The Huntingtin protein, well known for its involvement in the neurodegenerative Huntington’s disease, is also expressed in skeletal muscle. The work presented here is dedicated to a better understanding of its function in skeletal muscle through the development and characterization of KO models.

Control of muscle contraction is still not understood. Here, we image fluorescently tagged ATP with single-molecule precision to reveal the activity of individual myosins in different sarcomeric locations. We show how treatment with PKA and the FDA-approved drug mavacamten affects relaxed myofibrils.

The automaticity of human-induced pluripotent stem cell–derived cardiomyocytes is regulated by a coupled-clock system of the Ca²⁺ and membrane clocks. We found that the coupled-clock system is regulated by local Ca²⁺ releases and cAMP/PKA-dependent coupling of the Ca²⁺ clock to the membrane clock.

The dominant models explaining potassium channel gating often invoke widening and narrowing of the helix bundle crossing. This paper shows that a closely related channel, NaK, is not gated by this mechanism as the helix bundle crossing in the nonconducting channel is already open.

Optical activation of channel rhodopsin is used to increase neuronal activity. In cerebellar interneurons, it actually leads to a biphasic activation/inhibition sequence. In these cells, activation of KCa1.1 channels contributes to the post-stimulus inhibition.

Mutations in essential components for depolarization-induced Ca²⁺ release (DICR) are implicated into various skeletal muscle diseases. Murayama et al. establish a reconstituted DICR platform in nonmuscle cells for validation of disease-causing mutations and drug discovery.

Claudins in tight junctions form ion channels that regulate paracellular permeability. We use molecular dynamics simulations of claudin-15 strands formed by up to 300 monomers to uncover the molecular mechanism of strand flexibility.