Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “quantitative trait locus”

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 73 records · Page 4Linked to original sources
PubMed2000

Genetic dissection of collagen-induced arthritis in Chromosome 10 quantitative trait locus speed congenic rats: evidence for more than one regulatory locus and sex influences.

Rat Chromosome 10 (RNO10) harbors Cia5, a non-MHC quantitative trait locus (QTL) that regulates the severity of type II collagen-induced arthritis (CIA) in DAxF344 and DAxBN F2 rats. CIA is an animal model with many features that resemble rheumatoid arthritis. To facilitate analysis of Cia5 independently of the other CIA regulatory loci on other chromosomes, DA recombinant QTL speed congenic rats, DA.F344(Cia5), were generated. These QTL congenic rats have a large chromosomal segment containing Cia5 (interval size < or =80.1 cM) from CIA-resistant F344 rats introgressed into their genome. Phenotypic analyses of these rats for susceptibility and severity of CIA confirmed that Cia5 is an important disease-modifying locus. CIA severity was significantly lower in the Cia5 congenic rats than in DA controls. We also generated DA Cia5 speed sub-congenic rats, DA.F344(Cia5a), which had a smaller segment of the F344 genome, Cia5a, comprising only the distal q-telomeric end (interval size < or = 22.5 cM) of Cia5, introgressed into their genome. DA.F344(Cia5a) sub-congenic rats also exhibited reduced CIA disease severity compared with the parental DA rats. The regulatory effects in both congenic strains were sex influenced. The disease-ameliorating effect of the larger fragment, Cia5, was greater in males than in females, but the effect of the smaller fragment, Cia5a, was greater in females. We also present an improved genetic linkage map covering the Cia5/Cia5a region, which we have integrated with two rat radiation hybrid maps. Comparative homology analysis of this genomic region with mouse and human chromosomes was also undertaken. Regulatory loci for multiple autoimmune/inflammatory diseases in rats (RNO10), mice (MMU11), and humans (HSA17 and HSA5q23-q31) map to chromosomal segments homologous to Cia5 and Cia5a.

Animals↗
PubMed2003

Quantitative trait locus mapping for atherosclerosis susceptibility.

PURPOSE OF REVIEW: Atherosclerosis is a complex trait with both environmental and genetic aspects. Although some progress has been made in defining genes associated with atherosclerosis in humans, animal models have been useful in learning about pathways and genes involved in atherogenesis. This review describes an unbiased genetic mapping method called quantitative trait locus mapping and progress in using this method to identify genes that alter atherosclerosis susceptibility in mice. RECENT FINDINGS: Approximately 10 well defined genetic loci have been described that are associated with lesion severity in diet-induced or gene knockout mouse models of atherosclerosis. Recently, two of these genetic loci were narrowed considerably by analysis of genetic recombinants within these loci. In addition, a computational method to discover quantitative trait loci has been applied to atherosclerosis. However, none of the genes responsible for these atherosclerosis quantitative trait loci has been definitively identified. The recent completion of the mouse draft genome should facilitate the task of identifying these genes. SUMMARY: Quantitative trait locus mapping studies in mouse models of atherosclerosis have defined genetic regions that alter lesion severity. The identification of the responsible genes may lead to insights into the pathogenesis of atherosclerosis as well as to candidates for human genetic association studies.

Animals↗
PubMed2006

A quantitative trait locus for body fat on chromosome 1q43 in French Canadians: linkage and association studies.

OBJECTIVE: To explore a quantitative trait locus (QTL) on human chromosome 1q affecting BMI, adiposity, and fat-free mass phenotypes in the Quebec Family Study cohort. RESEARCH METHODS AND PROCEDURES: Non-parametric sibpair and variance component linkage analyses and family-based association studies were performed with a dense set of chromosome 1q43 microsatellites and single-nucleotide polymorphism markers in 885 adult individuals. RESULTS: Linkage was observed between marker D1S184 and BMI (p = 0.0004) and with body fat mass or percentage body fat (p < or = 0.0003), but no linkage was detected with fat-free mass. Furthermore, significant linkages (p < 0.0001) were achieved with subsamples of sibpairs at both ends of phenotype distributions. Association studies with quantitative transmission disequilibrium tests refined the linkage to a region overlapping the regulator of G-protein signaling 7 (RGS7) gene and extending to immediate upstream gene loci. DISCUSSION: The present study indicates that the QTL on chromosome 1q43 specifically affects total adiposity and provides a genetic mapping framework for the dissection of this adiposity locus.

