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ERGIC-53 gene structure and mutation analysis in 19 combined factors V and VIII deficiency families.

Combined factors V and VIII deficiency is an autosomal recessive bleeding disorder associated with plasma levels of coagulation factors V and VIII approximately 5% to 30% of normal. The disease gene was recently identified as the endoplasmic reticulum-Golgi intermediate compartment protein ERGIC-53 by positional cloning, with the detection of two founder mutations in 10 Jewish families. To identify mutations in additional families, the structure of the ERGIC-53 gene was determined by genomic polymerase chain reaction (PCR) and sequence analysis of bacterial artificial chromosome clones containing the ERGIC-53 gene. Nineteen additional families were analyzed by direct sequence analysis of the entire coding region and the intron/exon junctions. Seven novel mutations were identified in 10 families, with one additional family found to harbor one of the two previously described mutations. All of the identified mutations would be predicted to result in complete absence of functional ERGIC-53 protein. In 8 of 19 families, no mutation was identified. Genotyping data indicate that at least two of these families are not linked to the ERGIC-53 locus. Taken together, these results suggest that a significant subset of combined factors V and VIII deficiency is due to mutation in one or more additional genes.

Amino Acid Substitution↗

Primary B cell gastric lymphoma. A genotypic analysis.

A series of cases of gastric lymphoproliferative disease exhibiting the features of pseudolymphoma, frank lymphoma, or both was investigated immunohistochemically and genotypically for evidence of B cell clonality. Immunoperoxidase studies on frozen and paraffin sections showed that all cases clearly exhibited immunoglobulin light chain restriction (eight cases kappa, six cases lambda). Southern blotting using JH, Ck, and Cl probes to detect clonally rearranged gene fragments confirmed monoclonality in each case, and the immunohistochemical and genotypic data were in agreement in all cases except one (1 light chain restriction/k gene rearrangement). The study confirmed that light chain restriction in gastric lymphoid infiltrates is synonymous with monoclonality ant there is a histologic continuum between low grade B cell gastric lymphoma with features of pseudolymphoma and high grade B cell lymphoma. The authors believe that histologic and immunohistochemical features such as light chain restriction clearly discriminate reactive and neoplastic gastric lymphoid infiltration. Therefore, light chain-restricted lymphoid proliferation, previously termed pseudolymphoma is, in fact, an early stage of frank lymphoma, which obviates the need to use the term pseudolymphoma.

B-Lymphocytes↗

Multipoint linkage-disequilibrium mapping narrows location interval and identifies mutation heterogeneity.

Single-nucleotide polymorphism (SNP) genotypes were recently examined in an 890-kb region flanking the human gene CYP2D6. Single-marker and haplotype-based analyses identified, with genomewide significance (P < 10-7), a 403-kb interval displaying strong linkage disequilibrium (LD) with predicted poor-metabolizer phenotype. However, the width of this interval makes the location of causal variants difficult: for example, the interval contains seven known or predicted genes in addition to CYP2D6. We have developed the Bayesian fine-mapping software coldmap, which, applied to these genotype data, yields a 95% location interval covering only 185 kb and establishes genomewide significance for a causal locus within the region. Strikingly, our interval correctly excludes four SNPs, which individually display association with genomewide significance, including the SNP showing strongest LD (P < 10-34). In addition, coldmap distinguishes homozygous cases for the major CYP2D6 mutation from those bearing minor mutations. We further investigate a selection of SNP subsets and find that previously reported methods lead to a 38% savings in SNPs at the cost of an increase of <20% in the width of the location interval.

Bayes Theorem↗

Meat quality traits were unaffected by a quantitative trait locus affecting leg composition traits in Texel sheep.

A QTL affecting leg muscle and fat traits has been identified within the New Zealand Texel population. The QTL maps to a region on OAR 2 with a two-marker haplotype test established at markers BULGE20 and BM81124. These markers encompass the likely position of Growth Differentiation Factor 8 (GDF8). The pleiotropic effects of this QTL on meat quality traits are tested. Objective measures of meat quality including pH, color (L*, a*, and b*), and tenderness (as assessed by Warner-Bratzler shear force measurements) were assessed on longissimus and semi-membranosus muscles of 540 progeny from six Texel sires. Four of these sires were subsequently identified as segregating for leg muscle and fat traits. For these segregating sires, comparison of progeny that had inherited the favorable haplotype from their sire with those that had received the alternate haplotype revealed no significant differences in the meat quality traits assessed. This finding suggests that the muscling QTL does not have pleiotropic effects on meat quality. A general scan for meat quality QTL was carried out using genotype data for eight markers from FCB128 to RM356 flanking 122cM of OAR 2 using Haley-Knott regression. This analysis revealed two QTL for a single sire. A QTL detected in the region of Marker INRA40 for color L* mapped to a site close to the muscling QTL, but there was evidence to suggest it is at a distinct locus. The QTL in the region of Marker RM356 might map distal to Marker RM356, as no peak was observed. This QTL, which seems to affect pH, color a*, color b*, and Warner-Bratzler shear measurements, requires further characterization.

