Figure 10.

Models of bud neck abscission by ESCRT-III. The function of ESCRT-I-II (green and pink) and ESCRT-III (red, Vps2; yellow, Vps24; and blue, Snf7) are shown for different models for the mechanisms of membrane remodeling by ESCRT proteins. (A) Dome model—ESCRT-I/II complex initiates the formation of an Vps2/24 dome from the cytoplasm side. The membrane is remodeled as results of its wrapping up tightly around the dome. (B) Reverse dome model - same as the dome model only that the ESCRT-III structure is initiated from the bud lumen. The bud grows but then turn over to end up in a configuration similar to the one in the dome model. The driving force for membrane remodeling is again the tight binding to the ESCRT-III dome. (C) Stress-induced buckling model—polymerization of ESCRT-III polymers results in the accumulation of stress due to the deviation from the preferred curvature. As a result, the ESCRT-III structure is transformed from a flat 2D one to a 3D spiral. Reverse buckling than causes the abscission of the membrane. (D) Membrane-curvature deformation upon Vps2/Vps24 (light and dark gray) binding to an Snf7 filament. According to this model, the driving force for the deformation of the ESCRT-III structure is the binding of Vps2/Vps24 for the Snf7 polymer. The sporadic binding creates a locally preferred curvature that is different from that of the Snf7 polymer. This promotes the buckling of the ESCRT-III structure. Since the membrane binds the ESCRT-III structure, it is remodeled by its buckling. (E) Dynamical polymerization of ESCRT-III filaments leading to membrane ingression - In this model, the ESCRT-III structure is not static, but dynamic. Polymerization and depolymerization from the end of the ESCRT-III structure, as well as from its middle, continually contribute to monomers turnover and global structure deformation that results in the membrane remodeling.