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PubMed2005

Ncf1 (p47phox) polymorphism determines oxidative burst and the severity of arthritis in rats and mice.

Identifying genes that regulate polygenic diseases influenced by the environment such as rheumatoid arthritis (RA), has so far proven to be difficult. By using an alternative approach, i.e., linkage analysis using relevant animal models we succeeded in finding the Ncf1 gene residing in the Pia4 quantitative trait locus to be responsible for the severity of pristane induced arthritis in rats. The influence of another mutation in the mouse Ncf1 gene showed the same association between decreased oxidative burst and enhanced arthritis. In this case the mutation affected a splice site giving a non-detectable oxidative burst response and enhanced collagen induced arthritis as well as myelin oligodendrocyte protein induced experimental autoimmune encephalomyelitis. These findings open up new possibilities for new treatments for autoimmune diseases, i.e., RA, targeting the NADPH oxidase pathway.

Animals↗

PubMed2024

Genetic variants reduced POPs-related colorectal cancer risk via altering miRNA binding affinity and m6A modification.

Exposure to persistent organic pollutants (POPs) may contribute to colorectal cancer risk, but the underlying mechanisms of crucial POPs exposure remain unclear. Hence, we systematically investigated the associations among POPs exposure, genetics and epigenetics and their effects on colorectal cancer. A case-control study was conducted in the Chinese population for detecting POPs levels. We measured the concentrations of 24 POPs in the plasma using gas chromatography-tandem mass spectrometry (GC-MS/MS) and evaluated the clinical significance of POPs by calculating the area under the receiver operating characteristic curve (AUC). To assess the associations between candidate genetic variants and colorectal cancer risk, unconditional logistic regression was used. Compared with healthy control individuals, individuals with colorectal cancer exhibited higher concentrations of the majority of POPs. Exposure to PCB153 was positively associated with colorectal cancer risk, and PCB153 demonstrated superior accuracy (AUC=0.72) for predicting colorectal cancer compared to other analytes. On PCB153-related genes, the rs67734009 C allele was significantly associated with reduced colorectal cancer risk and lower plasma levels of PCB153. Moreover, rs67734009 exhibited an expression quantitative trait locus (eQTL) effect on ESR1, of which the expression level was negatively related to PCB153 concentration. Mechanistically, the risk allele of rs67734009 increased ESR1 expression via miR-3492 binding and m6A modification. Collectively, this study sheds light on potential genetic and epigenetic mechanisms linking PCB153 exposure and colorectal cancer risk, thereby providing insight into the accurate protection against POPs exposure.

Humans↗

PubMed2004

Lower body temperature as a potential mechanism of life extension in homeotherms.

Although best known for his studies on the anti-aging effects of dietary restriction, Dr Roy Walford began his career by studying the anti-aging effects of lowering body temperature. As a tribute to his long and productive career, we review these pioneering studies and the singular influence these have had on our own thinking about the potential for lower body temperature to extend the life span of homeotherms. We show our results from a study of six classical inbred strains of mice that depict marked strain variation in the body temperature response to dietary restriction. In addition, we show a genome scan from a recombinant inbred strain panel in which we identified a significant quantitative trait locus on murine chromosome 9 and a provisional locus on chromosome 17 that specify variation in the response of body temperature to dietary restriction. These discoveries suggest that we can now extend the studies of Dr Walford to critically test whether lower body temperature can prolong the life span of mammals.

Aging↗

PubMed2004

Genetic analysis of inherited hydrocephalus in a rat model.

Congenital hydrocephalus is a serious neurological disorder with a diverse etiology. Although there is strong evidence for genetic causes, few genes have been identified in humans. The rodent model, the H-Tx rat, has hydrocephalus with an onset in late gestation and a complex mode of inheritance. Ventricular dilatation is associated with abnormalities in the cerebral aqueduct and subcommissural organ. Quantitative trait locus (QTL) mapping was performed on DNA from the progeny of a backcross with the non-hydrocephalic Fischer F344 strain, using DNA microsatellite markers. The hydrocephalus trait was quantified by measuring the severity of the ventricular dilatation. Four chromosomes, each with a locus for hydrocephalus (Chrs 9, 10, 11, and 17), were mapped using additional markers and DNA from four subsets of backcross progeny with allelic recombination at or near each locus. The genetic positions for the markers and the loci were located using the Ensemble Rat Genome Browser. For each chromosome studied, the interval containing the locus was examined for known rat genes and for human genes identified from human-rat homology. Genes expressed in brain and with a function associated with known causes of hydrocephalus were identified as possible candidate genes. Future studies to characterize the causative genes in this animal model will improve the understanding of genetic causes in humans.

