Mutations in the gene encoding fragile X mental retardation protein (FMRP), an RNA-binding protein expressed during brain development, lead to fragile X sydrome (FXS). Bagni and colleagues show that, in embryonic mice, loss of FMRP delays the migration of new-born neurons to the cortical plate by reducing N-cadherin levels. This delay results in an imbalance in excitatory and inhibitory activity and altered structural connectivity in the postnatal brain. Thus, disrupted FMRP activity in early embryonic brain development may contribute to altered network connectivity in FXS.