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Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of mouse muscle satellite cell-derived myoblasts (MyoD-/-, p53-/-)

ABSTRACT: Muscle satellite cells are a self-renewing pool of stem cells that give rise to daughter myogenic precursor cells in adult skeletal muscle. Published and preliminary data indicated that MyoD and p53 genes are involved in satellite cell differentiation. We would like to know what downstream genes of both transcription factors are affected in satellite cell-derived myoblasts (MyoD-/-, p53 -/-). Experiment Overall Design: this experiment include 3 samples and 25 replicates

ORGANISM(S): Mus musculus

SUBMITTER: OGIC Info Ontario Genomics Innovation Centre (OGIC)

PROVIDER: E-GEOD-3244 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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MyoD induces myogenic differentiation through cooperation of its NH2- and COOH-terminal regions.

Ishibashi Jeff J Perry Robert L RL Asakura Atsushi A Rudnicki Michael A MA

The Journal of cell biology 20051101 3

MyoD and Myf5 are basic helix-loop-helix transcription factors that play key but redundant roles in specifying myogenic progenitors during embryogenesis. However, there are functional differences between the two transcription factors that impact myoblast proliferation and differentiation. Target gene activation could be one such difference. We have used microarray and polymerase chain reaction approaches to measure the induction of muscle gene expression by MyoD and Myf5 in an in vitro model. In ...[more]

PMID: 16275751

Similar Datasets

Muscle Satellite Cells: MyoD and p53 genes

Project description:Muscle satellite cells are a self-renewing pool of stem cells that give rise to daughter myogenic precursor cells in adult skeletal muscle. Published and preliminary data indicated that MyoD and p53 genes are involved in satellite cell differentiation. We would like to know what downstream genes of both transcription factors are affected in satellite cell-derived myoblasts (MyoD-/-, p53 -/-). Keywords: other

2005-09-07 | GSE3244 | GEO

Notch signaling/MyoD double deficient embryonic muscle progenitors

Project description:Skeletal muscle growth and regeneration rely on myogenic progenitor and satellite cells, the stem cells of postnatal muscle. Elimination of Notch signals during mouse development results in premature differentiation of myogenic progenitors and formation of very small muscle groups. Here we show that this drastic effect is rescued by mutation of the muscle differentiation factor MyoD. However, rescued myogenic progenitors do not assume a satellite cell position and contribute poorly to myofiber growth. The disrupted homing is due to a deficit in basal lamina assembly around emerging satellite cells and to their impaired adhesion to myofibers. On a molecular level, emerging satellite deregulate the expression of basal lamina components and adhesion molecules like integrin a7, collagen XVIIIa1, Megf10 and Mcam. We conclude that Notch signals control homing of satellite cells, stimulating them to contribute to their own microenvironment and to adhere to myofibers. Gene expression analysis using total RNA from FACS-isolated Vcam-1+/CD31-/CD45-/Sca1- embryonic muscle progenitor cells from E17.5 back muscle tissue of MyoD-/-, Pax3cre/+;Rbpjflox/flox;MyoD-/- and Pax3cre/+;DnMamlflox/flox;MyoD-/- mice.

2012-12-31 | E-GEOD-39379 | biostudies-arrayexpress

Expression data of satellite cells through muscle injury time course

Project description:Satellite cells are resident skeletal muscle stem cells responsible for muscle maintenance and repair. In resting muscle, satellite cells are maintained in a quiescent state. Satellite cell activation induces the myogenic commitment factor, MyoD, and cell cycle entry to facilitate transition to a population of proliferating myoblasts that eventually exit the cycle and regenerate muscle tissue. The molecular mechanism involved in the transition of a quiescent satellite cell to a transit-amplifying myoblast is poorly understood. We used microarrays to detail the global program of gene expression of in vivo satellite cell activation through muscle injury and identified RNA post-transcriptional regulation as a key component of satellite cell activation. Wild type or Sdc4-/- satellite cells were FACS isolated from resting muscle or from muscle 12h and 48h following barium chloride-induced muscle injury. 5000 cell equivalents of RNA was labeled and hybridized to MOE430v2 GeneChips (Affymetrix) and scanned as per manufacturers protocol. Probeset intensities were GCRMA normalized for further analysis including UPGMA hierarchical clustering, analysis of variance (ANOVA), and fold change.

2012-07-31 | E-GEOD-38870 | biostudies-arrayexpress

Expression data of satellite cells through muscle injury time course

2012-08-01 | GSE38870 | GEO

Mus musculus

Project description:Muscle Satellite Cells: MyoD and p53 genes

| PRJNA92787 | ENA

Notch signaling/MyoD double deficient embryonic muscle progenitors

2012-12-31 | GSE39379 | GEO

Klf5 regulates muscle differentiation via directly targeted muscle-specific genes in cooperation with MyoD in mice

Project description:Deletion of Klf5 in satellite cells impaired muscle regeneration due to a failure of differentiation. Mechanistically, Klf5 controls transcription of muscle genes by interacting with MyoD and Mef2. These findings provide a potential intervention into the process of muscle regeneration through modulation of Klf5.

2016-10-14 | GSE80812 | GEO

Myogenesis MyoD

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. Keywords: Time-Series

2006-12-13 | GSE6487 | GEO

Chromatin accessibility landscape of freshly-isolated human and murine muscle satellite cells and myoblasts

Project description:Muscle stem cells, also known as satellite cells, represent the main myogenic population accounting for skeletal muscle homeostasis and regeneration. Here, using the Assay for Transposase Accessible Chromatin followed by sequencing (ATAC-seq), we investigated the epigenetic landscape of activated human and murine satellite cells. Our analysis identified a compendium of putative regulatory elements defining activated satellite cells and myoblasts, respectively.

2021-08-20 | GSE165414 | GEO

Transcription profiling of mouse 2C5/7 myoD-/-;myf5-/- fibroblast cells expressing MyoD, Myf5, myogenin, or hrGFP

Project description:Gene expression changes induced by MyoD or Myf5 were examined in a double-knockout fibroblast cell line lacking endogenous functional myoD or myf5 genes. Use of this cell line precluded the possibility of auto- or cross-activation of endogenous myoD or myf5. Myogenin or hrGFP were expressed in parallel samples as controls. Following infection with retrovirus - expressing the relevant myogenic regulatory factor (MRF) from the viral LTR promoter and hrGFP through an IRES element in the same mRNA transcript - GFP+ cells were sorted by FACS and harvested for total RNA. Experiment Overall Design: this experiment include 4 samples and 12 replicates

2008-06-12 | E-GEOD-3245 | biostudies-arrayexpress

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