BAR domain proteins, actin polymerization, and myosin II control fusion pore dynamics to facilitate crumpling exocytosis. Schematic model of pore expansion, stabilization, and constriction as distinct steps in a sequence that facilitates exocytosis by actomyosin-mediated membrane crumpling (MC). The pore is regulated at each step by distinct components which include branched actin polymerization, myosin II and BAR domain proteins. The I-BAR protein MIM cooperates with actin and myosin II to control fusion pore dynamics of large secretory vesicles. MIM localizes to the future fusion site on the vesicle. After fusion, the pore expands in an Arp2/3, myosin II, MIM, and CIP4-dependent manner. The pore stabilizes with a wide diameter in a MIM-dependent manner, preventing full collapse and membrane integration. SNX1 is also essential for efficient pore stabilization. Pore constriction depends on myosin II and initiates during actomyosin-mediated membrane crumpling. Orchestrated dynamics of the fusion pore is essential for membrane crumpling and insulation of the apical cell membrane during exocytosis.