PubMed Health⌕ Search

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.

At least 37 records · Page 2Linked to original sources
PubMed2002

The nature of quantitative genetic variation for Drosophila longevity.

Longevity is a typical quantitative trait: the continuous variation in life span observed in natural populations is attributable to genetic variation at multiple quantitative trait loci (QTL), environmental sensitivity of QTL alleles, and truly continuous environmental variation. To begin to understand the genetic architecture of longevity at the level of individual QTL, we have mapped QTL for Drosophila life span that segregate between two inbred strains that were not selected for longevity. A mapping population of 98 recombinant inbred lines (RIL) was derived from these strains, and life span of virgin male and female flies measured under control culture conditions, chronic heat and cold stress, heat shock and starvation stress, and high and low density larval environments. The genotypes of the RIL were determined for polymorphic roo transposable element insertion sites, and life span QTL were mapped using composite interval mapping methods. A minimum of 19 life span QTL were detected by recombination mapping. The life span QTL exhibited strong genotype by sex, genotype by environment, and genotype by genotype (epistatic) interactions. These interactions complicate mapping efforts, but evolutionary theory predicts such properties of segregating QTL alleles. Quantitative deficiency mapping of four longevity QTL detected in the control environment by recombination mapping revealed a minimum of 11 QTL in these regions. Clearly, longevity is a complex quantitative trait. In the future, linkage disequilibrium mapping can be used to determine which candidate genes in a QTL region correspond to the genetic loci affecting variation in life span, and define the QTL alleles at the molecular level.

Animals↗
PubMed2002

Fluctuating environments and the role of mutation in maintaining quantitative genetic variation.

We study a class of genetic models in which a quantitative trait determined by several additive loci is subject to temporally fluctuating selection. Selection on the trait is assumed to be stabilizing but with an optimum that varies periodically and might be perturbed stochastically. The population mates at random, is infinitely large and has discrete generations. We pursue a statistical and numerical approach, covering a wide range of ecological and genetic parameters, to determine the potential of fluctuating environments to maintain quantitative genetic variation. Whereas, in contrast to some recent claims, this potential seems to be rather limited in the absence of recurrent mutation, fluctuating environments might, in combination with it, often generate high levels of additive genetic variation. We investigate how the genetic variation maintained depends on the ecological parameters and on the underlying genetics.

Genetic Variation↗
PubMed1991

Soft selection and quantitative genetic variation: a laboratory experiment.

The effect of environmental heterogeneity on the genetic variation of different quantitative characters was studied in two laboratory and two recently captured populations of Drosophila melanogaster. Two different culture media (habitats R and G) were used. Coarse-grained heterogeneity with independent density control in each habitat (R + G), and fine-grained (R/G) heterogeneity were simulated in population cages. Control populations in both R and G habitats were also maintained. Genetic differences for oviposition-site preference, larval preference and/or within-habitat viability were found between subpopulations sampled from different media. This happened in all four populations maintained on R + G, two populations maintained on R/G, and one control population. Thus, environmental heterogeneity seems to protect genetic variability responsible for between-habitat genetic differentiation, particularly when such heterogeneity corresponds to the 'soft selection' model (R + G). However, for the quasi-neutral trait sternopleural bristle number, no genetic between-habitat differentiation, nor increased heritability were observed in populations maintained under any kind of environmental heterogeneity. Hence, although soft selection seems to be a real force in determining adaptation to heterogeneous environments, the genetic variability maintained may be small in relation to the whole genome.

Animals↗
PubMed2005

Transforming growth factor-beta2 is involved in quantitative genetic variation in thymic involution.

