This article has been reviewed according to Science X's editorial process and policies. Editors have highlighted the following attributes while ensuring the content's credibility: Every movement we make, from blinking to sprinting, depends on the ability of muscle fibers to contract in a rapid and coordinated way. Achieving this precision requires an intricate internal membrane network known as the transverse tubule, or T-tubule, system.
These narrow membrane invaginations carry electrical signals from the cell surface deep into the muscle fiber, where they trigger the release of calcium needed for contraction. Defects in T-tubules are a common feature of several inherited and acquired muscle disorders. Yet a fundamental question has remained: How do these membrane structures grow during muscle development without becoming excessive or disorganized?
A new study from the group led by Edgar Gomes at GIMM provides an unexpected answer. Rather than promoting T-tubule growth, a specialized actin network acts as a molecular brake, preventing the membrane system from expanding excessively and helping muscle fibers develop the architecture required for coordinated contraction. The research is published in the journal Science Advances.
T-tubules dramatically increase the surface area of muscle fibers, allowing electrical impulses to rapidly reach the interior of these exceptionally large cells. They form highly organized structures called triads, where each T-tubule is flanked by two compartments of the sarcoplasmic reticulum. These structures create the sites where calcium is rapidly released to trigger muscle contraction.
Because this architecture is so precisely organized, its formation requires tight regulation. However, the molecular mechanisms controlling T-tubule growth have remained poorly understood. Using live-cell microscopy, cryo-electron tomography, genetic manipulation and functional analyses of muscle contraction, the researchers discovered that T-tubules are more dynamic than previously appreciated.
Rather than expanding continuously, their growth is tightly restrained by the cortical actin network, a dense meshwork of actin filaments located just beneath the plasma membrane. The team found that this restraint depends on a specific version of the Arp2/3 complex, a protein complex that organizes branched actin networks. In particular, Arp2/3 complexes containing the Arpc5 subunit act as gatekeepers, preventing excessive T-tubule growth.
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