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. 2014 Nov 25;15(12):21723–21739. doi: 10.3390/ijms151221723

Figure 1.

Figure 1

Schematic model for abscission in mammalian cells. In panel (A), CEP55 (Centrosomal protein of 55 kDa) has first recruited ESCRT-I components (Tumour susceptibility gene 101 (TSG101), apoptosis-linked gene 2-interacting protein (ALIX)) to the Flemming body, followed by the recruitment of ESCRT-III; (B) The Recruitment of the ATPase VPS4 to this assembly is proposed to mediate breakage or remodeling of the ESCRT-III, facilitating the appearance of ESCRT-III at the abscission zone (for details of different models for this event, see text); (C) Constriction at the secondary ingression site may be driven either by fusion of endosomal vesicles with the plasma membrane (inset), or by ESCRT-III interactions with the plasma membrane (see text). The possible role of lipid domains and the Rho GTPase activating protein (RhoGAP) (insert) is discussed in the text; and (D) Scission is thought to be driven by the ESCRT-III/VPS4 complex.