Knowing chops from chuck: roasting myoD redundancy.
The myf5 and myoD genes are implicated in the specification of vertebrate skeletal muscle. These genes have been thought to be functionally redundant because neonatal mice bearing homozygous null mutations in either gene show grossly normal muscle development. By analyzing the early embryonic development of the mutants, Michael Rudnicki and coworkers show that trunk muscle development is retarded in embryos bearing myf5 null mutations, while early limb and branchial arch muscle development is retarded by myoD null mutations. These results indicate that the myoD and myf5 genes are not redundant but that each controls the early specification of distinct muscle cell lineages.
Department of Anatomy and Cardiovascular Research Institute, University of California, San Francisco 94143, USA. ordahl@itsa.ucsf.edu
C P
CP
Ordahl
B A
BA
Williams
D000818:Animals; D002454:Cell Differentiation / Q000235:genetics; D004268:DNA-Binding Proteins; D018507:Gene Expression Regulation, Developmental / Q000235:genetics; D051379:Mice; D018345:Mice, Knockout; D008822:Mice, Transgenic; D009124:Muscle Proteins / Q000235:genetics*; D018482:Muscle, Skeletal / Q000196:embryology*; D017570:MyoD Protein / Q000235:genetics*; D051787:Myogenic Regulatory Factor 5; D015534:Trans-Activators; D014714:Vertebrates
D004268:DNA-Binding Proteins; D009124:Muscle Proteins; C497418:Myf5 protein, mouse; D017570:MyoD Protein; D051787:Myogenic Regulatory Factor 5; D015534:Trans-Activators