Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “quantitative trait”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,657 records · Page 92Linked to original sources
PubMed2006

Mating system and the evolution of quantitative traits: an experimental study of Mimulus guttatus.

The mating system of a population profoundly influences its evolution. Inbreeding alters the balance of evolutionary forces that determine the amount of genetic variation within a population. It redistributes that variation among individuals, altering heritabilities and genetic correlations. Inbreeding even changes the basic relationships between these genetic statistics and response to selection. If populations differing only in mating system are exposed to the same selection pressures, will they respond in qualitatively different ways? Here, we address this question by imposing selection on an index of two negatively correlated traits (flower size and development rate) within experimental populations that reproduce entirely by outcrossing, entirely by self-fertilizing, or by a mixture of outcrossing and selfing. Entirely selfing populations responded mainly by evolving larger flowers whereas outcrossing populations also evolved more rapid development. Divergence occurred despite an equivalent selection regime and no direct effect of mating system on fitness. The study provides an experimental demonstration of how the interaction of selection, genetic drift, and mating system can produce dramatic short-term changes in trait means, variances, and covariances.

Crosses, Genetic↗
PubMed1997

Multipoint analysis of quantitative traits.

Complete multipoint analysis as implemented by MAPMAKER/SIBS was used to identify the chromosomal regions with the strongest evidence of linkage. Three different quantitative sib-pair methods were compared. For each trait the maximum lod/Z score was used to implicate a chromosomal region. For trait Q5, chromosome 5, the analysis was repeated in a second data set to test for replication of the result from the first data set. The initial screen was carried out using complete parental information and the first sibling pair from each nuclear family. The effect of removing the parental genotypes and the use of multiple independent sibs was examined in the second data set for Q5, chromosome 5.

Chromosome Mapping↗
PubMed2005

Linkage analysis of chromosome 1 with essential hypertension and blood pressure quantitative traits in Chinese families.

Summary Several recent studies have linked human chromosome 1p to essential hypertension (EH) or blood pressure (BP) levels. In an independent population of 148 hypertensive families from China we tested these findings. Thirty highly informative microsatellite markers spanning about 284 cM were genotyped. Qualitative linkage analysis was conducted using non-parametric linkage analysis implemented within the GENEHUNTER 2.0 software, whereas quantitative analysis was performed with the variance-component method integrated in the S.O.L.A.R. 1.7.4. software with an additional Haseman-Elston method using the SAGE/SIBPAL2 program. We observed suggestive linkage between D1S2890 (1p31, 80.9 cM) and hypertension using the multipoint non-parametric linkage analysis (NPL = 2.19, P = 0.01). In the quantitative analysis we didn't observe a significant excess of identity-by-descent allele sharing between the systolic blood pressure levels and the markers. However, the D1S207 microsatellite marker (1p21) which is located about 107 cM from the telomere of 1p showed weak linkage evidence with the diastolic blood pressure levels (LOD = 1.42). These findings suggest linkage of 1p31 with essential hypertension in the ethnic Chinese, and provide a potential clue for future studies involving candidate genes for hypertension.

Adult↗
PubMed2003

A whole-genome screen of a quantitative trait of age-related maculopathy in sibships from the Beaver Dam Eye Study.

Age-related maculopathy (ARM) is a leading cause of visual impairment among the elderly in Western populations. To identify ARM-susceptibility loci, we genotyped a subset of subjects from the Beaver Dam (WI) Eye Study and performed a model-free genomewide linkage analysis for markers linked to a quantitative measure of ARM. We initially genotyped 345 autosomal markers in 325 individuals (N=263 sib pairs) from 102 pedigrees. Ten regions suggestive of linkage with ARM were observed on chromosomes 3, 5, 6, 12, 15, and 16. Prior to fine mapping, the most significant regions were an 18-cM region on chromosome 12, near D12S1300 (P=.0159); a region on chromosome 3, near D3S1763, with a P value of.0062; and a 6-cM region on chromosome 16, near D16S769, with a P value of.0086. After expanding our analysis to include 25 additional fine-mapping markers, we found that a 14-cM region on chromosome 12, near D12S346 (located at 106.89 cM), showed the strongest indication of linkage, with a P value of.004. Three other regions, on chromosomes 5, 6, and 15, that were nominally significant at P< or =.01 are also appropriate for fine mapping.

Adult↗
PubMed1998

Strategies to utilize marker-quantitative trait loci associations.