Adipose Tissue↗
PubMed1998

Congenic strain confirms putative quantitative trait locus for body weight in the rat.

Quantitative trait loci (QTLs) affecting body weight were investigated in the backcross population derived from non-diabetic BB/OK and spontaneously hypertensive rat (SHR) strains. The F1 hybrids were backcrossed onto SHR rats, and QTL analysis was performed separately with the resulting backcross populations for each sex on Chromosomes (Chrs) 1, 3, 4, 10, 13, and 18. The body weight was determined at the age of 14 weeks, and the statistical analysis was performed with MAPMAKER/QTL 1.1b computer program. According to the stringent threshold for a lod score of 3.0, markers on Chr 1 were found to be linked with body weight. The QTL with a peak lod score (5.1) on Chr 1 for a male population was located within markers Igf2 and D1Mgh12. In contrast, in the female population the body weight affecting QTL (lod = 5.7) on Chr 1 was located between the D1Mit3 and Lsn markers. The existence of QTLs on Chr 1 affecting body weight in the male population was confirmed by congenic BB.Sa rats, carrying chromosomal region of SHR (Sa-Igf2) on the genetic background of BB rat.

Animals↗
PubMed2003

Quantitative trait locus analysis of serum insulin, triglyceride, total cholesterol and phospholipid levels in the (SM/J x A/J)F2 mice.

Quantitative trait locus (QTL) analysis of serum insulin, triglyceride, total cholesterol and phospholipid levels at 10 weeks of age was performed in 321 F2 offspring from SM/J and A/J mice. Interval mapping revealed a total of 22 suggestive QTLs affecting the four traits: two insulin QTLs on Chromosomes (Chrs) 6 and 8; six triglyceride QTLs on Chrs 4, 8, 9, 11, 12 and 19; six total-cholesterol QTLs on Chrs 1, 3, 4, 14, 17 and 19; and eight phospholipid QTLs on Chrs 2, 3, 4, 6, 8, 10 and 19. Gender influenced the expression of eight of the suggestive QTLs. The total-cholesterol QTLs on Chrs 4, 14 and 17, the triglyceride QTL on Chr 9 and the phospholipid QTL on Chr 4 were specific to females. The phospholipid QTLs on Chrs 2 and 6 and the insulin QTL on Chr 8 were specific to males. In addition, common QTLs involved in the regulation of some of the traits were identified. The female-specific QTL on Chr 4 appeared to be involved in the regulation of total cholesterol and phospholipid levels. The QTL on Chr 8 affected insulin and phospholipid levels, whereas the Chr 19 QTL was common to the three lipid parameters.

Animals↗
PubMed2004

Quantitative trait locus analysis of plasma cholesterol and triglyceride levels in C57BL/6J x RR F2 mice.

A highly significant cholesterol quantitative trait locus (QTL) (Cq6) was identified on chromosome 1 in C57BL/6J x RR F2 mice. The Cq6 was located over the gene for apolipoprotein A-Il (Apoa2), and the RR allele was associated with increased plasma cholesterol. C57BL/6J has Apoa2a alleles and RR has Apoa2b alleles. Three different Apoa2 alleles are known on the basis of amino acid substitutions at four residues. Analysis with partial Apoa2 congenic strains possessing Apoa2a, Apoa2b, and Apoa2C alleles revealed that the Apoa2b allele is unique in the ability to increase cholesterol among the three Apoa2 alleles, and that the Ala-to-Val substitution at residue 61 may be crucial as far as cholesterol metabolism is concerned. We also investigated the question of whether the Apoa1 gene is responsible for the cholesterol QTLs (Cq4 and Cq5) that had been identified previously on chromosome 9 in C57BL/6J x KK-Ay/a F2 and in KK x RR F2, but not in C57BL/6J x RR F2 mice. Similar to Apoa2 alleles, three different Apoal alleles with two successive amino acid substitutions were revealed among the strains. However, we could not correlate Apoal polymorphisms with the occurrence of QTLs in these three sets of F2 mice.

Alleles↗
PubMed2003

Effects of including a quantitative trait locus in selection under different waiting plans of young bulls.

