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The sarcoplasmic reticulum in ventricular myocytes is a highly dynamic, motile organelle capable of structural changes driven by microtubules and molecular motor proteins.
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The sarcoplasmic reticulum in ventricular myocytes is a dynamic, motile organelle driven by molecular motor proteins, challenging the traditional model of static SR-sarcolemma junctions.
The fidelity of excitation-contraction (EC) coupling in ventricular myocytes is remarkable, with each action potential evoking a [Ca²⁺](i) transient. The prevalent model is that the consistency in EC coupling in ventricular myocytes is due to the formation of fixed, tight junctions between the sarcoplasmic reticulum (SR) and the sarcolemma where Ca²⁺ release is activated. Here, we tested the hypothesis that the SR is a structurally inert organelle in ventricular myocytes. Our data suggest that rather than being static, the SR undergoes frequent dynamic structural changes. SR boutons expressing functional ryanodine receptors moved throughout the cell, approaching or moving away from the sarcolemma of ventricular myocytes. These changes in SR structure occurred in the absence of changes in [Ca²⁺](i) during EC coupling. Microtubules and the molecular motors dynein and kinesin 1(Kif5b) were important regulators of SR motility. These findings support a model in which the SR is a motile organelle capable of molecular motor protein-driven structural changes.
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Vega et al. (2011) studied this question. The sarcoplasmic reticulum in ventricular myocytes is a highly dynamic, motile organelle capable of structural changes driven by microtubules and molecular motor proteins.
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