FB2025_01 , released February 20, 2025
Allele: Dmel\pblUAS.N.Tag:HA
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General Information
Symbol
Dmel\pblUAS.N.Tag:HA
Species
D. melanogaster
Name
FlyBase ID
FBal0280752
Feature type
allele
Associated gene
Dmel\pbl
Associated Insertion(s)
Carried in Construct
P{UAS-HA-pbl}
Key Links
Transgenic product class
cDNA
(Jeong et al., 2012)
wild_type
(Jeong et al., 2012)
Mutagen
Nature of the Allele
Transgenic product class
cDNA
(Jeong et al., 2012)
wild_type
(Jeong et al., 2012)
Mutagen
in vitro construct
(Jeong et al., 2012)
Progenitor genotype
Carried in construct
P{UAS-HA-pbl}
Cytology
Description

UASt regulatory sequences drive expression of pbl (cDNA clone SD01796) which is tagged at the N-terminal end with Tag:HA.

(Jeong et al., 2012)
Allele components
Component
Use(s)
Regulatory region(s)
UASt
Encoded product / tool
pbl
Tagged with
Tag:HA
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 ( 1 )
      Disease
      Interaction
      References
      exacerbates  tauopathy
      modeled by Hsap\MAPTUAS.cWa
      (Feuillette et al., 2020)
      Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
       
      Disease-implicated variant(s)
       
      Phenotypic Data
      Phenotypic Class
      Phenotype Manifest In
      Detailed Description
      Statement
      Reference

      Expression of pblScer\UAS.N.T:Ivir\HA1 under the control of Scer\GAL4elav.PLu in embryos leads to mildly increased frequency of defasciculation defects in intersegmental nerve b motor axons compared to controls and very lowly penetrant lateral axon tract disruptions in the central nervous system.

      (Jeong et al., 2017)
      External Data
      Interactions
      Show genetic interaction network for Enhancers & Suppressors
      Phenotypic Class
      Enhanced by
      NOT Enhanced by
      Suppressed by
      Enhancer of
      Other
      Phenotype Manifest In
      Enhanced by
      NOT Enhanced by
      Suppressed by
      NOT suppressed by
      Enhancer of
      Statement
      Reference

      pblUAS.N.Tag:HA, Scer\GAL4GMR.PF is an enhancer of eye phenotype of Hsap\MAPTUAS.cWa, Scer\GAL4GMR.PF

      (Feuillette et al., 2020)
      Other
      Additional Comments
      Genetic Interactions
      Statement
      Reference

      The moderate axon pathfinding defects (defasciculation defects in intersegmental nerve b, ISNb, motor axons very infrequent lateral axon tract disruptions in the central nervous system) characteristic for embryos expressing pblScer\UAS.N.T:Ivir\HA1 under the control of Scer\GAL4elav.PLu are strongly exacerbated by co-expression of Sema1aScer\UAS.cJa and to a lesser extent also by co-expression of Sema1aΔ5.Scer\UAS (increases the frequency of defects in the central nervous system but not in the ISNb) - in addition, both these embryos also display midline crossing defects. Co-expression with either Sema1aScer\UAS.T:Hsap\MYC or Sema1aΔ1-40.Scer\UAS does not enhance the phenotype.

      (Jeong et al., 2017)

      Co-expression of Sema-1aScer\UAS.cJa and pblScer\UAS.N.T:Ivir\HA1 under the control of Scer\GAL4elav.PLu results in ISNb defects in 46.1% of hemisegments. Defects in the lateral-most Fas2-positive longitudinal connectives are seen in 21.6% of hemisegments. An average of 3.6 ectopic midline crossings in the central nervous system are seen per embryo.

      Co-expression of Sema-1amICD.Scer\UAS and pblScer\UAS.N.T:Ivir\HA1 under the control of Scer\GAL4elav.PLu results in ISNb guidance defects in more than 40% of hemisegments, while only mild defects in central nervous system patterning are seen.

      Co-expression of Sema-1amICD.Scer\UAS.T:Hsap\Fc-IgG and pblScer\UAS.N.T:Ivir\HA1 under the control of Scer\GAL4elav.PLu results in ISNb guidance defects in more than 40% of hemisegments, while only mild defects in central nervous system patterning are seen.

      plexAMB09499/+ strongly suppresses the lateral longitudinal central nervous system defects seen in embryos co-expressing Sema-1aScer\UAS.cJa and pblScer\UAS.N.T:Ivir\HA1 under the control of Scer\GAL4elav.PLu, while the ISNb defects are not suppressed.

      plexAMB09499/+ significantly suppresses the central nervous system defects seen in embryos co-expressing Sema-1amICD.Scer\UAS.T:Hsap\Fc-IgG and pblScer\UAS.N.T:Ivir\HA1 under the control of Scer\GAL4elav.PLu, while the ISNb defects are not suppressed.

      (Jeong et al., 2012)
      Xenogenetic Interactions
      Statement
      Reference
      Complementation and Rescue Data
      Partially rescues

      Scer\GAL4sca-537.4/pblUAS.N.Tag:HA partially rescues pbl09645

      (Jeong et al., 2012)
      Fails to rescue

      Scer\GAL4how-24B/pblUAS.N.Tag:HA fails to rescue pbl09645

      (Jeong et al., 2012)
      Comments

      Expression of pblScer\UAS.N.T:Ivir\HA1 under the control of Scer\GAL4how-24B fails to rescue the motor axon pathfinding defects seen in pbl09645 embryos.

      Expression of pblScer\UAS.N.T:Ivir\HA1 under the control of Scer\GAL4sca-537.4 partially but significantly rescues the pathfinding defects in the ISNb and SNa, but not the ISN, motor axon pathways in pbl09645 embryos.

      (Jeong et al., 2012)
      Images (0)
      Mutant
      Wild-type
      Stocks (2)
      Notes on Origin
      Discoverer
      External Crossreferences and Linkouts ( 0 )
      Synonyms and Secondary IDs (2)
      Reported As
      Symbol Synonym
      pblScer\UAS.N.T:Ivir\HA1
      pblUAS.N.Tag:HA
      Name Synonyms
      Secondary FlyBase IDs
        References (4)