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PubMed2004

Discovering modes of action for therapeutic compounds using a genome-wide screen of yeast heterozygotes.

Modern medicine faces the challenge of developing safer and more effective therapies to treat human diseases. Many drugs currently in use were discovered without knowledge of their underlying molecular mechanisms. Understanding their biological targets and modes of action will be essential to design improved second-generation compounds. Here, we describe the use of a genome-wide pool of tagged heterozygotes to assess the cellular effects of 78 compounds in Saccharomyces cerevisiae. Specifically, lanosterol synthase in the sterol biosynthetic pathway was identified as a target of the antianginal drug molsidomine, which may explain its cholesterol-lowering effects. Further, the rRNA processing exosome was identified as a potential target of the cell growth inhibitor 5-fluorouracil. This genome-wide screen validated previously characterized targets or helped identify potentially new modes of action for over half of the compounds tested, providing proof of this principle for analyzing the modes of action of clinically relevant compounds.

Drug Evaluation, Preclinical↗

PubMed2002

A genome-wide screen for linkage in Nordic sib-pairs with multiple sclerosis.

Genetic factors influence susceptibility to multiple sclerosis but the responsible genes remain largely undefined, association with MHC class II alleles being the only established genetic feature of the disease. The Nordic countries have a high prevalence of multiple sclerosis, and to further explore the genetic background of the disease, we have carried out a genome-wide screen for linkage in 136 sibling-pairs with multiple sclerosis from Denmark, Finland, Norway and Sweden by typing 399 microsatellite markers. Seventeen regions where the lod score exceeds the nominal 5% significance threshold (0.7) were identified-1q11-24, 2q24-32, 3p26.3, 3q21.1, 4q12, 6p25.3, 6p21-22, 6q21, 9q34.3, 10p15, 10p12-13, 11p15.5, 12q21.3, 16p13.3, 17q25.3, 22q12-13 and Xp22.3. Although none of these regions reaches the level of genome-wide significance, the number observed exceeds the 10 that would be expected by chance alone. Our results significantly add to the growing body of linkage data relating to multiple sclerosis.

Denmark↗

PubMed2005

Genome-wide screen for inner nuclear membrane protein targeting in Saccharomyces cerevisiae: roles for N-acetylation and an integral membrane protein.

Appropriate nuclear membrane structure is important for all eukaryotic organisms as evidenced by the numerous human diseases and alterations in gene expression caused by inappropriate targeting of proteins to the inner nuclear membrane (INM). We report here the first genome-wide screen to identify proteins functioning in INM targeting. We transformed to near completion the 4850 members of the Saccharomyces cerevisiae deletion collection of unessential genes in the 96-well format with a plasmid encoding a reporter protein, Trm1-II-GFP, which normally resides at the INM. We found that deletion of genes encoding subunits of the N-terminal acetyltransferase, NatC, cause mislocation of Trm1-II-GFP from the INM to the nucleoplasm. Mass spectroscopic analysis indicates that Trm1-II-GFP is N-acetylated. N-terminal mutations of Trm1-II-GFP predicted to ablate N-acetylation cause nucleoplasmic location, whereas a variant with an N-terminal alteration predicted to allow N-acetylation by NatC is located at the INM, providing genetic support that Trm1p-II N-acetylation is necessary for its subnuclear INM location. However, because N-acetylation appears not to be sufficient for INM targeting, it may provide a necessary role for INM targeting by affecting Trm1-II-GFP structure and exposure of cis-acting INM targeting motifs. We also discovered that YIL090W/Ice2p, an integral membrane protein located in the endoplasmic reticulum, is necessary for efficient targeting of Trm1-II-GFP to the INM. YIL090W/Ice2p may serve as a tether for INM proteins or as a regulator of INM tethers. Our methodology can be extrapolated to obtain genome-wide perspectives of mechanisms necessary to achieve appropriate subcellular and/or suborganellar location for any resident protein.

Acetylation↗

PubMed2000

Genome-wide screening for radiation response factors in head and neck cancer.