Animals↗

PubMed2006

Structure, expression, and mapping of two nodule-specific genes identified by mining public soybean EST databases.

Numerous nodule-specific genes, which are involved in the root nodule development and function, have been known and are still being discovered. Here, we reported the structure, expression, and genetic map location of two novel nodule-specific genes. First, two EST groups, one obtained from a nodule library and the other from all aboveground tissue libraries, were clustered with regard to in silico expression profiles. We compiled a pool of 103 putative nodule-specific sequence clusters. Then, two representative ESTs were selected for further experimental analyses. According to the full-length cDNA sequences, one was an EST of a novel nodule-specific polygalacturonase gene, GmPGN, and the other was an EST of a new short nodule-specific gene, GmEKN. The results of expression analyses of the GmPGN cDNAs indicated that GmPGN expression was not detectable in any of the soybean tissues except in the nodule tissue and may be regulated via alternative splicing. GmEKN expression was the most strongly detected in the nodule. The predicted GmEKN protein is both glutamic acid- and lysine-rich, and is also highly hydrophilic. Genetic mapping located GmPGN near the known quantitative trait locus conferring resistance to soybean cyst nematode on soybean molecular linkage group (MLG) B1, and GmEKN on MLG A2. These results provide useful information for the use of these genes in research on the orchestration of numerous genes in nodule development and function.

Amino Acid Sequence↗

PubMed2005

QT interval is a heritable quantitative trait with evidence of linkage to chromosome 3 in a genome-wide linkage analysis: The Framingham Heart Study.

OBJECTIVES: To identify genomic regions linked to QT interval duration in an unselected population. BACKGROUND: QT interval prolongation is associated with increased risk of sudden cardiac death and coronary heart disease and may result from acquired conditions or inherited ion channel defects. The influence of genetic variants on QT interval length in apparently healthy individuals is uncertain. METHODS: We studied subjects from the Framingham Heart Study in whom 12-lead ECGs were available from regular clinic examinations. QT, QT-peak, and RR intervals were measured using digital calipers. A 10-centiMorgan (cM) density genome-wide scan was performed in a subset of the largest families having at least two members with ECG phenotypes (326 families). Variance components methods (Genehunter) were used. RESULTS: Evidence was observed for significant heritability of the QT interval (h(2) 0.35; 95% CI, 0.29-0.41), QT-peak interval (h(2) 0.37; 95% CI, 0.29-0.45), and calculated JT interval (h(2) 0.25; 95% CI, 0.19-0.31). In the genome-wide linkage analysis, we found suggestive evidence for linkage of the QT interval 19 to 48 cM from the tip of the short arm of chromosome 3 (maximum two-point LOD score 3.00, maximum multipoint LOD score 2.71). After fine-mapping with seven microsatellite markers, the peak multipoint LOD score rose to 2.84 at 24.4 cM. The region of linkage contains potassium and sodium channel genes, including the SCN5A gene, which has been implicated in one form of the long QT syndrome and in the Brugada syndrome. CONCLUSIONS: QT and related ECG intervals are heritable traits in a large unselected population. We provide suggestive evidence for a quantitative trait locus on chromosome 3 influencing QT interval duration. Further studies are warranted to identify genes that influence QT interval variation and to determine the role of heritable factors in life-threatening QT prolongation.

Aged↗

PubMed2005

Comparative analysis of BAC and whole genome shotgun sequences from an Anopheles gambiae region related to Plasmodium encapsulation.

