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MYOD Gene Expression Regulation during Myogenic Conversion of Fibroblasts

ABSTRACT: We provide here gene expression profile of IMR90 fibroblasts expressing or not MYOD culured in GM for 1 day or GM for 1 day and DM for 3 days

ORGANISM(S): Homo sapiens

PROVIDER: GSE98198 | GEO | 2019/09/10

REPOSITORIES: GEO

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MYOD Remodeling of the Genome Architecture during Myogenic Conversion of Somatic Cells

Project description:We provide here an unprecedented analysis of the three-dimensional re-organization of the genome during cellular reprograming of one cell type into another by the ectopic expression of one single transcription factor. By integrating Hi-C analysis with ChIPseq-based detection of MYOD genome-wide binding and RNAseq profiling of gene expression, we discovered that MYOD causes profound alterations in the high order chromatin structure during fibroblast reprogramming into skeletal muscle cells. We also used CTCF ChIPSeq in IMR90 GSE31477 (GSM935404); CTCF ChIPSeq in human myoblasts (hMB) GSE29611 (GSM733762); CTCF ChIPSeq human myotubes (hMT) GSE29611 (GSM733783); H3K27Ac in IMR90 GSE43070 (GSM1055818); H3K27Ac in hMB GSE29611 (GSM733755); H3K27Ac in hMT GSE29611 (GSM733666) Same number of reads was used for H3K27Ac ChIP comparison. ChIPSeq p300 IMR90 GSE43070 (GSM1055812). We also used RNASeq from GSE90895 (GSM2417196, GSM2417197, GSM2417198, GSM2417204, GSM2417203)

2019-09-10 | GSE98509 | GEO

Transcription profiling of mouse embryoic fibroblasts expressing wild type MyoD or its non-acetylatable version MyoD RRR to investigate how MyoD acetylation may contribute to differential gene activation.

Project description:The transcription factor MyoD can coax na?e fibroblasts or otherwise committed cells to adopt the skeletal muscle phenotype by activating the muscle gene expression program. Activation of muscle gene expression occurs in quantal steps with not all the target genes of MyoD being activated at the same time. Some genes are induced in the initial phases, others at later stages despite the fact that MyoD is present throughout the differentiation process. MyoD is post-translationally modified by phosphorylation, ubiquitination, and acetylation. Here, we have employed a model system in which MyoD and its non-acetylatable version were inducibly expressed in mouse embryonic fibroblasts derived from mice to investigate how MyoD acetylation may contribute to differential gene activation. Experiment Overall Design: Mouse embryos fibroblasts (MEFs) obtained from MyoD-/-/Myf5-/- animals will be transduced with retroviruses expressing an estrogen receptor hormone binding domain fused to either mouse MyoD wild type (ER-MyoD wt) or MyoD bearing three point mutations at lysine residues 99, 102, and 104 that render it no longer acetylatable ( ER-MyoD RRR). A retrovirus without the ER-MyoD insert was also employed as negative control.</p> Aim 2. We will compare genome-wide expression profiling of MEFs transduced with either ER-MyoD wt or ER-MyoD RRR cultured in the presence of a medium that promotes skeletal muscle differentiation (DM) supplemented with beta-estradiol for 0, 6, 12, and 24 hours, respectively.

2007-11-15 | E-GEOD-6487 | biostudies-arrayexpress

Epicatechin elicits MyoD-dependent myoblast differentiation and myogenic conversion of fibroblasts.

Project description:Prevention of age-associated reduction in muscle mass and function is required to manage a healthy life. Supplemental (-)-Epicatechin (EC) appears to act as a potential regulator for muscle growth and strength. However, its cellular and molecular mechanisms as a potential muscle growth agent have not been studied well. In the current study, we investigated a role of EC in differentiation of muscle progenitors to gain the molecular insight into how EC regulates muscle growth. EC enhanced myogenic differentiation in a dose-dependent manner through stimulation of promyogenic signaling pathways, p38MAPK and Akt. EC treatment elevated MyoD activity by enhancing its heterodimerization with E protein. Consistently, EC also positively regulated myogenic conversion and differentiation of fibroblasts. In conclusion, EC has a potential as a therapeutic or nutraceutical remedy to treat degenerative muscle diseases or age-related muscle weakness.

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Gene expression profiling on C3H/10T1/2 fibroblasts during their myogenic conversion in case of Six4 ablation

Project description:In this study, we used C3H/10T1/2 cells, a well known model of myogenic conversion, to study the effect of Six4 knockdown on the expression of genes during fibroblasts to myocytes conversion induced by ectopic expression of MyoD We established C3H/10T1/2 cell line with stable Six4 knockdown by short hairpin RNA (shSix4) vs a control cell line (shLuc) and converted these cells into myogenic lineage by retroviral transduction of plasmid encoding Flag-MyoD-myc (pBABE-MyoD) or empty plasmid (pBABE). Cells were then induced to differentiate for 24 hours before RNA extraction.

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Inducible expression of MyoD directly mediates myogenic conversion of human induced pluripotent stem cells (iPSCs) derived from Duchenne muscular dystrophy (DMD).

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2014-01-09 | E-GEOD-46633 | biostudies-arrayexpress

Inducible expression of MyoD directly mediates myogenic conversion of human induced pluripotent stem cells (iPSCs) derived from Duchenne muscular dystrophy (DMD).

2014-01-09 | GSE46633 | GEO

Gene expression profiling on C3H/10T1/2 fibroblasts during their myogenic conversion in case of Six4 ablation

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Myogenesis MyoD

2006-12-13 | GSE6487 | GEO

Transcriptome sequencing analysis of MyoD-induced transdifferentiation in 10T1/2 fibroblasts using RNA-seq

Project description:To understand the effect of LncMyod on MyoD-induced transdifferentiation of 10T1/2 fibroblast cells, we performed RNA-seq on LncMyoD-KO 10T1/2 fibroblasts with MyoD-induced transdifferentiation.

2020-12-08 | GSE159133 | GEO

Dissecting mechanisms by which MyoD and small molecules convert fibroblasts to muscle progenitor cells

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2021-07-28 | GSE171039 | GEO

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