| First Author | An Y | Year | 2017 |
| Journal | Dev Cell | Volume | 41 |
| Issue | 4 | Pages | 382-391.e5 |
| PubMed ID | 28535373 | Mgi Jnum | J:284020 |
| Mgi Id | MGI:6389901 | Doi | 10.1016/j.devcel.2017.04.012 |
| Citation | An Y, et al. (2017) A Molecular Switch Regulating Cell Fate Choice between Muscle Progenitor Cells and Brown Adipocytes. Dev Cell 41(4):382-391.e5 |
| abstractText | During mouse embryo development, both muscle progenitor cells (MPCs) and brown adipocytes (BAs) are known to derive from the same Pax7(+)/Myf5(+) progenitor cells. However, the underlying mechanisms for the cell fate control remain unclear. In Pax7-null MPCs from young mice, several BA-specific genes, including Prdm16 and Ucp1 and many other adipocyte-related genes, were upregulated with a concomitant reduction of Myod and Myf5, two muscle lineage-determining genes. This suggests a cell fate switch from MPC to BA. Consistently, freshly isolated Pax7-null but not wild-type MPCs formed lipid-droplet-containing UCP1(+) BA in culture. Mechanistically, MyoD and Myf5, both known transcription targets of Pax7 in MPC, potently repress Prdm16, a BA-specific lineage-determining gene, via the E2F4/p107/p130 transcription repressor complex. Importantly, inducible Pax7 ablation in developing mouse embryos promoted brown fat development. Thus, the MyoD/Myf5-E2F4/p107/p130 axis functions in both the Pax7(+)/Myf5(+) embryonic progenitor cells and postnatal myoblasts to repress the alternative BA fate. |
