Synaptic, transcriptional and chromatin genes disrupted in autism
The genetic architecture of autism spectrum disorder involves the interplay of common and rare variants and their impact on hundreds of genes. Using exome sequencing, here we show that analysis of rare coding variation in 3,871 autism cases and 9,937 ancestry-matched or parental controls implicates...
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| Published in | Nature (London) Vol. 515; no. 7526; pp. 209 - 215 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
London
Nature Publishing Group UK
13.11.2014
Nature Publishing Group |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0028-0836 1476-4687 1476-4687 |
| DOI | 10.1038/nature13772 |
Cover
| Abstract | The genetic architecture of autism spectrum disorder involves the interplay of common and rare variants and their impact on hundreds of genes. Using exome sequencing, here we show that analysis of rare coding variation in 3,871 autism cases and 9,937 ancestry-matched or parental controls implicates 22 autosomal genes at a false discovery rate (FDR) < 0.05, plus a set of 107 autosomal genes strongly enriched for those likely to affect risk (FDR < 0.30). These 107 genes, which show unusual evolutionary constraint against mutations, incur
de novo
loss-of-function mutations in over 5% of autistic subjects. Many of the genes implicated encode proteins for synaptic formation, transcriptional regulation and chromatin-remodelling pathways. These include voltage-gated ion channels regulating the propagation of action potentials, pacemaking and excitability–transcription coupling, as well as histone-modifying enzymes and chromatin remodellers—most prominently those that mediate post-translational lysine methylation/demethylation modifications of histones.
Whole-exome sequencing in a large autism study identifies over 100 autosomal genes that are likely to affect risk for the disorder; these genes, which show unusual evolutionary constraint against mutations, carry
de novo
loss-of-function mutations in over 5% of autistic subjects and many function in synaptic, transcriptional and chromatin-remodelling pathways.
Autism-linked genetic factors analysed
Autism spectrum disorder (ASD) is a broad group of brain development disorders, including autism, childhood disintegrative disorder and Asperger's syndrome, characterized by impaired social interaction and communication, repetitive behaviour and restricted interests. Two groups reporting in this issue of
Nature
have used large-scale whole-exome sequencing to examine the contribution of inherited and germline
de novo
mutations to ASD risk. Silvia De Rubeis
et al
. analysed DNA samples from 3,871 autism cases and 9,937 ancestry-matched or parental controls and identify more than 100 autosomal genes that are likely to affect risk for the disease.
De novo
loss-of-function mutations were detected in more than 5% of autistic subjects. Many of the associated gene products appear to function in synaptic, transcriptional, and chromatin remodelling pathways. Ivan Iossifov
et al
. sequenced exomes from more than 2,500 families, each with one child with ASD. They identify 27 high-confidence gene targets and estimate that 13% of
de novo
missense mutations and 43% of
de novo
'likely gene-disrupting' (LGD) mutations contribute to 12% and 9% of diagnoses, respectively. |
|---|---|
