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PubMed1991

Genetics and reproduction in fish culture.

Fish genetics has made major strides during the past 20 yr due both to improvements in the ability of fish culturists to manage reproduction and to deliberate experimentation and application. The general finding has been that the quantitative genetics of fish differ little from those of other animals and that the applications of animal improvement techniques are similar for fish and other animals. In addition, a number of novel techniques, such as ploidy manipulation and sex reversal, are relatively easy to achieve with a number of fish species. As a result, some very specialized approaches to research have been possible, and applications to fish production seem to be limited only to the imagination of the breeder. However, only limited application has occurred over a major portion of the industry, and genetic improvement of stocks has been achieved in very few instances. The reason for this apparent dichotomy between opportunity and reality seems to be related to the industry's lack of emphasis on genetic improvement.

Agriculture↗
PubMed1999

Genetic effects for plasma factor VII levels independent of and in common with triglycerides.

BACKGROUND: Coagulation factor VII has been demonstrated as a potential risk factor for cardiovascular disease. Both genes and non-genetic factors are related to plasma levels of factor VII. However, the extent to which genetic effects influence variability in plasma factor VII levels is unknown. Further, increased levels of plasma factor VII are associated with serum triglycerides, yet the reason for this association is not fully understood. METHODS AND RESULTS: Quantitative genetic analyses were applied to evaluate the relative importance of genetic and different environmental influences on plasma factor VII levels and to test the significance of genetic and environmental factors in common to factor VII and triglycerides in 215 pairs of middle-aged and elderly twins, of whom 104 were reared apart and 120 were women. Genetic influences were found to account for 57% of the individual differences in plasma factor VII levels, whereas shared-rearing and residual-familial environmental factors were not significant. Furthermore, a significant genetic correlation of 0.38 was found between factor VII and triglycerides, but the environmental correlation between these two measures was not significant. Genetic factors in common to factor VII and triglycerides explain about 7% of the total variance for factor VII. CONCLUSION: The present study suggests that there are substantial genetic influences on plasma factor VII levels. Furthermore, genetic effects explain the phenotypic association between factor VII and triglycerides.

Aged↗
PubMed2004

Multivariate genetic analysis of lifetime exercise and environmental factors.

PURPOSE: We investigated whether the association between exercise and individual-specific factors that correlate with exercise may be explained by genetic or common environmental factors. METHODS: Lifetime exercise data were available from 147 MZ and 153 DZ adult male twin pairs with a mean age of 50 yr (SD = 8 yr). RESULTS: The best-fitting quantitative genetic model for adulthood exercise level consisted of additive genetic effects, genetic effects due to dominance and unique environment effects, with genetic effects explaining 51% (95% CI = 29-63%) of the variance. Factors associated with adulthood exercise level were adolescent exercise, participation in competitive sports, perceived health, smoking status, and percent body fat. In bivariate models, approximately half of the covariation between those factors and adulthood exercise level was accounted for by unique environmental effects (i.e., factors not shared by the co-twins). Additive genetic effects explained less (3-20%) than dominance genetic effects (23-53%) of the covariation between those factors and adulthood exercise. Shared environmental effects were present only in the bivariate model of adulthood and adolescent exercise, explaining 11% of the covariance. CONCLUSIONS: : The genetic component shared in common by exercise and factors associated with exercise suggests that there may be a complex pathway of genetic selection and predisposition for a physically active lifestyle.

Adolescent↗
PubMedDate not supplied

[Accuracy of a real-time polymerase-chain-reaction assay for a quantitative estimation of genetically modified sources in food products].

The accuracy of a real-time polymerase-chain-reaction assay for genetically modified sources in food products was determined using two official test systems (kits) of primers and samples. These kits were recommended by the Federal Center of State Sanitary and Epidemiological Surveillance (Russian Ministry of Health) and the European Commission. We used the following three models of thermocyclers: iCycler iQ (BioRad, United States), Rotor-Gene 3000 (Corbett Research, Australia), and DT-322 (DNA-Technology, Russia). Studies of samples that contained 1% genetically modified sources showed that the error of a quantitative assay for genetically modified sources in food products corresponds to 20-30% and does not depend on the kit type and the thermocycler model used.

