Molecular mechanisms of selective autophagy in Drosophila

Gohel, Raksha; Kournoutis, Athanasios; Petridi, Stavroula; Nezis, Ioannis P.

doi:10.1016/bs.ircmb.2019.08.003

Cited by 13 publications

(12 citation statements)

References 200 publications

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“…Macroautophagy (henceforth referred to as autophagy; Box 1) is a form of autophagy in which the cellular cargo becomes sequestered within a double‐membraned vesicle, termed an autophagosome. The choice of the autophagosomal content can proceed in a relatively nonselective manner (known as “bulk autophagy”) or involve the tightly regulated elimination of individual cellular components (known as “selective autophagy”), depending on the inducing factor (He & Klionsky, 2009 ; Sica et al , 2015 ; Dikic & Elazar, 2018 ; Gohel et al , 2020 ). By contrast, chaperone‐mediated autophagy (CMA) operates as a protein‐exclusive type of autophagy in which KFERQ‐like motif‐bearing proteins are first recognized by the heat‐shock cognate protein HSPA8/HSC70 and enter the lysosome for degradation, upon binding LAMP2A (lysosomal‐associated membrane protein 2A) and translocation through a channel formed by oligomerization of this protein (Kaushik & Cuervo, 2018 ).…”

Section: Introductionmentioning

confidence: 99%

Autophagy in major human diseases

et al. 2021

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Autophagy is a core molecular pathway for the preservation of cellular and organismal homeostasis. Pharmacological and genetic interventions impairing autophagy responses promote or aggravate disease in a plethora of experimental models. Consistently, mutations in autophagy-related processes cause severe human pathologies. Here, we review and discuss preclinical data linking autophagy dysfunction to the pathogenesis of major human disorders including cancer as well as cardiovascular, neurodegenerative, metabolic, pulmonary, renal, infectious, musculoskeletal, and ocular disorders.

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Section: Introductionmentioning

confidence: 99%

Autophagy in major human diseases

et al. 2021

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“…Finally, autophagy-dependent cell death is finely controlled in insects, and its role in development has been largely studied in Drosophila [178,179]. To our knowledge, pyroptosis and necroptosis have not yet been described in insects.…”

Section: Interplay Between Cell Death and Susceptibility Of Mosquito mentioning

confidence: 99%

Infection of Mammals and Mosquitoes by Alphaviruses: Involvement of Cell Death

Cappuccio

Maisse

2020

Cells

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Alphaviruses, such as the chikungunya virus, are emerging and re-emerging viruses that pose a global public health threat. They are transmitted by blood-feeding arthropods, mainly mosquitoes, to humans and animals. Although alphaviruses cause debilitating diseases in mammalian hosts, it appears that they have no pathological effect on the mosquito vector. Alphavirus/host interactions are increasingly studied at cellular and molecular levels. While it seems clear that apoptosis plays a key role in some human pathologies, the role of cell death in determining the outcome of infections in mosquitoes remains to be fully understood. Here, we review the current knowledge on alphavirus-induced regulated cell death in hosts and vectors and the possible role they play in determining tolerance or resistance of mosquitoes.

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“…The process is headed by an initiation complex (aka. Atg1 kinase complex) that conveys AMPK and Tor signalling-mediated nutritional information to other components followed by a nucleation complex (Class III phosphatidylinositol-3-kinase, PI3K) with lipid kinase activity 20,24 . This prepares membranes with phosphatidylinositol-3-phosphate (PI3P) for expansion of cup-like double membrane structures called phagophores that finally close to form autophagosomes containing to-be-degraded cytoplasmic cargoes.…”

Section: Introductionmentioning

confidence: 99%

“…This involves conjugation of Atg8a to the phagophore/autophagosome membrane on phosphatidylethanolamine (PE). Thereafter, Atg8a also contributes to organizing autophagosome fusion with lysosomes 20,24 .…”

Section: Introductionmentioning

confidence: 99%

LC3-associated phagocytosis promotes glial degradation of axon debris after injury

Szabó

Vincze

Bognar

et al. 2022

Preprint

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Glial engulfment of dead neurons and neurites after trauma, during development and in neurodegenerative diseases plays a crucial role in nervous system maintenance. Axon debris generated after traumatic injury is cleared by phagocytic glia via Draper receptor signalling in Drosophila. However, mechanisms governing the efficiency of axon debris phagocytosis and degradation have remained largely unexplored. Here we show that glial LC3-associated phagocytosis (LAP), an engulfment pathway assisted by certain components of the macroautophagy machinery, promotes clearance of degenerating axons in the Drosophila wing nerve. A LAP-specific subset of autophagy-related (Atg) genes is required in glia for efficient debris elimination, which includes members of the Atg8a (LC3) conjugation system and the Vps34 lipid kinase complex subunits UVRAG and Rubicon but not Atg14 or the Atg1 kinase complex. Atg8a and Rubicon are recruited to Rab7-positive phagosomes and Atg8a lipid conjugation is essential for debris-containing phagosome maturation. Finally, Rubicon overexpression in glia accelerates axon debris elimination. Our results reveal the critical role of LAP in glia in the clearance of neuronal debris in vivo, with important implications for the recovery of the injured nervous system.

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Molecular mechanisms of selective autophagy in Drosophila

Cited by 13 publications

References 200 publications

Autophagy in major human diseases

Autophagy in major human diseases

Infection of Mammals and Mosquitoes by Alphaviruses: Involvement of Cell Death

LC3-associated phagocytosis promotes glial degradation of axon debris after injury

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