Marker-assisted selection holds promise because genetic markers provide completely heritable traits than can be measured at any age in either sex and that are potentially correlated with traits of economic value. Theoretical and simulation studies show that the advantage of using marker-assisted selection can be substantial, particularly when marker information is used, because normal selection is less effective, for example, for sex-limited or carcass traits. Assessment of the available information and its most effective use is difficult, but approaches such as crossvalidation may help in this respect. Marker systems are now becoming available that allow the high density of markers required for close associations between marker loci and trait loci. Emerging technologies could allow large numbers of polymorphic sites to be identified, practically guaranteeing that markers will be available that are in complete association with any trait locus. Identifying which polymorphism out of many that is associated with any trait will remain problematic, but multiple-locus disequilibrium measures may allow performance to be associated with unique marker haplotypes. This type of approach, combined with cheap and high density markers, could allow a move from selection based on a combination of "infinitesimal" effects plus individual loci to effective total genomic selection. In such a unified model, each region of the genome would be given its appropriate weight in a breeding program. However, the collection of good quality trait information will remain central to the use of these technologies for the foreseeable future.

Animals↗
PubMed2005

Mapping quantitative trait loci associated with leaf and stem pubescence in cotton.

Leaf pubescence in cotton have a potential for insect pest management. Varying degrees of leaf trichome density in Gossypium species and cultivars have been associated to a series of five genes, referred to as t(1)-t(5). We used two segregating interspecific G. hirsutum x G. barbadense backcross populations developed in our laboratory to assess qualitatively and quantitatively leaf and stem pubescence. QTL analyses were performed using simple and composite interval mapping. Based on both types of measurements and under both types of QTL analyses, nine QTLs met permutation-based thresholds. The nine QTLs mapped to four different chromosome regions. Highest LOD values corresponded to the QTLs detected on c6 (four colocalized QTLs) and on D03 (two QTLs) for which the higher pubescence in the progeny derived from the pubescent G. hirsutum parent alleles. Conversely, on c17 (one QTL) and A01 (two QTLs), the G. hirsutum parental alleles affected negatively pubescence. These results combined with another published study confirm (1) the location in a center region of chromosome 6 of the t(1) locus as a major locus/gene determining leaf pubescence, and (2) additional genes located on seven additional chromosomes have been shown to impart trichome density either positively or negatively. The existence of a high density of PCR-based loci in most of the regions identified as harboring leaf pubescence QTLs, particularly that on chromosome 6, will facilitate future efforts for map-based cloning.

Chromosome Mapping↗
PubMed2001

Putative quantitative trait locus affecting birth weight on bovine chromosome 2.

A genome scan for chromosomal regions influencing birth weight was performed using 151 progeny of a single Hereford x composite bull and 170 microsatellite markers spanning 2.497 morgans on 29 bovine autosomes. A QTL was identified at the telomeric end of bovine chromosome 2 (maximum effect at 114 cM) accounting for approximately 2.8 kg of birth weight or 0.64 residual standard deviations (after adjustment for sex of calf, age of dam, and breed of dam). No significant effect on growth from birth to weaning was detected in this region. The presence of this QTL within a resource herd composed of breeds common to the Northern Great Plains provides an opportunity to initiate marker-assisted selection to reduce birth weight with minimal effect on postnatal growth. Thus, potentially the amount and degree of dystocia can be reduced and the economic loss associated with calving difficulty lessened without compromise of subsequent growth performance. In addition, this finding indicates that significant genetic variation for birth weight (and presumably other production-related traits) exists within herds composed of commercially adapted Bos taurus germplasm.

Animals↗
PubMed2003

Quantitative trait loci for periosteal circumference (PC): identification of single loci and epistatic effects in F2 MRL/SJL mice.

To test the hypothesis that periosteal circumference (PC), which is associated with bone size through cross-sectional moment of inertia (CMI), has heritable components, we performed a linkage analysis using 633 MRL/SJL F(2) mice that have 14% difference in mean PC. PC was determined in femurs by use of peripheral quantitative computerized tomography (pQCT). The genome-wide scan identified nine QTL for PC adjusted by body weight on chromosomes 1 (2 QTL), 2 (2 QTL), 8, 11, 15, 17, and X, which accounted for 38.6% of phenotype variance. QTL on chromosomes 1 (D1Mit33), 8 (D8Mit125), 15 (D15Mit 62), 17 (D17Mit176), and X (DXMit208) were unique for PC adjusted by body weight and femur length, while the remaining PC QTL were shared with body weight but not femur length. Four epistatic interactions were identified which accounted for 37.6% of phenotype variance. There was also evidence of pleiotropic effects on chromosome 11 among four size phenotypes (PC, body length, body weight, bone mineral density, and muscle size), which may represent a common genetic mechanism that may regulate bone size and body size.

Animals↗
PubMed2006

Alpha-haemoglobin stabilising protein is a quantitative trait gene that modifies the phenotype of beta-thalassaemia.

