| http://purl.uniprot.org/citations/24055173 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/24055173 | http://www.w3.org/2000/01/rdf-schema#comment | "Skeletal myogenesis in the embryo is regulated by the coordinated expression of the MyoD family of muscle regulatory factors (MRFs). MyoD and Myf-5, which are the primary muscle lineage-determining factors, function in a partially redundant manner to establish muscle progenitor cell identity. Previous diphtheria toxin (DTA)-mediated ablation studies showed that MyoD+ progenitors rescue myogenesis in embryos in which Myf-5-expressing cells were targeted for ablation, raising the possibility that the regulative behavior of distinct, MRF-expressing populations explains the functional compensatory activities of these MRFs. Using MyoD(iCre) mice, we show that DTA-mediated ablation of MyoD-expressing cells results in the cessation of myogenesis by embryonic day 12.5 (E12.5), as assayed by myosin heavy chain (MyHC) and Myogenin staining. Importantly, MyoD(iCre/+);R26(DTA/+) embryos exhibited a concomitant loss of Myf-5+ progenitors, indicating that the vast majority of Myf-5+ progenitors express MyoD, a conclusion consistent with immunofluorescence analysis of Myf-5 protein expression in MyoD(iCre) lineage-labeled embryos. Surprisingly, staining for the paired box transcription factor, Pax7, which functions genetically upstream of MyoD in the trunk and is a marker for fetal myoblasts and satellite cell progenitors, was also lost by E12.5. Specific ablation of differentiating skeletal muscle in ACTA1Cre;R26(DTA/+) embryos resulted in comparatively minor effects on MyoD+, Myf-5+ and Pax7+ progenitors, indicating that cell non-autonomous effects are unlikely to explain the rapid loss of myogenic progenitors in MyoD(iCre/+);R26(DTA/+) embryos. We conclude that the vast majority of myogenic cells transit through a MyoD+ state, and that MyoD+ progenitors are essential for myogenesis and stem cell development."xsd:string |
| http://purl.uniprot.org/citations/24055173 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.ydbio.2013.09.012"xsd:string |
| http://purl.uniprot.org/citations/24055173 | http://purl.uniprot.org/core/author | "Yamamoto M."xsd:string |
| http://purl.uniprot.org/citations/24055173 | http://purl.uniprot.org/core/author | "Wood W.M."xsd:string |
| http://purl.uniprot.org/citations/24055173 | http://purl.uniprot.org/core/author | "Goldhamer D.J."xsd:string |
| http://purl.uniprot.org/citations/24055173 | http://purl.uniprot.org/core/author | "Etemad S."xsd:string |
| http://purl.uniprot.org/citations/24055173 | http://purl.uniprot.org/core/date | "2013"xsd:gYear |
| http://purl.uniprot.org/citations/24055173 | http://purl.uniprot.org/core/name | "Dev Biol"xsd:string |
| http://purl.uniprot.org/citations/24055173 | http://purl.uniprot.org/core/pages | "114-127"xsd:string |
| http://purl.uniprot.org/citations/24055173 | http://purl.uniprot.org/core/title | "MyoD-expressing progenitors are essential for skeletal myogenesis and satellite cell development."xsd:string |
| http://purl.uniprot.org/citations/24055173 | http://purl.uniprot.org/core/volume | "384"xsd:string |
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