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Results for “Expression quantitative trait locus”

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At least 109 records · Page 6Linked to original sources
PubMed2000

Synergistic gene interactions control the induction of the mitochondrial uncoupling protein (Ucp1) gene in white fat tissue.

Among a selected group of mouse strains susceptible to dietary obesity, those with an enhanced capacity for Ucp1 and brown adipocyte induction in white fat preferentially lost body weight following adrenergic stimulation. Based on the generality of this mechanism for reducing obesity, a genetic analysis was initiated to identify genes that control brown adipocyte induction in white fat depots in mice. Quantitative trait locus (QTL) analysis was performed using the variations of retroperitoneal fat Ucp1 mRNA expression in progeny of genetic crosses between the A/J and C57BL/6J parental strains and selected AXB recombinant inbred strains. Three A/J-derived loci on chromosomes 2, 3, and 8 and one C57BL/6J locus on chromosome 19 were linked to Ucp1 induction in retroperitoneal fat. Although A/J-derived alleles seemed to contribute to elevated Ucp1 expression, the C57BL/6J allele on chromosome 19 increased Ucp1 mRNA to levels higher than parental values. Thus, novel patterns of C57BL/6J and A/J recombinant genotypes among the four mapped loci resulted in a transgressive variation of Ucp1 phenotypes. Although the extent of the interchromosomal interactions have not been fully explored, strong synergistic interactions occur between a C57BL/6J allele on chromosome 19 and an A/J allele on chromosome 8. In addition to selective synergistic interactions between loci, variations in recessive and dominant effects also contribute to the final levels of Ucp1 expression.

Adipose Tissue↗
PubMed2005

Nucleotide sequence polymorphism within exon 4 of the bovine prolactin gene and its associations with milk performance traits.

Prolactin plays an important regulatory function in mammary gland development, milk secretion, and expression of milk protein genes. Hence the PRL gene is a potential quantitative trait locus and genetic marker of production traits in dairy cattle. We analysed the sequence of the PRL gene to investigate whether mutations in this sequence might be responsible for quantitative variations in milk yield and composition. Using SSCP and direct sequencing, we detected six single-nucleotide polymorphisms within a 294-bp prolactin gene fragment involving exon 4. All detected mutations were silent with respect to the amino acid sequence of the protein. PCR-RFLP genotyping of SNP 8398 R (RsaI) was used to assess allele frequencies in 186 Black-and-White cows (0.113 and 0.887 for A and G, respectively) and in 138 Jersey cows (0.706 and 0.294 for A and G, respectively). Black-and-White cows with genotype AG showed the highest milk yield, while cows with genotype GG showed the highest fat content.

Animals↗
PubMed2002

Expression, genomic structure and mapping of the thymus specific protease prss16: a candidate gene for insulin dependent diabetes mellitus susceptibility.

PRSS16 is a serine protease specifically expressed by epithelial cells in the thymic cortex. The human gene is encoded on 6p21.3-p22 where recent linkage analysis has identified an association with insulin dependent diabetes mellitus (IDDM) susceptibility independent of HLA-DR3. To further investigate its potential role in autoimmunity, we characterized the mouse orthologue, Prss16. The genomic structure of Prss16 shows conservation with the human gene in size, number of exons and chromosomal location. Mapping of Prss16 places it on mouse chromosome 13 centromeric of thesatin locus. This region is comparable to the PRSS16 region on human chromosome 6 and has also been linked to quantitative trait locus for IDDM in the nonobese diabetic mouse. Similar to the human gene, Prss16 expression is highly specific in the mouse with expression limited to the cortical thymic epithelium. Notably, embryonic expression coincides with population of the thymic anlage with T-cell precursors and initiation of T-cell development. We also show that NOD and New Zealand Black mice, which have a disrupted thymic architecture and autoimmune phenotype, have lower levels of Prss16 expression compared to C57BL/6 mice. These findings support the role of Prss16 in T-cell development and susceptibility to autoimmunity in the mouse.

