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General Information
Symbol
Dmel\Cdc424
Species
D. melanogaster
Name
FlyBase ID
FBal0062063
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
point mutation
Nucleotide change:

G19698306A

Reported nucleotide change:

G370A

Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

Nucleotide substitution: G370A. Mutation in splice acceptor consensus site.

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 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

After single cell wounding (by laser ablation), Cdc424/Cdc426 embryos show a wider actin ring than wild type and less orientated cortical actin flow toward the wound. Wound expansion and actin halo formation are not significantly affected.

Cdc424/Cdc426 embryos show defects in epithelial wound repair. The expansion and coalescence phases are not significantly delayed and by contraction, the wounds have become rounded, consistent with the presence of a functional actomyosin cable. There is a severe reduction of filopodia and lamellipodia protrusions in the leading edge cells throughout the wound repair process. The contraction phase is doubled in length compared to wild type. The wound cannot be sealed and a small hole remains at the end of the process.

26% of Cdc424 mutant R cell clones target normally, whereas 23% select inappropriate target columns and 51% fail to extend. Some photoreceptors display morphological defects in the retina, although this phenotype did not correlate with the axon targeting phenotype.

Homozygous tracheal terminal cells have very strong defects in branching and lumen formation.

Heterozygous and Cdc424/Cdc422 flies show normal resistance to infection with P.aeruginosa by septic injury.

VS1 neurons that are homozygous for Cdc423 often have defects in dendrite caliber; distal dendrites can be thicker than proximal dendrites and dendrites can also be thinner near major branches than wild-type. The dendrites of Cdc423 cells are also often misguided: for example, a dendrite can innervate the ventral region of the dendritic field, even though it has originated from a dorsal branch. Additionally, the most medial branch in the dendritic tree is shifted medially, resulting in a more pronounced split between the dorsal and ventral halves of the dendritic field. The axonal terminus of a Cdc423 VS1 neuron has an increase in the number of branches, is often tipped with enlarged structures and can have axons that turn laterally away from the midline. Dendrites are significantly longer in mutants than in wild type and there is a 50% reduction in numbers of well-developed dendritic spines.

Cdc424/Cdc426 combinations produce over 70% embryonic lethality, even when outcrossed to wild-type males. In Cdc424/Cdc426 germ-line clones, the specialised actin filaments that project outward from the nurse cell ring canals appear to be enhanced. Although Cdc424 germ-line clones fail to produce functional oocytes, their anterior posterior polarity appears to be unaffected.

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

Cdc42[+]/Cdc424 is a non-enhancer of abnormal neuroanatomy phenotype of PsGEFΔ21

Cdc42[+]/Cdc424 is a non-enhancer of visible | dominant phenotype of Sb70

Cdc42[+]/Cdc424 is a non-enhancer of visible | dominant phenotype of Sb63b

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

Cdc42[+]/Cdc424 is a non-enhancer of adult mushroom body alpha-lobe phenotype of PsGEFΔ21

Cdc42[+]/Cdc424 is a non-enhancer of leg phenotype of Sb70

Cdc42[+]/Cdc424 is a non-enhancer of leg phenotype of Sb63b

Cdc42[+]/Cdc424 is a non-enhancer of mitotic domain 1 | embryonic cycle 14 phenotype of CycB+t10

Suppressor of
Statement
Reference
NOT Suppressor of
Statement
Reference

Cdc42[+]/Cdc424 is a non-suppressor of intersegmental nerve | heat sensitive phenotype of Nl1N-ts1

Cdc42[+]/Cdc424 is a non-suppressor of intersegmental nerve branch ISNb of A1-7 | heat sensitive phenotype of Nl1N-ts1

Cdc42[+]/Cdc424 is a non-suppressor of segmental nerve branch SNa of A1-7 | heat sensitive phenotype of Nl1N-ts1

Cdc42[+]/Cdc424 is a non-suppressor of eye | adult stage phenotype of Scer\GAL4GMR.PU, pblDH-PH.UAS.Tag:HA

Cdc424 is a non-suppressor of wing phenotype of LIMK1UAS.cCa, Scer\GAL4en-e16E

Cdc42[+]/Cdc424 is a non-suppressor of mitotic domain 1 | embryonic cycle 14 phenotype of CycB+t10

Other
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

Cdc424 heterozygosity suppresses the quantal content and evoked junctional potential phenotypes of Dyb11 heterozygotes.

