FB2024_03 , released June 25, 2024
Allele: Dmel\beat-IaC163
Open Close
General Information
Symbol
Dmel\beat-IaC163
Species
D. melanogaster
Name
FlyBase ID
FBal0085881
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
beatC163
Key Links
Allele class
Mutagen
    Nature of the Allele
    Allele class
    Mutagen
    Progenitor genotype
    Caused by aberration
    Cytology
    Description

    Aberration breakpoint within beat-Ia.

    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

    beat-IaC163/Df(2L)BSC278 results in lethality with escapers.

    beat-Ia3/beat-IaC163 third instar larvae often lack neuromuscular junctions (NMJs) on dorsal muscles (the percentage of muscles lacking NMJs is given in parentheses); muscle 1 (31%), muscle 9 (34%), muscle 2 (8%), muscle 10 (13%).

    beat-Ia3/beat-IaC163 third instar larvae often lack neuromuscular junctions (NMJs) on ventral muscles (the percentage of muscles lacking NMJs is given in parentheses); muscle 12 (25%), muscle 13 (34%), muscle 6 (38%), muscle 7 (55%).

    Leaky allele.

    External Data
    Interactions
    Show genetic interaction network for Enhancers & Suppressors
    Phenotypic Class
    NOT Enhanced by
    Statement
    Reference
    NOT suppressed by
    Statement
    Reference
    Enhancer of
    Statement
    Reference

    unc-5[+], beat-IaC163, beat-Ia[+], unc-58 is an enhancer of abnormal neuroanatomy phenotype of eve3

    Suppressor of
    Phenotype Manifest In
    NOT Enhanced by
    NOT suppressed by
    Statement
    Reference

    beat-IaC163/beat-Ia3, unc-58 has motor neuron phenotype, non-suppressible by Nrgl10

    Enhancer of
    Statement
    Reference

    unc-5[+], beat-IaC163, beat-Ia[+], unc-58 is an enhancer of larval intersegmental nerve phenotype of eve3

    Suppressor of
    Additional Comments
    Genetic Interactions
    Statement
    Reference

    CNS exit from EW neurons misexpressing eveScer\UAS.cBa is partially suppressed in an unc-58 beat-IaC163/beat-Ia3 mutant background while midline crossing is partially restored (in 15% of hemisegments).

    Nrgl10/Y; beat-IaC163/beat-Ia3 double mutants exhibit intersegmental nerve axon stalling prior to the first branch point.

    unc-58, beat-IaC163/beat-Ia3 double mutants exhibit intersegmental nerve axon stalling prior to the first branch point.

    Nrgl10/Y; unc-58, beat-IaC163/beat-Ia3 triple mutants exhibit severe defects in the intersegmental nerve crossing in the ventral muscle field.

    Nrgl10/Y; beat-IaC163/beat-Ia3 double mutants do not exhibit any aCC or RP2 exit phenotypes.

    unc-58, beat-IaC163/beat-Ia3 mutants exhibit a failure of motor neurons to exit the CNS in 10% of hemisegments.

    The addition of a Nrgl10/Y background does not affect the unc-58, beat-IaC163/beat-Ia3 CNS exit failure seen in 10% of unc-58, beat-IaC163/beat-Ia3 hemisegments.

    A transheterozygous combination of eve3/+, unc-58/+ reduces beat-Ia levels to 50% and significantly increases the defects seen in intersegmental nerves, with the number of axons exhibiting stalling increasing from 8.1% to 23.1% in eve3/+, unc-58/+ transheterozygotes and eve3/+, unc-58/+, beat-IaC163/+ triple heterozygotes, respectively.

    A heterozygous beat-IaC163 background dominantly suppresses the ISNb pathfinding phenotypes from 64% in fracΔ1 homozygotes to 18% in double mutants.

    The neuromuscular junction innervation defects seen in the dorsal muscles of beat-Ia3/beat-IaC163 third instar larvae are not enhanced by expression of sideScer\UAS.cSa under the control of either Scer\GAL4how-24B or Scer\GAL4Mef2.PR.

    Xenogenetic Interactions
    Statement
    Reference
    Complementation and Rescue Data
    Images (0)
    Mutant
    Wild-type
    Stocks (2)
    Notes on Origin
    Discoverer
    External Crossreferences and Linkouts ( 0 )
    Synonyms and Secondary IDs (8)
    References (11)