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PubMed2000

Localization of a small genomic region associated with elevated ACE.

Defining the relationship between multiple polymorphisms in a small genomic region and an underlying quantitative trait locus (QTL) represents a major challenge in human genetics. Pedigree analyses have shown that angiotensin I-converting enzyme (ACE) levels are influenced by a QTL located within or close to the ACE gene and most likely resides in the 3' region of this locus. We genotyped seven polymorphisms spanning 13 kb in the 3' end of ACE in 159 Afro-Caribbean subjects to evaluate the linkage disequilibrium between these sites and to narrow the genomic region associated with an elevated ACE level using a cladistic analysis. The linkage disequilibrium measurement D' and a haplotype tree revealed three distinct haplotype segments, presumably because of recombination. The value of the linkage disequilibrium parameter p(excess) was highest for site 22982, which is located in the middle segment. A series of nested, cladistic analyses confirmed that the other two regions are unlikely to be the ACE-linked QTL and that the variant resides in the middle region. Analyses of the same polymorphisms in 98 unrelated Europeans in the Monitoring Trends and Determinants in Cardiovascular Diseases (MONICA) study resulted in fewer haplotypes than were observed among the Afro-Caribbean subjects, suggesting that populations with greater genetic diversity may be especially informative for fine-scale mapping.

Black People↗
PubMed2004

Genome-wide scan of reading ability in affected sibling pairs with attention-deficit/hyperactivity disorder: unique and shared genetic effects.

Attention-deficit/hyperactivity disorder (ADHD) and reading disability (RD) are common highly heritable disorders of childhood, which frequently co-occur. Data from twin and family studies suggest that this overlap is, in part, due to shared genetic underpinnings. Here, we report the first genome-wide linkage analysis of measures of reading ability in children with ADHD, using a sample of 233 affected sibling pairs who previously participated in a genome-wide scan for susceptibility loci in ADHD. Quantitative trait locus (QTL) analysis of a composite reading factor defined from three highly correlated reading measures identified suggestive linkage (multipoint maximum lod score, MLS>2.2) in four chromosomal regions. Two regions (16p, 17q) overlap those implicated by our previous genome-wide scan for ADHD in the same sample: one region (2p) provides replication for an RD susceptibility locus, and one region (10q) falls approximately 35 cM from a modestly highlighted region in an independent genome-wide scan of siblings with ADHD. Investigation of an individual reading measure of Reading Recognition supported linkage to putative RD susceptibility regions on chromosome 8p (MLS=2.4) and 15q (MLS=1.38). Thus, the data support the existence of genetic factors that have pleiotropic effects on ADHD and reading ability--as suggested by shared linkages on 16p, 17q and possibly 10q--but also those that appear to be unique to reading--as indicated by linkages on 2p, 8p and 15q that coincide with those previously found in studies of RD. Our study also suggests that reading measures may represent useful phenotypes in ADHD research. The eventual identification of genes underlying these unique and shared linkages may increase our understanding of ADHD, RD and the relationship between the two.

Adolescent↗
PubMed2002

An X-chromosome scan reveals a locus for fat distribution in chromosome region Xp21-22.

Several groups have completed autosomal genome scans for human obesity, but only two have examined the X chromosome. A French group reported linkage of BMI to Xp and Xq markers, and a Finnish group reported linkage of BMI to Xq. We scanned the X chromosome in two cohorts, 190 European-American families (940 members) and 43 African-American families (208 members). We examined five correlated obesity phenotypes, BMI, body fat percentage, hip and waist circumferences, and plasma leptin concentration. We also examined leptin resistance (leptin/BMI) and fat patterning (waist-to-hip ratio [WHR]). Variables were adjusted for age within generation, race, and sex. We genotyped 20 markers with average spacing of 10 cM and no interval >22 cM and conducted nonparametric analyses. Suggestive linkage was found for WHR only. Linkage was supported in both family sets, and support was especially strong for females. Z scores for analyses of female phenotypes were 2.69, 1.73, and 2.37 (P = 0.0036, 0.0418, and 0.0089) for African-Americans, European-Americans, and the combined sample, respectively. The peaks were 51-73 cM from the p terminus, 14-34 cM distal of the French report in Xp22. Our results suggest that a quantitative trait locus influencing fat distribution in women may lie in chromosome region Xp21-22; however, the linked interval is large and differs substantially from that of the French and Finnish groups. Given the positive but divergent results, it would be worthwhile for others to examine the X chromosome.

