ESCRT Machinery Is Required for Plasma Membrane Repair

Abstract

Plasma membrane damage can be triggered by numerous phenomena, and efficient repair is essential for cell survival. Endocytosis, membrane patching, or extracellular budding can be used for plasma membrane repair. We found that endosomal sorting complex required for transport (ESCRT), involved previously in membrane budding and fission, plays a critical role in plasma membrane repair. ESCRT proteins were recruited within seconds to plasma membrane wounds. Quantitative analysis of wound closure kinetics coupled to mathematical modeling suggested that ESCRTs are involved in the repair of small wounds. Real-time imaging and correlative scanning electron microscopy (SEM) identified extracellular buds and shedding at the site of ESCRT recruitment. Thus, the repair of certain wounds is ensured by ESCRT-mediated extracellular shedding of wounded portions.

The autophagic machinery ensures nonlytic transmission of mycobacteria

“…Recently, a new calcium-dependent wound healing mechanism has been discovered. The endosomal sorting complexes required for transport (ESCRT) machinery has been demonstrated to catalyze the shedding of small vesicles carrying membrane wounds (31). Even though no molecular mechanism has been proposed, autophagosome interactions with the plasma membrane have been suggested to allow the release of virus particles (32) and the cell-to-cell transmission of Brucella (2).…”

Vps4 Stimulatory Element of the Cofactor Vta1 Contacts the ATPase Vps4 α7 and α9 to Stimulate ATP Hydrolysis

“…The endosomal sorting complexes required for transport (ESCRTs) 2 participate in multivesicular body (MVB) sorting in the endocytic pathway, abscission of the cellular bridge during cytokinesis, the budding of enveloped viruses, and the repair of small wounds in the plasma membrane (1)(2)(3)(4)(5). Most of these processes are similar in that cytosolic machinery (i.e.…”

Hydraulic fracturing in cells and tissues: fracking meets cell biology

“…All these functions share in common the need to constrict, fuse, and/or sever lipid membranes. The mechanism proposed to heal nuclear fracture was analogous to that used to reseal the nuclear membrane after mitosis or to repair the plasma membrane after damage [32][33][34]. Briefly, a few tens of seconds after fracture of the nuclear envelope, the central ESCRT-III subunit CHMP4B is recruited to the site of damage.…”