| AbstractList | The genetic architecture of autism spectrum disorder involves the interplay of common and rare variants and their impact on hundreds of genes. Using exome sequencing, here we show that analysis of rare coding variation in 3,871 autism cases and 9,937 ancestry-matched or parental controls implicates 22 autosomal genes at a false discovery rate (FDR) < 0.05, plus a set of 107 autosomal genes strongly enriched for those likely to affect risk (FDR < 0.30). These 107 genes, which show unusual evolutionary constraint against mutations, incur de novo loss-of-function mutations in over 5% of autistic subjects. Many of the genes implicated encode proteins for synaptic formation, transcriptional regulation and chromatin-remodelling pathways. These include voltage-gated ion channels regulating the propagation of action potentials, pacemaking and excitability-transcription coupling, as well as histone-modifying enzymes and chromatin remodellers-most prominently those that mediate post-translational lysine methylation/demethylation modifications of histones. The genetic architecture of autism spectrum disorder involves the interplay of common and rare variants and their impact on hundreds of genes. Using exome sequencing, here we show that analysis of rare coding variation in 3,871 autism cases and 9,937 ancestry-matched or parental controls implicates 22 autosomal genes at a false discovery rate (FDR) < 0.05, plus a set of 107 autosomal genes strongly enriched for those likely to affect risk (FDR < 0.30). These 107 genes, which show unusual evolutionary constraint against mutations, incur de novo loss-of-function mutations in over 5% of autistic subjects. Many of the genes implicated encode proteins for synaptic formation, transcriptional regulation and chromatin-remodelling pathways. These include voltage-gated ion channels regulating the propagation of action potentials, pacemaking and excitability–transcription coupling, as well as histone-modifying enzymes and chromatin remodellers—most prominently those that mediate post-translational lysine methylation/demethylation modifications of histones. Whole-exome sequencing in a large autism study identifies over 100 autosomal genes that are likely to affect risk for the disorder; these genes, which show unusual evolutionary constraint against mutations, carry de novo loss-of-function mutations in over 5% of autistic subjects and many function in synaptic, transcriptional and chromatin-remodelling pathways. Autism-linked genetic factors analysed Autism spectrum disorder (ASD) is a broad group of brain development disorders, including autism, childhood disintegrative disorder and Asperger's syndrome, characterized by impaired social interaction and communication, repetitive behaviour and restricted interests. Two groups reporting in this issue of Nature have used large-scale whole-exome sequencing to examine the contribution of inherited and germline de novo mutations to ASD risk. Silvia De Rubeis et al . analysed DNA samples from 3,871 autism cases and 9,937 ancestry-matched or parental controls and identify more than 100 autosomal genes that are likely to affect risk for the disease. De novo loss-of-function mutations were detected in more than 5% of autistic subjects. Many of the associated gene products appear to function in synaptic, transcriptional, and chromatin remodelling pathways. Ivan Iossifov et al . sequenced exomes from more than 2,500 families, each with one child with ASD. They identify 27 high-confidence gene targets and estimate that 13% of de novo missense mutations and 43% of de novo 'likely gene-disrupting' (LGD) mutations contribute to 12% and 9% of diagnoses, respectively. The genetic architecture of autism spectrum disorder involves the interplay of common and rare variants and their impact on hundreds of genes. Using exome sequencing, here we show that analysis of rare coding variation in 3,871 autism cases and 9,937 ancestry-matched or parental