FB2024_03 , released June 25, 2024
Allele: Dmel\fraΔC.UAS.Tag:HA
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General Information
Symbol
Dmel\fraΔC.UAS.Tag:HA
Species
D. melanogaster
Name
FlyBase ID
FBal0244568
Feature type
allele
Associated gene
Dmel\fra
Associated Insertion(s)
Carried in Construct
P{UAS-fra.HA.ΔC}
Also Known As
P{UAS-FraΔC-HA}, UAS-FraΔC-HA
Key Links
Transgenic product class
inframe_deletion
(Garbe et al., 2007)
Mutagen
Nature of the Allele
Transgenic product class
inframe_deletion
(Garbe et al., 2007)
Mutagen
in vitro construct
(Garbe et al., 2007)
Progenitor genotype
Carried in construct
P{UAS-fra.HA.ΔC}
Cytology
Description

UAS regulatory sequences drive expression of fra lacking almost the entire cytoplasmic domain (amino acids 1109-1372), and tagged with a Tag:HA epitope.

(Garbe et al., 2007)
Allele components
Component
Use(s)
Regulatory region(s)
UAS
Encoded product / tool
fra
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 ( 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

      The expression of fraΔC.UAS.Tag:HA under the control of Scer\GAL4Pdf.PU results in adult sLNv neurons exhibiting significantly shorter axons compared to controls.

      (Oliva et al., 2016)

      Expression of a weak transgene of fraΔC.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4elav.PLu does not cause any defects in axon midline crossing.

      (O'Donnell and Bashaw, 2013)

      Expression of fraΔC.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4eg-Mz360 generates midline crossing defects, with most (approx. 90%) eg-axons mis-projecting.

      (O'Donnell and Bashaw, 2013)

      Neuronal expression of fraΔC.Scer\UAS.T:Ivir\HA under the control of Scer\GAL4eg-Mz360 leads to a dose dependent "commissureless" phenotype.

      (Yang et al., 2009)

      Overexpression of one copy of fraΔC.Scer\UAS.T:Ivir\HA under the control of Scer\GAL4elav.PLu causes commissures to become thin. Axon commissures are almost completely absent when two copies of fraΔC.Scer\UAS.T:Ivir\HA are expressed.

      The severity of the embryonic commissure phenotype resulting from the overexpression of one copy of fraΔC.Scer\UAS.T:Ivir\HA under the control of Scer\GAL4elav.PLu increases in fraunspecified heterozygotes. Homozygous fraunspecified mutants overexpressing one copy of fraΔC.Scer\UAS.T:Ivir\HA exhibit a near complete loss of axon commissures.

      Expression of fraΔC.Scer\UAS.T:Ivir\HA under the control of Scer\GAL4eg-Mz360 causes a decrease of EW attraction towards the midline, though in many segments the EW neurons cross normally. When fraScer\UAS.T:Myr1.T:Hsap\MYC is expressed in fraunspecified homozygous embryos, none of the EW neurons cross the midline. In some segments, EG axon guidance is also defective, a phenotype never observed in fraunspecified mutants.

      (Garbe et al., 2007)
      External Data
      Interactions
      Show genetic interaction network for Enhancers & Suppressors
      Phenotypic Class
      Enhanced by
      NOT Enhanced by
      Suppressed by
      NOT suppressed by
      NOT Enhancer of
      Statement
      Reference

      Scer\GAL4eg-Mz360/fraΔC.UAS.Tag:HA is a non-enhancer of abnormal neuroanatomy phenotype of Abl2

      (O'Donnell and Bashaw, 2013)
      Suppressor of
      NOT Suppressor of
      Phenotype Manifest In
      Enhanced by
      Statement
      Reference

      Scer\GAL4eg-Mz360, fraΔC.UAS.Tag:HA has larval EW neuron | embryonic stage phenotype, enhanceable by Tace17

      (Zang et al., 2022)

      Scer\GAL4eg-Mz360, fraΔC.UAS.Tag:HA has axon | embryonic stage phenotype, enhanceable by Tace17

