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Pax3 stimulates p53 ubiquitination and degradation independent of transcription
Xiao Dan Wang et al. PLoS One. 2011.
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Background: Pax3 is a developmental transcription factor that is required for neural tube and neural crest development. We previously showed that inactivating the p53 tumor suppressor protein prevents neural tube and cardiac neural crest defects in Pax3-mutant mouse embryos. This demonstrates that Pax3 regulates these processes by blocking p53 function. Here we investigated the mechanism by which Pax3 blocks p53 function.
Methodology/principal findings: We employed murine embryonic stem cell (ESC)-derived neuronal precursors as a cell culture model of embryonic neuroepithelium or neural crest. Pax3 reduced p53 protein stability, but had no effect on p53 mRNA levels or the rate of p53 synthesis. Full length Pax3 as well as fragments that contained either the DNA-binding paired box or the homeodomain, expressed as GST or FLAG fusion proteins, physically associated with p53 and Mdm2 both in vitro and in vivo. In contrast, Splotch Pax3, which causes neural tube and neural crest defects in homozygous embryos, bound weakly, or not at all, to p53 or Mdm2. The paired domain and homeodomain each stimulated Mdm2-mediated ubiquitination of p53 and p53 degradation in the absence of the Pax3 transcription regulatory domains, whereas Splotch Pax3 did not stimulate p53 ubiquitination or degradation.
Conclusions/significance: Pax3 inactivates p53 function by stimulating its ubiquitination and degradation. This process utilizes the Pax3 paired domain and homeodomain but is independent of DNA-binding and transcription regulation. Because inactivating p53 is the only required Pax3 function during neural tube closure and cardiac neural crest development, and inactivating p53 does not require Pax3-dependent transcription regulation, this indicates that Pax3 is not required to function as a transcription factor during neural tube closure and cardiac neural crest development. These findings further suggest novel explanations for PAX3 functions in human diseases, such as in neural crest-derived cancers and Waardenburg syndrome types 1 and 3.
© 2011 Wang et al.
Conflict of interest statement
Competing Interests: The authors have declared that no competing interests exist.
Figures

