The myf5 and myoD genes are implicated in the specification of vertebr
ate skeletal muscle. These genes have been thought to be functionally
redundant because neonatal mice bearing homozygous null mutations in e
ither gene show grossly normal muscle development, By analyzing the ea
rly embryonic develop ment of the mutants, Michael Rudnicki and cowork
ers show that trunk muscle development is retarded in embryos bearing
myf5 null mutations, while early limb and branchial arch muscle develo
pment 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. BioEssays 20:357
-362, 1998, (C) 1998 John Wiley & Sons, Inc.