INTRODUCTION: Radiation therapy is an integral part of the treatment of head and neck cancer. Factors predicting radiation response are ill defined. The aim of this study was to identify genetic aberrations associated with radiation response in cell lines derived from head and neck squamous cell carcinomas (HNSCC) using comparative genomic hybridization (CGH) for genome-wide screening. METHODS: Five cell lines derived from HNSCC were subjected to a single course of radiation (400 cGy) in parallel with a similarly handled, untreated control. Cellular response to radiation was determined on posttreatment days 1, 2, 3, 4, and 5 using a cell viability assay (MTT assay). Radiation response was defined as 35% or greater decrease in cell survival relative to control. Tumor doubling time was determined by cell counts performed at day 0 and 1 for each cell line. All experiments were done in quadruplicate. CGH analysis was performed by differentially labeling DNA from tumor and normal tissue with fluorescent agents. The labeled DNAs were simultaneously hybridized to normal metaphase chromosomes. Image analysis for fluorescence intensity along the entire length of each metaphase chromosome allowed generation of a color ratio, which was used to detect copy number changes. RESULTS: Radioresistance was identified in two of five cell lines. The tumor doubling time was not a predictor of radiation response. CGH identified a complex pattern of aberrations, with gain of 3q common to all cell lines. The number of genetic aberration was higher in radiation-sensitive cell lines than in radiation-resistant ones. No recurrent aberrations were unique to the radiation-resistant cell lines. Recurrent gains at 7p and 17q and losses at 5q, 7q, and 18q were unique to the radiation-sensitive cell lines. CONCLUSIONS: The number of aberrations identified by CGH analysis may be a predictor of radiation response. A large study of primary tumors is warranted to confirm this association and identify specific genetic aberrations associated with radiation response.

Carcinoma, Squamous Cell↗

PubMed2026

Genome-wide screening and functional analysis of protein glycosylation-related genes involved in tomato fruit ripening.

Protein glycosylation, an essential co- and post-translational modification, plays critical roles in plant growth, development, and stress responses. However, its functional role in tomato fruit ripening has not been extensively investigated. Here, key protein glycosylation-related genes involved in tomato fruit ripening were identified by genome-wide screen and subsequently functional characterization. First, a dataset comprising 242 glycosylation-related proteins was established based on Gene Ontology annotations in tomato, combined with sequence homology to protein glycosylation-related proteins from Arabidopsis thaliana and Homo sapiens. Then, Subsequently, 28 genes encoding highly expressed glycosylation-related proteins (RPKM > 30) at the breaker (BR) stage were selected for functional screening, and subsequently 6 genes were identified as regulators of fruit ripening by method of virus-induced gene silencing (VIGS). Among them, Solyc03g098600 (STT3B), Solyc01g109410 (OST48), Solyc04g082670 (RPN1), and Solyc08g076460 (DAD1) functioned as positive regulators of tomato fruit ripening, whereas Solyc04g005340 (UAM2) and Solyc08g075340 (XEG113), acted as negative regulators. The expression of these genes responded dynamically to multiple ripening-related cues, including temperature, light, ethylene, and transcription factors. Furthermore, silencing of these genes individually affected the expression of genes involved in fruit ripening, including ethylene biosynthesis genes (ACS2, ACS4, ACO1, and ACO3), ripening-associated transcription factors (RIN, NOR, NOR-LIKE1, FUL1, and FUL2), and the key gene (PSY1) of lycopene biosynthesis pathway. Collectively, these findings demonstrate that protein glycosylation plays an important role in tomato fruit ripening by modulating ethylene signaling, ripening-associated transcriptional regulation, and lycopene biosynthesis.

Fruit ripening↗

PubMed2004

Mutator genes for suppression of gross chromosomal rearrangements identified by a genome-wide screening in Saccharomyces cerevisiae.

Different types of gross chromosomal rearrangements (GCRs), including translocations, interstitial deletions, terminal deletions with de novo telomere additions, and chromosome fusions, are observed in many cancers. Multiple pathways, such as S-phase checkpoints, DNA replication, recombination, chromatin remodeling, and telomere maintenance that suppress GCRs have been identified. To experimentally expand our knowledge of other pathway(s) that suppress GCRs, we developed a generally applicable genome-wide screening method. In this screen, we identified 10 genes (ALO1, CDC50, CSM2, ELG1, ESC1, MMS4, RAD5, RAD18, TSA1, and UFO1) that encode proteins functioning in the suppression of GCRs. Moreover, the breakpoint junctions of GCRs from these GCR mutator mutants were determined with modified breakpoint-mapping methods. We also identified nine genes (AKR1, BFR1, HTZ1, IES6, NPL6, RPL13B, RPL27A, RPL35A, and SHU2) whose mutations generated growth defects with the pif1Delta mutation. In addition, we found that some of these mutations changed the telomere size.

