Bayesian Test for Colocalisation between Pairs of Genetic Association Studies Using Summary Statistics

Genetic association studies, in particular the genome-wide association study (GWAS) design, have provided a wealth of novel insights into the aetiology of a wide range of human diseases and traits, in particular cardiovascular diseases and lipid biomarkers. The next challenge consists of understandi...

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Veröffentlicht in:	PLoS genetics Jg. 10; H. 5; S. e1004383
Hauptverfasser:	Giambartolomei, Claudia, Vukcevic, Damjan, Schadt, Eric E., Franke, Lude, Hingorani, Aroon D., Wallace, Chris, Plagnol, Vincent
Format:	Journal Article
Sprache:	Englisch
Veröffentlicht:	United States Public Library of Science 01.05.2014 Public Library of Science (PLoS)
Schlagworte:	Bayes Theorem Bayesian statistical decision theory Biology and Life Sciences Biomarkers Biomedical research Computer and Information Sciences Disease Gene expression Gene loci Genome-wide association studies Genome-Wide Association Study Genomes Humans Lipids Medical research Medicine and Health Sciences Meta-analysis Methods Probability Sample Size Statistical analysis Statistical methods Statistics Studies
ISSN:	1553-7404, 1553-7390, 1553-7404
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Abstract	Genetic association studies, in particular the genome-wide association study (GWAS) design, have provided a wealth of novel insights into the aetiology of a wide range of human diseases and traits, in particular cardiovascular diseases and lipid biomarkers. The next challenge consists of understanding the molecular basis of these associations. The integration of multiple association datasets, including gene expression datasets, can contribute to this goal. We have developed a novel statistical methodology to assess whether two association signals are consistent with a shared causal variant. An application is the integration of disease scans with expression quantitative trait locus (eQTL) studies, but any pair of GWAS datasets can be integrated in this framework. We demonstrate the value of the approach by re-analysing a gene expression dataset in 966 liver samples with a published meta-analysis of lipid traits including >100,000 individuals of European ancestry. Combining all lipid biomarkers, our re-analysis supported 26 out of 38 reported colocalisation results with eQTLs and identified 14 new colocalisation results, hence highlighting the value of a formal statistical test. In three cases of reported eQTL-lipid pairs (SYPL2, IFT172, TBKBP1) for which our analysis suggests that the eQTL pattern is not consistent with the lipid association, we identify alternative colocalisation results with SORT1, GCKR, and KPNB1, indicating that these genes are more likely to be causal in these genomic intervals. A key feature of the method is the ability to derive the output statistics from single SNP summary statistics, hence making it possible to perform systematic meta-analysis type comparisons across multiple GWAS datasets (implemented online at http://coloc.cs.ucl.ac.uk/coloc/). Our methodology provides information about candidate causal genes in associated intervals and has direct implications for the understanding of complex diseases as well as the design of drugs to target disease pathways.
AbstractList	Genetic association studies, in particular the genome-wide association study (GWAS) design, have provided a wealth of novel insights into the aetiology of a wide range of human diseases and traits, in particular cardiovascular diseases and lipid biomarkers. The next challenge consists of understanding the molecular basis of these associations. The integration of multiple association datasets, including gene expression datasets, can contribute to this goal. We have developed a novel statistical methodology to assess whether two association signals are consistent with a shared causal variant. An application is the integration of disease scans with expression quantitative trait locus (eQTL) studies, but any pair of GWAS datasets can be integrated in this framework. We demonstrate the value of the approach by re-analysing a gene expression dataset in 966 liver samples with a published meta-analysis of lipid traits including >100,000 individuals of European ancestry. Combining all lipid biomarkers, our re-analysis supported 26 out of 38 reported colocalisation results with eQTLs and identified 14 new colocalisation results, hence highlighting the value of a formal statistical test. In three cases of reported eQTL-lipid pairs (SYPL2, IFT172, TBKBP1) for which our analysis suggests that the eQTL pattern is not consistent with the lipid association, we identify alternative colocalisation results with SORT1, GCKR, and KPNB1, indicating that these genes are more likely to be causal in these genomic intervals. A key feature of the method is the ability to derive the output statistics from single SNP summary statistics, hence making it possible to perform systematic meta-analysis type comparisons across multiple GWAS datasets (implemented online at http://coloc.cs.ucl.ac.uk/coloc/). Our methodology provides information about candidate causal genes in associated intervals and has direct implications for the understanding of complex diseases as well as the design of drugs to target disease pathways. Genetic association studies, in particular the genome-wide association study (GWAS) design, have provided a wealth of novel insights into