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Fig. 3 | BMC Biology

Fig. 3

From: Plasma membrane integrity: implications for health and disease

Fig. 3

Plasma membrane repair pathways to seal a physical breach. Depending on the extent of damage, several different pathways can cooperatively facilitate wound closure. (a) Exocytosis can relieve membrane tension at the wound site to promote wound closure. Vesicle recruitment to the cell surface occurs through kinesin- and myosin-dependent transport and may require additional support by proteins such as MG53. At the wound site, calcium-dependent fusion machinery such as synaptotagmins (SYT) or dysferlin (DYSF) mediate vesicle fusion. (b) Patching entails inter-vesicle fusion underneath the wound site to generate a membrane patch to seal large tears. (c) Lysosomal exocytosis can promote caveolar endocytosis upon the extracellular release of cathepsins and acid sphingomyelinase (ASM). The fate of endocytosed lesions is determined upon sorting in multivesicular bodies. (d) Concentric zones of actin regulators (e.g., RHOA, myosin-II, CDC42) can form around the wound site to facilitate closure by actomyosin contractions. (e) The accumulation of vesicles, calcium-sensitive proteins (e.g., ANXA1), and mitochondria at the wound site can form a temporary plug to limit diffusion of materials between the extra- and intra-cellular environment. (f) Different annexins can assemble along the wound edge to limit wound expansion (ANXA5), induce membrane curvature (ANXA4), and generate constriction force (ANXA6) to seal a breach. (g) The ANXA7-dependent recruitment of ESCRT-III machinery to the wound site can lead to membrane scission and the release of damaged membrane

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