EndophilinA-dependent coupling between activity-dependent calcium influx and synaptic autophagy is disrupted by a Parkinson-risk mutation

Bademosi, Adekunle T.; Decet, Marianna; Kuenen, Sabine; Calatayud, Carles; Swerts, Jef; Gallego, Sandra F; Schoovaerts, Nils; Louros, Nikolaos; Martin, Ella; Karamanou, Spyridoula; Sibarita, Jean‐Baptiste; Vints, Katlijn; Gounko, Natalia V.; Meunier, Frédéric A.; Economou, Anastassios; Versées, Wim; Rousseau, Frédéric; Schymkowitz, Joost; Soukup, Sandra‐Fausia; Verstreken, Patrik

doi:10.1101/2022.04.29.490010

Cited by 2 publications

(1 citation statement)

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“…The work from Decet and Verstreken summaries our current understanding of autophagosomal biogenesis at presynaptic terminals and how autophagy is connected to neurotransmission ( Decet and Verstreken ). Autophagosomal biogenesis is induced at presynaptic terminals by metabolic signals (e.g., Amino acid deprivation) and prolonged neuronal activity and it is locally regulated by presynaptic enriched proteins ( Soukup et al, 2016 ; Okerlundk et al, 2017 ; Vanhauwaert et al, 2017 ; Bademosi et al, 2022 ; Hernandez-Diaz et al, 2022 ). The authors discuss the complex relationship between autophagy and neurotransmission, and review how autophagy at presynaptic terminals modulates neurotransmission via synaptic vesicle turnover/recycling and intracellular calcium buffering via tubular ER.…”

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confidence: 99%

Editorial: Autophagy in the central nervous system: Focus on neurons, glia and neuron-glia interactions

Jimenez‐Sanchez

Pampliega²,

Soukup³

2022

Front. Cell Dev. Biol.

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Editorial on the Research Topic Autophagy in the central nervous system: Focus on neurons,glia and neuron-glia interactions Autophagy is a fundamental catabolic recycling process of the cell and plays an essential role in brain physiology and pathology. We can differentiate three major autophagy types that all degrade there cargo via the endo-lysosomal system; chaperone-mediated autophagy (CMA), microautophagy, and macroautophagy. CMA and microautophagy use cytosolic chaperone proteins to transport proteins directly to lysosomes or endosomes respectively. CMA requires the LAMP2A receptor on lysosomes for substrate binding, while microautophagy transfers the cargo by invagination of lysosomal and endosomal membranes. In contrast, macroautophagy (here after called autophagy) consists in the formation of an autophagic membrane that engulfs cytoplasmic material that than fuses with the lysosome to degrade the content.In this Research Topic, we bring together, a collection of articles that highlight the role of autophagy in the brain with particular view on neurons, neuroglia and synaptic compartments, dysregulation of autophagy in neurodegeneration, methods to detect, analyze and quantify autophagy as well as points of therapeutic opportunities in neurodegenerative disease.In neurons, autophagy presents cell specific adaptations. Neurons are highly polarized post-mitotic cells that are particularly sensitive to oxidative stress and the accumulation of dysfunctional and toxic proteins. Moreover, presynaptic compartments can lay sometimes fare away from the soma, have limited local translation mechanisms and these compartments host the areas where synaptic vesicles fuse with the plasma membrane to release neurotransmitter for communication with post synaptic site. The work from Decet and Verstreken summaries our current understanding of

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mentioning

confidence: 99%

Editorial: Autophagy in the central nervous system: Focus on neurons, glia and neuron-glia interactions

Jimenez‐Sanchez

Pampliega²,

Soukup³

2022

Front. Cell Dev. Biol.

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Synaptogyrin regulates neuronal activity dependent autophagy to degrade synaptic vesicle components and pathological Tau

Hernandez-Diaz,

Martinez-Olondo,

Sanchez-Mirasierra

et al. 2023

Preprint

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Synapses are specialized neuronal compartments essential for brain communication. Neuronal communication mostly relies on the adequate supply and renovation of synaptic vesicles that fuse with the plasma membrane and release neurotransmitters in response to action potentials. Autophagy is an evolutionary conserved cellular mechanism essential for homeostasis that can be locally regulated in the neuronal synapse. However, the precise mechanisms controlling synaptic autophagy, especially during neuronal communication and pathological scenarios, remain elusive. Here, we report that neuronal activity and amino-acid deprivation regulate synaptic autophagy via distinct molecular mechanisms. We show that Synaptogyrin, a highly abundant presynaptic protein found in synaptic vesicles, is a novel negative regulator of synaptic autophagy in response to neuronal activity without affecting autophagy induction via amino-acid deprivation. We demonstrate that loss of Synaptogyrin modifies the localization of the autophagy protein Atg9 and boosts autophagosome formation at the synapse. Furthermore, activation of synaptic autophagy by loss of Synaptogyrin, but not by amino acid deprivation, leads to the degradation of synaptic vesicle components via autophagy. Reducing the levels of Synaptogyrin results in the degradation of synaptic TAU via autophagy and restores autophagy dysfunction observed in a Drosophila Tau model of Frontotemporal Dementia (FTD). Our data provide novel and valuable information to understand how autophagy is regulated at the synapse in response to neuronal activity and how this process participates in neuronal (dys)function.

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EndophilinA-dependent coupling between activity-dependent calcium influx and synaptic autophagy is disrupted by a Parkinson-risk mutation

Cited by 2 publications

References 109 publications

Editorial: Autophagy in the central nervous system: Focus on neurons, glia and neuron-glia interactions

Editorial: Autophagy in the central nervous system: Focus on neurons, glia and neuron-glia interactions

Synaptogyrin regulates neuronal activity dependent autophagy to degrade synaptic vesicle components and pathological Tau

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