the aetiology of a wide range of human diseases and traits, in particular cardiovascular diseases and lipid biomarkers. The next challenge consists of understanding the molecular basis of these associations. The integration of multiple association datasets, including gene expression datasets, can contribute to this goal. We have developed a novel statistical methodology to assess whether two association signals are consistent with a shared causal variant. An application is the integration of disease scans with expression quantitative trait locus (eQTL) studies, but any pair of GWAS datasets can be integrated in this framework. We demonstrate the value of the approach by re-analysing a gene expression dataset in 966 liver samples with a published meta-analysis of lipid traits including >100,000 individuals of European ancestry. Combining all lipid biomarkers, our re-analysis supported 26 out of 38 reported colocalisation results with eQTLs and identified 14 new colocalisation results, hence highlighting the value of a formal statistical test. In three cases of reported eQTL-lipid pairs (SYPL2, IFT172, TBKBP1) for which our analysis suggests that the eQTL pattern is not consistent with the lipid association, we identify alternative colocalisation results with SORT1, GCKR, and KPNB1, indicating that these genes are more likely to be causal in these genomic intervals. A key feature of the method is the ability to derive the output statistics from single SNP summary statistics, hence making it possible to perform systematic meta-analysis type comparisons across multiple GWAS datasets (implemented online at http://coloc.cs.ucl.ac.uk/coloc/). Our methodology provides information about candidate causal genes in associated intervals and has direct implications for the understanding of complex diseases as well as the design of drugs to target disease pathways. Genetic association studies, in particular the genome-wide association study (GWAS) design, have provided a wealth of novel insights into the aetiology of a wide range of human diseases and traits, in particular cardiovascular diseases and lipid biomarkers. The next challenge consists of understanding the molecular basis of these associations. The integration of multiple association datasets, including gene expression datasets, can contribute to this goal. We have developed a novel statistical methodology to assess whether two association signals are consistent with a shared causal variant. An application is the integration of disease scans with expression quantitative trait locus (eQTL) studies, but any pair of GWAS datasets can be integrated in this framework. We demonstrate the value of the approach by re- analysing a gene expression dataset in 966 liver samples with a published meta-analysis of lipid traits including >100,000 individuals of European ancestry. Combining all lipid biomarkers, our re-analysis supported 26 out of 38 reported colocalisation results with eQTLs and identified 14 new colocalisation results, hence highlighting the value of a formal statistical test. In three cases of reported eQTL-lipid pairs (SYPL2, IFT172, TBKBP1) for which our analysis suggests that the eQTL pattern is not consistent with the lipid association, we identify alternative colocalisation results with SORT1, GCKR, and KPNB1, indicating that these genes are more likely to be causal in these genomic intervals. A key feature of the method is the ability to derive the output statistics from single SNP summary statistics, hence making it possible to perform systematic meta-analysis type comparisons across multiple GWAS datasets (implemented online at Genetic association studies, in particular the genome-wide association study (GWAS) design, have provided a wealth of novel insights into the aetiology of a wide range of human diseases and traits, in particular cardiovascular diseases and lipid biomarkers. The next challenge consists of understanding the molecular basis of these associations. The integration of multiple association datasets, including gene expression datasets, can contribute to this goal. We have developed a novel statistical methodology to assess whether two association signals are consistent with a shared causal variant. An application is the integration of disease scans with expression quantitative trait locus (eQTL) studies, but any pair of GWAS datasets can be integrated in this framework. We demonstrate the value of the approach by re-analysing a gene expression dataset in 966 liver samples with a published meta-analysis of lipid traits including >100,000 individuals of European ancestry. Combining all lipid biomarkers, our re-analysis supported 26 out of 38 reported colocalisation results with eQTLs and identified 14 new colocalisation results, hence highlighting the value of a formal statistical test. In three cases of reported eQTL-lipid pairs (SYPL2, IFT172, TBKBP1) for which our analysis suggests that the eQTL pattern is not consistent with the lipid association, we identify alternative colocalisation results with SORT1, GCKR, and KPNB1, indicating that these genes are more likely to be causal in these genomic intervals. A key feature of the method is the ability to derive the output statistics from single SNP summary statistics, hence making it possible to perform systematic meta-analysis type comparisons across multiple GWAS datasets (implemented online at http://coloc.cs.ucl.ac.uk/coloc/). Our methodology provides information about candidate causal genes in