The only natural mechanism of malaria transmission in sub-Saharan Africa is the mosquito, generally Anopheles gambiae. Blocking malaria parasite transmission by stopping the development of Plasmodium in the insect vector would provide a useful alternative to the current methods of malaria control. Toward this end, it is important to understand the molecular basis of the malaria parasite refractory phenotype in An. gambiae mosquito strains. We have selected and sequenced six bacterial artificial chromosome (BAC) clones from the Pen-1 region that is the major quantitative trait locus involved in Plasmodium encapsulation. The sequence and the annotation of five overlapping BAC clones plus one adjacent, but not contiguous clone, totaling 585kb of genomic sequence from the centromeric end of the Pen-1 region of the PEST strain were compared to that of the genome sequence of the same strain produced by the whole genome shotgun technique. This project identified 23 putative mosquito genes plus putative copies of the retrotransposable elements BEL12 and TRANSIBN1_AG in the six BAC clones. Nineteen of the predicted genes are most similar to their Drosophila melanogaster homologs while one is more closely related to vertebrate genes. Comparison of these new BAC sequences plus previously published BAC sequences to the cognate region of the assembled genome sequence identified three retrotransposons present in one sequence version but not the other. One of these elements, Indy, has not been previously described. These observations provide evidence for the recent active transposition of these elements and demonstrate the plasticity of the Anopheles genome. The BAC sequences strongly support the public whole genome shotgun assembly and automatic annotation while also demonstrating the benefit of complementary genome sequences and of human curation. Importantly, the data demonstrate the differences in the genome sequence of an individual mosquito compared to that of a hypothetical, average genome sequence generated by whole genome shotgun assembly.

Amino Acid Sequence↗

PubMed2026

Deep learning and statistical methods identify novel asthma risk variants in Europeans.

BACKGROUND: Asthma is a common heritable respiratory disorder with a complex genetic basis. Although large-scale genome-wide association studies have identified many risk loci, the full spectrum of its polygenic architecture remains to be defined. OBJECTIVE: We refined the genetic landscape of asthma in individuals of European ancestry and improve polygenic risk prediction through statistical and deep learning-based methods. METHODS: We conducted the largest genome-wide association study meta-analysis of asthma in individuals of European ancestry, combining data from the Global Biobank Meta-analysis Initiative (121,940 cases, 1,254,131 controls) and the Million Veteran Program (36,823 cases, 398,278 controls). To enhance discovery, we applied pleiotropy-informed multitrait analysis and conditional false discovery rate approaches, each incorporating eosinophil counts as a secondary trait. In parallel, we used a Transformer-based deep learning framework to further prioritize variants and improve polygenic risk prediction. RESULTS: The meta-analysis identified 69 independent genome-wide significant loci (P < 5 × 10-8) not previously reported in asthma. Multitrait analysis of genome-wide association studies, conditional false discovery rate, and deep learning approaches uncovered additional candidate loci. Functional annotation and expression quantitative trait locus mapping implicated novel genes in immune regulation, airway remodeling, and metabolic processes. Polygenic risk score models derived from deep learning-prioritized variants outperformed those based on conventional genome-wide association study and standard statistical approaches. CONCLUSIONS: Our study yields a comprehensive map of asthma-associated loci in European ancestry populations, improves genetic risk prediction, and informs future mechanistic studies.

Humans↗

PubMed2026

The bioinformatics approach to identifying pathogenic variants for colorectal cancer (CRC).

Colorectal cancer (CRC) is the third most prevalent cancer globally, accounting for 9.6% of newly diagnosed cases and 9.3% of cancer-related deaths. It develops from the uncontrolled proliferation of glandular cells in the colon and rectum and is categorized into three primary types: sporadic, hereditary, and colitis-associated. While genetic susceptibility is a key factor in CRC pathogenesis, identifying high-impact pathogenic variants remains a significant challenge. This study integrates bioinformatics and population genetics approaches to identify CRC-associated single-nucleotide polymorphisms (SNPs) with potential clinical significance. CRC-associated SNPs were extracted from the Genome-Wide Association Studies (GWAS) Catalog, functionally annotated via HaploReg, and validated via Ensembl. In addition, expression quantitative trait locus (eQTL) data from the GTEx database were used to assess the effects of these variants on gene expression across human tissues. Our analysis identified three high-priority SNPs (rs9379084, rs3184504, and rs11557154) associated with the RREB1, ATXN2, SH2B3, and DCAF12 genes, which exhibited marked allele frequency differences among populations. These findings suggest potential biomarkers for CRC risk assessment and highlight the importance of genetic screening across diverse populations.

Bioinformatics↗

PubMed2005

Correlation of susceptibility to 6-aminonicotinamide and hydrocortisone-induced cleft palate.

