In a previous study, protein distributions in normal and dystrophic soleus and EDL were examined using polyacrylamide isoelectric focusing. Whereas normally protein distributions in these two muscles were characteristically different, in dystrophic muscles they were strikingly similar. The soleus-specific proteins were identified as the myosin light chains LCls and LC2s. The EDL-amplified proteins were the myosin light chains LC1f, LC2f, the phosphorylated form of LC2f (LC2f-P), and LC3f. In addition, evidence is presented that one protein, which had not been identified in two-dimensional gels, is parvalbumin. The decreased proportion of parvalbumin, LC2f-P, and LC3f in the dystrophic EDL was also shown in other fast-twitch muscles of the mouse. We suggest that these changes in protein distributions in dystrophic muscles reflect a loss of their acquired state of differentiation.

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The postnatal development of extrafusal fibers in the slow-twitch soleus muscle of genetically dystrophic C57BL/6J dy2J/dy2J mice and their normal age-matched controls was investigated by histochemical and quantitative methods at selected ages of 4, 8, 12, and 32 weeks. The majority of fibers in the soleus consisted of two kinds, fast-twitch oxidative-glycolytic (FOG) and slow-twitch oxidative (SO), according to reactions for alkaline-stable and acid-stable myosin ATPase and the oxidative enzyme, NADH-tetrazolium reductase. A minor population of fibers, stable for both alkaline- and acid-preincubated ATPase, but variable in staining intensity for NADH-TR, were designated "atypical" fibers. With age, the normal soleus exhibited a gradual increase in the number and proportion of SO fibers and a reciprocal, steady decline in the percentage of FOG fibers. Atypical fibers were numerous at 4 weeks, but were substantially diminished at later ages. Since total extrafusal fiber number remained relatively constant between the periods examined, this change in relative proportions reflects an adaptive transformation of fiber types characteristic of normal postnatal growth. A striking alteration in the number and distribution of fiber types was associated with the dystrophic soleus. At 4 weeks an 18% reduction in total fiber number was already noted. Subsequently, by 32 weeks a further 22% diminution in overall fiber number had occurred. With age, the absolute number and proportion of dystrophic SO fibers were drastically reduced. In contrast, the percentage of dystrophic FOG fibers increased significantly while their absolute numbers between 4 and 32 weeks remained relatively constant. Atypical fibers in the dystrophic solei were found in elevated numbers at all age groups, particularly at 12 weeks. They may, in part, represent attempts at regeneration or an intermediate stage in fiber-type transformation. Microscopically, both of the major fiber types appeared affected, albeit differently, by the dystrophic process. We suggest that a failure or retardation in the normal postnatal conversion of fiber types within the soleus muscle occurs in this murine model for muscular dystrophy.