Synj¹/Synj² homozygous third instar larvae exhibit a significant decrease in synaptic vesicle loading (in FM1-43 loading assay) at neuromuscular junction synaptic boutons, as compared to controls.

Synj²/Synj¹ transheterozygotes are lethal at the third instar larval stage; mutant third instar larval neuromuscular junctions fail to sustain neurotransmission under high stimulation conditions (assessed by the amplitude of spontaneous excitatory junctional currents), and their presynaptic regions exhibit a significant decrease in the levels of endocytosis, exhibit a significant increase in the number of satellite boutons, exhibit a failure to starvation-induce mature autophagosomes (detected as fluorescent Atg8 puncta) and autolysosomes (detected as fluorescent Lamp1 puncta), and exhibit concomitant decrease in synaptic vesicles density and increase in cisternae density at boutons under starvation conditions, as compared to controls.

Synj²/Synj¹ transheterozygotes expressing Synj^RQ.Scer\UAS, but not Synj^Scer\UAS.cVa, under the control of Scer\GAL4^nSyb.PU present significant decreases in adult lifespan under starvation and significant decreases in the number of intact ommatidia upon 7 day exposure to constant light, but not to constant darkness, as compared to controls; transheterozygous third instar larval neuromuscular junctions expressing Synj^RQ.Scer\UAS, but not Synj^Scer\UAS.cVa, under the control of Scer\GAL4^Toll-6-D42 present a significantly decreased induction of mature autophagosomes (detected as fluorescent Atg8 puncta) in the presynaptic region in response to direct electric nerve stimulation or starvation, as compared to controls; transheterozygous third instar larval neuromuscular junctions expressing Synj^Scer\UAS.cVa also do not present neurotransmission defects, as shown by insignificant differences in the amplitude and frequency of miniature and spontaneous excitatory junctional currents under basal conditions, as compared to controls.

Synj¹/Synj² transheterozygotes have strongly decreased viability - only about 30% of control rate of survival to third instar larval stage. The mutant larvae show defects in active synaptic vesicle endocytosis (of both the exo/endo recycling pool and the reserve vesicle pool) as well as neurotransmission defects at high stimulation frequency. The normal evoked excitatory postsynaptic potential (EPSP) amplitude is comparable to controls, however the mutant larvae display a rapid rundown of the EPSP amplitude upon a high frequency stimulation sustained for a prolonged period of time.

When homozygous mutant somatic clones are made in the eye, the eyes appear morphologically wild-type. Electroretinogram (ERG) recordings show a depolarisation in response to light similar to controls. However almost all of these ERGs lack on/off transients, and those that are seen are very small. These animals perform as well as control flies in phototaxis assays. Photoreceptor cells and the lamina also appear grossly normal in mutant eyes. However the synaptic vesicles appear dense and cluster in highly organised rows. Other subcellular structures do not exhibit obvious defects. Homozygous mutant, or synj¹/Df(2R)R1-8 larvae move slowly, become paralysed and die as third instar larvae or early pupae. synj¹/synj² or synj²/Df(2R)R1-8 animals exhibit defects in endocytosis. The excitatory junctional potentials (EJPs) of mutants are not significantly different from controls. During repeated stimulation at low-frequency (1Hz) the EJP amplitude declines marginally, as do controls. At Higher-frequency stimulation (10Hz) the amplitude of the EJP declines rapidly (unlike controls) in mutants to about 25% to 30% of the original response and is then maintained for the remainder of the paradigm. Synaptic vesicles are somewhat depleted from the synaptic boutons from mutant terminals. ERGs starting from "lights on" performed on mutant eyes largely lack on/off transients. Occasionally a small and delayed off transient is observed.