Project description:To study the gene expression profile difference in the myoblast differentiation of normal and DM1 groups, we performed RNA-seq on the total RNA samples collected from the in vitro myoblast differentiation day 4 of normal and DM1 C2C12 cell models. Normal and DM1 cell models were bulit by stably transfecting C2C12 cells with GFP-CUG5 and GFP-CUG200 plasmids. Each group contained three biological replicates. The expression matrix was obtained by Hisat2 followed by Stringtie.
Project description:To study the gene expression profile difference caused by miR-322/-503 overexpression in the myoblast differentiation of DM1 group, we performed RNA-seq on the total RNA samples collected from the in vitro myoblast differentiation day 4 of control and miR-322/-503 overexpressing DM1 C2C12 cell models. The DM1 cell model was bulit by stably transfecting C2C12 cells with GFP-CUG200 plasmid. Each group contained three biological replicates. The expression matrix was obtained by Hisat2 followed by Stringtie.
Project description:We are investigating the transcriptional response of changes in RNA steady-state levels between normal and DM1. We used microarrays to detail the global programme of gene expression differences in normal or DM1 myoblasts. Keywords: comparison Two types of cells were analyzed, normal or DM1 deficient. The expression differences were compared to each other and we have deciphered a gene expression profile that is representative of DM1 deficiency.
Project description:We are investigating the transcriptional response of changes in RNA steady-state levels between normal and DM1. We used microarrays to detail the global programme of gene expression differences in normal or DM1 myoblasts. Keywords: comparison
Project description:DM1 and DM2 biopsies from patients were compared to Normal adult individuals Keywords: 3 groups of samples 10 DM1 biopsies, 20 DM2 biopsies, and 6 Normal individuals biopsies
Project description:Epigenetic defects caused by hereditary or de novo mutations are implicated in various human diseases. It remains uncertain whether correcting the underlying mutation can reverse these defects in patient cells. Focusing on myotonic dystrophy type 1 (DM1), we discovered a fundamental difference between undifferentiated and differentiated cells. While in mutant human embryonic stem cells (hESCs), DNA methylation and H3K9me3 enrichments are completely abolished by repeat excision (2000CTG), in patients' myoblasts (CTG2600 expansion) repeat deletion fails to do so. This distinction stems from cell differentiation, and can be set back by reprogramming gene-edited myoblasts. We demonstrate that abnormal methylation in DM1 is distinctively maintained in the undifferentiated state by the activity of the de novo DNMTs (DNMT3b and/or DNMT3a). Overall, these findings highlight a crucial difference in heterochromatin maintenance between undifferentiated (sequence-dependent) and differentiated (sequence-independent) cells, underscoring the role of differentiation as a locking mechanism for repressive epigenetic modifications at the DM1 locus.