A ribosomal defect in dystrophic hamsters.
Polysomes were isolated from the skeletal muscle, the heart, and the liver of dystrophic and normal hamsters and their protein synthesis activity was assessed in a cell-free wheat germ extract as a source factors and tRNAs. Our results show that there is a shift of the optimal magnesium concentration required for protein synthesis with polysomes from the skeletal muscle and the heart of dystrophic hamsters, as compared with control hamsters. As a consequence of this shift, polysomes from the skeletal muscle and the heart of dystrophic hamsters, were less active than normal ones at low magnesium concentrations, but more active at high magnesium concentrations. These changes in activity were age dependent since, with skeletal muscle, they were observed at 30 days and disappeared at 60 days but reappeared at 120 and 200 days. With heart polysomes, on the other hand, the changes in activity were observed at 60 days but not in younger or older animals. No change in activity was observed with liver polysomes. Similar results were obtained when endogenous mRNAs were replaced by an exogenous messenger such as poly(U). This suggests that the differences in protein synthesis activity between polysomes from dystrophic and normal hamsters are not due to changes in the endogenous mRNAs but result from a ribosomal abnormality.
D000818:Animals; D006224:Cricetinae; D007700:Kinetics; D008099:Liver / Q000648:ultrastructure; D008297:Male; D008647:Mesocricetus; D009132:Muscles / Q000648:ultrastructure; D009137:Muscular Dystrophy, Animal / Q000378:metabolism* / Q000473:pathology; D009206:Myocardium / Q000648:ultrastructure; D011072:Poly U / Q000378:metabolism; D011132:Polyribosomes / Q000378:metabolism*; D014176:Protein Biosynthesis; D012333:RNA, Messenger / Q000378:metabolism
D012333:RNA, Messenger; D011072:Poly U