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Electrokinetically based approach for single-nucleotide polymorphism discrimination using a microfluidic device.

In this work, we describe and implement an electrokinetic approach for single-nucleotide polymorphism (SNP) discrimination using a PDMS/glass-based microfluidic chip. The technique takes advantage of precise control of the coupled thermal (Joule heating), shear (electroosmosis), and electrical (electrophoresis) energies present at an array of probes afforded by the application of external electrical potentials. Temperature controllers and embedded thermal devices are not required. The chips can be easily and inexpensively fabricated using standard microarray printing methods combined with soft-lithography patterned PDMS fluidics, making these systems easily adaptable to applications using higher density arrays. Extensive numerical simulations of the coupled flow and thermal properties and microscale thermometry experiments are described and used to characterize the in-channel conditions. It was found that optimal conditions for SNP detection occur at a lower temperature on-chip than for typical microarray experiments, thereby revealing the importance of the electrical and shear forces to the overall process. To demonstrate the clinical utility of the technique, the detection of single-base pair mutations in the survival motor neuron gene, associated with the childhood disease spinal muscular atrophy, is conducted.

Cyclic AMP Response Element-Binding Protein↗

The causal element for the lactase persistence/non-persistence polymorphism is located in a 1 Mb region of linkage disequilibrium in Europeans.

Expression of lactase in the intestine persists into adult life in some people and not others, and this is due to a cis-acting regulatory polymorphism. Previous data indicated that a mutation leading to lactase persistence had occurred on the background of a 60 kb 11-site LCT haplotype known as A (Hollox et al. 2001). Recent studies reported a 100% correlation of lactase persistence with the presence of the T allele at a CT SNP at -14 kb from LCT, in individuals of Finnish origin, suggesting that this SNP may be causal of the lactase persistence polymorphism, and also reported a very tight association with a second SNP (GA -22 kb) (Enattah et al. 2002). Here we report the existence of a one megabase stretch of linkage disequilibrium in the region of LCT and show that the -14 kb T allele and the -22 kb A allele both occur on the background of a very extended A haplotype. In a series of Finnish individuals we found a strong correlation (40/41 people) with lactose digestion and the presence of the T allele. The T allele was present in all 36 lactase persistent individuals from the UK (phenotyped by enzyme assay) studied, 31/36 of whom were of Northern European ancestry, but not in 11 non-persistent individuals who were mainly of non-UK ancestry. However, the CT heterozygotes did not show intermediate lactase enzyme activity, unlike those previously phenotyped by determining allelic transcript expression. Furthermore the one lactase persistent homozygote identified by having equally high expression of A and B haplotype transcripts, was heterozygous for CT at the -14 kb site. SNP analysis across the 1 megabase region in this person showed no evidence of recombination on either chromosome between the -14 kb SNP and LCT. The combined data shows that although the -14 kb CT SNP is an excellent candidate for the cause of the lactase persistence polymorphism, linkage disequilibrium extends far beyond the region searched so far. In addition, the CT SNP does not, on its own, explain all the variation in expression of LCT, suggesting the possibility of genetic heterogeneity.

Alleles↗

Age at onset of Huntington disease is not modulated by the R72P variation in TP53 and the R196K variation in the gene coding for the human caspase activated DNase (hCAD).

BACKGROUND: TP53 is an attractive candidate for modifying age of onset (AO) in Huntington disease (HD): The amino-terminus of the mutated huntingtin (htt) exon 1 translation product has functional properties which may affect critically the TP53 pathway in HD neurons. The pathogenic domain of mutant htt interacts with nuclear transcription factors, and it potentially modulates TP53-induced transcriptional events. A single nucleotide polymorphism (SNP) resulting in the R72P exchange in TP53 protein might modulate the variation in AO. In addition, also the R196K replacement in human caspase activated DNase (hCAD) may theoretically affect the AO. METHODS: We have genotyped the polymorphisms R72P and R196K in a well established cohort of 167 unrelated HD patients. RESULTS: The expanded CAG repeat explained 30.8% of the variance in AO. Adding the genotypes of the SNPs investigated did not affect the variance of the AO variance explained. CONCLUSION: In this replication study, no association was found explaining a significant amount of the variability in AO of HD thus contradicting a recent report.