DNA Primers↗
PubMed1990

Population structure analysis using polygenic traits: estimation of migration matrices.

Many studies of subdivided populations have attempted to determine the underlying migration rates that generate observed patterns of genetic differentiation. Most previous analyses have yielded only qualitative inferences about migration. In this paper I present a new method for estimating the full migration matrix from information on polygenic trait variation. The method employs multivariate quantitative genetic theory to provide a matrix formulation of the expected covariance structure in multigenerational subdivided populations for which information is available at different points in the life cycle. I develop a restricted maximum likelihood technique (REML) to take account of this additional life-cycle information and to estimate both the migration matrix and the ratio of effective population size to census size. To make the problem computationally tractable, the migration matrix is modeled as a log-linear function of a few covariates, such as subdivision size and geographic distance. I apply the technique to data on dermatoglyphic ridge counts for 1015 individuals of the Jirel population of east Nepal, considering two different age cohorts. In the adult cohort (individuals over 21 years of age) I examine data by both birthplace and residence and for the subadult cohort (under 21 years of age), by birthplace. Results from the REML technique reveal that the best-fitting migration model is a finite island model with an estimated endemicity of 0.730 +/- 0.105 and an estimated ratio of effective size to census size of 0.287 +/- 0.095. Both estimates are reasonable given known demographic data. In addition, Fst values predicted by the migration model are concordant with REML estimates obtained directly from the dermatoglyphic variation.

Adolescent↗
PubMed2001

Genetic control of coordinated changes in HDL and LDL size phenotypes.

We investigated the correlation of high density lipoprotein (HDL) and low density lipoprotein (LDL) particle size distributions in samples from >1100 participants in the San Antonio Family Heart Study. By use of analyses of individual correlations of each HDL fraction with each LDL fraction, we devised new metrics for particle size phenotype, termed DeltaHDL and DeltaLDL, to optimally reflect the size correlations. Confirming previous studies, we found that the 2 size phenotype variables were positively correlated (r=0.51). Quantitative genetic analysis indicated that nearly half (44%) of the variance in DeltaHDL and in DeltaLDL was explained by the additive effects of genes. Bivariate genetic analyses indicated that a positive genetic correlation (rho(G)=0.56) exists between them and suggested that the pleiotropic effects of a gene or group of genes account for approximately 31% [ie, rho(G)(2) =(0.56)(2)=0.31] of the genetic variance in the 2 traits. Triglyceride (TG) levels were negatively related to DeltaHDL and DeltaLDL, with phenotypic correlations of -0.48 and -0.58, respectively, and genetic correlations of -0.45 and -0.76, respectively, suggesting that genes exert significant pleiotropic effects on the covariation of TGs with each of the size variables. Finally, we evaluated a bivariate model for DeltaHDL and DeltaLDL in which TG level was included as a covariate. This analysis indicated that a small but significant genetic correlation remains for DeltaHDL and DeltaLDL, even after accounting for the effects of TGs. Thus, our study demonstrates that the phenotypic correlation of HDL and LDL sizes results in part from the pleiotropic actions of a set of genes, some of which also influence TG levels and some of which do not.

Coronary Disease↗
PubMed1980

Multiple structural genes for mouse amylase.

Salivary and pancreatic amylases from the mouse show both structural and quantitative genetic variation encoded within a gene complex on chromosome 3. Two fundamental questions prompted by this variation are whether salivary and pancreatic amylases are derived from different structural genes and whether multiple structural genes are causing the quantitative variation observed in each of the two amylases. These questions were approached by comparing the amylase protein from 12 congenic lines carrying amylase gene complexes derived from different origins. The amylases were purified by affinity chromatography employing the inhibitor cyclohepta-amylose and characterized in terms of amino acid composition, specific activity, molecular weight, and heat stability. They were analyzed by native electrophoresis in polyacrylamide gels and by peptide mapping employing both cyanogen bromide cleavage and restricted proteolysis in the presence of dodecylsulfate. By these techniques, many differences in the structure of pancreatic amylase that were not reflected in the salivary amylase were found among mouse strains. Likewise, a distinct salivary amylase variant was found. These results suggest that independent structural genes exist for the two amylases. Furthermore, by all criteria used, pancreatic amylase from single strains exhibits molecular heterogeneity, whereas heterogeneity was never found for salivary amylase. We conclude that at least four structural genes code for pancreatic amylase while only a single gene, different from any of the pancreatic genes, codes for salivary amylase.

