Ank2f02001/Ank2f02001 mutant 1st, 2nd and 3rd instar larval neuromuscular junctions exhibit abberant microtubule organization, with aggregates of central microtubules; and a significant increase in synaptic retraction frequency at later larval stages, but no defect in the presence of microtubules at terminal boutons, as compared to controls.
Ank2f02001 mutants exhibit a significant increase in synaptic retractions compared with controls.
Sound-evoked compound action potentials in the antennal nerve are not significantly different from wild type in mutant flies. However, nonlinear mechanical amplification is significantly reduced compared to wild type.
Ank2f02001 mutant third instar larvae show severe NMJ degeneration, leading to complete elimination of the presynaptic nerve terminal at many NMJs. Loss of Ank2 also causes axonal blockages and severe disruption of the axonal and synaptic microtubule skeleton.
Homozygous egrΔ25 mutants show large defects in EPSP amplitude compared to wild-type. A large number of recording are seen that have average EPSPs below 25mV.
Neuromuscular junctions of mutant larvae have fewer but larger boutons than normal.
Neuromuscular junctions of Ank2RM5-1/Ank2f02001 larvae have fewer but larger boutons than normal. The synaptic span (the widest extension of synaptic branches along a muscle fibre) is reduced compared to wild type.
Homozygotes die at late larval/early pupal stages.
Homozygotes show severe synaptic retractions at more than 60% of all neuromuscular junctions (NMJs) on muscles 6/7.
Ank2f02001/Df(3L)RM5-2 and Ank2f02001/Ank2f00518 animals die as third instar larvae/early pupae, and they show severe synaptic retractions at the NMJs.
The severity of the synaptic retraction phenotype that is seen at the NMJs of Ank2f02001/Df(3L)RM5-2 animals increases progressively during larval development.
Ank2f02001/Df(3L)RM5-2 third instar larvae show defects in synaptic transmission and motoneuron excitability at the NMJ. Defects in in synapse morphology are also seen at the NMJ, with enlarged presynaptic membrane compartments. The presynaptic microtubule cytoskeleton shows abnormal organisation. Ultrastructurally, NMJs show hallmarks of synapse degeneration, including accumulations of endosomal/vacuole-like membrane profiles. In addition, giant synaptic boutons are seen at the NMJ. The boutons are elongated laterally, and multiple active zones can be detected. In addition, large vesicles are present. Large accumulations of microtubules can also be seen, with vesicles being absent from these regions.