Age of Onset↗

Genomic structure and organization of the high grade Myopia-2 locus (MYP2) critical region: mutation screening of 9 positional candidate genes.

PURPOSE: Myopia is a common complex eye disorder, with implications for blindness due to increased risk of retinal detachment, chorioretinal degeneration, premature cataracts, and glaucoma. A genomic interval of 2.2 centiMorgans (cM) was defined on chromosome band 18p11.31 using 7 families diagnosed with autosomal dominant high myopia and was designated the MYP2 locus. To characterize this region, we analyzed 9 known candidate genes localized to within the 2.2 cM interval by direct sequencing. METHODS: Using public databases, a physical map of the MYP2 interval was compiled. Gene expression studies in ocular tissues using complementary DNA library screens, microarray experiments, reverse transcription techniques, and expression data identified in external databases aided in prioritizing gene selection for screening. Coding regions, intron-exon boundaries and untranslated exons of all known genes [Clusterin-like 1 (CLUL1), elastin microfibril interfacer 2 (EMILIN2), lipin 2 (LPIN2), myomesin 1 (MYOM1), myosin regulatory light chain 3 (MRCL3), myosin regulatory light chain 2 (MRLC2), transforming growth beta-induced factor (TGIFbeta), large Drosophila homolog associated protein 1 (DLGAP1), and zinc finger protein 161 homolog (ZFP161)] were sequenced using genomic DNA samples from 9 affected and 6 unaffected MYP2 pedigree members, and from 5 external controls (4 unaffected and 1 affected). Gene sequence changes were compared to known variants from public single nucleotide polymorphism (SNP) databases. RESULTS: In total, 103 polymorphisms were found by direct sequencing; 10 were missense, 14 were silent, 26 were not translated, 49 were intronic, 1 insertion, and 3 were homozygous deletions. Twenty-seven polymorphisms were novel. Novel SNPs were submitted to the public database; observed frequencies were submitted for known SNPs. No sequence alterations segregated with the disease phenotype. CONCLUSIONS: Mutation analysis of 9 encoded positional candidate genes on MYP2 loci did not identify sequence alterations associated with the disease phenotype. Further studies of MYP2 candidate genes, including analysis of putative genes predicted in silico, are underway.

Chromosomes, Human, Pair 18↗

Genotyping single nucleotide polymorphisms by MALDI mass spectrometry in clinical applications.

Matrix-assisted laser desorption/ionization time-of-flight (MALDI-TOF) mass spectrometry has become one of the most powerful and widely applied technologies for SNP scoring and determination of allele frequencies in the post-genome sequencing era. Although different strategies for allele discrimination combined with MALDI were devised, in practice only primer extension methods are nowadays routinely used. This combination enables the rapid, quantitative, and direct detection of several genetic markers simultaneously in a broad variety of biological samples. In the field of molecular diagnostics, MALDI has been applied to the discovery of genetic markers, that are associated with a phenotype like a disease susceptibility or drug response, as well as an alternative means for diagnostic testing of a range of diseases for which the responsible mutations are already known. It is one of the first techniques with which whole genome scans based on single nucleotide polymorphisms were carried out. It is equally well suited for pathogen identification and the detection of emerging mutant strains as well as for the characterization of the genetic identity and quantitative trait loci mapping in farm animals. MALDI can also be used as a detection platform for a range of novel applications that are more demanding than standard SNP genotyping such as mutation/polymorphism discovery, molecular haplotyping, analysis of DNA methylation, and expression profiling. This review gives an introduction to the application of mass spectrometry for DNA analysis, and provides an overview of most studies using SNPs as genetic markers and MALDI mass spectrometric detection that are related to clinical applications and molecular diagnostics. Further, it aims to show specialized applications that might lead to diagnostic applications in the future. It does not speculate on whether this methodology will ever reach the diagnostic market.

Animals↗

Fast detection of single nucleotide polymorphisms (SNPs) by primer elongation with monitoring of supercritical-angle fluorescence.