The advantage of using the genotype of a quantitative trait locus (QTL) in selection schemes of dairy cattle was quantified using stochastic simulation. Three selection plans were studied. In the first plan, young bulls waited for 3 yr until their sisters completed a lactation and then were evaluated and selected based on an animal model. In a second plan, young bulls waited for 5 yr until their daughters completed a lactation. An intermediate 4-yr waiting plan was also studied. Simulation was for 16 yr with overlapping generations. Population and model parameters were proportional to the U.S. Holstein population. The advantage of using a QTL was quantified as the percentage of superiority of QTL-assisted over QTL-free selection using cumulative genetic response. Percentage of superiority was reported for four selection pathways: active sires, young bulls, bull dams, and first lactation cows. A general trend was observed: low superiority in early years of selection that increased to a plateau in later years and then decreased. The superiority of the QTL information was greatest in the 3-yr waiting plan and least in the 4-yr waiting plan. Superiority at plateau for selection pathways ranged from 16 to 26% for the 3-yr waiting plan, from 3 to 12% for the 4-yr waiting plan, and from 5 to 13% for the 5-yr waiting plan. The contribution to selection response attributed to the QTL and the polygenes was quantified. The rate at which the favorable allele approached fixation and the accuracy of predicting breeding values on the percentage of superiority were studied.

Animals↗
PubMed2026

Integration of Genome-Wide Association Studies With Single-Cell and Bulk Expression Quantitative Trait Locus to Identify Stroke Susceptibility Genes.

BACKGROUND: Previous studies have integrated genome-wide association studies with expression quantitative trait locus (eQTL) data from bulk tissues to identify stroke susceptibility genes. However, eQTL data exhibit high cell-type specificity, and genetic variants may have distinct effects across stroke subtypes. METHODS: We applied the summary-data-based Mendelian randomization (MR) method to integrate eQTL data from 7 brain cell types with genome-wide association studies data for 5 stroke phenotypes (stroke, ischemic stroke, cardioembolic stroke, large artery stroke, and small vessel stroke). Results were compared with summary-data-based MR using eQTL data from 49 tissues in the Genotype-Tissue Expression project. Robustness of significant single-cell summary-data-based MR associations was assessed via MR and colocalization analyses. Further evaluations included single-cell RNA-seq differential expression, protein-protein interaction, druggability, and phenome-wide association studies. RESULTS: Single-cell summary-data-based MR identified many novel significant genes not detected using bulk tissue eQTL data. Validated associations revealed 2 stroke risk genes (LRCH1, ICA1L), 3 stroke protective genes (AHI1, LYRM9, CENPQ), 2 large artery stroke risk genes (LIPA, ELL), and 1 ischemic stroke protective gene (CENPQ). Single-cell RNA-seq showed significantly increased LIPA expression in mouse stroke samples compared with controls. Protein-protein interaction and druggability analyses, along with phenome-wide association studies, prioritized LIPA and LRCH1 as potential therapeutic targets for stroke while indicating possible adverse effects. CONCLUSIONS: Integrating single-cell eQTL with stroke-subtype genome-wide association studies uncovers novel cell-type-specific causal genes and highlights promising therapeutic targets, advancing understanding of stroke pathogenesis.

Genome-Wide Association Study↗
PubMed2006

Haplotype variation in structure and expression of a gene cluster associated with a quantitative trait locus for improved yield in rice.

By constructing nearly isogenic lines (NILs) that differ only at a single quantitative trait locus (QTL), we fine-mapped the yield-improving QTL qGY2-1 to a 102.9-kb region on rice chromosome 2. Comparison analysis of the genomic sequences in the mapped QTL region between the donor (Dongxiang wild rice, Oryza rufipogon Griff.) and recurrent (Guichao2, Oryza sativa ssp. indica) parents used for the development of NILs identified the haplotypes of a leucine-rich repeat receptor kinase gene cluster, which showed extensive allelic variation. The sequences between genes in the cluster had a very high rate of divergence. More importantly, the genes themselves also differed between two haplotypes: Only 92% identity was observed for one allele, and another allele was found to have completely lost its allelic counterpart in Guichao2. The other six shared genes all showed >98% identity, and four of these exhibited obvious regulatory variation. The same haplotype segments also differed in length (43.9-kb in Guichao2 vs. 52.6-kb in Dongxiang wild rice). Such extensive sequence variation was also observed between orthologous regions of indica (cv. 93-11) and japonica (cv. Nipponbare) subspecies of Oryza sativa. Different rates of sequence divergence within the cluster have resulted in haplotype variability in 13 rice accessions. We also detected allelic expression variation in this gene cluster, in which some genes gave unequal expression of alleles in hybrids. These allelic variations in structure and expression suggest that the leucine-rich repeat receptor kinase gene cluster identified in our study should be a particularly good candidate for the source of the yield QTL.

