X-ray-mediated deletion of P{GT1}BG01221, resulting in deletion of the entire CadN2 gene, part of the CadN gene and sequences in between the two genes (including the P{GT1}BG01221 element).
When large clones of CadNΔ14 mutant cells are generated in the eye, R4 axons frequently fail to extend, or extend aberrantly.
Using MARCM, mistargeting of CadNΔ14 mutant L1-L5 cells is seen at the following percentages: 29% of L1 neurons, typically terminating in M10 rather than M5; 0% of L2 neurons; 81% of L3 neuron, typically terminating in M5 and M6 rather than M3; 81% of L4 neurons, terminating in M2 or, less frequently, M8 instead of M4; 0% of L5 terminals, but 100% of L5 interstitial branches fail to extend from M1 into M2. 100% of CadNΔ14 mutant R7 cells mistarget. 4% of R8 cells extend significantly deeper into the medulla than the remaining R8 cells, similar to controls.
At 25hrs APF, the centres of CadNΔ14 L3 growth cones are located in the R7 temporary layer about 2υm more proximal than in wild-type L3s. Mutant L3 terminals continue to exhibit incorrect layer choice, and remain elongated along one side of the column with only some diffuse lateral processes.
When using a reverse MARCM approach, 44/825 wildtype L5 neurons, neighboured by mutant cells, are observed in which almost no interstitial branches extend into M2 but instead send branches into adjacent columns, compared to controls which show no targeting defects.
CadNΔ14 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 CadNΔ14 mutants, R7 axons frequently stop at abnormally distal positions within the R8 recipient layer, leaving gaps in the array of otherwise regular R7 termini. However the ganglion-specific targeting of R1-R6 axons to the lamina nor the layer-specific targeting of R8 axons within the medulla are affected.
In CadNΔ14 homozygous mutants, the pattern of cartridges (where the R cell axons and lamina neuron processes form a highly organised fascicle) is severely disrupted.
In CadNΔ14 mutant target clones, the array of R4 axons appear disrupted, with many axons failing to extend, while others target inappropriately.
CadNΔ14 has abnormal neuroanatomy | adult stage | somatic clone phenotype, enhanceable by Sema1ak13702/Sema1ak13702
CadNΔ14 has abnormal neuroanatomy | P-stage | somatic clone phenotype, enhanceable by Sema1ak13702/Sema1ak13702
CadNΔ14 has abnormal neuroanatomy | somatic clone | pupal stage phenotype, non-suppressible by Scer\GAL4elav-C155/LarUAS.cKa
CadNΔ14/CadNΔ14 is an enhancer of abnormal neuroanatomy | adult stage | somatic clone phenotype of Sema1ak13702
CadNΔ14/CadNΔ14 is an enhancer of abnormal neuroanatomy | P-stage | somatic clone phenotype of Sema1ak13702
CadN[+]/CadNΔ14 is a non-enhancer of abnormal planar polarity phenotype of Scer\GAL4hs.2sev, nmoUAS.cUa
CadN[+]/CadNΔ14 is a non-suppressor of abnormal planar polarity phenotype of Scer\GAL4hs.2sev, nmoUAS.cUa
CadNΔ14, Rich1 has abnormal neuroanatomy | somatic clone phenotype
CadN[+]/CadNΔ14, Lar2127/Lar[+], Liprin-αF has partially lethal - majority die | dominant phenotype
CadNΔ14 has lamina monopolar neuron L2 | adult stage | somatic clone phenotype, enhanceable by Sema1ak13702/Sema1ak13702
CadNΔ14 has lamina monopolar neuron L4 | adult stage | somatic clone phenotype, enhanceable by Sema1ak13702/Sema1ak13702
CadNΔ14 has lamina monopolar neuron L3 | adult stage | somatic clone phenotype, enhanceable by Sema1ak13702/Sema1ak13702
CadNΔ14 has lamina monopolar neuron L3 | P-stage | somatic clone phenotype, enhanceable by Sema1ak13702/Sema1ak13702
CadNΔ14 has lamina monopolar neuron L1 | P-stage | somatic clone phenotype, enhanceable by Sema1ak13702/Sema1ak13702
CadNΔ14 has lamina monopolar neuron L1 | adult stage | somatic clone phenotype, enhanceable by Sema1ak13702/Sema1ak13702
CadNΔ14 has lamina monopolar neuron L5 | P-stage | somatic clone phenotype, enhanceable by Sema1ak13702/Sema1ak13702
CadNΔ14 has photoreceptor neuron | somatic clone | pupal stage phenotype, non-suppressible by Scer\GAL4elav-C155/LarUAS.cKa
CadNΔ14/CadNΔ14 is an enhancer of lamina monopolar neuron L3 | adult stage | somatic clone phenotype of Sema1ak13702
CadNΔ14/CadNΔ14 is an enhancer of lamina monopolar neuron L1 | P-stage | somatic clone phenotype of Sema1ak13702
CadNΔ14/CadNΔ14 is an enhancer of lamina monopolar neuron L1 | adult stage | somatic clone phenotype of Sema1ak13702
CadNΔ14/CadNΔ14 is an enhancer of lamina monopolar neuron L5 | P-stage | somatic clone phenotype of Sema1ak13702
CadNΔ14/CadNΔ14 is an enhancer of lamina monopolar neuron L5 | adult stage | somatic clone phenotype of Sema1ak13702
CadN[+]/CadNΔ14 is a non-enhancer of ommatidium phenotype of Scer\GAL4hs.2sev, nmoUAS.cUa
CadN[+]/CadNΔ14 is a non-suppressor of ommatidium phenotype of Scer\GAL4hs.2sev, nmoUAS.cUa
CadNΔ14 is a non-suppressor of ommatidium phenotype of ecspok
CadNΔ14, Rich1 has photoreceptor cell R7 | somatic clone phenotype
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 Lar2127 and CadNΔ14 are generated in the eye, R4 axon targeting errors are more frequently observed than in single mutants.
Expression of LarScer\UAS.cKa under the control of Scer\GAL4elav-C155 in CadNΔ14 somatic mutant clones does not rescue the photoreceptor targeting defects.
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.