We describe the rapid detection of single nucleotide polymorphisms (SNPs) by real-time observation of primer elongation. The enzymatic elongation of surface-bound primers is monitored by detecting the increase of surface-bound fluorescence caused by the incorporation of Cy5-labelled deoxycytidine 5'-triphosphate residues (Cy5-dCTPs) into the corresponding strand. In order to discriminate against the fluorescence from unbound Cy5-dCTPs, the detection volume was restricted to the surface by collecting supercritical-angle fluorescence. The efficiency of enzymatic double-stranded DNA synthesis is governed by the complementarity of the primer and template. An SNP in the sequence of the primer obstructs its elongation increasingly with decreased distance of the mismatch to the 3' end of the primer. By real-time fluorescence detection during primer elongation, SNPs can be detected within a few minutes, which is significantly faster than in experiments where the fluorescence is measured after completion of the reaction. We demonstrate the efficiency of the method by detecting an SNP in the ErbB2 gene that is involved in causing a higher risk of breast cancer.

Base Pair Mismatch↗

Quantification of single nucleotide polymorphisms by automated DNA sequencing.

Single nucleotide polymorphisms (SNPs) are linked to phenotypes associated with diseases and drug responses. Many techniques are now available to identify and quantify such SNPs in DNA or RNA pools, although the information on the latter is limited. The majority of these methodologies require prior knowledge of target sequences, normally obtained through DNA sequencing. Direct quantitation of SNPs from DNA sequencing raw data will save time and money for large amount sample analysis. A high throughput DNA sequencing assay, in combination with a SNP quantitative algorithm, was developed for the quantitation of a SNP present in HCV RNA sequences. For a side-by-side comparison, a Pyrosequencing assay was also developed. Quantitation performance was evaluated for both methods. The direct DNA sequencing quantitation method was shown to be more linear, accurate, sensitive, and reproducible than the Pyrosequencing method for the quantitation of the SNP present in HCV RNA molecules.

Algorithms↗

No association was found between a functional SNP in ZDHHC8 and schizophrenia in a Japanese case-control population.

ZDHHC8 is a new and attractive candidate for a schizophrenia-susceptibility factor. First, several lines of linkage studies showed that 22q11, on which ZDHHC8 is located, is a "hot" region. Second, fine linkage disequilibrium mapping revealed a significant association around ZDHHC8. Moreover, a very recent study reported that one single nucleotide polymorphism (SNP: rs175174) in ZDHHC8 might affect the splicing process, the ZDHHC8 knock-out mice showed the gender-specific phenotype, and the transmission disequilibrium test (TDT) using this SNP also showed significant association with human female schizophrenia. Thus, we attempted a replication study of this SNP using relatively large Japanese case-control samples (561 schizophrenics and 529 controls). No association was found between schizophrenia and controls even after dividing samples by gender. Because our sample size provided quite high power, ZDHHC8 may not play a major role in Japanese schizophrenia. And our results did not support the gender-specific effect of this SNP.

Acyltransferases↗

Candidate gene analysis of IP-10 gene in patients with Alzheimer's disease.

Interferon-gamma-inducible Protein-10 (IP-10) is supposed to play a role in Alzheimer's disease (AD) development, as demonstrated by increased levels in cerebrospinal fluid from patients with AD. A mutation scanning of IP-10 exonic region was carried out in 10 patients with AD and 10 age-matched controls, demonstrating the presence of two previously reported single nucleotide polymorphisms (SNPs) in exon 4 (G-->C and T-->C) as well as a novel SNP in exon 2 (C-->T). Exon 4 G-->C and T-->C allelic variants were next evaluated in a population of 279 AD patients and 251 controls, in order to determine whether their presence could influence the susceptibility towards the development of the disease. These two SNPs were in complete linkage disequilibrium. No differences in haplotype frequencies were found in AD patients as compared with controls, even stratifying according to the presence of Apolipoprotein E varepsilon4 allele, gender or age at onset. A new protocol was developed to easily determine the C-->T SNP in exon 2. A preliminary analysis revealed a very low frequency of this allelic variant (1%). Therefore, the complete association study was not carried out because the size of our population was not sufficient to draw reliable conclusions. According to these results, IP-10 does not seem to be a risk factor for AD. However, a novel rare polymorphism has been identified, which could exert a role in AD susceptibility. Thus, further studies on larger populations are needed before confidently excluding IP-10 as a susceptibility gene for AD.