controls implicates 22 autosomal genes at a false discovery rate (FDR) < 0.05, plus a set of 107 autosomal genes strongly enriched for those likely to affect risk (FDR < 0.30). These 107 genes, which show unusual evolutionary constraint against mutations, incur de novo loss-of-function mutations in over 5% of autistic subjects. Many of the genes implicated encode proteins for synaptic formation, transcriptional regulation and chromatin-remodelling pathways. These include voltage-gated ion channels regulating the propagation of action potentials, pacemaking and excitability-transcription coupling, as well as histone-modifying enzymes and chromatin remodellers-most prominently those that mediate post-translational lysine methylation/demethylation modifications of histones.The genetic architecture of autism spectrum disorder involves the interplay of common and rare variants and their impact on hundreds of genes. Using exome sequencing, here we show that analysis of rare coding variation in 3,871 autism cases and 9,937 ancestry-matched or parental controls implicates 22 autosomal genes at a false discovery rate (FDR) < 0.05, plus a set of 107 autosomal genes strongly enriched for those likely to affect risk (FDR < 0.30). These 107 genes, which show unusual evolutionary constraint against mutations, incur de novo loss-of-function mutations in over 5% of autistic subjects. Many of the genes implicated encode proteins for synaptic formation, transcriptional regulation and chromatin-remodelling pathways. These include voltage-gated ion channels regulating the propagation of action potentials, pacemaking and excitability-transcription coupling, as well as histone-modifying enzymes and chromatin remodellers-most prominently those that mediate post-translational lysine methylation/demethylation modifications of histones. The genetic architecture of autism spectrum disorder involves the interplay of common and rare variants and their impact on hundreds of genes. Using exome sequencing, here we show that analysis of rare coding variation in 3,871 autism cases and 9,937 ancestry-matched or parental controls implicates 22 autosomal genes at a false discovery rate (FDR) < 0.05, plus a set of 107 autosomal genes strongly enriched for those likely to affect risk (FDR < 0.30). These 107 genes, which show unusual evolutionary constraint against mutations, incur de novo loss-of-function mutations in over 5% of autistic subjects. Many of the genes implicated encode proteins for synaptic formation, transcriptional regulation and chromatin-remodelling pathways. These include voltage-gated ion channels regulating the propagation of action potentials, pacemaking and excitability-transcription coupling, as well as histone-modifying enzymes and chromatin remodellers-most prominently those that mediate post-translational lysine methylation/demethylation modifications of histones. The genetic architecture of autism spectrum disorder involves the interplay of common and rare variation and their impact on hundreds of genes. Using exome sequencing, analysis of rare coding variation in 3,871 autism cases and 9,937 ancestry-matched or parental controls implicates 22 autosomal genes at a false discovery rate (FDR) < 0.05, and a set of 107 autosomal genes strongly enriched for those likely to affect risk (FDR < 0.30). These 107 genes, which show unusual evolutionary constraint against mutations, incur de novo loss-of-function mutations in over 5% of autistic subjects. Many of the genes implicated encode proteins for synaptic, transcriptional, and chromatin remodeling pathways. These include voltage-gated ion channels regulating propagation of action potentials, pacemaking, and excitability-transcription coupling, as well as histone-modifying enzymes and chromatin remodelers, prominently histone post-translational modifications involving lysine methylation/demethylation. |
