MiRNA expression data from skeletal muscle stem cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Takahiko Sato
PROVIDER: E-GEOD-48412 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:It has been shown recently that non-coding RNAs including miRNAs are involved in the development of skeletal muscle progenitors and to maintain the quiescent condition of adult skeletal muscle stem cells. To identify the difference among developing skeletal muscle-committed progenitors or stem cells detected by Pax3-GFP; MyoD-primed RFP expressions, miRNA microarray was performed.
2014-08-01 | GSE48412 | GEO
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
Project description:In skeletal myogenesis, the transcription factor MyoD activates distinct transcriptional programs in progenitors compared to terminally differentiated cells. Using ChIP-seq and gene expression analyses, we show that in primary myoblasts, Snail-HDAC1/2 repressive complex bind and exclude MyoD from its targets. Notably, Snail binds E-box motifs that are G/C-rich in their central dinucleotides, and such sites are almost exclusively associated with genes expressed during differentiation. By contrast, Snail does not bind the A/T-rich E-boxes associated with MyoD targets in myoblasts. Thus, Snai1-HDAC1/2 prevents MyoD occupancy on differentiation-specific regulatory elements and the change from Snail- to MyoD-binding often results in enhancer switching during differentiation. Furthermore, we show that a regulatory network involving Myogenic Regulatory Factors (MRFs), Snail/2, miR-30a and miR-206 acts as a molecular switch that controls entry into myogenic differentiation. Together, these results reveal a regulatory paradigm that directs distinct gene expression programs in progenitors versus terminally differentiated cells. Genome wide binding sites of various transcription factors and chromatin modifiers in muscle cells
2012-07-04 | E-GEOD-24852 | biostudies-arrayexpress
Project description:The skeletal myogenic lineage in developing embryos is specified within the somites and requires members of the Paired box (Pax) family of transcription factors. In particular, Pax3 is the first member of this family expressed in the central region of the dermomyotome and it is necessary for specification, migration and survival of the myogenic progenitors that will form the muscles of the limbs, diaphragm and tongue. To investigate Pax3 molecular functions in the developing mesoderm, we generated doxycycline-inducible mouse embryonic stem (ES) cells expressing untagged and HaFlag-tagged-Pax3. These cell lines were used to unbiasedly identify its interacting partners by tandem affinity purification followed by mass spectrometry.
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Project description:We report skeletal muscle developmental defects in SRSF2 MyoD-Cre mice, in which SRSF2 is ablated in skeletal muscle.
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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.
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Project description:Alveolar rhabdomyosarcoma (aRMS) is an aggressive sarcoma of skeletal muscle characterized by expression of the PAX3-FOXO1 fusion gene. Despite its discovery over almost 20 years ago, PAX3-FOXO1 remains an enigmatic tumor driver. Previously, we reported that PAX3-FOXO1 supports aRMS initiation by enabling bypass of cellular senescence. Here, we show that bypass occurs in part by PAX3-FOXO1-mediated upregulation of RASSF4, a Ras-association domain family (RASSF) member, which then suppresses the evolutionarily conserved mammalian Hippo/Mst1 pathway. RASSF4 loss-of-function activates Hippo/Mst1 and inhibits downstream YAP, causing aRMS cell cycle arrest and senescence. This is the first evidence for an oncogenic role for RASSF4, and a novel mechanism for Hippo signaling suppression in human cancer. Human skeletal muscle myoblasts (HSMMs) were retrovirally transduced with either an empty vector (Vp, pK1) or PAX3-FOXO1 (PFp, pK1-PAX3-FOXO1) and selected on puromycin. Presenescent (presen) cells were harvested before the senescence checkpoint. Since cells expressing PAX3-FOXO1 can bypass the senescence checkpoint, postsenescent (postsen) cells expressing PAX3-FOXO1 were also harvested. the gene expression affected by the introduction of PAX3-FOXO1
