FB2024_03 , released June 25, 2024
Allele: Dmel\hpoMGH4
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General Information
Symbol
Dmel\hpoMGH4
Species
D. melanogaster
Name
FlyBase ID
FBal0193408
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Mutagen
    Nature of the Allele
    Mutagen
    Progenitor genotype
    Cytology
    Description
    Mutations Mapped to the Genome
    Curation Data
    Type
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    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
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    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

    Heterozygous larvae show no significant defects in dendrite morphology of ddaC neurons.

    Heterozygous males do not have ectopic sex combs on the second or third legs.

    ddaC clones mutant for hpoMGH4 exhibit simplified dendritic trees in third instar larvae, but show more extensive dendritic arborisations in earlier larval stages (second to early third instar), consistent with the involvement of hpo in the maintenance of dendrites. In hpoMGH4 mutant clones at earlier developmental stages, dendritic branches are often found to overlap.

    hpoMGH4/+ heterozygotes exhibit wild-type dendritic tiling, with wild-type levels of dendritic crossing points per υm[2].

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

    hpoMGH4 has abnormal neuroanatomy phenotype, non-enhanceable by wtsx1/wts[+]

    Suppressed by
    NOT suppressed by
    Statement
    Reference
    Enhancer of
    Statement
    Reference

    hpoMGH4/hpo[+] is an enhancer of visible | dominant phenotype of Pc3

    Other
    Phenotype Manifest In
    NOT Enhanced by
    Statement
    Reference

    hpoMGH4 has multidendritic dendrite phenotype, non-enhanceable by wtsx1/wts[+]

    Suppressed by
    NOT suppressed by
    Statement
    Reference
    Enhancer of
    Statement
    Reference

    hpoMGH4/hpo[+] is an enhancer of sex comb | ectopic phenotype of Pc3

    hpoMGH4/hpo[+] is an enhancer of mesothoracic leg phenotype of Pc3

    hpoMGH4/hpo[+] is an enhancer of metathoracic leg phenotype of Pc3

    Other
    Statement
    Reference

    Pc3, hpoMGH4/hpo[+] has dendrite & dorsal multidendritic neuron ddaC | somatic clone phenotype

    Additional Comments
    Genetic Interactions
    Statement
    Reference

    Pc3/hpoMGH4 double heterozygous larvae show dendritic defects in ddaC neurons; there is a significant reduction in the number of dendritic branchpoints.

    The ectopic sex comb phenotype seen on the second and third legs of Pc3/+ males is enhanced by hpoMGH4/+.

    hpoMGH4 allows recovery of Df(1)su(s)R194/+ clones in the adult eye in animals with mosaic eyes containing two genotypes of cells with respect to RpL36; cells which are Df(1)su(s)R194/+ and cells in which the haplo-insufficiency of Df(1)su(s)R194/+ for RpL36 has been rescued by RpL36+t4 (in a wild-type background the Df(1)su(s)R194/+ clones are eliminated by cell competition and are not seen in the adult eye in these animals). hpoMGH4 does not prevent loss of Df(1)su(s)R194/+ clones in the wing disc.

    Transheterozygotes for trc1/hpoMGH4 exhibit obvious iso-neuronal as well as hetero-neuronal tiling defects, including a significant increase in dendritic crossing-points compared to single mutants.

    Transheterozygotes for trc2/hpoMGH4 exhibit obvious iso-neuronal as well as hetero-neuronal tiling defects, including a significant increase in dendritic crossing-points compared to single mutants.

    Transheterozygotes for fry1/hpoMGH4 exhibit obvious iso-neuronal as well as hetero-neuronal tiling defects, including a significant increase in dendritic crossing-points compared to single mutants.

    Transheterozygotes for wtsx1/hpoMGH4 display simplified dendrites similar to wtsx1 mutants.

    Overexpression of trcScer\UAS.T:Zzzz\FLAG, under the control of Scer\GAL4elav-C155 in hpoMGH4 MARCM clones partially suppresses the dendritic tiling defects in class IV neurons.

    Overexpression of wtsScer\UAS.L.T:Hsap\MYC, under the control of Scer\GAL4elav-C155 in hpoMGH4 MARCM clones does not suppress the dendritic tiling defects in class IV neurons.

    Xenogenetic Interactions
    Statement
    Reference
    Complementation and Rescue Data
    Comments

    Both the dendritic tiling and maintenance phenotypes of hpoMGH4 mutant clones are rescued by expression of hpoScer\UAS.cEa under the control of Scer\GAL4elav-C155 or Scer\GAL4ppk.PG (MARCM).

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    External Crossreferences and Linkouts ( 0 )
    Synonyms and Secondary IDs (2)
    Reported As
    Name Synonyms
    Secondary FlyBase IDs
      References (5)