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

ABSTRACT: 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

ORGANISM(S): Mus musculus

SUBMITTER: OGIC Info Ontario Genomics Innovation Centre (OGIC)

PROVIDER: E-GEOD-3245 | 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

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MyoD, Myf5, myogenin, or hrGFP expressed in 2C5/7 myoD-/-;myf5-/- fibroblast cells

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. Keywords: other

2005-09-07 | GSE3245 | GEO

ChIP-seq of Active Histone Mark (H3K27ac) and Myogenic Regulatory Factors (MYF5 and MYOD) in Fusion Negative Rhabdomyosarcoma Cell Lines

Project description:We performed Chip-seq analysis of Myogenic Regulatory Transcription Factors (MYF5 and MYOD) in Fusion Negative Rhabdomyosarcoma cell lines. Endogenous MYF5/H3K27ac Chip-seq was performed in Rh18 cells and MYOD-H3K27ac Chip-seq was performed in RD cells, given that these cell lines express these proteins in a mutually-exclusive manner. Analysis revealed a common subset of enhancer and promoter regions bound by these transcription factors that are enriched for cell cycle regulation and embryonic muscle development pathways. Keywords: rhabdomyiosarcoma, Chip-seq, chromatin, Transcription factos, MYF5, MYOD

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Distinct activities of Myf5 and MyoD indicate sequential roles in skeletal muscle lineage specification and differentiation (ChIP-Seq)

Project description:In this work we compare the molecular functions of Myf5 and MyoD, two highly related bHLH transcription factors that regulate skeletal muscle specification and differentiation. We find MyoD and Myf5 bind the same sites genome-wide but have distinct functions: Myf5 induces histone acetylation without Pol II recruitment or robust gene activation, whereas MyoD induces histone acetylation, recruits PolII and robustly activates gene transcription. Chip-seq profiling of MyoD, Myf5, Histone H4 acetylation (H4Ac), and Pol II in MyoD-/-; Myf5-/- MEFs (M&M MEFs)

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Distinct activities of Myf5 and MyoD indicate sequential roles in skeletal muscle lineage specification and differentiation (ChIP-Seq)

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Mus musculus

Project description:MyoD, Myf5, myogenin, or hrGFP expressed in 2C5/7 myoD-/- myf5-/- fibroblast cells

| PRJNA92789 | ENA

MyoD and myogenin ChIP-seq in differentiated C2C12 cells

Project description:The submitted files contain ChIP-seq data for the MyoD and myogenin muscle regulatory factors in diffrentiated C2C12 cells as well as two different sonicated input samples (one from a regular 1% formaldehyde fixation and one from a dual 1%FA + 1.5 mM EGS fix). Characterization of genome-wide MyoD and myogenin binding in C2C12 cells

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Novel RNA-binding activity of MYF5 enhances Ccnd1/Cyclin D1 mRNA translation during myogenesis

Project description:Skeletal muscle contains long multinucleated and contractile structures known as muscle fibers, which arise from the fusion of myoblasts into nucleated myotubes during myogenesis. The myogenic regulatory factor (MRF) MYF5 is the earliest to be expressed during myogenesis and functions as a transcription factor in muscle progenitor cells (satellite cells) and myocytes. In mouse C2C12 myocytes, MYF5 is implicated in the initial steps of myoblast differentiation into myotubes. Ribonucleoprotein immunoprecipitation (RIP) analysis showed that MYF5 bound a subset of myoblast mRNAs; prominent among them was Ccnd1 mRNA, which encodes the key cell cycle regulator CCND1 (Cyclin D1). Biotin-RNA pulldown, UV-crosslinking, and gel shift experiments indicated that MYF5 was capable of binding the 3' untranslated region (UTR) and the coding region (CR) of Ccnd1 mRNA. MYF5 silencing in proliferating growing myoblasts revealed that and MYF5 promoted CCND1 translation, and it also modestly increased transcription of Ccnd1 mRNA. Importantly, silencing MYF5 reduced myoblast growth as well as differentiation of myoblasts into myotubes, while overexpressing MYF5 in C2C12 cells upregulated CCND1 expression. We propose that MYF5 enhances early myogenesis in part by coordinately elevating Ccnd1 transcription and Ccnd1 mRNA translation.

2016-08-08 | GSE73704 | GEO

Novel RNA-binding activity of MYF5 enhances Ccnd1/Cyclin D1 mRNA translation during myogenesis

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