to estimate a mutational genetic component of variance for the infinitesimal model of many genes of small effect. Assuming that the inbred base population was at a mutation-drift equilibrium, it is estimated that the heritability for body size has increased by 1.0% per generation, with lower and upper confidence limits of 0.6% and 1.6%, respectively. A model which includes a mutational genetic component of variance fits the data much better than one involving only base population genetic variance. A model with no genetic component fits the data very poorly. An environmental covariance of body size of mother and offspring was included in the model and accounts for 10% of the variance. By using information only from the observed response to selection, the estimated increase in heritability from mutation is 0.3% per generation. These values are higher than published estimates for the increase in variance from spontaneous mutations in bristle traits of Drosophila, for which there are extensive data, but similar to estimates for various skeletal traits in mice.
Animals↗
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↗
Quantitative genetic variation in CD19 expression correlates with autoimmunity.
Signaling thresholds influence the balance between humoral immunity and autoimmunity. Cell surface CD19 regulates intrinsic and Ag receptor-induced B lymphocyte signaling thresholds, and transgenic mice that overexpress CD19 by 3-fold generate spontaneous autoantibodies in a genetic background not associated with autoimmunity. To quantify the extent that genetically determined differences in expression of a single cell surface molecule can influence autoantibody production, we have assessed autoimmunity in a C57BL/6-transgenic mouse line with subtle 15-29% increases in CD19 cell surface expression (CD19 transgenic). Antinuclear Abs, especially anti-spindle pole Abs, rheumatoid factor, and autoantibodies for ssDNA, dsDNA, and histone were produced in these transgenic mice, but not littermate controls. This demonstrates that small changes in CD19 expression can induce autoantibody production. Remarkably, similar changes in CD19 expression were found on B cells from patients with systemic sclerosis, a multisystem disorder of connective tissue with autoantibody production. CD19 density on blood B cells from systemic sclerosis patients was significantly ( approximately 20%) higher compared with normal individuals, whereas CD20, CD22, and CD40 expression were normal. These results suggest that modest changes in the expression or function of regulatory molecules such as CD19 may shift the balance between tolerance and immunity to autoimmunity. Thereby autoimmune disease may result from a collection of subtle multigenic alterations that could include incremental density changes in cell surface signaling molecules.
Adult↗
Quantitative genetic variations and essential hypertension.
Explore the source record for details and available documents.
Angiotensin-Converting Enzyme Inhibitors↗
Patterns of genetic architecture for life-history traits and molecular markers in a subdivided species.
Understanding the utility and limitations of molecular markers for predicting the evolutionary potential of natural populations is important for both evolutionary and conservation genetics. To address this issue, the distribution of genetic variation for quantitative traits and molecular markers is estimated within and among 14 permanent lake populations of Daphnia pulicaria representing two regional groups from Oregon. Estimates of population subdivision for molecular and quantitative traits are concordant, with QST generally exceeding GST. There is no evidence that microsatellites loci are less informative about subdivision for quantitative traits than are allozyme loci. Character-specific comparison of QST and GST support divergent selection pressures among populations for the majority of life-history traits in both coast and mountain regions. The level of within-population variation for molecular markers is uninformative as to the genetic variation maintained for quantitative traits. In D. pulicaria, regional differences in the frequency of sex may contribute to variation in the maintenance of expressed within-population quantitative-genetic variation without substantially impacting diversity at the genic level. These data are compared to an identical dataset for 17 populations of the temporary-pond species, D. pulex.
Animals↗
Naturally occurring variation in bristle number and DNA polymorphisms at the scabrous locus of Drosophila melanogaster.
The association between quantitative genetic variation in bristle number and molecular variation at a candidate neurogenic locus, scabrous, was examined in Drosophila melanogaster. Approximately 32 percent of the genetic variation in abdominal bristle number (21 percent for sternopleural bristle number) among 47 second chromosomes from a natural population was correlated with DNA sequence polymorphisms at this locus. Several polymorphic sites associated with large phenotypic effects occurred at intermediate frequency. Quantitative genetic variation in natural populations caused by alleles that have large effects at a few loci and that segregate at intermediate frequencies conflicts with the classical infinitesimal model of the genetic basis of quantitative variation.
Alleles↗
Comparative losses of quantitative and molecular genetic variation in finite populations of Drosophila melanogaster.
Quantitative genetic variation, the main determinant of the ability to evolve, is expected to be lost in small populations, but there are limited data on the effect, and controversy as to whether it is similar to that for near neutral molecular variation. Genetic variation for abdominal and sternopleural bristle numbers and allozyme heterozygosity were estimated in 23 populations of Drosophila melanogaster maintained at effective population sizes of 25, 50, 100, 250 or 500 for 50 generations, as well as in 19 highly inbred populations and the wild outbred base population. Highly significant negative regressions of proportion of initial genetic variation retained on inbreeding due to finite population size were observed for both quantitative characters (b = -0.67 +/- 0.14 and -0.58 +/- 0.11) and allozyme heterozygosity (b = -0.79 +/- 0.10), and the regression coefficients did not differ significantly. Thus, quantitative genetic variation is being lost at a similar rate to molecular genetic variation. However, genetic variation for all traits was lost at rates significantly slower than predicted by neutral theory, most likely due to associative overdominance. Positive, but relatively low correlations were found among the different measures of genetic variation, but their low magnitudes were attributed to large sampling errors, rather than differences in the underlying processes of loss.
