FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\kelneo2
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General Information
Symbol
Dmel\kelneo2
Species
D. melanogaster
Name
FlyBase ID
FBal0031527
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
kelchneo
Key Links
Genomic Maps

Nature of the Allele
Progenitor genotype
Associated Insertion(s)
Cytology
Description
Mutations Mapped to the Genome
Curation Data
Variant Molecular Consequences
Associated Sequence Data
DNA sequence
Protein sequence
 
Expression Data
Reporter Expression
Additional Information
Statement
Reference

kel transcripts are absent in males, females and ovaries in kelneo2 mutants.

No kel protein is observed in kelneo2 mutant egg chambers.

 
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

Mid- and late-stage ring canals of homozygous females are disorganised and have a reduced lumen.

Ring canal diameter and length of stage 5 to 8 egg chambers are greater than those measured in wild type females. Ring canal diameter and length increase ahead of schedule. Nurse cells degenerate prematurely variably between stage 8 and 10, well before nurse cell dumping should occur. Actin filament bundles stray away from the margins into the canal proper. The canal proper looks like it contains a network of bundles and is never completely occluded but does allow movement of organelles through the canal. Results suggest the failure to produce eggs is not simply due to occlusion but is instead somehow related to the degeneration of the nurse cells and oocyte at stages before nurse cell dumping.

kel mutant egg chambers have ring canals that are obstructed by disordered actin and hts product.

Egg chambers defective for early, slow, and late, fast cytoplasm transport into the oocyte. As early as stage 7 of oogenesis oocyte is smaller than wild type. Mutant egg cytoplasm looks rough and irregular. The small oocytes are surrounded by egg shell where dorsal appendages are shorter and fatter than wild type and sometimes fused dorsally. In the most extreme cases the anterior of the egg is open forming a cup shape. The small eggs usually degenerate in the ovary.

External Data
Interactions
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Phenotypic Class
Phenotype Manifest In
Additional Comments
Genetic Interactions
Statement
Reference
Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments

The sterility of homozygous females is rescued by kelotu.PR, kelORF1.otu, kelUAA.otu, kelORF1.otu.T:Hsap\MYC and kelAla.otu, but not by kelΔUGA.otu or kelSer.otu. The ring canal phenotype is rescued by kelORF1.otu and kelORF1.otu.T:Hsap\MYC, but not by kelΔUGA.otu or kelSer.otu. kelAla.otu partially rescues the morphology of late stage ring canals. kelneo2/kelPL25 flies carrying kelORF1.otu produce eggs at approximately wild-type rates. 97.6% of these eggs survive to hatching.

Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
Comments
Comments

Dysgenesis induced revertants restore female fertility.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (4)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (10)