Chromosome Aberrations↗

PubMed2002

A simple method for genome-wide screening for advantageous insertions of mobile DNAs in Escherichia coli.

Laboratory evolution in Escherichia coli has revealed that fitness typically increases in experimental populations. These changes are sometimes associated with changes in insertion sequence positions, some of which may themselves cause advantageous phenotypes. We have a novel and general method for identifying genes in Escherichia coli, whose knockout by mobile DNA insertions is beneficial in experimental evolution. Insertion sites in favored clones can be identified by reference to genomic information. We have implemented the method using modified Tn10 transposons bearing kanamycin and chloramphenicol resistance cassettes. Results are consistent across replicated experiments, demonstrating that the insertions are themselves creating selective advantages, rather than hitch-hiking with favorable base substitutions. The successful clones have subsequently been confirmed to have a fitness advantage relative to the progenitor strain. In experiments in shaking culture, we find that advantageous insertions usually fall in operons required in the pathways creating flagella. The method allows a rapid genome-wide screening for advantageous insertions in arbitrary environmental conditions. It allows investigation of the extent to which transient mutations generating environment-dependent selective advantages may help to explain the persistence of mobile DNAs in primarily clonal organisms, such as E. coli.

Chloramphenicol Resistance↗

PubMed1984

Human genomic library screened with 17-base oligonucleotide probes yields a novel interferon gene.

A method is presented that has permitted a human genomic library to be screened for low-copy genes using 17-base synthetic oligonucleotides as probes. Parallel screening with two different 17-base probes permitted the unambiguous identification of clones containing interferon-alpha (IFN-alpha) genes. The isolated human IFN-alpha genes were sequenced, and one appears to be IFN-alpha L; the other is one not previously described, which we have designated IFN-alpha WA. The IFN-alpha WA sequence differs from those of IFN-alpha genes A-L at approximately equal to 10% of the positions and is most similar to IFN-alpha C, -alpha F, and -alpha H. IFN-alpha WA has been found to encode amino acids that differ from those conserved at each of five positions in all previously reported IFN-alpha species. The IFN-alpha WA gene codes for an active interferon, which has been expressed in Escherichia coli using an M13-lacZ fusion as an expression vector. About 5 X 10(6) units of IFN-alpha WA were obtained per liter of bacterial culture. The described screening procedure using short probes should permit the isolation of genes for which sequence information is available from animal or plant genomic libraries.

Base Sequence↗

PubMed2004

A genome-wide screen identifies a single beta-defensin gene cluster in the chicken: implications for the origin and evolution of mammalian defensins.

BACKGROUND: Defensins comprise a large family of cationic antimicrobial peptides that are characterized by the presence of a conserved cysteine-rich defensin motif. Based on the spacing pattern of cysteines, these defensins are broadly divided into five groups, namely plant, invertebrate, alpha-, beta-, and theta-defensins, with the last three groups being mostly found in mammalian species. However, the evolutionary relationships among these five groups of defensins remain controversial. RESULTS: Following a comprehensive screen, here we report that the chicken genome encodes a total of 13 different beta-defensins but with no other groups of defensins being discovered. These chicken beta-defensin genes, designated as Gallinacin 1-13, are clustered densely within a 86-Kb distance on the chromosome 3q3.5-q3.7. The deduced peptides vary from 63 to 104 amino acid residues in length sharing the characteristic defensin motif. Based on the tissue expression pattern, 13 beta-defensin genes can be divided into two subgroups with Gallinacin 1-7 being predominantly expressed in bone marrow and the respiratory tract and the remaining genes being restricted to liver and the urogenital tract. Comparative analysis of the defensin clusters among chicken, mouse, and human suggested that vertebrate defensins have evolved from a single beta-defensin-like gene, which has undergone rapid duplication, diversification, and translocation in various vertebrate lineages during evolution. CONCLUSIONS: We conclude that the chicken genome encodes only beta-defensin sequences and that all mammalian defensins are evolved from a common beta-defensin-like ancestor. The alpha-defensins arose from beta-defensins by gene duplication, which may have occurred after the divergence of mammals from other vertebrates, and theta-defensins have arisen from alpha-defensins specific to the primate lineage. Further analysis of these defensins in different vertebrate lineages will shed light on the mechanisms of host defense and evolution of innate immunity.

