IN-VIVO PROTEIN-SYNTHESIS IN DEVELOPING HEARTS OF NORMAL AND CARDIAC MUTANT AXOLOTLS (AMBYSTOMA-MEXICANUM)

Recessive mutant gene c in axolotls causes a failure of the hearts of affected embryos to function. The mutant hearts (c/c) lack organized s arcomeric myofibrils. The present study was undertaken to determine th e overall pattern of in vivo protein synthesis and subsequent accumula tion of the newly synthesized proteins for a 24-h period in normal (+/ + or +/c) and cardiac mutant (c/c) axolotl hearts at various stages of development. Additionally, selected cytoskeletal/myofibrillar protein s were analyzed in detail for their synthesis during heart development . For such analyses, the hearts were radiolabeled with S-35-methionine for 24 h and subjected to SDS-PAGE and autoradiography. Quantitative densitometric analyses of the bands show that, even though the overall protein pattern is similar in normal and mutant heart tissues, a gene ral reduction in the synthesis of the proteins in mutant hearts is obs erved even at the earlier stages of development (stages 35-36 and 37-3 8), Synthesis and accumulation of most of the proteins is significantl y inhibited in mutant hearts at later stages (stages 41-42), Tropomyos in synthesis in mutant hearts is at a level of only 72.6% of that in n ormal embryonic hearts at stage 35. The synthesis and the accumulation of the tropomyosin in mutant hearts decreases further with increasing age until the protein essentially stops being synthesized by stage 41 .