The third instar larval neuromuscular junction of Liprin-αF3ex15/Liprin-αR60 transheterozygotes exhibit a significant decrease in active zone density (identified by Bruchpilot puncta), as compared to controls.
Liprin-αF3ex15 mutant larvae exhibit a vesicle localization phenotype, with ectopic aggregates of VGlut present at distal axon regions just proximal to the synaptic nerve terminal. This ectopic accumulation near synaptic termini occurs early in synaptic development and is not attributable to a gradual accumulation of synaptic vesicles during synaptic terminal growth.
Liprin-αF3ex15/Liprin-αR60 adults do not show defects in locomotion (assayed both by walking ability on a flat surface and in a negative geotaxis assay).
Evoked excitatory junctional currents (EJCs) are significantly reduced in amplitude in Liprin-αF3ex15/Liprin-αR60 third instar larvae compared to controls, while the amplitude of spontaneous miniature EJCs is normal.
The overall size of the neuromuscular junction is reduced in Liprin-αF3ex15/Liprin-αR60 third instar larvae compared to controls.
Mutant neuromuscular junctions show reliable homeostatic compensation (increase in quantal content) after treatment with philanthotoxin-433 for 10 minutes.
Liprin-αF3ex15/Liprin-α1J-0 mutant peripheral nerves have an accumulation of clear-core vesicles along the axon, compared to wild-type axons. Visualization of synaptic vesicle precursor transport along motor axons in intact third instar larva shows that the flux of cargo in the anterograde direction is significantly decreased in the mutants, while the flux is increased in the retrograde direction. However, the total flux is unchanged. There are no ectopic presynaptic specializations, breakdowns in the plasma membrane, or obvious changes in microtubule density or morphology along motor axons of Liprin-αF3ex15/Liprin-α1J-0 mutants.
Liprin-αF3ex15/Df(2L)Liprin-α-77ex63 embryos do not show defects in motor axon pathfinding. Liprin-αF3ex15/Liprin-αR60 larval neuromuscular junctions frequently lack small nascent boutons ("buds") surrounding a large end bouton (which are seen in wild-type animals). Overall neuromuscular junction ultrastructure looks relatively normal in Liprin-αF3ex15/Liprin-αR60 larvae, but active zones are always abnormal in either total size or shape, with the mean maximum dimension being nearly double that of wild type. Excitatory junctional potentials (EJPs) are reduced 36% in Liprin-αF3ex15/Liprin-αR117 larvae compared to controls. The mean amplitude and the frequency of unitary mRJPs is normal. The resting potential of the muscle is normal. The quantal content of evoked release is reduced by over 50%.
Df(2L)Exel7027/Liprin-αF3ex15 has increased mortality during development phenotype, suppressible | partially by Hsap\PPFIA3UAS.Tag:HA/Scer\GAL4da.PU
Df(2L)Exel7027/Liprin-αF3ex15 has increased mortality during development phenotype, suppressible | partially by Scer\GAL4da.PU/Hsap\PPFIA3W546C.UAS.Tag:HA
Df(2L)Exel7027/Liprin-αF3ex15 has increased mortality during development phenotype, suppressible | partially by Scer\GAL4da.PU/Hsap\PPFIA3R784W.UAS.Tag:HA
Liprin-αR60/Liprin-αF3ex15 is a non-suppressor of abnormal neuroanatomy | third instar larval stage phenotype of Nlg1Δcyto.UAS.EGFP, Scer\GAL4Mef2.PR
Df(2L)Exel7027/Liprin-αF3ex15, Hsap\PPFIA3R39C.UAS.Tag:HA, Scer\GAL4da.PU has lethal phenotype
Df(2L)Exel7027/Liprin-αF3ex15, Hsap\PPFIA3R784W.UAS.Tag:HA, Scer\GAL4da.PU has short lived phenotype
Df(2L)Exel7027/Liprin-αF3ex15, Hsap\PPFIA3UAS.Tag:HA, Scer\GAL4da.PU has partially lethal phenotype
Df(2L)Exel7027/Liprin-αF3ex15, Hsap\PPFIA3R415W.UAS.Tag:HA, Scer\GAL4da.PU has short lived phenotype
Liprin-αR60/Liprin-αF3ex15 has synaptic vesicle phenotype, suppressible by Scer\GAL4BG380/sggA81T.UAS
Liprin-αR60/Liprin-αF3ex15 has synapse phenotype, suppressible by Scer\GAL4BG380/sggA81T.UAS
Liprin-αF3ex15 has synaptic vesicle phenotype, suppressible by wrdUAS.EGFP/Scer\GAL4Toll-6-D42
Liprin-αF3ex15 has synapse phenotype, suppressible by wrdUAS.EGFP/Scer\GAL4Toll-6-D42
Liprin-αR60/Liprin-αF3ex15 is a non-suppressor of NMJ bouton | third instar larval stage phenotype of Nlg1Δcyto.UAS.EGFP, Scer\GAL4Mef2.PR
Df(2L)Exel7027/Liprin-αF3ex15, Hsap\PPFIA3UAS.Tag:HA, Scer\GAL4da.PU has NMJ bouton | larval stage | decreased number phenotype
Neuronal expression of PP2A-B'Scer\UAS.T:Avic\GFP-EGFP under the control of Scer\GAL4D42 substantially clears VGlut accumulation at the distal axons of Liprin-αF3ex15 mutants.
Expression of dominant negative sggA81T.Scer\UAS under the control of Scer\GAL4BG380 suppresses the Liprin-αR60/Liprin-αF3ex15 mutant distal axon phenotype.
The reduction in bouton number per muscle area seen in third instar larvae expressing Nlg1Δcyto.Scer\UAS.T:Avic\GFP-EGFP under the control of Scer\GAL4Mef2.PR is not suppressed by Liprin-αR60/Liprin-αF3ex15.
Liprin-αF3ex15 is rescued by Scer\GAL4elav.PU/Liprin-αUAS.GFP
Neuronal expression of Liprin-αScer\UAS.T:Zzzz\TAP under the control of Scer\GAL4elav.PU completely rescues the active zone morphological defects found in Liprin-αF3ex15 mutants.