Minor sarcoplasmic reticulum membrane components that modulate excitation–contraction coupling in striated muscles

Authors


  • This review was presented at The Journal of Physiology Symposium on Calsequestrin, triadin and more: the proteins that modulate calcium release in cardiac and skeletal muscle, which took place at the 53rd Biophysical Society Annual Meeting at Boston, MA, USA on 27 February 2009. It was commissioned by the Editorial Board and reflects the views of the authors.

Corresponding author F. Zorzato: Department of Experimental and Diagnostic Medicine, University of Ferrara, Via Borsari 46, 44100 Ferrara, Italy. Email: zor@unife.it

Abstract

In striated muscle, activation of contraction is initiated by membrane depolarisation caused by an action potential, which triggers the release of Ca2+ stored in the sarcoplasmic reticulum by a process called excitation–contraction coupling. Excitation–contraction coupling occurs via a highly sophisticated supramolecular signalling complex at the junction between the sarcoplasmic reticulum and the transverse tubules. It is generally accepted that the core components of the excitation–contraction coupling machinery are the dihydropyridine receptors, ryanodine receptors and calsequestrin, which serve as voltage sensor, Ca2+ release channel, and Ca2+ storage protein, respectively. Nevertheless, a number of additional proteins have been shown to be essential both for the structural formation of the machinery involved in excitation–contraction coupling and for its fine tuning. In this review we discuss the functional role of minor sarcoplasmic reticulum protein components. The definition of their roles in excitation–contraction coupling is important in order to understand how mutations in genes involved in Ca2+ signalling cause neuromuscular disorders.

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