Induction of Myofibrillogenesis in Cardiac Mutant Axolotls by RNA from Normal Embryonic Endoderm a

Recessive mutant gene c, for “cardiac nonfunction” in the axolotl results in an absence of heart function.’ Skeletal muscle does not appear to be defective. Morphological studies comparing normal and mutant heart development from stage 34 (heart beat stage) through 41 (when mutant embryos die) have been reported? Electron microscopy reveals that normal ventricular heart myocytes contain organized sarcomeric myofibrils at stage 34-35. By stage 41, the normal ventricular myocardium shows trabeculae formation and contains well-differentiated muscle cells. The mutant myocardium does not trabeculate and remains a single cell layer in thickness. Mutant heart ventricular cells contain a few scattered thin (6 nm) and thick ( 15 nm) filaments and occasional Z bodies. Some mutant cells show a partial organization of myofilaments; however, distinct sarcomeric myofibrils are not observed. Mutant cells, instead, show amorphous proteinaceous collections in their peripheral cytoplasm where myofibrils initially organize in normal cells. Humphrey ’ performed heart transplant experiments and showed that mutant hearts transplanted into the heart regions of normal embryos began to beat. In reciprocal transplants, normal into mutant, the normal organs failed to beat. These experiments suggested that gene c might exert its effect by way of abnormal induction or inhibitory processes in the heart region of mutant embryos. It is well-established that anterior endoderm in amphibians is an important heart inductor tissue?-’ Inasmuch as Humphrey’s ’ transplantation experiments were suggestive of abnormal inductive processes in cardiac mutant embryos, we performed experiments to determine whether the cardiac defect could be corrected by culturing mutant (c/c) hearts with normal ( + / + ) anterior endoderm or by medium conditioned by the preculture of normal