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Predicting quantitative trait levels by modeling SNP interaction.

Predicting phenotype from genotype is difficult when the phenotype is affected by a gene with numerous weakly penetrant alleles that differ only in the pattern of their single nucleotide polymorphisms (SNPs). While it is probable that SNP interactions affect phenotype, to our knowledge no one has determined the most effective way of evaluating whether SNPs interact and of modeling the interaction. Therefore, to explore this issue, we investigate here three methods of modeling SNP interaction using data from Genetic Analysis Workshop 12. Since major gene 5 (MG5) has sequence information and explains 37% of the variation in quantitative trait 5 (Q5), we focus on using SNPs within MG5 to predict Q5 among individuals who married into the pedigree. As a preliminary screening step, we reduced the number of SNPs from 269 to 34 based on their association with Q5. In our first models we assumed that SNPs affected Q5 in a simple additive manner. These models explained 34% and 15% of the variation in Q5 in women and men, respectively. Our second model was a linear model, which used individual SNPs and simple interaction terms as predictors. These models explained 36% and 16% of the variation in Q5 levels for women and men, respectively. Our last model was a "hit"-based model which was motivated by the hypothesis that disequilibrium between SNPs may reflect the fact that SNPs affect phenotype by acting in concert with other SNPs within their "disequilibrium set." Thus, the number of hits within the disequilibrium sets were used as predictors. These models explained 35% and 19% of the variation in Q5 for women and men, respectively. Our results suggest that phenotype can be predicted from complex patterns of weakly penetrant SNPs using relatively simple models. We concluded that SNP interaction either was not included in the simulation model, or had only a weak impact on Q5 levels.

Female↗

Using denaturing HPLC for SNP discovery and genotyping, and establishing the linkage disequilibrium pattern for the all-trans-retinol dehydrogenase (RDH8) gene.

All-trans-retinol dehydrogenase (RDH8) is a visual cycle enzyme that reduces all-trans-retinal to all-trans-retinol. As part of an on-going effort to map genes involved in complex eye diseases, myopia in particular, using association studies, single nucleotide polymorphisms (SNPs) were identified and linkage disequilibrium (LD) pattern was established within and around the RDH8 gene. We used denaturing high-performance liquid chromatography (DHPLC) to screen SNPs in four DNA pools each consisting of DNA from five individuals and genotyped the identified SNPs in 150 Chinese subjects from Hong Kong. Fifteen SNPs were identified: seven were common with the minor allele frequency >0.05 and ten were novel. Common SNPs were included in LD and haplotype analysis using the ASSOCIATE and EH programmes. Four SNPs in the 3' region exhibited significant LD and formed a haplotype block, while three common SNPs in the 5' region did not exhibit useful LD. The LD pattern around the RDH8 gene suggested that one SNP from the 3'region and two to three SNPs from the 5' region were needed in association studies involving RDH8. Our results demonstrated the efficiency of DHPLC in screening SNPs when coupled with DNA pooling strategy and in genotyping SNPs.

Alcohol Oxidoreductases↗

Single-nucleotide polymorphisms in the public domain: how useful are they?

There is a concerted effort by a number of public and private groups to identify a large set of human single-nucleotide polymorphisms (SNPs). As of March 2001, 2.84 million SNPs have been deposited in the public database, dbSNP, at the National Center for Biotechnology Information (http://www.ncbi.nlm.nih.gov/SNP/). The 2.84 million SNPs can be grouped into 1.65 million non-redundant SNPs. As part of the International SNP Map Working Group, we recently published a high-density SNP map of the human genome consisting of 1.42 million SNPs (ref. 3). In addition, numerous SNPs are maintained in proprietary databases. Our survey of more than 1,200 SNPs indicates that more than 80% of TSC and Washington University candidate SNPs are polymorphic and that approximately 50% of the candidate SNPs from these two sources are common SNPs (with minor allele frequency of > or =20%) in any given population.

DNA↗

Bioinformatic and experimental tools for identification of single-nucleotide polymorphisms in genes with a potential role for the development of the insulin resistance syndrome.

