FB2024_03 , released June 25, 2024
Allele: Dmel\oskA87
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General Information
Symbol
Dmel\oskA87
Species
D. melanogaster
Name
FlyBase ID
FBal0141009
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Mutagen
    Nature of the Allele
    Mutagen
    Progenitor genotype
    Associated Insertion(s)
    Cytology
    Description

    Contains a ZAM element in the first exon of the osk gene.

    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 ( 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

    Segmentation defects are observed in embryos from oskA87/Df(3R)osk mothers expressing oskM1R.Δ118-135.T:Ivir\HA1.

    Segmentation defects are observed in embryos from oskA87/Df(3R)osk mothers expressing oskM1R.Δ121-150.T:Ivir\HA1.

    Segmentation defects are observed in embryos from oskA87/Df(3R)osk mothers expressing oskM1R.Δ91-120.T:Ivir\HA1.

    Segmentation defects are observed in embryos from oskA87/Df(3R)osk mothers expressing oskM1R.INV121-182.T:Ivir\HA1.

    Expression of oskt.WT in osk1/Df(3R)p-XT103 mutant mothers results in embryos containing an average of 24 pole cells, as in wild-type.

    One copy of oskt.WT suppresses the arrest in oogenesis found in oskA87/Df(3R)p-XT103. However, 10% of the resulting embryos are missing abdominal segments, displaying a weak posterior group phenotype.

    oskA87/Df(3R)p-XT103 females fail to lay eggs and are sterile owing to the early arrest of oogenesis.

    osk1/oskA87, osk2/oskA87 and osk9/oskA87 transheterozygous embryos show the 'posterior group' phenotype as they lack an abdomen and germline.

    oskA87/Df(3R)p-XT103 females fail to lay eggs although oocytes are determined and begin to develop, but then arrest. Defects become evident in the egg chambers at stage 2, when fragmentation of the normally compact karyosome is observed. oskA87/Df(3R)p-XT103 egg chambers continue to develop until stage 7, when they begin to degenerate.

    oskA87/Df(3R)p-XT103 females that carry either the oskmM1mM2 or the oskmM1SLmM2 transgene are able to lay eggs but the resulting embryos lack abdomens.

    Embryos produced by oskA87/Df(3R)p-XT103 females that express osk3'UTR.Scer\UAS.P\T, under the control of both Scer\GAL4otu.T:Hsim\VP16 and Scer\GAL4nos.UTR.T:Hsim\VP16, show the 'posterior group' phenotype.

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

    osk[+]/oskA87 is a suppressor of embryonic head phenotype of miraαTub67C.mGFP6

    Other
    Statement
    Reference
    Additional Comments
    Genetic Interactions
    Statement
    Reference

    The bicaudal phenotype of embryos derived from miraαTub67C.T:Avic\GFP-m6/+ females is almost completely suppressed (99.2%) if the females are also heterozygous for oskA87. Although these embryos form normal heads, only 0.6% of them hatch.

    Females double heterozygous for pAbp37-2 and oskA87 produce much more frequently embryos with strong posterior phenotypes than females heterozygous for each of these mutations alone.

    Xenogenetic Interactions
    Statement
    Reference
    Complementation and Rescue Data
    Comments

    Almost all embryos from oskA87/Df(3R)osk mothers expressing oskΔ121-150.T:Ivir\HA1 display normal segmentation.

    Embryos from oskA87/Df(3R)osk mothers expressing oskM1R.Δ40-84.Δ196-423.T:Ivir\HA1 display normal segmentation.

    Almost all embryos from oskA87/Df(3R)osk mothers expressing oskM1R.Δ40-84.Δ196-423.T:Ivir\HA1 display normal segmentation.

    Segmentation defects are observed in embryos from oskA87/Df(3R)osk mothers expressing oskM1R.Δ118-135.T:Ivir\HA1.

    Almost all embryos from oskA87/Df(3R)osk mothers expressing oskM1R.Δ151-180.T:Ivir\HA1 display normal segmentation.

    Segmentation defects are observed in embryos from oskA87/Df(3R)osk mothers expressing oskM1R.Δ121-150.T:Ivir\HA1.

    Segmentation defects are observed in embryos from oskA87/Df(3R)osk mothers expressing oskM1R.Δ91-120.T:Ivir\HA1.

