FB2024_03 , released June 25, 2024
Allele: Dmel\Cdc426
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General Information
Symbol
Dmel\Cdc426
Species
D. melanogaster
Name
FlyBase ID
FBal0062061
Feature type
allele
Associated gene
Dmel\Cdc42
Associated Insertion(s)
Carried in Construct
Key Links
Genomic Maps

Allele class

hypomorphic allele - genetic evidence

Mutagen
Nature of the Allele
Allele class

hypomorphic allele - genetic evidence

(Stramer et al., 2005)
Mutagen
ethyl methanesulfonate
(Fehon et al., 1997)
Progenitor genotype
Cytology
Description

Nucleotide substitution: C269T. Amino acid replacement: S83L.

(Genova et al., 2000)
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
point_mutation
X:19,698,205..19,698,205 [+]
Nucleotide change:

C19698205T

Reported nucleotide change:

G269A

Amino acid change:

S83L | Cdc42-PA; S83L | Cdc42-PC; S83L | Cdc42-PD

Reported amino acid change:

S83L

(Genova et al., 2000)
Variant Molecular Consequences
Associated Sequence Data
DDBJ / EMBL / GenBank
DNA sequence
Protein sequence
AF153429
AAD43793
 
UniProtKB/Swiss-Prot
    UniProtKB/TrEMBL
      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

      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.

      (Abreu-Blanco et al., 2014)

      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.

      (Abreu-Blanco et al., 2012)

      Hemocytes in embryos derived 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 derived 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.

      (Stramer et al., 2005)

      Cdc423/Cdc426 or Cdc424/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. In Cdc424/Cdc426 germ-line clones, the specialised actin filaments that project outward from the nurse cell ring canals appear to be enhanced.

      (Genova et al., 2000)
      External Data
      Interactions
      Show genetic interaction network for Enhancers & Suppressors
      Phenotypic Class
      Phenotype Manifest In
      Additional Comments
      Genetic Interactions
      Statement
      Reference

      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).

      (Kamiyama et al., 2015)

      .

      (Stramer et al., 2005)
      Xenogenetic Interactions
      Statement
      Reference
      Complementation and Rescue Data
      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 (2)
      References (11)