Back

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.

2024-08-13 cell biology
10.1101/2024.08.13.607563 bioRxiv
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.

Matching journals

The top 5 journals account for 50% of the predicted probability mass.

50% of probability mass above

"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.