      (Zang et al., 2022)

      Scer\GAL4eg-Mz360, fraΔC.UAS.Tag:HA has larval EW neuron | embryonic stage phenotype, enhanceable by Tace19

      (Zang et al., 2022)

      Scer\GAL4eg-Mz360, fraΔC.UAS.Tag:HA has axon | embryonic stage phenotype, enhanceable by Tace19

      (Zang et al., 2022)

      Scer\GAL4eg-Mz360, fraΔC.UAS.Tag:HA has larval EW neuron | embryonic stage phenotype, enhanceable by Scer\GAL4eg-Mz360/Tace10xUAS.Tag:HA

      (Zang et al., 2022)

      Scer\GAL4eg-Mz360, fraΔC.UAS.Tag:HA has axon | embryonic stage phenotype, enhanceable by Scer\GAL4eg-Mz360/Tace10xUAS.Tag:HA

      (Zang et al., 2022)

      Scer\GAL4eg-Mz360, fraΔC.UAS.Tag:HA has larval EW neuron | embryonic stage phenotype, enhanceable by Df(3R)BSC794

      (Zang et al., 2022)

      Scer\GAL4eg-Mz360, fraΔC.UAS.Tag:HA has axon | embryonic stage phenotype, enhanceable by Df(3R)BSC794

      (Zang et al., 2022)

      Scer\GAL4eg-Mz360, fraΔC.UAS.Tag:HA has larval EW neuron phenotype, enhanceable by unc-5[+]/unc-52

      (O'Donnell and Bashaw, 2013)

      Scer\GAL4eg-Mz360, fraΔC.UAS.Tag:HA has symmetrical commissure phenotype, enhanceable by unc-5[+]/unc-52

      (O'Donnell and Bashaw, 2013)

      Scer\GAL4eg-Mz360, fraΔC.UAS.Tag:HA has larval EW neuron phenotype, enhanceable by mys1

      (O'Donnell and Bashaw, 2013)

      Scer\GAL4eg-Mz360, fraΔC.UAS.Tag:HA has symmetrical commissure phenotype, enhanceable by mys1

      (O'Donnell and Bashaw, 2013)

      Scer\GAL4eg-Mz360, fraΔC.UAS.Tag:HA has larval EW neuron phenotype, enhanceable by robo11

      (O'Donnell and Bashaw, 2013)

      Scer\GAL4eg-Mz360, fraΔC.UAS.Tag:HA has symmetrical commissure phenotype, enhanceable by robo11

      (O'Donnell and Bashaw, 2013)

      Scer\GAL4eg-Mz360, fraΔC.UAS.Tag:HA has larval EW neuron phenotype, enhanceable by Scer\GAL4eg-Mz360/Src64BYF.UAS

      (O'Donnell and Bashaw, 2013)

      Scer\GAL4eg-Mz360, fraΔC.UAS.Tag:HA has symmetrical commissure phenotype, enhanceable by Scer\GAL4eg-Mz360/Src64BYF.UAS

      (O'Donnell and Bashaw, 2013)
      NOT Enhanced by
      Suppressed by
      NOT suppressed by
      NOT Enhancer of
      Suppressor of
      NOT Suppressor of
      Additional Comments
      Genetic Interactions
      Statement
      Reference

      Expression of a weak transgene of fraΔC.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4eg-Mz360 has no effect on the number and severity of midline crossing defects found in Abl2 homozygous mutants. The presence of AblScer\UAS.T:Avic\GFP reduces the number of midline crossing defects (to a statistically significant level) in Abl2 homozygous mutants in a fraΔC.Scer\UAS.T:Ivir\HA1-expressing background. The presence of AblK417N.Scer\UAS.T:Avic\GFP reduces (although not to a statistically significant level) the number of midline crossing defects in Abl2 homozygous mutants in a fraΔC.Scer\UAS.T:Ivir\HA1-expressing background.

