Dysbindin links presynaptic proteasome function to homeostatic recruitment of low release probability vesicles

Abstract

At the fly neuromuscular junction, postsynaptic receptor perturbation induces homeostatic enhancement of neurotransmitter release. Here, the authors show that the presynaptic proteasome controls a vesicle pool required for homeostatic plasticity and that dysbindin is required to access this pool.