Mapping genomic loci implicates genes and synaptic biology in schizophrenia
Schizophrenia has a heritability of 60–80% 1 , much of which is attributable to common risk alleles. Here, in a two-stage genome-wide association study of up to 76,755 individuals with schizophrenia and 243,649 control individuals, we report common variant associations at 287 distinct genomic loci....
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| Veröffentlicht in: | Nature (London) Jg. 604; H. 7906; S. 502 - 508 |
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| Format: | Journal Article |
| Sprache: | Englisch |
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London
Nature Publishing Group UK
21.04.2022
Nature Publishing Group |
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| ISSN: | 0028-0836, 1476-4687, 1476-4687 |
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| Abstract | Schizophrenia has a heritability of 60–80%
1
, much of which is attributable to common risk alleles. Here, in a two-stage genome-wide association study of up to 76,755 individuals with schizophrenia and 243,649 control individuals, we report common variant associations at 287 distinct genomic loci. Associations were concentrated in genes that are expressed in excitatory and inhibitory neurons of the central nervous system, but not in other tissues or cell types. Using fine-mapping and functional genomic data, we identify 120 genes (106 protein-coding) that are likely to underpin associations at some of these loci, including 16 genes with credible causal non-synonymous or untranslated region variation. We also implicate fundamental processes related to neuronal function, including synaptic organization, differentiation and transmission. Fine-mapped candidates were enriched for genes associated with rare disruptive coding variants in people with schizophrenia, including the glutamate receptor subunit
GRIN2A
and transcription factor
SP4
, and were also enriched for genes implicated by such variants in neurodevelopmental disorders. We identify biological processes relevant to schizophrenia pathophysiology; show convergence of common and rare variant associations in schizophrenia and neurodevelopmental disorders; and provide a resource of prioritized genes and variants to advance mechanistic studies.
A genome-wide association study including over 76,000 individuals with schizophrenia and over 243,000 control individuals identifies common variant associations at 287 genomic loci, and further fine-mapping analyses highlight the importance of genes involved in synaptic processes. |
|---|---|
| AbstractList | Schizophrenia has a heritability of 60–80%, much of which is attributable to common risk alleles. Here, in a 2-stage genome-wide association study of up to 76,755 people with schizophrenia and 243,649 controls, we report common variant associations at 287 distinct genomic loci. Associations were concentrated in genes expressed in CNS neurons, excitatory and inhibitory, but not other tissues or cell types. Using fine-mapping and functional genomic data, we identify 120 genes (106 protein-coding) as likely to underpin associations at some of these loci, including 16 genes with credible causal non-synonymous or UTR variation. We also implicate fundamental processes related to neuronal function, including synaptic organisation, differentiation, and transmission. Fine-mapped candidates were enriched for genes associated with rare disruptive coding variants in people with schizophrenia, including the glutamate receptor subunit GRIN2A and transcription factor SP4, and were also enriched for genes implicated by such variants in neurodevelopmental disorders. We identify biological processes relevant to schizophrenia pathophysiology, show convergence of common and rare variant associations in schizophrenia and neurodevelopmental disorders, and provide a rich resource of prioritised genes and variants to advance mechanistic studies. Schizophrenia has a heritability of60-80%1, much of which is attributable to common risk alleles. Here, in a two-stage genome-wide association study of up to 76,755 individuals with schizophrenia and 243,649 control individuals, we report common variant associations at 287 distinct genomic loci. Associations were concentrated in genes that are expressed in excitatory and inhibitory neurons of the central nervous system, but not in other tissues or cell types. Using fine-mapping and functional genomic data, we identify 120 genes (106 protein-coding) that are likely to underpin associations at some of these loci, including 16 genes with credible causal non-synonymous or untranslated region variation. We also implicate fundamental processes related to neuronal function, including synaptic organization, differentiation and transmission. Fine-mapped candidates were enriched for genes associated with rare disruptive coding variants in people with schizophrenia, including the glutamate receptor subunit