Immunofluorescence studies for myosin, alpha-actinin and tropomyosin in developing hearts of normal and cardiac lethal mutant Mexican axolotls, Ambystoma mexicanum.
Recessive mutant gene c in axolotl embryos results in an absence of normal heart function. Immunofluorescence studies were done to determine the distributions of myosin, tropomyosin and alpha-actinin in the hearts of normal and mutant siblings. Anti-myosin specifically stains the A bands of myofibrils in normal hearts and reveals a progressive increase in myofibril organization with development. Mutant hearts display less staining for myosin than normal and localization is mainly in amorphous collections. Anti-alpha-actinin stains the Z lines of myofibrils in normal myocytes. Mutant cells also have significant staining for alpha-actinin but show no striations. Antitropomyosin intensely stains the I bands of myofibrils in normal cells; however, there is very little staining for tropomyosin in mutant hearts. Thus, mutant myocardial cells have reduced but significant amounts of actin (Lemanski, Mooseker, Peachey & Iyengar, 1976) and myosin, even though non-filamentous, and substantial amounts of alpha-actinin. The cells appear to contain little tropomyosin.
D000185:Actinin / Q000378:metabolism*; D000557:Ambystoma / Q000196:embryology* / Q000235:genetics; D000818:Animals; D005455:Fluorescent Antibody Technique; D006321:Heart / Q000196:embryology*; D008854:Microscopy, Electron; D009124:Muscle Proteins / Q000378:metabolism*; D009154:Mutation; D009206:Myocardium / Q000648:ultrastructure; D009210:Myofibrils / Q000648:ultrastructure; D009218:Myosins / Q000378:metabolism*; D014335:Tropomyosin / Q000378:metabolism*
D009124:Muscle Proteins; D014335:Tropomyosin; D000185:Actinin; D009218:Myosins