Amylases↗
PubMed1993

A third source of developmental differences.

An illustrative list is presented of human and animal studies which each point to the existence of a third source, in addition to genetic and environmental factors, underlying phenotypic differences in development. It is argued that this third source may consist of nonlinear epigenetic processes that can create variability at all phenotypical-somatic and behavioral-levels. In a quantitative genetic analysis with human subjects, these processes are confounded with within-family environmental influences. A preliminary model to quantify these influences is introduced.

Animals↗
PubMed2005

Conservation genetics of amphibians.

Amphibians are good models for investigating the genetics of wild animal populations because they are: (1) widely distributed in most ecosystems; (2) easy to sample in breeding assemblages; (3) often philopatric to breeding sites, generating high levels of population genetic structure; (4) amenable to controlled crossings in the laboratory; and (5) of major conservation concern. Neutral genetic markers, mostly microsatellites, have been used successfully in studies of amphibian effective population sizes and structures, and in assessing the consequences of hybridisation. Phylogeography has provided important insights into population histories and the fates of introductions. Quantitative genetic methods have demonstrated adaptive variation in life history traits of importance to fitness and therefore to population viability.

Amphibians↗
PubMed2005

Invasion success and genetic diversity of introduced populations of guppies Poecilia reticulata in Australia.

High genetic diversity is thought to characterize successful invasive species, as the potential to adapt to new environments is enhanced and inbreeding is reduced. In the last century, guppies, Poecilia reticulata, repeatedly invaded streams in Australia and elsewhere. Quantitative genetic studies of one Australian guppy population have demonstrated high additive genetic variation for autosomal and Y-linked morphological traits. The combination of colonization success, high heritability of morphological traits, and the possibility of multiple introductions to Australia raised the prediction that neutral genetic diversity is high in introduced populations of guppies. In this study we examine genetic diversity at nine microsatellite and one mitochondrial locus for seven Australian populations. We used mtDNA haplotypes from the natural range of guppies and from domesticated varieties to identify source populations. There were a minimum of two introductions, but there was no haplotype diversity within Australian populations, suggesting a founder effect. This was supported by microsatellite markers, as allelic diversity and heterozygosity were severely reduced compared to one wild source population, and evidence of recent bottlenecks was found. Between Australian populations little differentiation of microsatellite allele frequencies was detected, suggesting that population admixture has occurred historically, perhaps due to male-biased gene flow followed by bottlenecks. Thus success of invasion of Australia and high additive genetic variance in Australian guppies are not associated with high levels of diversity at molecular loci. This finding is consistent with the release of additive genetic variation by dominance and epistasis following inbreeding, and with disruptive and negative frequency-dependent selection on fitness traits.

Animals↗
PubMed1987

Genetic differentiation of quantitative characters between populations or species. II: Optimal selection in infinite populations.

Using a new and more general genetic model called the discrete-allelic state model and assuming discrete-time process, the evolutionary changes of genetic variation of quantitative characters, controlled by a few loci, within and between populations during the process of genetic differentiation of populations or species, are studied under the effects of mutation and centripetal selection in infinitely large populations. While in a finite population and ignoring selection, the rate of change of additive genetic variance depends on mutation and effective population size, traits under optimal selection in infinitely large populations go through the dynamics of a rather complicated form depending on the relative intensities of selection and mutation. When a population, which has reached steady-state by mutation-selection balance, splits into two, in one of which the same optimum genotype holds but in the other the optimum shifts a few standard deviations away from the original optimum, the corresponding daughter population starts differentiating from its sister population by favouring certain class of mutant alleles and discarding others which were originally favoured. During this process of turn over of genes, both the intra- and inter-populational variances undergo a complicated change, and the ratio of the former to the latter is a non-linear function of time of divergence. This pattern is qualitatively very different from the case when selection is absent. The intra-population distribution of genotypic values, during this transition, is shown to deviate considerably from normality. The presence of linkage seems to retard the accumulation of intra-populational genetic variance. The implications of these results are discussed in comparison with the earlier findings of evolutionary models of quantitative traits.

