Gene expression elucidates functional impact of polygenic risk for schizophrenia View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2016-11

AUTHORS

Menachem Fromer, Panos Roussos, Solveig K Sieberts, Jessica S Johnson, David H Kavanagh, Thanneer M Perumal, Douglas M Ruderfer, Edwin C Oh, Aaron Topol, Hardik R Shah, Lambertus L Klei, Robin Kramer, Dalila Pinto, Zeynep H Gümüş, A Ercument Cicek, Kristen K Dang, Andrew Browne, Cong Lu, Lu Xie, Ben Readhead, Eli A Stahl, Jianqiu Xiao, Mahsa Parvizi, Tymor Hamamsy, John F Fullard, Ying-Chih Wang, Milind C Mahajan, Jonathan M J Derry, Joel T Dudley, Scott E Hemby, Benjamin A Logsdon, Konrad Talbot, Towfique Raj, David A Bennett, Philip L De Jager, Jun Zhu, Bin Zhang, Patrick F Sullivan, Andrew Chess, Shaun M Purcell, Leslie A Shinobu, Lara M Mangravite, Hiroyoshi Toyoshiba, Raquel E Gur, Chang-Gyu Hahn, David A Lewis, Vahram Haroutunian, Mette A Peters, Barbara K Lipska, Joseph D Buxbaum, Eric E Schadt, Keisuke Hirai, Kathryn Roeder, Kristen J Brennand, Nicholas Katsanis, Enrico Domenici, Bernie Devlin, Pamela Sklar

ABSTRACT

Over 100 genetic loci harbor schizophrenia-associated variants, yet how these variants confer liability is uncertain. The CommonMind Consortium sequenced RNA from dorsolateral prefrontal cortex of people with schizophrenia (N = 258) and control subjects (N = 279), creating a resource of gene expression and its genetic regulation. Using this resource, ∼20% of schizophrenia loci have variants that could contribute to altered gene expression and liability. In five loci, only a single gene was involved: FURIN, TSNARE1, CNTN4, CLCN3 or SNAP91. Altering expression of FURIN, TSNARE1 or CNTN4 changed neurodevelopment in zebrafish; knockdown of FURIN in human neural progenitor cells yielded abnormal migration. Of 693 genes showing significant case-versus-control differential expression, their fold changes were ≤ 1.33, and an independent cohort yielded similar results. Gene co-expression implicates a network relevant for schizophrenia. Our findings show that schizophrenia is polygenic and highlight the utility of this resource for mechanistic interpretations of genetic liability for brain diseases. More... »

PAGES

1442-1453

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/nn.4399

    DOI

    http://dx.doi.org/10.1038/nn.4399

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1022499785

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/27668389


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