Title | Dissecting the Causal Mechanism of X-Linked Dystonia-Parkinsonism by Integrating Genome and Transcriptome Assembly. |
Publication Type | Journal Article |
Year of Publication | 2018 |
Authors | Aneichyk, T, Hendriks, WT, Yadav, R, Shin, D, Gao, D, Vaine, CA, Collins, RL, Domingo, A, Currall, B, Stortchevoi, A, Multhaupt-Buell, T, Penney, EB, Cruz, L, Dhakal, J, Brand, H, Hanscom, C, Antolik, C, Dy, M, Ragavendran, A, Underwood, J, Cantsilieris, S, Munson, KM, Eichler, EE, Acuña, P, Go, C, R Jamora, DG, Rosales, RL, Church, DM, Williams, SR, Garcia, S, Klein, C, Müller, U, Wilhelmsen, KC, Timmers, HTMarc, Sapir, Y, Wainger, BJ, Henderson, D, Ito, N, Weisenfeld, N, Jaffe, D, Sharma, N, Breakefield, XO, Ozelius, LJ, D Bragg, C, Talkowski, ME |
Journal | Cell |
Volume | 172 |
Issue | 5 |
Pagination | 897-909.e21 |
Date Published | 2018 02 22 |
ISSN | 1097-4172 |
Keywords | Alternative Splicing, Alu Elements, Base Sequence, Cohort Studies, CRISPR-Cas Systems, Dystonic Disorders, Family, Female, Genetic Diseases, X-Linked, Genetic Loci, Genome, Human, Haplotypes, High-Throughput Nucleotide Sequencing, Histone Acetyltransferases, Humans, Induced Pluripotent Stem Cells, Introns, Male, Minisatellite Repeats, Models, Genetic, Nerve Degeneration, Neural Stem Cells, Neurons, RNA, Messenger, Short Interspersed Nucleotide Elements, TATA-Binding Protein Associated Factors, Transcription Factor TFIID, Transcriptome |
Abstract | X-linked Dystonia-Parkinsonism (XDP) is a Mendelian neurodegenerative disease that is endemic to the Philippines and is associated with a founder haplotype. We integrated multiple genome and transcriptome assembly technologies to narrow the causal mutation to the TAF1 locus, which included a SINE-VNTR-Alu (SVA) retrotransposition into intron 32 of the gene. Transcriptome analyses identified decreased expression of the canonical cTAF1 transcript among XDP probands, and de novo assembly across multiple pluripotent stem-cell-derived neuronal lineages discovered aberrant TAF1 transcription that involved alternative splicing and intron retention (IR) in proximity to the SVA that was anti-correlated with overall TAF1 expression. CRISPR/Cas9 excision of the SVA rescued this XDP-specific transcriptional signature and normalized TAF1 expression in probands. These data suggest an SVA-mediated aberrant transcriptional mechanism associated with XDP and may provide a roadmap for layered technologies and integrated assembly-based analyses for other unsolved Mendelian disorders. |
DOI | 10.1016/j.cell.2018.02.011 |
Alternate Journal | Cell |
PubMed ID | 29474918 |
PubMed Central ID | PMC5831509 |
Grant List | P01 NS087997 / NS / NINDS NIH HHS / United States UM1 HG008900 / HG / NHGRI NIH HHS / United States / HH / Howard Hughes Medical Institute / United States R01 NS102423 / NS / NINDS NIH HHS / United States S10 RR023440 / RR / NCRR NIH HHS / United States S10 RR020936 / RR / NCRR NIH HHS / United States S10 OD016372 / OD / NIH HHS / United States S10 OD012027 / OD / NIH HHS / United States |