The mechanisms regulating thymic involution are unclear. In inbred mouse strains the rate of thymic involution and the function of the hematopoietic stem cell (HSC) compartment are subject to quantitative genetic variation. We have shown previously that transforming growth factor-beta2 (TGF-beta2) is a genetically determined positive regulator of HSCs. Here, we demonstrate that genetic variation in the rate of thymic involution correlates with genetic variation in the responsiveness of hematopoietic stem and progenitor cells to TGF-beta2. Corroborating these correlations, thymic cellularity and peripheral naive T-cell frequency were higher in old Tgfb2+/- mice than in wild-type littermates. The frequency of early T-cell precursors was increased in Tgfb2+/- mice, suggesting that TGF-beta2 affects the earliest stages of T-cell development in old mice. Reciprocal transplantation experiments indicated that TGF-beta2 expressed both in the (micro)environment and in the hematopoietic system can accelerate thymic involution; however, the age of the stem cells appeared irrelevant. Thus, although thymic involution is largely determined by the aged environment, TGF-beta2 plays a major modulatory role that is subject to genetic variation and is possibly mediated through its regulatory effects on early hematopoiesis.

Aging↗
PubMed2000

Quantitative genetic variation in Daphnia: temporal changes in genetic architecture.

Nonadditive genetic variation and genetic disequilibrium are two important factors that influence the evolutionary trajectory of natural populations. We assayed quantitative genetic variation in a temporary-pond-dwelling population of Daphnia pulex over a full season to examine the role of nonadditive genetic variation and genetic disequilibrium in determining the short-term evolutionary trajectory of a cyclic parthenogen. Quantitative traits were influenced by three factors: (1) clonal selection significantly changed the population mean phenotype during the course of the growing season; (2) sexual reproduction and recombination led to significant changes in life-history trait means and the levels of expressed genetic variation, implying the presence of substantial nonadditive genetic variation and genetic disequilibrium; and (3) Egg-bank effects were found to be an important component of the realized year-to-year change. Additionally, we examined the impact of genetic disequilibria induced by clonal selection on the genetic (co)variance structure with a common principal components model. Clonal selection caused significant changes in the (co)variance structure that were eliminated by a single bout of random mating, suggesting that a build-up of disequilibria was the primary source of changes in the (co)variance structure. The results of this study highlight the complexity of natural selection operating on populations that undergo alternating phases of sexual and asexual reproduction.

Animals↗
PubMed2004

Quantitative genetic variation: a post-modern view.

It has become commonplace to map individual quantitative trait loci (QTL) in experimental organisms; the means (line-crosses and dense maps of markers) and motivation (the close relationship between continuous physiological traits and common, complex diseases) are self-evident. Progress in mapping human QTL has been more gradual, an inevitable consequence of genetic mapping in a natural population setting. The common objective of these studies has been to understand the molecular mechanisms underlying individual QTL. Recent theoretical and practical advances shift this focus to a more comprehensive or genomic perspective on quantitative variation. Fisher's infinitesimal model of adaptive evolution, which satisfied quantitative geneticists for over 50 years, has been modified in the light of data from QTL mapping experiments in plants and animals. The resulting exponential model provides a pleasing empirical fit to the distribution of QTL effect sizes, predicts that a large amount of quantitative variation will be explained by a limited number of genes and suggests a new mathematical framework for linkage mapping. Molecular analysis of QTL suggests that coding variants (e.g. allozymes) underlie a fraction of quantitative variation and that variants that affect gene expression (expression QTL, eQTL) have a substantial role. This is supported by genomic experiments that combine expression profiling with classical genetic mapping approaches to reveal a remarkable wealth of quantitative heritable variation in the transcriptome and that cis-and trans-acting regulatory factors are organized in networks reflecting pleiotropy. It is hoped that these advances will enhance our understanding of the genetic basis of complex inherited diseases.

Animals↗
PubMed2004

Quantitative genetic variation in an island population of the speckled wood butterfly (Pararge aegeria).