Adipose Tissue↗
PubMed2003

Quantitative trait loci with opposing blood pressure effects demonstrating epistasis on Dahl rat chromosome 3.

Our previous linkage studies indicated that there might be a blood pressure (BP) quantitative trait locus (QTL) on chromosome 3 (Chr 3) contrasting between the Dahl salt-sensitive (S) strain and the Lewis (LEW) strain. To prove and then to narrow down the segment containing this QTL, five congenic strains have been generated by replacing various segments of the S rats with the homologous segments of the LEW rats. They are designated as S.L1, S.L2, S.L3, S.L4, and S.L5, respectively. S.L2, S.L3, S.L4, and S.L5 are substrains of S.L1, i.e., they contain substitutions of smaller sections within the large fragment defined by S.L1. The construction of these congenic strains was facilitated by a genome-wide marker screening process. BPs of the rats were measured by telemetry. S.L2 and S.L3 shared a fragment of Chr 3 in common and both showed a BP-lowering effect, indicating the existence of "-BP" QTL alleles from LEW compared with S. In contrast, S.L4 involves a section with no overlap with either S.L2 or S.L3, and S.L4 showed a BP significantly higher than that of S rats, indicating the presence of "+BP" QTL alleles from LEW compared with S. Interestingly, the combined effect of the -BP QTL and +BP QTL alleles was "-" in S.L1, implying that the "-" QTL is epistatic to "+" QTL.

Animals↗
PubMed2006

Gene flow's effect on the genetic architecture of a local adaptation and its consequences for QTL analyses.

This paper uses computer simulations to determine how gene flow between populations affects (1) the genetic architecture of a local adaptation and (2) properties of alleles segregating in quantitative trait locus (QTL) mapping populations. Results suggest that the average magnitude of an allele that causes a phenotypic difference between populations declines as the migration rate increases, but with an increase in migration, alleles of larger magnitude cause proportionally more of the phenotypic difference between populations. Gene flow between populations that are used in a QTL study tends to cause the average magnitude and percent variance explained (PVE) of an allele in a mapping population to increase. Thus, although the average magnitude of an allele causing a difference declines with migration the average magnitude or PVE of an allele in a QTL mapping population may increase. The reason is that the probability an allele is sampled for a QTL mapping population is in direct proportion to its frequency and alleles of larger magnitude tend to segregate at relatively higher frequencies than alleles of smaller effect with an increased migration. As the rate of gene flow between populations increases, the proportion of the phenotypic difference explained by alleles that are segregating in a QTL mapping population (and therefore potentially detected) decreases. Lastly, results suggest QTL alleles of large effect (>20% PVE) should be commonly found, provided the divergence time between populations is not too long or optima of populations are not too far apart.

Crosses, Genetic↗
PubMed2006

Quantitative trait loci for BMD identified by autosome-wide linkage scan to chromosomes 7q and 21q in men from the Amish Family Osteoporosis Study.

UNLABELLED: Using autosome-wide linkage analysis in 964 Amish, strong evidence was found for the presence of genes affecting hip and spine BMD in men on chromosomes 7q31 and 21q22 (LOD = 4.15 and 3.36, respectively). INTRODUCTION: BMD is highly heritable, with genetic factors accounting for 60-88% of variation. The goal of this study was to localize genes contributing to BMD variation. MATERIALS AND METHODS: The Amish Family Osteoporosis Study was designed to identify genes affecting bone health. The Amish are a genetically closed population with a homogeneous lifestyle. BMD was measured at the spine, hip, and radius using DXA in 964 participants (mean age, 50.2 +/- 16.3 [SD] years; range, 18-99 years) from large multigenerational families. Genotyping of 731 highly polymorphic microsatellite markers (average spacing of 5.4 cM) and autosome-wide multipoint linkage analysis were performed. RESULTS: In the overall study population, no strong evidence for linkage was detected to any chromosomal region (peak LOD: 2.11 for radius BMD on chromosome 3q26). In a subgroup analysis of men (n = 371), strong evidence was detected for a quantitative trait locus (QTL) influencing BMD variation on chromosome 7q31 at the total hip (LOD = 4.15) and femoral neck (LOD = 3.09) and for a second QTL influencing spine BMD at 21q22 (LOD = 3.36). Suggestive evidence of linkage was found in men for a QTL at 12q24 affecting total hip BMD (LOD = 2.60) and at 18p11 for femoral neck (LOD = 2.07), and in women (n = 593) at 1p36 for femoral neck BMD (LOD = 2.02) and at 1q21 for spine BMD (LOD = 2.11). In age subgroup analyses, suggestive evidence for linkage was found for those <50 years of age (n = 521) on chromosomes 11q22 and 14q23 (LODs = 2.11 and 2.16, respectively) and for those >50 years of age (n = 443) on 3p25.2 (LOD = 2.32). CONCLUSIONS: These results strongly suggest the presence of genes affecting hip and spine BMD in men on chromosomes 7q31 and 21q22. Modest evidence was found for genes affecting BMD in women on chromosomes 1p36 and 1q21 and in men at 12q24, replicating results from other populations.

