FB2024_03 , released June 25, 2024
Allele: Dmel\hb15
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General Information
Symbol
Dmel\hb15
Species
D. melanogaster
Name
FlyBase ID
FBal0005406
Feature type
allele
Associated gene
Dmel\hb
Associated Insertion(s)
Carried in Construct
Also Known As
hbFB, hbFB92
Key Links
Genomic Maps

Allele class

amorphic allele - genetic evidence

Mutagen
Nature of the Allele
Allele class

amorphic allele - genetic evidence

(Hulskamp et al., 1994, Tautz, 1988)
Mutagen
X ray
(Hulskamp et al., 1994, Lehmann and Nusslein-Volhard, 1987, Tearle and Nusslein-Volhard, 1987)
Progenitor genotype
Cytology
Description

Deletion of 10 nucleotides starting at amino acid 150 resulting in a nonsense frameshift before the first zinc finger domain.

(Hulskamp et al., 1994)
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
deletion
3R:8,693,698..8,693,707 [-]
Comment:

A deletion of 10 nucleotides starting at amino acid 150 (exact position unspecified) results in a frameshift and early translation termination before the first finger domain.

(Hulskamp et al., 1994)
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

      embryonic/larval tracheal dorsal trunk

      (Wolf and Schuh, 2000)

      embryonic abdominal segment 7

      (Wimmer et al., 2000)

      embryonic abdominal segment 8

      (Wimmer et al., 2000)

      embryonic ganglion mother cell | embryonic stage 13, with hbP1only

      (Bahrampour et al., 2017)

      embryonic labial segment

      (Wimmer et al., 2000, Hulskamp et al., 1994)

      embryonic mesothoracic segment

      (Wimmer et al., 2000, Hulskamp et al., 1994)

      embryonic metathoracic segment

      (Wimmer et al., 2000, Hulskamp et al., 1994)

      embryonic neuroblast | embryonic stage 13, with hbP1only

      (Bahrampour et al., 2017)

      embryonic neuroblast | embryonic stage 14, with hbP1only

      (Bahrampour et al., 2017)

      embryonic prothoracic segment

      (Wimmer et al., 2000, Hulskamp et al., 1994)

      larval DA2 motor neuron | increased number (with hbP1only), with Scer\GAL4en-e16E, hbΔD.VP16.UAS

      (Tran et al., 2010)

      larval DA2 motor neuron | increased number (with hbP1only), with Scer\GAL4en-e16E, hbΔDMZ.VP16.UAS

      (Tran et al., 2010)

      larval DO1 motor neuron (with hbP1only), with Scer\GAL4en-e16E, hbΔD.VP16.UAS

      (Tran et al., 2010)

      larval DO1 motor neuron (with hbP1only), with Scer\GAL4en-e16E, hbΔDMZ.VP16.UAS

      (Tran et al., 2010)

      larval DO2 motor neuron (with hbP1only), with Scer\GAL4en-e16E, hbΔD.VP16.UAS

      (Tran et al., 2010)

      larval DO2 motor neuron (with hbP1only), with Scer\GAL4en-e16E, hbΔDMZ.VP16.UAS

      (Tran et al., 2010)

      U neuron (with hbP1only), with Scer\GAL4en-e16E, hbUAS.VP16

      (Tran et al., 2010)

      U neuron | increased number (with hbP1only), with Scer\GAL4en-e16E, hbUAS.cWa

      (Tran et al., 2010)

      U neuron | increased number (with hbP1only), with Scer\GAL4en-e16E, hbΔAB.VP16.UAS

      (Tran et al., 2010)

      U neuron | increased number (with hbP1only), with Scer\GAL4en-e16E, hbΔB.VP16.UAS

      (Tran et al., 2010)

      U neuron | increased number (with hbP1only), with Scer\GAL4en-e16E, hbΔE.VP16.UAS

      (Tran et al., 2010)
      Detailed Description
      Statement
      Reference

      hbP1only/hb15 transheterozygotes present a significant decrease in the number of dividing neuroblasts during stages 13 and 14 of embryogenesis and present a significant decrease in the number of dividing neuroblast daughters during stage 13, but not stage 14, of embryogenesis, as compared to controls; these embryos, however, show no significant differences in the number of neuroblasts, as compared to controls.

      (Bahrampour et al., 2017)

      In wild-type, neuroblast NB7-1 generates five U motoneurons. Overexpression of hbScer\UAS.T:Hsim\VP16 in hb15/hbP1only mutant NB7-1 under the control of Scer\GAL4en-e16E produces an average of six U neurons per hemisegment.

      In wild-type, neuroblast NB7-1 generates five U motoneurons. Overexpression of hbScer\UAS.cWa in hb15/hbP1only mutant NB7-1 under the control of Scer\GAL4en-e16E produces an average of 12 U neurons per hemisegment.