Age of Onset↗

A double-screening method to identify reliable candidate non-synonymous SNPs from chicken EST data.

Discovery of non-synonymous single nucleotide polymorphisms (nsSNP), which cause amino acid substitutions, is important because they are more likely to alter protein function than synonymous SNPs (sSNP) or those SNPs that do not result in amino acid changes. By changing the coding sequences, nsSNP may play a role in heritable differences between individual organisms. In the chicken and many other vertebrates, the main obstacle for identifying nsSNP is that there is insufficient protein and mRNA sequence information for self-species referencing and thus, determination of the correct reading frame for expressed sequence tags (ESTs) is difficult. Therefore, in order to estimate the correct reading frame at nsSNP in chicken ESTs, a double-screening approach was designed using self- or cross-species protein referencing, in addition to the ESTScan coding region estimation programme. Starting with 23 427 chicken ESTs, 1210 potential SNPs were discovered using a phred/phrap/polyphred/consed pipeline process and among these, 108 candidate nsSNP were identified with the double screening method. A searchable SNP database (chicksnps) for the candidate chicken SNPs, including both nsSNPs and sSNPs is available at http://chicksnps.afs.udel.edu. The chicken SNP data described in this paper have been submitted to the data base SNP under National Center for Biotechnology Information assay ID ss4387050-ss4388259.

Animals↗

Superimposing polymorphism: the case of a point mutation within a polymorphic Alu insertion.

The COL3A1 Alu insertion is a member of the AluY subfamily. It has been found to be absent in non-human primates and polymorphic in worldwide human populations. The integration of the element into the human genome seems to have preceded the initial migration(s) of anatomically modern humans out of the African continent. Although the insertion has been detected in populations from all the continents, its highest frequency values are located within sub-Saharan Africa. The sequence alignment of the COL3A1 insertion from several African individuals revealed a bi-allelic single nucleotide polymorphism (SNP) at the downstream terminus of the element's poly-A tract. Once discovered, a selective PCR procedure was designed to determine the frequency of both alleles in 19 worldwide populations. The A-allele in this binary SNP experiences a clinal increase in the eastward direction from Africa to Southeast Asia and Mongolia, reaching fixation in the two latter regions. The T variant, on the other hand, exhibits a westward clinal increase outside of Africa, with its lowest frequency in Asia and achieving fixation in northern Europe. The presence of this internal SNP extends the usefulness provided by the polymorphic Alu insertion (PAI). It is possible that superimposing polymorphisms like this one found in the COL3A1 locus may accentuate signals from genetic drift events allowing for visualization of recent dispersal patterns.

Africa↗

A polymorphism in the CDKN1B gene is associated with increased risk of hereditary prostate cancer.

The loss of cell cycle control is believed to be an important mechanism in the promotion of carcinogenesis. CDKN1B (p27) belongs to the Cip/Kip family and functions as an important cell cycle gatekeeper. Several lines of evidence from clinical studies and laboratory experiments demonstrate that CDKN1B is an important tumor suppressor gene in prostate cancer etiology. In addition, a case-control study has shown that the 326T/G (V109G) polymorphism in CDKN1B is associated with advanced prostate cancer. In light of the evidence for linkage between the chromosomal location of the CDKN1B gene (12p13) and prostate cancer susceptibility in several hereditary prostate cancer (HPC) populations, we hypothesized that sequence variants of CDKN1B play a role in HPC. To test this hypothesis, we first resequenced this gene in 96 HPC probands to identify germ-line mutations and sequence variants. We then genotyped the identified sequence variants among all family members of 188 HPC families and tested for their cosegregation with prostate cancer. In total, 10 sequence variants were identified, including three nonsynonymous changes. A family-based test, which is free from the effects of population stratification, revealed a significant association between single nucleotide polymorphism (SNP) -79C/T and prostate cancer (with a nominal P of 0.0005). The C allele of -79C/T was overtransmitted from parents to their affected offspring. Evidence for this association was primarily contributed by affected offspring whose age at diagnosis was <65 years. Together with the previous association study in a sporadic prostate cancer population, our new findings additionally suggest that germ-line variants of this gene play a role in prostate cancer susceptibility.

