In:
PLOS Genetics, Public Library of Science (PLoS), Vol. 18, No. 10 ( 2022-10-24), p. e1010211-
Abstract:
Changes in neurotransmitter receptor abundance at post-synaptic elements play a pivotal role in regulating synaptic strength. For this reason, there is significant interest in identifying and characterizing the scaffolds required for receptor localization at different synapses. Here we analyze the role of two C . elegans post-synaptic scaffolding proteins (LIN-2/CASK and FRM-3/FARP) at cholinergic neuromuscular junctions. Constitutive knockouts or muscle specific inactivation of lin-2 and frm-3 dramatically reduced spontaneous and evoked post-synaptic currents. These synaptic defects resulted from the decreased abundance of two classes of post-synaptic ionotropic acetylcholine receptors (ACR-16/CHRNA7 and levamisole-activated AChRs). LIN-2’s AChR scaffolding function is mediated by its SH3 and PDZ domains, which interact with AChRs and FRM-3/FARP, respectively. Thus, our findings show that post-synaptic LIN-2/FRM-3 complexes promote cholinergic synaptic transmission by recruiting AChRs to post-synaptic elements.
Type of Medium:
Online Resource
ISSN:
1553-7404
DOI:
10.1371/journal.pgen.1010211
DOI:
10.1371/journal.pgen.1010211.g001
DOI:
10.1371/journal.pgen.1010211.g002
DOI:
10.1371/journal.pgen.1010211.g003
DOI:
10.1371/journal.pgen.1010211.g004
DOI:
10.1371/journal.pgen.1010211.g005
DOI:
10.1371/journal.pgen.1010211.g006
DOI:
10.1371/journal.pgen.1010211.g007
DOI:
10.1371/journal.pgen.1010211.g008
DOI:
10.1371/journal.pgen.1010211.g009
DOI:
10.1371/journal.pgen.1010211.t001
DOI:
10.1371/journal.pgen.1010211.s001
DOI:
10.1371/journal.pgen.1010211.s002
DOI:
10.1371/journal.pgen.1010211.s003
DOI:
10.1371/journal.pgen.1010211.s004
DOI:
10.1371/journal.pgen.1010211.s005
DOI:
10.1371/journal.pgen.1010211.s006
DOI:
10.1371/journal.pgen.1010211.s007
DOI:
10.1371/journal.pgen.1010211.s008
DOI:
10.1371/journal.pgen.1010211.s009
DOI:
10.1371/journal.pgen.1010211.s010
DOI:
10.1371/journal.pgen.1010211.s011
DOI:
10.1371/journal.pgen.1010211.s012
DOI:
10.1371/journal.pgen.1010211.s013
DOI:
10.1371/journal.pgen.1010211.r001
DOI:
10.1371/journal.pgen.1010211.r002
DOI:
10.1371/journal.pgen.1010211.r003
DOI:
10.1371/journal.pgen.1010211.r004
Language:
English
Publisher:
Public Library of Science (PLoS)
Publication Date:
2022
detail.hit.zdb_id:
2186725-2
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