Animals↗
Developmental interactions and the constituents of quantitative variation.
Development is the process by which genotypes are transformed into phenotypes. Consequently, development determines the relationship between allelic and phenotypic variation in a population and, therefore, the patterns of quantitative genetic variation and covariation of traits. Understanding the developmental basis of quantitative traits may lead to insights into the origin and evolution of quantitative genetic variation, the evolutionary fate of populations, and, more generally, the relationship between development and evolution. Herein, we assume a hierarchical, modular structure of trait development and consider how epigenetic interactions among modules during ontogeny affect patterns of phenotypic and genetic variation. We explore two developmental models, one in which the epigenetic interactions between modules result in additive effects on character expression and a second model in which these epigenetic interactions produce nonadditive effects. Using a phenotype landscape approach, we show how changes in the developmental processes underlying phenotypic expression can alter the magnitude and pattern of quantitative genetic variation. Additive epigenetic effects influence genetic variances and covariances, but allow trait means to evolve independently of the genetic variances and covariances, so that phenotypic evolution can proceed without changing the genetic covariance structure that determines future evolutionary response. Nonadditive epigenetic effects, however, can lead to evolution of genetic variances and covariances as the mean phenotype evolves. Our model suggests that an understanding of multivariate evolution can be considerably enriched by knowledge of the mechanistic basis of character development.
Animals↗
Additive genetic variation and the distribution of QTN effects among sites.
Early quantitative genetic theories emphasize the distribution of gene effects at individual loci or the distribution of mutant effects in maintaining quantitative genetic variation, but infrequently stress the distribution of gene effects among loci. In this study, we analyse the effects of the distribution of quantitative trait nucleotides (QTN) effects among sites under artificial and stabilizing selection. Wright's formula is applied to describing the density distribution of allele frequencies of multiple diallelic QTN at the equilibrium of mutation-drift-selection. Our results demonstrate that the distribution of QTN effects among sites can affect additive genetic variation in terms of total additive variance, average gene diversity, per-class contribution of QTN effects and per-QTN contribution. When the distribution of QTN effects among sites is changed from L-shaped to bell-shaped or to be a flatter, both the total additive variance and the average gene diversity are changed. Per-class and per-QTN contributions exhibit different distribution patterns. The L-shaped distribution indicates the predominant role of the aggregative effects from the QTN of small finite effects. The bell-shaped or flatter distributions indicate the predominance of the QTN of intermediate and large effects. These predictions highlight the significance of the distribution of QTN effects among sites in interpreting the maintenance of quantitative genetic variation at the fine genome scale.
Animals↗
How closely correlated are molecular and quantitative measures of genetic variation? A meta-analysis.
The ability of populations to undergo adaptive evolution depends on the presence of quantitative genetic variation for ecologically important traits. Although molecular measures are widely used as surrogates for quantitative genetic variation, there is controversy about the strength of the relationship between the two. To resolve this issue, we carried out a meta-analysis based on 71 datasets. The mean correlation between molecular and quantitative measures of genetic variation was weak (r = 0.217). Furthermore, there was no significant relationship between the two measures for life-history traits (r = -0.11) or for the quantitative measure generally considered as the best indicator of adaptive potential, heritability (r = -0.08). Consequently, molecular measures of genetic diversity have only a very limited ability to predict quantitative genetic variability. When information about a population's short-term evolutionary potential or estimates of local adaptation and population divergence are required, quantitative genetic variation should be measured directly.
Animals↗
Precision and high-resolution mapping of quantitative trait loci by use of recurrent selection, backcross or intercross schemes.
Dissecting quantitative genetic variation into genes at the molecular level has been recognized as the greatest challenge facing geneticists in the twenty-first century. Tremendous efforts in the last two decades were invested to map a wide spectrum of quantitative genetic variation in nearly all important organisms onto their genome regions that may contain genes underlying the variation, but the candidate regions predicted so far are too coarse for accurate gene targeting. In this article, the recurrent selection and backcross (RSB) schemes were investigated theoretically and by simulation for their potential in mapping quantitative trait loci (QTL). In the RSB schemes, selection plays the role of maintaining the recipient genome in the vicinity of the QTL, which, at the same time, are rapidly narrowed down over multiple generations of backcrossing. With a high-density linkage map of DNA polymorphisms, the RSB approach has the potential of dissecting the complex genetic architecture of quantitative traits and enabling the underlying QTL to be mapped with the precision and resolution needed for their map-based cloning to be attempted. The factors affecting efficiency of the mapping method were investigated, suggesting guidelines under which experimental designs of the RSB schemes can be optimized. Comparison was made between the RSB schemes and the two popular QTL mapping methods, interval mapping and composite interval mapping, and showed that the scenario of genomic distribution of QTL that was unlocked by the RSB-based mapping method is qualitatively distinguished from those unlocked by the interval mapping-based methods.
Animals↗
Theoretical models of selection and mutation on quantitative traits.
Empirical studies of quantitative genetic variation have revealed robust patterns that are observed both across traits and across species. However, these patterns have no compelling explanation, and some of the observations even appear to be mutually incompatible. We review and extend a major class of theoretical models, 'mutation-selection models', that have been proposed to explain quantitative genetic variation. We also briefly review an alternative class of 'balancing selection models'. We consider to what extent the models are compatible with the general observations, and argue that a key issue is understanding and modelling pleiotropy. We discuss some of the thorny issues that arise when formulating models that describe many traits simultaneously.
Evolution, Molecular↗