Figure 1. Pax3 negatively regulates p53 protein,…

Figure 2. Pax3 stimulates p53 degradation and…

Figure 3. Pax3 stimulates Mdm2-mediated ubiquitination of…

Figure 4. The Pax3 domains that associate…
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The role of Pax3 and Pax7 in development and cancer.
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References
Robson EJ, He SJ, Eccles MR. A PANorama of PAX genes in cancer and development. Nat Rev Cancer. 2006;6:52–62. - PubMed
Stuart ET, Kioussi C, Gruss P. Mammalian Pax Genes. Ann Rev Genet. 1994;28:219–236. - PubMed
Goulding MD, Chalepakis G, Deutsch U, Erselius JR, Gruss P. Pax-3, a novel murine DNA binding protein expressed during early neurogenesis. EMBO J. 1991;10:1135–1147. - PMC - PubMed
Auerbach R. Analysis of the developmental effects of a lethal mutation in the house mouse. J Exp Zool. 1954;127:305–329.
Bober E, Franz T, Arnold HH, Gruss P, Tremblay P. Pax-3 is required for the development of limb muscles: a possible role for the migration of dermomyotomal muscle progenitor cells. Development. 1994;120:603–612. - PubMed
Show all 60 references
Publication types
Research Support, N.I.H., Extramural
MeSH terms
Animals
Embryonic Stem Cells / metabolism
Immunoprecipitation
Mice
Microscopy, Fluorescence
PAX3 Transcription Factor
Paired Box Transcription Factors / physiology*
Proteolysis
Proto-Oncogene Proteins c-mdm2 / physiology
Real-Time Polymerase Chain Reaction
Transcription, Genetic / physiology*
Tumor Suppressor Protein p53 / metabolism*
Ubiquitination
Substances
PAX3 Transcription Factor
Paired Box Transcription Factors
Tumor Suppressor Protein p53
Pax3 protein, mouse
Mdm2 protein, mouse
Proto-Oncogene Proteins c-mdm2
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Natural products, PGC-1 α , and Duchenne muscular dystrophy
Ipek Suntar et al. Acta Pharm Sin B. 2020 May.
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Peroxisome proliferator-activated receptor γ (PPARγ) is a transcriptional coactivator that binds to a diverse range of transcription factors. PPARγ coactivator 1 (PGC-1) coactivators possess an extensive range of biological effects in different tissues, and play a key part in the regulation of the oxidative metabolism, consequently modulating the production of reactive oxygen species, autophagy, and mitochondrial biogenesis. Owing to these findings, a large body of studies, aiming to establish the role of PGC-1 in the neuromuscular system, has shown that PGC-1 could be a promising target for therapies targeting neuromuscular diseases. Among these, some evidence has shown that various signaling pathways linked to PGC-1α are deregulated in muscular dystrophy, leading to a reduced capacity for mitochondrial oxidative phosphorylation and increased reactive oxygen species (ROS) production. In the light of these results, any intervention aimed at activating PGC-1 could contribute towards ameliorating the progression of muscular dystrophies. PGC-1α is influenced by different patho-physiological/pharmacological stimuli. Natural products have been reported to display modulatory effects on PPARγ activation with fewer side effects in comparison to synthetic drugs. Taken together, this review summarizes the current knowledge on Duchenne muscular dystrophy, focusing on the potential effects of natural compounds, acting as regulators of PGC-1α.
Keywords: AAV, adeno-associated virus; AMP, adenosine monophosphate; AMPK, 5′ adenosine monophosphate-activated protein kinase; ASO, antisense oligonucleotides; ATF2, activating transcription factor 2; ATP, adenosine triphosphate; BMD, Becker muscular dystrophy; COPD, chronic obstructive pulmonary disease; CREB, cyclic AMP response element-binding protein; CnA, calcineurin a; DAGC, dystrophin-associated glycoprotein complex; DGC, dystrophin–glycoprotein complex; DMD, Duchenne muscular dystrophy; DRP1, dynamin-related protein 1; DS, Down syndrome; ECM, extracellular matrix; EGCG, epigallocatechin-3-gallate; ERRα, estrogen-related receptor alpha; FDA, U. S. Food and Drug Administration; FGF, fibroblast growth factor; FOXO1, forkhead box class-O1; GABP, GA-binding protein; GPX, glutathione peroxidase; GSK3b, glycogen synthase kinase 3b; HCT, hydrochlorothiazide; HDAC, histone deacetylase; HIF-1α, hypoxia-inducible factors; IL, interleukin; LDH, lactate dehydrogenase; MCP-1, monocyte chemoattractant protein-1; MD, muscular dystrophy; MEF2, myocyte enhancer factor 2; MSCs, mesenchymal stem cells; Mitochondrial oxidative phosphorylation; Muscular dystrophy; MyoD, myogenic differentiation; NADPH, nicotinamide adenine dinucleotide phosphate; NF-κB, nuclear factor kappa-light-chain-enhancer of activated B cells; NMJ, neuromuscular junctions; NO, nitric oxide; NOS, NO synthase; Natural product; PDGF, platelet derived growth factor; PGC-1, peroxisome proliferator-activated receptor γ coactivator 1; PPARγ activation; PPARγ, peroxisome proliferator-activated receptor γ; Peroxisome proliferator-activated receptor γ coactivator 1α; ROS, reactive oxygen species; Reactive oxygen species; SIRT1, silent mating type information regulation 2 homolog 1; SOD, superoxide dismutase; SPP1, secreted phosphoprotein 1; TNF-α, tumor necrosis factor-α; UCP, uncoupling protein; VEGF, vascular endothelial growth factor; cGMP, cyclic guanosine monophosphate; iPSCs, induced pluripotent stem cells; p38 MAPK, p38 mitogen-activated protein kinase.
© 2020 Chinese Pharmaceutical Association and Institute of Materia Medica, Chinese Academy of Medical Sciences. Production and hosting by Elsevier B.V.
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Graphical abstract

