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Comparative expression profiling identifies differential roles for Myogenin and p38α MAPK signaling in myogenesis

ABSTRACT: Mitogen activated protein kinase (MAPK) signaling regulates differentiation of many cell types. During myogenesis in particular, p38a MAPK (MAPK14) phosphorylates multiple transcriptional regulators to modulate muscle-specific gene expression. Among the p38a MAPK modulated genes is the muscle-specific transcriptional regulator Myogenin (Myog) that is also essential to complete the muscle differentiation program, and while it is known that both p38a MAPK and Myog are critically required for myogenesis, the individual contribution of each of these proteins is poorly defined. Here we show that Myog expression (in the absence of p38a MAPK signaling) is sufficient to establish expression of many late markers of muscle differentiation and to mediate cell migration. However, Myog expression alone did not led to the formation of multinucleated muscle cells, highlighting a critical role for p38a MAPK in myoblast fusion. Using comparative microarray analysis we identified p38a MAPK-dependent genes that are not regulated by Myog

ORGANISM(S): Mus musculus

PROVIDER: GSE25763 | GEO | 2012/08/02

SECONDARY ACCESSION(S): PRJNA134061

REPOSITORIES: GEO

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Comparative expression profiling identifies differential roles for Myogenin and p38M-NM-1 MAPK signaling in myogenesis

Project description:Mitogen activated protein kinase (MAPK) signaling regulates differentiation of many cell types. During myogenesis in particular, p38a MAPK (MAPK14) phosphorylates multiple transcriptional regulators to modulate muscle-specific gene expression. Among the p38a MAPK modulated genes is the muscle-specific transcriptional regulator Myogenin (Myog) that is also essential to complete the muscle differentiation program, and while it is known that both p38a MAPK and Myog are critically required for myogenesis, the individual contribution of each of these proteins is poorly defined. Here we show that Myog expression (in the absence of p38a MAPK signaling) is sufficient to establish expression of many late markers of muscle differentiation and to mediate cell migration. However, Myog expression alone did not led to the formation of multinucleated muscle cells, highlighting a critical role for p38a MAPK in myoblast fusion. Using comparative microarray analysis we identified p38a MAPK-dependent genes that are not regulated by Myog We generated a stable C2C12-derived cell line (C2i-Myog) that expresses a Doxycycline (Dox)-inducible cDNA encoding Flag-tagged Myog. In this system, the chemical induction of exogenous Myog (Dox) combined with the pharmacological inhibition of p38a/b MAPK signaling by SB203580 (SB) would allow us to assess the functional contribution of these two pathways during myogenesis

2012-08-01 | E-GEOD-25763 | biostudies-arrayexpress

Muscle regeneration controlled by a designated DNA dioxygenase (Methylation-Seq)

Project description:DNA methylation plays critical roles in regulating muscle cell fate determination and myogenesis. Tet dioxygenases are responsible for active DNA demethylation. The functions of Tet proteins in muscle regeneration have not been well characterized. Here we find that Tet2 is required for complete regeneration after muscle injury. Loss of Tet2 in myoblasts leads to reduced fusion index and thinner myofibers. Tet2 activates transcription of key differentiation modulator Myogenin (MyoG) further promoting myoblast differentiation and fusion. Re-expressing of MyoG in Tet2 KO myoblasts rescues the differentiation and fusion defects. Further mechanistic analysis reveals that Tet2 facilitates the recruitment of H3K4me1 and H3K27ac, increases the chromatin accessibility, and MyoD binding on MyoG enhancer. These functions are specifically executed by Tet2, but not Tet1 and Tet3. We identified the Tet2 specific function during myogenesis and shed new lights on DNA methylation and pioneer transcription factor transcription activation.

2021-06-01 | GSE158647 | GEO

Muscle regeneration controlled by a designated DNA dioxygenase (RNA-Seq)

2021-06-01 | GSE158646 | GEO

Muscle regeneration controlled by a designated DNA dioxygenase (ATAC-Seq)

2021-06-01 | GSE158648 | GEO

Gene Expression Profiling of siRNA Knock-Down of Six1, Six4 and Myogenin in C2C12

Project description:Six1, Six4 and Myogenin are transcription factors that are known to be required for skeletal myogenesis. Currently, very little is known about the genes targeted by Six1 and Six4. Gene expression profiling when one or both transcription factors were knock-down by siRNA was performed to identify genes affected by their absence. We also hypothesized that Six1 and Six4 can work in cooperation with the myogenic regulatory factor (MRFs) family of transcription factors, such as Myogenin. Therefore, we performed the same type of experiment where the myogenin was knocked-down by siRNA to identify genes that are possibly regulated by the Six1 or Six4 in conjunction with Myogenin. C2C12 Myoblasts were transfected with siRNA against Six1, Six4, Six1 with Six4, Myogenin, or control 24h before start of differentiation. The cells were allowed to differentiate in differentiation medium for 24h and were harvested for gene expression profiling. Four replicates per siRNA were performed.