Alleles↗
PubMed2006

Estimating maternal genetic effects in livestock.

This study investigates the estimation of direct and maternal genetic (co)variances, accounting for environmental covariances between direct and maternal effects. Estimated genetic correlations between direct and maternal effects presented in the literature have often been strongly negative, and their validity has been questioned. Explanations of extreme estimates have focused on the existence of environmental covariances between dam and offspring. As a solution, models including a regression on dam-phenotype have been proposed, but have yielded biased estimates. The performance of models that implement the variance structure arising from the classical model of Willham, however, has not been evaluated. This study investigated the covariance structure of the parts of the residual term that arise from Willham's model. Results show that a correlation between the residual of the record of an individual and that of its dam is a direct consequence of combining Willham's model with the usual assumption that phenotypic covariances between different traits are the sum of additive genetic and environmental covariances. Stochastic simulations show that fitting this structure yields unbiased estimates of the genetic (co)variances. When correlated residuals were ignored in the cases investigated, the bias in the estimated genetic correlations was approximately equal to the value of the environmental correlation. In contrast to models including a regression on dam-phenotype, there were no difficulties with interpretation of results, and the approach was consistent with standard quantitative genetic theory. The use of Willham's model while accounting for correlated residuals is conceptually appealing and yields unbiased results, with no need for regression on dam phenotype. Inclusion of the ability to fit the residual variance structure required for maternal effects into existing software packages would be helpful to animal breeders.

Animals↗
PubMed2001

Three loci modify growth of a transgene-induced mammary tumor: suppression of proliferation associated with decreased microvessel density.

In earlier studies it was observed that the genetic background significantly affected the phenotype of a transgene-induced mammary tumor. Tumors arising in an (I/LnJ x PyMT) F1 hybrid background appeared earlier than in the FVB/N-TgN(MMTV-PyVT)(634Mul) parent, but accumulated less tumor mass, indicating a net decrease in tumor growth. Quantitative genetic mapping in a backcross identified three loci that were associated with the decreased proliferative capacity of the I/LnJ F1 tumors. Molecular analysis of the tumors suggests that these loci may act by restricting the tumor's ability to recruit microvessels. The three loci, designated Mmtg1-3, are unlinked to the angiogenic genes Fgf2, Flt1, Flk4, Flk1, Vegf, and Vegfc, as well as the precursors of the endogenous antiangiogenic molecules angiostatin and endostatin. The Mmtg loci may therefore provide novel targets for antiangiogenic therapeutic strategies.

Animals↗
PubMed2003

Selective and genetic constraints on the evolution of body size in a stream-dwelling salmonid fish.

To examine constraints on evolution of larger body size in two stunted populations of brook charr (Salvelinus fontinalis) from a single river in Cape Race, Newfoundland, Canada, we measured viability selection acting on length-at-age traits, and estimated quantitative genetic parameters in situ (following reconstruction of pedigree information from microsatellite data). Furthermore we tested for phenotypic differentiation between the populations, and for association of high juvenile growth with early maturity that is predicted by life history theory. Within each population, selection differentials and estimates of heritabilities for length-at-age traits suggested that evolution of larger size is prevented by both selective and genetic constraints. Between the populations, phenotypic differentiation was found in length-at-age and age of maturation traits, whereas early maturation was associated with increased juvenile growth (relative to adult growth) both within and between populations. The results suggest an adaptive plastic response in age of maturation to juvenile growth rates that have a largely environmental basis of determination.

Adaptation, Physiological↗
PubMed2001

The genetic architecture of quantitative traits.

