Autophagy and the endolysosomal system in presynaptic function
| Autor: | Michael R. Kreutz, Maria Andres-Alonso, Anna Karpova |
|---|---|
| Rok vydání: | 2020 |
| Předmět: |
metabolism [Nerve Growth Factors]
Proteostasis Autophagy Synaptic plasticity Endolysosomal system Axonal boutons Presynaptic Terminals Review Synaptic vesicle metabolism [Lysosomes] 03 medical and health sciences Cellular and Molecular Neuroscience 0302 clinical medicine medicine Animals Humans ddc:610 Nerve Growth Factors Axon Molecular Biology metabolism [Synaptic Vesicles] 030304 developmental biology Pharmacology Neurons 0303 health sciences Neuronal Plasticity Chemistry Protein turnover Cell Biology metabolism [Synapses] Cell biology medicine.anatomical_structure metabolism [Neurons] metabolism [Presynaptic Terminals] Synapses Molecular Medicine Soma Synaptic Vesicles Lysosomes 030217 neurology & neurosurgery Biogenesis |
| Zdroj: | Cellular and Molecular Life Sciences Cellular and molecular life sciences, 78(6):2621-2639 Cellular and molecular life sciences 78(6), 2621-2639 (2021). doi:10.1007/s00018-020-03722-5 |
| ISSN: | 1420-9071 |
| DOI: | 10.1007/s00018-020-03722-5 |
| Popis: | The complex morphology of neurons, the specific requirements of synaptic neurotransmission and the accompanying metabolic demands create a unique challenge for proteostasis. The main machineries for neuronal protein synthesis and degradation are localized in the soma, while synaptic junctions are found at vast distances from the cell body. Sophisticated mechanisms must, therefore, ensure efficient delivery of newly synthesized proteins and removal of faulty proteins. These requirements are exacerbated at presynaptic sites, where the demands for protein turnover are especially high due to synaptic vesicle release and recycling that induces protein damage in an intricate molecular machinery, and where replacement of material is hampered by the extreme length of the axon. In this review, we will discuss the contribution of the two major pathways in place, autophagy and the endolysosomal system, to presynaptic protein turnover and presynaptic function. Although clearly different in their biogenesis, both pathways are characterized by cargo collection and transport into distinct membrane-bound organelles that eventually fuse with lysosomes for cargo degradation. We summarize the available evidence with regard to their degradative function, their regulation by presynaptic machinery and the cargo for each pathway. Finally, we will discuss the interplay of both pathways in neurons and very recent findings that suggest non-canonical functions of degradative organelles in synaptic signalling and plasticity. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full text from SpringerLink