OBJECTIVES: Genes with a possible role for the development of the insulin resistance syndrome (IRS) were scanned for novel single-nucleotide polymorphisms (SNPs) using bioinformatics. METHODS: GenBank mRNA sequences were compared to the human EST database using gapped BLAST, software that is available on the internet. Mismatches between the search and the EST sequences indicated potential SNPs. Thirty-two SNPs in 13 genes were randomly chosen for experimental verification. PCR and direct sequencing were used to determine the 'true' SNPs. A random sample of 30 Swedish men with slightly elevated diastolic blood pressure (85-94 mmHg) obtained from a population-based study was selected for the sequencing. After completion of these stages, the potential SNPs were checked against the large and rapidly expanding SNP databases HGBASE and NCBI. RESULTS: EST searches of 146 genes revealed 106 potential SNPs in 44 genes. Experimental analysis of 32 of these potential SNPs verified two SNPs; endothelin receptor A 1471 G/C (3' UTR) and PAI-1 Trp514Arg from a T/C exchange. These two SNPs were also identified in the NCBI and HGBASE databases together with two polymorphisms that were not experimentally identified in our homogeneous Swedish population. Overall, the HGBASE and NCBI databases contained entries of 22% (23 out of 106) of the SNPs identified through our EST searches. CONCLUSIONS: In the search for genetic variations causing complex diseases like IRS in homogeneous populations (such as the Swedish one used here), important information can be obtained through bioinformatic searches of human genome databases and experimental verification.

Adult↗

Association between two mu-opioid receptor gene (OPRM1) haplotype blocks and drug or alcohol dependence.

We examined 13 single nucleotide polymorphisms (SNPs) spanning the coding region of the mu-opioid receptor gene (OPRM1), among 382 European Americans (EAs) affected with substance dependence [alcohol dependence (AD) and/or drug dependence (DD)] and 338 EA healthy controls. These SNPs delineated two haplotype blocks. Genotype distributions for all SNPs were in Hardy-Weinberg equilibrium (HWE) in controls, but in cases, four SNPs in Block I and three SNPs in Block II showed deviation from HWE. Significant differences were found between cases and controls in allele and/or genotype frequencies for six SNPs in Block I and two SNPs in Block II. Association of SNP4 in Block I with DD (allele: P=0.004), SNP5 in Block I with AD and DD (allele: P< or =0.005 for both) and two SNPs in Block II with AD (SNP11 genotype: P=0.002; SNP12 genotype: P=0.001) were significant after correction for multiple testing. Frequency distributions of haplotypes (constructed by five tag SNPs) differed significantly for cases and controls (P<0.001 for both AD and DD). Logistic regression analyses confirmed the association between OPRM1 variants and substance dependence, when sex and age of subjects and alleles, genotypes, haplotypes or diplotypes of five tag SNPs were considered. Population structure analyses excluded population stratification artifact. Additional supporting evidence for association between OPRM1 and AD was obtained in a smaller Russian sample (247 cases and 100 controls). These findings suggest that OPRM1 intronic variants play a role in susceptibility to AD and DD in populations of European ancestry.

Adult↗

Experimental validation of data mined single nucleotide polymorphisms from several databases and consecutive dbSNP builds.

Rapid development in the annotation of human genetic variation has increased the numbers of single nucleotide polymorphisms (SNPs) in candidate genes by several orders of magnitude. The selection of both useful target SNPs for disease-gene association studies and SNPs associated with the treatment response is therefore an increasingly challenging task. We describe a workflow for selecting SNPs based on their putative function and frequency in candidate genes extracted from PubMed resources. The annotation of each SNP and its frequency in a Caucasian population was assessed in several databases. Approximately 4000 SNPs were identified from an initial 233 candidate genes. In a case study, we performed actual genotyping of 1030 of these SNPs in 213 genes and obtained 710 successfully genotyped SNPs. Using the flow-chart outlined here, only 87 SNPs were monomorphic (approximately 12%). This study reports the frequency of SNPs in a Caucasian population, selected in silico, using a candidate gene approach and validated by actually genotyping 193 individuals. The selected genotypes represent a valuable set of verified candidate SNPs for pharmacogenetic studies in Caucasian populations.

Breast Neoplasms↗

Effect of MDR1 haplotype on risk of Parkinson disease.