Animals↗

Molecular characterization of Streptococcus pyogenes isolates to investigate an outbreak of puerperal sepsis.

OBJECTIVE: To describe microbiological characteristics and epidemiologic features of an outbreak of postpartum endometritis. METHODS: Various markers were investigated in five patients and three throat carriage isolates of Streptococcus pyogenes obtained during an outbreak of endometritis occurring in a 13-week period. Molecular characterization included biotyping, T-serotyping, emm gene sequence and restriction, pulsed-field gel electrophoresis (PFGE), and random amplified polymorphic DNA (RAPD) analysis. RESULTS: Biotype, T-serotype, and genotypic data (emm analysis, PFGE, and RAPD analysis) revealed a close relationship among the isolates from three patients, suggesting that cross-contamination had occurred. These isolates were biotype 1, T type 28, and emm type 28. The isolates from one patient and one carrier differed from those of the index patient by minor variations of the emm amplicon restriction pattern, PFGE pattern, or RAPD pattern. The remaining isolates were phenotypically and genetically different. CONCLUSION: Identification of different isolates demonstrated that different strains may circulate simultaneously during a true outbreak and that the predominant strain might persist for several months.

Carrier State↗

The 5HT1Dbeta receptor gene in bipolar disorder: a family-based association study.

The serotonin (5HT) receptor genes are considered good candidates for Major Depression (MD), Bipolar Disorder (BP), and Obsessive-Compulsive Disorder (OCD). The 5HT1Dbeta receptor gene has at least three polymorphisms known: G861C, T-261G, and the functional T371G (Phe-124-Cys). The aim of this study was to investigate for the presence of linkage disequilibrium between the 5HT1Dbeta receptor gene and BP. Two hundred and ninety probands with DSM-IV BPI, BPII, or Schizoaffective Disorder (Bipolar type) with their living parents were recruited. Genotyping data for the G861C and T371G polymorphisms were analyzed using the Transmission Disequilibrium Test (TDT). One hundred and sixty triads were informative for the TDT on the G861C polymorphism, which showed no preferential transmission of either allele (chi-square = 0.438, df = 1, p =.508). Only four triads were suitable for the analysis on the T371G variant, with the T allele transmitted once and the G allele transmitted four times to the affected. These findings validate further the results of pharmacological studies excluding a direct involvement of the 5HT1Dbeta receptor in the pathogenesis of BP. Further investigations combining genetic and pharmacological strategies are warranted.

Adult↗

[Association of angiotensin I converting enzyme 2 gene polymorphism with essential hypertension in Chinese].

OBJECTIVE: To identify the genetic variants of angiotensin I converting enzyme 2 (ACE2) gene in a Chinese population and to determine whether the ACE2 gene polymorphisms are associated with essential hypertension (EH). METHODS: Seven hundred and forty-five patients with EH and 362 normal blood pressure controls were included in the study to assess the contribution of polymorphism of ACE2 gene. Direct DNA sequencing was performed to detect the single nucleotide polymorphisms (SNPs) in 20 subjects who were randomly selected from the EH patients. RESULTS: One SNP named G8790A located in the 4th base of the third intron was found in the 20 patients. The genotyping data indicate that the A allele frequency in male EH patients complicated with cardiac incompetence(55%) is significantly different from that in the control group(43.3%)(P<0.01). The A allele frequency in female patients with cardiac incompetence (56.1%) is higher than that in the controls (50.5%), but the difference does not reach statistical significance. CONCLUSION: The G8790A polymorphism may be related to the essential hypertension with cardiac incompetence in Chinese population. Additional investigation will be need to confirm the association.

Aged↗

Exclusion of AR-CHED from the chromosome 20 region containing the PPMD and AD-CHED loci.

