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* Department of Molecular Genetics, The three adult fast myosin heavy chains
(MyHCs) constitute the vast majority of the myosin in
adult skeletal musculature, and are >92% identical.
We describe mice carrying null mutations in each of
two predominant adult fast MyHC genes, IIb and IId/x. Both null strains exhibit growth and muscle defects, but
the defects are different between the two strains and do
not correlate with the abundance or distribution of
each gene product. For example, despite the fact that
MyHC-IIb accounts for >70% of the myosin in skeletal
muscle and shows the broadest distribution of expression, the phenotypes of IIb null mutants are generally
milder than in the MyHC-IId/x null strain. In addition,
in a muscle which expresses both IIb and IId/x MyHC
in wild-type mice, the histological defects are completely different for null expression of the two genes. Most striking is that while both null strains exhibit
physiological defects in isolated muscles, the defects are
distinct. Muscle from IIb null mice has significantly reduced ability to generate force while IId null mouse
muscle generates normal amounts of force, but has altered kinetic properties. Many of the phenotypes demonstrated by these mice are typical in human muscle
disease and should provide insight into their etiology.
Department of Microbiology and Immunology, Albert Einstein College of Medicine, New
York 10461; § Department of Cell Biology and Physiology, University of Pittsburgh, Pittsburgh, Pennsylvania 15261; Department
of Physiology, University of Michigan Medical School, Ann Arbor, Michigan 48109; ¶ Department of Molecular Cellular and
Developmental Biology, University of Colorado, Boulder, Colorado 80309
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