FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\Dysdet-1
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General Information
Symbol
Dmel\Dysdet-1
Species
D. melanogaster
Name
Dysdetached-1
FlyBase ID
FBal0002369
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
det1, Dysdet1
Key Links
Mutagen
Nature of the Allele
Progenitor genotype
Cytology
Description
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
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 ( 1 )
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

Dysdet-1 homozygous larvae show decreased locomotion, namely decreased frequency of peristaltic waves.

Indirect flight muscle myofibril integrity is disrupted in 3-5 days old Dysdet-1 mutant flies, and this phenotype becomes significantly more penetrant in older animals (13-15 days). The myofibril defects are significantly suppressed when the flies are given food supplemented with either 2-acetyl-4(5)-tetrahydroxybutyl imidazole (THI) or THI oxime.

Overall activity of Dysdet-1 mutant flies is reduced compared to controls.

Myofibril integrity is disrupted in 3-5 days old Dysdet-1/Df(3R)Exel6184 mutant flies, and this phenotype becomes significantly more penetrant in older animals (13-15 days). The myofibril defects are significantly suppressed when the flies are given food supplemented with either 2-acetyl-4(5)-tetrahydroxybutyl imidazole (THI) or the S1P analog FTY720.

DysE6/Dysdet-1 heterozygotes display posterior crossvein abnormalities.

No obvious tergal depressor of trochanter (TDT) muscle fiber defect is observed in homozygous Dysdet-1 animals.

Homozygotes have a crossvein phenotype with incomplete penetrance and variable expressivity; 78% of mutant flies have at least one wing with a defective posterior crossvein. 39% of mutant wings have a complete posterior crossvein, 42% have a "gapped" phenotype (the crossvein is detached from either vein L4 or L5, but not both), 18% have a "detached" phenotype (the crossvein is detached from both L4 and L5) and 1% have a "point" phenotype (the crossvein is reduced to a point).

det1/Df(3R)Exel6184 transheterozygotes show a posterior crossvein phenotype with 100% penetrance. 18% of mutant wings have a complete posterior crossvein, 49% have a "gapped" phenotype and 33% have a "detached" phenotype.

det1/detEP3397 transheterozygotes show a posterior crossvein phenotype with 100% penetrance.

Homozygotes exhibit truncation of the posterior crossvein.

Posterior crossveins detached from longitudinals at one or both ends and may be absent. Wings occasionally folded back under or folded flat at middle. Eyes sometimes rough and bulging. Wings slightly spread. Bristles tend to break; scutellars occasionally doubled. RK3.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Enhanced by
Statement
Reference

Dysdet-1 has posterior crossvein phenotype, enhanceable by dpps1

Other
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

Introduction of dpps1 into a det1 background causes severe truncation of the posterior crossvein and wing vein L4.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (6)
Reported As
Name Synonyms
Dysdetached-1
Secondary FlyBase IDs
    References (10)