FB2024_03 , released June 25, 2024
Allele: Dmel\Psn+14.UAS
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General Information
Symbol
Dmel\Psn+14.UAS
Species
D. melanogaster
Name
FlyBase ID
FBal0101586
Feature type
allele
Associated gene
Dmel\Psn
Associated Insertion(s)
Carried in Construct
P{UAS-Psn.+14}
Also Known As
UAS-Psn+14, UAS-psn, UAS-DPsn
Key Links
Transgenic product class
wild_type
(Ye and Fortini, 1999)
Mutagen
Nature of the Allele
Transgenic product class
wild_type
(Ye and Fortini, 1999)
Mutagen
in vitro construct
(Ye and Fortini, 1999)
Progenitor genotype
Carried in construct
P{UAS-Psn.+14}
Cytology
Description

UASt regulatory sequences drive expression of the wild-type long isoform of Psn.

(Ye and Fortini, 1999)
Allele components
Component
Use(s)
Regulatory region(s)
UASt
Encoded product / tool
Psn
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 ( 1 )
      Modifiers Based on Experimental Evidence ( 1 )
      Disease
      Interaction
      References
      model of  neurodegenerative disease
      is ameliorated by UbqnUAS.cLa
      (Li et al., 2007)
      is exacerbated by UbqnRNAi.Ex2.UAS
      (Li et al., 2007)
      Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
       
      Disease-implicated variant(s)
       
      Phenotypic Data
      Phenotypic Class
      Phenotype Manifest In

      adult heart, with Scer\GAL4how-24B

      (Li et al., 2011)

      adult thorax & macrochaeta, with Scer\GAL4c625

      (Ye and Fortini, 1999)

      adult thorax & microchaeta, with Scer\GAL419A

      (Ye and Fortini, 1999)

      campaniform sensillum of dorsal radius | ectopic, with Scer\GAL4Hc

      (Ye and Fortini, 1999)

      campaniform sensillum of proximal dorsal radius | ectopic, with Scer\GAL4Hc

      (Ye and Fortini, 1999)

      cardiac myofibril, with Scer\GAL4how-24B

      (Li et al., 2011)

      crossvein, with Scer\GAL4en-e16E

      (Ye and Fortini, 1999)

      eye, with Scer\GAL4GMR.PF

      (Li et al., 2007, Ye and Fortini, 1999)

      eye, with Scer\GAL4hs.2sev

      (Ye and Fortini, 1999)

      interommatidial bristle, with Scer\GAL4GMR.PF

      (Li et al., 2007, Ye and Fortini, 1999)

      interommatidial bristle, with Scer\GAL4hs.2sev

      (Ye and Fortini, 1999)

      lens, with Scer\GAL4GMR.PF

      (Ye and Fortini, 1999)

      macrochaeta | ectopic, with Scer\GAL419A

      (Ye and Fortini, 1999)

      macrochaeta | ectopic, with Scer\GAL4c625

      (Ye and Fortini, 1999)

      mitochondrion, with Scer\GAL4how-24B

      (Li et al., 2011)

      ommatidium, with Scer\GAL4GMR.PF

      (Li et al., 2007, Ye and Fortini, 1999)

      ommatidium, with Scer\GAL4hs.2sev

      (Ye and Fortini, 1999)

      pigment cell, with Scer\GAL4GMR.PF

      (Ye and Fortini, 1999)

      pigment cell, with Scer\GAL4hs.2sev

      (Ye and Fortini, 1999)

      posterior crossvein, with Scer\GAL4ptc-559.1

      (Li et al., 2011)

      primary pigment cell, with Scer\GAL4GMR.PF

      (Ye and Fortini, 1999)

      scutum & macrochaeta, with Scer\GAL419A

      (Ye and Fortini, 1999)

      scutum & macrochaeta, with Scer\GAL4c625

      (Ye and Fortini, 1999)

      secondary pigment cell, with Scer\GAL4GMR.PF

      (Ye and Fortini, 1999)

      tertiary pigment cell, with Scer\GAL4GMR.PF

      (Ye and Fortini, 1999)

      wing, with Scer\GAL4ptc-559.1

      (Li et al., 2011)

      wing, with Scer\GAL4sd.PU

      (Li et al., 2011)

      wing, with Scer\GAL4T80

      (Ye and Fortini, 1999)

      wing | distal, with Scer\GAL4dpp.blk1

      (Ye and Fortini, 1999)

      wing | posterior, with Scer\GAL4en-e16E

      (Ye and Fortini, 1999)

      wing margin bristle | ectopic, with Scer\GAL4dpp.blk1

      (Ye and Fortini, 1999)

      wing vein, with Scer\GAL4T80

      (Ye and Fortini, 1999)

      wing vein L1, with Scer\GAL4Hc

      (Ye and Fortini, 1999)

      wing vein L3, with Scer\GAL4Hc

      (Ye and Fortini, 1999)
      Detailed Description
      Statement
      Reference

      Expression of Psn+14.UAS under the control of Scer\GAL4Appl.G1a does not lead to axonal blockages in third instar larval segmental nerves compared to controls.

      (Banerjee et al., 2018)

      Expression of Psn+14.Scer\UAS under the control of Scer\GAL4how-24B leads to an increased heart rate and irregular heartbeat rhythms, accompanied by cardiomyofibril defects and mitochondrial impairment.

