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Akt is also an integral element of PI3Kinase\u2010target of rapamycin (TOR)\u2010Rheb signaling, a pathway that affects synapse assembly in both vertebrates and <jats:italic>Drosophila<\/jats:italic>. Our recent findings demonstrated that disruption of this pathway in <jats:italic>Drosophila<\/jats:italic> is responsible for a number of neurodevelopmental deficits that may also affect phenotypes associated with tuberous sclerosis complex, a disorder resulting from mutations compromising the TSC1\/TSC2 complex, an inhibitor of TOR (Dimitroff et al., 2012). Therefore, we examined the role of Akt in the assembly and physiological function of the <jats:italic>Drosophila<\/jats:italic> neuromuscular junction (NMJ), a glutamatergic synapse that displays developmental and activity\u2010dependent plasticity. The single <jats:italic>Drosophila Akt<\/jats:italic> family member, <jats:italic>Akt1<\/jats:italic> selectively altered the postsynaptic targeting of one glutamate receptor subunit, GluRIIA, and was required for the expansion of a specialized postsynaptic membrane compartment, the subsynaptic reticulum (SSR). Several lines of evidence indicated that <jats:italic>Akt1<\/jats:italic> influences SSR assembly by regulation of Gtaxin, a <jats:italic>Drosophila<\/jats:italic> t\u2010SNARE protein (Gorczyca et al., 2007) in a manner independent of the mislocalization of GluRIIA. Our findings show that <jats:italic>Akt1<\/jats:italic> governs two critical elements of synapse development, neurotransmitter receptor localization, and postsynaptic membrane elaboration. \u00a9 2013 The Authors. Developmental Neurobiology Published by Wiley Periodicals, Inc. 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