| Literature DB >> 30561649 |
Eric T Wang1,2,3,4,5, Daniel Treacy1, Katy Eichinger6, Adam Struck7, Joseph Estabrook1,2,3,4,5, Hailey Olafson3,4,5, Thomas T Wang1, Kirti Bhatt6, Tony Westbrook8, Sam Sedehizadeh8, Amanda Ward9, John Day10, David Brook8, J Andrew Berglund3,4,5,7, Thomas Cooper9,11,12, David Housman1,2, Charles Thornton6, Christopher Burge1,2.
Abstract
Myotonic dystrophy (dystrophia myotonica, DM) is a multi-systemic disease caused by expanded CTG or CCTG microsatellite repeats. Characterized by symptoms in muscle, heart and central nervous system, among others, it is one of the most variable diseases known. A major pathogenic event in DM is the sequestration of muscleblind-like proteins by CUG or CCUG repeat-containing RNAs transcribed from expanded repeats, and differences in the extent of MBNL sequestration dependent on repeat length and expression level may account for some portion of the variability. However, many other cellular pathways are reported to be perturbed in DM, and the severity of specific disease symptoms varies among individuals. To help understand this variability and facilitate research into DM, we generated 120 RNASeq transcriptomes from skeletal and heart muscle derived from healthy and DM1 biopsies and autopsies. A limited number of DM2 and Duchenne muscular dystrophy samples were also sequenced. We analyzed splicing and gene expression, identified tissue-specific changes in RNA processing and uncovered transcriptome changes strongly correlating with muscle strength. We created a web resource at http://DMseq.org that hosts raw and processed transcriptome data and provides a lightweight, responsive interface that enables browsing of processed data across the genome.Entities:
Mesh:
Substances:
Year: 2019 PMID: 30561649 PMCID: PMC6452195 DOI: 10.1093/hmg/ddy432
Source DB: PubMed Journal: Hum Mol Genet ISSN: 0964-6906 Impact factor: 6.150