Impaired glycerophosphorylcholine synthesis in murine muscular dystrophy.

A test of some of the tenets of a proposed hypothesis on muscle phospholipid synthesis, and its possible defect in murine muscular dystrophy, shows that the cytidine pathways for the synthesis of phosphatidylcholine and phosphatidylethanolamine have a negligible flux in differentiated mouse gastrocnemius, while that of the respective proposed de novo glycerophosphodiester pathways is normally high in this muscle. Evidence is presented that de novo glycerophosphorylcholine synthesis in dystrophic mouse gastrocnemius is about half that of the wild type homozygotes, while that of the heterozygotes is near the mean of the two homozygous groups. No significant differences in rates of glycerophosphorylcholine or glycerophosphorylethanolamine synthesis were observed in brain and liver tissues among the three genotypes. These results suggest that defective de novo synthesis of glycerophosphorylcholine may be the primary biochemical lesion in murine muscular dystrophy.