FlyBase Allele Report: Dmel\kel[DE1]

General Information

Symbol

Dmel\kel^DE1

Species

D. melanogaster

Name

FlyBase ID

FBal0031520

Feature type

allele

Associated gene

Dmel\kel

Associated Insertion(s)

Carried in Construct

Also Known As

kelch^DE1

Key Links

Genomic Maps

JBrowse

Allele class

loss of function allele

Mutagen

ethyl methanesulfonate

Nature of the Allele

Allele class

loss of function allele

(Robinson and Cooley, 1997, Robinson and Cooley, 1997, Xue and Cooley, 1993)

Mutagen

ethyl methanesulfonate

(Xue and Cooley, 1993, Schupbach and Wieschaus, 1991)

Progenitor genotype

Cytology

Description

Amino acid replacement: Q109term.

(Hudson et al., 2015)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

point_mutation

2L:18,137,607..18,137,607 [-]

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.

(Hudson et al., 2015)

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

abnormal cell shape

(Djagaeva et al., 2005)

abnormal cell size | adult stage | female

(Hudson et al., 2015)

decreased cell size | oogenesis

(Hudson et al., 2019)

female sterile

(Hudson et al., 2015, Schupbach and Wieschaus, 1991)

female sterile | recessive

(Robinson and Cooley, 1997, Xue and Cooley, 1993)

increased cell death

(Djagaeva et al., 2005)

Phenotype Manifest In

actin cytoskeleton | adult stage | female

(Hudson et al., 2015)

actin filament

(Djagaeva et al., 2005)

egg

(Hudson et al., 2019)

egg chamber

(Djagaeva et al., 2005)

filamentous actin

(Hudson and Cooley, 2010)

filamentous actin | oogenesis

(Hudson et al., 2019)

karyosome

(Djagaeva et al., 2005)

nurse cell

(Foley and Cooley, 1998)

nurse cell & actin filament

(Kelso et al., 2002)

nurse cell & nucleus

(Djagaeva et al., 2005)

nurse cell fusome

(Djagaeva et al., 2005)

nurse cell ring canal

(Hudson et al., 2019, Hudson et al., 2015, Wahlstrom et al., 2004, Kelso et al., 2002, Robinson and Cooley, 1997)

nurse cell ring canal | oogenesis stage S6

(Hudson and Cooley, 2010)

nurse cell ring canal | oogenesis stage S7

(Hudson and Cooley, 2010)

nurse cell ring canal | oogenesis stage S8

(Hudson and Cooley, 2010)

nurse cell ring canal | oogenesis stage S9

(Hudson and Cooley, 2010)

nurse cell ring canal | oogenesis stage S10

(Hudson and Cooley, 2010)

nurse cell ring canal | oogenesis stage S11

(Hudson and Cooley, 2010)

nurse cell ring canal | oogenesis stage S12

(Hudson and Cooley, 2010)

nurse cell ring canal | oogenesis stage S13

(Hudson and Cooley, 2010)

nurse cell ring canal | oogenesis stage S14

(Hudson and Cooley, 2010)

nurse cell ring canal rim

(Robinson and Cooley, 1997)

oocyte

(Hudson et al., 2015, Djagaeva et al., 2005)

oocyte & actin filament

(Kelso et al., 2002)

stalk follicle cell

(Djagaeva et al., 2005)

Detailed Description

Statement

Reference

kel^DE1 homozygosity induces very thick F-actin rim in egg chamber ring canals. Eggs laid are significantly smaller than controls.

(Hudson et al., 2019)

kel^DE1 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.

(Hudson et al., 2015)

kel^DE1 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.

(Hudson and Cooley, 2010)

kel^DE1 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 kel^DE1 nurse cells have greater levels of F-actin than wild type and appear abnormal. Additionally, in 10-15% of kel^DE1 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.

(Djagaeva et al., 2005)

At stage 9 of oogenesis kel^DE1 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.

(Kelso et al., 2002)

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

(Foley and Cooley, 1998)

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

(Robinson and Cooley, 1997)

Actin filaments in the ring canals are disorganised in homozygous females. This phenotype is rescued by kel^{ORF1.otu.T:Hsap\MYC} and kel^{ΔNORF1.otu.T:Hsap\MYC} but not by kel^{KREP.otu.T:Hsap\MYC}.

