Opendata, web and dolomites

SynDegrade SIGNED

The Role of Local Protein Degradation in Neurotransmitter Release and Homeostatic Plasticity

Total Cost €


EC-Contrib. €






Project "SynDegrade" data sheet

The following table provides information about the project.


Organization address
address: RAMISTRASSE 71
city: Zürich
postcode: 8006

contact info
title: n.a.
name: n.a.
surname: n.a.
function: n.a.
email: n.a.
telephone: n.a.
fax: n.a.

 Coordinator Country Switzerland [CH]
 Total cost 1˙489˙340 €
 EC max contribution 1˙489˙340 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2015-STG
 Funding Scheme ERC-STG
 Starting year 2016
 Duration (year-month-day) from 2016-05-01   to  2021-04-30


Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    UNIVERSITAT ZURICH CH (Zürich) coordinator 1˙489˙340.00


 Project objective

While many neurons live for decades, the proteins that determine neural function have half-lives of hours to weeks. On the one hand, this allows for plastic changes during development and learning. On the other hand, this poses the question of how stable neural function can be achieved and maintained at all. Several neurological diseases, such as epilepsy or migraine, have been linked to uncontrolled neural function. However, the molecular mechanisms that stabilize nervous system function are poorly understood. The major site of regulation of neural activity is the chemical synapse. Synaptic function is tightly linked to the specific composition and abundance of proteins at synapses. However, the molecular pathways underlying the homeostatic control of protein levels at synapses, henceforth called synaptic proteostasis, are largely unknown.

The main objective of this proposal is to unravel the molecular signaling systems underlying synaptic proteostasis through local protein degradation, and its role in regulating a key step in synaptic transmission: neurotransmitter release. We propose to systematically analyze Ubiquitin Proteasome System (UPS)-dependent modulation of synaptic transmission in mutants of all major classes of synaptic genes, with a focus on homeostatic plasticity genes. This will be realized by employing a unique combination of forward genetics and electrophysiological analysis of synaptic transmission in Drosophila. Novel genetically-encoded probes will be used and developed to study synaptic transmission and protein degradation, and to acutely perturb protein function. Finally, this new information will be translated into the mammalian CNS by studying UPS-dependent modulation of release at a CNS synapse that allows for a detailed biophysical description of this phenomenon. Together, this approach should be ideally suited to dissect the molecular signaling systems underlying presynaptic proteostasis, and its role in neural physiology and pathology.


year authors and title journal last update
List of publications.
2019 Igor Delvendahl, Martin Müller
Homeostatic plasticity—a presynaptic perspective
published pages: 155-162, ISSN: 0959-4388, DOI: 10.1016/j.conb.2018.10.003
Current Opinion in Neurobiology 54 2019-02-11

Are you the coordinator (or a participant) of this project? Plaese send me more information about the "SYNDEGRADE" project.

For instance: the website url (it has not provided by EU-opendata yet), the logo, a more detailed description of the project (in plain text as a rtf file or a word file), some pictures (as picture files, not embedded into any word file), twitter account, linkedin page, etc.

Send me an  email ( and I put them in your project's page as son as possible.

Thanks. And then put a link of this page into your project's website.

The information about "SYNDEGRADE" are provided by the European Opendata Portal: CORDIS opendata.

More projects from the same programme (H2020-EU.1.1.)

DimorphicCircuits (2019)

Elucidating the development of sexually-dimorphic circuits: from molecular mechanisms to synapses and behavior

Read More  

FICOMOL (2019)

Field Control of Cold Molecular Collisions

Read More  



Read More