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PubMed2001

Power and robustness of a score test for linkage analysis of quantitative traits using identity by descent data on sib pairs.

Identification of genes involved in complex traits by traditional (lod score) linkage analysis is difficult due to many complicating factors. An unfortunate drawback of non-parametric procedures in general, though, is their low power to detect genetic effects. Recently, Dudoit and Speed [2000] proposed using a (likelihood-based) score test for detecting linkage with IBD data on sib pairs. This method uses the likelihood for theta, the recombination fraction between a trait locus and a marker locus, conditional on the phenotypes of the two sibs to test the null hypothesis of no linkage (theta = (1/2)). Although a genetic model must be specified, the approach offers several advantages. This paper presents results of simulation studies characterizing the power and robustness properties of this score test for linkage, and compares the power of the test to the Haseman-Elston and modified Haseman-Elston tests. The score test is seen to have impressively high power across a broad range of true and assumed models, particularly under multiple ascertainment. Assuming an additive model with a moderate allele frequency, in the range of p = 0.2 to 0.5, along with heritability H = 0.3 and a moderate residual correlation rho = 0.2 resulted in a very good overall performance across a wide range of trait-generating models. Generally, our results indicate that this score test for linkage offers a high degree of protection against wrong assumptions due to its strong robustness when used with the recommended additive model.

Computer Simulation↗
PubMedDate not supplied

Adjusting for confounding due to population admixture when estimating the effect of candidate genes on quantitative traits.

When analyzing the relationship between allelic variability and traits, a potential source of confounding is population admixture. An approach to adjusting for potential confounding due to population admixture when estimating the influence of allelic variability at a candidate gene is presented. The approach involves augmenting linear regression models with additional regressors. Family genotype data are used to define the regressors, and inclusion of the regressors ensures that, even in the presence of population admixture, the estimates of the regression coefficients that parameterize the influence of allelic variability on the trait are unbiased. The approach is illustrated through an analysis of the influence of apolipoprotein E genotype on plasma low density lipoprotein cholesterol concentrations.

Alleles↗
PubMed2005

Identification of carcass and meat quality quantitative trait loci in a Landrace pig population selected for growth and leanness.

The identification of QTL related to production traits that are relevant for the pig industry has been mostly performed by using divergent crosses. The main objective of the current study was to investigate whether these growth, fatness, and meat quality QTL, previously described in diverse experimental populations, were segregating in a Landrace commercial population selected for litter size, backfat thickness, and growth performance. We have found QTL for carcass weight (posterior P > 0.75), cutlet weight (posterior P > 0.99), weight of ham (posterior P > 0.75), shoulders weight (posterior probability > 0.99), and shear firm-ness (posterior P > 0.99) on pig Chromosome 2. Moreover, QTL with posterior P > 0.75 for fat thickness between the 3rd and 4th ribs (Chromosome 7), rib weights (Chromosome 8), backfat thickness (Chromosomes 8, 9, and 10), and b Minolta color component (Chromosome 7) were identified. These results indicate that commercial purebred populations retain a significant amount of genetic variation, even for traits that have been selected for many generations.

Adipose Tissue↗
PubMed1998

Quantitative trait loci analysis of human event-related brain potentials: P3 voltage.

The P3 event-related brain potential (ERP) is a positive-going voltage change of scalp-recorded electroencephalographic activity that occurs between 300-500 ms after stimulus onset. It is elicited when a stimulus is perceived, memory operations are engaged, and attentional resources are allocated toward its processing. Because this ERP component reflects fundamental cognitive processing, it has found wide utility as an assessment of human mental function in basic and clinical studies. In particular, P3 attributes are heritable and have demonstrated considerable promise as a means to identify individuals at genetic risk for alcoholism. We have conducted a quantitative linkage analysis on a large sample from families with a high density of affected individuals. The analyses suggest that several regions of the human genome contain genetic loci related to the generation of the P3 component of the ERP, which are possible candidate loci underlying the functional organization of human neuroelectric activity.

