Syncrip/hnRNP Q influences synaptic transmission and regulates BMP signaling at the Drosophila neuromuscular synapse
James M. Halstead,
Yong Qi Lin,
Lita Durraine,
Russell S. Hamilton,
Graeme Ball,
Greg G. Neely,
Hugo J. Bellen,
Ilan Davis
Affiliations
James M. Halstead
Department of Biochemistry, South Parks Road, The University of Oxford, Oxford OX1 3QU, UK
Yong Qi Lin
Howard Hughes Medical Institute, Department of Molecular and Human Genetics, Department of Neuroscience, Program in Developmental Biology, Neurological Research Institute at Baylor College of Medicine, Houston, TX 77030, USA
Lita Durraine
Howard Hughes Medical Institute, Department of Molecular and Human Genetics, Department of Neuroscience, Program in Developmental Biology, Neurological Research Institute at Baylor College of Medicine, Houston, TX 77030, USA
Russell S. Hamilton
Department of Biochemistry, South Parks Road, The University of Oxford, Oxford OX1 3QU, UK
Graeme Ball
Micron Imaging Facility, Department of Biochemistry, South Parks Road, The University of Oxford, Oxford OX1 3QU, UK
Greg G. Neely
Neuroscience Program, Garvan Institute of Medical Research, Darlinghurst, Sydney, NSW 2010, Australia
Hugo J. Bellen
Howard Hughes Medical Institute, Department of Molecular and Human Genetics, Department of Neuroscience, Program in Developmental Biology, Neurological Research Institute at Baylor College of Medicine, Houston, TX 77030, USA
Ilan Davis
Department of Biochemistry, South Parks Road, The University of Oxford, Oxford OX1 3QU, UK
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.
