Exocytosis articles from across Nature Portfolio

SNARE-dependent membrane fusion underlies neurotransmission in the nervous system. Here, the authors demonstrate how, in mammalian neurons, the synaptic protein tomosyn controls secretion by increasing the energy barrier for fusion.

This study reveals functional heterogeneity at the level of exocytosis among β cells and identifies a subpopulation of β cells that make a disproportionally large contribution to insulin release from mouse islets.

Insulin secretion adapts to metabolic needs, but how this happens over the short term is not clear. Here the authors show this involves upregulation of beta-cell exocytosis and requires the SUMO-protease SENP1, which responds to redox state in a zinc-dependent manner.

Synaptotagmin-1 and -7 are calcium sensors that distinctly drive vesicular exocytosis. Here, using wild-type proteins but manipulating the composition of the target membranes, the authors show that synaptotagmin-7 is unusually robust at penetrating membranes.

Release of glutamate at high frequency involves a distinct subset of synaptic vesicles made by adaptor protein AP-3. Sorting of the phospholipid flippase ATP8A1 by AP-3 confers release at high frequency by recruiting synapsin to synaptic vesicles.

High neuronal proteostress can trigger the production of aggregate-filled exophers in C. elegans. Here authors show that such extrusion relies on aggregate-associated intermediate filaments and adaptors.

Here, we reveal functional heterogeneity among β cells and discover that readily releasable β cells (RRβs) are a subpopulation that disproportionally contributes to biphasic glucose-stimulated insulin secretion. We further show that the dysfunction of RRβs has a crucial role in the progression of diabetes.

Chiara Zurzolo brings to attention the pioneering work that established virus-infected cells as a model to study cell polarity.

Wozniak and colleagues reveal that cleavage of the lysosomal protein RILP following activation of the inflammasome enhances exosome release and regulates the trafficking of miRNAs into exosomes by FMR1.

It is now clear that key autophagy proteins possess alternative functions, distinct from their conventional roles in autophagy. Adding to this emerging field, a new study shows how ATG16L1 acts to promote plasma membrane repair following damage by pore-forming bacteria.