(Robinson and Cooley, 1997)

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.

(Xue and Cooley, 1993)

Abnormalities in follicle cell migration: open ended chorion.

(Schupbach and Wieschaus, 1991)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

NOT Enhancer of

Statement

Reference

kel^DE1/kel^DE1 is a non-enhancer of decreased cell size phenotype of hts^R913fs

(Hudson et al., 2019)

kel^DE1 is a non-enhancer of visible phenotype of Scer\GAL4^en-e16E, arm^UAS.cWa

(Greaves et al., 1999)

kel^DE1 is a non-enhancer of visible phenotype of Scer\GAL4^en-e16E, shg^{i.UAS.Tag:SS(aos),Tag:MYC}

(Greaves et al., 1999)

NOT Suppressor of

Statement

Reference

kel^DE1/kel^DE1 is a non-suppressor of decreased cell size phenotype of hts^R913fs

(Hudson et al., 2019)

kel^DE1 is a non-suppressor of visible phenotype of Scer\GAL4^en-e16E, arm^UAS.cWa

(Greaves et al., 1999)

kel^DE1 is a non-suppressor of visible phenotype of Scer\GAL4^en-e16E, shg^{i.UAS.Tag:SS(aos),Tag:MYC}

(Greaves et al., 1999)

Other

Statement

Reference

dbo^Δ25.1, kel^DE1 has abnormal planar polarity phenotype

(Strutt et al., 2013)

Phenotype Manifest In

NOT Enhanced by

Statement

Reference

kel^DE1 has nurse cell ring canal phenotype, non-enhanceable by Actn^Δ233/Actn^Δ208

(Wahlstrom et al., 2004)

Suppressed by

Statement

Reference

kel^DE1 has filamentous actin | oogenesis phenotype, suppressible by hts^R913fs/hts^R913fs

(Hudson et al., 2019)

kel^DE1 has nurse cell ring canal phenotype, suppressible by hts^R913fs/hts^R913fs

(Hudson et al., 2019)

NOT suppressed by

Statement

Reference

kel^DE1 has nurse cell ring canal phenotype, non-suppressible by Actn^Δ233/Actn^Δ208

(Wahlstrom et al., 2004)

Enhancer of

Statement

Reference

kel^DE1/kel[+] is an enhancer of filamentous actin | oogenesis phenotype of Prosβ5^HMS00119, Scer\GAL4^{VP16.mat.αTub67C}, hts^{Ovhts.UASp.GFP(S65T)}

(Hudson et al., 2019)

kel^DE1/kel[+] is an enhancer of nurse cell ring canal phenotype of Prosβ5^HMS00119, Scer\GAL4^{VP16.mat.αTub67C}, hts^{Ovhts.UASp.GFP(S65T)}

(Hudson et al., 2019)

kel^DE1/kel[+] is an enhancer of nurse cell ring canal phenotype of Prosβ5^HMS00119, Scer\GAL4^{VP16.mat.αTub67C}

(Hudson et al., 2015)

kel^DE1/kel[+] is an enhancer of actin cytoskeleton | adult stage | female phenotype of Prosβ5^HMS00119, Scer\GAL4^{VP16.mat.αTub67C}

(Hudson et al., 2015)

NOT Enhancer of

Statement

Reference

kel^DE1/kel^DE1 is a non-enhancer of egg phenotype of hts^R913fs

(Hudson et al., 2019)

kel^DE1 is a non-enhancer of wing phenotype of Scer\GAL4^en-e16E, arm^UAS.cWa

(Greaves et al., 1999)

kel^DE1 is a non-enhancer of wing phenotype of Scer\GAL4^en-e16E, shg^{i.UAS.Tag:SS(aos),Tag:MYC}

(Greaves et al., 1999)

NOT Suppressor of

Statement

Reference

kel^DE1/kel^DE1 is a non-suppressor of nurse cell ring canal phenotype of hts^R913fs

(Hudson et al., 2019)

kel^DE1/kel^DE1 is a non-suppressor of filamentous actin | oogenesis phenotype of hts^R913fs

