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Autophagy and the endolysosomal system in presynaptic function. | LitMetric

Autophagy and the endolysosomal system in presynaptic function.

Cell Mol Life Sci

Research Group Neuroplasticity, Leibniz Institute for Neurobiology, 39118, Magdeburg, Germany.

Published: March 2021

AI Article Synopsis

  • Neurons face a unique challenge in maintaining protein balance due to their complex structure and the distance between protein synthesis (in the soma) and synaptic sites, which require efficient transport and removal of proteins.
  • The primary systems involved in managing this protein turnover at presynaptic sites are autophagy and the endolysosomal system, both crucial for handling damaged proteins generated during synaptic activity.
  • Recent research highlights not only the roles of these pathways in degradation but also their new non-conventional functions in synaptic signaling and plasticity, showing a complex interplay in neuronal function.

Article Abstract

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.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8004491PMC
http://dx.doi.org/10.1007/s00018-020-03722-5DOI Listing

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