      (Tran et al., 2010)

      85% of the progeny of hb15 germ-line clone mothers mated to wild-type fathers hatch into first instar larvae.

      (Deshpande et al., 2005)

      Mutant embryos show normal filopodia-like cell extensions of the tracheal cells at stage 12.

      (Wolf et al., 2002)

      When one copy of hbP1only is supplied zygotically (via the father) to hb12/hb15 embryos the A7/A8 fusion mutant phenotype is rescued. When one copy of hbP1only is supplied maternally both the A7/A8 and anterior labial and T1 segments are rescued; only T2 and T3 remain unrescued. When the maternal contribution of hbP1only is increased (three copies) 30% rescued embryos show only the maternal rescue of labial and T1 segments. Most show additional rescue of thoracic segments of mostly T3 character. 5-10% of embryos show rescue of all thoracic segments.

      (Wimmer et al., 2000)

      In hb15 mutant embryos initial tracheal development appears normal up to stage 12. Subsequently the trunk branches become stalled and misrouted, whereas the other primary branches are formed as in wild-type embryos. Despite the strong dorsal trunk phenotype, the dorsal trunk branches occasionally fuse in mutant embryos and form dorsal trunk rudiments.

      (Wolf and Schuh, 2000)

      The effects of loss of maternal and zygotic nos product on germ cell migration is studied in females with hb15 nosBN mutant germ line clones crossed to nos18/Df(3R)Dl-FX3 males.

      (Forbes and Lehmann, 1998)

      All thoracic segments and the most posterior gnathal segment are missing.

      (Hulskamp et al., 1994)

      Embryos derived from hb15 bcd6 females show a mirror image duplication of abdominal segments, centered around A6. Embryos derived from hb15 bcd6 females, and also zygotically mutant for hb8 show a mirror image duplication of abdominal segments, centered around A6, and segments A7 and A8 are fused.

      (Hulskamp et al., 1990)
      External Data
      Interactions
      Show genetic interaction network for Enhancers & Suppressors
      Phenotypic Class
      Enhanced by
      Other
      Phenotype Manifest In
      Enhanced by
      Enhancer of
      Suppressor of
      Statement
      Reference

      hb15/hb12 is a suppressor | partially of EW3 neuron phenotype of Kr1, KrmCD, svp2/svp1

      (Kanai et al., 2005)

      hb15/hb12 is a suppressor | partially of larval DA3 motor neuron phenotype of Kr1, KrmCD, svp2/svp1

      (Kanai et al., 2005)

      hb15/hb12 is a suppressor | partially of larval LL1 motor neuron phenotype of Kr1, KrmCD, svp2/svp1

      (Kanai et al., 2005)
      Other
      Statement
      Reference

      hb15, nanosL7 has germline cell phenotype

      (Arrizabalaga and Lehmann, 1999)
      Additional Comments
      Genetic Interactions
      Statement
      Reference

      Only about 55% of the progeny of hb15; nosBN germ-line clone mothers mated to wild-type fathers hatch into first instar larvae, but most of those that hatch make it to adulthood (42% of all progeny).. Of the unhatched embryos, about 25% have kni-like posterior defects while the remainder have cuticle defects ranging from near normal, through segment fusion and deletion to a few that form only scraps of cuticle. This increased embryonic lethality is rescued by nos+t5.7.

      (Deshpande et al., 2005)

      KrmCD; Kr1/Kr1 enhances the reduction in later born neurons of the NB7-1 an NB2-3 lineages see in svp1/svp2 embryos so that U4 and U5 are almost completely eliminated, as are EW2 and EW3. This enhanced phenotype is partially suppressed if the embryos are also hb12/hb15.

      (Kanai et al., 2005)

      hb15 mutant embryos that express bnlScer\UAS.cSa ectopically have no signs of dorsal trunk outgrowth at all.

      (Wolf and Schuh, 2000)

      nosL7 homozygous embryos derived from nosL7 hb15 homozygous female germline clones form germ cells normally, but show defects after stage 10 of embryogenesis. At this stage, many germ cells fail to leave the gut (in contrast to wild type) and tightly associate into clusters of cells. Some germ cells follow a normal migratory pattern, the morphology of the germ cells is normal and the embryos develop into fertile flies.

      (Arrizabalaga and Lehmann, 1999)
      Xenogenetic Interactions
      Statement
      Reference
      Complementation and Rescue Data
      Partially rescued by

      hb15/hb12 is partially rescued by hbP1only

      (Wimmer et al., 2000)
      Comments
      Images (0)
      Mutant
      Wild-type
      Stocks (0)
      Notes on Origin
      Discoverer

      Lehmann.

      Comments
      Comments

      Class I allele.

      Phenotypic class I.

      (Lehmann and Nusslein-Volhard, 1987)
      External Crossreferences and Linkouts ( 0 )
      Synonyms and Secondary IDs (3)
      References (30)