GRIN2A and transcription factor SP4, and were also enriched for genes implicated by such variants in neurodevelopmental disorders. We identify biological processes relevant to schizophrenia pathophysiology; show convergence of common and rare variant associations in schizophrenia and neurodevelopmental disorders; and provide a resource of prioritized genes and variants to advance mechanistic studies. Schizophrenia has a heritability of 60-80%1, much of which is attributable to common risk alleles. Here, in a two-stage genome-wide association study of up to 76,755 individuals with schizophrenia and 243,649 control individuals, we report common variant associations at 287 distinct genomic loci. Associations were concentrated in genes that are expressed in excitatory and inhibitory neurons of the central nervous system, but not in other tissues or cell types. Using fine-mapping and functional genomic data, we identify 120 genes (106 protein-coding) that are likely to underpin associations at some of these loci, including 16 genes with credible causal non-synonymous or untranslated region variation. We also implicate fundamental processes related to neuronal function, including synaptic organization, differentiation and transmission. Fine-mapped candidates were enriched for genes associated with rare disruptive coding variants in people with schizophrenia, including the glutamate receptor subunit GRIN2A and transcription factor SP4, and were also enriched for genes implicated by such variants in neurodevelopmental disorders. We identify biological processes relevant to schizophrenia pathophysiology; show convergence of common and rare variant associations in schizophrenia and neurodevelopmental disorders; and provide a resource of prioritized genes and variants to advance mechanistic studies.Schizophrenia has a heritability of 60-80%1, much of which is attributable to common risk alleles. Here, in a two-stage genome-wide association study of up to 76,755 individuals with schizophrenia and 243,649 control individuals, we report common variant associations at 287 distinct genomic loci. Associations were concentrated in genes that are expressed in excitatory and inhibitory neurons of the central nervous system, but not in other tissues or cell types. Using fine-mapping and functional genomic data, we identify 120 genes (106 protein-coding) that are likely to underpin associations at some of these loci, including 16 genes with credible causal non-synonymous or untranslated region variation. We also implicate fundamental processes related to neuronal function, including synaptic organization, differentiation and transmission. Fine-mapped candidates were enriched for genes associated with rare disruptive coding variants in people with schizophrenia, including the glutamate receptor subunit GRIN2A and transcription factor SP4, and were also enriched for genes implicated by such variants in neurodevelopmental disorders. We identify biological processes relevant to schizophrenia pathophysiology; show convergence of common and rare variant associations in schizophrenia and neurodevelopmental disorders; and provide a resource of prioritized genes and variants to advance mechanistic studies. Schizophrenia has a heritability of 60-80% , much of which is attributable to common risk alleles. Here, in a two-stage genome-wide association study of up to 76,755 individuals with schizophrenia and 243,649 control individuals, we report common variant associations at 287 distinct genomic loci. Associations were concentrated in genes that are expressed in excitatory and inhibitory neurons of the central nervous system, but not in other tissues or cell types. Using fine-mapping and functional genomic data, we identify 120 genes (106 protein-coding) that are likely to underpin associations at some of these loci, including 16 genes with credible causal non-synonymous or untranslated region variation. We also implicate fundamental processes related to neuronal function, including synaptic organization, differentiation and transmission. Fine-mapped candidates were enriched for genes associated with rare disruptive coding variants in people with schizophrenia, including the glutamate receptor subunit GRIN2A and transcription factor SP4, and were also enriched for genes implicated by such variants in neurodevelopmental disorders. We identify biological processes relevant to schizophrenia pathophysiology; show convergence of common and rare variant associations in schizophrenia and neurodevelopmental disorders; and provide a resource of prioritized genes and variants to advance mechanistic studies. Schizophrenia has a heritability of 60-80% 1 , much of which is attributable to common risk alleles. Here, in a two-stage genome-wide association study of up to 76,755 individuals with schizophrenia and 243,649 control individuals, we report common variant associations at 287 distinct genomic loci. Associations were concentrated