2010-07-30 | E-GEOD-19967 | biostudies-arrayexpress

Expression data from exercised-trained, myog-deleted adult mice

Project description:Although skeletal muscle metabolism is a well-studied physiological process, little is known about how it is regulated at the transcriptional level. The myogenic transcription factor myogenin is required for skeletal muscle development during embryonic and fetal life, but myogeninâs role in adult skeletal muscle is unclear. We sought to determine myogeninâs function in adult muscle metabolism. A Myog conditional allele and Cre-ER transgene were used to delete Myog in adult mice. Mice were analyzed for exercise capacity by involuntary treadmill running. To assess oxidative and glycolytic metabolism, we monitored blood glucose and lactate levels and performed histochemical analysis on muscle fibers. Surprisingly, we found that Myog-deleted mice performed significantly better than controls in high- and low-intensity treadmill running. This enhanced exercise capacity was due to more efficient oxidative metabolism during low-intensity exercise and more efficient glycolytic metabolism during high-intensity exercise. Furthermore, Myog-deleted mice had an enhanced response to long-term voluntary exercise training on running wheels. We identified several candidate genes whose expression was altered in exercise-stressed muscle of mice lacking myogenin. The results suggest that myogenin plays a critical role as a high-level transcriptional regulator to control the energy balance between aerobic and anaerobic metabolism in adult skeletal muscle. We used microarrays to detail the global program of gene expression underlying enhanced exercise endurance associated with myog-deletion and long-term exercise training. Mouse gastrocnemius muscles were selected after 6 months of myog-deletion and exercise training for RNA extraction and hybridization on Affymetrix microarrays. We chose 3 wild type and 3 myog-deleted mice that best represented the average of each larger group that was tested during our mouse exercise studies.

2010-06-08 | E-GEOD-22046 | biostudies-arrayexpress

ChIP-seq profiling of myogenin and p300 occupancy in the context of rexinoid signaling during early myogenic differentiation

Project description:Deciphering the molecular mechanisms underpinning myoblast differentiation is a critical step in developing the best strategy to promote muscle regeneration in patients suffering from muscle-related diseases. We have previously established that a rexinoid x receptor (RXR)-selective agonist enhances the differentiation and fusion of myoblasts through a direct regulation of MyoD expression, coupled with an augmentation of myogenin protein. Here, we found that RXR signaling modifies the chromatin state distribution of myogenin, promoting the binding preference of myogenin for poised enhancers and a distinct motif. We also found an association of myogenin with rexinoid-responsive gene expression and identified an epigenetic signature related to histone acetyltransferase p300. Moreover, RXR signaling instigates residue-specific histone acetylation at enhancers co-occupied by p300 and myogenin. Thus, genomic distribution of transcriptional regulators is an important designate for identifying novel targets as well as developing therapeutics that modulate epigenetic landscape in a selective manner to promote muscle regeneration.

2020-06-24 | GSE139942 | GEO

Gene Expression Profiling of siRNA Knock-Down of Six1, Six4 and Myogenin in C2C12

2010-07-05 | GSE19967 | GEO

Global and gene-specific analyses show distinct roles for Myod and Myog at a common set of promoters

Project description:We used a combination of genome-wide and promoter-specific DNA binding and expression analyses to assess the functional roles of Myod and Myog in regulating the program of skeletal muscle gene expression. Our findings indicate that Myod and Myog have distinct regulatory roles at a similar set of target genes. At genes expressed throughout the program of myogenic differentiation, Myod can bind and recruit histone acetyltransferases. At early targets, Myod is sufficient for near full expression; whereas, at late expressed genes Myod initiates regional histone modification but is not sufficient for gene expression. At these late genes, Myog does not bind efficiently without Myod, however, transcriptional activation requires the combined activity of Myod and Myog. Therefore, the role of Myog in mediating terminal differentiation is, in part, to enhance expression of a subset of genes previously initiated by Myod. Keywords: Myod, Myogenin, muscle differentiation, regulatory network, gene expression

2006-03-01 | GSE3858 | GEO

Expression data from exercised-trained, myog-deleted adult mice

Project description:Although skeletal muscle metabolism is a well-studied physiological process, little is known about how it is regulated at the transcriptional level. The myogenic transcription factor myogenin is required for skeletal muscle development during embryonic and fetal life, but myogenin’s role in adult skeletal muscle is unclear. We sought to determine myogenin’s function in adult muscle metabolism. A Myog conditional allele and Cre-ER transgene were used to delete Myog in adult mice. Mice were analyzed for exercise capacity by involuntary treadmill running. To assess oxidative and glycolytic metabolism, we monitored blood glucose and lactate levels and performed histochemical analysis on muscle fibers. Surprisingly, we found that Myog-deleted mice performed significantly better than controls in high- and low-intensity treadmill running. This enhanced exercise capacity was due to more efficient oxidative metabolism during low-intensity exercise and more efficient glycolytic metabolism during high-intensity exercise. Furthermore, Myog-deleted mice had an enhanced response to long-term voluntary exercise training on running wheels. We identified several candidate genes whose expression was altered in exercise-stressed muscle of mice lacking myogenin. The results suggest that myogenin plays a critical role as a high-level transcriptional regulator to control the energy balance between aerobic and anaerobic metabolism in adult skeletal muscle. We used microarrays to detail the global program of gene expression underlying enhanced exercise endurance associated with myog-deletion and long-term exercise training.

2010-05-29 | GSE22046 | GEO

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