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Letters to Nature
Nature 346, 567 - 569 (09 August 1990); doi:10.1038/346567a0

Regions of the skeletal muscle dihydropyridine receptor critical for excitation–contraction coupling

Tsutomu Tanabe*, Kurt G. Beam, Brett A. Adams, Tetsuhiro Niidome* & Shosaku Numa*

* Departments of Medical Chemistry and Molecular Genetics, Kyoto University Faculty of Medicine, Kyoto 606, Japan
Department of Physiology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, Colorado 80523, USA
To whom correspondence should be addressed.

IT is thought that in skeletal muscle excitation–contraction (EC) coupling, the release of Ca2+ from the sarcoplasmic reticulum is controlled by the dihydropyridine (DHP) receptor in the transverse tubular membrane, where it serves as the voltage sensor1–3. We have shown previously4 that injection of an expression plasmid carrying the skeletal muscle DHP receptor complementary DNA3 restores EC coupling and L-type calcium current that are missing in skeletal muscle myotubes from mutant mice with muscular dysgenesis5–9. This restored coupling resembles normal skeletal muscle EC coupling4, which does not require entry of extracellular Ca2+ (refs 10, 11). By contrast, injection into dysgenic myotubes of an expression plasmid carrying the cardiac DHP receptor cDNA12 produces L-type calcium current and cardiac-type EC coupling13, which does require entry of extracellular Ca2+ (refs 14–16). To identify the regions responsible for this important functional difference between the two structurally similar DHP receptors, we have expressed various chimaeric DHP receptor cDNAs in dysgenic myotubes. The results obtained indicate that the putative cytoplasmic region between repeats II and III of the skeletal muscle DHP receptor3 is an important determinant of skeletal-type EC coupling.

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