Alcoholism↗
PubMed2004

Inheritable nature of enological quantitative traits is demonstrated by meiotic segregation of industrial wine yeast strains.

Wine yeast strains exhibit a wide variability in their technological properties. The large number of allelic variants and the high degree of heterozygosity explain this genetic variability found among the yeast flora. Furthermore, most enological traits are controlled by polygenic systems presenting complex interactions between the alleles. Taking this into account, we hypothesized that the meiotic segregation of such alleles from a given strain might generate a progeny population with very different technological properties. In this work, a population of 50 progeny clones derived from four industrial wine strains of Saccharomyces cerevisiae was characterized for three major enological traits: ethanol tolerance, volatile-acidity production and hydrogen sulphide production. For this purpose, reliable laboratory fermentation tests were developed in accordance with enological practice. A wide variability in the values of the various parameters was found among spore clones obtained after sporulation. Many clones presenting better aptitudes than the parental strains were obtained. Moreover, analysis of the progeny demonstrated that: (1) traits are in part inheritable; (2) traits are clearly polygenic; (3) broad relations of dominance/recessivity can be established. All these findings constitute an initial step for establishing breeding strategies for wine yeast improvement.

Culture Media↗
PubMed2005

A directed search in the region of GDF8 for quantitative trait loci affecting carcass traits in Texel sheep.

A directed search for QTL affecting carcass traits was carried out in the region of growth differentiation factor 8 (GDF8, also known as myostatin) on ovine chromosome 2 in seven Texel-sired half-sib families totaling 927 progeny. Weights were recorded at birth, weaning, ultrasound scanning, and slaughter. Ultrasonic measures of LM cross-sectional dimensions and s.c. fat above the LM were made, with the same measurements made on the LM after slaughter. Following slaughter, linear measurements of carcass length and width were made on all carcasses, and legs and loins from 540 lambs were dissected. Genotyping was carried out using eight microsatellite markers from FCB128 to RM356 on OAR 2 and analyzed using Haley-Knott regression. There was no evidence for QTL for growth rates or linear carcass traits. There was some evidence for QTL affecting LM dimensions segregating in some sire families, although it was not consistent between ultrasound and carcass measures of the same traits. There was strong and consistent evidence for a QTL affecting muscle and fat traits in the leg that mapped between markers BM81124 and BULGE20 for the four sires that were heterozygous in this region, but not for the three sires that were homozygous. The size of the effect varied across the four sires, ranging from 0.5 to 0.9 of an adjusted SD for weight-adjusted leg muscle traits, and ranging from 0.6 to 1.2 of an adjusted SD for weight-adjusted leg fat traits. The clearest effect shown was for multivariate analysis combining all leg muscle and fat traits analyzed across sires, where the -log(10) probability was 14. Animals carrying the favorable haplotype had 3.3% more muscle and 9.9% less fat in the leg relative to animals carrying other haplotypes. There was evidence for a second peak in the region of marker TEXAN2 for one sire group. It seems that a QTL affecting muscle and fat traits exists within the New Zealand Texel population, and it maps to the region of GDF8 on OAR2.

Adipose Tissue↗
PubMed2006

Identification of quantitative trait loci for carcass composition and pork quality traits in a commercial finishing cross.

A QTL study for carcass composition and meat quality traits was conducted on finisher pigs of a cross between a synthetic Piétrain/Large White boar line and a commercial sow cross. The mapping population comprised 715 individuals evaluated for a total of 30 traits related to growth and fatness (4 traits), carcass composition (11 traits), and meat quality (15 traits). Offspring of 8 sires (n = 715) were used for linkage analysis and genotyped for 73 microsatellite markers covering 14 chromosomal regions representing approximately 50% of the pig genome. The regions examined were selected based on previous studies suggesting the presence of QTL affecting carcass composition or meat quality traits. Thirty-two QTL exceeding the 5% chromosome-wise significance level were identified. Among these, 5 QTL affecting 5 different traits were significant at the 1% chromosome-wise level. The greatest significance levels were found for a QTL affecting loin weight on SSC11 and a QTL with an effect on the Japanese color scale score of the loin on SSC4. About one-third of the identified QTL were in agreement with QTL previously reported. Results showed that QTL affecting carcass composition and meat quality traits segregated within commercial lines. Use of these results for marker-assisted selection offers opportunities for improving pork quality by within-line selection.