Adolescent↗
PubMed2005

Meta-analysis of four new genome scans for lipid parameters and analysis of positional candidates in positive linkage regions.

Lipid levels in plasma strongly influence the risk for coronary heart disease. To localise and subsequently identify genes affecting lipid levels, we performed four genome-wide linkage scans followed by combined linkage/association analysis. Genome-scans were performed in 701 dizygotic twin pairs from four samples with data on plasma levels of HDL- and LDL-cholesterol and their major protein constituents, apolipoprotein AI (ApoAI) and Apolipoprotein B (ApoB). To maximise power, the genome scans were analysed simultaneously using a well-established meta-analysis method that was newly applied to linkage analysis. Overall LOD scores were estimated using the means of the sample-specific quantitative trait locus (QTL) effects inversely weighted by the standard errors obtained using an inverse regression method. Possible heterogeneity was accounted for with a random effects model. Suggestive linkage for HDL-C was observed on 8p23.1 and 12q21.2 and for ApoAI on 1q21.3. For LDL-C and ApoB, linkage regions frequently coincided (2p24.1, 2q32.1, 19p13.2 and 19q13.31). Six of the putative QTLs replicated previous findings. After fine mapping, three maximum LOD scores mapped within 1 cM of major candidate genes, namely APOB (LOD=2.1), LDLR (LOD=1.9) and APOE (LOD=1.7). APOB haplotypes explained 27% of the QTL effect observed for LDL-C on 2p24.1 and reduced the LOD-score by 0.82. Accounting for the effect of the LDLR and APOE haplotypes did not change the LOD score close to the LDLR gene but abolished the linkage signal at the APOE gene. In conclusion, application of a new meta-analysis approach maximised the power to detect QTLs for lipid levels and improved the precision of their location estimate.

Adolescent↗
PubMed2006

Unexpected high polymorphism at the FABP4 gene unveils a complex history for pig populations.

Fatty acid bing protein 4 (FABP4) plays a key role in fat regulation in mammals and is a strong positional candidate gene for the FAT1 quantitative trait locus located on porcine chromosome 4. DNA resequencing of the FABP4 gene region in 23 pigs from 10 breeds and wild boar revealed 134 variants in 6.4 kb, representing a silent nucleotide diversity of piS=0.01, much higher than reported so far in animal domestic species. Moreover, this diversity was highly structured. Also strikingly, the FABP4 phylogenetic tree did not show any geographical or breed origin clustering, with distant breeds sharing similar haplotypes and some of the most heterozygous samples pertaining to highly inbred animals like Iberian Guadyerbas (inbreeding coefficient approximately 0.3) or British Tamworth. In contrast, the cytochrome b (mtDNA) phylogenetic tree was coherent with geographical origin. The estimated age of the most recent common ancestor for the most divergent Iberian or Tamworth haplotypes was much older than domestication. An additional panel of 100 pigs from 8 different breeds and wild boar from Spain, Tunisia, Sardinia, and Japan was genotyped for seven selected single nucleotide polymorphisms and shows that high variability at the porcine FABP4 is the rule rather than the exception. Pig populations, even highly inbred, can maintain high levels of variability for surprisingly long periods of time.

Animals↗
PubMed1998

A factor preventing melanization of sephadex CM C-25 beads in Plasmodium-susceptible and refractory anopheles gambiae.