BACKGROUND: MDR1, a multidrug transporter, encodes a P-glycoprotein that regulates the bioavailability of xenobiotics and is highly expressed at the blood-brain-barrier. Two single nucleotide polymorphisms (SNPs) (e21/2677[G/T/A] and e26/3435[C/T]) in the MDR1 gene can lead to differences in MDR1 expression and function. Specific MDR1 alleles of the 2 SNPs are positively selected among ethnic Chinese but not in the white population. OBJECTIVE: To determine whether specific haplotypes formed by SNPs e21/2677 and e26/3435 may protect against Parkinson disease (PD) among ethnic Chinese in Hong Kong. DESIGN: Case-control study. SETTING: Tertiary referral centers in Hong Kong. SUBJECTS: One hundred eighty-five patients with PD and 206 control subjects. INTERVENTIONS: The two SNPs were amplified in a single multiplex polymerase chain reaction. Five other SNPs that span 100 kilobases of the gene were also analyzed. MAIN OUTCOME MEASURES: Haplotypes frequencies, degree of haplotype association with the disease status, and estimated odds ratio for each haplotype with associated 95% confidence intervals. RESULTS: In addition to 2677 G-->T/A (exon 21) and 3435 C-->T (exon 26), the other SNPs that were analyzed were -41 A-->G (intron -1), -145 C-->G (exon 1), -129 T-->C (exon 1), 1236 T-->C (exon 12), and 4036 A-->G (exon 28). Haplotypes containing SNPs e21/2677 and e26/3435 were found to be significantly associated with risk of PD. In particular, the 2677T-3435T haplotype was strongly associated with a reduced risk of PD (P<.001; chi(2) = 14.521; odds ratio, 0.33; 95% confidence interval, 0.19-0.59). CONCLUSIONS: An MDR1 haplotype containing SNPs e21/2677T and e26/3435T protects against PD in ethnic Chinese, compatible with the observation of a recent positive selection of the T alleles of these 2 SNPs in this ethnic population.

Adult↗

Informativity assessment for biallelic single nucleotide polymorphisms.

Common single nucleotide polymorphisms (SNPs) have the potential to provide a widely used means of simple and robust kinship testing. Suitable measures of polymorphism informativity are therefore required in order to guide the search for the most efficient combinations of SNPs. In the context of kinship testing, such measures should preferably be related to Z, the power of excluding false paternity in trios comprising mother, child and alleged father. Since the bulk of SNPs is expected to be biallelic, a Z-related measure of informativity can be defined for SNPs in a particularly elegant manner: allele frequency vectors of sets of n biallelic SNPs that give rise to the same Z value approximate to an n-dimensional sphere around (1/2,...,1/2). Owing to this relationship, it can be shown that the number N of maximally informative SNPs (i.e., of SNPs with allele frequencies 1/2), providing the same Z value as a given set of n SNPs, approximates to 2n times the average gene diversity of the latter. Linear regression analysis of a large number of simulated SNP sets reveals that only a minor linear correction of Nis required for large n. Since Z= 1-(13/16)N, Ncan also be calculated easily for multiallelic markers with known Z. The "equivalent number of maximally informative SNPs", N, is therefore suggested as a measure of marker informativity in the context of kinship testing.

Alleles↗

KCNQ4: a gene for age-related hearing impairment?

Age-related hearing impairment (ARHI) is the most common sensory impairment among the elderly. It is a complex disorder influenced by genetic as well as environmental factors. SNPs in a candidate susceptibility gene, KCNQ4, were examined in two independent Caucasian populations. Two quantitative trait locus (QTL) values were investigated: Zhigh and Zlow, a measure of high and respectively low frequency hearing loss. In the first population, the statistical analysis of 23 genotyped SNPs spread across KCNQ4 resulted in significant p-values for two SNPs for Zhigh-SNP9 (NT_004511:g.11244177A > T) and SNP15 (NT_004511:g.11257005C > T; NP_004691:p.Ala259Ala), and one SNP for Zlow-SNP12 (NT_004511:g.11249550A > T). The linkage disequilibrium (LD) structure of KCNQ4 was subsequently determined in a 34-kb region surrounding the significant SNPs, resulting in three LD-blocks. LD-block 1 contains SNP9 and covers an area of 5 kb, LD-block 2 measures 5 kb and surrounds SNP13 (NT_004511:g.11253513A > G) to SNP18 (NT_004511:g.11257509G > A; NP_004691:p.Thr293Thr), and LD-block 3 spans 7 kb. Five tag-SNPs of block 1 and 2, and 2 extra SNPs were subsequently genotyped in the second population. Again, several SNPs were positively associated with ARHI: one SNP (SNP18) for the high frequencies and three SNPs (SNP9, SNP12, and SNP18) for the low frequencies, although only a single SNP (SNP12) resulted in significant p-values in both populations. Nevertheless, the associated SNPs of both populations were all located in the same 13-kb region in the middle of the KCNQ4 gene.

