Protein condensates as flexible platforms for membrane traffic.

With an essential role in nearly every physiological process and disease state, trafficking vesicles are fundamental to cell biology. Canonical understanding of membrane traffic has been driven by key achievements in structural biology. Nonetheless, discoveries over the past few years progressively point to the critical role of intrinsically disordered domains and proteins, which lack a well-defined secondary structure. From the initiation of endocytosis and the sequestration of synaptic vesicles to the stabilization of endoplasmic reticulum exit sites and the extension of the autophagic cup, flexible protein condensates, rich in intrinsic disorder, are increasingly implicated. While important debates about the physical nature and mechanistic interpretation of these findings remain, the significance of transient, multivalent protein assemblies in membrane traffic is increasingly clear.