Co-expression of sra^{Scer\UAS.T:Ivir\HA1} suppresses aggregate formation in axons at the Scer\GAL4^elav.PU>Appl^Scer\UAS.cUa third instar larval NMJ.

The evoked excitatory postsynaptic potential (EPSP) amplitude during a 5 minute stimulation at 10 Hz shows a significantly steeper decline in triple transgenic synj^+tKa Dap160^Scer\UAS.cMa sra^Scer\UAS.cCa Scer\GAL4^elav.PLu flies compared to controls. (This effect is not seen when double or single transgenes are expressed.) No significant difference is seen in miniature EPSP frequency or amplitude between the triple transgenics and controls.

Dye uptake/unloading assays demonstrate that neuromuscular junctions of triple transgenic synj^+tKa Dap160^Scer\UAS.cMa sra^Scer\UAS.cCa Scer\GAL4^elav.PLu larvae show a delay in the rate of vesicle uptake, generating an overall defect in endocytosis. Exocytosis and vesicle pool size are unaffected.

Triple transgenic synj^+tKa Dap160^Scer\UAS.cMa sra^Scer\UAS.cCa Scer\GAL4^elav.PLu larvae show significantly impaired locomotor activity compared to controls. Triple transgenic adult flies fall more frequently and fail to climb the sides of the vial when mechanical stress is applied - their movement becomes normal after some recovery time.

Neuromuscular junctions of triple transgenic synj^+tKa Dap160^Scer\UAS.cMa sra^Scer\UAS.cCa Scer\GAL4^elav.PLu larvae exhibit a ~2.5-fold increase in small satellite boutons. Double transgenic synj^+tKa sra^Scer\UAS.cCa Scer\GAL4^elav.PLu larvae show a similar phenotype, though double transgenic synj^+tKa Dap160^Scer\UAS.cMa Scer\GAL4^elav.PLu or Dap160^Scer\UAS.cMa sra^Scer\UAS.cCa Scer\GAL4^elav.PLu do not.

Neuromuscular junctions of triple transgenic synj^+tKa Dap160^Scer\UAS.cMa sra^Scer\UAS.cCa Scer\GAL4^elav.PLu larvae exhibit an increase in number but a decrease in size of synaptic boutons.

Co-expression of sra^Scer\UAS.cCa and Hsap\APP^{695.Scer\UAS.T:Hsap\MYC} (under the control of Scer\GAL4^c739) fully rescues the short term memory defect in young (< 10 day old) adult flies, but not in older (> 30 day old) flies, as compared to flies with either construct alone, and does not affect gross morphology of the mushroom body.

Co-expression of sra^Scer\UAS.cCa partially rescues performance after 10-trial spaced training in flies with Hsap\APP^{695.Scer\UAS.T:Hsap\MYC} under the control of Scer\GAL4^c739.

Co-expression of sra^Scer\UAS.cCa fully rescues the short term memory defects of flies expressing Hsap\APP^{695.Scer\UAS.T:Hsap\MYC} under the control of transient activation of Scer\GAL4^{Mef2.247.Switch}.

Co-expression of sra^{Scer\UAS.T:Ivir\HA1} significantly delays the onset of age-dependent retinal degeneration and suppresses age-dependent phototaxis defects in flies with expression of Hsap\APP^{695.Scer\UAS.T:Hsap\MYC} driven by Scer\GAL4^GMR.PU. Co-expression of sra^{Scer\UAS.T:Ivir\HA1} suppresses formation of Hsap\APP aggregates in photoreceptor axons in flies with Hsap\APP^{695.Scer\UAS.T:Hsap\MYC} driven by Scer\GAL4^GMR.PU, likely alleviating blocked transport and delivering protein to synaptic terminals in the medulla.

Co-expression of sra^{Scer\UAS.T:Ivir\HA1} significantly partially suppresses aggregate formation in axons at the NMJ and locomotion defects in Scer\GAL4^elav.PU>Hsap\APP^{695.Scer\UAS.T:Hsap\MYC} third instar larvae; Syt1 vesicle or mitochondrial anterograde and retrograde transport is also facilitated in larval motor axons. Co-expression of Pp2B-14D^{Act.Δ.Scer\UAS} suppresses the ability of sra^{Scer\UAS.T:Ivir\HA1} to protect against Scer\GAL4^elav.PU>Hsap\APP^{695.Scer\UAS.T:Hsap\MYC} induced larval axonal transport and locomotion defects.

Co-expression of sra^{Scer\UAS.T:Ivir\HA1} significantly suppresses the increases in bouton number (synapse proliferation), but not satellite bouton number at the NMJ in Scer\GAL4^elav.PU>Hsap\APP^{695.Scer\UAS.T:Hsap\MYC} larvae.