sterile (with CadNM19), with CadN7b-13a-18a.UAS, Scer\GAL4elav.PU
sterile (with CadNM19), with CadN7b-13b-18a.UAS, Scer\GAL4elav.PU
Homozygous embryos show mild central nervous system defects.
Proximal arborization is occasionally eliminated in neuron clones homozygous for CadN405. The defect is adult brains are diverse.
In CadN405 mutant homozygous clones, R7 cells terminate their axon projections in the outer M3 layer, rather than the M6 layer.
At 48% after pupal formation (APF), all R cell axons homozygous for CadN405 extend aberrantly (64%), or do not extend at all (36%).
At 17% APF, 21% of CadN405 R7 growth cones (analysed as single cell mutant clones) fail to reach the R7-temporary layer in the medulla; the mutant axons either expand their growth cones incorrectly at the R8-temporary layer or between the R7 and R8 temporary layers. In addition, over half of the mutant growth cones show severe morphological defects. At 25% APF, 55% of the mutant R7 axons terminate at the R8 temporary layer or between the R7 and R8 temporary laters. Some of the mutant axons leave a small filopodium connecting to the R7 temporary layer.
Mosaic flies in which the photoreceptor cells are homozygous show defects in the optomotor response.
The ability of mutant flies to detect motion is approximately 5 times worse than wild-type. The response of mutant flies to a UV/Vis choice test is approximately 8 fold worse than wild-type. Mutants perform well, though less well than wild-type, in counter-current fast phototaxis assays. In CadN405 mosaic eyes, the R7 and R8 projections that normally form a regular array in the medulla fail to form this array and often terminate at the outer edge of the medulla. Individual R cells do not make the characteristic projections seen in the wild-type. In the optic lobe of CadN405 mosaic eyes, the lamina plexus forms irregular clumps, rather than the smooth line of uniform thickness seen in wild-type. R8 termini exhibit defects in local topographical mapping failing to form the regular array in the medulla normally seen. The array of R4 termini is also disrupted, also R4 growth cones do not expand fully within the lamina plexus. The array of R7 termini is also disrupted and their termini exhibit elongated thickening along the terminal region. However ganglion specificity is not affected and the columnar organisation of the lamina neurons is normal. Glial cells differentiate and migrate normally into the lamina, however the organisation of glial cells is disrupted such that in some regions of the lamina, they fail to form the three layers seen in wild-type. When individual R7 axons are mutant, they fail to terminate at the R7 target layer, M6, and stop instead at the R8 layer, M3. However topographic mapping of the R7 in the medulla appears normal in these animals. When homozygous somatic clones are made in the eye so that only mutant R7 cells persist, the response from these flies to a UV/Vis choice test is several times worse than wild-type.
CadN405 has abnormal neuroanatomy phenotype, non-suppressible by seqUAS.cBa/Scer\GAL4GMR.long
CadN[+]/CadN405 is an enhancer of abnormal neuroanatomy | somatic clone phenotype of Rich2
CadN[+]/CadN405 is a non-enhancer of abnormal neuroanatomy | somatic clone phenotype of Rich1
CadN405 is a suppressor of abnormal neuroanatomy phenotype of Scer\GAL4GMR.long, seqUAS.cBa
CadN405 has photoreceptor cell R7 phenotype, non-suppressible by seqUAS.cBa/Scer\GAL4GMR.long
CadN405 has medulla layer M6 phenotype, non-suppressible by seqUAS.cBa/Scer\GAL4GMR.long
CadN405 has medulla layer M3 phenotype, non-suppressible by seqUAS.cBa/Scer\GAL4GMR.long
CadN[+]/CadN405 is an enhancer of photoreceptor cell R7 | somatic clone phenotype of Rich2
CadN[+]/CadN405 is a non-enhancer of photoreceptor cell R7 | somatic clone phenotype of Rich1
CadN405 is a suppressor of photoreceptor cell R8 phenotype of Scer\GAL4GMR.long, seqUAS.cBa
CadN405 is a suppressor of medulla layer M6 phenotype of Scer\GAL4GMR.long, seqUAS.cBa
CadN405 is a suppressor of medulla layer M3 phenotype of Scer\GAL4GMR.long, seqUAS.cBa
CadN405 suppresses the R8 cell targeting defects seen when seqScer\UAS.cBa is expressed under the control of Scer\GAL4GMR.long. The R8 axons no longer terminate in the M6 layer of the medulla and correctly target the M3 layer. However the flies do show an R7 targeting phenotype; the R7 photoreceptors target the M3 layer rather than the M6 layer, as is seen in CadN405 mutants alone.
CadN405/CadNM19 is partially rescued by Scer\GAL4elav.PU/CadN7b-13a-18a.UAS
CadN405/CadNM19 is partially rescued by Scer\GAL4elav.PU/CadN7b-13b-18a.UAS
CadN405 is partially rescued by Scer\GAL4Tub.PU/CadN18B.UAS
CadN405 is partially rescued by CadN18A.UAS/Scer\GAL4Tub.PU
CadN405 is partially rescued by Scer\GAL4Tub.PU/CadNUAS.cIa
CadN405 is partially rescued by Scer\GAL4elav-C155/CadN7b-13a-18a.UAS
CadN405 is partially rescued by Scer\GAL4elav-C155/CadN7b-13b-18a.UAS
CadN405 is partially rescued by Scer\GAL4elav-C155/CadN7b-13a-18b.UAS
CadN405 is partially rescued by Scer\GAL4elav-C155/CadNUAS.cIa
CadN405/CadNM19 is not rescued by Scer\GAL4how-24B/CadN7b-13a-18a.UAS
CadN405/CadNM19 is not rescued by Scer\GAL4how-24B/CadN7b-13b-18a.UAS
Scer\GAL4how-24B-mediated expression of CadN7b-13a-18a.Scer\UAS has no effect on the lethality of CadNM19/CadN405.
Scer\GAL4elav.PU-mediated expression of CadN7b-13a-18a.Scer\UAS partially rescues the lethality of CadNM19/CadN405 - animals now survive through to the adult stage, but fail to produce progeny.
Found in a screen using a retina dependant behavioural test - an optomotor assay to assess the function of photoreceptor cells R1 to R6.