Little is known about how CFTR, the Cl⁻ channel that is mutated in cystic fibrosis, interacts with lipids. Abu-Arish et al. show that agents that stimulate salt and fluid secretion reduce CFTR lateral mobility and promote its clustering into ceramide-rich platforms, thereby increasing its surface expression.

Ca²⁺ flux into axon terminals via Ca_V2.1 is the trigger for neurotransmitter release at neuromuscular junctions and many central synapses. Our data raise the possibility that an arginine to proline substitution at residue 1,673 causes a severe neurodevelopmental disorder by making Ca_V2.1 less sensitive to changes in membrane potential.

Muscle fiber contraction involves chemical reactions and structural changes that are sensitive to temperature. Ishii et al. show that rapid heating causes cardiac thin filament sliding, and the data could indicate that thin filaments are partially activated during diastole at mammalian body temperature.