Animals↗
PubMed1998

Quantitative trait loci affecting 4-nitroquinoline 1-oxide-induced tongue carcinogenesis in the rat.

The incidence of tongue carcinomas (TCs) induced by oral administration of 4-nitroquinoline 1-oxide in rats is strain dependent. The inbred Dark-Agouti (DA) strain showed a much higher susceptibility to large mass-forming infiltrative TCs than did the Wistar-Furth (WF) strain. Our previous study (M. Kitano et al, Jpn. J. Cancer Res., 87: 1097-1101, 1996) on crosses between these two strains postulated a dominant susceptibility gene in DA and a dominant resistance gene in WF rats. The present study mapped these loci by analyzing the backcrosses to each parent with simple sequence repeat polymorphisms. Five quantitative parameters were analyzed: (a) the number of TCs > 5 mm in diameter; (b) the total number of TCs per rat; (c) the diameter of the largest TCs (DTCmax values); (d) the number of non-TC cancers per rat; and (e) and the number of cancers of any site per rat. All of these parameters were closely correlated (P < 0.0001). DA rats had a semidominant gene (Stc1) favoring the development of 4-nitroquinoline 1-oxide-induced cancers on chromosome 19, closely linked to D19Mit9. Peak linkage was observed 4 cM distal from D19Mit9, with a logarithm of the odds (lod) score of 5.72 for the number of large TCs and 6.08 for the DTCmax. On the other hand, WF rats had a semidominant gene (Rtc1) mapped between D1Mit1 and D1Mit3, approximately 20 cM from D1Mit1, with a peak lod score of 3.30 for both the number of large TCs and the DTCmax. The main effect of Rtc1 seemed to be to reduce the size of the TCs. The action of these genes was dose dependent and cooperative. The final incidence of TC in DA, WF, F1, and backcross rats seemed to be explained by combinations of genotype at these two loci. Possible candidate genes for Stc1 and Rtc1 are discussed.

4-Nitroquinoline-1-oxide↗
PubMed1999

A genome-wide screen for asthma-associated quantitative trait loci in a mouse model of allergic asthma.

Asthma is the most common illness of childhood, affecting one child in seven in the UK. Asthma has a genetic basis, but genetic studies of asthma in humans are confounded by uncontrolled environmental factors, varying penetrance and phenotypic pleiotropy. An animal model of asthma would offer controlled exposure, limited and consistent genetic variation, and unlimited size of sibships. Following immunization and subsequent challenge with ovalbumin, the Biozzi BP2 mouse shows features of asthma, including airway inflammation, eosinophil infiltration and non-specific bronchial responsiveness. In order to identify genetic loci influencing these traits, a cross was made between BP2 and BALB/c mice, and a genome-wide screen carried out in the F2progeny of the F1intercross. Five potentially linked loci were identified, four of which corresponded to human regions of syntenic homology that previously have shown linkage to asthma-associated traits.

Airway Resistance↗
PubMed2003

Quantitative trait symmetry independent of Hsp90 buffering: distinct modes of genetic canalization and developmental stability.

