Mutations in the latheo (laf) gene disrupt associative learning in Drosophi
la, but a role for LAT in regulating neuronal function has not been demonst
rated. Here, we report that LAT plays a central role in regulating Ca2+- an
d activity-dependent synaptic plasticity. Immunological localization of the
LAT protein indicates it is present at synaptic connections of the larval
neuromuscular junction (NMJ) and is enriched in presynaptic boutons. Basal
synaptic transmission amplitude at the laf mutant NMJ is elevated 3- to 4-f
old, and Ca2+ dependence of transmission is significantly reduced. Multiple
forms of synaptic facilitation and posttetanic potentiation (PTP) are stro
ngly depressed or absent at the mutant synapse. Our results suggest that LA
T is a novel presynaptic protein with a role in the Ca2+-dependent synaptic
modulation mechanisms necessary for behavioral plasticity.