Key result
The recessive mutant gene c in axolotl embryos causes precardiac mesoderm to fail to complete differentiation into functional muscle tissue, affecting the accumulation of actin, myosin, and tropomyosin.
Population
Embryonic myocardial cells of cardiac lethal mutant Mexican axolotls (Ambystoma mexicanum) and normal siblings
Comparison
Heavy meromyosin binding and sodium dodecyl… vs Normal embryonic hearts, nonmuscle tissues, and…
Design
Preclinical
Authors
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Axolotl c mutation models cardiac myogenesis failure; leaves open relevance to mammalian or human cardiogenesis.
The cardiac lethal mutation in Mexican axolotls impairs the accumulation and organization of key muscle proteins, including myosin and tropomyosin, leading to a failure of functional muscle tissue differentiation.
Lemanski et al. (1976) studied Cardiac lethal mutant Mexican axolotls (Ambystoma mexicanum). Recessive mutant gene c vs. Normal siblings was evaluated on Muscle protein differentiation and organization (actin, myosin, and tropomyosin). The recessive mutant gene c in axolotl embryos causes precardiac mesoderm to fail to complete differentiation into functional muscle tissue, affecting the accumulation of actin, myosin, and tropomyosin.
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