    Segmentation defects are observed in embryos from oskA87/Df(3R)osk mothers expressing oskM1R.INV121-182.T:Ivir\HA1.

    Almost all embryos from oskA87/Df(3R)osk mothers expressing oskM1R.T:Ivir\HA1 display normal segmentation.

    Expression of osk3'UTR.attB.Scer\UAS.P\T driven by a combination of Scer\GAL4nos.UTR.T:Hsim\VP16 and Scer\GAL4mat.αTub67C.T:Hsim\VP16 is sufficient to rescue the early oogenesis arrest and egg-less phenotype of oskA87/Df(3R)p-XT103 females.

    Expression of osk3'UTR.ΔAR-a.Scer\UAS.P\T driven by a combination of Scer\GAL4nos.UTR.T:Hsim\VP16 and Scer\GAL4mat.αTub67C.T:Hsim\VP16 fails to rescue the egg-less phenotype of oskA87/Df(3R)p-XT103 females and egg chambers do not develop beyond stage 7.

    Expression of osk3'UTR.ΔAR-b.Scer\UAS.P\T driven by a combination of Scer\GAL4nos.UTR.T:Hsim\VP16 and Scer\GAL4mat.αTub67C.T:Hsim\VP16 fails to rescue the egg-less phenotype of oskA87/Df(3R)p-XT103 females and egg chambers do not develop beyond stage 7.

    The cuticle defects of embryos derived from oskA87/Df(3R)osk females are rescued by osk+t8.

    oskBRE.AB- almost completely rescues the cuticle defects of embryos derived from oskA87/Df(3R)osk females; 96% have wild-type cuticles, while 4% have head defects.

    83% of embryos derived from oskA87/Df(3R)osk females carrying oskBRE.C- have 0-1 abdominal segments, and 14% have 2-7 abdominal segments.

    Expression of the either the oskmM1mM2 or the oskmM1SLmM2 transgene rescues the egg-less phenotype of oskA87/Df(3R)p-XT103 females but the embryos produced lack an abdomen.

    Expression of oskScer\UAS.P\T.cJa, under the control of both Scer\GAL4otu.T:Hsim\VP16 and Scer\GAL4nos.UTR.T:Hsim\VP16, rescues the early oogenesis arrest of oskA87/Df(3R)p-XT103 females, as well as the 'posterior group' phenotype of the progeny (lack of abdomen and germline).

    Expression of the intronless oskΔi.123.Scer\UAS.P\T, under the control of both Scer\GAL4otu.T:Hsim\VP16 and Scer\GAL4nos.UTR.T:Hsim\VP16, rescues the early oogenesis arrest of oskA87/Df(3R)p-XT103 females.

    Expression of osk3'UTR.Scer\UAS.P\T, under the control of both Scer\GAL4otu.T:Hsim\VP16 and Scer\GAL4nos.UTR.T:Hsim\VP16, rescues the early oogenesis and egg-less phenotype of oskA87/Df(3R)p-XT103 females and the karyosome defect. However, the 'posterior group' phenotype of the embryos produced from these females is not rescued.

    osk13TTTAY rescues the stage 6 oocyte arrest phenotype of oskA87/Df(3R)p-XT103 females.

    osk13TTgAY rescues the stage 6 oocyte arrest phenotype of oskA87/Df(3R)p-XT103 females. However, embryos derived from oskA87/Df(3R)p-XT103;osk13TTgAY mothers display a fully penetrant osk mutant maternal-effect phenotype in which the abdomen fails to form.

    Expression of oskTTgAY.A, oskTTgAY.C or oskTTgAY.D fails to rescue the osk RNA and protein localisation defects observed in oskA87/Df(3R)p-XT103 oocytes.

    Expression of the oskTTgAY.B transgene fully rescues the osk RNA and protein localisation defects observed in oskA87/Df(3R)p-XT103 oocytes.

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

    M. Erdelyi D. St Johnston A. Ephrussi

    Mutagen comment: this allele was discovered in an EMS mutagenesis screen, although it was found to have a ZAM insertion.

    External Crossreferences and Linkouts ( 0 )
    Synonyms and Secondary IDs (3)
    References (33)