Abstract
The actin cytoskeleton is essential for the structural changes in dendritic spines that lead to the formation of new synapses. Although the molecular mechanisms underlying spine formation are well characterized, the events that drive spine maturation during development are largely unknown. In this study, we demonstrate that Angiomotin (AMOT-130) is necessary for spine stabilization. AMOT-130 is enriched in mature dendritic spines and functions to stabilize the actin cytoskeleton by coupling F-actin to postsynaptic protein scaffolds. These functions of AMOT are transiently restricted during postnatal development by phosphorylation imposed by the kinase Lats1. Our study proposes that AMOT-130 is essential for normal spine morphogenesis and identifies Lats1 as an upstream regulator in this process. Moreover, our findings may link AMOT-130 loss and the related spine defects to neurological disorders.