A possible mechanism of phenotypic expression of normal and dystrophic genomes on succinic dehydrogenase activity and fiber size within a single myofiber of muscle transplants.

Muscle transplantation was used to evaluate the ability of normal and dystrophic chickens to support regeneration of both normal and dystrophic muscle fragments. Pectoralis muscles were grafted into the site of the biceps muscle of host chickens. Identification of dystrophic characteristics of intact and regenerating muscle fibers was made by cytochemical analysis of mitochondrial succinic dehydrogenase (SDH) and by fiber size. In the biceps muscle of dystrophic chicks at 40 days ex ovo, the mean size of muscle fibers with low activity of SDH and fibers with high SDH activity was 29.0 +/- 5.9 micrometers and 42.0 +/- 10.4 micrometers, respectively. The mean size of normal muscle fibers was notably smaller than in dystrophic muscle and was 17.8 + 3.1 micrometers. The hypertrophy of fibers coupled with elevation of SDH activity tended to increase with age. Transplants were examined at 56 days postoperatively. The results of cross-transplantation between normal and dystrophic genotypes were similar to unoperated muscles in the correlation between SDH activity and fiber size. Donor muscles determined the type of myofibers regenerated in transplants regardless of whether the host was normal or dystrophic. In addition, combined transplantation was attempted to produce a single hybrid myofiber in which normal and dystrophic pectoralis muscle were mixed in equal volume. The mixtures were then allowed to regenerate in host chicks. A number of mosaic myofibers appeared in transplants and had regional differences in SDH activity along their length. It was concluded that: (1) The characteristics of high SDH activity and fiber hypertrophy are an expression of dystrophic nuclei, (2) combined transplantation of both normal and dystrophic muscle fragments can produce mosaic myofibers in SDH reaction; and (3) the local control of SDH activity and fiber size within nuclear territories in mosaic myofibers seems likely to be due to phenotypic expression of either normal or dystrophic genomes.