The general aim of our group is to understand the pathophysiology of Planar Cell Polarity (PCP) in mammals, and more specifically to identify and define the molecular and cellular mechanisms of PCP, and the consequences of early and late deletion of PCP signaling.
PCP is mostly understood and studied in epithelia, and notably the inner ear, which is accepted as one of the best model to analyze PCP in mammals. It is more challenging to understand how PCP mechanisms affect non-epithelial cells such as neurons or glial cells, because of the absence of a referent epithelial plane, and the inherent 3D structure of the brain. We know however that mutations in PCP genes affect dramatically the nervous system, and some have been associated with neurodevelopmental disorders (autism syndrome disorders), sensory impairments and neurological disorders (epilepsy or ataxia). In 2011, we created the "Planar Polarity and Plasticity" team which combines complementary expertises and uses an epithelial model (the cochlea) in order to decipher and study the role(s) of PCP signaling in mammalian brain, during development and in adulthood. This original combination of scientific expertise (epithelial and neuronal), together with a multidisciplinary approach of PCP integrating cellular, developmental and functional approaches and a series of specific conditional mutants has allowed our group to significantly contribute to the understanding of how PCP signaling regulates critical processes such as cytoskeleton dynamic, neuronal dendritic arborization, synaptogenesis, and synaptic plasticity. We have also shown that modification of PCP protein can be involved in learning and social deficit, opening new insight on the pathophysiological process of cognitive perturbances.
These goals have been achieved thanks to the solid expertise of our group in cell biology and development, the strong local and international network of collaborators, and the state-of-the-art facilities in Magendie or in the Bordeaux Neurocampus.
Planar cell polarity (PCP) signaling is well known to play a critical role during prenatal brain development; whether it plays specific roles at postnatal stages remains rather unknown. Here, we inve
GPR88 is a neuronal cerebral orphan G-protein-coupled receptor (GPCR) that has been linked to various psychiatric disorders. However, no extensive description of its localization has been provided so
Levodopa (L-DOPA)-induced dyskinesias (LIDs) represent the major side effect in Parkinson's disease (PD) therapy. Leucine-rich repeat kinase 2 (LRRK2) mutations account for up to 13 % of familial case
Synapses and nuclei are connected by bidirectional communication mechanisms that enable information transfer encoded by macromolecules. Here, we identified RNF10 as a novel synaptonuclear protein mess
L-3,4-dihydroxyphenylalanine (L-DOPA)-induced dyskinesias (LIDs) represent the main side effect of Parkinson's Disease (PD) therapy. Among the various pharmacological targets for novel therapeutic app