Liprin-αF 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-αF eye-specific mosaics and display normal morphological differentiation during pupal and adult stages. Liprin-αF 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-αF 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-αF mutant R cells typically display specific defects in axon extension toward their targets. Two types of defect are observed. Approximately 64% of Liprin-αF 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.
CadN[+]/CadNΔ14, Lar2127/Lar[+], Liprin-αF has partially lethal - majority die | dominant phenotype
