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Expression data from normal or DM1 myoblasts

ABSTRACT: 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

ORGANISM(S): Homo sapiens

PROVIDER: GSE22498 | GEO | 2010/10/01

SECONDARY ACCESSION(S): PRJNA128661

REPOSITORIES: GEO

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Expression data from normal or DM1 myoblasts

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.

2010-10-01 | E-GEOD-22498 | biostudies-arrayexpress

Expression data from DM1, DM2 and Normal Adult Skeletal Muscle Biopsies

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

2010-01-28 | E-GEOD-7014 | biostudies-arrayexpress

the myoblast differentiation difference in normal and DM1 murine cell models

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.

2021-09-08 | GSE174119 | GEO

Expression data from DM1, DM2 and Normal Adult Skeletal Muscle Biopsies

Project description:DM1 and DM2 biopsies from patients were compared to Normal adult individuals Keywords: 3 groups of samples

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Myotonic dystrophy type 1 (DM1) leads to altered mRNA expression in heart tissue

Project description:Myotonic dystrophy type 1 (DM1) is a dominantly inherited disease that affects multiple organ systems. Cardiac dysfunction is the second leading cause of death in DM1. We quantified gene expression in heart tissue from a heart-specific DM1 mouse model (EpA960/MCM) which inducibly expresses human DMPK exon 15 containing 960 CUG expanded repeats and that reproduced Celf1 up regulation. To assess if, in addition to splicing and miRNA defects, CUGexp RNA also perturbed the steady state mRNA levels of genes, we carried out a microarray study on wildtype E14, adult, MCM controls and DM1 mouse hearts. As anticipated we noted a large number of genes to be developmentally regulated in wildtype hearts, however, within 72h of induction of CUGexp RNA there appeared to be a coordinate adult-to-embryonic shift in steady state levels of many genes. We identified transcripts over-expressed or under-expressed in hearts of wildtype adult mice, wildtype embryonic day 14 (E14), and DM1 mice induced to express CUGexp RNA for 72h and 1wk, when compared to MCM controls. Multiple group comparison.

2014-01-24 | E-GEOD-48991 | biostudies-arrayexpress

Expression data from C2C12 myoblasts transduced with PRDM16 or vector

2009-07-31 | GSE15895 | GEO

Expression data from C2C12 myoblasts transduced with PRDM16 or vector

Project description:PRDM16 is a 140 kDa transcriptional coregulatory protein. PRDM16 has been shown to function as a bi-directional switch in brown fat cell fate by stimulating the development of brown fat cells from myf-5 positive myoblastic precursors. We used microarrays to detail the global programme of gene expression underlying the myoblasts-brown fat conversion induced by PRDM16. undifferentiated C2C12 myoblasts were stably expressed with retroviral PRDM16 or vector control. Total RNAs were isolated by Trizol, and subjected to Affymetrix microarrays.

2010-03-03 | E-GEOD-15895 | biostudies-arrayexpress

Myotonic dystrophy type 1 (DM1) leads to altered mRNA expression in heart tissue

2014-01-24 | GSE48991 | GEO

Differentiation Shifts from a Reversible to an Irreversible Heterochromatin State at the DM1 locus

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.

2024-02-06 | GSE128901 | GEO

Recovery in the intrinsic myogenic program of congenital myotonic dystrophy myoblasts after excision of the expanded (CTG)n repeat

Project description:The congenital form of myotonic dystrophy type 1 (cDM) is caused by large-scale expansion of a (CTG•CAG)n repeat in DMPK and DM1-AS. Production of toxic transcripts with long trinucleotide tracts from these genes results in impediment of myogenic differentiation capacity as cDM’s most prominent morpho-phenotypic hallmark. In the current in vitro study, we compared the early differentiation programs of isogenic cDM myoblasts with and without a (CTG)2600 repeat obtained by gene editing. We found that excision of the repeat restored the ability of cDM myoblasts to engage in myogenic fusion, preventing that the ensuing myotubes remained immature. Although the cDM-typical epigenetic status of the DM1 locus and the expression of genes therein were not altered upon removal of the repeat, analyses at the transcriptome and proteome level revealed that early abnormalities in the temporal expression of differentiation regulators, myogenic progression markers and alternative splicing patterns before and immediately after the onset of differentiation became normalized. Our observation that molecular and cellular features of cDM are reversible and can be corrected by repeat-directed genome editing in muscle progenitors is important information for future development of gene therapy for different forms of DM1.

2019-11-20 | PXD016056 | Pride

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