Arp2/3 iso-complexes limit t-tubule overgrowth to ensure myofiber formation and synchronous contraction
Pereira, A. R.; Soares, A. d. R.; Liu, T.; Ferreira, J. L.; Leal, G.; Faleiro, I.; Kogata, N.; Way, M.; Moores, C.; Gomes, E. R.
Show abstract
Muscle cells form a network of plasma membrane invaginations called t-tubules that control calcium release from the endoplasmic reticulum at the triads during muscle contraction. Although the importance of t-tubules for muscle physiology is well established, and abnormalities are found in multiple disorders, the mechanisms that mediate t-tubule growth are unknown. We show that the actomyosin cortex beneath the plasma membrane, regulated by Arp2/3 complexes containing Arpc5, acts as a gatekeeper for the membrane availability required for t-tubule growth. Enlarged t-tubules are formed upon disruption of Arpc5, impairing the synchronisation between plasma membrane depolarization and calcium release. Additionally, ablation of Arpc5 postnatally in myofibers results in muscle fatigue and t-tubule abnormalities, as observed in muscle disorders. We propose that the actomyosin cortex impacts muscle function, offering a potential pathophysiological mechanism for muscle disorders.
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