FB2024_03 , released June 25, 2024
Allele: Dmel\zfh175.26
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General Information
Symbol
Dmel\zfh175.26
Species
D. melanogaster
Name
FlyBase ID
FBal0086260
Feature type
allele
Associated gene
Dmel\zfh1
Associated Insertion(s)
Carried in Construct
Also Known As
zfh-175.26
Key Links
Allele class

amorphic allele - molecular evidence

amorphic allele - genetic evidence

Mutagen
Nature of the Allele
Allele class

amorphic allele - genetic evidence

(Broihier et al., 1998)

amorphic allele - molecular evidence

(Leatherman and DiNardo, 2008)
Mutagen
ethyl methanesulfonate
(Broihier et al., 1998)
Progenitor genotype
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

      Very few zfh175.26 mutant cyst progenitor cell clones are recovered compared to controls. The mutant cyst progenitor cells that are recovered have begun to express differentiation markers. Germline stem cell clones are recovered at similar levels to controls.

      (Leatherman and DiNardo, 2008)

      zfh15 and zfh15/zfh175.26 embryos show defects in the formation of ventral motor nerves. The ISN nerve is always present in these mutants but has branching defects. This nerve exits the CNS, but the ISNb and SNa nerves are truncated or absent. The SNc and ISNd nerves are not identifiable in these mutant embryos and it may be that the CNS stops developing before the formation of these minor nerves.

      (Layden et al., 2006)

      In male stage 13 embryos double mutant for zfh175.26 and Df(3R)GC14, male-specific somatic gonadal precursors are still specified, even though the somatic gonadal precursors fail to develop in parasegment 10-12.

      (DeFalco et al., 2003)

      Mutant embryos have mild defects in the development of the tracheal dorsal trunk.

      (Franch-Marro and Casanova, 2000)

      Germ cells in mutant embryos do not successfully navigate to the somatic gonadal precursors (SGPs): the majority of the germ cells do not attach to the SGPs at stage 11. Germ cells migrate past their target mesodermal cells, into posterior or ectodermal regions. Occasionally small gonads may form. Embryos derived from homozygous germline clones develop normally as long as a wild-type copy of zfh1 is zygotically provided. The germ cell migration phenotype is not exacerbated when the embryos are derived from a zfh1 homozygous mutant germline. Germ cells are unable to transfer between germ layers in double mutant embryos with tin (Df(3R)GC14). Most germ cells adhere to the endoderm throughout embryogenesis, some scatter near the gut at late stages.

      (Broihier et al., 1998)

      The number of fat body precursor cells is reduced in zfh165.34/zfh175.26 embryos, often resulting in gaps within the developing tissue.

      (Moore et al., 1998)
      External Data
      Interactions
      Show genetic interaction network for Enhancers & Suppressors
      Phenotypic Class
      Phenotype Manifest In
      Additional Comments
      Genetic Interactions
      Statement
      Reference

      Pole cells occasionally aggregate and form pseudo-gonads at the level of the fifth abdominal segment in zfh175.26 Df(3R)GC14 double mutant embryos.

      (Marhold et al., 2003)

      The addition of tinEC40 to mutants leads to a tracheal dorsal trunk that is almost completely absent.

      (Franch-Marro and Casanova, 2000)

      zfh175.26; Df(3R)GC14 double mutant embryos completely lack gonadal mesoderm, and the number of fat body precursors is virtually abolished. The gonadal mesoderm and fat body defects seen in zfh175.26; eyacli-IID double mutant embryos are identical to that seen in zfh165.34/zfh175.26 single mutant embryos.

      (Moore et al., 1998)
      Xenogenetic Interactions
      Statement
      Reference
      Complementation and Rescue Data
      Rescued by

      zfh165.34/zfh175.26 is rescued by zfh1hs.PL

      (Broihier et al., 1998)
      Partially rescued by

      zfh15/zfh175.26 is partially rescued by Scer\GAL4elav-C155/zfh1UAS.cLa

      (Layden et al., 2006)
      Not rescued by

      zfh15/zfh175.26 is not rescued by Scer\GAL4s.gcm/zfh1UAS.cLa

      (Layden et al., 2006)
      Comments

      zfh15/zfh175.26 embryos expressing zfh1Scer\UAS.cLa under the control of Scer\GAL4elav-C155 show a substantial rescue in the ability of the ISNb and SNa nerves to exit the CNS, but does not rescue the ISN projection defects.

      (Layden et al., 2006)

      Germ cell migration phenotype is rescued by heat induced ectopic expression of zfh1hs.PL.

      (Broihier et al., 1998)
      Images (0)
      Mutant
      Wild-type
      Stocks (0)
      Notes on Origin
      Discoverer
      External Crossreferences and Linkouts ( 0 )
      Synonyms and Secondary IDs (2)
      References (13)