The Hsp90 chaperone buffers development against a wide range of morphological changes in many organisms and in Drosophila masks the effects of hidden genetic variation. Theory predicts that genetic and nongenetic buffering will share common mechanisms. For example, it is argued that Hsp90 genetic buffering evolved solely as a by-product of environmental buffering, and that Hsp90 should mask morphological deviations from any source. To test this idea, we examined the effect of Hsp90 on purely nongenetic variation in phenotype, measured as differences between the left and right sides of several bilaterally symmetrical bristle and wing traits in individual flies. Consistent with previous reports, Hsp90 buffered the expression of rare morphogenic variants specific to particular genetic backgrounds. However, neither trait-by-trait nor global asymmetry was affected in outbred flies treated with an Hsp90 inhibitor or across a series of inbred genetic backgrounds from a wild population tested in isogenic F1 heterozygotes carrying either (i) a dominant negative Hsp90 allele on a mutant 3rd chromosome or (ii) a null P-insertion mutation, which was introgressed into the control genetic background on all chromosomes. By contrast, Hsp90-regulated trait means and significant effects of sex, temperature, and genetic background on trait symmetry were clearly detected. We conclude that, by maintaining the function of signaling proteins, Hsp90 masks variation affecting target pathways and traits in populations independent of purely nongenetic sources of variation, refuting the idea that a single Hsp90-dependent process generally controls genetic canalization and developmental stability.

Alleles↗
PubMed2003

Identification of quantitative trait loci for receiving pecks in young and adult laying hens.

Feather pecking (FP) is a major problem in cage and free-range housing systems. In free-range systems, FP is more difficult to control. It is not known why a victim is being pecked. It could be that a bird is genetically predisposed to be pecked. To study the genetics of FP behavior, a large F2 population of 630 hens was generated from a cross between two commercial laying lines differing in their propensity to feather peck. The traits measured at 6 and 30 wk of age were receiving gentle FP, receiving severe FP, and receiving aggressive pecking. In addition, receiving toe pecking (TP) was also measured at 30 wk of age. For receiving gentle FP at 6 wk of age, a significant QTL on GGA1 and three different suggestive QTL were identified on GGA2, GGA6, and GGA7, respectively. For receiving gentle FP at 30 wk of age, a suggestive QTL on GGA5 was detected. For receiving aggressive pecking, a suggestive QTL was detected on GGA3. For receiving TP, three suggestive QTL were detected on GGA1, GGA5, and GGA23, respectively. The different QTL detected for receiving gentle FP at different ages indicate that this trait is regulated by different genes in young and adult hens.

Aggression↗
PubMed2004

Localization and identification of human quantitative trait loci: king harvest has surely come.

The scientific process of localization and subsequent identification of genes influencing risk of common diseases is still in its infancy. Initial localization of disease-related loci has traditionally been performed using family-based linkage methods to scan the genome. Early pronouncements of the failure of this approach for common diseases were premature and based on comparing suboptimal linkage designs with overly optimistic and empirically unproven association-based designs. On the contrary, substantial recent progress in the positional cloning of genes influencing such complex phenotypes suggests that modern approaches based around a family-based linkage paradigm will be successful. In particular, the rapidly growing emphasis on the analysis of the genetic basis of quantitative correlates of disease risk represents a novel and promising approach in which initial localization is performed using linkage and subsequent identification utilizes association approaches in positional candidate genes.

Gene Frequency↗
PubMed2003

Diet-dependent obesity and hypercholesterolemia in the New Zealand obese mouse: identification of a quantitative trait locus for elevated serum cholesterol on the distal mouse chromosome 5.

AIMS: New Zealand obese (NZO) mice exhibit a polygenic syndrome of obesity, insulin resistance, and hypercholesterolemia that resembles the human metabolic syndrome. This study was performed in order to locate genes responsible for elevated serum cholesterol and to compare their effects under a standard and high fat diet. METHODS: A backcross population of NZO with SJL mice (NZO x F1(SJL x NZO)) was generated. Mice were raised on a normal or high fat diet and were monitored for 22 weeks (body weight, serum cholesterol, and blood glucose). A genome-wide scan was performed by genotyping of approximately 200 polymorphic microsatellite markers by PCR and linkage analysis was performed with the MAPMAKER program. RESULTS: In the genome-wide scan, a single susceptibility locus for hypercholesterolemia (Chol1/NZO, maximum LOD score 14.5 in a combined population of 523 backcross mice) was identified on chromosome 5. Cholesterol levels were significantly elevated in both male and female homozygous carriers of the Chol1/NZO allele. The locus maps 40cM distal of the previously described obesity locus Nob1 in the vicinity of the marker D5Mit244 and in the vicinity of hypercholesterolemia QTL previously identified in the NZB, CAST, and C57BL/6J strains. Chol1/NZO was not associated with elevated body weight, serum insulin, or hyperglycemia. The high fat diet significantly increased serum cholesterol levels, but the fat content of the diet did not alter the absolute effect of Chol1/NZO. CONCLUSIONS: Chol1/NZO is a major susceptibility locus on the distal mouse chromosome 5, which produces gender-independent hypercholesterolemia in NZO mice. The effect of Chol1/NZO was independent of the dietary fat content and was not associated with the other traits of the metabolic syndrome. Thus, it is suggested that the responsible gene might be involved in cholesterol metabolism.