associated intervals and has direct implications for the understanding of complex diseases as well as the design of drugs to target disease pathways. Genome-wide association studies (GWAS) have found a large number of genetic regions (“loci”) affecting clinical end-points and phenotypes, many outside coding intervals. One approach to understanding the biological basis of these associations has been to explore whether GWAS signals from intermediate cellular phenotypes, in particular gene expression, are located in the same loci (“colocalise”) and are potentially mediating the disease signals. However, it is not clear how to assess whether the same variants are responsible for the two GWAS signals or whether it is distinct causal variants close to each other. In this paper, we describe a statistical method that can use simply single variant summary statistics to test for colocalisation of GWAS signals. We describe one application of our method to a meta-analysis of blood lipids and liver expression, although any two datasets resulting from association studies can be used. Our method is able to detect the subset of GWAS signals explained by regulatory effects and identify candidate genes affected by the same GWAS variants. As summary GWAS data are increasingly available, applications of colocalisation methods to integrate the findings will be essential for functional follow-up, and will also be particularly useful to identify tissue specific signals in eQTL datasets. Genetic association studies, in particular the genome-wide association study (GWAS) design, have provided a wealth of novel insights into the aetiology of a wide range of human diseases and traits, in particular cardiovascular diseases and lipid biomarkers. The next challenge consists of understanding the molecular basis of these associations. The integration of multiple association datasets, including gene expression datasets, can contribute to this goal. We have developed a novel statistical methodology to assess whether two association signals are consistent with a shared causal variant. An application is the integration of disease scans with expression quantitative trait locus (eQTL) studies, but any pair of GWAS datasets can be integrated in this framework. We demonstrate the value of the approach by re-analysing a gene expression dataset in 966 liver samples with a published meta-analysis of lipid traits including >100,000 individuals of European ancestry. Combining all lipid biomarkers, our re-analysis supported 26 out of 38 reported colocalisation results with eQTLs and identified 14 new colocalisation results, hence highlighting the value of a formal statistical test. In three cases of reported eQTL-lipid pairs (SYPL2, IFT172, TBKBP1) for which our analysis suggests that the eQTL pattern is not consistent with the lipid association, we identify alternative colocalisation results with SORT1, GCKR, and KPNB1, indicating that these genes are more likely to be causal in these genomic intervals. A key feature of the method is the ability to derive the output statistics from single SNP summary statistics, hence making it possible to perform systematic meta-analysis type comparisons across multiple GWAS datasets (implemented online at http://coloc.cs.ucl.ac.uk/coloc/). Our methodology provides information about candidate causal genes in associated intervals and has direct implications for the understanding of complex diseases as well as the design of drugs to target disease pathways.Genetic association studies, in particular the genome-wide association study (GWAS) design, have provided a wealth of novel insights into the aetiology of a wide range of human diseases and traits, in particular cardiovascular diseases and lipid biomarkers. The next challenge consists of understanding the molecular basis of these associations. The integration of multiple association datasets, including gene expression datasets, can contribute to this goal. We have developed a novel statistical methodology to assess whether two association signals are consistent with a shared causal variant. An application is the integration of disease scans with expression quantitative trait locus (eQTL) studies, but any pair of GWAS datasets can be integrated in this framework. We demonstrate the value of the approach by re-analysing a gene expression dataset in 966 liver samples with a published meta-analysis of lipid traits including >100,000 individuals of European ancestry. Combining all lipid biomarkers, our re-analysis supported 26 out of 38 reported colocalisation results with eQTLs and identified 14 new colocalisation results, hence highlighting the value of a formal statistical test. In three cases of reported eQTL-lipid pairs (SYPL2, IFT172, TBKBP1) for which our analysis suggests that the eQTL pattern is not consistent with the lipid association, we identify alternative colocalisation results with SORT1, GCKR, and KPNB1, indicating that these genes are more likely to be causal in these genomic intervals. A key feature of the method is the ability to derive the output statistics from single SNP summary statistics, hence making it possible to perform systematic meta-analysis type comparisons across multiple GWAS datasets (implemented online at http://coloc.cs.ucl.ac.uk/coloc/). Our methodology provides information about candidate causal genes in associated intervals and has direct implications for the understanding of complex diseases as well as the design of drugs to target disease pathways.