in genes that are expressed in excitatory and inhibitory neurons of the central nervous system, but not in other tissues or cell types. Using fine-mapping and functional genomic data, we identify 120 genes (106 protein-coding) that are likely to underpin associations at some of these loci, including 16 genes with credible causal non-synonymous or untranslated region variation. We also implicate fundamental processes related to neuronal function, including synaptic organization, differentiation and transmission. Fine-mapped candidates were enriched for genes associated with rare disruptive coding variants in people with schizophrenia, including the glutamate receptor subunit GRIN2A and transcription factor SP4, and were also enriched for genes implicated by such variants in neurodevelopmental disorders. We identify biological processes relevant to schizophrenia pathophysiology; show convergence of common and rare variant associations in schizophrenia and neurodevelopmental disorders; and provide a resource of prioritized genes and variants to advance mechanistic studies. Schizophrenia has a heritability of 60–80% 1 , much of which is attributable to common risk alleles. Here, in a two-stage genome-wide association study of up to 76,755 individuals with schizophrenia and 243,649 control individuals, we report common variant associations at 287 distinct genomic loci. Associations were concentrated in genes that are expressed in excitatory and inhibitory neurons of the central nervous system, but not in other tissues or cell types. Using fine-mapping and functional genomic data, we identify 120 genes (106 protein-coding) that are likely to underpin associations at some of these loci, including 16 genes with credible causal non-synonymous or untranslated region variation. We also implicate fundamental processes related to neuronal function, including synaptic organization, differentiation and transmission. Fine-mapped candidates were enriched for genes associated with rare disruptive coding variants in people with schizophrenia, including the glutamate receptor subunit GRIN2A and transcription factor SP4 , and were also enriched for genes implicated by such variants in neurodevelopmental disorders. We identify biological processes relevant to schizophrenia pathophysiology; show convergence of common and rare variant associations in schizophrenia and neurodevelopmental disorders; and provide a resource of prioritized genes and variants to advance mechanistic studies. A genome-wide association study including over 76,000 individuals with schizophrenia and over 243,000 control individuals identifies common variant associations at 287 genomic loci, and further fine-mapping analyses highlight the importance of genes involved in synaptic processes. |
| Author | Marder, Stephen R. Cordeiro, Quirino Terao, Chikashi Sugar, Catherine A. Wray, Naomi R. Witt, Stephanie H. Petryshen, Tracey L. Bene, Judit Sim, Kang Scott, Rodney J. Jablensky, Assen V. Myin-Germeys, Inez Mallet, Jacques Castle, David Herms, Stefan Henskens, Frans A. Thibaut, Florence Moran, Jennifer L. Albus, Margot Gadelha, Ary Muntané, Gerard Mortensen, Preben B. Yue, Weihua Waddington, John Buxbaum, Joseph D. Alizadeh, Behrooz Z. McGrath, John J. Ge, Tian Kučinskiene, Zita Ausrele Baune, Bernhard T. Davidson, Michael Kučinskas, Vaidutis Williams, Nigel M. Szatkiewicz, Jin P. Giusti-Rodríguez, Paola Zimprich, Fritz Gejman, Pablo V. Landi, Stefano Kennedy, James L. Gratten, Jacob Black, Donald W. Hakonarson, Hakon Joa, Inge Stahl, Eli A. Svrakic, Dragan M. Swerdlow, Neal R. Turetsky, Bruce I. Pato, Michele T. Gur, Ruben C. Steen, Nils Eiel Bonassi, Stefano Arango, Celso Lubinski, Jan Freedman, Robert Li, Miaoxin Kim, Sung-Wan DeLisi, Lynn E. Rapaport, Mark H. McCarroll, Steven A. Roffman, Joshua L. Porteous, David Werge, Thomas Bromet, Evelyn |
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| ContentType | Journal Article |
| Contributor | Ashley-Koch, Allison Gandal, Mike Arsianti, Tiana Polioudakis, Damon Purcell, Shaun Henuhili, Supiyani Diatri, H Pochareddy, Sirisha Li, Mingfeng Amir, Nurmiati Fromer, Menachem Won, Hyejung Nasrun, Martina W Warrell, Jonathan Reddy, Tim Kusumaningrum, Profitasari Siste, Kristiana Tobing, Heriani Grennan, Kay Hoffman, Gabriel Breen, Michael Brown, Miguel Sanders, Stephan Weng, Zhiping Lay, Fides Semen, G Irmansyah, Irmansyah Abyzov, Alexej Jiang, Shan Navarro, Fabio Szekely, Anna Sethi, Anurag Khalimah, Siti Akbarian, Schahram Djatmiko, Prianto Galeev, Timur van Bakel, Harm Wang, Daifeng Wulandari, D Wiguna, Tjhin Antoni, Ronald Mattei, Eugenio Wiseman, Jennifer Pratt, Henry Giase, Gina Pan, Xinghua Liu, Chunyu Rhie, Suhn Marini, T M Asmarahadi, Asmarahadi Hyde, Thomas Liu, Shuang Goes, Fernando Witt, Heather Peters, Mette A Safyuni, N S Prasetyawan, Prasetyawan Guerra, Brittney Evalina, None Dracheva, Stella Carlyle, Becky Bryois, Julien Reza, Muhammad Shieh, Annie Kusumadewi, Irmia Ismoyo, Joni H Rozowsky, Joel Gursoy, Gamze Emani, Prashant Gerstein, |