Animals↗
PubMed2005

Quantitative trait locus analysis reveals two intragenic sites that influence O6-alkylguanine-DNA alkyltransferase activity in peripheral blood mononuclear cells.

The repair of specific types of DNA alkylation damage by O6-alkylguanine-DNA alkyltransferase (MGMT) is a major mechanism of resistance to the carcinogenic and chemotherapeutic effects of certain alkylating agents. MGMT expression levels vary widely between individuals but the underlying causes of this variability are not known. To address this, we used an expressed single nucleotide polymorphism (SNP) and demonstrated that the MGMT alleles are frequently expressed at different levels in peripheral blood mononuclear cells (PBMC). This suggests that there is a genetic component of inter-allelic variation of MGMT levels that maps close to or within the MGMT locus. We then used quantitative trait locus (QTL) analysis using intragenic SNPs and found that there are at least two sites influencing inter-individual variation in PBMC MGMT activity. One is characterized by an SNP at the 3' end of the first intron and the second by two SNPs in the last exon. The latter are in perfect disequilibrium and both result in amino acid substitutions-one of them, Ile143Val, affecting an amino acid close to the Cys145 residue at the active site of MGMT. Using in vitro assays, we further showed that while the Val143 variant did not affect the activity of the protein on methylated DNA substrate, it was more resistant to inactivation by the MGMT pseudosubstrate, O6-(4-bromothenyl)guanine. These findings suggest that further investigations of the potential epidemiological and clinical significance of inherited differences in MGMT expression and activity are warranted.

Base Sequence↗
PubMed2003

Functional divergence of a syntenic invertase gene family in tomato, potato, and Arabidopsis.

Comparative analysis of complex developmental pathways depends on our ability to resolve the function of members of gene families across taxonomic groups. LIN5, which belongs to a small gene family of apoplastic invertases in tomato (Lycopersicon esculentum), is a quantitative trait locus that modifies fruit sugar composition. We have compared the genomic organization and expression of this gene family in the two distantly related species: tomato and Arabidopsis. Invertase family members reside on segmental duplications in the near-colinear genomes of tomato and potato (Solanum tuberosum). These chromosomal segments are syntenically duplicated in the model plant Arabidopsis. On the basis of phylogenetic analysis of genes in the microsyntenic region, we conclude that these segmental duplications arose independently after the separation of the tomato/potato clade from Arabidopsis. Rapid regulatory divergence is characteristic of the invertase family. Interestingly, although the processes of gene duplication and specialization of expression occurred separately in the two species, synteny-based orthologs from both clades acquired similar organ-specific expression. This similar expression pattern of the genes is evidence of comparable evolutionary constraints (parallel evolution) rather than of functional orthology. The observation that functional orthology cannot be identified through analysis of expression similarity highlights the caution that needs to be exercised in extrapolating developmental networks from a model organism.

Arabidopsis↗
PubMed2026

Mapping the causal chain from genetic risk variants to lipid dysmetabolism in Parkinson's disease.

The molecular pathways linking genetic variants to Parkinson's disease (PD) onset and progression remain incompletely defined; however, risk alleles in multiple genes, including GBA1, strongly implicate lipid metabolism. To systematically identify causal biomarker signatures, we analysed comprehensive metabolome profiles from blood plasma in 149 PD patients and 150 controls, along with complementary genetic, RNA-sequencing and metabolic data from other available clinical and pathologic cohorts. Using colocalization and summary-data-based Mendelian randomization, we tested whether expression and metabolic quantitative trait loci mediate the association between implicated genetic variants and PD risk. We further integrated differential metabolomics and proteomics from blood and brain to reveal pertinent mechanisms. We show that common PD risk variants at the serine palmitoyltransferase small subunit B (SPTSSB) locus, a key regulator of de novo sphingolipid biosynthesis, are associated with increased SPTSSB brain expression and elevated plasma ceramides. Additional analyses strongly support our hypothesis that a common SPTSSB causal variant is responsible for PD risk as well as the expression and metabolic quantitative trait loci. Multiple sphingolipids and fatty acid derivatives were perturbed in PD, and we identified both unique and shared features with the Alzheimer's disease metabolome. A PD acylcarnitine signature was further replicated in human post-mortem brain tissue, when comparing those with or without preclinical Lewy body pathology. Integrated analysis of complementary brain proteomic profiles revealed dysregulation of mitochondrial processes dependent on acylcarnitines, including fatty acid beta-oxidation, the tricarboxylic acid cycle and oxidative phosphorylation. Our results identify promising biomarkers and reveal a causal chain linking genetic variation to altered gene/protein expression, lipid dysmetabolism, and the manifestation of PD.