Animals↗
PubMed1997

The effects of spontaneous mutation on quantitative traits. II. Dominance of mutations with effects on life-history traits.

We studied the dominance of the effects of chromosomes carrying unselected mutations on five life-history traits in Drosophila melanogaster. Mutations were accumulated on the second chromosome for 44 generations in the absence of natural selection. Traits studied were female fecundity early and late in adult life, male mating ability, and male and female longevity. Homozygous effects were estimated for 50 mutant lines, and heterozygous effects were estimated by crossing these lines in a partial diallel scheme. Direct estimates of dominance showed that the effects of mutants are at least partially recessive. Heterozygotes had higher trait means than homozygotes in all five cases, and these differences were significant for late fecundity and female longevity. For all traits, genetic variance was larger among homozygous crosses than among heterozygous crosses. These results are consistent with those of many other studies that suggest that both unselected mutations and those found segregating in natural populations are partially recessive.

Animals↗
PubMed2001

[Construction of a genetic map and location of quantitative trait loci for yield component traits in maize by SSR markers].

Using 230 F2:3 lines derived from the hybrid of ND3138, a SSR genetic linkage map of maize (Zea mays L.) was constructed on which 80 markers distribute among 10 linkage groups and spanning maize genome about 2033.4 cM with average distance between markers being 25.42 cM. The 230 F2:3 lines were grown in a random design of one-row plot with three replication, and evaluated for ear length, bared tip, ear diameter, row number, kernel number row-1, one thousand grains weight, ear weight and grain weight plant-1. With interval mapping procedure, 30 QTLs were revealed for all traits, which distributed on 9 of 10 chromosomes of maize except chromosome 6 and accounted for from 9.5% to 55.3% of the total phenotypic variation. Genetic effects and gene action were also determined.

Chromosome Mapping↗
PubMed2005

Comparison of linkage and association strategies for quantitative traits using the COGA dataset.

Genome scans using dense single-nucleotide polymorphism (SNP) data have recently become a reality. It is thought that the increase in information content for linkage analysis as a result of the denser scans will help refine previously identified linkage regions and possibly identify new regions not identifiable using the sparser, microsatellite scans. In the context of the dense SNP scans, it is also possible to consider association strategies to provide even more information about potential regions of interest. To circumvent the multiple-testing issues inherent in association analysis, we use a recently developed strategy, implemented in PBAT, which screens the data to identify the optimal SNPs for testing, without biasing the nominal significance level. We compare the results from the PBAT analysis to that of quantitative linkage analysis on chromosome 4 using the Collaborative Study on the Genetics of Alcoholism data, as released through Genetic Analysis Workshop 14.

Alcoholism↗
PubMed2002

Integrating sibship data for mapping quantitative trait loci.

Sibship methods have been shown to be more powerful than traditional sib-pair methods in mapping quantative trait loci. We propose a statistical procedure which integrates data on sibships into a so-called 'contrast function', a natural extension of the classical squared sib-pair trait difference proposed by Haseman & Elston (1972). We also develop a combined mean and contrast function which provides more information on linkage compared to the contrast function. Our method is extended to multiple, epistatically interacting trait loci. Monte-Carlo simulations are included to compare the efficiencies of the proposed procedures with some currently used methods. An application of our proposed method is presented using data on alcohol dependence.

Alcoholism↗