FB2025_01 , released February 20, 2025
Allele: Dmel\foiC887
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General Information
Symbol
Dmel\foiC887
Species
D. melanogaster
Name
FlyBase ID
FBal0319773
Feature type
allele
Associated gene
Dmel\foi
Associated Insertion(s)
Carried in Construct
Key Links
Genomic Maps

Allele class
Mutagen
    Nature of the Allele
    Allele class
    Mutagen
    Progenitor genotype
    Cytology
    Description

    Nucleotide substitution: C2503T.

    (Carrasco-Rando et al., 2016)
    Mutations Mapped to the Genome
    Curation Data
    Type
    Location
    Additional Notes
    References
    point_mutation
    3L:8,532,800..8,532,800 [+]
    Nucleotide change:

    C8532800T

    Reported nucleotide change:

    C2614T

    Amino acid change:

    Q628term | foi-PA; Q628term | foi-PB; Q628term | foi-PC; Q628term | foi-PD

    Comment:

    Reported as a C to T change at nucleotide 2503 of the foi cDNA, assumed to be RE41071. Mutation mapped to position 2504 of the cDNA, which corresponds to the C of a Glutamine codon.

    (Carrasco-Rando et al., 2016)
    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
        Phenotype Manifest In
        Detailed Description
        Statement
        Reference

        foiC887/foiC887 and foiC887/Df(3L)BSC13 mutant embryos display defective muscle patterning with missing muscles, morphological defects in dorsal, lateral and ventral groups of muscles, and a fusion defect shown by reduced size of the remaining muscles. In foiC887/foiC887 mutant embryos, the visceral mesoderm is defective, with loss of the gastric caeca and anterior gut constriction, misplaced middle constriction, in many cases a delay in the formation or failure to complete the posterior gut constriction, and the DA1 muscle displays myoblast fusion defects, as compared to wild type. Mutants also display failure of the SNb nerve branch to defasciculate from the dorsal ISN leaving ventral muscles without innervation, as compared with controls. Founder cell segregation is unaffected in foiC887/foiC887 mutants, but there appears to be failed specification and/or segregation of fusion-competent myoblasts (FCMs), and an increase in the number of apoptotic FCMs.

        (Carrasco-Rando et al., 2016)
        External Data
        Interactions
        Show genetic interaction network for Enhancers & Suppressors
        Phenotypic Class
        Suppressed by
        Statement
        Reference

        foiC887 has abnormal cell death | embryonic stage phenotype, suppressible by Df(3L)H99/Df(3L)H99

        (Carrasco-Rando et al., 2016)
        Phenotype Manifest In
        Suppressed by
        NOT suppressed by
        Additional Comments
        Genetic Interactions
        Statement
        Reference

        foiC887/foiC887, Df(3L)H99/Df(3L)H99 double mutants do not exhibit apoptosis of fusion-competent myoblasts (FCMs), but otherwise still exhibit defective differentiation of FCMs and do not appear phenotypically different to foiC887/foiC887 mutants.

        Expression of ZnT63CScer\UAS.cWa or lmdScer\UAS.cRa under the control of Scer\GAL4Mef2.PU fails to rescue the faulty specification of fusion-competent myoblasts in foiC887/foiC887 mutants.

        Expression of CatsupScer\UAS.cCa under the control of Scer\GAL4Mef2.PU fails to rescue the faulty specification of fusion-competent myoblasts nor the DA1 myoblast fusion defect in foiC887/foiC887 mutants.

        Expression of Zip42C.1Scer\UAS.T:Avic\GFP-EGFP under the control of Scer\GAL4Mef2.PU significantly rescues the faulty specification of fusion-competent myoblasts, and partially rescues the DA1 fusion defects of foiC887/foiC887 mutants.

        Expression of Zip71BScer\UAS.cCa under the control of Scer\GAL4Mef2.PU significantly rescues the faulty specification of fusion-competent myoblasts, but does not rescue the myoblast fusion defects, including in the DA1 muscle, of foiC887/foiC887 mutants.

        (Carrasco-Rando et al., 2016)
        Xenogenetic Interactions
        Statement
        Reference

        Expression of Hsap\SLC39A6Scer\UAS.cCa under the control of Scer\GAL4Mef2.PU fails to rescue the faulty specification of fusion-competent myoblasts nor the DA1 myoblast fusion defect in foiC887/foiC887 mutants.

        (Carrasco-Rando et al., 2016)
        Complementation and Rescue Data
        Rescued by

        foiC887 is rescued by foiUAS.cCa/Scer\GAL4Mef2.PU

        (Carrasco-Rando et al., 2016)
        Partially rescued by

        foiC887 is partially rescued by Scer\GAL4sns.PU/foiUAS.cCa

        (Carrasco-Rando et al., 2016)

        foiC887 is partially rescued by foiUAS.cCa/Scer\GAL4kirre.PU

        (Carrasco-Rando et al., 2016)

        foiC887 is partially rescued by foiUAS.cCa

        (Carrasco-Rando et al., 2016)
        Comments

        Expression of foiScer\UAS.cCa under the control of Scer\GAL4Mef2.PU fully rescues the muscle patterning and fusion, visceral mesoderm, and defective fusion-competent myoblast differentiation phenotypes of foiC887/foiC887 mutants.

        Expression of foiScer\UAS.cCa under the control of Scer\GAL4sns.PU partially rescues the defective fusion-competent myoblast differentiation and DA1 fusion phenotypes of foiC887/foiC887 mutants.

        Expression of foiScer\UAS.cCa under the control of Scer\GAL4kirre.PU fails to rescue the defective fusion-competent myoblast differentiation, but does rescue the muscle patterning defects of foiC887/foiC887 mutants.

        Expression of foiScer\UAS.cCa with no GAL4 driver is sufficient to reduce the defective fusion-competent myoblast differentiation phenotype, and partially rescue the DA1 fusion phenotype of foiC887/foiC887 mutants.

        (Carrasco-Rando et al., 2016)
        Images (0)
        Mutant
        Wild-type
        Stocks (0)
        Notes on Origin
        Discoverer
        External Crossreferences and Linkouts ( 0 )
        Synonyms and Secondary IDs (1)
        Reported As
        Symbol Synonym
        foiC887
        (Carrasco-Rando et al., 2016)
        Name Synonyms
        Secondary FlyBase IDs
          References (1)