Humans↗
PubMed2002

Evidence of genetic interaction between the beta-globin complex and chromosome 8q in the expression of fetal hemoglobin.

During human development, the switch from fetal to adult hemoglobin (Hb) is not complete with the residual gamma-globin expression being restricted to a subset of erythrocytes termed "F cells" (FC). Statistical analyses have shown the FC trait to be influenced by a common sequence variant (C-->T) at position -158 upstream of the Ggamma-globin gene, termed the "XmnI-Ggamma polymorphism." The XmnI-Ggamma site is believed to be involved in the expression of the Ggamma-globin gene through interaction with transcription factors, and polymorphisms in the transcription factors could be influencing fetal Hb expression, conditional on the XmnI-Ggamma site. Using a two-locus model, in which the second locus was the known quantitative-trait locus (QTL) at the XmnI-Ggamma site, we showed suggestive linkage to chromosome 8q. A maximum single-point LOD score of 4.33 and a multipoint LOD score of 4.75 were found in a 15-20 cM region of chromosome 8q. A single-locus analysis failed to show linkage of FC to the region when the XmnI-Ggamma site was accounted for by removing its effects from the data or including it as a covariate. Results of the single-locus analysis were significant when the effects of the XmnI-Ggamma site were not accounted for in any way. The results of analysis in a large Indian kindred indicate that there is an interaction between the XmnI-Ggamma site and a QTL on chromosome 8q that is influencing the production of fetal Hb.

Chromosome Mapping↗
PubMed2000

Genetics of adaptive radiation in Hawaiian species of Tetramolopium (Asteraceae). III. Evolutionary genetics of sex expression.

Despite numerous studies of speciation on oceanic islands, few insights exist on the genetic changes involved in the origin and diversification of island taxa. Here we report a genetic analysis of the evolutionary change in sex expression in Hawaiian Tetramolopium. The most diverse clade in the genus is characterized by a monoecious breeding system. The breeding system resulted from a change in sex expression in disc florets from the ancestral hermaphroditic condition to the derived male state. Analysis of an F2 population from a cross between the two forms of sex expression indicates two regions of the Tetramolopium linkage map are associated with the loss of female function in disc florets. Quantitative trait locus mapping of the two linkage groups confirms that two loci control 56% of the phenotypic variation of the trait in the F2 population. Additive and dominance effects are apparent but no statistical evidence of epistasis was found. Several related reproductive traits also have few genetic associations on the linkage map, but are generally distinct from the control of sex expression. Although modifier loci are likely to be involved, the apparent simple genetic change underlying sex expression parallels a major evolutionary diversification in Hawaiian Tetramolopium and may have initiated the divergence of this novel clade.

Adaptation, Biological↗
PubMed2005

Integrating QTL and high-density SNP analyses in mice to identify Insig2 as a susceptibility gene for plasma cholesterol levels.

The use of inbred strains of mice to dissect the genetic complexity of common diseases offers a viable alternative to human studies, given the control over experimental parameters that can be exercised. Central to efforts to map susceptibility loci for common diseases in mice is a comprehensive map of DNA variation among the common inbred strains of mice. Here we present one of the most comprehensive high-density, single nucleotide polymorphism (SNP) maps of mice constructed to date. This map consists of 10,350 SNPs genotyped in 62 strains of inbred mice. We demonstrate the utility of these data via a novel integrative genomics approach to mapping susceptibility loci for complex traits. By integrating in silico quantitative trait locus (QTL) mapping with progressive QTL mapping strategies in segregating mouse populations that leverage large-scale mapping of the genetic determinants of gene expression traits, we not only facilitate identification of candidate quantitative trait genes, but also protect against spurious associations that can arise in genetic association studies due to allelic association among unlinked markers. Application of this approach to our high-density SNP map and two previously described F2 crosses between strains C57BL/6J (B6) and DBA/2J and between B6 ApoE(-/-) and C3H/HeJ ApoE(-/-) results in the identification of Insig2 as a strong candidate susceptibility gene for total plasma cholesterol levels.

