FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\CRMPsupK1
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General Information
Symbol
Dmel\CRMPsupK1
Species
D. melanogaster
Name
FlyBase ID
FBal0277232
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Genomic Maps

Allele class
Nature of the Allele
Allele class
Progenitor genotype
Cytology
Description

Deletion of 153 bp of exon E4-intron I4 sequences of CRMP with an insertion of six nucleotides (Genbank GU452677). The predicted open reading frame created by the E4-I4 fusion terminates at an in-frame nonsense codon within intron I4, probably resulting in a severely truncated product consisting of only the N-terminal 10% of the CRMP protein.

Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Comment:

5381 bp deletion associated with the imprecise excision of P{EP}CRMPEP3238, which removes the 3' end of exon 4 and the first nucleotide of intron 4 of CRMP.

Variant Molecular Consequences
Associated Sequence Data
DNA sequence
Protein sequence
 
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

CRMPsupK1 adults show circadian arrhythmicity. Their l-LNvs show a split POT.

Homozygous, hemizygous, or heteroallelic CRMPsupK1 mutants are viable, fertile, and morphologically normal when grown under standard laboratory conditions.

When tested for short term memory performance 2 minutes after a single aversive Pavlovian training session, CRMPsupK1/CRMPsupIa1 as well as homozygous CRMPsupK1 mutants exhibit significantly reduced performance compared with wild-type control flies. Medium-term memory performance measured 3 hours after a single aversive Pavlovian training session is also reduced in homozygous mutants and heteroallelic mutant animals.

Homozygous CRMPsupK1 mutants exhibit significantly reduced long-term memory performance compared with control animals.

Under free-running conditions (constant darkness), wild-type and CRMPsupK1 mutant animals exhibit similar overall activity. Period length is similar for all tested animals, indicating that the length of the circadian clock is not affected by CRMPsupK1. Compared with wild-type and heterozygous animals, significantly reduced arrhythmic power values indicating the relative strength of rhythmicity of free-running behaviours are observed among CRMPsupK1 homozygotes, CRMPsupK1/Df(3R)noi-B hemizygotes and CRMPsupK1/CRMPsupIa1 heteroallelic animals. Some individual CRMPsupK1 homozygotes and CRMPsupK1/Df(3R)noi-B hemizygotes lack significantly rhythmic behaviours (arrhythmic).

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhancer of
Statement
Reference
NOT Enhancer of
Statement
Reference
Suppressor of
NOT Suppressor of
Statement
Reference

CRMPsupK1 is a non-suppressor of visible phenotype of Rac1N17.UAS, Scer\GAL4sev.EP

Other
Phenotype Manifest In
Enhancer of
Statement
Reference
NOT Enhancer of
Statement
Reference

CRMPsupK1 is a non-enhancer of eye phenotype of Rac1N17.UAS, Scer\GAL4sev.EP

Suppressor of
NOT Suppressor of
Statement
Reference

CRMPsupK1 is a non-suppressor of eye phenotype of Rac1N17.UAS, Scer\GAL4sev.EP

Other
Additional Comments
Genetic Interactions
Statement
Reference

The rough eye phenotype resulting from the expression of Ras85DScer\UAS.cKa via Scer\GAL4GMR.PF is suppressed by homozygous CRMPsupK1.

CRMPsupK1 homozygotes expressing sggScer\UAS.cBa under the control of either Scer\GAL4GMR.PF or Scer\GAL4ey.PH regularly survive to the pharate adult stage and frequently eclose as adults displaying reduced rough eyes.

Severely reduced eyes are produced in homozygous CRMPsupK1 animals also expressing Rac1V12.Scer\UAS under the control of Scer\GAL4sev.EP.

Animals expressing dominant-negative Rac1N17.Scer\UAS under the control of Scer\GAL4sev.EP display no discernible differences in the presence or absence of homozygous CRMPsupK1.

The eye phenotype resulting from the expression of Rac2EP3118 under the control of Scer\GAL4GMR.PF is enhanced in CRMPsupK1 animals that have reduced eyes with extensively fused ommatidia.

The Scer\GAL4ey.PH driver produces irregular ommatidial arrangements and reduced eyes in Rac2EP3118 animals that are homozygous for CRMPsupK1.

Pan-neural expression of Rac2EP3118 with Scer\GAL4elav-C155 in CRMPsupK1 homozygotes results in rough eyes.

CRMPT:Avic\GFP-EGFP supports the suppression of the body colour phenotype of bunspecified, CRMPsupK1 double mutants by rSu(b).cSa resulting in a brownish cuticle.

CRMPfs9a.T:Avic\GFP-EGFP fails to support the suppression of the body colour phenotype of bunspecified, CRMPsupA4/CRMPsupK1 double mutants by rSu(b).cSa resulting in a dark gray cuticle.

CRMPfs9b.T:Avic\GFP-EGFP supports the suppression of the body colour phenotype of bunspecified, CRMPsupA4/CRMPsupK1 double mutants by rSu(b).cSa resulting in a brownish cuticle.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (2)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (5)