FB2024_03 , released June 25, 2024
Allele: Dmel\foiC887
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General Information
Symbol
Dmel\foiC887
Species
D. melanogaster
Name
FlyBase ID
FBal0319773
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
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Allele class
Mutagen
    Nature of the Allele
    Allele class
    Mutagen
    Progenitor genotype
    Cytology
    Description

    Nucleotide substitution: C2503T.

    Mutations Mapped to the Genome
    Curation Data
    Type
    Location
    Additional Notes
    References
    Nucleotide change:

    C8532800T

    Reported nucleotide change:

    C2614T

    Amino acid change:

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

    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.

    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

    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.

    External Data
    Interactions
    Show genetic interaction network for Enhancers & Suppressors
    Phenotypic Class
    Suppressed by
    Statement
    Reference
    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.

    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.

    Complementation and Rescue Data
    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.

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    Mutant
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    External Crossreferences and Linkouts ( 0 )
    Synonyms and Secondary IDs (1)
    Reported As
    Symbol Synonym
    Name Synonyms
    Secondary FlyBase IDs
      References (1)