One major quantitative trait locus controls melanization of both malaria ookinetes and Sephadex CM beads in a refractory strain of the mosquito, Anopheles gambiae. Hemolymph transferred from a nonmelanizing, Plasmodium-susceptible strain (4arr) to a melanizing, Plasmodium-refractory strain (L35) caused a reduction in the melanization of CM beads. In addition, when beads were first incubated in vivo in susceptible mosquitoes and then recovered, washed, and transferred to refractory mosquitoes, a strong reduction in melanization was observed. No changes in melanization were observed when beads or hemolymph were transferred in the opposite direction or within a strain. Incubation of beads in vitro in refractory or susceptible hemolymph resulted in a reduction of melanization when these beads were subsequently transferred to refractory mosquitoes. This reduction was significantly stronger when susceptible hemolymph was used as the incubating medium. Protection from melanization was observed after 3-, 6-, and 24-h incubations of beads in susceptible mosquitoes with longer incubations resulting in greater protection. Treatment of protected beads with 1 M NaOH resulted in the loss of the protection but treatment with 1% sodium dodecyl sulfate (SDS), 1% SDS/DTT/boiling, or 1 M NaOAc (pH 8.9) did not. These results show that a melanization-preventing factor covalently binds to the surface of CM beads in susceptible mosquitoes and can subsequently prevent melanization in refractory mosquitoes.

Animals↗
PubMed1999

Asymptotic power of likelihood-ratio tests for detecting quantitative trait loci using the COGA data.

We investigated the asymptotic power of the likelihood-ratio test for detecting linkage to a quantitative trait locus (QTL) using the data set from the Collaborative Study on the Genetics of Alcoholism (COGA). Assuming a total trait heritability of 50% as determined for the COGA Cz P300 phenotype, we determined the minimum QTL heritability required at each point in the genome to achieve 80% power to detect linkage with a lod of 3.0. We find that there are regions of the genome where it is not possible to detect a QTL of any effect with 80% power, and that the overall minimum detectable QTL heritability for the COGA data is 0.35-0.40.

Alcoholism↗
PubMed2004

Comparative map and trait viewer (CMTV): an integrated bioinformatic tool to construct consensus maps and compare QTL and functional genomics data across genomes and experiments.

In the past few decades, a wealth of genomic data has been produced in a wide variety of species using a diverse array of functional and molecular marker approaches. In order to unlock the full potential of the information contained in these independent experiments, researchers need efficient and intuitive means to identify common genomic regions and genes involved in the expression of target phenotypic traits across diverse conditions. To address this need, we have developed a Comparative Map and Trait Viewer (CMTV) tool that can be used to construct dynamic aggregations of a variety of types of genomic datasets. By algorithmically determining correspondences between sets of objects on multiple genomic maps, the CMTV can display syntenic regions across taxa, combine maps from separate experiments into a consensus map, or project data from different maps into a common coordinate framework using dynamic coordinate translations between source and target maps. We present a case study that illustrates the utility of the tool for managing large and varied datasets by integrating data collected by CIMMYT in maize drought tolerance research with data from public sources. This example will focus on one of the visualization features for Quantitative Trait Locus (QTL) data, using likelihood ratio (LR) files produced by generic QTL analysis software and displaying the data in a unique visual manner across different combinations of traits, environments and crosses. Once a genomic region of interest has been identified, the CMTV can search and display additional QTLs meeting a particular threshold for that region, or other functional data such as sets of differentially expressed genes located in the region; it thus provides an easily used means for organizing and manipulating data sets that have been dynamically integrated under the focus of the researcher's specific hypothesis.

Adaptation, Physiological↗
PubMed2006

Population and systems genetics analyses of cortisol in pigs divergently selected for stress.

This study presents a systems genetic analysis on the physiology of cortisol in mice and pigs with an aim to show the potential of a comprehensive computational approach to quickly identify candidate genes and avoid a costly whole-genome quantitative trait locus (QTL) mapping. Population genetics analyses were performed on measurements of cortisol from a pig selection experiment. Expression QTL were mapped and gene networks were built using gene expressions for Crhr1 (corticotrophin-releasing hormone receptor) gene and single nucleotide polymorphisms from public mouse data. Results from mouse data were used to infer potential candidate regulatory genes involved in pig cortisol regulation, using a comparative or translational systems genetics approach. The pig data used were from a 10-yr divergent genetic selection experiment, providing data on 417 individuals. Population genetics analysis showed that cortisol is highly genetically determined with heritabilities of 0.40-0.70. Furthermore, a major gene with an additive effect of 86 ng/ml is segregating. Genetical-genomics investigations revealed two trans-acting eQTL for Crhr1 gene expression on chromosomes 2 and 13. Candidate gene search under trans-eQTL peaks yielded 63 genes for Crhr1 expression phenotypes. Functional links for Crhr1 genes with other genes/proteins in the gene network using mouse data were shown for the first 10 statistically significant genes involved. Results show translational or comparative systems genetics approaches reduce costs and time in large-scale genetics and "-omics" investigations. This is the first study to report a strong genetic basis for cortisol physiology using a systems approach.