Figure 1
Speculative model of the role…

Figure 2
DMD pathogenesis and PGC-1 α…
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References
Handschin C., Spiegelman B.M. Peroxisome proliferator-activated receptor gamma coactivator 1 coactivators, energy homeostasis, and metabolism. Endocr Rev. 2006;27:728–735. - PubMed
Arany Z. PGC-1 coactivators and skeletal muscle adaptations in health and disease. Curr Opin Genet Dev. 2008;18:426–434. - PMC - PubMed
Eisele P.S., Salatino S., Sobek J., Hottiger M.O., Handschin C. The PGC-1 coactivators repress the transcriptional activity of NF-κB in skeletal muscle cells. J Biol Chem. 2012;288:2246–2260. - PMC - PubMed
Chen S.D., Yang D.I., Lin T.K., Shaw F.Z., Liou C.W., Chuang Y.C. Roles of oxidative stress, apoptosis, PGC-1α and mitochondrial biogenesis in cerebral ischemia. Int J Mol Sci. 2011;12:7199–7215. - PMC - PubMed
Lin J., Wu H., Tarr P.T., Zhang C.Y., Wu Z., Boss O. Transcriptional co-activator PGC-1α drives the formation of slow-twitch muscle fibres. Nature. 2002;418:797–801. - PubMed
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Transcriptome and epigenome diversity and plasticity of muscle stem cells following transplantation
Brendan Evano et al. PLoS Genet. 2020.
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Adult skeletal muscles are maintained during homeostasis and regenerated upon injury by muscle stem cells (MuSCs). A heterogeneity in self-renewal, differentiation and regeneration properties has been reported for MuSCs based on their anatomical location. Although MuSCs derived from extraocular muscles (EOM) have a higher regenerative capacity than those derived from limb muscles, the molecular determinants that govern these differences remain undefined. Here we show that EOM and limb MuSCs have distinct DNA methylation signatures associated with enhancers of location-specific genes, and that the EOM transcriptome is reprogrammed following transplantation into a limb muscle environment. Notably, EOM MuSCs expressed host-site specific positional Hox codes after engraftment and self-renewal within the host muscle. However, about 10% of EOM-specific genes showed engraftment-resistant expression, pointing to cell-intrinsic molecular determinants of the higher engraftment potential of EOM MuSCs. Our results underscore the molecular diversity of distinct MuSC populations and molecularly define their plasticity in response to microenvironmental cues. These findings provide insights into strategies designed to improve the functional capacity of MuSCs in the context of regenerative medicine.
Conflict of interest statement
I have read the journal's policy and the authors of this manuscript have the following competing interests: W.R. is a consultant and shareholder of Cambridge Epigenetix. T.S. is CEO and shareholder of Chronomics. All other authors declare no competing interests.
Figures