Evidence of changes in levels of genetic variation in the field is scarce. Theoretically, selection and a bottleneck may lead to the depletion of additive genetic variance (V(A)) but not of nonadditive, dominance variance (V(D)), although a bottleneck may converse V(D) to V(A). Here we analyse quantitative genetic variation for the Speckled Wood butterfly Pararge aegeria on the island of Madeira about 120 generations after first colonisation. Colonisation of the island involved both a bottleneck and strong natural selection, changing the average value of traits. Several life history and morphological traits with varying levels of change since colonisation were analysed. In accordance with expectations, all traits except one showed relatively low levels of V(A), with an average heritability (h(2)) of 0.078. Levels of V(D) for these traits were relatively high, 20-94% of total variance and on average 80% of V(G). The exception was a morphological trait that probably had not experienced strong natural selection after colonisation, for which a h(2) of 0.27 was found. Another interesting observation is that the population seems resistant to inbreeding effects, which may be the result of purging of deleterious alleles.

Animals↗
PubMed1991

Quantitative genetic variation of esterase activity associated with a gene amplification in Culex quinquefasciatus.

Amplification of the esterase B1 gene is responsible for insecticide resistance in the mosquito Culex quinquefasciatus. We used a mating scheme to isolate chromosomes carrying amplified esterase genes from a long-selected laboratory strain (Tem-R) to determine whether observed variation in esterase activity had a genetic basis. The amplified esterase genes segregated as a block and a possible newly arisen esterase B1 copy-number variant was found among the progeny of females which carried amplified B1 genes on only one homologue. A quantitative genetic analysis found significant genetic variation of esterase activity among families which carried different amplification-bearing chromosomes from the Tem-R strain. Esterase B1 copy-number variation among these Tem-R chromosomes is the most likely basis for the observed genetic variation in esterase activity.

Analysis of Variance↗
PubMed2000

Importance of quantitative genetic variations in the etiology of hypertension.

Recent progress has been remarkable in identifying mutations which cause diseases (mostly uncommon) that are inherited simply. Unfortunately, the common diseases of humankind with a strong genetic component, such as those affecting cardiovascular function, have proved less tractable. Their etiology is complex with substantial environmental components and strong indications that multiple genes are implicated. In this article, we consider the genetic etiology of essential hypertension. After presenting the distribution of blood pressures in the population, we propose the hypothesis that essential hypertension is the consequence of different combinations of genetic variations that are individually of little consequence. The candidate gene approach to finding relevant genes is exemplified by studies that identified potentially causative variations associated with quantitative differences in the expression of the angiotensinogen gene (AGT). Experiments to test causation directly are possible in mice, and we describe their use to establish that blood pressures are indeed altered by genetic changes in AGT expression. Tests of differences in expression of the genes coding for the angiotensin-converting enzyme (ACE) and for the natriuretic peptide receptor A are also considered, and we provide a tabulation of all comparable experiments in mice. Computer simulations are presented that resolve the paradoxical finding that while ACE inhibitors are effective, genetic variations in the expression of the ACE gene do not affect blood pressure. We emphasize the usefulness of studying animals heterozygous for an inactivating mutation and a wild-type allele, and briefly discuss a way of establishing causative links between complex phenotypes and single nucleotide polymorphisms.

Animals↗
PubMed2000

Quantitative genetic variation of leaf size and shape in a mixed diploid and triploid population of Populus.

In the interspecific cross of Populus trichocarpa x P. deltoides, unexpected simultaneous occurrence of diploid hybrids and triploid hybrids (with two alleles from the female parent and one from the male parent at each locus) led us to examine the evolutionary genetic significance of this phenomenon. As expected, leaf size and shape of the triploid progeny are closer to the female P. trichocarpa than male P. deltoides parent. Although the pure triploid progeny population did not have higher genetic variance in leaf traits than the pure diploid population, the former appears to hide much non-additive genetic variance and display strong genetic control over the phenotypic plasticity of leaf traits. It is suggested that the cryptic non-additive variance, especially epistasis, can be released when a population is disturbed by changes in the environment. A mixed diploid and triploid progeny population combines phenotypic and genetic characteristics of both pure hybrids and is considered to be of adaptive significance for populars to survive and evolve in a fluctuating environment. The significant effect due to general and specific combining ability differences at the population level suggests that the population divergence of these two species is under additive and non-additive genetic control.

