BEGIN:VCALENDAR VERSION:2.0 PRODID:-//132.216.98.100//NONSGML kigkonsult.se iCalcreator 2.20.4// BEGIN:VEVENT UID:20260312T132601EDT-8237rVOnOG@132.216.98.100 DTSTAMP:20260312T172601Z DESCRIPTION:Mechanisms of load adaptation by endocytic actin networks\n\nMa tthew Akamatsu\, University of Washington\n Tuesday March 24\, 12-1pm\n Zoom Link: https://mcgill.zoom.us/j/87078928687\n In Person: 550 Sherbrooke\, R oom 189\n \n Abstract: Self-organization is a hallmark of biological process es wherein local (neighboring) interactions constrained by the geometrical environment and physical laws give rise to emergent architectures and ada ptive behaviors. In clathrin-mediated endocytosis\, branched actin cytoske letal networks deform the cell’s plasma membrane against tension to intern alize cargo. Characteristic of self-organizing systems\, these networks ad apt their size and architecture under high load to increase force-producin g capability. However\, the mechanisms that govern this mechano-adaptation remain poorly understood. Our lab combines biophysical modeling\, quantit ative microscopy of gene-edited human stem cells\, and high-resolution ima ge analysis to investigate cytoskeletal self-organization and load adaptat ion in mammalian endocytosis.\n\nA minimal biophysical model recapitulated the mechano-adaptive behavior of these endocytic cytoskeletal networks. S imulations predicted that under elevated load\, endocytic actin networks r espond by nucleating actin filaments and shifting their orientations to a more load-bearing arrangement. To test this prediction\, we used quantitat ive lattice light-sheet microscopy of gene-edited human induced pluripoten t stem cells and transient osmotic shocks to increase membrane tension. In deed\, elevating membrane tension increased branched actin assembly and th e fraction of endocytic sites assembling an actin cytoskeleton\, specifica lly at the basal cellular surface. With simulations\, we identified severa l putative factors that contribute to load adaptation\, including the tran sient stalling of endocytic sites and force-dependent association rates be tween capping protein and actin filaments. These adaptive behaviors allow a dynamic actin cytoskeleton to robustly and reliably deform cellular memb ranes in the stochastic cellular environment.\n DTSTART:20260324T160000Z DTEND:20260324T170000Z SUMMARY:QLS Seminar Series - Matthew Akamatsu URL:/arts/channels/event/qls-seminar-series-matthew-ak amatsu-371875 END:VEVENT END:VCALENDAR