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@ARTICLE{Gundelfinger:163766,
author = {Gundelfinger, Eckart D and Karpova, Anna and Pielot, Rainer
and Garner, Craig C. and Kreutz, Michael R.},
title = {{O}rganization of {P}resynaptic {A}utophagy-{R}elated
{P}rocesses},
journal = {Frontiers in synaptic neuroscience},
volume = {14},
issn = {1663-3563},
address = {Lausanne},
publisher = {Frontiers Research Foundation},
reportid = {DZNE-2022-00505},
pages = {829354},
year = {2022},
abstract = {Brain synapses pose special challenges on the quality
control of their protein machineries as they are far away
from the neuronal soma, display a high potential for plastic
adaptation and have a high energy demand to fulfill their
physiological tasks. This applies in particular to the
presynaptic part where neurotransmitter is released from
synaptic vesicles, which in turn have to be recycled and
refilled in a complex membrane trafficking cycle. Pathways
to remove outdated and damaged proteins include the
ubiquitin-proteasome system acting in the cytoplasm as well
as membrane-associated endolysosomal and the autophagy
systems. Here we focus on the latter systems and review what
is known about the spatial organization of autophagy and
endolysomal processes within the presynapse. We provide an
inventory of which components of these degradative systems
were found to be present in presynaptic boutons and where
they might be anchored to the presynaptic apparatus. We
identify three presynaptic structures reported to interact
with known constituents of membrane-based
protein-degradation pathways and therefore may serve as
docking stations. These are (i) scaffolding proteins of the
cytomatrix at the active zone, such as Bassoon or Clarinet,
(ii) the endocytic machinery localized mainly at the
peri-active zone, and (iii) synaptic vesicles. Finally, we
sketch scenarios, how presynaptic autophagic cargos are
tagged and recruited and which cellular mechanisms may
govern membrane-associated protein turnover in the
presynapse.},
subtyp = {Review Article},
cin = {AG Düzel / AG Garner},
ddc = {610},
cid = {I:(DE-2719)5000006 / I:(DE-2719)1810001},
pnm = {353 - Clinical and Health Care Research (POF4-353) / 351 -
Brain Function (POF4-351)},
pid = {G:(DE-HGF)POF4-353 / G:(DE-HGF)POF4-351},
typ = {PUB:(DE-HGF)16},
pmc = {pmc:PMC8968026},
pubmed = {pmid:35368245},
doi = {10.3389/fnsyn.2022.829354},
url = {https://pub.dzne.de/record/163766},
}