A yeast functional screen predicts new candidate ALS disease genes

Julien Couthouis(University of Pennsylvania), Michael P. Hart, James Shorter(Institute of Molecular Biology and Biophysics), Mariely DeJesus‐Hernandez, Renske Erion, Rachel Oristano, Annie X. Liu, Daniel M. Ramos, Niti Jethava, Divya Hosangadi(Bucks County Intermediate Unit), James Epstein, Ashley Chiang(Elwyn), Zamia Diaz(Institute of Molecular Biology and Biophysics), Tadashi Nakaya, Fadia Ibrahim, Hyung‐Jun Kim(Howard Hughes Medical Institute), Jennifer A. Solski(Anzac Research Institute), Kelly L. Williams(The University of Sydney), Jelena Mojsilovic‐Petrovic(Children's Hospital of Philadelphia), Caroline Ingre(Umeå University), Khrista Boylan(Mayo Clinic), Neill R. Graff‐Radford(Mayo Clinic), Dennis W. Dickson, Dana Clay-Falcone(University of Pennsylvania), Lauren Elman(Neurology, Inc), Leo McCluskey(Neurology, Inc), Robert A. Greene(University of Pennsylvania), Robert G. Kalb(Children's Hospital of Philadelphia), Virginia M.‐Y. Lee(University of Pennsylvania), John Q. Trojanowski(University of Pennsylvania), Albert C. Ludolph(Universität Ulm), Wim Robberecht(KU Leuven), Peter M. Andersen(Umeå University), Garth A. Nicholson(The University of Sydney), Ian P. Blair(The University of Sydney), Oliver D. King(Boston Biomedical Research Institute), Nancy M. Bonini(Howard Hughes Medical Institute), Vivianna M. Van Deerlin(University of Pennsylvania), Rosa Rademakers, Zissimos P. Mourelatos, Aaron D. Gitler
Proceedings of the National Academy of Sciences
November 7, 2011
Cited by 398

Abstract

Amyotrophic lateral sclerosis (ALS) is a devastating and universally fatal neurodegenerative disease. Mutations in two related RNA-binding proteins, TDP-43 and FUS, that harbor prion-like domains, cause some forms of ALS. There are at least 213 human proteins harboring RNA recognition motifs, including FUS and TDP-43, raising the possibility that additional RNA-binding proteins might contribute to ALS pathogenesis. We performed a systematic survey of these proteins to find additional candidates similar to TDP-43 and FUS, followed by bioinformatics to predict prion-like domains in a subset of them. We sequenced one of these genes, TAF15, in patients with ALS and identified missense variants, which were absent in a large number of healthy controls. These disease-associated variants of TAF15 caused formation of cytoplasmic foci when expressed in primary cultures of spinal cord neurons. Very similar to TDP-43 and FUS, TAF15 aggregated in vitro and conferred neurodegeneration in Drosophila, with the ALS-linked variants having a more severe effect than wild type. Immunohistochemistry of postmortem spinal cord tissue revealed mislocalization of TAF15 in motor neurons of patients with ALS. We propose that aggregation-prone RNA-binding proteins might contribute very broadly to ALS pathogenesis and the genes identified in our yeast functional screen, coupled with prion-like domain prediction analysis, now provide a powerful resource to facilitate ALS disease gene discovery.


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