Animals↗
PubMed2001

Genetic loci determining bone density in mice with diet-induced atherosclerosis.

This study investigates the phenotypic and genetic relationships among bone-density-related traits and those of adipose tissue and plasma lipids in mice with diet-induced atherosclerosis. Sixteen-month-old female F2 progeny of a C57BL/6J and DBA/2J intercross, which had received an atherogenic diet for 4 mo, were examined for multiple measures of femoral bone mass, density, and biomechanical properties using both computerized tomographic and radiographic methods. In addition, body weight and length, adipose tissue mass, plasma lipids and insulin, and aortic fatty lesions were assessed. Bone mass was inversely correlated with extent of atherosclerosis and with a prooxidant lipid profile and directly correlated with body weight, length, and, most strongly, adipose tissue mass. Quantitative trait locus (QTL) analysis, using composite interval mapping (CIM) and multi-trait analysis, identified six loci with multi-trait CIM LOD scores > 5. Three of these coincided with loci linked with adipose tissue and plasma high-density lipoprotein. Application of statistical tests for distinguishing close linkage vs. pleiotropy supported the presence of a potential pleiotropic effect of two of the loci on these traits. This study shows that bone mass in older female mice with atherosclerosis has multiple genetic determinants and provides phenotypic and genetic evidence linking the regulation of bone density with adipose tissue and plasma lipids.

Adipose Tissue↗
PubMed2004

Cloning and characterization of FAM13A1--a gene near a milk protein QTL on BTA6: evidence for population-wide linkage disequilibrium in Israeli Holsteins.

A cluster of genes coding for proteins of the extracellular matrix (ECM) containing sequence motifs essential for integrin-receptor interactions is located on HSA4q21 and on BTA6, within the critical region of a quantitative trait locus (QTL) affecting milk protein production. Genes within this cluster are involved in the formation of bone and lobuloalveolar structures in mammary gland and in kidney function. We cloned a bovine gene neighboring this ECM cluster, termed FAM13A1, the first member of a novel gene family (FAM13). A short predominant 5.1-kb mRNA variant capable of encoding 697 amino acids is transcribed from 18-exon orthologous genes in human and mouse. All putative protein orthologs contained a bipartite nuclear-localization signal and two coil-coiled domains. We detected two other FAM13 paralogs, C5ORF5 and FAM13C1, on HSA5q31 and HSA10q21, respectively. All FAM13 paralogs produce transcripts that are complementary to adjacent genes, suggesting that antisense transcription may regulate their functions. The structure of a longer 5.9-kb variant, FAM13A1_v2, that has an extra 7-exon putative RhoGAP domain at the N-terminus provides further clues to FAM13 function. Analysis of 400 bulls revealed a population-wide linkage disequilibrium between FAM13A1 polymorphisms and the QTL.

Amino Acid Sequence↗
PubMed1998

Genetic determinants of autoimmune disease and coronary vasculitis in the MRL-lpr/lpr mouse model of systemic lupus erythematosus.

MRL-lpr/lpr (MRL/lpr) mice are a model of human autoimmune disease. They exhibit a number of characteristics of systemic lupus erythematosus, including anti-DNA Abs, anti-cardiolipin Abs, immune complex-mediated vasculitis, lymphadenopathy, and severe glomerulonephritis. Although the autoimmune disorder is mediated primarily by mutation of the Fas gene (lpr), which interferes with lymphocyte apoptosis, MRL/lpr mice also have other predisposing genetic factors. In an effort to identify these additional factors, we have applied quantitative trait locus (QTL) mapping using an intercross between MRL/lpr mice and the nonautoimmune inbred strain BALB/cJ. A complete linkage map spanning the entire genome was constructed for 189 intercross progeny, and genetic loci contributing to features of the autoimmunity were identified using statistical analytic procedures. As expected, the primary genetic determinant of autoimmune disease in this cross was the Fas gene on mouse chromosome 19, exhibiting a lod score of 60. In addition, two novel loci, one on chromosome 2 (lod score, 4.3) and one on chromosome 11 (lod score, 3.1), were found to contribute to levels of anti-DNA Abs. Interestingly, the chromosome 19 and chromosome 11 QTLs, but not the chromosome 2 QTL, also exhibited associations with anti-cardiolipin Abs (lod scores, 38.4 and 2.6). We further examined the effects of these QTLs on the development of coronary vasculitis in the F2 mice. Our results indicate that the QTLs on chromosomes 11 and 19 also control the development of vasculitis, demonstrating common genetic determinants of autoantibody levels and vasculitis.