It has been suggested that altered levels or function of alpha-haemoglobin stabilising protein (AHSP), an erythroid-specific protein that binds specifically to free alpha-(haemo)globin, might account for some of the clinical variability in beta-thalassaemia. To assess the variation of AHSP expression, mRNA levels in circulating reticulocytes of 103 healthy individuals were measured by quantitative reverse transcription-polymerase chain reaction. AHSP expression varied up to threefold, and did not correlate with age or sex. A systematic survey of the AHSP locus identified eight sequence variants, of which six were common. Four common variants, including the longer homopolymer (T18) in the putative promoter, are strongly associated with AHSP expression. Reporter assays in K562 cells showed that the activity of the shorter (T15) reporter was relatively lower than that of the T18 reporter. In a study of nine anaemic patients who were heterozygous for beta-thalassaemia and also heterozygous for the triplicated alpha-globin gene (alpha alpha alpha/alpha alpha), frequency of the shorter homopolymer was higher than expected. AHSP expression is variable, with cis control accounting for some of its variance. In some families, the subtle altered levels in AHSP related to the AHSP genotype appears to be a relevant contributory factor in the haematological phenotype.

Adult↗
PubMed2006

Identification of quantitative trait loci (QTL) for oil and protein contents and their relationships with other seed quality traits in Brassica juncea.

A detailed RFLP-genomic map was used to study the genetics of oil, seed and meal protein and sum of oil and seed/meal protein contents in a recombinant doubled-haploid population developed by crossing black- and yellow-seeded Brassica juncea lines. Two yellow seed color genes (SC-B4, SC-A6) and one QTL for erucic acid content (E(1b)) showed pleiotropic effect for oil, protein and sum of oil and seed/meal protein contents. Six (O-A1, O-A6, O-A9, O-B3, O-B4, O-B5) and five (SP-A1, SP-A9, SP-B4, SP-B6, SP-C) QTLs were significant for oil and seed protein contents, respectively. Tight linkage of three of these QTLs (SP-A1, SP-A9, SP-B4, O-A1, O-A9, O-B4), with opposite effects, poses challenge to the plant breeders for simultaneous improvement of negatively correlated (r = -0.7**) oil and seed protein contents. However, one QTL for oil content (O-B3) and two for seed protein content (SP-B6, SP-C) were found to be unlinked, which offer the possibility for simultaneous improvement of these two traits. QTLs significant for meal protein (MP-A1, MP-A6, MP-A9, MP-B5, MP-B6) were significant at least for oil, seed protein or sum of oil and seed/meal protein contents (T-A6, T-A7, T-B4, T-B5). Sum of oil and seed protein contents and sum of oil and meal protein contents had a perfect correlation, as well as same epistatic interactions and QTLs with similar additive effect. This indicates that protein in seed or meal has practically the same meaning for breeding purposes. Epistatic interactions were significant for the quality traits, and their linkage reflected association among the traits.

Agriculture↗
PubMed1999

Properties of spontaneous mutations affecting quantitative traits.

Recent mutation accumulation results from invertebrate species suggest that mild deleterious mutation is far less frequent than previously thought, implying smaller expressed mutational loads. Although the rate (lambda) and effect (s) of very slight deleterious mutation remain unknown, most mutational fitness decline would come from moderately deleterious mutation (s approximately 0.2, lambda approximately 0.03), and this situation would not qualitatively change in harsh environments. Estimates of the average coefficient of dominance (h) of non-severe deleterious mutations are controversial. The typical value of h = 0.4 can be questioned, and a lower estimate (about 0.1) is suggested. Estimated mutational parameters are remarkably alike for morphological and fitness component traits (excluding lethals), indicating low mutation rates and moderate mutational effects, with a distribution generally showing strong negative asymmetry and little leptokurtosis. New mutations showed considerable genotype-environment interaction. However, the mutational variance of fitness-component traits due to non-severe detrimental mutations did not increase with environmental harshness. For morphological traits, a class of predominantly additive mutations with no detectable effect on fitness and relatively small effect on the trait was identified. This should be close to that responsible for standing variation in natural populations.

Adaptation, Physiological↗
PubMed2001

Genetic and nongenetic bases for the L-shaped distribution of quantitative trait loci effects.

The L-shaped distribution of estimated QTL effects (R(2)) has long been reported. We recently showed that a metabolic mechanism could account for this phenomenon. But other nonexclusive genetic or nongenetic causes may contribute to generate such a distribution. Using analysis and simulations of an additive genetic model, we show that linkage disequilibrium between QTL, low heritability, and small population size may also be involved, regardless of the gene effect distribution. In addition, a comparison of the additive and metabolic genetic models revealed that estimates of the QTL effects for traits proportional to metabolic flux are far less robust than for additive traits. However, in both models the highest R(2)'s repeatedly correspond to the same set of QTL.

Linkage Disequilibrium↗