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General Information
Symbol
Dmel\Cdc423
Species
D. melanogaster
Name
FlyBase ID
FBal0062064
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
cdc42-3
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
point mutation
Nucleotide change:

G19698359A

Reported nucleotide change:

G423A

Amino acid change:

G114D | Cdc42-PA; G114D | Cdc42-PC; G114D | Cdc42-PD

Reported amino acid change:

G114D

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

Nucleotide substitution: G423A. Amino acid replacement: G114D.

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

Homozygous germline clones result in the arrest of oogenesis and mutant egg chambers develop only until stage 5. From stage 4 onwards, the mutant egg chambers contain 16 polyploid nurse cells instead of the normal 15 nurse cells plus one oocyte. Marker analysis indicates that the oocyte is correctly specified during early stages, but that its fate is not maintained.

Cdc423/+ flies do not exhibit a significantly increased pacing-induced heart failure rate or arrhythmia, do not have significantly different diastolic or systolic intervals, nor any significant disruption in cellular architecture of cardiomyocytes as compared to controls.

Homozygous clones in the wing result in a multiple wing hair phenotype.

Cdc423 mutants have normal embryonic and early larval neuroblast polarity. Third instar larval central brain neuroblasts display polarity defects.

Homozygous Cdc423 mutant embryos do not exhibit a myoblast fusion phenotype.

Hemocytes in embryos dervied from Cdc423/Cdc426 mothers show normal developmental dispersal and normal recruitment to sites of laser-induced tissue damage. However, during the migratory phase and after arrival at the wound site, the mutant hemocytes often possess several leading edges suggesting that they cannot maintain a persistent polarity.

The failure of hemocytes to maintain polarity in embryos dervied from Cdc423/Cdc426 mothers leads the hemocytes to adopt a haphazard migratory route. This defect is countered by the mutant hemocytes migrating at approximately twice the normal speed so that they reach the wound as rapidly as in wild type embryos. On reaching the wound, the mutant hemocytes appear to remain more active than wild type hemocytes, and exhibit exuberant protrusive activity.

In Cdc423/Cdc423 embryos the ectodermal keyhole cells fail to invaginate into the proventricular endoderm.

Mutant embryos exhibit arrested ganglionic branches (GBs), and GBs turning prematurely away from the midline.

Cdc423/Cdc426 combinations produce over 70% embryonic lethality, even when outcrossed to wild-type males. Embryos produced by Cdc423/Cdc426 mothers display disruptions in epidermal development, including incomplete germband retraction, ventral holes in the epidermis, ventral holes in cuticle produced by epidermal cells, and anterior open phenotypes. Ventral holes range in size from isolated disruptions to openings in the entire ventral surface of the embryo. Patterns of neuronal differentiation are largely normal, even in areas where the integrity of the overlying epidermis is disrupted. In certain embryos defects in the central nervous system, such as incomplete formation and midline fusion of the longitudinal connectives are observed. However, in all embryos the axons of the peripheral nervous system appear to extend properly. Cdc423 somatic clones generated early in larval development do not survive until the wandering third instar larval stage, those generated later (72h AEL) are smaller than sister control clones. No clones survive to adulthood. Even in a Minute background clones in the eye are only visible as scars, not producing any adult ommatidia. Clones in the eye disc do initiate differentiation as photoreceptor cells in the larval eye imaginal disc. In Cdc423 germ-line clones, the cytoplasmic actin filaments that normally form in the nurse cells, although still present are reduced in number compared to wild-type.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhancer of
Statement
Reference

Cdc42[+]/Cdc423 is an enhancer of visible phenotype of Scer\GAL4en-e16E, kermitGS2053

NOT Enhancer of
Statement
Reference

Cdc42[+]/Cdc423 is a non-enhancer of neuroanatomy defective phenotype of DAAMEx1

Cdc423 is a non-enhancer of neuroanatomy defective phenotype of SNF4Aγloe

Cdc42[+]/Cdc423 is a non-enhancer of visible | dominant phenotype of Sb70

Cdc42[+]/Cdc423 is a non-enhancer of visible | dominant phenotype of Sb63b

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

Cdc42[+]/Cdc423 is an enhancer of wing hair phenotype of Scer\GAL4en-e16E, kermitGS2053

NOT Enhancer of
Statement
Reference

Cdc42[+]/Cdc423 is a non-enhancer of mushroom body alpha-lobe phenotype of DAAMEx1

Cdc42[+]/Cdc423 is a non-enhancer of mushroom body beta-lobe phenotype of DAAMEx1

Cdc423 is a non-enhancer of photoreceptor cell | precursor & nucleus phenotype of Scer\GAL4unspecified, msnDN.UAS

Cdc42[+]/Cdc423 is a non-enhancer of leg phenotype of Sb70

Cdc42[+]/Cdc423 is a non-enhancer of leg phenotype of Sb63b

Suppressor of
Statement
Reference
NOT Suppressor of
Statement
Reference

Cdc423 is a non-suppressor of wing phenotype of LIMK1UAS.cCa, Scer\GAL4en-e16E

Cdc423 is a non-suppressor of ommatidium phenotype of Rac1V12.hs.sev

Cdc423 is a non-suppressor of phenotype of dshhs.sev.B

Other
Additional Comments
Genetic Interactions
Statement
Reference

One copy of Cdc423 does not enhance the axonal growth defects seen in the α and β lobes of DAAMEx1 mutant mushroom bodies.

There is no significant difference in the nervous system degeneration seen in SNF4Aγloe mutants in a Cdc423 heterozygous background.

Cdc423/+; Pak6/+ double heterozygotes display severe cardiomyocyte organization abnormalities and contractile abnormalities as compared with either single heterozygote, but no differences in heart beat defects and overall rhythmicity.

Cdc423/+; Df(2L)Exel6012/+ double heterozygotes do not display defects in heart rhythm as compared to controls.

Cdc423/+; Df(2L)Exel9032/+ double heterozygotes and Cdc423/+; Df(3R)BSC397/+ double heterozygotes show significant defects in cardiomyocyte structure, significantly increased arrhythmia, but no significant differences in the overall length of diastolic and systolic intervals.

tin346/+; Cdc423/+ double heterozygotes exhibit a significantly increased pacing-induced heart failure rate, significantly increased arrhythmia and a tendency toward longer diastolic intervals, in addition to severe misalignment of cardiac myofibrils, as compared with controls. These flies do not exhibit differences in systolic intervals.

tinEC40/+; Cdc423/+ double heterozygotes exhibit a significantly increased pacing-induced heart failure rate.

The Cdc423/+ heterozygous mutation does not suppress or enhance the GluRIIASP16 NMJ synaptic homeostasis phenotype. There is no deficit in synaptic bouton number in Cdc423/+ , GluRIIASP16 double mutants, compared to wild-type or GluRIIASP16 controls.

Synaptic homeostasis is completely blocked in larvae that are double heterozygotes for Cdc423/+ and ExnEY01953/+ in a GluRIIASP16 mutant genetic background. There is no deficit in synaptic bouton number in Cdc423/+ , ExnEY01953/+, GluRIIASP16 triple mutants, compared to wild-type or GluRIIASP16 controls.

The combination of Cdc423/+ and cacS/+ heterozygous mutations blocks the synaptic homeostatic compensation at the neuromuscular junction (NMJ) in a homozygous GluRIIASP16 genetic background.

Cdc423/+ 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 Cdc423/+ (3%). The frequency of the malformed leg phenotype seen in Sb70/+ heterozygotes (7%) is not increased if the flies are also heterozygous for Cdc423/+ (7%).

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Fails to complement
Comments
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 (30)