Diploidy↗
PubMed1993

Population structure in Daphnia obtusa: quantitative genetic and allozymic variation.

Quantitative genetic analyses for body size and for life history characters within and among populations of Daphnia obtusa reveal substantial genetic variance at both hierarchical levels for all traits measured. Simultaneous allozymic analysis on the same population samples indicate a moderate degree of differentiation: GST = 0.28. No associations between electrophoretic genotype and phenotypic characters were found, providing support for the null hypothesis that the allozymic variants are effectively neutral. Therefore, GST can be used as the null hypothesis that neutral phenotypic evolution within populations led to the observed differentiation for the quantitative traits, which I call QST. The results of this study provide evidence that natural selection has promoted diversification for body size among populations, and has impeded diversification for relative fitness. Analyses of population differentiation for clutch size, age at reproduction, and growth rate indicate that neutral phenotypic evolution cannot be excluded as the cause.

Analysis of Variance↗
PubMed2004

The effect of temperature and wing morphology on quantitative genetic variation in the cricket Gryllus firmus, with an appendix examining the statistical properties of the Jackknife-MANOVA method of matrix comparison.

We investigated the effect of temperature and wing morphology on the quantitative genetic variances and covariances of five size-related traits in the sand cricket, Gryllus firmus. Micropterous and macropterous crickets were reared in the laboratory at 24, 28 and 32 degrees C. Quantitative genetic parameters were estimated using a nested full-sib family design, and (co)variance matrices were compared using the T method, Flury hierarchy and Jackknife-manova method. The results revealed that the mean phenotypic value of each trait varied significantly among temperatures and wing morphs, but temperature reaction norms were not similar across all traits. Micropterous individuals were always smaller than macropterous individuals while expressing more phenotypic variation, a finding discussed in terms of canalization and life-history trade-offs. We observed little variation between the matrices of among-family (co)variation corresponding to each combination of temperature and wing morphology, with only one matrix of six differing in structure from the others. The implications of this result are discussed with respect to the prediction of evolutionary trajectories.

Analysis of Variance↗
PubMed2001

Effects of bottlenecks on quantitative genetic variation in the butterfly Bicyclus anynana.

The effects of a single population bottleneck of differing severity on heritability and additive genetic variance was investigated experimentally using a butterfly. An outbred laboratory stock was used to found replicate lines with one pair, three pairs and 10 pairs of adults, as well as control lines with approximately 75 effective pairs. Heritability and additive genetic variance of eight wing pattern characters and wing size were estimated using parent-offspring covariances in the base population and in all daughter lines. Individual morphological characters and principal components of the nine characters showed a consistent pattern of treatment effects in which average heritability and additive genetic variance was lower in one pair and three pair lines than in 10 pair and control lines. Observed losses in heritability and additive genetic variance were significantly greater than predicted by the neutral additive model when calculated with coefficients of inbreeding estimated from demographic parameters alone. However, use of molecular markers revealed substantially more inbreeding, generated by increased variance in family size and background selection. Conservative interpretation of a statistical analysis incorporating this previously undetected inbreeding led to the conclusion that the response to inbreeding of the morphological traits studied showed no significant departure from the neutral additive model. This result is consistent with the evidence for minimal directional dominance for these traits. In contrast, egg hatching rate in the same experimental lines showed strong inbreeding depression, increased phenotypic variance and rapid response to selection, highly indicative of an increase in additive genetic variance due to dominance variance conversion.

Analysis of Variance↗
PubMed1996

A comparison of isozyme and quantitative genetic variation in Pinus contorta ssp. latifolia by FST.

