Fragile X syndrome (FXS), a neurodevelopmental disorder, arises due to malfunctions in the RNA binding protein FMRP, Fragile X Messenger Ribonucleoprotein 1. Our findings illustrate that, in a mouse model of FXS, alterations in the composition of the actin-cytoskeleton within the PSD significantly affect the striatum, a brain region particularly susceptible to such changes. On a behavioral level, these modifications are associated with a reduced flexibility in behavior driven by the striatum, a common trait among individuals with FXS. Our work underscores the critical role of actin-dynamics dysregulation in the striatum in contributing to the main characteristics of FXS and opened promising avenues for addressing pharmacologically specific traits of FXS through the regulation of actin-dynamics in specific brain regions. The speaker will also share additional unpublished data on the molecular and behavioural aspects of ASD.<\/p>\n