Membrane fusion and budding mediate fundamental processes like intracellular trafficking, exocytosis, and endocytosis. Fusion is thought to open a nanometer-range pore that may subsequently close or dilate irreversibly, whereas budding transforms flat membranes into vesicles. Reviewing recent breakthroughs in real-time visualization of membrane transformations well exceeding this classical view, we synthesize a new model and describe its underlying mechanistic principles and functions. Fusion involves hemi-to-full fusion, pore expansion, constriction and/or closure while fusing vesicles may shrink, enlarge, or receive another vesicle fusion; endocytosis follows exocytosis primarily by closing Ω-shaped profiles pre-formed through the flat-to-Λ-to-Ω-shape transition or formed via fusion. Calcium/SNARE-dependent fusion machinery, cytoskeleton-dependent membrane tension, osmotic pressure, calcium/dynamin-dependent fission machinery, and actin/dynamin-dependent force machinery work together to generate fusion and budding modes differing in pore status, vesicle size, speed and quantity, controls release probability, synchronization and content release rates/amounts, and underlies exo-endocytosis coupling to maintain membrane homeostasis. These transformations, underlying mechanisms, and functions may be conserved for fusion and budding in general.

膜融合和出芽介导细胞内运输、胞吐作用和内吞作用等基本过程。融合被认为会打开一个纳米范围的孔，随后可能会不可逆地关闭或扩张，而出芽则将扁平膜转变为囊泡。回顾最近在膜转变实时可视化方面取得的突破，远远超出了这种经典观点，我们综合了一个新模型并描述了其基本机制原理和功能。融合涉及半到完全融合、孔扩张、收缩和/或闭合，同时融合囊泡可能收缩、扩大或接受另一个囊泡融合；胞吐作用之后的内吞作用主要是通过闭合通过扁平到Λ到Ω形状过渡预先形成的Ω形轮廓或通过融合形成。钙/SNARE依赖的融合机制、细胞骨架依赖的膜张力、渗透压、钙/动力依赖的裂变机制和肌动蛋白/动力依赖的力机制共同作用，产生孔状态、囊泡大小、速度不同的融合和出芽模式和数量，控制释放概率、同步和内容释放速率/量，并作为胞吐耦合以维持膜稳态的基础。这些转化、潜在机制和功能通常可以为融合和出芽而保守。