Quantification of tropomyosin by radioimmunoassay in developing hearts of cardiac mutant axolotls, Ambystoma mexicanum.
Recessive mutant gene c in axolotls results in a failure of embryonic heart function. Earlier morphological studies showed that the mutant myocardial cells lack organized sarcomeric myofibrils. Electrophoresis and immunofluorescent studies suggested that the mutant heart cells contain substantial amounts of actin, myosin and alpha-actinin; however, tropomyosin appeared deficient. In the present study, we employed a newly developed extremely sensitive solid-phase radioimmunoassay method to quantitate very accurately the tropomyosin levels in normal and mutant sibling hearts at early (stage 35), intermediate (stage 39) and late (stage 41) developmental stages. Our results demonstrate that cardiac mutant hearts contain significantly lower than normal quantities of antigenically detectable tropomyosin at all of the developmental stages examined. This insufficiency of tropomyosin in mutant hearts may be a primary cause at the cell level for their failure to form organized myofibrils.
D000557:Ambystoma / Q000235:genetics; D000818:Animals; D006321:Heart / Q000254:growth & development*; D009154:Mutation; D009206:Myocardium / Q000032:analysis*; D011863:Radioimmunoassay / Q000379:methods; D014335:Tropomyosin / Q000032:analysis* / Q000276:immunology
D014335:Tropomyosin