Alleles↗
PubMed1999

Quantitative trait locus analysis of plasma lipoprotein levels in an autoimmune mouse model : interactions between lipoprotein metabolism, autoimmune disease, and atherogenesis.

The autoimmune MRL/lpr mouse strain, a model for systemic lupus erythematosus, exhibited an unusual plasma lipoprotein profile, suggesting a possible interaction of autoimmune disease and lipoprotein metabolism. In an effort to examine the genetic basis of such interactions, and to study their relationship to atherogenesis, we performed a quantitative trait locus analysis using a total of 272 (MRL/lprxBALB/cJ) second generation (F2) intercross mice. These mice were examined for levels of total plasma cholesterol, HDL cholesterol, VLDL and LDL cholesterol, unesterified cholesterol, autoantibodies, and aortic fatty streak lesions. Using a genome scan approach, we identified 4 quantitative trait loci controlling plasma lipoprotein levels on chromosomes (Chrs) 5, 8, 15, and 19. The locus on Chr 15 exhibited lod scores of 11.1 for total cholesterol and 6.7 for VLDL and LDL cholesterol in mice fed an atherogenic diet, and it contains a candidate gene, the sterol regulatory element binding protein-2. The locus on Chr 5 exhibited lod scores of 3.8 for total cholesterol and 4.1 for unesterified cholesterol in mice fed an atherogenic diet, and this locus has been observed in 2 previous studies. The locus on Chr 8 exhibited a lod score of 3.1 for unesterified cholesterol in mice fed a chow diet. This locus contains the lecithin-cholesterol acyltransferase gene, and decreased activity of the enzyme in the MRL strain suggests that this gene underlies the quantitative-trait locus. The locus on Chr 19 exhibited a lod score of 8.4 for HDL cholesterol and includes the Fas gene, which is mutated in MRL/lpr mice and is primarily responsible for the autoimmune phenotype in this cross. That the Fas gene is responsible for the HDL quantitative-trait loci is supported by the finding that autoantibody levels were strongly correlated with HDL cholesterol levels (rho=-0.37, P<0.0001) among the F2 mice. HDL cholesterol levels were in turn significantly associated with aortic fatty streak lesions among the F2 mice (rho=-0.17, P=0.006). Further, there was a threshold effect of autoantibody levels on the development of fatty streak lesions (rho=0.45, P=0.004 for 42 F2 mice with anti-dsDNA Ab over 0.5 OD). Our results support the concept that the high prevalence of coronary artery disease in systemic lupus erythematosus is due in part to a reduction of HDL cholesterol levels resulting from the autoimmune disease.

Animals↗
PubMed2005

Locating a blood pressure quantitative trait locus within 117 kb on the rat genome: substitution mapping and renal expression analysis.

Previously, a blood pressure (BP) quantitative trait locus (QTL) on rat chromosome 9 (RNO9) was localized to a <2.4 cM interval using congenic strains generated by introgressing segments of RNO9 from the Dahl salt-resistant (R) rat into the background of the Dahl salt-sensitive (S) rat. Renal gene expression using Affymetrix gene chips was profiled on S and a congenic strain spanning the 2.4-cM BP QTL interval. This analysis identified 20 differentially expressed genes/expressed sequence tags. Of these, the locus with the greatest differential expression (30- to 35-fold) was regulated endocrine-specific protein 18 (Resp18), which also mapped in the 2.4-cM BP QTL interval. Additional substitution mapping located the QTL to <0.4 cM or approximately 493 kb. This newly defined QTL region still included Resp18. Nucleotide variants were identified between S and R genomic DNA of Resp18 in the coding, 5' regulatory and 3' untranslated regions. The coding sequence variation (T/C) occurs in exon 2 and predicts an amino acid change (Ile/Val) in the protein product. Resp18 was considered a differentially expressed positional candidate for the QTL. To fine-map the BP QTL, we constructed a congenic strain with a smaller introgressed region. Compared with the S rat, this strain (1) had significantly lower BP, (2) did not contain the R form of Resp18, and (3) did not retain the rather spectacular differential expression of Resp18. Together, these results demonstrate that a BP QTL independent of Resp18 exists within the newly defined 117-kb QTL region on RNO9.