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| Copyright | The Author(s), under exclusive licence to Springer Nature Limited 2022 2022. The Author(s), under exclusive licence to Springer Nature Limited. Copyright Nature Publishing Group Apr 21, 2022 licence_http://creativecommons.org/publicdomain/zero |
| Copyright_xml | – notice: The Author(s), under exclusive licence to Springer Nature Limited 2022 – notice: 2022. The Author(s), under exclusive licence to Springer Nature Limited. – notice: Copyright Nature Publishing Group Apr 21, 2022 – notice: licence_http://creativecommons.org/publicdomain/zero |
| CorporateAuthor | The SynGO Consortium PsychENCODE Indonesia Schizophrenia Consortium Schizophrenia Working Group of the Psychiatric Genomics Consortium Psychosis Endophenotypes International Consortium SynGO Consortium |
| CorporateAuthor_xml | – name: Indonesia Schizophrenia Consortium – name: Psychosis Endophenotypes International Consortium – name: PsychENCODE – name: The SynGO Consortium – name: Schizophrenia Working Group of the Psychiatric Genomics Consortium – name: SynGO Consortium |
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| DOI | 10.1038/s41586-022-04434-5 |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 GWAS meta-analyses (SA, GP, SR, VT); Replication data (SMag, HS, KSt [deCODE]); African-American and Latino sample analyses (EGA, TB, GG, SR, VT); Bioinformatics (JBr, JCH, AFP, AJP, DPos, PFS, KW, SynGO consortium); Comparison of males and females (SR, JSi, VT, PMV); Heritability and Polygenic Prediction (OAA, OF, TG, HHu, BMN, MOD, AFP, ALR, SR, VT, JTRW, NRW, JZ); Phenotype stratification (CAD, EVa); Cellular and Tissue analysis (JBr, MOD, DPos, PFS, JTRW, KW); Gene Ontology (JCH, MOD, AFP, AJP, DPos, JTRW, KW); Fine-mapping (CB, MJD, HHu, MLa, MOD, GP, AFP, MP, SR, JTRW); SMR (LSH, MOD, TQ, NRW, YW, JY); Hi-C (DPos, ALR, PFS, JTRW, KW); Other TWAS (MJG, LSH, MKi, PR, GV, WZha); Integration of fine-mapping, gene expression, Hi-C informatics, rare variants (LSH, MOD, AFP, TQ, ALR, PFS, JTRW, NRW, YW, JY); SynGO (FK, MOD, AFP, ABS, MV, JTRW); Additional statistical advice (PAH). The remaining authors contributed to the recruitment, phenotyping, genotyping, or data processing for the contributing components of the meta-analysis, or provided other forms of functional annotation data. Primary drafting and editing of the manuscript was coordinated by SR, JTRW, and MOD. The primary draft sections were written by JBr, CYC, CAD, LSH, HHu, BMN, MOD, MJO, AFP, AJP, SR, ABS, PFS, VT, EVa, MV, JTRW, NRW, JY. Additional edits were from OAA, MJD, KSK. Numerous other authors provided edits, comments and suggestions, and all authors saw and approved the contents of the manuscript. The Chair of the Psychiatric Genomics Consortium is PFS and the Schizophrenia Working Group of the PGC is led MOD and JTRW. AUTHOR CONTRIBUTIONS The management group for this paper was led by MOD and JTRW with SR responsible for primary analytic matters supported by BMN and MJD. The management group was comprised of a subset of the PIs of the component studies, bioinformaticians, and analysts and were responsible for study design, conduct, management, primary and final interpretation and included OAA, BTB, SIB, ADB, DB, EB, SC, ACor, DCu, MJD, MDF, ED, HE, AHF, PVG, MGi, SJG, KSH, HHu, NI, RSK, KSK, JAK, JLe, TL, DFL, JLi, AMcI, AMcQ, VAM, DWM, BJM, BMN, MOD, RAO, MJO, AP, DPos, SQ, BPR, SR, DR, SGS, ASe, YS, EAS, PFS, MTT, MPV, JTRW, DRW, TW, NRW, XY, WY. These authors jointly supervised this work: Stephan Ripke, James T. R. Walters, Michael C. O‘Donovan Deceased: Robert W. McCarley |
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| Snippet | Schizophrenia has a heritability of 60–80%
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, much of which is attributable to common risk alleles. Here, in a two-stage genome-wide association study of up... Schizophrenia has a heritability of 60-80% , much of which is attributable to common risk alleles. Here, in a two-stage genome-wide association study of up to... Schizophrenia has a heritability of60-80%1, much of which is attributable to common risk alleles. Here, in a two-stage genome-wide association study of up to... Schizophrenia has a heritability of 60-80%1, much of which is attributable to common risk alleles. Here, in a two-stage genome-wide association study of up to... Schizophrenia has a heritability of 60–80%, much of which is attributable to common risk alleles. Here, in a 2-stage genome-wide association study of up to... Schizophrenia has a heritability of 60-80% 1 , much of which is attributable to common risk alleles. Here, in a two-stage genome-wide association study of up... |
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| Title | Mapping genomic loci implicates genes and synaptic biology in schizophrenia |
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