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General Information
Symbol
Dmel\cknK.Δ324-331
Species
D. melanogaster
Name
FlyBase ID
FBal0265796
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
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

Deletion which removes ckn residues 324-331, but does not result in a frameshift.

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

cknK.Δ324-331 homozygous or cknK.Δ324-331/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.

cknK.Δ324-331 heterozygous embryos do not exhibit ISNb guidance defects.

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

cknK.Δ324-331 has neuroanatomy defective | embryonic stage phenotype, non-enhanceable by Ptp69D1/Ptp69D[+]

cknK.Δ324-331 has neuroanatomy defective | embryonic stage phenotype, non-enhanceable by Ptp69D[+]/Ptp69D7

NOT suppressed by
Statement
Reference

cknK.Δ324-331 has neuroanatomy defective | embryonic stage phenotype, non-suppressible by Ptp69D1/Ptp69D[+]

cknK.Δ324-331 has neuroanatomy defective | embryonic stage phenotype, non-suppressible by Ptp69D[+]/Ptp69D7

Enhancer of
Statement
Reference
Other
Phenotype Manifest In
NOT Enhanced by
Statement
Reference
NOT suppressed by
Statement
Reference
Enhancer of
Other
Additional Comments
Genetic Interactions
Statement
Reference

Lar5.5 cknK.Δ324-331 double heterozygous embryos display bypass phenotypes with 39% penetrance.

A heterozygous or homozygous Ptp69D1 background fails to affect the penetrance of the ISNb bypass phenotype found in cknK.Δ324-331 heterozygotes or homozygotes.

A heterozygous or homozygous Ptp69D7 background fails to affect the penetrance of the ISNb bypass phenotype found in cknK.Δ324-331 heterozygotes or homozygotes.

ISNb pathfinding is delayed in approximately 23% of dock3 cknK.Δ324-331 double heterozygotes.

A heterozygous cknK.Δ324-331 background enhances ISNb pathfinding defects in dock3 homozygotes, from 6% to 43% of hemisegments.

dock3 cknK.Δ324-331 double homozygotes exhibit delayed 'immature' ISNb axons in 65% 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.

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
cknK.Δ324-331
Name Synonyms
Secondary FlyBase IDs
    References (1)