Amino Acid Motifs↗

PubMed2002

Autoimmune thyroid disease susceptibility loci in a large Chinese family.

OBJECTIVES: The autoimmune thyroid diseases (AITDs) comprising Graves' disease (GD) and Hashimoto's thyroiditis (HT) are complex genetic diseases, which result from an interaction between predisposing genes and environmental triggers. The aim of our study was to dissect the genetic predisposition to GD and HT in one large Chinese family with multiple members affected with AITD. PATIENTS: We completed a whole genome screen of a large multiplex Chinese-American family. We enrolled 27 family members from three generations. Eight members were affected with AITD, six had GD and two had HT. DESIGN: We determined the information limits of the family. Power calculations indicated that the maximum attainable LOD scores were 5.1 assuming dominant inheritance, and 3.4 assuming recessive inheritance. These estimates both assumed 100% penetrance and one gene. Whole genome screening was performed using 400 highly polymorphic and densely spaced microsatellite markers spanning the entire human genome (intermarker distance < 10 cM). Linkage analysis was performed using two-point and multipoint parametric and nonparametric methods. RESULTS: Initial whole genome screening performed with 400 microsatellite markers identified two markers that showed evidence for linkage to AITD in this family, D11S4191 and D9S175, with two-point LOD scores of 2.31 and 2.05, respectively. Multipoint linkage analysis focusing on the regions containing these markers revealed a maximum multipoint LOD score (MLS) of 2.13 and a nonparametric linkage score (NPL) of 6.1 for D11S4191 and an MLS of 2.01 and NPL of 7.5 for D9S175. CONCLUSIONS: These results showed that this Chinese family harboured susceptibility loci for AITD which were distinct from those previously found in the Caucasian population. This suggests that different susceptibility loci exist between different ethnic groups. Furthermore, even within a single family from a genetically homogenous population, more than one gene was involved in the genetic susceptibility to AITD, supporting the notion that AITDs are caused by multiple genes of varying influences.

Adolescent↗

PubMed2004

Genome-wide screening for prognosis-predicting genes in early-stage non-small-cell lung cancer.

In early-stage non-small-cell lung cancer (NSCLC), a substantial proportion of patients can be cured by surgery. Development of distant metastases is the most frequent cause of therapeutic failure. The possibility to accurately predict a patient's risk for developing distant metastasis would help to identify patients that are candidates for further intervention such as conventional adjuvant chemotherapy or experimental drugs. Current molecular biology techniques allow the genome-wide screening for differentially expressed genes; and adequate bioinformatics approaches are developed at a rapid pace to improve prognosis prediction. Genes associated with metastasis do not necessarily play a role in disease pathogenesis but rather reflect the activation of specific signal-transduction pathways that are associated with enhanced migration and invasion capability. In our own work, we have identified several genes (e.g. thymosin beta-4, elF4A1), including a novel non-coding RNA (MALAT-1) to be expressed at significantly higher levels in stage-I and stage-II NSCLC primary tumours that subsequently metastasised. As a consequence, patients with high-level expression of these genes were shown to have significantly worse survival compared to patients with low-level expression of these genes. These data support the hypothesis that gene-expression patterns in primary tumours determine the tumours' likelihood to metastasise. In the near future, this information will be used for tailored therapy approaches for patients with early-stage NSCLC.

Biomarkers, Tumor↗

PubMed2026

A multicenter survey on BRAF screening for the implementation of perioperative cancer genomic medicine for resectable colorectal oligometastases.