Aged↗

Inference of population genetic parameters in metagenomics: a clean look at messy data.

Metagenomic projects generate short, overlapping fragments of DNA sequence, each deriving from a different individual. We report a new method for inferring the scaled mutation rate, theta = 2Neu, and the scaled exponential growth rate, R = Ner, from the site-frequency spectrum of these data while accounting for sequencing error via Phred quality scores. After obtaining maximum likelihood parameter estimates for theta and R, we calculate empirical Bayes quality scores reflecting the posterior probability that each apparently polymorphic site is truly polymorphic; these scores can then be used for other applications such as SNP discovery. For realistic parameter ranges, analytic and simulation results show our estimates to be essentially unbiased with tight confidence intervals. In contrast, choosing an arbitrary quality score cutoff (e.g., trimming reads) and ignoring further quality information during inference yields biased estimates with greater variance. We illustrate the use of our technique on a new project analyzing activated sludge from a lab-scale bioreactor seeded by a wastewater treatment plant.

Bacteria↗

Direct micro-haplotyping by multiple double PCR amplifications of specific alleles (MD-PASA).

Analysis of haplotypes is an important tool in population genetics, familial heredity and gene mapping. Determination of haplotypes of multiple single nucleotide polymorphisms (SNPs) or other simple mutations is time consuming and expensive when analyzing large populations, and often requires the help of computational and statistical procedures. Based on double PCR amplification of specific alleles, described previously, we have developed a simple, rapid and low-cost method for direct haplotyping of multiple SNPs and simple mutations found within relatively short specific regions or genes (micro-haplotypes). Using this method, it is possible to directly determine the physical linkage of multiple heterozygous alleles, by conducting a series of double allele-specific PCR amplification sets with simple analysis by gel electrophoresis. Application of the method requires prior information as to the sequence of the segment to be haplotyped, including the polymorphic sites. We applied the method to haplotyping of nine sites in the chicken HSP108 gene. One of the haplotypes in the population apparently arose by recombination between two existing haplotypes, and we were able to locate the point of recombination within a segment of 19 bp. We anticipate rapidly growing needs for SNP haplotyping in human (medical and pharmacogenetics), animal and plant genetics; in this context, the multiple double PCR amplifications of specific alleles (MD-PASA) method offers a useful haplotyping tool.

Alleles↗

Risk of cerebral venous thrombosis and novel gene polymorphisms of the coagulation and fibrinolytic systems.

BACKGROUND AND PURPOSE: Genetic thrombophilic conditions such as those associated with Factor V Leiden (FVL) and the prothrombin mutant (PT G20210A) have been identified as risk factors for cerebral venous thrombosis (CVT). Recently, a single nucleotide polymorphism (SNP) of the thrombin activatable fibrinolysis inhibitor (TAFI G-438A) has been shown to be associated with lower TAFI levels and to decrease the risk for peripheral venous thrombosis. Furthermore, a protective role in juvenile stroke was shown for a SNP of the vitamin K dependent protein Z (PZ Intron F G79A) which is linked with low PZ levels. PATIENTS AND METHODS: In 77 consecutive patients with CVT and in 203 randomly selected population controls from the same region of Southern Germany, we investigated the following functional SNPs using PCR and restriction fragment analysis techniques: TAFI G-438A, PZ Intron F G79A, FVL and PT G20210A. RESULTS: The prevalence of FVL tended to be higher (OR 2.08, 95 % CI 0.91-4.75, p = 0.06) and that of PT G20210A (OR 4.57, 95 % CI 1.45-14.44, p = 0.007) was significantly higher in patients with CVT than in controls. The A-allele frequency of the TAFI G-438A polymorphism did not significantly differ between patients (21.3 %) and controls (26.9%; OR 0.71, 95 % CI 0.45-1.12; p = 0.17). For the PZ G79A SNP, the frequency of the A-allele was 19.5% in CVT and 24.6% in controls (OR 0.77, 95 % CI 0.49-1.21; p = 0.31). CONCLUSIONS: In this large series of CVT patients, a positive association with established thrombophilic risk factors FVL and especially the PT G20210A mutation was confirmed. In contrast, our study found no significant association of CVT with SNPs of the TAFI and the PZ genes. Other than testing for FVL and the PT G20210A mutation, exploration of these potential thrombophilic variants seems to be of limited value in the investigation of CVT.