Congenital hereditary endothelial dystrophy (CHED) is a disorder of the corneal endothelium and has been recognized to segregate in families with both autosomal dominant (AD) and autosomal recessive (AR) modes of transmission. AD-CHED has been previously linked to the pericentric region of chromosome 20. Posterior polymorphous dystrophy (PPMD), a corneal endothelial disorder showing phenotypic overlap with CHED, has also been previously genetically mapped to this region. The genetic interval containing AD-CHED is within the larger genetic interval containing the PPMD locus. This study sought to determine whether AR-CHED segregating in a consanguineous Saudi Arabian pedigree is linked to the previously mapped and overlapping loci for AD-CHED and PPMD on the pericentric region of chromosome 20. Forty members of a consanguineous Saudi Arabian pedigree segregating AR-CHED were ascertained. Short tandem-repeat polymorphic markers from the 20 cM interval on chromosome 20 containing both the PPMD and AD-CHED loci were used to genotype these individuals. LOD score analysis of the genotype data with the MENDEL software package utilizing a model of autosomal recessive inheritance with complete penetrance showed exclusion of CHED from the entire PPMD/AD-CHED interval by utilizing overlapping intervals of LOD scores of at least -2. The results obtained demonstrate that AR-CHED is not allelic to either AD-CHED or PPMD, although it has been proposed that AD-CHED may be allelic to PPMD. Thus, there are at least two genes responsible for CHED and PPMD.

Chromosome Mapping↗

Human p53 tumor suppressor gene (TP53) and schizophrenia: case-control and family studies.

The human p53 tumor suppressor gene (TP53) is considered as a candidate susceptibility gene for schizophrenia because of its functions in neurodevelopment. To test for an association between TP53 and schizophrenia, both the case-control study and the transmission disequilibrium test (TDT) were performed on genotype data from eight polymorphisms in TP53. Our samples included 286 Toronto schizophrenia cases and 264 controls, and 163 Portuguese nuclear families. In the Toronto case-control study significant differences of allele frequencies of the CAA Ins/Del (p=0.027) and the 16bp Ins/Del (p=0.022) were detected. In TDT analysis we found significant differences for transmission of the CAA Ins/Del (p=0.017) in Portuguese schizophrenia families. Haplotype analysis also showed a significant association between TP53 and schizophrenia. These results provide further evidence that TP53 may play a role in the pathogenesis of schizophrenia.

Brain Chemistry↗

Kleine-Levin syndrome: an autoimmune hypothesis based on clinical and genetic analyses.

BACKGROUND: Kleine-Levin syndrome (KLS) is a rare disorder of unknown etiology. Pathophysiologic hypotheses include a hypothalamic dysfunction and abnormalities in the central serotonin and dopamine metabolism. Several clinical symptoms also suggest an underlying autoimmune process. OBJECTIVE: To systematically investigate patients with KLS with reference to the available hypotheses. METHODS: The authors collected clinical, polysomnographic, CSF, CT, and MRI records and analyzed gene polymorphisms of HLA-DQB1, tryptophan hydroxylase (TpH), and catechol-O-methyltransferase (COMT) in 30 unrelated patients with KLS and their families. The genotype data were contrasted with data from a normal control population. RESULTS: Only human leukocyte antigen (HLA)-DQB1*0201 allele frequency was significantly increased in patients with KLS. Three patients with KLS but none of the control subjects were DQB1*0201 homozygous. Two affected subjects from the same family were DQB1*0201 homozygous. In 17 DQB1*0201 heterozygous parents, 11 (64.7%) had transmitted this allele, suggesting a preferential transmission. CONCLUSION: These findings, together with the young age at onset, the recurrence of symptoms, and the frequent infectious precipitating factors, suggest an autoimmune etiology for Kleine-Levin syndrome.

Adolescent↗

Effect of alpha thalassaemia trait and enhanced gamma chain production on disease severity in beta thalassaemia major and intermedia.

One hundred and twenty patients with homozygous beta thalassaemia were selected to determine the clinical effects of certain genetic factors which may modify disease severity. Genetic analysis defined specific beta thalassaemia mutations, the alpha thalassaemia genotype, and the presence of an XmnI restriction enzyme site, associated with increased fetal haemoglobin (HbF) production under certain conditions. Genotypic data with globin chain synthesis were related to the age when regular transfusions began and subsequent pubertal development. This study showed that the major determinants of disease severity in beta thalassaemia were the beta thalassaemia mutations, with co-inheritance of alpha thalassaemia trait and coinheritance of a high HbF determinant acting as ameliorating factors. The presence of an alpha thalassaemia deletion significantly reduced initial disease severity, although the effect on pubertal development was less clear. It is concluded that detailed genetic analysis should be performed in all newly diagnosed patients with thalassaemia. This, in conjunction with clinical assessment, will help to predict disease severity and prognosis.

Adolescent↗

A genome screen for genes predisposing to bipolar affective disorder detects a new susceptibility locus on 8q.