Audience	Academic
Author	Vukcevic, Damjan Schadt, Eric E. Franke, Lude Hingorani, Aroon D. Giambartolomei, Claudia Wallace, Chris Plagnol, Vincent
AuthorAffiliation	4 Department of Genetics, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands 5 Institute of Cardiovascular Science, University College London, London, United Kingdom 6 JDRF/Wellcome Trust Diabetes and Inflammation Laboratory, Cambridge, Institute for Medical Research, Department of Medical Genetics, NIHR, Cambridge Biomedical Research Centre, University of Cambridge, Addenbrooke's Hospital, Cambridge, United Kingdom 1 UCL Genetics Institute, University College London (UCL), London, United Kingdom 2 Murdoch Childrens Research Institute, Royal Children's Hospital, Melbourne, Australia 3 Department of Genetics and Genomics Sciences, Mount Sinai School of Medicine, New York, New York, United States of America Dartmouth College, United States of America
AuthorAffiliation_xml	– name: 6 JDRF/Wellcome Trust Diabetes and Inflammation Laboratory, Cambridge, Institute for Medical Research, Department of Medical Genetics, NIHR, Cambridge Biomedical Research Centre, University of Cambridge, Addenbrooke's Hospital, Cambridge, United Kingdom – name: 4 Department of Genetics, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands – name: 3 Department of Genetics and Genomics Sciences, Mount Sinai School of Medicine, New York, New York, United States of America – name: 5 Institute of Cardiovascular Science, University College London, London, United Kingdom – name: 2 Murdoch Childrens Research Institute, Royal Children's Hospital, Melbourne, Australia – name: 1 UCL Genetics Institute, University College London (UCL), London, United Kingdom – name: Dartmouth College, United States of America
Author_xml	– sequence: 1 givenname: Claudia surname: Giambartolomei fullname: Giambartolomei, Claudia – sequence: 2 givenname: Damjan surname: Vukcevic fullname: Vukcevic, Damjan – sequence: 3 givenname: Eric E. surname: Schadt fullname: Schadt, Eric E. – sequence: 4 givenname: Lude surname: Franke fullname: Franke, Lude – sequence: 5 givenname: Aroon D. surname: Hingorani fullname: Hingorani, Aroon D. – sequence: 6 givenname: Chris surname: Wallace fullname: Wallace, Chris – sequence: 7 givenname: Vincent surname: Plagnol fullname: Plagnol, Vincent
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/24830394$$D View this record in MEDLINE/PubMed
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Notes	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Conceived and designed the experiments: CG DV CW VP LF. Performed the experiments: CG CW VP. Analyzed the data: CG CW. Contributed reagents/materials/analysis tools: EES LF ADH. Wrote the paper: CG CW DV VP ADH. The authors have declared that no competing interests exist.
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Snippet	Genetic association studies, in particular the genome-wide association study (GWAS) design, have provided a wealth of novel insights into the aetiology of a... Genetic association studies, in particular the genome-wide association study (GWAS) design, have provided a wealth of novel insights into the aetiology of a...
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StartPage	e1004383
SubjectTerms	Bayes Theorem Bayesian statistical decision theory Biology and Life Sciences Biomarkers Biomedical research Computer and Information Sciences Disease Gene expression Gene loci Genome-wide association studies Genome-Wide Association Study Genomes Humans Lipids Medical research Medicine and Health Sciences Meta-analysis Methods Probability Sample Size Statistical analysis Statistical methods Statistics Studies
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Title	Bayesian Test for Colocalisation between Pairs of Genetic Association Studies Using Summary Statistics
URI	https://www.ncbi.nlm.nih.gov/pubmed/24830394 https://www.proquest.com/docview/1525771594 https://pubmed.ncbi.nlm.nih.gov/PMC4022491 https://doaj.org/article/8ad130264f4e4f78ab943d9f044089cd http://dx.doi.org/10.1371/journal.pgen.1004383
Volume	10
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