Our previous genome-wide Quantitative Trait Locus (QTL) mapping study using mouse A/J by C57BL/6J recombinant inbred (RI) lines suggested several chromosomal regions contain genes influencing susceptibility to phenytoin (PT)-induced cleft lip with or without cleft palate [CL(P)] and 6-aminonicotinamide (6-AN)-induced isolated cleft palate (CP). Importantly, the same chromosomal regions but different RI parental strain alleles were sometimes implicated in susceptibility to these different kinds of orofacial clefting. Here we report the susceptibility to hydrocortisone (HC)-induced CP in these RI lines. We treated pregnant females with HC and studied the incidence of CP in day 17 fetuses. RI lines showed highly correlated responses to HC and 6-AN. The A/J parental line and five RI lines showed very high levels of clefting in response to both of these teratogens. The C57BL/6J parental line and five other RI lines exhibited low incidence of CP for these teratogens. In contrast, there was no significant correlation between incidence of PT-induced CL(P) and HC-induced CP.

6-Aminonicotinamide↗

PubMed2006

Lack of significant association between -1021C-->T polymorphism in the dopamine beta hydroxylase gene and attention deficit hyperactivity disorder.

Recent trends in medications for attention deficit hyperactivity disorder (ADHD) suggest that norepinephrine (NE) deficiency may contribute to the disease etiology. Dopamine beta hydroxylase (DBH) is the key enzyme which converts dopamine to NE and since DBH gene is considered a major quantitative trait locus for plasma DBH activity, genetic polymorphism may lead to altered NE neurotransmission. Several polymorphisms including a 5' flanking -1021C-->T polymorphism, was reported to be associated with changed DBH activity and an association between -1021C-->T polymorphism with ADHD was observed in Han Chinese children. We have carried out family-based studies with three polymorphisms in the DBH gene, -1021C-->T polymorphism, exon 2*444g/a and intron 5 TaqI RFLP, to explore their association with Indian ADHD cases. Allele and genotype frequency of these polymorphisms in ADHD cases were compared with that of their parents and a control group. Haplotypes obtained were analyzed for linkage disequilibrium (LD). Haplotype-based haplotype relative risk analysis and transmission disequilibrium test showed lack of significant association between transmission of the polymorphisms and ADHD. A haplotype comprising of allele 1 of all polymorphisms showed a slight positive trend towards transmission from parents to ADHD probands. Strong LD was observed between *444g/a and TaqI RFLP in all the groups. However, low D' values and corresponding log of odds scores in the control group as compared to the ADHD families indicated that, the incidence of the two polymorphisms being transmitted together could be higher in ADHD families.

Adolescent↗

PubMed2026

Genetic dissection of cardiac iron regulation using transcriptome network analysis and systems genetics in BXD mice.

Cardiac iron homeostasis is essential for myocardial energy metabolism and contractile function, yet the genetic and molecular mechanisms governing iron levels within the heart remain poorly understood. We used a systems genetics approach to dissect the transcriptional regulation of cardiac iron homeostasis. Myocardial iron level varies substantially across BXD strains (40-112 μg/g) and is under heritable genetic control (H2 = 0.38). Elevated cardiac iron is associated with reduced ventricular mass, increased ventricular ectopy, and prolonged atrioventricular conduction in the BXD population. Weighted gene co-expression network analysis of the BXD heart transcriptome identified a co-expression module that was significantly and negatively correlated with cardiac iron levels in both young and old BXD mice and enriched for pathways related to metabolic regulation, cyclic AMP (cAMP) signaling, circadian entrainment, and cardiovascular physiology. The module showed substantial overlap with a curated cardiac iron gene set, and cross-species enrichment analysis confirmed its conservation in human cardiomyopathy differentially expressed genes (enrichment ratio = 1.49; false discovery rate [FDR] = 0.0342). Quantitative trait locus (QTL) mapping of the first principal component of the overlapping module iron genes (n = 38), corroborated by individual gene mapping, identified trans-eQTL hotspots on multiple chromosomes, implicating Fcho2, Gcc2, and Rmdn1 as candidate upstream regulators operating through sequential steps of intracellular iron trafficking. Together, these findings establish a systems-level map of cardiac iron gene regulation, identify candidate genetic regulators, and provide a molecular framework linking disruption of iron-related transcriptional networks to structural and electrical cardiac dysfunction with implications for iron-related heart diseases.