Bipolar affective disorder (BPAD), also known as manic depressive illness, is a severe psychiatric disorder characterized by episodes of mania and depression. It has a lifetime prevalence of approximately 1% in all human populations. In order to identify chromosomal regions containing genes that play a role in determining susceptibility to this psychiatric condition, we have conducted a complete genome screen with 382 markers (average marker spacing of 9.3 cM) in a sample of 75 BPAD families which were recruited through an explicit ascertainment scheme. Pedigrees were of German, Israeli and Italian origin, respectively. Parametric and non-parametric linkage analysis was performed. The highest two-point LOD score was obtained on 8q24 (D8S514; LOD score = 3.62), in a region that has not attracted much attention in previous linkage studies of BPAD. The second best finding was seen on 10q25-q26 (D10S217; LOD score = 2.86) and has been reported in independent studies of BPAD. Other regions showing 'suggestive' evidence for linkage localized to 1p33-p36, 2q21-q33, 3p14, 3q26-q27, 6q21-q22, 8p21, 13q11 and 14q12-q13. In addition, we aimed at detecting possible susceptibility loci underlying genomic imprinting by analyzing the autosomal genotype data with the recently developed extension of the GENEHUNTER program, GENEHUNTER-IMPRINTING. Putative paternally imprinted loci were identified in chromosomal regions 2p24-p21 and 2q31-q32. Maternally imprinted susceptibility genes may be located on 14q32 and 16q21-q23.

Bipolar Disorder↗

Genetic studies of syndromes with severe periodontitis and palmoplantar hyperkeratosis.

The Papillon-Lefèvre and Haim Munk syndromes are characterized by the presence of both palmoplantar hyperkeratosis (PPK) and severe early onset periodontitis. It is the early onset periodontal disease component that distinguishes these from other more common forms of PPK. It has been proposed that the periodontal disease component may be a casual association in individuals with PPK. Genetic syndromes with palmoplantar keratosis and severe ealry onset periodontitis may be due to specific bacterial infections in individuals with PPK. Recently, keratin gene mutations have been identified in several conditions typified by palmoplantar keratosis. The present study sought to test the hypothesis that a keratin gene defect similar to those previously identified in other PPK conditions is responsible for the Haim Munk and the Papillon. Lefèvre syndromes. We have performed genetic linkage studies to test for linkage between polymorphic DNA loci within 2 cytokeratin gene families and the disease phenotype in Haim Munk syndrome and Papillon-Lefèvre syndrome. Families with individuals segregating for the Haim Munk syndrome and the Papillon-Lefèvre syndrome were examined to determine disease status, and genotyped for microsatellite DNA markers closely linked to the acidic (type I) and the basic (type II) cytokeratin genes on chromosomes 12 and 17. Genotype data were evaluated for microsatellite allele homozygosity in affected individuals. Results of these preliminary genetic studies suggest that the gene defect in Haim Munk syndrome is not due to a gene defect in either the type I or the type II keratin gene clusters. These findings suggest that Haim Munk syndrome may be genetically distinct from other more common forms of PPK that have been linked to the cytokeratin gene families, and suggest that mutations in genes other than keratin genes are responsible. Additional family studies are needed to confirm these preliminary findings.

Adult↗

[The Estonian Genome Project in the context of European genome research].

It is the aim of the Estonian Genome Project to establish a database which compiles phenotype and genotype data of a large part of the Estonian population. The Gene Bank will only be used for scientific and public health research. Researchers hope that it will help identify disease genes and prepare the ground for the personalized medicine of the future. Additionally, the project will improve Estonian's international competitiveness in high technology and have a strong educational effect on the population. The legal framework, the Human Genes Research Act, was passed by the Estonian parliament in December 2000. It had been drafted by a group of experts who took into account all available international guidance documents on genetic research. With the pilot project involving three selected regions successfully finished, the main project has now started.

Databases, Nucleic Acid↗

Combined effects of the p53 and p73 polymorphisms on lung cancer risk.

