| 2006 |
MYOG and MYOD have distinct regulatory roles at a common set of target genes in skeletal muscle. MYOD binds first and recruits histone acetyltransferases to initiate regional histone modification at late-expressed genes, but is not sufficient for their full expression. MYOG does not bind these late genes efficiently without prior MYOD binding; transcriptional activation of late genes requires the combined activity of MYOD and MYOG. Thus MYOG's role in terminal differentiation is to enhance expression of a subset of genes previously initiated by MYOD. |
Genome-wide ChIP, promoter-specific DNA binding assays, expression analysis, histone modification profiling in myoblasts/myotubes |
The EMBO journal |
High |
16437161
|
| 2018 |
Oncogenic RAS, acting through the RAF-MEK-ERK MAPK pathway, represses MYOG expression by causing ERK2-dependent promoter-proximal stalling of RNA polymerase II at the MYOG locus. MEK inhibition with trametinib removes ERK2 from the MYOG promoter, releases transcriptional stalling, and restores MYOG expression. Restored MYOG subsequently opens chromatin and establishes super-enhancers at genes required for late myogenic differentiation. |
ChIP for ERK2 and Pol II at MYOG promoter, small-molecule inhibitor treatment (trametinib), RNA-seq, ATAC-seq, xenograft tumor models |
Science translational medicine |
High |
29973406
|
| 1991 |
The MYOG (Myf4) promoter is regulated by multiple signaling pathways: (1) MyoD1, Myf5, and Myf6 transactivate the Myf4 promoter in fibroblasts; (2) serum components, bFGF, TGF-β, and EGF down-regulate Myf4 gene activity; (3) cAMP-elevating agents (dibutyryl-cAMP, forskolin, cholera toxin) inhibit the Myf4 promoter; (4) pertussis toxin (which inactivates Gi protein) stimulates Myf4 expression, indicating positive control through a Gi protein-dependent pathway. A minimal ~200 bp upstream region is sufficient for cell-type-specific expression. |
CAT/LacZ reporter assays with 5' deletion constructs, forced expression of MRFs in 10T1/2 fibroblasts, pharmacological perturbation with pertussis toxin, cholera toxin, forskolin, dibutyryl-cAMP |
The Journal of cell biology |
Medium |
1659574
|
| 2008 |
The proto-oncogene Ski is required for muscle terminal differentiation and directly activates transcription of MYOG. Ski occupies the endogenous MYOG regulatory region and activates its transcription primarily through a MEF3 site bound by Six1, not through MyoD or MEF2 binding sites. This requires direct physical interaction of Ski with Six1 and Eya3, mediated by the Dachshund homology domain of Ski. |
Conditional retroviral overexpression and knockdown of Ski in C2C12 myoblasts, ChIP at the MYOG locus, transcriptional reporter assays, co-immunoprecipitation of Ski-Six1-Eya3 complex |
The Journal of biological chemistry |
High |
19008232
|
| 2015 |
MYOD and MYOG bind to a conserved E-box element proximal to the Myomaker transcription start site and induce Myomaker transcription, thereby promoting myoblast fusion. |
Luciferase reporter assays with E-box mutants, ChIP for MYOD and MYOG at the Myomaker promoter in chicken primary myoblasts |
International journal of molecular sciences |
Medium |
26540045
|
| 2022 |
Actin-related protein 5 (Arp5) acts as an inhibitory regulator of MYOG (and MYOD) by binding to their cysteine-rich (CR) region, which overlaps with the region essential for their epigenetic/chromatin-remodeling functions. Arp5 competes with the Pbx1-Meis1 homeodomain heterodimer for binding to the CR region of MYOG, thereby disturbing MyoD-mediated chromatin remodeling. This inhibitory function is independent of the INO80 chromatin remodeling complex. In rhabdomyosarcoma, elevated Arp5 expression contributes to dysregulation of MYOG activity. |
Co-immunoprecipitation, overexpression and siRNA knockdown of Arp5 in myoblasts and RMS cells, chromatin remodeling assays, myotube formation assays, in vivo overexpression in mouse hind limbs |
eLife |
High |
35348112
|
| 2011 |
PTPLa (protein tyrosine phosphatase-like A) is required for myoblast differentiation; cells lacking PTPLa fail to differentiate into myotubes due to repressed MYOG expression. PTPLa loss does not affect MyoD levels but specifically impairs MYOG induction, placing PTPLa upstream of MYOG in the myogenic differentiation pathway. |
siRNA knockdown of PTPLa in myoblasts, Western blot and qPCR for MYOG expression, differentiation assays |
Molecular and cellular biology |
Medium |
22106411
|
| 2023 |