Adult↗

A comprehensive association study for genes in inflammation pathway provides support for their roles in prostate cancer risk in the CAPS study.

BACKGROUND: Recently identified associations of prostate cancer risk with several genes involved in innate immunity support a role of inflammation in the etiology of prostate cancer. Considering inflammation is regulated by a complex system of gene products, we hypothesize sequence variants in many other genes of this pathway are associated with prostate cancer. METHODS: We evaluated 9,275 SNPs in 1,086 genes of the inflammation pathway using a MegAllele genotyping system among 200 familial cases and 200 unaffected controls selected from a large Swedish case-control population (CAPS). RESULTS: We found that significantly more than the expected numbers of SNPs were significant at a nominal P-value of 0.01, 0.05, and 0.1, providing overall support for our hypothesis. The excess was largest when using a more liberal nominal P-value (0.1); we observed 992 significant SNPs compared with the 854 significant SNPs expected by chance, and this difference was significant based on a permutation test (P = 0.0025). We also began the effort of differentiating true associated SNPs by selecting a small subset of significant SNPs (N = 26) and genotyped these in an independent sample of approximately 1,900 CAPS1 subjects. We were able to confirm 3 of these 26 SNPs. It is expected that many more true associated SNPs will be confirmed among the 992 significant SNPs identified in our pathway screen. CONCLUSIONS: Our study provides the first objective support for an association between prostate cancer and multiple modest-effect genes in inflammatory pathways.

Aged↗

Identification of regulatory polymorphisms in the TNF-TNF receptor superfamily.

The tumor necrosis factor and TNF receptor (TNF-TNFR) superfamily plays very important roles in the pathogenesis of many immune-mediated diseases. Regulation of TNF-TNFR superfamily gene expression influences many aspects of the pathology associated with these diseases. In order to investigate genetic variations in the regulatory regions of the TNF-TNFR superfamily genes, promoter regions were screened by sequencing DNA samples from 24 unrelated Korean individuals. We identified a total of 68 single-nucleotide polymorphisms (SNPs) in the regulatory regions of the known TNF-TNFR superfamily genes, including 50 SNPs in the promoter regions, 16 SNPs in the 5'-UTR regions, and two SNPs in the coding regions of these genes. Among the 68 SNPs identified in this study, 25 SNPs were novel SNPs. Interestingly, the sequence alteration created by 11 SNPs completely abolished putative transcription factor binding sites in these alleles. These results suggest that these SNP sites can regulate gene expression by controlling the binding of transcription factors. The identification of function-altering SNPs in the promoter regions of the TNF-TNFR superfamily will facilitate efforts to understand the association of TNF-TNFR superfamily genes with several immune-mediated human diseases.

Binding Sites↗

The study of neighboring nucleotide composition and transition/transversion bias.

Base substitution is one of the raw fuels that produce genetic variation and drive evolution. Recent studies have shown that the genome components affect mutation patterns to some extent. In order to infer the correlation between the Transition/Transversion ratio (Ts/Tv) and the number of immediately adjacent A and T nucleotides, we investigated 3611007 Oryza sativa SNPs (including 45462 coding SNPs, and 242811 intronic SNPs) and 32019 Arabidopsis SNPs. The results show that Ts/Tv is negatively correlated with the number of immediately adjacent A and T in O. sativa and Arabidopsis. We further calculated AT2 (the number of SNPs whose immediately adjacent nucleotides are either A or T) and AT0 (the number of SNPs whose immediately adjacent nucleotides are either C or G) for all 6 types of SNPs. C/G SNP of O. sativa and Arabidopsis has the highest AT2/AT0, which denotes C/G SNP may be influenced by the adjacent A and T nucleotides mostly. For SNPs in O. sativa, the neighboring effect of A and T nucleotides is limited to 2 nucleotides on both sides; for SNPs in Arabidopsis, the effect extends no more than 4 nucleotides on both sides.

Arabidopsis↗

High-density single-nucleotide polymorphism maps of the human genome.

