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Syncrip/hnRNP Q influences synaptic transmission and regulates BMP signaling at the Drosophila neuromuscular synapse
Author(s) -
James M. Halstead,
Yong Lin,
Lita Durraine,
Russell S. Hamilton,
Graeme Ball,
G. Gregory Neely,
Hugo J. Bellen,
Ilan Davis
Publication year - 2014
Publication title -
biology open
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.936
H-Index - 41
ISSN - 2046-6390
DOI - 10.1242/bio.20149027
Subject(s) - biology , synapse , neurotransmission , neuromuscular junction , synaptic vesicle recycling , neuroscience , synaptic vesicle , postsynaptic potential , microbiology and biotechnology , synaptic pharmacology , synaptic plasticity , synaptic fatigue , vesicle , inhibitory postsynaptic potential , excitatory postsynaptic potential , receptor , genetics , membrane
Synaptic plasticity involves the modulation of synaptic connections in response to neuronal activity via multiple pathways. One mechanism modulates synaptic transmission by retrograde signals from the post-synapse that influence the probability of vesicle release in the pre-synapse. Despite its importance, very few factors required for the expression of retrograde signals, and proper synaptic transmission, have been identified. Here, we identify the conserved RNA binding protein Syncrip as a new factor that modulates the efficiency of vesicle release from the motoneuron and is required for correct synapse structure. We show that syncrip is required genetically and its protein product is detected only in the muscle and not in the motoneuron itself. This unexpected non-autonomy is at least partly explained by the fact that Syncrip modulates retrograde BMP signals from the muscle back to the motoneuron. We show that Syncrip influences the levels of the Bone Morphogenic Protein ligand Glass Bottom Boat from the post-synapse and regulates the pre-synapse. Our results highlight the RNA-binding protein Syncrip as a novel regulator of synaptic output. Given its known role in regulating translation, we propose that Syncrip is important for maintaining a balance between the strength of presynaptic vesicle release and postsynaptic translation.

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