The transcriptional repressor TRPS1 directly restricts MYOG expression and thereby inhibits terminal myogenic differentiation. TRPS1 and MYOD1 share common genomic binding sites including the MYOG promoter; TRPS1 occupancy at the MYOG promoter represses MYOG transcription. In embryonal rhabdomyosarcoma, elevated TRPS1 (sustained by miR-1 suppression) impairs myogenic differentiation through this mechanism. |
ChIP for TRPS1 and MYOD1 at the MYOG promoter, luciferase reporter assays, TRPS1 overexpression and knockdown in myoblasts and RD cells, in vivo xenograft experiments |
Molecular therapy : the journal of the American Society of Gene Therapy |
High |
37452493
|
| 2018 |
DEC1 (Bhlhe40/STRA13) overexpression inhibits myogenic differentiation in bovine satellite cells by inhibiting MYOG promoter activity, as demonstrated by luciferase reporter assays. DEC1 overexpression reduces MYOG mRNA and protein levels. |
Adenovirus-mediated DEC1 overexpression, luciferase reporter assay of MYOG promoter, Western blot and qPCR for MYOG in bovine satellite cells |
Journal of cellular physiology |
Medium |
29350420
|
| 2022 |
CREB1 directly binds to the proximal promoter region of MYOG and activates its transcription, promoting myogenic differentiation in bovine myoblasts, as shown by dual-luciferase reporter assays. |
Dual-luciferase reporter assay with MYOG promoter constructs, CREB1 overexpression/knockdown, ChIP (inferred from promoter analysis) |
International journal of biological macromolecules |
Low |
35777504
|
| 2017 |
MYOG drives transcription of the bovine SIX1 gene indirectly via the MEF3 motif in the SIX1 promoter, as shown by EMSA, ChIP, serial deletion constructs, site-directed mutation, and siRNA interference experiments. |
EMSA, ChIP, luciferase reporter with deletion constructs and site-directed mutations, siRNA knockdown |
Scientific reports |
Medium |
28974698
|
| 2022 |
MYOG binds to E-box elements in the core promoter region (-159/+1) of the bovine Myoz2 gene and cooperates with MYOD to regulate its transcription, as demonstrated by ChIP, dual-luciferase assay, site-directed mutagenesis, and siRNA interference. |
ChIP, dual-luciferase reporter with deletion constructs and site-directed mutagenesis, siRNA interference |
Research in veterinary science |
Medium |
36191510
|
| 2022 |
MEF2A and MYOG cooperate to bind the core promoter region (-248/-56) of the bovine LATS2 gene and regulate its transcription, as identified by site-directed mutations, siRNA interference, and chromatin immunoprecipitation. |
Dual-luciferase reporter with deletion/mutation constructs, siRNA interference, ChIP |
Research in veterinary science |
Medium |
36126508
|
| 2022 |
Vitamin C (VC) promotes muscle differentiation by upregulating nuclear translocation of CSRP3, which then interacts physically with MYOG (and MYOD), linking CSRP3-MYOG interaction to VC-mediated myogenesis. |
Co-immunoprecipitation/interaction assay, nuclear fractionation, C2C12 differentiation assays, mouse muscle injury model |
Journal of agricultural and food chemistry |
Low |
35652451
|
| 2014 |
Sheep MyoG protein localizes to the nucleus when expressed in transfected cells, and forced expression of MyoG in goat embryonic fibroblasts induces desmin expression, demonstrating its myogenic trans-differentiation activity. MyoG contains a bHLH domain and lacks a signal peptide, identifying it as a non-secretory nuclear transcription factor. |
EGFP-tagged MyoG transfection with subcellular localization by fluorescence microscopy, Western blot, RT-PCR; forced expression in GEF cells with desmin immunodetection |
Molecular biology reports |
Medium |
24385300
|
| 2009 |
In zebrafish, myog (unlike mrf4) cannot rescue myogenesis in myod/myf5 double morphants, demonstrating that myog is not sufficient to activate myogenesis de novo in the absence of upstream MRFs. This places myog downstream of myod/myf5 in the zebrafish myogenic hierarchy. |
Morpholino knockdown of myod and myf5 in zebrafish, rescue experiments with forced early expression of mrf4 or myog, in vivo imaging of muscle development |
Journal of cell science |
Medium |
19193870
|
| 1999 |
No causative mutations were detected in the MYOG (myf4) coding region in 37 patients with severe congenital myopathy, indicating that coding mutations in MYOG are not a common cause of severe congenital myopathy. Additional intronic sequences (659 bp in intron 1, 498 bp in intron 2) and a variable (CA)-dinucleotide repeat in intron 2 were characterized. |
PCR amplification and automated sequencing of all three MYOG exons in 37 patients and 40 controls |
Genomics |
Low |
10329008
|