|Feature type||allele||Associated gene||Dmel\Lar|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
|Phenotype Manifest In|
photoreceptor cell & growth cone | somatic clone
photoreceptor cell R2 & axon | somatic clone
photoreceptor cell R3 & axon | somatic clone
photoreceptor cell R4 & axon | somatic clone
photoreceptor cell R5 & axon | somatic clone
photoreceptor cell R7 & axon | somatic clone
Using the MARCM method, in 100% of cartridges in which lamina neurons are homozygous for Lar451, normal spacing and structure is observed. The projections of R4 axons are invariably unaffected by the presence of mutant target cells.
Mosaic flies in which the photoreceptor cells are homozygous show defects in the optomotor response (72% fail to respond to a motion stimulus) and the UV/visual light choice test (34% show phototaxis towards visible light, compared to only 12% of wild-type flies). Initial photoreceptor cell projections (in third instar larvae) are largely normal in mosaic animals in which the photoreceptor cells are homozygous. A small number of R2-R5 axons overshoot the lamina and terminate aberrantly in the medulla. Targetting of R8 axons to the medulla appears normal at this stage. R7 growth cones form a regular array of 8-10 rows in the medulla, as in wild type. Photoreceptor cell growth cones in the lamina often fail to extend out of the ommatidial bundle towards their normal neuronal targets. Those growth cones that fail to leave the bundle are abnormally thin and have few filopodia. The regular array of photoreceptor cell terminals in the lamina plexus that is normally seen during mid-pupal development is only slightly disrupted in the mosaic animals. R7 growth cones extend beyond the R8 layer in early pupae in which the photoreceptor cells are homozygous (as occurs in wild type) but the R7 growth cones have an abnormal bush-like structure. In the older part of the medulla some R7 growth cones fail to stay in the R7 recipient layer and retract towards the R8 recipient layer. In mid-pupae the rows of R7 termini have gaps, and the termini often show an aberrant "collapsed" morphology, with only a thin process remaining at the normal termination site. The expressivity of the R7 morphology defects correlates strongly with the age of the R7 terminus. 50% of single homozygous R1-R6 photoreceptor cells in the lamina (induced in a heterozygous background) fail to extend out from the ommatidial bundle before elaborating the presynaptic terminal, producing a presynaptic terminal in an inappropriate position. In the remaining cases, the axon fibre extends to an apparently normal position before thickening to form the presynaptic terminal. The morphology of the presynaptic terminal is largely normal. Mutant R1-R6 axon termini extend into the lamina plexus (as in wild type) but are somewhat more irregular in thickness than controls. Single homozygous R7 photoreceptor cells in the lamina (induced in a heterozygous background) often (68%) fail to terminate at their normal target layer (M6) and instead terminate at the M3 layer or at variable positions in the medulla neuropil between M3 and M6. Those mutant R7 axons that terminate in the appropriate layer have abnormal morphology, with the mutant termini assuming a spear-like morphology (instead of the normal button-like appearance). Mosaic adults in which the whole eye is homozygous show 78% mistargeted R7 axons.
|Phenotype Manifest In|
|Complementation & Rescue Data|
|Stocks ( 0 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 4 )|
|Secondary FlyBase IDs|
|References ( 3 )|