Liprin-αE homozygous MARCM clones of R7 photoreceptor neurons at 40-60 percent through pupal development (P40-60) have significantly reduced lifespan of bulbous growth cone filopodia (bulbs) at axon terminals, with significantly more transient bulbs, significantly fewer stable bulbs and no change in the total number of bulbs, compared to controls, with no effect on other filopodia; unlike controls there are timepoints during P60 where no bulbs are present; at P70, significantly fewer synapses are present, compared to controls; axons begin to retract at P40, and there is a moderate level of retraction by P70, unlike controls, which do not retract.
When large clones of Liprin-αE mutant cells are generated in the eye, R4 axons frequently fail to extend, or extend aberrantly.
Liprin-αE 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.
In Liprin-αE mutants, R7 axons frequently stop at abnormally distal positions within the R8 recipient layer. However the ganglion-specific targeting of R1-R6 axons to the lamina nor the layer-specific targeting of R8 axons within the medulla are unaffected.
R-cells proliferate normally during the third instar larval stage in Liprin-αE eye-specific mosaics and display normal morphological differentiation during pupal and adult stages. Liprin-αE 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.
In Liprin-αE mutant clones, R7 axons sometimes stop in the R8 recipient layer instead of the R7 recipient layer, leaving gaps in the array of otherwise regular R7 termini.
The behaviour of Liprin-αE 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-αE mutant R cells typically display specific defects in axon extension toward their targets. Two types of defect are observed. Approximately 64% of Liprin-αE 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.
When large clones of cells mutant for both Liprin-αE and CadNΔ14 are generated in the eye, R4 axon targeting errors are more frequently observed than in single mutants.
When large clones of cells mutant for both Liprin-αE and Lar2127 are generated in the eye, R4 axon targeting errors are more frequently observed than in single mutants.
When large clones of cells mutant for Liprin-αE, Lar2127, and CadNΔ14 are generated in the eye, R4 axon targeting errors are observed, but the frequency of defects is similar to Liprin-αE; Lar2127, Lar2127; CadNΔ14, or Liprin-αE; CadNΔ14 double mutant combinations.
