FB2024_03 , released June 25, 2024
Allele: Dmel\CadNΔ14
Open Close
General Information
Symbol
Dmel\CadNΔ14
Species
D. melanogaster
Name
FlyBase ID
FBal0193539
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
ncadΔ14
Key Links
Allele class
Mutagen
Nature of the Allele
Allele class
Progenitor genotype
Caused by aberration
Cytology
Description

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).

Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Variant Molecular Consequences
Associated Sequence Data
DNA sequence
Protein sequence
 
Expression Data
Reporter Expression
Additional Information
Statement
Reference
 
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 0 )
Disease
Evidence
References
Modifiers Based on Experimental Evidence ( 0 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

chp staining of the medulla of CadNΔ14 eye clones (made using the 'eyFLP' system) reveals a few 'gaps' as if some R7 terminals are missing.

CadNΔ14 eye clones (made using the 'eyFLP' system) have R7 targeting phenotypes.

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.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
NOT suppressed by
Enhancer of
NOT Enhancer of
Statement
Reference
Suppressor of
Statement
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

NOT Suppressor of
Statement
Reference
Other
Phenotype Manifest In
Enhanced by
NOT suppressed by
Enhancer of
NOT Enhancer of
Statement
Reference

CadN[+]/CadNΔ14 is a non-enhancer of ommatidium phenotype of Scer\GAL4hs.2sev, nmoUAS.cUa

NOT Suppressor of
Statement
Reference

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

Other
Additional Comments
Genetic Interactions
Statement
Reference

CadNΔ14, Rich1 double mutant eye clones (made using the 'eyFLP' system) have R7 targeting phenotypes similar to CadNΔ14 single mutants.

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.

The ommatidial rotation defects observed in ecspok hemizygous adult eyes are not suppressed by CadNΔ14/+.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (6)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (11)