PRESENTATION
LES EQUIPES
RESSOURCES
ENSEIGNEMENT
COMMUNICATION

Bienvenue à l'Institut de Pharmacologie Moléculaire et Cellulaire


Annuaire     Contact     Intranet    CNRS    UCA    Autres sites CNRS
 

Stéphane MARTIN
Chef d'équipe

L'EQUIPE

Bendjafer

Chato

Gwizdek

Kieffer

Lacagne

Martin

Poupon-silvestre
LES PUBLICATIONS

 
 Pronot M. et al. (2021). Proteomic Identification of an Endogenous Synaptic SUMOylome in the Developing Rat Brain. Front Mol Neurosci

 Prieto M. et al. (2021). Missense mutation of Fmr1 results in impaired AMPAR-mediated plasticity and socio-cognitive deficits in mice. Nat Commun

 Schorova L. et al. (2019). The synaptic balance between sumoylation and desumoylation is maintained by the activation of metabotropic mGlu5 receptors. Cell Mol Life Sci

 Khayachi A. et al. (2018). Sumoylation regulates FMRP-mediated dendritic spine elimination and maturation. Nat Commun

 Loriol C. et al. (2014). mGlu5 receptors regulate synaptic sumoylation via a transient PKC-dependent diffusional trapping of Ubc9 into spines. Nat Commun

 Martin S. et al. (2007). SUMOylation regulates kainate-receptor-mediated synaptic transmission. Nature

CONTACTS
Stéphane MARTIN
Chef d'équipe, 04 93 95 34 61 - CV

Belinda BENDJAFER
Gestionnaire, 04 93 95 77 17
 

Equipe du Dr Stphane Martin
Implication physiologique et physiopathologique de la sumoylation neuronale

Public
expert

Grand
public

Activités de l'équipe

The communication between neurons takes place in highly specialized structures called synapses. The synaptic compartment is a very dynamic area where all the molecular processes relevant to neuronal communication and plasticity are orchestrated in a spatiotemporal manner. In the past years, the post-translational modification SUMOylation has emerged as an essential regulator of neuronal communication by dynamically regulating the molecular processes at the synapse.
 
SUMOylation consists in the covalent, but reversible, enzymatic conjugation of the Small Ubiquitin-like MOdifier (SUMO1-3) polypeptides (~100 amino acids; ~11 kDa) to specific lysine residues of target proteins. More specifically, the SUMOylation/deSUMOylation balance is orchestrated by the coordinated action of the sole SUMO-conjugating enzyme Ubc9 and SUMO-deconjugating enzymes called SENPs. SUMOylation participates in the dynamic regulation of multi-protein complexes by creating new binding sites for specific interactors or alternatively, by disrupting or preventing protein-protein interactions. SUMOylation regulates the function of many proteins involved in neuronal excitability, postsynaptic differentiation as well as in synaptic communication and plasticity. A tight regulation of the SUMOylation/deSUMOylation balance is therefore critical to the brain function.
 
The overall objective of the ‘SUMOylation in neuronal function & dysfunction’ team is to decode the physiological and pathophysiological consequences of SUMOylation at the mammalian synapse. We pioneered the work on the SUMO process at the synapse and our effort over the past years clearly established that SUMOylation is developmentally and activity-dependently regulated in the brain. In the lab, we combine the use of molecular tools, advanced biochemistry and state-of-the-art live-imaging approaches to:
  1. Decipher the molecular mechanisms driving the regulation of the activity-dependent SUMOylation / deSUMOylation balance at synapses.
  2. Identify and characterize the synaptic network of SUMOylated proteins.
  3. Define the physiological role of selected SUMOylated proteins important for the synaptic function, and investigate how disruption or alteration of their SUMOylation can participate in the etiology of brain disorders.
These data will advance our understanding of how neurons regulate the activity-dependent and synapse-specific SUMOylation of target proteins. In addition, this work provides additional insights for complementary studies on the role of SUMOylation in animal models of diseases characterized by synaptic dysfunction. In the longer term, these data will inform on strategies that may lead to tractable targets for therapeutic intervention.

 

Récompenses

  •  
  •  
Prix Jérôme Lejeune « Jeunes Chercheurs » décerné à Marta PRIETO GARCIA pour sa thèse intitulée « Conséquences physiopathologiques d'une mutation faux sens X-fragile (Pathophysiological consequences of a Fragile X missense mutation) »
 

Communiqués de presse

2021 - Exploring Drug Repurposing to Restore Hippocampal Function in FXS Mouse Models

 
2021 - Conséquences physiopathologiques de la mutation faux sens X-fragile FMRP-R138Q 
2018 - Un nouveau mécanisme moléculaire de la maturation des neurones
2014 - SUMO: un acteur clé du dialogue neuronal    


L'équipe est membre de :

This project will thus contribute to establishing an interactive network of regional institutes in the life sciences, focused on the study of signaling pathways in animal and plants, essential to our understanding of human health and fundamental biological processes.

 

Financements

IPMC UMR7275
660 Route des Lucioles
SOPHIA ANTIPOLIS
06560 VALBONNE

tél : 04 93 95 77 77 - fax : 04 93 95 77 08

 

INSTITUT DE PHARMACOLOGIE MOLECULAIRE ET CELLULAIRE

mentions légales
données personnelles