Here we report a large, extensively characterized set of single-nucleotide polymorphisms (SNPs) covering the human genome. We determined the allele frequencies of 55,018 SNPs in African Americans, Asians (Japanese-Chinese), and European Americans as part of The SNP Consortium's Allele Frequency Project. A subset of 8333 SNPs was also characterized in Koreans. Because these SNPs were ascertained in the same way, the data set is particularly useful for modeling. Our results document that much genetic variation is shared among populations. For autosomes, some 44% of these SNPs have a minor allele frequency > or =10% in each population, and the average allele frequency differences between populations with different continental origins are less than 19%. However, the several percentage point allele frequency differences among the closely related Korean, Japanese, and Chinese populations suggest caution in using mixtures of well-established populations for case-control genetic studies of complex traits. We estimate that approximately 7% of these SNPs are private SNPs with minor allele frequencies <1%. A useful set of characterized SNPs with large allele frequency differences between populations (>60%) can be used for admixture studies. High-density maps of high-quality, characterized SNPs produced by this project are freely available.

Alleles↗

Single nucleotide polymorphism spectra in newborns and centenarians: identification of genes coding for rise of mortal disease.

Some single-nucleotide polymorphisms (SNPs) increase the risk of mortal disease. Identifying these SNPs and the genes in which they reside is an important area in human genomics. Such qualitative observations are important in themselves. However, an accurate assessment of the numerical distribution and age-dependent decline of SNPs in the population would permit calculation of the rises represented by each SNP. Such analyses have not been attempted because of a lack of an efficient and cost-effective method to detect multiple SNPs in a large number of individuals and a large number of genes. Here, we suggest the use of an analytical procedure that can scan for SNPs in 100-bp DNA sequences from as many as 10000 donors' blood cell samples, or 20000 alleles, simultaneously. Our suggestion is based on technology developed for studies of somatic mutations in human tissue DNA for point mutations at frequencies equal to or greater than 10(-6). In a simplified version of this technology, any SNP arising at frequencies at or above 5x10(-4) would be identified with useful precision. A gene would be represented by 10 or more sections of 100bp. This strategy includes splice-site mutations that represent a significant fraction of gene inactivating point mutations and would not be observed in strategies using cDNA. To illustrate the logic of the suggested approach, we use American mortality records to calculate the expected decrease in SNPs coding for premature mortality in newborns and centenarians. We consider several elementary cases: SNPs in one gene only, any of several genes, or all of several genes that create a risk of death by pancreatic cancer. The fraction of expressed polymorphisms affecting mortality should be simultaneously increased in probands and decreased in the aged relative to newborns. Silent polymorphisms in the same gene would remain unchanged in all three groups and serve as internal standards. A key point is that scanning a gene, in which loss of gene function creates the risk of mortality is expected to reveal not one, but multiple SNPs, which decline with age, as carriers die earlier in life than non-carriers. Several SNPs in a scanned gene would suggest that the decreasing SNP was genetically linked to a different polymorphism that creates the disease risk.

Age Factors↗

Identification and characterization of single-nucleotide polymorphisms in MCH-R1 and MCH-R2.

OBJECTIVE: To identify and functionally characterize single-nucleotide polymorphisms (SNPs) in melanin-concentrating hormone (MCH)-R1 and -R2. RESEARCH METHODS AND PROCEDURES: The entire coding regions and intron/exon splice junction regions of MCH-R1 and MCH-R2 were sequenced from anonymous white (n=45) and African-American (n=46) individuals. DNA was analyzed, and SNPs were identified using Phred, Phrap, and Consed software. DNA constructs containing MCH-R1 and MCH-R2 SNPs were generated and expressed in CHO cells. The effect of the SNPs in MCH-R1 and MCH-R2 were assessed in receptor binding assays and functional assays measuring changes in intracellular cAMP and Ca2+ levels. RESULTS: We identified 12 SNPs in the MCH-R1 gene. Two of these SNPs are in coding regions, and one produces an arginine-for-glycine substitution at residue 34 in the MCH-R1 sequence. This SNP is present at a minor allele frequency of 15% in the African-American population tested in this study. We identified eight SNPs in the MCH-R2 gene. Four of these SNPs are in coding regions, and two produce amino acid substitutions. Lysine substitutes for arginine at residue 63 of the African-American population, and glutamine substitutes for arginine at residue 152 in whites (minor allele frequency of 2% for both SNPs). No changes in receptor binding or functional signaling were observed with the SNP mutations in MCH-R1 or MCH-R2. DISCUSSION: These data indicate that potential therapeutics designed to act at the MCH receptor are unlikely to have altered effects in subpopulations that express variant forms of MCH-R1 or MCH-R2.