Animals↗
PubMed2006

QTL analysis of intraspecific differences between two Silene vulgaris ecotypes.

BACKGROUND AND AIMS: Serpentine soils provide a highly selective substrate for plant colonization and growth and represent an ideal system for studying the evolution of plant-ecotypes. In the present study the aim was to identify the genetic architecture of morphological traits distinguishing serpentine and non-serpentine ecotypes of Silene vulgaris. METHODS: Using an F(2) mapping population derived from an intraspecific cross between a serpentine and a non-serpentine ecotype of S. vulgaris, the genetic architecture of 12 morphological traits was explored using a quantitative trait locus (QTL) analysis. KEY RESULTS: The QTL analysis identified a total of 49 QTLs, of which 24 were classified as major QTLs. The mean number of QTLs per trait category was found to correspond well with numbers reported in the literature for similar crosses. Clustering of QTLs for different traits was found on several linkage groups. CONCLUSIONS: Morphological traits that differentiate the two ecotypes are strongly correlated, presumably as a consequence of the joint effects of extensive linkage of QTLs for different traits and directional selection. The signature of consistent directional selection was found for leaf and shoot trait divergence. Intraspecific ecotype differences in S. vulgaris were found to be distributed across the entire genome. The study shows that QTL analyses on non-model organisms can provide novel insights into the genetic basis of plant diversification.

Chromosome Mapping↗
PubMedDate not supplied

Bayes factors for detection of quantitative trait loci.

A fundamental issue in quantitative trait locus (QTL) mapping is to determine the plausibility of the presence of a QTL at a given genome location. Bayesian analysis offers an attractive way of testing alternative models (here, QTL vs. no-QTL) via the Bayes factor. There have been several numerical approaches to computing the Bayes factor, mostly based on Markov Chain Monte Carlo (MCMC), but these strategies are subject to numerical or stability problems. We propose a simple and stable approach to calculating the Bayes factor between nested models. The procedure is based on a reparameterization of a variance component model in terms of intra-class correlation. The Bayes factor can then be easily calculated from the output of a MCMC scheme by averaging conditional densities at the null intra-class correlation. We studied the performance of the method using simulation. We applied this approach to QTL analysis in an outbred population. We also compared it with the Likelihood Ratio Test and we analyzed its stability. Simulation results were very similar to the simulated parameters. The posterior probability of the QTL model increases as the QTL effect does. The location of the QTL was also correctly obtained. The use of meta-analysis is suggested from the properties of the Bayes factor.

Algorithms↗
PubMed2006

Identification and molecular mapping of PdR1, a primary resistance gene to Pierce's disease in Vitis.

A major quantitative trait locus (QTL) controlling resistance to Pierce's disease (PD) of grape, caused by the bacterium Xylella fastidiosa (Xf), was identified on a Vitis linkage map and denoted as 'Pierce's disease resistance 1' (PdR1). Placement of the locus was accomplished by evaluating a family of full-sib progeny from a cross of two PD-resistant interspecific hybrids with resistance inherited from Vitis arizonica. Resistance was measured under greenhouse conditions by direct quantification of Xf numbers in stem tissues as well as by evaluation of disease symptoms based on leaf scorch and a cane maturation index (CMI). A large QTL (LOD 17.2) accounting for 72% of the phenotypic variance in bacterial numbers was localized to linkage group 14 of the male parent F8909-17. The approximate 95% confidence interval around the QTL peak extended 5.7 cM when using composite interval mapping. The other disease evaluation methods (leaf scorch and CMI, respectively) placed the resistance QTL to the same region on linkage group 14, although at wider 95% confidence intervals (6.0 and 7.5 cM), lower peak LOD scores (11.9 and 7.7) and accounting for less phenotypic variance (59 and 42%). This is the first report of an Xf resistance QTL mapped in any crop species. The relevance of the markers located in the region spanning the QTL will be discussed, addressing their usefulness for the development of PD-resistant grape cultivars.

Chromosome Mapping↗