|Feature type||allele||Associated gene||Dmel\gek|
|Mutagen||in vitro construct - regulatory fusion, in vitro construct - deletion|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
|Carried in construct|
neuroanatomy defective | third instar larval stage, with gekomb1080/Df(2R)e03819-f02302, Scer\GAL4Glass38-1
|Phenotype Manifest In|
embryonic/larval optic stalk | third instar larval stage, with gekomb1080/Df(2R)e03819-f02302, Scer\GAL4Glass38-1
eye photoreceptor cell | third instar larval stage, with gekomb1080/Df(2R)e03819-f02302, Scer\GAL4Glass38-1
Expression of gek[ΔPH.Scer\UAS] under the control of Scer\GAL4[Glass38-1] results in normal R cell axon targeting in third instar larvae. No photoreceptor morphology defects are seen in the eye discs, but adult animals have rough eyes. Expression of gek[ΔPH.Scer\UAS] under the control of Scer\GAL4[Glass38-1] in gek[omb1080]/Df(2R)e03819-f02302 mutant third instar larvae results in early termination of many R cell growth cones, with large clumps appearing in the optic stalk and the distal lamina.
|Phenotype Manifest In|
|Complementation & Rescue Data|
Expression of gek[ΔPH.Scer\UAS] in pupal stage R cells under the control of Scer\GAL4[elav-C155] rescues the axon targeting phenotypes seen in gek[omb1080] homozygous clones. 83% of axons extend correctly, 12% mistarget and 5% do not extend. Premature stopping of R1-R6 axons above the lamina plexus is not observed. However, approximately 18% of R cells exhibit morphological defects, with apical domains extending too far towards the center of the ommatidium or being located basally. 6% of all R cell bodies are below the plane of the ommatidium. All remaining R cells appear normal.
|Stocks ( 0 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 1 )|
|Secondary FlyBase IDs|
|References ( 1 )|