Animals↗
PubMed1996

Extensions to quantitative trait locus mapping in experimental organisms.

Quantitative trait locus (QTL) mapping studies involving inbred model organisms have become important and often-used investigative tools in contemporary genetics research. As a result, a number of statistical methods and study designs have been developed that have made it relatively easy for researchers to determine the rough locations of a number of QTLs that influence traits of all types, including a great many of relevance to hypertension and blood pressure regulation. However, as a whole, these methods and designs are limited in that they are not flexible enough to accommodate many of the complexities associated with quantitative trait expression. In this review, we describe a number of extensions to QTL mapping designs that should make QTL mapping experiments more insightful and compelling. These extensions include multiple QTL modeling with an emphasis on epistatic locus interaction and additive locus effects, the use of multiple phenotypic end points, the design of pharmacogenetic studies, the use of whole-genome parameters in quantitative trait investigations, and issues in mapping QTLs that influence traits that exhibit developmental trends. We use studies investigating the genetic basis of blood pressure regulation to exemplify relevant issues.

Animals↗
PubMed2006

Mapping quantitative trait loci for hearing loss in Black Swiss mice.

In common inbred mouse strains, hearing loss is a highly prevalent quantitative trait, which is mainly controlled by the Cdh23(753A) variant and alleles at numerous other strain-specific loci. Here, we investigated the genetic basis of hearing loss in non-inbred strains. Mice of Swiss Webster, CF-1, NIH Swiss, ICR, and Black Swiss strains exhibited hearing profiles characteristic of progressive, sensorineural hearing impairment. In particular, CF-1, Black Swiss, and NIH Swiss mice showed early-onset hearing impairment, ICR and Swiss Webster mice expressed a delayed-onset hearing loss, and NMRI mice had normal hearing. By quantitative trait locus (QTL) mapping, two significant QTLs were identified underlying hearing loss in Black Swiss mice: one QTL mapped to chromosome (chr) 10 (named ahl5, LOD 8.9, peak association 35-42 cM) and a second QTL localized to chr 18 (ahl6, LOD 3.8, 38-44 cM). Ahl5 and ahl6 account for 61% and 32% of the variation in the backcross, respectively. Cadherin 23 (Cdh23) and protocadherin 15 (Pcdh15), mapping within the 95% confidence interval of ahl5, bear nucleotide polymorphisms in coding exons, but these appear to be unrelated to the hearing phenotype. Haplotype analyses across the Cdh23 locus demonstrated the phylogenetic relationship between Black Swiss and common inbred strains.

Age Factors↗
PubMed2025

Cross-Phenotype Genome-Wide Association Study on the Shared Genetic Susceptibility to Systemic Sclerosis and Primary Biliary Cholangitis.