| Audience | Academic |
| Author | Klauck, Sabine M. Guter, Stephen J. Wang, Li-San Schellenberg, Gerard D. Walsh, Christopher A. Liu, Li Tammimies, Kristiina Curran, Sarah R. Marshall, Christian R. Purcell, Shaun Crooks, Lucy Ercument Cicek, A. Yuen, Ryan K. C. Gallagher, Louise Jeremy Willsey, A. Reichenberg, Abraham Fromer, Menachem Lee, Irene Scherer, Stephen W. Ma’ayan, Avi He, Xin Rajagopalan, Deepthi Stevens, Christine Skuse, David Sanders, Stephan J. Parr, Jeremy R. Brownfeld, Jessica M. Barrett, Jeffrey C. Duketis, Eftichia Singh, Tarjinder State, Matthew W. Aleksic, Branko Dawson, Geraldine Samocha, Kaitlin Klei, Lambertus Geller, Evan Lei, Jing Valladares, Otto Fu, Shih-Chen Campbell, Nicholas G. Neale, Benjamin Voran, Annette Lehtimäki, Terho Kilpinen, Helena Sean Hill, R. Buxbaum, Joseph D. Goldberg, Arthur P. Sklar, Pamela Hultman, Christina M. Chahrour, Maria H. Yu, Timothy W. Coon, Hilary Lehner, Thomas Schulte-Rüther, Martin Cai, Jinlu McInnes, Alison L. Ozaki, Norio De Rubeis, Silvia Roeder, Kathryn Lin, Chiao-Feng Sabo, Aniko Walker, Susan Szatmari, Peter Cook, E |
| AuthorAffiliation | 10 Department of Psychiatry, Graduate School of Medicine, Nagoya University, Nagoya, Japan 17 Harvard Medical School, Boston, Massachusetts, USA 24 Department of Psychiatry, School of Medicine, Trinity College Dublin, Dublin, Ireland 33 Department of Clinical Chemistry, Fimlab Laboratories, Tampere, Finland SF-33100 49 National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland, USA 4 Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, New York, USA 43 Department of Psychiatry, University of California at San Francisco, San Francisco, California, USA 27 Department of Biostatistics, Columbia University, New York, New York, USA 3 Ray and Stephanie Lane Center for Computational Biology, Carnegie Mellon University, Pittsburgh, Pennsylvania, USA 1 Seaver Autism Center for Research and Treatment, Icahn School of Medicine at Mount Sinai, New York, New York, USA 54 McLaughlin Centre, University of Toronto, Toronto, Ontario M5S 1A1, C |
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University of Santiago de Compostela and Galician Foundation of Genomic Medicine (SERGAS). 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C. surname: Yuen fullname: Yuen, Ryan K. C. organization: Program in Genetics and Genome Biology, The Centre for Applied Genomics, The Hospital for Sick Children, Toronto, Ontario M5G 0A4, Canada – sequence: 77 givenname: Edwin H. surname: Cook fullname: Cook, Edwin H. organization: Department of Psychiatry, Institute for Juvenile Research, University of Illinois at Chicago – sequence: 78 givenname: Christine M. surname: Freitag fullname: Freitag, Christine M. organization: Department of Child and Adolescent Psychiatry, Psychosomatics and Psychotherapy, Goethe University Frankfurt, 60528 Frankfurt, Germany – sequence: 79 givenname: Michael surname: Gill fullname: Gill, Michael organization: Department of Psychiatry, School of Medicine, Trinity College Dublin, Dublin 8, Ireland – sequence: 80 givenname: Christina M. surname: Hultman fullname: Hultman, Christina M. organization: Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, SE-171 77 Stockholm, Sweden – sequence: 81 givenname: Thomas surname: Lehner fullname: Lehner, Thomas organization: National Institute of Mental Health, National Institutes of Health – sequence: 82 givenname: Aarno surname: Palotie fullname: Palotie, Aarno