(Hudson et al., 2019)

kel^DE1/kel^DE1 is a non-suppressor of egg phenotype of hts^R913fs

(Hudson et al., 2019)

kel^DE1 is a non-suppressor of wing phenotype of Scer\GAL4^en-e16E, arm^UAS.cWa

(Greaves et al., 1999)

kel^DE1 is a non-suppressor of wing phenotype of Scer\GAL4^en-e16E, shg^{i.UAS.Tag:SS(aos),Tag:MYC}

(Greaves et al., 1999)

Other

Statement

Reference

dbo^Δ25.1, kel^DE1 has ommatidium phenotype

(Strutt et al., 2013)

dbo^Δ25.1, kel^DE1 has wing hair phenotype

(Strutt et al., 2013)

Additional Comments

Genetic Interactions

Statement

Reference

kel^DE1, hts^R913fs double homozygotes exhibit the same thinner egg chamber ring canal F-actin rim phenotype observed in hts^R913fs single homozygotes rather than the very thick F-actin rim phenotype observed in kel^DE1 single homozygotes.

(Hudson et al., 2019)

kel^DE1 dbo^Δ25.1 double mutant wings show trichome swirls only below vein 4. Approximately 1% of ommatidia in the eye are mispolarised.

(Strutt et al., 2013)

Ring canal morphology in Actn^Δ208/Actn^Δ233 ; kel^DE1/kel^DE1 double mutant females is the same as in kel^DE1 single mutants.

(Wahlstrom et al., 2004)

Rescue of actin cytoskeleton organization and ring canal localization in the oocyte and nurse cells of kel^DE1 homozygotes by kel^Y627A.otu is unaffected by Src64B^Δ17/Src64B^Δ17. Neither is the abnormal ring canal morphology in these animals.

(Kelso et al., 2002)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Rescued by

kel^DE1 is rescued by Scer\GAL4^VP16.otu/kel^UASp.cHa

(Hudson et al., 2015)

kel^DE1 is rescued by kel^UASp.cHa/Scer\GAL4^{VP16.mat.αTub67C}

(Hudson et al., 2015)

kel^DE1 is rescued by Scer\GAL4^VP16.otu/kel^K0.UASp

(Hudson et al., 2015)

kel^DE1 is rescued by Scer\GAL4^{VP16.mat.αTub67C}/kel^K0.UASp

(Hudson et al., 2015)

kel^DE1 is rescued by kel^QSTN.UASp/Scer\GAL4^{VP16.mat.αTub67C}

(Hudson et al., 2015)

kel^DE1 is rescued by kel^{K414R.K428R.UASp}/Scer\GAL4^{VP16.mat.αTub67C}

(Hudson et al., 2015)

kel^DE1 is rescued by kel^{K414R.K428R.UASp}/Scer\GAL4^VP16.otu

(Hudson et al., 2015)

kel^DE1 is rescued by kel^6KR.UASp/Scer\GAL4^{VP16.mat.αTub67C}

(Hudson et al., 2015)

kel^DE1 is rescued by Scer\GAL4^VP16.otu/kel^6KR.UASp

(Hudson et al., 2015)

kel^DE1 is rescued by kel^ORF1.otu

(Kelso et al., 2002)

kel^DE1 is rescued by kel^ORF1.otu

(Robinson and Cooley, 1997)

kel^DE1 is rescued by kel^{ORF1.otu.Tag:MYC}

(Robinson and Cooley, 1997)

kel^DE1 is rescued by kel^otu.PR

(Robinson and Cooley, 1997)

kel^DE1 is rescued by kel^{ORF1.otu.Tag:MYC}

(Robinson and Cooley, 1997)

kel^DE1 is rescued by kel^{ΔNORF1.otu.Tag:MYC}

(Robinson and Cooley, 1997)

Partially rescued by

kel^DE1 is partially rescued by Scer\GAL4^VP16.otu/kel^QSTN.UASp

(Hudson et al., 2015)

kel^DE1 is partially rescued by kel^Y627A.otu

(Kelso et al., 2002)