Adolescent↗

Analysis of variation in expression of autosomal dominant osteopetrosis type 2: searching for modifier genes.

INTRODUCTION: Autosomal Dominant Osteopetrosis type II (ADO2) is a heritable osteosclerotic disorder that results from heterozygous mutations in the ClCN7 gene. Analysis of ADO2 in our pedigrees indicates that the penetrance is 66%, with a highly variable phenotype. METHODS: To identify genes that modify disease status, we performed a 10 cM genome-wide scan using 400 microsatellite markers in 112 subjects from our 8 largest ADO2 families with mutations in the ClCN7 gene. Results were analyzed by parametric linkage analysis using autosomal dominant and recessive models for affects on disease status. Follow-up genotyping with additional microsatellite markers was performed for regions with LOD scores over 1.5. In addition, we compared the frequency of two nonsynonymous SNPs, rs12926089 (V418M) and rs11559208 (K691E), and one promoter SNP rs960467 in the normal ClCN7 allele between a sample of unaffected gene carriers and clinically affected subjects to test the hypothesis that genetic variation in the non-disease allele within the ClCN7 gene might influence disease expression. RESULTS: We found potential evidence of linkage for a modifier gene(s) on 9q21-22 with a LOD score of 1.89, which is not statistically significant, but interesting. We also found that, for SNP V418M on the non-disease allele with the wild-type ClCN7 sequence, 94.92% (56/59) of clinically affected subjects and 78.13% (25/32) of unaffected gene carriers had a valine while 5.08% (3/59) of the affected subjects and 21.88% (7/32) of unaffected gene carriers had a methionine (P < 0.03). Unfortunately, SNP K691E was not informative in our families. For SNP rs960467, on the non-disease allele with the wild-type ClCN7 gene, 87.93% (51/58) of clinically affected subjects and 62.50% (20/32) of unaffected gene carriers had a C allele while 12.07% (7/58) of the clinically affected subjects and 37.50% (12/32) of unaffected gene carriers had a T allele (P < 0.007). As expected, the polymorphisms on the disease allele were not associated with disease status. CONCLUSIONS: Chromosome 9q21-22 may harbor a modifier gene(s) that affect(s) ADO2 disease status and severity. Additionally, we find the associations between the polymorphisms on the non-disease allele and unaffected gene carrier status.

Alleles↗

Association analysis of the dopamine receptor D2 (DRD2) SNP rs1076560 in alcoholic patients.

The dopamine system plays a well-established role in alcoholism. In this study, we examined the association between the single-nucleotide polymorphism (SNP) rs1076560 of the dopamine receptor D2 (DRD2) gene and susceptibility to alcoholism. SNP rs1076560 (C/A) is located in intron 6 of DRD2, where it is 1.4 kb downstream from alternative exon 6 and 83 bp upstream from exon 7. A total of 248 alcoholic patients and 322 healthy controls, all Japanese males, were genotyped for rs1076560 polymorphism by direct sequencing and allele-specific PCR. Data were analyzed using standard chi(2) statistics and a backwards logistic regression approach to adjust for the contribution of aldehyde dehydrogenase-2 (ALDH2) genotype status. The DRD2 risk allele A was more prevalent in the alcoholic patients (40.1%) than in the healthy controls (34.0%) (P=0.034, odds ratio=1.300, 95% confidence interval=1.020-1.657). These data identify SNP rs1076560 as a potentially important variable in the development of alcoholism.

Alcoholism↗

SNP discovery using advanced algorithms and neural networks.

UNLABELLED: Forage is an application which uses two neural networks for detecting single nucleotide polymorphisms (SNPs). Potential SNP candidates are identified in multiple alignments. Each candidate is then represented by a vector of features, which is classified as SNP or monomorphic by the networks. A validated dataset of SNPs was constructed from experimentally verified SNP data and used for network training and method evalutation. AVAILABILITY: The package is available at biobase.biotech.kth.se/forage/

Algorithms↗