Lemanski L F, Fuldner R A, Paulson D J
J Embryol Exp Morphol. 1980 Feb;55:1-15.
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.
美西螈胚胎中的隐性突变基因c会导致心脏无法正常运作。我们进行了免疫荧光研究,以确定肌球蛋白、原肌球蛋白和α-辅肌动蛋白在正常和突变体同胞心脏中的分布情况。抗肌球蛋白抗体在正常心脏中特异性地标记肌原纤维的A带,并显示随着发育肌原纤维组织逐渐增加。突变体心脏的肌球蛋白染色比正常心脏少,且定位主要在无定形聚集体中。抗α-辅肌动蛋白抗体标记正常心肌细胞中肌原纤维的Z线。突变体细胞对α-辅肌动蛋白也有明显染色,但无条纹。抗原肌球蛋白抗体强烈标记正常细胞中肌原纤维的I带;然而,突变体心脏中原肌球蛋白的染色很少。因此,突变体心肌细胞中的肌动蛋白(Lemanski、Mooseker、Peachey和Iyengar,1976)和肌球蛋白含量减少但仍有可观数量,即使是非丝状的,且α-辅肌动蛋白含量也相当可观。细胞中似乎几乎没有原肌球蛋白。