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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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RNA-seq data from healthy and DMD human cells, along skeletal muscle differentiation from induced pluripotent stem cells

ABSTRACT: 3 healthy cells - 3 DMD cells - 7 time points (tissue-derived myoblasts, tissue-derived myotubes, hiPSCs, Day 3 of differentiation, Day 10 of differentiation, Day 17 of differentiation, Day 25 of differentiation) - 1 replicate per cell line for the tissue-derived samples and 3 biological replicates per cell line for the hiPSC-derived samples.

INSTRUMENT(S): Illumina HiSeq 4000

ORGANISM(S): Homo sapiens

SUBMITTER: Virginie Mournetas

PROVIDER: E-MTAB-8321 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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miRNA-seq data from healthy and DMD human cells, along skeletal muscle differentiation from induced pluripotent stem cells

Project description:3 or 4 healthy cells - 3 DMD cells - 7 time points (tissue-derived myoblasts, tissue-derived myotubes, hiPSCs, Day 3 of differentiation, Day 10 of differentiation, Day 17 of differentiation, Day 25 of differentiation).

2020-10-05 | E-MTAB-8293 | biostudies-arrayexpress

Comparison of Genome-Wide Binding of MyoD in Normal Human Myogenic Cells and Rhabdomyosarcomas Identifies Regional and Local Suppression of Promyogenic Transcription Factors (expression profiling).

Project description:Rhabdomyosarcoma is a pediatric tumor of skeletal muscle that expresses the myogenic basic helix-loop-helix protein MyoD but fails to undergo terminal differentiation. Prior work has determined that DNA binding by MyoD occurs in the tumor cells, but myogenic targets fail to activate. Using MyoD chromatin immunoprecipitation coupled to high-throughput sequencing and gene expression analysis in both primary human muscle cells and RD rhabdomyosarcoma cells, we demonstrate that MyoD binds in a similar genome-wide pattern in both tumor and normal cells but binds poorly at a subset of myogenic genes that fail to activate in the tumor cells. Binding differences are found both across genomic regions and locally at specific sites that are associated with binding motifs for RUNX1, MEF2C, JDP2, and NFIC. These factors are expressed at lower levels in RD cells than muscle cells and rescue myogenesis when expressed in RD cells. MEF2C is located in a genomic region that exhibits poor MyoD binding in RD cells, whereas JDP2 exhibits local DNA hypermethylation in its promoter in both RD cells and primary tumor samples. These results demonstrate that regional and local silencing of differentiation factors contributes to the differentiation defect in rhabdomyosarcomas. ChIP-Seq profiling of MyoD in human myotube, myoblast and rhabdomyosarcoma cells

2013-08-29 | E-GEOD-50413 | biostudies-arrayexpress

DUX4-induced gene expression is the major molecular signature in FSHD skeletal muscle

Project description:Facioscapulohumeral dystrophy (FSHD) is caused by decreased epigenetic repression of the D4Z4 macrosatellite array and recent studies have shown that this results in the expression of low levels of the DUX4 mRNA in skeletal muscle. Several other mechanisms have been suggested for FSHD pathophysiology and it remains unknown whether DUX4 expression can account for most of the molecular changes seen in FSHD. Since DUX4 is a transcription factor, we used RNA-seq to measure gene expression in muscle cells transduced with DUX4, and in muscle cells and biopsies from control and FSHD individuals. We show that DUX4 target gene expression is the major molecular signature in FSHD muscle together with a gene expression signature consistent with an immune cell infiltration. In addition, one unaffected individual without a known FSHD-causing mutation showed expression of DUX4 target genes. This individual has a sibling with FSHD and also without a known FSHD-causing mutation, suggesting the presence of yet unidentified modifier locus for DUX4 expression and FSHD. These findings demonstrate that expression of DUX4 accounts for the majority of the gene expression changes in FSHD skeletal muscle together with an immune cell infiltration. RNA-seq for muscle cells and biopsies from control and FSHD individuals.

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Expression data from untreated vs. BMP4-treated cultured wild-type and MuSK null muscle cells (myoblasts and myotubes)

Project description:Bone morphogenic proteins (BMPs) function in virtually all tissues with cell-type specific outcomes. Since there are a relatively small number of BMP receptors this exquisite signaling specificity requires additional molecules to regulate the output of this pathway. We demonstrated that the receptor tyrosine kinase MuSK that is selectively expressed in muscle and plays a critical role in synapse formation and maintenance binds to BMP4 and related BMPs. Since BMPs regulate the transcription of a set of genes, we performed microarrays for wild-type and MuSK null muscle cells to test if MuSK regulates BMP responses in muscle cells. We shought to determine if MuSK regulates BMP responses in muscle cells and if the cell context made any difference in MuSK regulation of BMP pathway. To test this, expression profiles of untreated vs. BMP4-treated undifferentiated myoblast and differentiated myotube cultures were generated for both wild-type and MuSK-null genotypes. All conditions were done in triplicates. In total 24 arrays were analyzed.

2015-08-03 | E-GEOD-59567 | biostudies-arrayexpress

Comparison of Genome-Wide Binding of MyoD in Normal Human Myogenic Cells and Rhabdomyosarcomas Identifies Regional and Local Suppression of Promyogenic Transcription Factors

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-08-29 | E-GEOD-50415 | biostudies-arrayexpress

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Genome-wide mapping of Sox6 binding sites in mouse fetal myotubes

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2011-10-06 | E-GEOD-32627 | biostudies-arrayexpress

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Project description:The nuclear organization of the genome is accepted as an important feature of gene expression regulation. However, it has remained unknown what the spatial organization of a single transcribed gene is. Here, we made use of several long highly expressed mammalian genes to describe their structure and spatial arrangement during transcription. We demonstrate that an expressed gene forms a transcription loop with RNA polymerases moving along the loop and carrying nascent RNAs that undergo co-transcriptional splicing. Transcription loops dynamically modify their harboring loci and extend into the nuclear interior due to their intrinsic stiffness. We hypothesize that the stiffness of the transcription loop arises due to a dense decoration of gene-axis with multiple voluminous nascent ribonucleoprotein particles, thus creating a stiff polymer bottlebrush. and provide supporting evidence to this hypothesis. Our work suggests that transcription loop formation is a universal principle of eukaryotic gene expression.

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2013-04-01 | E-GEOD-43183 | biostudies-arrayexpress

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