Fig 1. Head and limb-derived MuSCs display…

Fig 2. Head and limb-derived MuSCs display…

Fig 3. Head-derived MuSCs adopt a limb-like…

Fig 4. DNA methylation at enhancers partially…
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References
von Maltzahn J, Jones AE, Parks RJ, Rudnicki MA. Pax7 is critical for the normal function of satellite cells in adult skeletal muscle. Proc Natl Acad Sci. 2013;110:16474–16479. 10.1073/pnas.1307680110 - DOI - PMC - PubMed
Sambasivan R, Yao R, Kissenpfennig A, Van Wittenberghe L, Paldi A, Gayraud-Morel B et al. Pax7-expressing satellite cells are indispensable for adult skeletal muscle regeneration. Development. 2011;138:3647–3656. 10.1242/dev.067587 - DOI - PubMed
Lepper C, Partridge TA, Fan C-M. An absolute requirement for Pax7-positive satellite cells in acute injury-induced skeletal muscle regeneration. Development. 2011;138:3639–3646. 10.1242/dev.067595 - DOI - PMC - PubMed
Webster C, Blau HM. Accelerated age-related decline in replicative life-span of Duchenne muscular dystrophy myoblasts: implications for cell and gene therapy. Somat Cell Mol Genet. 1990;16:557–565. 10.1007/BF01233096 - DOI - PubMed
Blau HM, Webster C, Pavlath GK. Defective myoblasts identified in Duchenne muscular dystrophy. Proc Natl Acad Sci U S A. 1983;80:4856–4860. 10.1073/pnas.80.15.4856 - DOI - PMC - PubMed
Show all 97 references
Publication types
Research Support, Non-U.S. Gov't
MeSH terms
Animals
Cell Differentiation / genetics
Cell Lineage / genetics
Cell Plasticity / genetics*
Cell Proliferation / genetics
Epigenome / genetics*
Extremities / growth & development
Genetic Variation / genetics
Humans
Mice
Mice, Inbred C57BL
Muscle Cells / cytology
Muscle Fibers, Skeletal
Muscle, Skeletal / cytology
Myoblasts / cytology
Regeneration / genetics
Stem Cell Transplantation*
Stem Cells / cytology
Stem Cells / metabolism
Transcriptome / genetics*
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Extraocular muscle satellite cells are high performance myo-engines retaining efficient regenerative capacity in dystrophin deficiency
Pascal Stuelsatz et al. Dev Biol. 2015.
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Extraocular muscles (EOMs) are highly specialized skeletal muscles that originate from the head mesoderm and control eye movements. EOMs are uniquely spared in Duchenne muscular dystrophy and animal models of dystrophin deficiency. Specific traits of myogenic progenitors may be determinants of this preferential sparing, but very little is known about the myogenic cells in this muscle group. While satellite cells (SCs) have long been recognized as the main source of myogenic cells in adult muscle, most of the knowledge about these cells comes from the prototypic limb muscles. In this study, we show that EOMs, regardless of their distinctive Pax3-negative lineage origin, harbor SCs that share a common signature (Pax7(+), Ki67(-), Nestin-GFP(+), Myf5(nLacZ+), MyoD-positive lineage origin) with their limb and diaphragm somite-derived counterparts, but are remarkably endowed with a high proliferative potential as revealed in cell culture assays. Specifically, we demonstrate that in adult as well as in aging mice, EOM SCs possess a superior expansion capacity, contributing significantly more proliferating, differentiating and renewal progeny than their limb and diaphragm counterparts. These robust growth and renewal properties are maintained by EOM SCs isolated from dystrophin-null (mdx) mice, while SCs from muscles affected by dystrophin deficiency (i.e., limb and diaphragm) expand poorly in vitro. EOM SCs also retain higher performance in cell transplantation assays in which donor cells were engrafted into host mdx limb muscle. Collectively, our study provides a comprehensive picture of EOM myogenic progenitors, showing that while these cells share common hallmarks with the prototypic SCs in somite-derived muscles, they distinctively feature robust growth and renewal capacities that warrant the title of high performance myo-engines and promote consideration of their properties for developing new approaches in cell-based therapy to combat skeletal muscle wasting.
Keywords: Clonal growth; Cre/loxP; Duchenne muscular dystrophy; Engraftment; Extraocular muscles; FACS; Mdx(4cv); Myf5; MyoD; Myosin light chain 3F-nLacZ; Nestin-GFP; Pax3; Pax7; Renewal; Retractor bulbi; Satellite cells.
Copyright © 2014 Elsevier Inc. All rights reserved.
Figures

Fig. 1
In-situ detection, isolation and cell…

Fig. 2
Growth analysis of LIMB, DIA…

Fig. 3
Clonal analysis of LIMB, DIA…

Fig. 4
Assessment of in-vivo proliferative activity…

Fig. 5
H&E stained cross sections of…

Fig. 6
EOM SCs from dystrophin-null mdx…
All figures (7)
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Publication types
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
MeSH terms
Animals
Cell Lineage
Cell Proliferation
Cell Separation
Cell Transplantation
Disease Models, Animal
Dystrophin / deficiency
Dystrophin / physiology*
Extremities / embryology
Female
Flow Cytometry
Gene Expression Regulation, Developmental*
Male
Mice
Mice, Inbred C57BL
Mice, Inbred mdx
Mice, Transgenic
Muscle, Skeletal / embryology*
Muscular Dystrophy, Duchenne / genetics
Regeneration / physiology*
Satellite Cells, Skeletal Muscle / cytology*
Stem Cells / cytology*
Substances
Dystrophin
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