Abstract
The ESCRT machinery drives a diverse collection of membrane remodeling events, including multivesicular body biogenesis, release of enveloped retroviruses and both reformation of the nuclear envelope and cytokinetic abscission during mitotic exit. These events share the requirement for a topologically equivalent membrane remodeling for their completion and the cells deployment of the ESCRT machinery in these different contexts highlights its functionality as a transposable membrane-fission machinery. Here, we will examine recent data describing ESCRT-III dependent membrane remodeling and explore new roles for the ESCRT-III complex at the nuclear envelope.
Highlights
The Endosomal Sorting Complex Required for Transport (ESCRT) machinery is an evolutionarily-conserved, multisubunit membrane remodeling complex (Table 1)
Identified in yeast for its essential role in the biogenesis of intraluminal vesicles (ILVs) upon a class of endosome called the multivesicular body (MVB) [1,2,3], its roles in mammalian cells have been expanded to encompass a number of topologically equivalent membrane remodeling events
It is thought that the ESCRT-III complex provides this activity, whilst upstream ESCRT-components (ESCRT-I and ESCRT-II) coordinate this fission with the forming and sorting of ubiquitinated cargo onto the nascent ILV [4,5]
Summary
The Endosomal Sorting Complex Required for Transport (ESCRT) machinery is an evolutionarily-conserved, multisubunit membrane remodeling complex (Table 1). The ESCRT-III complex, recruited via TSG101 and ESCRT-I or by the ESCRT-III accessory protein ALIX [13,14], functions to sever the membranous stalks connecting budded virions with the plasma membrane in a manner topologically analogous to the membrane fission reaction performed to release ILVs at the MVB (Figure 1a). In addition to a pathophysiological role in viral replication, the ESCRT proteins TSG101 and ALIX are recruited to the midbody of dividing cells through interaction with the midbody protein CEP55 [17,18,19] They function to recruit the ESCRT-III complex to perform a topologically equivalent membrane fission during cytokinetic abscission (Figure 1a), allowing the separation of daughter cells and the completion of cell division [18,20,21]. This article will not focus on these www.sciencedirect.com
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