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Biophys J, June 2002, p. 3144-3149, Vol. 82, No. 6


*Department of Cell and Developmental Biology, University of
Pennsylvania, Philadelphia, Pennsylvania 19104-6058; and
Department of Anesthesiology, Brigham and Woman's
Hospital, Boston, Massachusetts 02115 USA
Calcium release during excitation-contraction coupling of
skeletal muscle cells is initiated by the functional interaction of the
exterior membrane and the sarcoplasmic reticulum (SR), mediated by the
"mechanical" coupling of ryanodine receptors (RyR) and
dihydropyridine receptors (DHPR). RyR is the sarcoplasmic reticulum
Ca2+ release channel and DHPR is an L-type calcium channel
of exterior membranes (surface membrane and T tubules), which acts as
the voltage sensor of excitation-contraction coupling. The two proteins communicate with each other at junctions between SR and exterior membranes called calcium release units and are associated with several
proteins of which triadin and calsequestrin are the best characterized.
Calcium release units are present in diaphragm muscles and hind limb
derived primary cultures of double knock out mice lacking both DHPR and
RyR. The junctions show coupling between exterior membranes and SR, and
an apparently normal content and disposition of triadin and
calsequestrin. Therefore SR-surface docking, targeting of triadin and
calsequestrin to the junctional SR domains and the structural
organization of the two latter proteins are not affected by lack of
DHPR and RyR. Interestingly, simultaneous lack of the two major
excitation-contraction coupling proteins results in decrease of calcium
release units frequency in the diaphragm, compared with either single
knockout mutation.
Biophys J, June 2002, p. 3144-3149, Vol. 82, No. 6
© 2002 by the Biophysical Society 0006-3495/02/06/3144/06 $2.00
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