Functional redundancy of the muscle-specific transcription factors Myf5 and myogenin (original) (raw)
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- Published: 29 February 1996
Nature volume 379, pages 823–825 (1996)Cite this article
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Abstract
THE myogenic basic helix–loop–helix transcription factors, Myf5, MyoD, myogenin and MRF4, play key roles in skeletal muscle development1,2. All of them induce myogenic differentiation in cultured non-muscle cells, suggesting that they might be functionally redundant. But the genes are expressed at different times during embryogenesis3–6 and mice carrying a mutation in any of the genes have different phenotypes7–13. A rib cage defect was observed in Myf5-deficient mice, which die perinatally7. We investigated whether the rib cage defect was due to the failure of the early activation of the gene or to the unique interactions of Myf5 with specific downstream targets. For this we inserted a myogenin complementary DNA into the Myf5 locus by homologous recombination which simultaneously disrupted Myf5 function. We report here that mice homozygous for this myogenin gene knock-in (ki) developed a normal rib cage and were viable, therefore demonstrating functional redundancy of Myf5 and myogenin for rib formation.
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Authors and Affiliations
- Whitehead Institute for Biomedical Research and Department of Biology, Massachusetts Institute of Technology, Nine Cambridge Center, Cambridge, Massachusetts, 02142, USA
Yukang Wang, Patrick N. J. Schnegelsberg, Jessica Dausman & Rudolf Jaenisch
Authors
- Yukang Wang
You can also search for this author inPubMed Google Scholar - Patrick N. J. Schnegelsberg
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Wang, Y., Schnegelsberg, P., Dausman, J. et al. Functional redundancy of the muscle-specific transcription factors Myf5 and myogenin.Nature 379, 823–825 (1996). https://doi.org/10.1038/379823a0
- Received: 25 October 1995
- Accepted: 08 January 1996
- Issue Date: 29 February 1996
- DOI: https://doi.org/10.1038/379823a0