organization: Department of Medicine, Analytic and Translational Genetics Unit, Massachusetts General Hospital, Program in Medical and Population Genetics, Broad Institute of MIT and Harvard, Institute for Molecular Medicine Finland, University of Helsinki, FI-00014 Helsinki, Finland., Department of Psychiatry, Psychiatric & Neurodevelopmental Genetics Unit, Massachusetts General Hospital, Boston, Massachusetts 02114, USA – sequence: 83 givenname: Gerard D. surname: Schellenberg fullname: Schellenberg, Gerard D. organization: Department of Pathology and Laboratory Medicine, University of Pennsylvania Perelman School of Medicine – sequence: 84 givenname: Pamela surname: Sklar fullname: Sklar, Pamela organization: Department of Psychiatry, Icahn School of Medicine at Mount Sinai, Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, Department of Neuroscience, Icahn School of Medicine at Mount Sinai – sequence: 85 givenname: Matthew W. surname: State fullname: State, Matthew W. organization: Department of Psychiatry, University of California at San Francisco – sequence: 86 givenname: James S. surname: Sutcliffe fullname: Sutcliffe, James S. organization: Vanderbilt Brain Institute, Vanderbilt University School of Medicine, Department of Molecular Physiology and Biophysics and Psychiatry, Vanderbilt University School of Medicine – sequence: 87 givenname: Christopher A. surname: Walsh fullname: Walsh, Christopher A. organization: Harvard Medical School, Division of Genetics and Genomics, Boston Children’s Hospital – sequence: 88 givenname: Stephen W. surname: Scherer fullname: Scherer, Stephen W. organization: Program in Genetics and Genome Biology, The Centre for Applied Genomics, The Hospital for Sick Children, Toronto, Ontario M5G 0A4, Canada., McLaughlin Centre, University of Toronto, Toronto, Ontario M5S 1A1, Canada – sequence: 89 givenname: Michael E. surname: Zwick fullname: Zwick, Michael E. organization: Department of Human Genetics, Emory University School of Medicine – sequence: 90 givenname: Jeffrey C. surname: Barrett fullname: Barrett, Jeffrey C. organization: The Wellcome Trust Sanger Institute, Cambridge, CB10 1SA, UK – sequence: 91 givenname: David J. surname: Cutler fullname: Cutler, David J. organization: Department of Human Genetics, Emory University School of Medicine – sequence: 92 givenname: Kathryn surname: Roeder fullname: Roeder, Kathryn organization: Ray and Stephanie Lane Center for Computational Biology, Carnegie Mellon University, Department of Statistics, Carnegie Mellon University – sequence: 93 givenname: Bernie surname: Devlin fullname: Devlin, Bernie organization: Department of Psychiatry, University of Pittsburgh School of Medicine – sequence: 94 givenname: Mark J. surname: Daly fullname: Daly, Mark J. email: mjdaly@broadinstitute.org organization: Harvard Medical School, The Broad Institute of MIT and Harvard, Department of Medicine, Center for Human Genetic Research, Massachusetts General Hospital – sequence: 95 givenname: Joseph D. surname: Buxbaum fullname: Buxbaum, Joseph D. email: joseph.buxbaum@mssm.edu organization: Seaver Autism Center for Research and Treatment, Icahn School of Medicine at Mount Sinai, Department of Psychiatry, Icahn School of Medicine at Mount Sinai, Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, Department of Neuroscience, Icahn School of Medicine at Mount Sinai, Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, The Mindich Child Health and Development Institute, Icahn School of Medicine at Mount Sinai |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/25363760$$D View this record in MEDLINE/PubMed http://kipublications.ki.se/Default.aspx?queryparsed=id:130112455$$DView record from Swedish Publication Index |
