Loss of full-length dystrophin expression causes major cell-autonomous abnormalities in proliferating myoblasts

ABSTRACT: Duchenne muscular dystrophy (DMD) is a severely debilitating and incurable neuromuscular disease. Its conspicuous feature is the absence of dystrophin in myofibers and therefore most therapeutic approaches focus on some form of its re-expression there. However, increasing body of evidence points at an early developmental onset of DMD and severe abnormalities were uncovered in dystrophic muscle stem cells. In this study, we explore gene expression changes in primary myoblasts from mice lacking expression of the full length dystrophin transcript. Total RNA extracted from primary myoblasts isolated from gastrocnemii of 8 week old male Dmd-mdx (MDX - lacking the full length dystrophin transcript), Dmd-mdx-βgeo (BGEO - lacking all dystrophin expression) and control mice (WT) were subjected to RNA sequencing following ribodepletion, and analysed for the differential expression of genes between groups and the enrichment of gene ontology categories or pathways.

INSTRUMENT(S): Illumina HiSeq 2500

ORGANISM(S): Mus musculus

SUBMITTER: Maxime Gosselin 

PROVIDER: E-MTAB-10322 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress