Résumé :
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Communication n° 104. We are studying the cellular function of triadin, a muscle protein localized specifically in the triad, but with a still obscure function. We have shown that Trisk 95 is part of a "calcium release complex", with the two calcium channels, ryanodine receptor (RyR) and dihydropyridine receptor (DHPR), and that triadin could regulate the calcium release through the RyR, stabilizing the closed state of RyR. But this function is still not clearly understood. In order to address more precisely the question "what is the role and the function of triadin", we overexpress Trisk 95 in myogenic cells. We have developed adenovirus (in collaboration with Genethon) able to express Trisk 95 in sense or antisense orientation. Using Trisk 95-adenovirus, we have induced over-expression of Trisk 95 in primary culture of rat skeletal muscle. We performed calcium imaging on infected myotubes, to study the modification of calcium release in these modified cells. We observed that in these cells, RyR and DHPR are still functional. Nevertheless, in cells over-expressing Trisk 95, the communication between both induced by cell depolarization was abolished and excitation-contraction coupling was no more functional. This effect was reverse by infection of the cells with antisense-Trisk 95 virus. This could be a new function for Trisk 95.
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