Animals↗
PubMed2004

Quantitative trait locus analyses and the study of evolutionary process.

The past decade has seen a proliferation of studies that employ quantitative trait locus (QTL) approaches to diagnose the genetic basis of trait evolution. Advances in molecular techniques and analytical methods have suggested that an exact genetic description of the number and distribution of genes affecting a trait can be obtained. Although this possibility has met with some success in model systems such as Drosophila and Arabidopsis, the pursuit of an exact description of QTL effects, i.e. individual gene effect, in most cases has proven problematic. We discuss why QTL methods will have difficulty in identifying individual genes contributing to trait variation, and distinguish between the identification of QTL (or marker intervals) and the identification of individual genes or nucleotide differences within genes (QTN). This review focuses on what ecologists and evolutionary biologists working with natural populations can realistically expect to learn from QTL studies. We highlight representative issues in ecology and evolutionary biology and discuss the range of questions that can be addressed satisfactorily using QTL approaches. We specifically address developing approaches to QTL analysis in outbred populations, and discuss practical considerations of experimental (cross) design and application of different marker types. Throughout this review we attempt to provide a balanced description of the benefits of QTL methodology to studies in ecology and evolution as well as the inherent assumptions and limitations that may constrain its application.

Adaptation, Biological↗
PubMed2006

Investigation of two candidate genes for meat quality traits in a quantitative trait locus region on SSC6: the porcine short heterodimer partner and heart fatty acid binding protein genes.

A highly significant quantitative trait locus (QTL) on pig chromosome 6, affecting intramuscular fat (IMF), has previously been detected by our group and others. Two genes of positional and biological interest, the small heterodimer partner (SHP; NR0B2) and the heart fatty acid binding protein (FABP3; H-FABP), were investigated for meat quality traits and IMF respectively. SHP was partially sequenced (GenBank: DQ002896 and DQ002897) and mapped to the QTL region on porcine chromosome 6, affecting IMF. The map shows no recombination between SHP and FABP3, which was previously mapped to the same QTL region. Twelve single nucleotide polymorphisms were detected in the sequenced region of SHP gene. Haplotype information was used to investigate association between genetic variation and different meat quality traits. SHP haplotype combinations were found to have significant effect on connective tissue. However, further studies are needed to evaluate this possible association more effectively. The FABP3 is involved in fatty acid transport and has been studied as a candidate gene for IMF by several research groups. In our study, FABP3 genotypes were confirmed to be significantly associated with IMF in pigs. The average content of IMF in our population was 1.6%, which may indicate that the FABP3 polymorphism explains as much as 30-35% of the variation in IMF in our pig cross-population.

Animals↗
PubMed2006

Stability over genetic backgrounds, generations and years of quantitative trait locus (QTLs) for organoleptic quality in tomato.

The efficiency of marker-assisted backcross for the introgression of a quantitative trait locus (QTL) from a donor line into a recipient line depends on the stability of QTL expression. QTLs for six quality traits in tomato (fruit weight, firmness, locule number, soluble solid content, sugar content and titratable acidity) were studied in order to investigate their individual effect and their stability over years, generations and genetic backgrounds. Five chromosome regions carrying fruit quality QTLs were transferred following a marker-assisted backcross scheme from a cherry tomato line into three modern lines with larger fruits. Three sets of genotypes corresponding to three generations were compared: (1) an RIL population, which contained 50% of each parental genome, (2) three BC3S1 populations which segregated simultaneously for the five regions of interest but were almost fully homozygous for the recipient genome on the eight chromosomes carrying no QTL and (3) three sets of QTL-NILs (BC3S3 lines) which differed from the recipient line only in one of the five regions. QTL detection was performed in each generation, in each genetic background and during 2 successive years for QTL-NILs. About half of the QTLs detected in QTL-NILs were detected in both years. Eight of the ten QTLs detected in RILs were recovered in the QTL-NILs with the genetic background used for the initial QTL mapping experiment, with the exception of two QTLs for fruit firmness. Several new QTLs were detected. In the two other genetic backgrounds, the number of QTLs in common with the RILs was lower, but several new QTLs were also detected in advanced generations.

Fruit↗
PubMed2000

Bovine CAPN1 maps to a region of BTA29 containing a quantitative trait locus for meat tenderness.