BXD mouse population↗

PubMed2005

A comprehensive radiation hybrid map of the bovine genome comprising 5593 loci.

A bovine whole genome 7000-rad radiation hybrid (RH) panel, SUNbRH(7000-rad), was constructed to build a high-resolution RH map. The Shirakawa-USDA linkage map served as a scaffold to construct a framework map of 3216 microsatellites on which 2377 ESTs were ordered. The resulting RH map provided essentially complete coverage across the genome, with 1 cR7000 corresponding to 114 kb, and a cattle-human comparative map of 1716 bovine genes and sequences annotated in the human genome, which covered 79 and 72% of the bovine and human genomes, respectively. We then integrated the bovine RH and comparative maps with BAC fingerprint information in to construct a detailed, BAC-based physical map covering a reported 40-cM quantitative trait locus region for intramuscular fat or "marbling" on BTA 4. In summary, the new, high-resolution SUNbRH7000-rad, comparative, Shirakawa-USDA linkage, and BAC fingerprint maps provide a set of genomic tools for fine mapping regions of interest in cattle.

Animals↗

PubMed2003

Genetic susceptibility to nickel-induced acute lung injury.

Human exposure to insoluble and soluble nickel compounds is extensive. Besides wide usage in many industries, nickel compounds are contained in cigarette smoke and, in low levels, in ambient particulate matter. Soluble nickel particulate, especially nickel sulfate (NiSO(4)), has been associated with acute lung injury. To begin identifying genes controlling susceptibility to NiSO(4), mean survival times (MSTs) of eight inbred mouse strains were determined after aerosol exposure. Whereas A/J (A) mice were sensitive, C57BL/6J (B6) mice survived nearly twice as long (resistant). Their offspring were similarly resistant, demonstrating heritability as a dominant trait. Quantitative trait locus (QTL) analysis of backcross mice generated from these strains identified a region on chromosome 6 significantly linked to survival time. Regions on chromosomes 1 and 12 were suggestive of linkage and regions on chromosomes 8, 9, and 16 contributed to the response. Haplotype analysis demonstrated that QTLs on chromosomes 6, 9, 12, and 16 could explain the MST difference between the parental strains. To complement QTL analysis results, cDNA microarray analysis was assessed following NiSO(4) exposure of A and B6 mice. Significant expression changes were identified in one or both strains for >100 known genes. Closer evaluation of these changes revealed a temporal pattern of increased cell proliferation, extracellular matrix repair, hypoxia, and oxidative stress, followed by diminished surfactant proteins. Certain expressed sequence tags clustered with known genes, suggesting possible co-regulation and novel roles in pulmonary injury. Together, results from QTL and microarray analyses of nickel-induced acute lung injury survival allowed us to generate a short list of candidate genes.

Adaptation, Physiological↗

PubMed1999

Linkage between IgE receptor-mediated histamine releasability from basophils and gene marker of chromosome 11q13.

BACKGROUND: The genetics of the regulation of the release of mediators involving the interaction of IgE with cells and their ability to release mediators have not been extensively investigated. With use of the candidate gene approach, it was reported that the gene regulating the beta chain of the high-affinity receptor for IgE is on chromosome 11q13. OBJECTIVE: To determine whether gene(s) in chromosome 11q13 may control the expression of maximal histamine release from basophil to anti-IgE stimuli, linkage analysis between this phenotype and the gene marker of chromosome 11q13 was performed. METHODS: Maximal histamine release to anti-IgE and calcium ionophore A23187 and genotyping chromosome 11q13 with use of microsatellite marker (D11S97) were performed in 56 probands with asthma and 59 of their siblings. The linkage was analyzed by affected sib-pair analysis and the quantitative trait locus approach. RESULTS: Maximal histamine release (mean +/- SE) to anti-IgE and A23187 was 43.3% +/- 3.5% and 30.9 +/- 3.4% in probands and 29.5% +/- 2.6% and 22.2% +/- 2.7 in siblings, respectively. Of 20 sib-pairs with the maximal histamine release to anti-IgE more than 33% (mean plus 1 SD of nonasthmatic controls), 11 (55%) shared 2 D11S97 alleles, 9 (45%) shared 1 allele, and neither sib-pair shared identical alleles, which indicates a significant linkage of maximal histamine to anti-IgE and gene marker of chromosome 11q13 (P =.02). The difference (mean +/- SE) of the maximal histamine release to anti-IgE between each proband and sibling was smaller in sib-pairs with 2 identical alleles than in those with 1 identical allele and with no identical allele (14.1% +/- 2.6% vs 25.8% +/- 3.1% vs 41.0% +/- 4.9%). However, the difference (mean +/- SE) to A23187 between each proband and sibling was not different among the 3 groups (9.7% +/- 1.8% vs 17.9% +/- 3.6% vs 10.4% +/- 4.8%). CONCLUSION: Maximal histamine release from basophils to anti-IgE stimuli was linked to the gene marker of chromosome 11q13.

