FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\CASKX-313
Open Close
General Information
Symbol
Dmel\CASKX-313
Species
D. melanogaster
Name
FlyBase ID
FBal0048071
Feature type
allele
Associated gene
Dmel\CASK
Associated Insertion(s)
Carried in Construct
Key Links
Allele class
Mutagen
Nature of the Allele
Allele class
Mutagen
X ray
(Martin and Ollo, 1996)
Progenitor genotype
tsl604
(Martin and Ollo, 1996)
Caused by aberration
Df(3R)cakiX-313
Cytology
Description

Imprecise excision of the P-element causing deletion of Caki coding sequences.

(Martin and Ollo, 1996)
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

      CASKX-307/CASKX-313 flies have reduced reactivity to electric shock compared to controls.

      CASKX-307/CASKX-313 flies show normal learning (measured as 2 minute memory) in an olfactory aversive conditioning assay. However, middle-term memory (measured 3 hours after one cycle of training) is completely abolished in the mutant flies.

      (Malik et al., 2013)

      Mature CASKX-307/CASKX-313 males show a extremely low overall level of immature-male courtship than the control. Courtship initiation latency of this mutant is also significantly longer than the control, with many males never initiating courtship during a 10 minute observation.

      Mature CASKX-307/CASKX-313 males fail to habituate to immature male pheromones.

      CASKP18/CASKX-313 flies exhibit significantly less movement than control flies.

      CASKX-307/CASKX-313 flies exhibit significantly less movement than control flies.

      CASKX-307/CASKX-313 flies have normal circadian locomotor rhythms and wild type free running periods.

      (Slawson et al., 2011)

      CASKX-313/CASKX-307 larvae display a severe defect in locomotion and a 20% increase in bouton number at neuromuscular junctions.

      CASKX-313/CASKX-307 neuromuscular junctions show a dramatic reduction in synaptic vesicle trafficking.

      Induced excitatory potential (EJP) amplitude at CASKX-313/CASKX-307 neuromuscular junctions is significantly decreased compared to wild type.

      Both the spontaneous miniature excitatory potential (mEJP) amplitude and frequency at CASKX-313/CASKX-307 neuromuscular junctions are significantly increased compared to wild type.

      (Sun et al., 2009)

      CASKX-307/CASKX-313 mutant flies exhibit an impairment in their flight ability compared to wild-type flies. Indirect flight muscle action potentials display significantly longer short- and long-latencies compared to wild-type controls. In some indirect flight muscles (approximately 5%) displaying a normal resting membrane potential, the stimulation of the giant fiber pathway fails to evoke a clear repsonse, which intead appears as a small depolarization. This lack of response remains unchanged with time as well as with increasing stimulus voltage or duration, suggesting that synaptic transmission is impaired in these fibers. The ability of the giant fiber pathway to follow continuous stimulation is also impaired. In contrast to wild-type flies, short-latency responses show a significant response decrement even at low stimulation frequencies in CASKX-307/CASKX-313 mutant flies. Long-latency responses show habituation, as in wild-type. At stimulation frequencies between 1 and 3 Hz the onset of habituation occurs significantly earlier in CASKX-307/CASKX-313 mutant flies than in wild-type. The percentage of CASKX-307/CASKX-313 mutant flies that show habituation is lower than in wild-type controls. These flies are also less responsive to dishabituation.

      The resting membrane potential of indirect flight muscle fibers from CASKX-307/CASKX-313 mutant flies is not significantly different from wild-type. Average miniature end-plate potentials (MEPPs) frequency in CASKX-307/CASKX-313 mutant flies is significantly higher than in wild-type. Furthermore, average MEPPs amplitude is greater in CASKX-307/CASKX-313 mutants. Latency values are much shorter in CASKX-307/CASKX-313 mutants than in wild-type.

      In a walking optomotor assay, the frequency of correct turns is significantly lower in CASKX-307/CASKX-313 mutants compared to wild-type flies. In a light intensity assay, the response of CASKX-307/CASKX-313 mutants to decreasing light intensity mirrors that of wild-type flies. However, the response of CASKX-307/CASKX-313 mutants at lower light intensities (below intermediate levels) suggest an impairment of visual function at low light intensity.

      CASKX-307/CASKX-313 mutants exhibit a higher sustained ERG respones than in wild-type individuals. Although the ON transient amplitude is similar in both wild-type and CASKX-307/CASKX-313 flies, OFF transients are significantly higher in CASKX-307/CASKX-313 mutants than in wild-type individuals. These differences remain even when a high-intensity light stimulus is used instead of a low-intensity stimulus. Adaptation of the sustained response, induced by continuous 1Hz stimulation, is qualitatively similar in both CASKX-307/CASKX-313 mutants and wild-type flies, whereas the amplitudes of the ERG sustained responses are significantly higher in CASKX-307/CASKX-313 flies during the whole stimulation period.

      (Zordan et al., 2005)

      Walking speed and path length of CakiX-307/CakiX-313 transheterozygotes is considerably reduced, as studied in Buridan's paradigm. Vision seems not to be dramatically altered.

      (Martin and Ollo, 1996)
      External Data
      Interactions
      Show genetic interaction network for Enhancers & Suppressors
      Phenotypic Class
      Phenotype Manifest In
      Additional Comments
      Genetic Interactions
      Statement
      Reference
      Xenogenetic Interactions
      Statement
      Reference
      Complementation and Rescue Data
      Rescued by

      CASKX-307/CASKX-313 is rescued by Scer\GAL4elav-C155/CASKUAS.cZa

      (Zordan et al., 2005)
      Not rescued by

      CASKX-307/CASKX-313 is not rescued by Scer\GAL4elav-C155/CASKUAS.cZa

      (Zordan et al., 2005)
      Comments

      Expression of CASKScer\UAS.cZa pan-neuronally under the control of Scer\GAL4elav-C155 fully rescues the neuromuscular junction miniature end-plate potential as well as the giant fiber habituation response defects found in CASKX-307/CASKX-313 mutant females but does not rescue any of these defects in male progeny.

      (Zordan et al., 2005)
      Images (0)
      Mutant
      Wild-type
      Stocks (1)
      Notes on Origin
      Discoverer
      Comments
      Comments

      CakiX-307/CakiX-313 transheterozygote is referred to as 'caki1', a deletion of genomic DNA encoding approximately 100 amino acids of the C-terminal part of Caki.

      (Martin and Ollo, 1996)
      External Crossreferences and Linkouts ( 0 )
      Synonyms and Secondary IDs (7)
      Reported As
      Symbol Synonym
      313
      (Slawson et al., 2011)
      CASKX-313
      CakiX-313
      Df(3)x313
      (Slawson et al., 2011)
      Df(3R)x313
      (Slawson et al., 2011)
      caki313
      (Sun et al., 2009)
      cakiX-313
      (Zordan et al., 2005)
      Name Synonyms
      Secondary FlyBase IDs
        References (6)