AP2 Regulates Thickveins Trafficking to Attenuate NMJ Growth Signaling in .

Compromised endocytosis in neurons leads to synapse overgrowth and altered organization of synaptic proteins. However, the molecular players and the signaling pathways which regulate the process remain poorly understood. Here, we show that σ2-adaptin, one of the subunits of the AP2-complex, genetically interacts with Mad, Medea and Dad (components of BMP signaling) to control neuromuscular junction (NMJ) growth in Ultrastructural analysis of mutants show an accumulation of large vesicles and membranous structures akin to endosomes at the synapse. We found that mutations in lead to an accumulation of Tkv receptors at the presynaptic membrane. Interestingly, the level of small GTPase Rab11 was significantly reduced in the mutant synapses. However, expression of Rab11 does not restore the synaptic defects of mutations. We propose a model in which AP2 regulates Tkv internalization and endosomal recycling to control synaptic growth.