FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\cknC.Δ750-806
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General Information
Symbol
Dmel\cknC.Δ750-806
Species
D. melanogaster
Name
FlyBase ID
FBal0265793
Feature type
allele
Associated gene
Dmel\ckn
Associated Insertion(s)
Carried in Construct
Key Links
Allele class
Mutagen
Nature of the Allele
Allele class
Mutagen
ethyl methanesulfonate
(Weng et al., 2011)
Progenitor genotype
P{GSV1}GS1205
(Weng et al., 2011)
Cytology
Description

Deletion removing ckn residues 752-806, resulting in a frameshift and truncated protein.

(Weng et al., 2011)
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Variant Molecular Consequences
Associated Sequence Data
DDBJ / EMBL / GenBank
DNA sequence
Protein sequence
 
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

      cknA.R305Q homozygous or cknA.R305Q/Df(2R)BSC330 mutant embryos display consistent motor axon projection defects, exhibiting classic ISNb 'bypass' phenotypes, where ISNb axons fail to innervate the ventrolateral muscle field. These axons appear to defasciculate normally from the primary ISN branch at the exit junction, but fail to enter the ventral muscle field, instead bypassing their targets as they extend parallel to the primary ISN fascicle. Frequently, mis-targeted ISNb axons reach back from the dorsal edge of muscle 12 to innervate the ventrolateral muscle field. In the majority of affected nerves, ISNb axons are visible as a distinct fascicle next to the ISN.

      (Weng et al., 2011)
      External Data
      Interactions
      Show genetic interaction network for Enhancers & Suppressors
      Phenotypic Class
      Enhanced by
      Statement
      Reference

      cknC.Δ750-806 has abnormal neuroanatomy | embryonic stage phenotype, enhanceable by dock04723

      (Weng et al., 2011)
      Phenotype Manifest In
      Additional Comments
      Genetic Interactions
      Statement
      Reference

      dock04723 cknC.Δ750-806 double homozygotes exhibit delayed 'immature' ISNb axons in 59% of hemisegments. Motor axons in the affected nerves are loosely organised with multiple projections and resemble wild-type axons at earlier stages. Furthermore, the ISNd branch is frequently absent or reduced in size. Examination of the ISNb/d choice point reveals defects in ISNb/d branch segregation. The lateral two longitudinal Fas2-positive fascicles are poorly fasciculated and discontinuous in these double mutants.

      (Weng et al., 2011)
      Xenogenetic Interactions
      Statement
      Reference
      Complementation and Rescue Data
      Images (0)
      Mutant
      Wild-type
      Stocks (0)
      Notes on Origin
      Discoverer
      External Crossreferences and Linkouts ( 0 )
      Synonyms and Secondary IDs (2)
      Reported As
      Symbol Synonym
      cknC.Δ750-806
      cknC
      (Weng et al., 2011)
      Name Synonyms
      Secondary FlyBase IDs
        References (1)