Author
Listed:
- Karzan Muhammad
(Freie Universität Berlin, Institute for Biology/Genetics
NeuroCure, Charité
Present address: Max Planck Institute for Brain Research, Neocortical Circuits Lab, Max-von-Laue-Str. 4, 60438 Frankfurt, Germany)
- Suneel Reddy-Alla
(Freie Universität Berlin, Institute for Biology/Genetics
NeuroCure, Charité)
- Jan H Driller
(Freie Universität Berlin, Institut für Chemie und Biochemie /Strukturbiochmie)
- Dietmar Schreiner
(Biozentrum, University of Basel)
- Ulises Rey
(NeuroCure, Charité)
- Mathias A. Böhme
(NeuroCure, Charité)
- Christina Hollmann
(NeuroCure, Charité)
- Niraja Ramesh
(Freie Universität Berlin, Institute for Biology/Genetics)
- Harald Depner
(Freie Universität Berlin, Institute for Biology/Genetics
NeuroCure, Charité)
- Janine Lützkendorf
(NeuroCure, Charité)
- Tanja Matkovic
(Freie Universität Berlin, Institute for Biology/Genetics
NeuroCure, Charité)
- Torsten Götz
(Freie Universität Berlin, Institute for Biology/Genetics
NeuroCure, Charité)
- Dominique D. Bergeron
(NeuroCure, Charité)
- Jan Schmoranzer
(Freie Universität Berlin, Institut für Chemie und Biochemie /Strukturbiochmie
Leibniz Institut für Molekulare Pharmakologie)
- Fabian Goettfert
(Max Planck Institute for Biophysical Chemistry)
- Mathew Holt
(VIB Center for the Biology of Disease)
- Markus C. Wahl
(Freie Universität Berlin, Institut für Chemie und Biochemie /Strukturbiochmie)
- Stefan W. Hell
(Max Planck Institute for Biophysical Chemistry)
- Peter Scheiffele
(Biozentrum, University of Basel)
- Alexander M. Walter
(NeuroCure, Charité
Leibniz Institut für Molekulare Pharmakologie)
- Bernhard Loll
(Freie Universität Berlin, Institut für Chemie und Biochemie /Strukturbiochmie)
- Stephan J. Sigrist
(Freie Universität Berlin, Institute for Biology/Genetics
NeuroCure, Charité)
Abstract
Assembly and maturation of synapses at the Drosophila neuromuscular junction (NMJ) depend on trans-synaptic neurexin/neuroligin signalling, which is promoted by the scaffolding protein Syd-1 binding to neurexin. Here we report that the scaffold protein spinophilin binds to the C-terminal portion of neurexin and is needed to limit neurexin/neuroligin signalling by acting antagonistic to Syd-1. Loss of presynaptic spinophilin results in the formation of excess, but atypically small active zones. Neuroligin-1/neurexin-1/Syd-1 levels are increased at spinophilin mutant NMJs, and removal of single copies of the neurexin-1, Syd-1 or neuroligin-1 genes suppresses the spinophilin-active zone phenotype. Evoked transmission is strongly reduced at spinophilin terminals, owing to a severely reduced release probability at individual active zones. We conclude that presynaptic spinophilin fine-tunes neurexin/neuroligin signalling to control active zone number and functionality, thereby optimizing them for action potential-induced exocytosis.
Suggested Citation
Karzan Muhammad & Suneel Reddy-Alla & Jan H Driller & Dietmar Schreiner & Ulises Rey & Mathias A. Böhme & Christina Hollmann & Niraja Ramesh & Harald Depner & Janine Lützkendorf & Tanja Matkovic & Tor, 2015.
"Presynaptic spinophilin tunes neurexin signalling to control active zone architecture and function,"
Nature Communications, Nature, vol. 6(1), pages 1-15, December.
Handle:
RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms9362
DOI: 10.1038/ncomms9362
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