BACKGROUND: Genomic screening is an essential, but potentially time-consuming procedure, especially in neoadjuvant settings. We evaluated the preoperative screening of the BRAF V600E mutation for recruitment to a clinical trial among patients with resectable colorectal oligometastases (CRM). METHODS: In April 2022, an investigator-initiated trial was launched to investigate the efficacy and safety of perioperative use of the BEACON triplet regimen for BRAF V600E mutant resectable CRM. BRAF screening was retrospectively conducted in patients with resected colorectal liver metastases in 2019 for planning the trial and prospectively conducted in preoperative patients with resectable CRM from January 2022 to June 2025 for patient recruitment to the trial. RESULTS: BRAF V600E mutation was detected in 12 (3.2%) of 379 postoperative patients retrospectively and in 36 (1.7%) of 2140 preoperative patients prospectively, with 1840 patients (86.0%) carrying the wild-type and 264 patients (12.3%) classified as untested. The detection rate of the BRAF V600E mutation was significantly lower when the screening was performed prospectively in preoperative patients (P < 0.001). The untested rates varied across metastatic organs, with 10.3% in the liver, 18.1% in the lungs, 12.0% in the lymph nodes, 16.7% in the peritoneum, and 7.8% in other organs. The untested rates decreased consistently across semiannual comparisons: 28.5% in the first evaluation, followed by 15.0%, 12.0%, 8.4%, 9.1%, 7.3%, and 7.1% (P < 0.01 when compared with the first period). CONCLUSION: Raising physician awareness, as reflected by the untested rate, is a crucial factor in conducting clinical trials to implement perioperative cancer genomic medicine.

Humans↗

PubMed2000

The haplotype linkage disequilibrium test for genome-wide screens: its power and study design.

The focus of human genetics continues to shift toward the dissection of complex phenotypes. Integral to these endeavors is the development of powerful analytical tools. To this end, we propose a novel method designated the haplotype linkage disequibrium (LD) test for identifying diseases genes. The basic structure of the haplotype test statistic is a chi-square in which haplotypes, as opposed to individual marker data, are compared between cases and controls. Specifically, we performed power calculations and demonstrate that the use of haplotypes improves the power of mapping disease genes. We show that this approach can be used for initial genome-wide screens in mapping disease genes. Furthermore, we investigated the factors influencing statistical power of the method and discussed basic principals underlying study design. Published data from the Hereditary Hemochromatosis region was used to illustrate the utility of the haplotype test. Also discussed is its relationship with linkage disequibrium.

Alleles↗

PubMed2005

A genome-wide screen in 1119 relative pairs with autoimmune thyroid disease.

CONTEXT: Autoimmune thyroid diseases (AITD), comprising Graves' disease and autoimmune hypothyroidism, are characterized by loss of immunological self-tolerance to thyroid antigens. These are complex diseases arising from a combination of genetic and environmental factors. An understanding of the genetic susceptibility factors for AITD could help to target treatments more effectively and identify people at risk for these conditions. OBJECTIVE: The objective of this study was to identify regions of genetic linkage to AITD that could potentially harbor genetic susceptibility factors for these conditions. DESIGN: The study design was a genome-wide screen performed on affected relative pairs with AITD. SETTING: Patients were recruited through hospital endocrinology clinics. PARTICIPANTS: Some 1119 Caucasian relative pairs affected with AITD (Graves' disease or autoimmune hypothyroidism) were recruited into the study. INTERVENTION: Blood samples were obtained from each participant for DNA analysis, and clinical questionnaires were completed. MAIN OUTCOME MEASURE: The study aimed to identify regions of genetic linkage to AITD. RESULTS: Three regions of suggestive linkage were obtained on chromosomes 18p11 (maximum LOD score, 2.5), 2q36 (maximum LOD score, 2.2), and 11p15 (maximum LOD score, 2.0). No linkage to human leukocyte antigen was found. CONCLUSIONS: The absence of significant evidence of linkage at any one locus in such a large dataset argues that genetic susceptibility to AITD reflects a number of loci, each with a modest effect. Linkage analysis may be limited in defining such loci, and large-scale association studies may prove to be more useful in identifying genetic susceptibility factors for AITD.

Chromosome Mapping↗

PubMed1999

A genome-wide screen for asthma-associated quantitative trait loci in a mouse model of allergic asthma.

