Functional redundancy of the muscle-specific transcription factors Myf5 and myogenin

THE myogenic basic helix–loop–helix transcription factors, Myf5, MyoD, myogenin and MRF4, play key roles in skeletal muscle development 1,2 . All of them induce myogenic differentiation in cultured non-muscle cells, suggesting that they might be functionally redundant. But the genes are expressed at...

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Bibliographic Details
Published in:Nature (London) 1996-02, Vol.379 (6568), p.823-825
Main Authors: Wang, Yukang, Schnegelsberg, Patrick N. J, Dausman, Jessica, Jaenisch, Rudolf
Format: Article
Language:English
Subjects:
Animals
Base Sequence
Biological and medical sciences
Cell Line
Classical genetics, quantitative genetics, hybrids
DNA Primers
DNA, Complementary
DNA-Binding Proteins
Embryonic growth stage
Fundamental and applied biological sciences. Psychology
Genetics
Genetics of eukaryotes. Biological and molecular evolution
Helix-Loop-Helix Motifs
Humanities and Social Sciences
letter
Mice
Molecular Sequence Data
multidisciplinary
Muscle Proteins - deficiency
Muscle Proteins - genetics
Muscle Proteins - physiology
Muscular system
Myogenic Regulatory Factor 5
Myogenin - genetics
Myogenin - physiology
Ribs - abnormalities
Ribs - embryology
Rodents
Science
Science (multidisciplinary)
Skeletal system
Trans-Activators
Transcription Factors - deficiency
Transcription Factors - genetics
Transcription Factors - physiology
Vertebrata
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Summary:THE myogenic basic helix–loop–helix transcription factors, Myf5, MyoD, myogenin and MRF4, play key roles in skeletal muscle development 1,2 . 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 embryogenesis 3–6 and mice carrying a mutation in any of the genes have different phenotypes 7–13 . A rib cage defect was observed in Myf5-deficient mice, which die perinatally 7 . 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.
ISSN:0028-0836
1476-4687
DOI:10.1038/379823a0