Adolescent↗

PubMed1996

Identification and characterization of the mouse obesity gene tubby: a member of a novel gene family.

The mutated gene responsible for the tubby obesity phenotype has been identified by positional cloning. A single base change within a splice donor site results in the incorrect retention of a single intron in the mature tub mRNA transcript. The consequence of this mutation is the substitution of the carboxy-terminal 44 amino acids with 24 intron-encoded amino acids. The normal transcript appears to be abundantly expressed in the hypothalamus, a region of the brain involved in body weight regulation. Variation in the relative abundance of alternative splice products is observed between inbred mouse strains and appears to correlate with an intron length polymorphism. This allele of tub is a candidate for a previously reported diet-induced obesity quantitative trait locus on mouse chromosome 7.

Adaptor Proteins, Signal Transducing↗

PubMed2000

WKHA rats with genetic hyperactivity and hyperreactivity to stress: a review.

WKHA rats are a homozygous strain of hyperactive rats developed by successive selected inbreedings, starting from a cross of spontaneously hypertensive (SHR) rats with their normotensive control strain, WKY. WKHA express hyperactivity in a novel environment, as do SHRs, however their blood pressure is normotensive, thus they are potentially a more promising model of hyperactivity than the SHR. WKHA became homozygous in 1990 (20 strict brother/sister inbreedings), and they are currently in the F36 generation. Studies in collaboration with numerous colleagues have allowed us to describe a limited behavioral and neurochemical profile of WKHA rats. Their most prominent behaviors include hyperactivity in a novel environment, and a marked hyperreactivity to stress, both of which are also characteristic of SHRs. They differ from SHRs in other respects: WKHA are less aggressive, habituate more readily to a novel environment, and are less exploratory in a familiar environment than the SHR. Neurochemical studies have revealed changes in brain monoamine function in WKHA rats, particularly in frontal cortical norepinephrine and dopamine uptake, and they show marked changes in neuroendocrine responses in the hypothalamic/pituitary/adrenal axis, as well as altered POMC peptides in the pituitary anterior and posterior lobes. Molecular genetic studies by colleagues in Bordeaux have identified a quantitative trait locus for the hyperactivity/hyperreactivity trait of WKHA rats.

Animals↗

PubMed2002

Norepinephrine transporter gene polymorphism is not associated with susceptibility to alcohol dependence.

Abnormalities in monoamine neurotransmission have been implicated in the pathogenesis of alcoholism, mood disorders and schizophrenia. Murine norepinephrine transporter gene (NET) has been mapped to a region on chromosome 8 where a quantitative trait locus for ethanol sensitivity. Therefore we tested whether norepinephrine transporter (NET) gene variants confer susceptibility to either alcohol dependence or severe alcohol withdrawal symptoms. There is a highly polymorphic silent G1287A mutation in the NET gene. In our study 157 alcoholics and 185 healthy unrelated matched control subjects were analyzed for a silent G1287A mutation. No significant differences in allele and genotype distribution between control subjects f(A)=0.33 and alcoholics f(A)=0.29 were found. No significant results were found in more homogenous subgroups, i.e. alcoholics with severe alcohol withdrawal (seizures, delirium), early onset age<26 nor dependent patients with positive familial history of alcoholism. These results suggest that the NET gene polymorphism in exon 9 accession number: mRNA: NM_001043, genomic contig.: NT_019610, is unlikely to be involved in the susceptibility to alcoholism and severe alcohol withdrawal.

Adult↗