Phenotypic variation for quantitative traits results from the segregation of alleles at multiple quantitative trait loci (QTL) with effects that are sensitive to the genetic, sexual, and external environments. Major challenges for biology in the post-genome era are to map the molecular polymorphisms responsible for variation in medically, agriculturally, and evolutionarily important complex traits; and to determine their gene frequencies and their homozygous, heterozygous, epistatic, and pleiotropic effects in multiple environments. The ease with which QTL can be mapped to genomic intervals bounded by molecular markers belies the difficulty in matching the QTL to a genetic locus. The latter requires high-resolution recombination or linkage disequilibrium mapping to nominate putative candidate genes, followed by genetic and/or functional complementation and gene expression analyses. Complete genome sequences and improved technologies for polymorphism detection will greatly advance the genetic dissection of quantitative traits in model organisms, which will open avenues for exploration of homologous QTL in related taxa.

Animals↗
PubMed2006

The genetics of attention deficit hyperactivity disorder.

Over the past 15 years, considerable progress has been made in understanding the etiology of childhood Attention Deficit Hyperactivity Disorder (ADHD), largely due to the publication of numerous twin studies which are consistent in suggesting substantial genetic influences (i.e., heritabilities ranging from 60% to 90%), non-shared environmental influences that are small-to-moderate in magnitude (i.e., ranging from 10% to 40%), and little-to-no shared environmental influences. Following from these quantitative genetic findings, numerous molecular genetic studies of association and linkage between ADHD and a variety of candidate genes have been conducted during the past 10 years. The majority of the candidate genes studied underlie various facets of the dopamine, norepinephrine, and serotonin neurotransmitter systems, although the etiological role of candidate genes outside of neurotransmitter systems (e.g., involved in various aspects of brain and nervous system development) have also been examined. In this paper, we review recent findings from candidate gene studies of childhood ADHD and highlight those candidate genes for which associations are most replicable and which thus appear most promising. We conclude with a consideration of some of the emerging themes that will be important in future studies of the genetics of ADHD.

Attention Deficit Disorder with Hyperactivity↗
PubMed1991

A genetic-correlational study of hippocampal neurochemical variation and variation in exploratory activities of mice.

Previously, we have demonstrated that hippocampal mossy fibers, containing the opioid peptide dynorphin B, are functionally connected with the gene-dependent exploratory behavior of mice. In order to seek further evidence of causal relationships between dynorphin B action and exploration, a quantitative-genetic method was chosen. For this purpose, mice from the inbred strains C57BL/6, DBA/2, BLN, and CPB-K were used. By means of radioimmunoassay, the hippocampal level of dynorphin B was monitored in mice that had been exposed to environmental novelty, as compared to naive animals. Clear evidence was obtained that novelty induces the release of hippocampal dynorphin B. Furthermore, low tissue content was found to be causally connected with high exploratory scores.

Animals↗
PubMed2002

Genetic analyses of endoreduplication in Zea mays endosperm: evidence of sporophytic and zygotic maternal control.

Flow cytometry was used to assess the variability of endoreduplication in endosperms of maize inbred lines. Little variation was found between midwestern dent types, and high levels of endoreduplication were observed in popcorns. Endoreduplication is different between inbred lines by 13-18 days after pollination, and flow cytometric analysis of ploidy level was feasible until 20 DAP. To study the genetic regulation of endoreduplication, four inbreds were crossed to B73 and developing endosperms from both parental, reciprocal F(1), and backcross generations were subjected to flow cytometric analysis. Three measurements of endoreduplication were calculated from these data and analyzed as quantitative genetic traits. Multiple models of trait inheritance were considered including triploid, diploid, sporophytic maternal, and maternal and paternal zygotic nuclear inheritance. Maternal zygotic effects, often considered a form of parental imprinting, and maternal sporophytic effects were detected. To test the feasibility of introgressing a high endoreduplication phenotype into a midwestern dent inbred line, a backcross population was generated from B73 x Sg18. Parental and progeny endoreduplication levels were compared and heritabilities assessed. The heritabilities calculated from these data generally agree with the values calculated in the larger crossing experiments.

Analysis of Variance↗