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Project description:Skeletal muscle development requires the coordinated expression of numerous transcription factors to control the specification of the muscle fate in mesodermal cells and the differentiation of the committed myoblasts into functional contractile fibers. The bHLH transcription factor MyoD plays a key role in these processes, since its forced expression is sufficient to induce the myogenesis in a variety of non-muscle cells in culture. Consistent with this observation, the majority of skeletal muscle genes requires MyoD to activate their own transcription. In order to identify novel MyoD-target genes we generated C2C12 MyoD-silenced clones, and used a muscle-specific cDNA microarray to study the induced modifications of the transcriptional profile. Gene expression was analyzed at three different stages in differentiating MyoD(-)C2C12 myoblasts. These microarray data sets identified many additional uncharacterized downstream MyoD transcripts that may play important functions in muscle cell differentiation. Among these genes, we concentrated our study on the cell cycle regulators Cdkn1c and calcyclin and on the muscle-specific putative myogenic regulator Ankrd2. Bioinformatic and functional studies on the promoters of these genes clarified their dependence on MyoD activity. Clues of other regulatory mechanisms that might interact with the principal bHLH transcription factor have been revealed by the unexpected up regulation in MyoD(-) cells of these novel (and other) target transcripts, at the differentiation stage in which MyoD became normally down regulated. Keywords: MyoD, cell cycle regulation, cDNA microarray, myogenic differentiation, gene regulation
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Project description:Optimal cell-based therapies for the treatment of muscle degenerative disorders should not only regenerate fibers, but provide a quiescent satellite cell pool ensuring long-term maintenance and regeneration. Conditional expression of Pax3/Pax7 in differentiating pluripotent stem cells (PSC) allows the generation of myogenic progenitors endowed with satellite cell-like abilities. To identify the molecular determinants underlying their regenerative potential, we performed transcriptome analyses of these cells along with primary myogenic cells from several developmental stages. Here we show that in vitro generated PSC-derived myogenic progenitors possess a molecular signature similar to embryonic/fetal myoblasts. However, compared to fetal myoblasts, following transplantation they show superior myofiber engraftment and ability to seed the satellite cell niche, respond to multiple re-injuries and contribute to long-term regeneration. Upon engraftment, the transcriptome of Pax3/Pax7-induced PSC-derived myogenic progenitors changes dramatically, acquiring similarity to that of satellite cells, particularly in genes involved in extracellular matrix remodeling. Single cell profiling reveals that these changes are induced, not selected, by the in vivo environment. These findings demonstrate that Pax3/Pax7-induced PSC-derived myogenic progenitors possess proliferative and migratory abilities characteristic of earlier developmental stages, and an intrinsic ability to respond to environmental cues upon skeletal muscle regeneration.
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Project description:Optimal cell-based therapies for the treatment of muscle degenerative disorders should not only regenerate fibers, but provide a quiescent satellite cell pool ensuring long-term maintenance and regeneration. Conditional expression of Pax3/Pax7 in differentiating pluripotent stem cells (PSC) allows the generation of myogenic progenitors endowed with satellite cell-like abilities. To identify the molecular determinants underlying their regenerative potential, we performed transcriptome analyses of these cells along with primary myogenic cells from several developmental stages. Here we show that in vitro generated PSC-derived myogenic progenitors possess a molecular signature similar to embryonic/fetal myoblasts. However, compared to fetal myoblasts, following transplantation they show superior myofiber engraftment and ability to seed the satellite cell niche, respond to multiple re-injuries and contribute to long-term regeneration. Upon engraftment, the transcriptome of Pax3/Pax7-induced PSC-derived myogenic progenitors changes dramatically, acquiring similarity to that of satellite cells, particularly in genes involved in extracellular matrix remodeling. Single cell profiling reveals that these changes are induced, not selected, by the in vivo environment. These findings demonstrate that Pax3/Pax7-induced PSC-derived myogenic progenitors possess proliferative and migratory abilities characteristic of earlier developmental stages, and an intrinsic ability to respond to environmental cues upon skeletal muscle regeneration.
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