      Expression of AblΔFABD.Scer\UAS.T:Avic\GFP in EW neurons, under the control of Scer\GAL4eg-Mz360 fails to rescue EW midline-crossing defects in Abl2 neurons expressing fraΔC.Scer\UAS.T:Ivir\HA1.

      (O'Donnell and Bashaw, 2013)

      A Src42Ak10108 heterozygous background partially suppresses the eg-positive neuron midline crossing defects found upon expression of fraΔC.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4eg-Mz360.

      A Src64Bko heterozygous background partially suppresses the eg-positive neuron midline crossing defects found upon expression of fraΔC.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4eg-Mz360.

      A Src42Ak10108/+ ; Src64Bko/+ trans-heterozygous background partially suppresses the eg-positive neuron midline crossing defects found upon expression of fraΔC.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4eg-Mz360.

      Src42Ak10108/+;Src64Bko heterozygous background suppresses the eg-positive neuron midline crossing defects found upon expression of fraΔC.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4eg-Mz360.

      Co-expression of Src64BYF.Scer\UAS with fraΔC.Scer\UAS.T:Ivir\HA1 in eg-expressing neurons, under the control of Scer\GAL4eg-Mz360 enhances the midline crossing defects found when fraΔC.Scer\UAS.T:Ivir\HA1 alone is expressed under the control of Scer\GAL4eg-Mz360.

      A unc-52 heterozygous background increases the percentage of embryonic segments displaying eg-positive axon midline crossing defects in flies expressing fraΔC.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4eg-Mz360. However, this increase isn't considered statistically significant.

      A mys1/Y background increases the percentage of embryonic segments displaying eg-positive axon midline crossing defects in flies expressing fraΔC.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4eg-Mz360. However, this increase isn't considered statistically significant.

      A robo1 homozygous background increases the percentage of embryonic segments displaying eg-positive axon midline crossing defects in flies expressing fraΔC.Scer\UAS.T:Ivir\HA1 under the control of Scer\GAL4eg-Mz360. However, this increase isn't considered statistically significant.

      (O'Donnell and Bashaw, 2013)

      The midline crossing defects of axons seen in Scer\GAL4eg-Mz360-driven fraΔC.Scer\UAS.T:Ivir\HA-expressing embryos are enhanced in a heterozygous communspecified/+ genetic background.

      (Yang et al., 2009)

      Expression of fraΔC.Scer\UAS.T:Ivir\HA driven by Scer\GAL4elav.PLu does not cause a commissureless phenotype in either Df(1)NP5 or Df(1)NetABΔ mutant background.

      Expression of fraΔC.Scer\UAS.T:Ivir\HA driven by Scer\GAL4elav.PLu still causes a commissureless phenotype in a fraunspecified unc-5unspecified double mutant background.

      Expression of fraΔC.Scer\UAS.T:Ivir\HA driven by Scer\GAL4elav.PLu in a fraunspecified sli2 double mutant background results in a phenotype similar to the phenotype observed for overexpression of fraΔC.Scer\UAS.T:Ivir\HA in a fraunspecified single mutant background, where many axons fail to cross the midline.

      Expression of fraΔC.Scer\UAS.T:Ivir\HA driven by Scer\GAL4elav.PLu in a fraunspecified robo1 double mutant background dramatically repels axons, though the defect is less severe than seen in a fraunspecified single mutant background.

      Expression of fraΔC.Scer\UAS.T:Ivir\HA driven by Scer\GAL4elav.PLu leads to a partial suppression of the robo1 single mutant phenotype.

      (Garbe et al., 2007)
      Xenogenetic Interactions
      Statement
      Reference
      Complementation and Rescue Data
      Images (0)
      Mutant
      Wild-type
      Stocks (0)
      Notes on Origin
      Discoverer
      External Crossreferences and Linkouts ( 0 )
      Synonyms and Secondary IDs (3)
      Reported As
      Symbol Synonym
      fraΔC.Scer\UAS.T:Ivir\HA1
      fraΔC.Scer\UAS.T:Ivir\HA
      fraΔC.UAS.Tag:HA
      Name Synonyms
      Secondary FlyBase IDs
        References (10)