FB2024_03 , released June 25, 2024
Allele: Dmel\Hs6std770
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General Information
Symbol
Dmel\Hs6std770
Species
D. melanogaster
Name
FlyBase ID
FBal0212981
Feature type
allele
Associated gene
Dmel\Hs6st
Associated Insertion(s)
Carried in Construct
Key Links
Allele class

loss of function allele

Mutagen
Nature of the Allele
Allele class

loss of function allele

(Kamimura et al., 2006)
Mutagen
Delta2-3 transposase
(Kamimura et al., 2006)
Progenitor genotype
Hs6stA201.1M3
(Kamimura et al., 2006)
Cytology
Description
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
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

      Zygotic Hs6std770 mutants survive to the adult stage without showing obvious morphological defects.

      A fraction (39%) of maternal and zygotic Hs6std770 mutants exhibit abnormal tracheal development. Tracheal development is incomplete, revealed by the presence of large gaps in the dorsal trunks, as well as stalled tracheal branches. The migration defects in these embryos are observed in all primary branches, but most commonly in the dorsal branch and the dorsal trunk. Tracheal morphology is indistinguishable from that of wild-type embryos in the remaining 61% of embryos.

      Normal development of tracheoblasts is observed in the majority of Hs6std770 mutants, although the tracheoblast is slightly reduced in size in a small fraction (18%) of Hs6std770 mutant discs.

      (Kamimura et al., 2006)
      External Data
      Interactions
      Show genetic interaction network for Enhancers & Suppressors
      Phenotypic Class
      Enhanced by
      Statement
      Reference

      Hs6std770 has increased mortality during development phenotype, enhanceable by Hsepid12

      (Dejima et al., 2013)

      Hs6std770 has lethal phenotype, enhanceable by Hsepid12

      (Dejima et al., 2013)
      Suppressor of
      Statement
      Reference

      Hs6std770 is a suppressor of visible phenotype of Sulf1ΔP1

      (Kleinschmit et al., 2010)
      Other
      Phenotype Manifest In
      Suppressor of
      Statement
      Reference

      Hs6st[+]/Hs6std770 is a suppressor of wing vein L5 phenotype of Hsepid12

      (Dejima et al., 2013)

      Hs6std770 is a suppressor of anterior wing margin phenotype of Sulf1ΔP1

      (Kleinschmit et al., 2010)

      Hs6std770 is a suppressor of wing margin bristle | increased number phenotype of Sulf1ΔP1

      (Kleinschmit et al., 2010)
      Other
      Additional Comments
      Genetic Interactions
      Statement
      Reference

      Hsepid12/Hsepid12; Hs6std770/+ mutants show a reduction of the wing vein L5.

      (Dejima et al., 2013)

      Hs6std770 suppresses the increased chemosensory bristle phenotype observed at the anterior dorsal wing margin of Sulf1ΔP1 mutant animals.

      (Kleinschmit et al., 2010)

      Embryos that are maternal and zygotic mutant for Hs6std770 and Hs2std267 are partial lethal during development. However, significant fractions of these null mutants survive to the adult stage without visible phenotypes.

      Hs2std267/Hs6std770 zygotic double mutants are completely lethal. Although invagination seems to occur normally in Hs2std267/Hs6std770 embryos, they exhibit several characteristic defects in branching morphogenesis. First, mutant tracheal precursor cells fail to migrate to form the primary branches. Second, clusters of mutant tracheal cells tend to extend dorsally and ventrally, forming long, skinny sacs of tracheal precursor cells of various sizes. Finally, approximately 16% of mutant embryos show fusion of the tracheal sacs to those in the neighboring segments.

      (Kamimura et al., 2006)
      Xenogenetic Interactions
      Statement
      Reference
      Complementation and Rescue Data
      Rescued by

      Hs6std770 is rescued by Scer\GAL4btl.PS/Hs6stUAS.cKa

      (Kamimura et al., 2006)
      Comments

      The small tracheoblast phenotype of Hs6std770 mutants is completely rescued by expression of Hs6stScer\UAS.cKa under the control of Scer\GAL4btl.PS.

      (Kamimura et al., 2006)
      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
      Hs6std770
      (Dejima et al., 2013, Sekine et al., 2013, Kleinschmit et al., 2010, Kamimura et al., 2006)
      Name Synonyms
      Secondary FlyBase IDs
        References (4)