Amino Acid Sequence↗

Evidence for non-additive influence of single nucleotide polymorphisms within the apolipoprotein E gene.

We analyzed 13 single nucleotide polymorphisms (SNPs) within the apolipoprotein E (APOE) gene, to identify pairs of SNPs that interact in a non-additive manner to influence genotypic mean levels of the ApoE protein in blood. An overparameterized general linear model of two-SNP genotype means was applied to data from 456 female and 398 male unrelated European Americans from Rochester, MN, USA. We found statistically significant evidence for non-additivity between SNPs within the male sample, but not within the female sample. We observed nine pairs of SNPs with evidence of non-additivity at the alpha=0.05 level of statistical significance within the male sample, when approximately three were expected by chance. Five of the nine pairs involved three SNPs (560, 624 and 1163) that did not have a statistically significant influence when considered separately in a single-site analysis. Three of the nine pairs involving four SNPs (832, 1998, 3937 and 4951) showed significant evidence for non-additivity in at least one of two other male samples from Jackson, MS, USA and North Karelia, Finland. Although all four of these SNPs had a statistically significant influence in Rochester when considered separately, only SNP 3937 gave a significant result in the other male samples. The four SNPs are located in the promoter, intronic and exonic regions, and 3' to the polyadenylation signal in the APOE gene. Our study suggests that analyses that only consider SNPs located in exons and ignore contexts such as those indexed by gender and population, and disregard non-additivity of SNP effects, may inappropriately model the contribution of a gene to the genetic architecture of a trait that has a complex multifactorial etiology.

Apolipoproteins E↗

Genetic variation in putative regulatory loci controlling gene expression in breast cancer.

Candidate single-nucleotide polymorphisms (SNPs) were analyzed for associations to an unselected whole genome pool of tumor mRNA transcripts in 50 unrelated patients with breast cancer. SNPs were selected from 203 candidate genes of the reactive oxygen species pathway. We describe a general statistical framework for the simultaneous analysis of gene expression data and SNP genotype data measured for the same cohort, which revealed significant associations between subsets of SNPs and transcripts, shedding light on the underlying biology. We identified SNPs in EGF, IL1A, MAPK8, XPC, SOD2, and ALOX12 that are associated with the expression patterns of a significant number of transcripts, indicating the presence of regulatory SNPs in these genes. SNPs were found to act in trans in a total of 115 genes. SNPs in 43 of these 115 genes were found to act both in cis and in trans. Finally, subsets of SNPs that share significantly many common associations with a set of transcripts (biclusters) were identified. The subsets of transcripts that are significantly associated with the same set of SNPs or to a single SNP were shown to be functionally coherent in Gene Ontology and pathway analyses and coexpressed in other independent data sets, suggesting that many of the observed associations are within the same functional pathways. To our knowledge, this article is the first study to correlate SNP genotype data in the germ line with somatic gene expression data in breast tumors. It provides the statistical framework for further genotype expression correlation studies in cancer data sets.

Breast Neoplasms↗

Linkage disequilibrium and allele-frequency distributions for 114 single-nucleotide polymorphisms in five populations.

Single-nucleotide polymorphisms (SNPs) may be extremely important for deciphering the impact of genetic variation on complex human diseases. The ultimate value of SNPs for linkage and association mapping studies depends in part on the distribution of SNP allele frequencies and intermarker linkage disequilibrium (LD) across populations. Limited information is available about these distributions on a genomewide scale, particularly for LD. Using 114 SNPs from 33 genes, we compared these distributions in five American populations (727 individuals) of African, European, Chinese, Hispanic, and Japanese descent. The allele frequencies were highly correlated across populations but differed by >20% for at least one pair of populations in 35% of SNPs. The correlation in LD was high for some pairs of populations but not for others (e.g., Chinese American or Japanese American vs. any other population). Regardless of population, average minor-allele frequencies were significantly higher for SNPs in noncoding regions (20%-25%) than for SNPs in coding regions (12%-16%). Interestingly, we found that intermarker LD may be strongest with pairs of SNPs in which both markers are nonconservative substitutions, compared to pairs of SNPs where at least one marker is a conservative substitution. These results suggest that population differences and marker location within the gene may be important factors in the selection of SNPs for use in the study of complex disease with linkage or association mapping methods.

Alleles↗