stnB¹² mutant flies expressing an insertion of stnB^Scer\UAS.cMa that results in very low levels of stnB (P{UAS-stnB.M}vl) under the control of Scer\GAL4^elav.PU barely reach the adult stage due to an inability to eclose from the pupal case. Surviving animals are highly uncoordinated and live only for a few days. This phenotype is enhanced when flies are raised at 18[o]C; surviving adults are rare and extremely uncoordinated, with the majority of animals failing to eclose. When stnB¹² mutant flies express a line producing slightly higher expression (P{UAS-stnB.M}l) survival is at a near-normal rate, while flies carrying an insertion that results in a moderate level of stnB (P{UAS-stnB.M}m) appear indistinguishable from controls with respect to survival and coordinated movement.

stnB¹² mutant third instar larvae expressing (P{UAS-stnB.M}vl) show defects in basal synaptic transmission (0.2Hz), with a 40% reduction in average excitatory junctional current (EJC) amplitude at neuromuscular junctions (muscle 6, segment 3) compared to controls. The amplitude is decreased further when the flies are raised at 18[o]C rather than 22[o]C. These larvae also show altered synaptic depression; when synapses are subjected to high-frequency stimulation (HFS) at 10Hz the initial reduction in amplitude is less pronounced than in wild-type and recovery is dramatically slowed. Raising the larvae at 18[o]C accentuates the slowing of the initial depression, but the recovery rate is improved slightly. A reduction in amplitude depression is also seen when flies are exposed to short trains of stimuli at frequencies greater than or equal to 5Hz and in response to paired stimuli with intervals of 50ms or 100ms. No difference is seen with intervals of 25ms, or at low calcium concentrations. No changes in either basal synaptic transmission of frequency-dependent synaptic depression are seen in third instar larvae expressing either the P{UAS-stnB.M}l or P{UAS-stnB.M}m insertion lines.

Overall vesicle density is reduced by 22% in the boutons of stnB¹² mutant larvae expressing P{UAS-stnB.M}vl, but the numbers of clustered vesicles and docked vesicles at presynaptic active zones do not differ significantly from controls. The boutons in terminal regions of axonal branches are frequently not normally shaped - the oval bouton shape is lost and aggregates of smaller boutons seem to form instead. In many cases, the spacing of normally shaped boutons is decreased and boutons do not follow the size distribution patterns of Is and Ib boutons. In contrast, the majority of synaptic boutons in the central regions of the axonal branches have normal morphological features. The average bouton area is reduced by 30% compared with controls. The morphology of boutons in stnB¹² mutant larvae expressing P{UAS-stnB.M}m is comparable to wild type.

Mutant nmjs appear morphologically wild type though the nerve terminals are slightly smaller than normal. In electrophysiological recordings at the embryonic nmj nerve stimulation produces muscle contraction demonstrating that presynaptic depolarization evokes transmitter release and that muscle excitation-secretion response is intact. However evoked EJC peak amplitudes are significantly reduced and the release of neurotransmitter at mutant synapses is markedly asynchronous due to delayed presynaptic vesicle fusion. Mutants have an impaired ability to synchronously trigger calcium-mediated vesicle fusion. The overall level of neurotransmitter release is reduced. Variability in EJC peak amplitudes is increased, compared to wild type. Transmission fidelity is lost. Calcium sensitivity is unaltered. MEJC frequency is not significantly altered, though amplitude is increased, perhaps because of increased quantity of neurotransmitter in some vesicles. Mutant synapses exhibit severe fatigue after prolonged stimulation. Synapses show decreased synaptic vesicle density and accumulate membrane-recycling intermediates.

stnB¹² has lethal phenotype, suppressible by Scer\GAL4^elav.PU/AP-2μ::stnB^{UAS.Tag:polyHis.Tag:MYC}

stnA¹², stnB¹² has lethal | recessive | embryonic stage phenotype, suppressible by Scer\GAL4^insc-Mz1407/Syt1^UAS.cLa

stnA¹², stnB¹² has lethal | recessive | embryonic stage phenotype, suppressible by Scer\GAL4^4G/Syt1^UAS.cLa

stnA¹², stnB¹² has lethal phenotype

Scer\GAL4^shi.PS, stnA¹², stnA^AB.UAS, stnB¹², stnB^AB.UAS has viable phenotype

Scer\GAL4^elav-C155, stnA¹², stnA^AB.UAS, stnB¹², stnB^AB.UAS has viable phenotype

Scer\GAL4^elav-C155, stnA¹², stnB¹², stnB^AB.UAS has viable phenotype

Scer\GAL4^Mhc.PW, stnA¹², stnA^AB.UAS, stnB¹², stnB^AB.UAS has lethal phenotype

Scer\GAL4^Mhc.PW, stnA¹², stnB¹², stnB^UAS.cEa has lethal phenotype

Scer\GAL4^elav-C155, stnA¹², stnA^UAS.cEa, stnB¹² has lethal phenotype

stnA¹², stnB¹² has lethal | recessive | embryonic stage phenotype

Scer\GAL4^insc-Mz1407, Syt1^UAS.cLa, stnA¹², stnB¹² has lethal | larval stage phenotype

Scer\GAL4^4G, Syt1^UAS.cLa, stnA¹², stnB¹² has viable phenotype

stnA¹²/stnA¹, stnB¹/stnB¹² has lethal phenotype