OBJECTIVE: An increased risk of primary biliary cholangitis (PBC) has been reported in patients with systemic sclerosis (SSc). Our study aims to investigate the shared genetic susceptibility between the two disorders and to define candidate causal genes using cross-phenotype genome-wide association study (GWAS) meta-analysis. METHODS: We performed cross-phenotype GWAS meta-analysis and Bayesian colocalization analysis for patients with SSc and patients with PBC. We performed both genome-wide and locus-based analysis, including tissue and pathway enrichment analyses, fine-mapping, Bayesian colocalization analyses with expression quantitative trait loci and protein quantitative trait loci (pQTL) datasets, and phenome-wide association studies. Finally, we used an integrative approach to prioritize candidate causal genes from the novel loci. RESULTS: We detected a strong genetic correlation between SSc and PBC (global genetic correlation = 0.84, P = 1.7 &#xd7; 10-6). In the cross-phenotype GWAS meta-analysis, we identified 44 nonhuman leukocyte antigens loci that reached genome-wide significance (P < 5 &#xd7; 10-8). Evidence of shared causal variants between patients with SSc and patients with PBC was found for nine loci, five of which were novel. Integrating multiple sources of evidence, we prioritized CD40, ERAP1, PLD4, SPPL3, and CCDC113 as novel candidate causal genes. The CD40 risk locus colocalized with trans-pQTLs of multiple plasma proteins involved in B cell function. CONCLUSION: Our study supports a strong shared genetic susceptibility between SSc and PBC. Using cross-phenotype analyses, we have prioritized several novel candidate causal genes and pathways for these disorders.

Humans↗
PubMed2005

Angiogenesis in prolactinomas: regulation and relationship with tumour behaviour.

Tumours are dependent on angiogenesis for growth and inhibition of angiogenesis has become a target for antineoplastic therapy. In the pituitary, unlike other tissues, vascularization is lower in adenomas compared to the normal gland. Despite this finding, a relationship between increased vascularity and several aspects of prolactinoma behaviour such as size, invasiveness, surgical outcome and malignancy, has been demonstrated. The process of angiogenesis is the result of a balance of stimulating and inhibiting factors. It is likely that an interaction between gene expression (such as pituitary tumour transforming gene (PTTG) and a novel gene located within the Edpm5 quantitative trait locus), hormonal stimuli including oestrogens, dopamine, 16 kDa fragments of prolactin and proangiogenic and antiangiogenic growth factors (for example, vascular endothelial growth factor (VEGF) and fibroblast growth factor (FGF-2), determine the final angiogenic phenotype of prolactinomas, and thus subsequent tumour behaviour. The elucidation of all the factors involved in the regulation of angiogenesis and their interactions might open new possibilities in the treatment of prolactinomas, especially in those cases with resistance or intolerance to dopamine agonists.

Dopamine↗
PubMed2003

Molecular characterization and expression of porcine bone morphogenetic protein receptor-IB in the uterus of cyclic and pregnant gilts.

Previous gene mapping analyses revealed a quantitative trait locus for uterine capacity on chromosome 8. Comparison of porcine and human genetic maps suggests that the bone morphogenetic protein receptor IB (BMPR-IB) gene may be located near this region. The objectives of this study were to 1) clone the full coding region for BMPR-IB, 2) examine BMPR-IB gene expression by the endometrium and its cellular localization in cyclic and pregnant gilts, and 3) map the BMPR-IB gene. By iterative screening of an expressed sequence tag library, we obtained a 3559-base pair cDNA clone including the full coding region of BMPR-IB. Endometrial BMPR-IB mRNA expression of White composite gilts was determined by Northern blotting in Days 10, 13, and 15 cyclic and Days 10, 13, 15, 20, 30, and 40 pregnant gilts. In cyclic gilts, endometrial BMPR-IB mRNA expression was elevated on Days 13 and 15 (P < 0.01) compared with Day 10. Expression of BMPR-IB mRNA was localized in both luminal and glandular epithelium on Day 15. However, in pregnant gilts, BMPR-IB mRNA expression was not significantly different in the endometrium from Day 10 to Day 20, and it was significantly decreased on Days 30 and 40 (P = 0.011). The BMPR-IB gene was mapped to 108 cM on chromosome 8. These findings show that BMPR-IB mRNA expression is regulated differently in cyclic and pregnant gilts; this pattern of gene expression may be important for endometrial function during the luteal phase of the estrous cycle as compared with early pregnancy.

Amino Acid Sequence↗
PubMed2001

Modulations in gene expression and mapping of genes associated with cyst nematode infection of soybean.

