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General Information
Symbol
Dmel\kelDE1
Species
D. melanogaster
Name
FlyBase ID
FBal0031520
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
kelchDE1
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
point mutation
Nucleotide change:

C18137607T

Amino acid change:

Q109term | kel-PA; Q109term | kel-PB

Reported amino acid change:

Q109term

Comment:

Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.

Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

Amino acid replacement: Q109term.

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

kelDE1 homozygosity induces very thick F-actin rim in egg chamber ring canals. Eggs laid are significantly smaller than controls.

kelDE1 homozygote mutant females display a ring canal phenotype in the egg chambers (thickening of the F-actin cytoskeleton and significantly smaller lumen diameter) and produce smaller oocytes compared to wild-type.

kelDE1 mutant ring canals in egg chambers display small lumen and F-actin disorganization. The ring canal phenotype first appears at approximately stage 6 of oogenesis. From stage 6 until the end of oogenesis, the growth of the outer diameters of the mutant ring canals is similar to wild-type. However, the inner diameter fail to expand, leaving a small lumen similar in size to ring canals of very young egg chambers.

kelDE1 mutants display multiple defects in oogenesis, including fusion of neighbouring egg chambers in 10-15% of ovarioles, mislocalization of the oocyte, defects in cellular shape and morphology, occasional apoptosis and a lack of stalk cells. The fusomes of kelDE1 nurse cells have greater levels of F-actin than wild type and appear abnormal. Additionally, in 10-15% of kelDE1 oocytes, karyosome morphology is abnormal. The nurse cells of these mutants occasionally show an aberrant accumulation of G-actin in the nuclei. Finally, the microtubule-dependent transport of proteins from the nurse cells to the oocyte appears to be affected.

At stage 9 of oogenesis kelDE1 homozygotes show massive disorganization the nurse cell and oocyte actin cytoskeleton, and partial occlusion of ring canal lumens. Ring canals are also mis-localized, sometimes ending up in the oocyte cytoplasm.

DNA fragmentation occurs in homozygous nurse cells, but is delayed with respect to wild-type.

Homozygous females have disorganised ring canal rims with a reduced lumen.

Actin filaments in the ring canals are disorganised in homozygous females. This phenotype is rescued by kelORF1.otu.T:Hsap\MYC and kelΔNORF1.otu.T:Hsap\MYC but not by kelKREP.otu.T:Hsap\MYC.

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.

Abnormalities in follicle cell migration: open ended chorion.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
NOT Enhancer of
Statement
Reference
NOT Suppressor of
Statement
Reference
Other
Phenotype Manifest In
NOT Enhanced by
Statement
Reference
Suppressed by
Statement
Reference
NOT suppressed by
Statement
Reference
Enhancer of
NOT Enhancer of
Statement
Reference

kelDE1/kelDE1 is a non-enhancer of egg phenotype of htsR913fs

kelDE1 is a non-enhancer of wing phenotype of Scer\GAL4en-e16E, armUAS.cWa

NOT Suppressor of
Statement
Reference

kelDE1/kelDE1 is a non-suppressor of nurse cell ring canal phenotype of htsR913fs

kelDE1/kelDE1 is a non-suppressor of egg phenotype of htsR913fs

kelDE1 is a non-suppressor of wing phenotype of Scer\GAL4en-e16E, armUAS.cWa

Other
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

kelDE1, htsR913fs double homozygotes exhibit the same thinner egg chamber ring canal F-actin rim phenotype observed in htsR913fs single homozygotes rather than the very thick F-actin rim phenotype observed in kelDE1 single homozygotes.

kelDE1 dboΔ25.1 double mutant wings show trichome swirls only below vein 4. Approximately 1% of ommatidia in the eye are mispolarised.

Ring canal morphology in ActnΔ208/ActnΔ233 ; kelDE1/kelDE1 double mutant females is the same as in kelDE1 single mutants.

Rescue of actin cytoskeleton organization and ring canal localization in the oocyte and nurse cells of kelDE1 homozygotes by kelY627A.otu is unaffected by Src64BΔ17/Src64BΔ17. Neither is the abnormal ring canal morphology in these animals.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Partially rescued by
Comments

Expression of any of the following: kelK414R.K428R.Scer\UAS.P\T, kel6KR.Scer\UAS.P\T, kelScer\UAS.P\T.cHa, kelK0.Scer\UAS.P\T, kelQSTN.Scer\UAS.P\T under the control of either Scer\GAL4mat.αTub67C.T:Hsim\VP16 or Scer\GAL4otu.T:Hsim\VP16 rescues the female sterility of kelDE1 mutants.

Expression of either kelScer\UAS.P\T.cHa or kelK0.Scer\UAS.P\T under the control of either Scer\GAL4otu.T:Hsim\VP16 (resulting in a low-level expressing) or Scer\GAL4mat.αTub67C.T:Hsim\VP16 (resulting in a high-level expression) fully rescues the nurse cell ring canal (thickening of the F-actin cytoskeleton) and small oocyte phenotypes characteristic for kelDE1 homozygote females.

Expression of kelQSTN.Scer\UAS.P\T under the control of Scer\GAL4otu.T:Hsim\VP16 (resulting in a low-level expressing) fully restores the small oocyte phenotype but only partially rescues the nurse cell ring canal phenotype (thickening of the F-actin cytoskeleton) characteristic for kelDE1 homozygote mutant females, while expression under the Scer\GAL4mat.αTub67C.T:Hsim\VP16 driver (resulting in a high-level expression) fully rescues both the ring canal and small oocyte phenotypes.

Expression of kelFE.Scer\UAS.P\T under the control of either Scer\GAL4otu.T:Hsim\VP16 driver (resulting in a low-level expressing) or Scer\GAL4mat.αTub67C.T:Hsim\VP16 (resulting in a high-level expression) does not rescue either the nurse cell ring canal phenotype (thickening of the F-actin cytoskeleton) or the small oocyte phenotype characteristic for kelDE1 homozygote females and neither rescues their sterility.

Organization of the actin cytoskeleton and ring canal localization in the oocyte and nurse cells of kelDE1 homozygotes is rescued by kelY627A.otu. However, the morphology of these ring canals (as assessed by actin localization in the canal) is not wild-type: they are significantly narrower than in wild-type, and have a much more concave rim.

The sterility of homozygous females is rescued by kelotu.PR, kelORF1.otu.T:Hsap\MYC and kelORF1.otu, but not by kelAla.otu, kelΔUGA.otu or kelSer.otu. The ring canal phenotype is largely rescued by kelotu.PR, kelORF1.otu.T:Hsap\MYC and kelORF1.otu, is partially rescued by kelAla.otu, and is not rescued by kelΔUGA.otu or kelSer.otu. Hemizygous kelDE1 flies carrying kelORF1.otu produce eggs at nearly wild-type rates, which is significantly higher than the rate of egg production of hemizygous kelDE1 flies that do not carry kelORF1.otu. 91.5% of the eggs laid by hemizygous kelDE1 flies carrying kelORF1.otu survive to hatching.

Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer

Schupbach and Wieschaus.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (2)
References (19)