same cell. While the full scope of causes for this diversity is unknown, tension on the plasma membrane is a likely contributor, as each endocytosis event necessitates induced membrane curvature. Our results demonstrate that increased membrane tension impedes clathrin-mediated endocytosis (CME) through inhibition of initiation, formation and dissolution of clathrin-coated structures, and endocytic dynamics rapidly and locally reflect changes in membrane tension due to pharmacological and mechanical stimuli. We found that spatial and temporal heterogeneities in clathrin coat dynamics mark the tension gradients arising during cell spreading and migration. Spatiotemporal variations in CME are also observed during morphological changes shaping development of multicellular organisms. Collectively, our findings suggest that tension gradients in tissues can lead to patterning and differentiation through mechanoregulation of CME.

No abstract

Many diseases are associated with aberrant protein aggregation. Recently, there has been resurgent interest in co-opting the framework of phase transitions to understand the distinct concentration thresholds separating different phases of aggregation-prone molecules. This analogy, which was purely conceptual, has now been shown to have quantitative significance.