Force-expression of Cardiac Troponin I in C2C12 Skeletal Myoblasts Suppresses Myoblast Fusion and Induces Actin Bundle Network Formation
In cardiac muscle of the chicken, slow skeletal form of troponin I (STnI) is initially expressed in the embryo, but it is later replaced by the cardiac form (CTnI). In contrast, in fast and slow skeletal muscles, CTnI is never expressed throughout the course of development. To examine how such a nor...
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Published in | Proceedings of the Japan Academy, Series B Vol. 73; no. 10; pp. 215 - 218 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
The Japan Academy
1997
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Subjects | |
Online Access | Get full text |
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Summary: | In cardiac muscle of the chicken, slow skeletal form of troponin I (STnI) is initially expressed in the embryo, but it is later replaced by the cardiac form (CTnI). In contrast, in fast and slow skeletal muscles, CTnI is never expressed throughout the course of development. To examine how such a normally absent cardiac isoform behaves in embryonic skeletal muscle if force-expressed, we established several C2C12 skeletal muscle cell lines that stably express CTnI. We used CTnI/9, whose amino acid sequence corresponds to 90% of that of CTnI. In all of these clones, fusion of myoblasts to form myotubes was inhibited. In a clone expressing CTnI/9 at the highest level, networks of thick actin bundles were found. Thus, expression of the TnI isoform, specific for adult cardiac muscle and absent in embryonic skeletal muscle, disturbs normal myogenic differentiation and myofibrillogenesis in skeletal muscle cells. |
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ISSN: | 0386-2208 1349-2896 |
DOI: | 10.2183/pjab.73.215 |