Imprecise excision of P{EP}EP2141, removing most of the upstream region of Liprin-α.
synapse (with Liprin-αF3ex15)
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-αR60 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.
Axon terminals of homozygous R7 photoreceptor cell clones often fail to contact the M6 layer of the medulla.
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-αR60 mutants exhibit a specific pattern of disruption in the structure of the cartridge, the synaptic unit in the lamina. Some cartridges have either >6 or <6 R cells axons, and some adjacent cartridges fuse.
R-cells proliferate normally during the third instar larval stage in Liprin-αR60 eye-specific mosaics and display normal morphological differentiation during pupal and adult stages. Liprin-αR60 mutant R cell axons select appropriate ganglion-specific targets in the lamina and the medulla and induce appropriate neuronal differentiation in the lamina target field. These axons also elaborate topographically appropriate maps in each region, with glial cell differentiation in these areas also appearing largely normal.
The behaviour of Liprin-αR60 mutant axons (generated through MARCM) is indistinguishable from wild-type along their trajectories into the lamina plexus, with each axon remaining tightly associated with the axon bundle of its wild-type neighbours from the same ommatidium. However, once within the lamina plexus, unlike wild-type R cells, Liprin-αR60 mutant R cells typically display specific defects in axon extension toward their targets. Two types of defect are observed. Approximately 64% of Liprin-αR60 mutant axons completely fail to extend away from the ommatidial bundle, whereas 21% make weak, morphologically abnormal extensions; the remaining axons extend normally. All R cell subtypes are equally affected.
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).
Liprin-αR60/Liprin-αF3ex15 is a non-suppressor of abnormal neuroanatomy | third instar larval stage phenotype of Nlg1Δcyto.UAS.EGFP, Scer\GAL4Mef2.PR
Liprin-αR60, RhoGAP100Fw46 has abnormal neuroanatomy | somatic clone | adult stage phenotype
Liprin-αR60 has synaptic vesicle phenotype, suppressible by wrdUAS.EGFP/Scer\GAL4Toll-6-D42
Liprin-αR60 has synapse phenotype, suppressible by wrdUAS.EGFP/Scer\GAL4Toll-6-D42
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-αR60/Liprin-αF3ex15 is a non-suppressor of NMJ bouton | third instar larval stage phenotype of Nlg1Δcyto.UAS.EGFP, Scer\GAL4Mef2.PR
Liprin-αR60, RhoGAP100Fw46 has retina | somatic clone 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-αR60 mutants.
Expression of dominant negative sggA81T.Scer\UAS under the control of Scer\GAL4BG380 suppresses the Liprin-αR60/Liprin-αF3ex15 mutant distal axon phenotype.
Retinas double mutant for Liprin-αR60 and RhoGAP100Fw46 are severely reduced in size, and the remaining photoreceptor neuron axons in the medulla are extremely disorganised.
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-αR60 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-αR60 mutants.