Micromolar calcium activated neural protease (CAPN1) was investigated as a potential candidate gene for a quantitative trait locus (QTL) on BTA29 affecting meat tenderness. A 2,948-bp bovine cDNA containing the entire coding region of the gene was obtained, showing 91% identity to human CAPN1. The 716 AA protein predicted from this sequence shows 97% similarity (95% identity) to the 714 AA human protein. Analysis of the gene structure revealed that CAPN1 mRNA is encoded by at least 19 exons, and 11,055 bp of the gene were sequenced, including 17 introns. Two single nucleotide polymorphisms (SNP) were detected in intron 12 and were used to map bovine CAPN1 to the telomeric end of the BTA29 linkage group. This approximately coincides with the position of the QTL, demonstrating that CAPN1 protease is a positional candidate gene potentially affecting variation in meat tenderness in a bovine resource mapping population.

Amino Acid Sequence↗
PubMed2003

Substitution mapping of a blood pressure quantitative trait locus to a 2.73 Mb region on rat chromosome 1.

OBJECTIVE: To improve the localization of a blood pressure quantitative trait locus (BP QTL) on rat chromosome (RNO) 1. METHODS: Congenic substrains were derived from the progenitor congenic strains S.LEW(D1Mco4X1) and S.LEW(D1Mco4X5) which previously localized a BP QTL (region 2) to a 17cM interval on RNO1. The newly developed congenic substrains, along with control Dahl salt-sensitive (S) rats were fed a 2% NaCl diet for 24 days before their BP was compared by both tail-cuff and radiotelemetry methods. RESULTS: By comparing BP of these congenic substrains to that of S rats, we have refined the location of the BP QTL2 region to a 2.73 Mb genomic interval that contains 19 annotated genes in the latest rat genome assembly (version 2.1). Slc9a3, the gene encoding the Na(+)/H(+) exchanger 3, originally a candidate gene in the BP QTL2 region, is excluded based on its map location. CONCLUSION: Substitution mapping was used to reduce a BP QTL on RNO1 from 17 centimorgans (cM) to approximately 1.4 cM (= 2.73 Mb). This region now contains 19 annotated rat candidate genes.

Animals↗
PubMed1999

An empirical test of the significance of an observed quantitative trait locus effect that preserves additive genetic variation.

We propose a constrained permutation test that assesses the significance of an observed quantitative trait locus effect against a background of genetic and environmental variation. Permutations of phenotypes are not selected at random, but rather are chosen in a manner that attempts to maintain the additive genetic variability in phenotypes. Such a constraint maintains the nonindependence among observations under the null hypothesis of no linkage. The empirical distribution of the lod scores calculated using permuted phenotypes is compared to that obtained using phenotypes simulated from the assumed underlying multivariate normal model. We make comparisons of univariate analyses for both a quantitative phenotype that appears consistent with a multivariate normal model and a quantitative phenotype containing pronounced outliers. An example of a bivariate analysis is also presented.

Alcoholism↗
PubMed1990

Using molecular markers to estimate quantitative trait locus parameters: power and genetic variances for unreplicated and replicated progeny.

Many of the progeny types used to estimate quantitative trait locus (QTL) parameters can be replicated, e.g., recombinant inbred, doubled haploid, and F3 lines. These parameters are estimated using molecular markers or QTL genotypes estimated from molecular markers as independent variables. Experiment designs for replicated progeny are functions of the number of replications per line (r) and the number of replications per QTL genotype (n). The value of n is determined by the size of the progeny population (N), the progeny type, and the number of simultaneously estimated QTL parameters (q - 1). Power for testing hypotheses about means of QTL genotypes is increased by increasing r and n, but the effects of these factors have not been quantified. In this paper, we describe how power is affected by r, n, and other factors. The genetic variance between lines nested in QTL genotypes (sigma 2n:q) is the fraction of the genetic variance between lines (sigma 2n) which is not explained by simultaneously estimated intralocus and interlocus QTL parameters (phi 2Q); thus, sigma 2n:q = sigma 2n - phi 2Q. If sigma 2n:q not equal to 0, then power is not efficiently increased by increasing r and is maximized by maximizing n and using r = 1; however, if sigma 2n:q = 0, then r and n affect power equally and power is efficiently increased by increasing r and is maximized by maximizing N.r. Increasing n efficiently increases power for a wide range of values of sigma 2n:q.sigma 2n:q = 0 when the genetic variance between lines is fully explained by QTL parameters (sigma 2n = phi 2Q).(ABSTRACT TRUNCATED AT 250 WORDS)

Alleles↗