The dendritogenesis defects in the embryonic aCC motoneurons characteristic for embryos expressing either Dscam1HMS01859 or dockJF02810 RNAi under the control of Scer\GAL4eve.RN2 are partially suppressed by co-expression of PakScer\UAS.T:Myr-Src64B : the reduced dendritic number is fully restored but the region containing primary dendritic processes is expanded compared to controls. This rescue effect is however blocked in the presence of either Cdc426 or Cdc424 (in hemizygous state). No suppression of the loss of dendritic tips is observed upon co-expression with PakScer\UAS.T:Lhem\EosFP-m2.

Expression of gekScer\UAS.cGa under the control of Scer\GAL4elav-C155 fails to suppress the axon targeting phenotypes seen in Cdc424 mutant clones.

Heterozygosity for Cdc424 in a cv-c1/+ mutant background restores quantal content (QC) to wild-type levels.

Heterozygosity for Cdc424 in a DysE6/+ mutant background restores quantal content (QC) to wild-type levels.

Heterozygosity for Cdc424 fails to suppress the axonal defects found in Nl1N-ts1 mutants.

The Cdc424/+ heterozygous mutation does not suppress or enhance the GluRIIASP16 NMJ synaptic homeostasis phenotype. There is no deficit in synaptic bouton number in Cdc424/+ , GluRIIASP16 double mutants, compared to wild-type or GluRIIASP16 controls.

Synaptic homeostasis is completely blocked in larvae that are double heterozygotes for Cdc424/+ and ExnEY01953/+ in a GluRIIASP16 mutant genetic background.

Heterozygosity for Cdc424 has no effect on the phenotype in the alpha lobes of the mushroom bodies that is seen in PsGEFΔ21 animals.

Expression of Rho11.dsRNA.Scer\UAS under the control of Scer\GAL4Act5C.PI does not affect the adherens junctions between Cdc424 mutant cells.

One copy of Cdc424 fails to suppress the rough eye phenotype seen when pblDH-PH.Scer\UAS.T:Ivir\HA1 is expressed under the control of Scer\GAL4GMR.PU.

The Cdc424 mutation fails to modify the cv-cM62 phenotype in the Malpighian tubules.

Cdc424/+ has very little effect on the mutant wing phenotype caused by expression of LIMK1Scer\UAS.cCa under the control of Scer\GAL4en-e16E (the % of wings with normal morphology at 18oC is 10% compared to 9% for control flies expressing LIMK1Scer\UAS.cCa under the control of Scer\GAL4en-e16E in an otherwise wild-type background). The frequency of the malformed leg phenotype seen in Sb63b/+ heterozygotes (8%) is not increased if the flies are also heterozygous for Cdc424/+ (6%). The frequency of the malformed leg phenotype seen in Sb70/+ heterozygotes (7%) is not increased if the flies are also heterozygous for Cdc424/+ (8%).

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Fails to complement
Partially rescued by
Comments

Expression of Cdc42Scer\UAS.cLa under the control of Scer\GAL4elav.PLu rescues the dendritic caliber and branching pattern phenotype of Cdc424 mutants in VS1 neurons. However, this expression is unable to rescue many of the VS1 defects such as dendrites being significantly longer than in wild-type and reduction of well developed dendritic spines.

Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 2 )
Crossreferences
GenBank Nucleotide - A collection of sequences from several sources, including GenBank, RefSeq, TPA, and PDB.
GenBank Protein - A collection of sequences from several sources, including translations from annotated coding regions in GenBank, RefSeq and TPA, as well as records from SwissProt, PIR, PRF, and PDB.
Synonyms and Secondary IDs (3)
References (36)