Infection of the soybean root by the soybean cyst nematode (SCN) (Heterodera glycines Ichinohe) induces a well-documented, yet poorly understood, response by the host plant. The plant response, involving the differentiation of a feeding structure, or "syncytium," facilitates the feeding and reproduction of the nematode to the detriment of the host. We used a genetic system involving a single dominant soybean gene conferring susceptibility to an inbred nematode strain, VL1, to characterize the nematode-host interaction in susceptible line PI 89008. The restriction fragment length polymorphism marker pB053, shown to map to a major SCN resistance locus, cosegregates with resistance among F2 progeny from the PI 89008 x PI 88287 cross. Cytological examination of the infection process confirmed that syncytium development in this genetic system is similar to that reported by others who used noninbred nematode lines. Our study of infected root tissue in the susceptible line PI 89008 revealed a number of genes enhanced in expression. Among these are catalase, cyclin, elongation factor 1alpha, beta-1,3-endoglucanase, hydroxy-methylglutaryl coenzyme A reductase, heat shock protein 70, late embryonic abundant protein 14, and formylglycinamidine ribonucleotide synthase, all of which we have genetically positioned on the public linkage map of soybean. Formylglycinamidine ribonucleotide synthase was found to be tightly linked with a major quantitative trait locus for SCN resistance. Our observations are consistent with the hypothesis proposed by others that feeding site development involves the dramatic modulation of gene expression relative to surrounding root cells.

Animals↗
PubMed2006

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

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

Animals↗
PubMed2006

Stability over genetic backgrounds, generations and years of quantitative trait locus (QTLs) for organoleptic quality in tomato.

The efficiency of marker-assisted backcross for the introgression of a quantitative trait locus (QTL) from a donor line into a recipient line depends on the stability of QTL expression. QTLs for six quality traits in tomato (fruit weight, firmness, locule number, soluble solid content, sugar content and titratable acidity) were studied in order to investigate their individual effect and their stability over years, generations and genetic backgrounds. Five chromosome regions carrying fruit quality QTLs were transferred following a marker-assisted backcross scheme from a cherry tomato line into three modern lines with larger fruits. Three sets of genotypes corresponding to three generations were compared: (1) an RIL population, which contained 50% of each parental genome, (2) three BC3S1 populations which segregated simultaneously for the five regions of interest but were almost fully homozygous for the recipient genome on the eight chromosomes carrying no QTL and (3) three sets of QTL-NILs (BC3S3 lines) which differed from the recipient line only in one of the five regions. QTL detection was performed in each generation, in each genetic background and during 2 successive years for QTL-NILs. About half of the QTLs detected in QTL-NILs were detected in both years. Eight of the ten QTLs detected in RILs were recovered in the QTL-NILs with the genetic background used for the initial QTL mapping experiment, with the exception of two QTLs for fruit firmness. Several new QTLs were detected. In the two other genetic backgrounds, the number of QTLs in common with the RILs was lower, but several new QTLs were also detected in advanced generations.

Fruit↗
PubMed2003

Selective breeding, quantitative trait locus analysis, and gene arrays identify candidate genes for complex drug-related behaviors.

Acute functional tolerance to ethanol develops during a single exposure to ethanol; it has been suggested to be a predisposing factor for the development of ethanol dependence. Genetic determinants of acute functional tolerance, as well as of ethanol dependence, have been clearly demonstrated. We describe a novel approach that uses a combination of selective breeding (to segregate genes contributing to the phenotype of interest, i.e., acute functional tolerance to the incoordinating effect of ethanol), quantitative trait locus analysis (to define chromosomal regions associated with acute functional tolerance), and DNA microarray technology (to identify differentially expressed genes in the brains of the selected lines of mice) to identify candidate genes for the complex phenotype of ethanol tolerance. The results indicate the importance of a signal transduction cascade that involves the glutamate receptor delta2 protein, the Ephrin B3 ligand, and the NMDA receptor, as well as a transcriptional regulatory protein that may be induced by activation of the NMDA receptor (zinc finger protein 179) and a protein that can modulate downstream responses to NMDA receptor activation (peroxiredoxin), in mediating acute tolerance to the incoordinating effect of ethanol.

Alcohol-Induced Disorders↗