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| ContentType | Journal Article |
| Contributor | Rappaport, Leonard Bastaki, Laila Firth, Helen Fitzpatrick, David van Kogelenberg, Margriet King, Daniel Akawi, Nadia Lim, Elaine T Hurles, Matthew Krishnappa, Netravathi Chang, Bernard S Parthiban, Vijaya Martin, Madelena Wu, Bai-Lin Niaz, Saima Yoo, Seung-Yun Fitzgerald, Tomas Harmin, David A Barrett, Daniel Gererty, Sebastian Stevens, Christine R Al-Turki, Saeed Ware, Janice Rajab, Anna Prigmore, Elena Khuri-Bulos, Najwa Gascon, Generoso G Coomber, Eve Poduri, Annapurna Rodriguez, Jacqueline Hanson, Ellen McRae, Jeremy Khalil, Samir Michael, Parker Miller, Ray Gabriel, Stacey B Rajan, Diana Al-Awadi, Sadika Morley, Katherine Nasir, Ramzi H Schmitz-Abe, Klaus Mukaddes, Nahit M Hashmi, Asif Al-Gazali, Lihadh Clayton, Stephen Herguner, Sabri Barkovich, A James Ben-Omran, Tawfeg Mason, Laura Yu, Timothy Sifrim, Alejandro Bayzetinova, Tanya Allub, Zeinab I Morrow, Eric M D'Gama, Alissa m Ambridge, Kirsty Hisama, Fuki M Barrett, Jeffrey Meyer, Brian Braverman, Nancy E Jones, Wendy Greenberg, Michael E LeClair, Elaine Carter, Nigel Middleton, Anna Al-Sa |
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40 givenname: Soher surname: Balkhy fullname: Balkhy, Soher – sequence: 41 givenname: A James surname: Barkovich fullname: Barkovich, A James – sequence: 42 givenname: Brendy J surname: Barry fullname: Barry, Brendy J – sequence: 43 givenname: Laila surname: Bastaki fullname: Bastaki, Laila – sequence: 44 givenname: Margaret surname: Bauman fullname: Bauman, Margaret – sequence: 45 givenname: Tawfeg surname: Ben-Omran fullname: Ben-Omran, Tawfeg – sequence: 46 givenname: Nancy E surname: Braverman fullname: Braverman, Nancy E – sequence: 47 givenname: Maria H surname: Chahrour fullname: Chahrour, Maria H – sequence: 48 givenname: Bernard S surname: Chang fullname: Chang, Bernard S – sequence: 49 givenname: Haroon R surname: Chaudhry fullname: Chaudhry, Haroon R – sequence: 50 givenname: Michael surname: Coulter fullname: Coulter, Michael – sequence: 51 givenname: Alissa m surname: D'Gama fullname: D'Gama, Alissa m – sequence: 52 givenname: Azhar surname: Daoud fullname: Daoud, Azhar – sequence: 53 givenname: Valsamma surname: Eapen fullname: Eapen, Valsamma – sequence: 54 givenname: Jillian M surname: Felie fullname: Felie, Jillian M – sequence: 55 givenname: Stacey B surname: Gabriel fullname: Gabriel, Stacey B – sequence: 56 givenname: Generoso G surname: Gascon fullname: Gascon, Generoso G – sequence: 57 givenname: Michael E surname: Greenberg fullname: Greenberg, Michael E – sequence: 58 givenname: Ellen surname: Hanson fullname: Hanson, Ellen – sequence: 59 givenname: David A surname: Harmin fullname: Harmin, David A – sequence: 60 givenname: Asif surname: Hashmi fullname: Hashmi, Asif – sequence: 61 givenname: Sabri surname: Herguner fullname: Herguner, Sabri – sequence: 62 givenname: R Sean surname: Hill fullname: Hill, R Sean – sequence: 63 givenname: Fuki M surname: Hisama fullname: Hisama, Fuki M – sequence: 64 givenname: Sarn surname: Jiralerspong fullname: Jiralerspong, Sarn – sequence: 65 givenname: Robert M surname: Joseph fullname: Joseph, Robert M – 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Stoler, Joan M – sequence: 92 givenname: Christine M surname: Sunu fullname: Sunu, Christine M – sequence: 93 givenname: Wen-Hann surname: Tan fullname: Tan, Wen-Hann – sequence: 94 givenname: Hisaaki surname: Taniguchi fullname: Taniguchi, Hisaaki – sequence: 95 givenname: Ahmad surname: Teebi fullname: Teebi, Ahmad – sequence: 96 givenname: Christopher A surname: Walsh fullname: Walsh, Christopher A – sequence: 97 givenname: Janice surname: Ware fullname: Ware, Janice – sequence: 98 givenname: Bai-Lin surname: Wu fullname: Wu, Bai-Lin – sequence: 99 givenname: Seung-Yun surname: Yoo fullname: Yoo, Seung-Yun – sequence: 100 givenname: Timothy surname: Yu fullname: Yu, Timothy |
