In the human CFTR anion channel, an hR117-hE1124 H-bond stabilizes the bursting state, and the hR117H mutation causes cystic fibrosis. Instead, in zebrafish CFTR, a zS109-zN120 H-bond stabilizes bursts through an alternative mechanism. Although serine and arginine are conserved, their interactions have evolved to increase the open probability in hCFTR.

The effect of RLC phosphorylation on Ca²⁺ sensitivity of contraction is amplified when cMyBP-C is absent from the sarcomere. These data indicate that cMyBP-C and RLC may act in concert to regulate contractility in healthy and diseased cardiac muscles.

Membrane stretch activates mechanosensitive PIEZO1 channels, but how this stimulus modulates microscopic open and shut states to increase open probability is unknown. Here, Wijerathne et al. investigate this mechanism using single channel dwell time analysis and Markov-chain modeling.

Cardiomyocyte sarcomere length (SL) variability assessed by second-harmonic generation (SHG) was significantly less than that by ANEPPS confocal fluorescence. We conclude that SHG-derived SL variability may reflect the true relaxed myocyte sarcomeric ultrastructure.

Infield and co-authors introduce an approach whereby the individual functional contribution of phosphoserine residues can be observed in real time via site-specific encoding of a caged-serine unnatural amino acid.

Charge-voltage curves of many voltage-gated ion channels exhibit hysteresis but such curves are also a direct measure of free energy of channel gating and, hence, should be path-independent. Here, we identify conditions to measure steady-state charge-voltage curves and show that these are curves are not hysteretic. ...

Striated muscle functional regulation occurs through the sequestration of myosin into the super-relaxed (SRX) state. Observing the turnover of single ATP molecules within cardiac sarcomeres defines the spatial arrangement of SRX myosin and their regulation by myosin-binding protein C.