The ESCRT-III isoforms CHMP2A and CHMP2B display different effects on membranes upon polymerization

Alqabandi, Maryam; Franceschi, Nicola De; Maity, Sourav; Miguet, Nolwenn; Bally, Marta; Roos, Wouter H.; Weissenhorn, Winfríed; Bassereau, Patricia; Mangenot, Stéphanie

doi:10.1186/s12915-021-00983-9

Cited by 21 publications

(12 citation statements)

References 89 publications

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“…1(a). Additionally, although monomers of different types share a similar molecular structure [2,5], polymers of different ESCRT-III monomers have been observed to have different shapes and different membrane binding interfaces, depending on their precise monomer composition [5,[12][13][14][15][16][17]. Therefore, as the copolymers change in composition, their geometry and mechanical properties are also expected to change, allowing the ESCRT-III to perform work on the membrane [8,[18][19][20][21].…”

mentioning

confidence: 99%

Mechanochemical Rules for Shape-Shifting Filaments that Remodel Membranes

et al. 2022

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mentioning

confidence: 99%

Mechanochemical Rules for Shape-Shifting Filaments that Remodel Membranes

et al. 2022

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“…In the last few years, a great deal of research work has been performed in order to understand how membrane constriction and scission is mediated by the ESCRT-III machinery (reviewed in [40,61,62]). Important advances in the field were achieved by using in vitro reconstitution studies using purified ESCRT subunits [44,47,59,[63][64][65]. These allowed investigation of the structures, molecular properties, and interplay of various ESCRT-III filaments.…”

Section: Mechanism Of Escrt-iii Membrane Remodelingmentioning

confidence: 99%

The ESCRT Machinery: Remodeling, Repairing, and Sealing Membranes

Olmos

2022

Membranes

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The ESCRT machinery is an evolutionarily conserved membrane remodeling complex that is used by the cell to perform reverse membrane scission in essential processes like protein degradation, cell division, and release of enveloped retroviruses. ESCRT-III, together with the AAA ATPase VPS4, harbors the main remodeling and scission function of the ESCRT machinery, whereas early-acting ESCRTs mainly contribute to protein sorting and ESCRT-III recruitment through association with upstream targeting factors. Here, we review recent advances in our understanding of the molecular mechanisms that underlie membrane constriction and scission by ESCRT-III and describe the involvement of this machinery in the sealing and repairing of damaged cellular membranes, a key function to preserve cellular viability and organellar function.

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“…CHMP3/Vps24 is an ESCRT-III protein that interacts with CHMP2A and promotes CHMP2A binding to membranes [73]. CHMP2A and CHMP3 form helical polymers that contribute the ability of ESCRT-III proteins to constrict membranes to facilitate membrane fission events in the cell [74].…”

Section: Escrt-iii Alternative Splicing Inhibits Autophagy-mediated Cell Death In Yeastmentioning

confidence: 99%

Adding Some “Splice” to Stress Eating: Autophagy, ESCRT and Alternative Splicing Orchestrate the Cellular Stress Response

Habib

Cook

Mathavarajah

et al. 2021

Genes

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Autophagy is a widely studied self-renewal pathway that is essential for degrading damaged cellular organelles or recycling biomolecules to maintain cellular homeostasis, particularly under cellular stress. This pathway initiates with formation of an autophagosome, which is a double-membrane structure that envelopes cytosolic components and fuses with a lysosome to facilitate degradation of the contents. The endosomal sorting complexes required for transport (ESCRT) proteins play an integral role in controlling autophagosome fusion events and disruption to this machinery leads to autophagosome accumulation. Given the central role of autophagy in maintaining cellular health, it is unsurprising that dysfunction of this process is associated with many human maladies including cancer and neurodegenerative diseases. The cell can also rapidly respond to cellular stress through alternative pre-mRNA splicing that enables adaptive changes to the cell’s proteome in response to stress. Thus, alternative pre-mRNA splicing of genes that are involved in autophagy adds another layer of complexity to the cell’s stress response. Consequently, the dysregulation of alternative splicing of genes associated with autophagy and ESCRT may also precipitate disease states by either reducing the ability of the cell to respond to stress or triggering a maladaptive response that is pathogenic. In this review, we summarize the diverse roles of the ESCRT machinery and alternative splicing in regulating autophagy and how their dysfunction can have implications for human disease.

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The ESCRT-III isoforms CHMP2A and CHMP2B display different effects on membranes upon polymerization

Cited by 21 publications

References 89 publications

Mechanochemical Rules for Shape-Shifting Filaments that Remodel Membranes

Mechanochemical Rules for Shape-Shifting Filaments that Remodel Membranes

The ESCRT Machinery: Remodeling, Repairing, and Sealing Membranes

Adding Some “Splice” to Stress Eating: Autophagy, ESCRT and Alternative Splicing Orchestrate the Cellular Stress Response

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