Not rescued by

kel^DE1 is not rescued by kel^FE.UASp/Scer\GAL4^VP16.otu

(Hudson et al., 2015)

kel^DE1 is not rescued by kel^FE.UASp/Scer\GAL4^{VP16.mat.αTub67C}

(Hudson et al., 2015)

kel^DE1 is not rescued by kel^ΔUGA.otu

(Robinson and Cooley, 1997)

kel^DE1 is not rescued by kel^Ala.otu

(Robinson and Cooley, 1997)

kel^DE1 is not rescued by kel^{ORF2.otu.Tag:MYC}

(Robinson and Cooley, 1997)

kel^DE1 is not rescued by kel^Ser.otu

(Robinson and Cooley, 1997)

kel^DE1 is not rescued by kel^{KREP.otu.Tag:MYC}

(Robinson and Cooley, 1997)

kel^DE1 is not rescued by kel^{IVRKREP.otu.Tag:MYC}

(Robinson and Cooley, 1997)

kel^DE1 is not rescued by kel^{BTBIVR.otu.Tag:MYC}

(Robinson and Cooley, 1997)

kel^DE1 is not rescued by kel^{ORF1-R.otu.Tag:MYC}

(Robinson and Cooley, 1997)

Comments

Expression of any of the following: kel^{K414R.K428R.Scer\UAS.P\T}, kel^{6KR.Scer\UAS.P\T}, kel^{Scer\UAS.P\T.cHa}, kel^{K0.Scer\UAS.P\T}, kel^{QSTN.Scer\UAS.P\T} under the control of either Scer\GAL4^{mat.αTub67C.T:Hsim\VP16} or Scer\GAL4^{otu.T:Hsim\VP16} rescues the female sterility of kel^DE1 mutants.

Expression of either kel^{Scer\UAS.P\T.cHa} or kel^{K0.Scer\UAS.P\T} under the control of either Scer\GAL4^{otu.T:Hsim\VP16} (resulting in a low-level expressing) or Scer\GAL4^{mat.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 kel^DE1 homozygote females.

Expression of kel^{QSTN.Scer\UAS.P\T} under the control of Scer\GAL4^{otu.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 kel^DE1 homozygote mutant females, while expression under the Scer\GAL4^{mat.αTub67C.T:Hsim\VP16} driver (resulting in a high-level expression) fully rescues both the ring canal and small oocyte phenotypes.

Expression of kel^{FE.Scer\UAS.P\T} under the control of either Scer\GAL4^{otu.T:Hsim\VP16} driver (resulting in a low-level expressing) or Scer\GAL4^{mat.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 kel^DE1 homozygote females and neither rescues their sterility.

(Hudson et al., 2015)

Organization of the actin cytoskeleton and ring canal localization in the oocyte and nurse cells of kel^DE1 homozygotes is rescued by kel^Y627A.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.

(Kelso et al., 2002)

The sterility of homozygous females is rescued by kel^otu.PR, kel^{ORF1.otu.T:Hsap\MYC} and kel^ORF1.otu, but not by kel^Ala.otu, kel^ΔUGA.otu or kel^Ser.otu. The ring canal phenotype is largely rescued by kel^otu.PR, kel^{ORF1.otu.T:Hsap\MYC} and kel^ORF1.otu, is partially rescued by kel^Ala.otu, and is not rescued by kel^ΔUGA.otu or kel^Ser.otu. Hemizygous kel^DE1 flies carrying kel^ORF1.otu produce eggs at nearly wild-type rates, which is significantly higher than the rate of egg production of hemizygous kel^DE1 flies that do not carry kel^ORF1.otu. 91.5% of the eggs laid by hemizygous kel^DE1 flies carrying kel^ORF1.otu survive to hatching.

(Robinson and Cooley, 1997)

Images (0)

Mutant

Wild-type

Stocks (2)

4893

107933

Notes on Origin

Discoverer

Schupbach and Wieschaus.

(Xue and Cooley, 1993)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (3)

Reported As

Symbol Synonym

Kelch^ED1

(Molina López et al., 2023)

kel^DE1

(Hudson et al., 2019, Mannix et al., 2019, Wang et al., 2016, Hudson et al., 2015, Rudrapatna et al., 2014, Strutt et al., 2013, Hudson and Cooley, 2010, Djagaeva and Doronkin, 2009, Christensen and Cook, 2007.3.22)

kelch^DE1

(Gorjanacz et al., 2002, Sokol and Cooley, 1999, Foley and Cooley, 1998)

Name Synonyms

Secondary FlyBase IDs

References (21)

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