A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Allele Dmel\CadNΔ14

General Information
SymbolDmel\CadNΔ14SpeciesD. melanogaster
NameFlyBase IDFBal0193539
Feature typealleleAssociated geneDmel\CadN
Also Known AsNcadΔ14
Allele class
MutagenX ray
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Description
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FB2013_03
FB2013_02
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Allele class
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Mutations Mapped to the Genome
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Protein sequence
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Nature of the lesion
Statement
Reference
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).
Caused by aberration
Cytology
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Statement
Reference
chp staining of the medulla of CadN[Δ14] eye clones (made using the 'eyFLP' system) reveals a few 'gaps' as if some R7 terminals are missing. CadN[Δ14] eye clones (made using the 'eyFLP' system) have R7 targeting phenotypes.
When large clones of CadN[Δ14] mutant cells are generated in the eye, R4 axons frequently fail to extend, or extend aberrantly.
Using MARCM, mistargeting of CadN[Δ14] 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 CadN[Δ14] 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 CadN[Δ14] 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.
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Statement
Reference
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Statement
Reference
CadN[+]/CadNΔ14 is an enhancer of lethal phenotype of Lar2127/Lar451
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Reference
CadN[+]/CadNΔ14 is a suppressor | partially of lethal phenotype of Liprin-αE/Liprin-α1
CadN[+]/CadNΔ14 is a suppressor | partially of lethal phenotype of Liprin-αF/Liprin-αE
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Reference
CadN[+]/CadNΔ14 is a non-enhancer of ommatidium phenotype of Scer\GAL4hs.2sev, nmoScer\UAS.cUa
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Statement
Reference
CadN[+]/CadNΔ14 is a non-suppressor of ommatidium phenotype of Scer\GAL4hs.2sev, nmoScer\UAS.cUa
CadNΔ14 is a non-suppressor of ommatidium phenotype of ecspok
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Reference
CadN[Δ14], Rich[1] double mutant eye clones (made using the 'eyFLP' system) have R7 targeting phenotypes similar to CadN[Δ14] single mutants.
When large clones of cells mutant for both Liprin-α[E] and CadN[Δ14] 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 Lar[2127] and CadN[Δ14] are generated in the eye, R4 axon targeting errors are more frequently observed than in single mutants. Expression of Lar[Scer\UAS.cKa] under the control of Scer\GAL4[elav-C155] in CadN[Δ14] somatic mutant clones does not rescue the photoreceptor targeting defects. When large clones of cells mutant for Liprin-α[E], Lar[2127], and CadN[Δ14] are generated in the eye, R4 axon targeting errors are observed, but the frequency of defects is similar to Liprin-α[E]; Lar[2127], Lar[2127]; CadN[Δ14], or Liprin-α[E]; CadN[Δ14] double mutant combinations.
The ommatidial rotation defects observed in ec[spok] hemizygous adult eyes are not suppressed by CadN[Δ14]/+.
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Reported As
Symbol Synonym
N-cadherinΔ14
Name Synonym
Secondary FlyBase IDs
hide References ( 8 )
Research paper
Gontang et al., 2011, Development 138(22): 4899--4909
The cytoskeletal regulator Genghis khan is required for columnar target specificity in the Drosophila visual system. [FBrf0216508]
Tong et al., 2011, Neuron 71(3): 447--459
Rich Regulates Target Specificity of Photoreceptor Cells and N-Cadherin Trafficking in the Drosophila Visual System via Rab6. [FBrf0214681]
Prakash et al., 2009, Dev. Biol. 336(1): 10--19
Complex interactions amongst N-cadherin, DLAR, and Liprin-alpha regulate Drosophila photoreceptor axon targeting. [FBrf0209258]
Nern et al., 2008, Neuron 58(1): 34--41
Local N-cadherin interactions mediate distinct steps in the targeting of lamina neurons. [FBrf0204173]
Montrasio et al., 2007, Dev. Dyn. 236(10): 2936--2942
A new allele uncovers the role of echinus in the control of ommatidial rotation in the Drosophila eye. [FBrf0202297]
Choe et al., 2006, Proc. Natl. Acad. Sci. U.S.A. 103(31): 11601--11606
Liprin-alpha is required for photoreceptor target selection in Drosophila. [FBrf0195369]
Prakash et al., 2005, Nat. Neurosci. 8(4): 443--450
Drosophila N-cadherin mediates an attractive interaction between photoreceptor axons and their targets. [FBrf0184200]
Supplementary material
Mirkovic et al., 2011, Nat. Struct. Mol. Biol. 18(6):
Supplemental Data. [FBrf0213975]