Asthma is the most common illness of childhood, affecting one child in seven in the UK. Asthma has a genetic basis, but genetic studies of asthma in humans are confounded by uncontrolled environmental factors, varying penetrance and phenotypic pleiotropy. An animal model of asthma would offer controlled exposure, limited and consistent genetic variation, and unlimited size of sibships. Following immunization and subsequent challenge with ovalbumin, the Biozzi BP2 mouse shows features of asthma, including airway inflammation, eosinophil infiltration and non-specific bronchial responsiveness. In order to identify genetic loci influencing these traits, a cross was made between BP2 and BALB/c mice, and a genome-wide screen carried out in the F2progeny of the F1intercross. Five potentially linked loci were identified, four of which corresponded to human regions of syntenic homology that previously have shown linkage to asthma-associated traits.

Airway Resistance↗

PubMed2004

Identification of a novel polymorphism involving a CGG repeat in the PTCH gene and a genome-wide screening of CGG-containing genes.

Mutations in the human homologue of the Drosophila patched gene (PTCH) are responsible for the hereditary disorder called nevoid basal cell carcinoma syndrome (NBCCS). PTCH has a CGG triplet repeat located 4 bp upstream of the first methionine codon. Here we report a novel polymorphism involving the number of the CGG-repeat. The major allele (86.3%) contained a repeat size of seven, whereas the minor allele contained eight. No significant difference in the distributions of genotypes was observed between normal and NBCCS individuals. However, when the repeat was inserted between a heterologous promoter and the luciferase gene, the longer repeats tended to induce higher luciferase activities, suggesting that the repeat length potentially affects the levels of gene expression. A genome-wide screening revealed that 68 and 146 genes contained a CGG/CCG repeat in the coding region and in the 5'-untranslated region (5'-UTR), respectively. None of the genes had this repeat in 3'-UTR. Interestingly, the number of genes with a CGG repeat in the 5'-UTR was significantly higher than that with a CCG repeat in the 5'-UTR. The localization of a CGG/CCG repeat in PTCH is quite unique in that only four other genes have been found in which the repeat is localized up to 4 bp upstream of the first methionine.

Alleles↗

PubMed2005

Genome-wide screen for prostate cancer susceptibility genes in men with clinically significant disease.

BACKGROUND: One of the difficulties confronting genetic studies of prostate cancer is the complex and heterogeneous etiology. Given the high population frequency of lesions meeting the histological definition of prostate cancer, a significant portion of men with a positive family history may be diagnosed due to increased surveillance and associated higher likelihood of biopsy. Over diagnosis decreases power to detect genes that increase susceptibility to a clinically significant prostate cancer. METHODS: We re-evaluated all 623 men with prostate cancer in our 188 hereditary prostate cancer families and identified a subset of 244 men with more aggressive disease based upon meeting at least one of the following clinical and/or pathologic criteria: tumor grade Gleason score > or = 7, tumor stage T2c or higher, pretreatment PSA > or = 20 ng/ml, rising PSA after treatment, evidence of metastasis, or death from prostate cancer. RESULTS: Genome-wide screens were re-performed by defining men as affected only if they met the criteria for clinically significant disease. The new analyses identified stronger evidence for linkage in Xq27-28 and 22q, as well as several novel loci, including 3p and 9p. CONCLUSIONS: Although, these results need to be confirmed in independent studies, our approach represents an important step to overcome the impact of over diagnosis in genetic studies of prostate cancer. Larger studies that incorporate this approach are needed.

Family Health↗

PubMed1997

Expression cloning of different bacterial phosphatase-encoding genes by histochemical screening of genomic libraries onto an indicator medium containing phenolphthalein diphosphate and methyl green.

A system for expression cloning of bacterial phosphatase-encoding genes has been developed, and its potential has been investigated. The system is based on histochemical screening of bacterial genomic libraries, constructed in an Escherichia coli multicopy plasmid vector, for phosphatase-producing clones using an indicator medium (named TPMG) made of Tryptose-Phosphate agar supplemented with the phosphatase substrate phenolphthalein diphosphate and the stain methyl green. To test the performance of this system, three genomic libraries were constructed from bacterial strains of different species which showed different patterns of phosphatase activity, and were screened using the TPMG medium. Following a partial screening, three different phosphatase-encoding genes (respectively encoding a class A non-specific acid phosphatase, an acid-hexose phosphatase and a non-specific alkaline phosphatase) were shotgun-cloned from the above libraries, indicating that the TPMG-based expression cloning system can be useful for rapid isolation of different bacterial phosphatase-encoding genes.

Acid Phosphatase↗