INS Topical Seminar – Christine Métin (Paris)
“Cellular mechanisms regulating the cortical distribution of GABAergic interneurons”
The p21 activated kinases (PAKs) are activated by Rac1 and Cdc42 and regulate the dynamics and contractility of the acto-myosin cytoskeleton, and the turnover of adhesive contacts. Mutations in one isoform, PAK3, are responsible in humans of X-linked non-syndromic intellectual disability. Pak3 is expressed in tangentially migrating interneurons in the developing cortex. By overexpressing mutants that mimic human mutations (kinase dead or defective for GTPase binding) or a constitutively active mutant, we have analyzed the influence of PAK3 activity on the morphology, dynamic behavior and on the trajectories of migrating interneurons in the developing cortex.
Christine Métin, DR2 INSERM, co-leads with P. Gaspar the team ”Developmental mechanisms of brain disorders” at Institut du Fer à Moulin (IFM) in Paris. With her group, C. Métin analyzes the cellular mechanisms that regulate the long distance migration of cortical interneurons from the basal forebrain to the developing cortex. She uses in vivo models to study how the migratory defects of interneurons alter their final distribution in the cortical target. In collaboration with the team of C. Bernard, she studies the consequences of interneuron migratory defects on the activity of cortical networks.
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