We employed F-statistics to analyze quantitative and isozyme variation among five populations of Pinus contorta ssp. latifolia, a wind-pollinated outcrossing conifer with wide and continuous distribution in west North America. Estimates of population differentiation (FST) for six quantitative traits were compared with the overall estimate of the differentiation (F*ST) from 19 isozymes that tested neutral to examine whether similar evolutionary processes were involved in morphological and isozyme differentiation. While the FST estimates for specific gravity, stem diameter, stem height and branch length were significantly greater than the F*ST estimate, as judged from the 95% confidence intervals by bootstrapping, the FST estimates for branch angle and branch diameter were indistinguishable from the F*ST estimate. Differentiation in stem height and stem diameter might reflect the inherent adaptation of the populations for rapid growth to escape suppression by neighboring plants during establishment and to regional differences in photoperiod, precipitation and temperature. In contrast, divergences in wood specific gravity and branch length might be correlated responses to population differentiation in stem growth. Possible bias in the estimation of FST due to Hardy-Weinberg disequilibrium (FIS not equal to 0), linkage disequilibrium, maternal effects and nonadditive genetic effects was discussed with special reference to P. contorta ssp. latifolia.

Genetic Variation↗
PubMed1996

Genetic markers and quantitative genetic variation in Medicago truncatula (Leguminosae): a comparative analysis of population structure.

Two populations of the selfing annual Medicago truncatula Gaertn. (Leguminoseae), each subdivided into three subpopulations, were studied for both metric traits (quantitative characters) and genetic markers (random amplified polymorphic DNA and one morphological, single-locus marker). Hierarchical analyses of variance components show that (1) populations are more differentiated for quantitative characters than for marker loci, (2) the contribution of both within and among subpopulations components of variance to overall genetic variance of these characters is reduced as compared to markers, and (3) at the population level, within population structure is slightly but not significantly larger for markers than for quantitative traits. Under the hypothesis that most markers are neutral, such comparisons may be used to make hypotheses about the strength and heterogeneity of natural selection in the face of genetic drift and gene flow. We thus suggest that in these populations, quantitative characters are under strong divergent selection among populations, and that gene flow is restricted among populations and subpopulations.

Biological Evolution↗
PubMed1980

Unequal crossing over at the rRNA tandon as a source of quantitative genetic variation in Drosophila.

Abdominal bristle selection lines (three high and three low) and controls were founded from a marked homozygous line to measure the contribution of sex-linked "mutations" to selection response. Two of the low lines exhibited a period of rapid response to selection in females, but not in males. There were corresponding changes in female variance, in heritabilities in females, in the sex ratio (a deficiency of females) and in fitness, as well as the appearance of a mutant phenotype in females of one line. All of these changes were due to bb alleles (partial deficiencies for the rRNA tandon) in the X chromosomes of these lines, while the Y chromosomes remained wild-type bb+. We argue that the bb alleles arose by unequal crossing over in the rRNA tandon.--A prediction of this hypothesis is that further changes can occur in the rRNA randon as selection is continued. This has now been shown to occur.--Our minimum estimate of the rate of occurrence of changes at the rRNA tandom is 3 X 10(-4). As this is substantially higher than conventional mutation rates, the questions of the mechanisms and rates of origin of new quantitative gaenetic variation require careful re-examination.

Animals↗
PubMed1986

Quantitative genetic variation in the skeleton of the mouse: II. Description of variation within and between inbred strains.

Variation in the skeletons of over 400 male and female mice from 12 genotypes was investigated by using multivariate statistical methods. A series of discriminant functions explains the differences in the shape of six bones: mandible, os coxae, femur, tibia-fibula, scapula, and humerus. The anatomical features of bone shape described by these functions are summarized together with illustrations of the typical shapes of each bone from the 12 genotypes. Variability within genotypes was investigated by using the Mahalanobis D2 distance--a measure of the difference between two points representing multivariate data--from the group mean. A series of variants were detected ranging from grossly abnormal bones to bones showing subtle differences localized to specific regions. Examples of the variants found are illustrated.

Animals↗