Lung cancer is a multigenic disease where one variant single nucleotide polymorphism may have only a modest independent effect on the disease phenotype, yet in aggregate, multiple biologically relevant single nucleotide polymorphisms may provide a more accurate representation of risk. Polymorphisms in members of the p53 family, such as p53 and p73, that have a functional relevance would be predicted to contribute to the disease phenotype. In this analysis, we used genotype data from 863 lung cancer cases and 852 healthy controls to test for multigenetic effects of polymorphisms at p53 exon 4, introns 3 and 6, and at p73 exon 2. All individuals in this analysis were self-reported non-Hispanic Caucasians. When the p73 and p53 variant alleles were combined and analyzed as a continuous variable, there was a 13% increase [odds ratios (OR), 1.13; 95% confidence intervals (CI), 1.05-1.21] in lung cancer risk for each additional variant allele. Furthermore, when the number of variant alleles was categorized into three groups (zero, one to three, and four or more variants), there was evidence of a gene-dosage effect with increased risks for individuals with one to three variants (OR, 1.30; 95% CI, 1.05-1.61) and four or more variants (OR, 1.78; 95% CI, 1.23-2.56). When the data were stratified by smoking status, an increased risk for lung cancer was evident only in current (OR, 2.32; 95% CI, 1.25-4.33) and former smokers (OR, 1.73; 95% CI, 1.02-2.94) with four or more variants. Younger individuals with four or more variants were also at a significantly increased risk for lung cancer (OR, 3.15; 95% CI, 1.62-6.12). This study provides support for the multigenetic effects of variant alleles from p53 exon 4, and introns 3 and 6, and p73, and their interplay with smoking, resulting in a significantly increased risk for lung cancer in this Caucasian population.

Aged↗

Association studies of polymorphisms of CYP2E1 gene in alcoholics with cirrhosis, antisocial personality, and normal controls.

To determine the role of CYP2E1 gene in susceptibility to alcoholism and alcohol cirrhosis, we gentoyped a sample of alcoholics with and without cirrhosis, alcoholics with antisocial personality, alcoholic families, and normal controls with RsaI, PstI, and DraI polymorphisms in the gene. Relative risk and haplotype relative risk approaches were used in genotype data analysis. The PstI polymorphism data were excluded from further analysis due to strong linkage disequilibrium with RsaI. For the RsaI polymorphism, comparison of total alcoholics, alcoholics with and without cirrhosis, and alcoholics with antisocial personality with normal controls were negative. The results of the same analysis with the above groups for DraII were also negative. Using the haplotype relative risk method, the result for DraI was positive, meaning that the mutated allele (D2) was significantly more transmitted than nontransmitted. However, the result of the same analysis for the RsaI polymorphism was not statistically significant. We conclude that the CYP2E1 gene plays no substantial role in susceptibility to alcohol cirrhosis or alcoholism.

Adult↗

Specific BACE1 genotypes provide additional risk for late-onset Alzheimer disease in APOE epsilon 4 carriers.

Alzheimer disease (AD) is characterized neuropathologically by neurofibrillary tangles and senile plaques. A key component of plaques is A beta, a polypeptide derived from A beta-precursor protein (APP) through proteolytic cleavage catalyzed by beta and gamma-secretase. We hypothesized that sequence variation in genes BACE1 (on chromosome 11q23.3) and BACE2 (on chromosome 21q22.3), which encode two closely related proteases that seem to act as the APP beta-secretase, may represent a genetic risk factor for AD. We analyzed the frequencies of single nucleotide polymorphisms (SNPs) in BACE1 and BACE2 genes in a community-based sample of 96 individuals with late-onset AD and 170 controls selected randomly among residents of the same community. The genotype data in both study groups did not demonstrate any association between AD and BACE1 or BACE2. After stratification for APOE status, however, an association between a BACE1 polymorphism located within codon V262 and AD in APOE epsilon 4 carriers was observed (P = 0.03). We conclude that sequence variation in the BACE1 or BACE 2 gene is not a significant risk factor for AD; however, a combination of a specific BACE1 allele and APOE epsilon 4 may increase the risk for Alzheimer disease over and above that attributed to APOE epsilon 4 alone.

Alzheimer Disease↗

Evidence and characteristics of putative human alpha recombination hotspots.

Understanding recombination rate variation is very important for studying genome diversity and evolution, and for investigation of phenotypic association and genetic diseases. Recombination hotspots have been observed in many species and are well studied in yeast. Recent study demonstrated that recombination hotspots are also a ubiquitous feature of the human genome. But the nature of human hotspots remains largely unknown. We have developed and validated a novel computational method for testing the existence of hotspots as well as for localizing them with either unphased or phased genotyping data. To study the characteristics of hotspots within or close to genes, we scanned for unusually high levels of recombination using the European population samples in the SeattleSNPs database, and found evidence for the existence of human alpha hotspots similar to those of yeast. This type of hotspots, found at promoter regions, accounts for about half of the total detected and appears to depend on some specific transcription factor binding sites (such as CGCCCCCGC). These characteristics can explain the observed weak correlation between hotspots and GC-content, and their variation may contribute to the diversity of hotspot distribution among different individuals and species. These long-sought putative human alpha recombination hotspots should deserve further experimental investigations.

Binding Sites↗