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| References | Lachmann (CR43) 2010; 26 Ronan, Wu, Crabtree (CR44) 2013; 14 Glessner (CR10) 2009; 459 Vatta (CR38) 2002; 11 Iossifov (CR15) 2012; 74 Poultney (CR8) 2013; 93 Yu (CR6) 2013; 77 Liu (CR36) 2014; 5 Smrt (CR26) 2010; 28 Girirajan (CR21) 2013; 92 Ripke (CR27) 2013; 45 Volkers (CR39) 2011; 34 Khare (CR41) 2012; 40 Pinto (CR3) 2010; 466 Yoon (CR25) 2008; 58 Zoghbi (CR47) 2003; 302 Klei (CR4) 2012; 3 O’Roak (CR12) 2012; 338 Helsmoortel (CR23) 2014; 46 Fromer (CR30) 2014; 506 Robinson, Lichtenstein, Anckarsater, Happe, Ronald (CR28) 2013; 110 Voineagu (CR34) 2011; 474 Neale (CR14) 2012; 485 Sebat (CR2) 2007; 316 DePristo (CR17) 2011; 43 He (CR20) 2013; 9 Darnell (CR31) 2011; 146 Collins (CR35) 2006; 97 Tan, Chen, Dannenfelser, Clark, Ma’ayan (CR37) 2013; 29 Pinto (CR22) 2014; 94 Jacquemont (CR29) 2014; 94 Willsey (CR16) 2013; 155 Rauch (CR45) 2012; 380 Gaugler (CR5) 2014; 46 Lim (CR7) 2013; 77 Long (CR24) 2013; 23 Sanders (CR11) 2012; 485 Scholl (CR40) 2013; 45 Adzhubei (CR18) 2010; 7 Ronald, Hoekstra (CR1) 2011; 156 Ascano (CR32) 2012; 492 Samocha (CR19) 2014; 46 Betancur (CR9) 2011; 1380 Feng (CR42) 2014; 15 Penzes, Cahill, Jones, VanLeeuwen, Woolfrey (CR46) 2011; 14 O’Roak (CR13) 2012; 485 Weyn-Vanhentenryck (CR33) 2014; 6 A Lachmann (BFnature13772_CR43) 2010; 26 J Feng (BFnature13772_CR42) 2014; 15 J Sebat (BFnature13772_CR2) 2007; 316 M Ascano Jr. (BFnature13772_CR32) 2012; 492 IA Adzhubei (BFnature13772_CR18) 2010; 7 L Volkers (BFnature13772_CR39) 2011; 34 SP Khare (BFnature13772_CR41) 2012; 40 AJ Willsey (BFnature13772_CR16) 2013; 155 C Betancur (BFnature13772_CR9) 2011; 1380 CM Tan (BFnature13772_CR37) 2013; 29 P Penzes (BFnature13772_CR46) 2011; 14 D Pinto (BFnature13772_CR22) 2014; 94 S Ripke (BFnature13772_CR27) 2013; 45 MO Collins (BFnature13772_CR35) 2006; 97 A Ronald (BFnature13772_CR1) 2011; 156 TW Yu (BFnature13772_CR6) 2013; 77 SM Weyn-Vanhentenryck (BFnature13772_CR33) 2014; 6 KJ Yoon (BFnature13772_CR25) 2008; 58 H Long (BFnature13772_CR24) 2013; 23 SJ Sanders (BFnature13772_CR11) 2012; 485 M Vatta (BFnature13772_CR38) 2002; 11 BJ O’Roak (BFnature13772_CR12) 2012; 338 HY Zoghbi (BFnature13772_CR47) 2003; 302 S Jacquemont (BFnature13772_CR29) 2014; 94 M Fromer (BFnature13772_CR30) 2014; 506 L Klei (BFnature13772_CR4) 2012; 3 BJ O’Roak (BFnature13772_CR13) 2012; 485 T Gaugler (BFnature13772_CR5) 2014; 46 UI Scholl (BFnature13772_CR40) 2013; 45 JT Glessner (BFnature13772_CR10) 2009; 459 JL Ronan (BFnature13772_CR44) 2013; 14 I Iossifov (BFnature13772_CR15) 2012; 74 JC Darnell (BFnature13772_CR31) 2011; 146 L Liu (BFnature13772_CR36) 2014; 5 S Girirajan (BFnature13772_CR21) 2013; 92 EB Robinson (BFnature13772_CR28) 2013; 110 C Helsmoortel (BFnature13772_CR23) 2014; 46 X He (BFnature13772_CR20) 2013; 9 CS Poultney (BFnature13772_CR8) 2013; 93 RD Smrt (BFnature13772_CR26) 2010; 28 BM Neale (BFnature13772_CR14) 2012; 485 I Voineagu (BFnature13772_CR34) 2011; 474 A Rauch (BFnature13772_CR45) 2012; 380 ET Lim (BFnature13772_CR7) 2013; 77 MA DePristo (BFnature13772_CR17) 2011; 43 D Pinto (BFnature13772_CR3) 2010; 466 KE Samocha (BFnature13772_CR19) 2014; 46 |
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| Title | Synaptic, transcriptional and chromatin genes disrupted in autism |
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