      Expression of Psn+14.Scer\UAS in the wing disc under the control of Scer\GAL4sd.PU results in loss of both wings. Compared with control flies Fig. (6C), wing discs of flies expressing Psn+14.Scer\UAS are thinner and reduced in size, especially in the dorsal/ventral compartment.

      Compared with control flies, expression of Psn+14.Scer\UAS driven by Scer\GAL4ptc-559.1 results in severe loss of intervein cells, narrowing the intervein sector between L3 and L4 vein and forming extra vein cells to fill the intervein region. The intervein sector between L4 and L5 is enlarged and the posterior crossvein vein is extended.

      (Li et al., 2011)

      Expression of Psn+14.Scer\UAS under the control of Scer\GAL4Bx-MS1096 does not result in a mutant phenotype in the wing.

      (Ganguly et al., 2008)

      Overexpression of two copies of Psn+14.Scer\UAS, driven by Scer\GAL4GMR.PF results in a small, rough eye phenotype. At eclosion, these flies possess significantly fewer and well as malformed interommatidial bristles compared with controls. Most parts of the eye lack the mechanosensory bristles normally surrounding each facet of the compound eye. Additionally, some bristles on the edge of the eye are abnormal in shape, characterized by bubble- and balloon-like lesions (as well as some double spindles), roughly 3-5υm in diameter.

      (Li et al., 2007)

      Flies that express Psn+14.Scer\UAS under the control of Scer\GAL4Act5C.PI show normal survival rates and normal wing patterns.

      (Greeve et al., 2004)

      Flies carrying one copy of Psn+14.Scer\UAS expressed under the control of Scer\GAL4hs.2sev or Scer\GAL4GMR.PF are morphologically

      indistinguishable from wild type.

      Flies carrying two copies of Psn+14.Scer\UAS expressed under the

      control of Scer\GAL4hs.2sev have a rough eye phenotype, consisting

      of irregular ommatidial packing, occasional ommatidial fusions and

      missing bristles. Pigment cells are missing, while the photoreceptor

      cell array is largely normal.

      Flies carrying two copies of Psn+14.Scer\UAS expressed under the

      control of Scer\GAL4GMR.PF have a rough eye phenotype, characterised

      by fusion of the lens material of adjacent ommatidia and loss of interommatidial

      bristles, producing a glossy external eye surface. Most pigment cells

      are missing. Almost all pupal ommatidia have the normal number of

      cone cells, but have missing primary, secondary and tertiary pigment

      cells.

      The rough eye phenotype caused by expression of two copies of Psn+14.Scer\UAS

      under the control of Scer\GAL4GMR.PF is enhanced if the flies are

      also carrying one copy of Psn-14.Scer\UAS, PsnM146V.Scer\UAS,

      PsnN141I.Scer\UAS, PsnL235P.Scer\UAS, PsnE280A.Scer\UAS

      or a third copy of Psn+14.Scer\UAS, is weakly enhanced if the flies

      are also carrying one copy of PsnD-ALG3.Scer\UAS and is not affected

      if the flies are also carrying one copy of Psn+14.loop.Scer\UAS

      or Psn-14.loop.Scer\UAS.

      A significant increase in apoptosis in the eye disc compared to wild

      type is seen in flies carrying two copies of Psn+14.Scer\UAS expressed

      under the control of Scer\GAL4hs.2sev or Scer\GAL4GMR.PF.

      The cell death induced by expression of Psn+14.Scer\UAS under the

      control of Scer\GAL4hs.2sev is cell-autonomous. The assembly of

      photoreceptor cell clusters is largely unperturbed, despite the increase

      in cell death.

      Flies carrying two copies of Psn+14.Scer\UAS expressed under the

      control of Scer\GAL4dpp.blk1 show distal wing blade notching and

      ectopic margin bristles.

      Flies carrying two copies of Psn+14.Scer\UAS expressed under the

      control of Scer\GAL4T80 have thickened wing veins and Dl-like

      vein tip phenotypes.

      Flies carrying two copies of Psn+14.Scer\UAS expressed under the

      control of Scer\GAL4Hc have multiple campaniform sensilla along

      wing veins L1 and L3 (in contrast to wild type where single campaniform

      sensilla arise at defined positions along wing veins L1 and L3).

      Flies carrying two copies of Psn+14.Scer\UAS expressed under the

      control of Scer\GAL4en-e16E have missing crossveins and posterior

      wing blade scalloping.

      Flies carrying two copies of Psn+14.Scer\UAS expressed under the

      control of Scer\GAL4c625 have ectopic macrochaetae on the notum

      and thorax.

      Flies carrying two copies of Psn+14.Scer\UAS expressed under the

      control of Scer\GAL419A have ectopic macrochaetae on the notum

      and missing microchaetae on the thorax.

      (Ye and Fortini, 1999)
      External Data
      Interactions
      Show genetic interaction network for Enhancers & Suppressors
      Phenotypic Class
      Enhanced by
      Statement
      Reference

      Psn+14.UAS has increased cell death phenotype, enhanceable by Scer\GAL4GMR.PF/UbqnRNAi.Ex2.UAS

      (Li et al., 2007)

      Psn+14.UAS, Scer\GAL4GMR.PF has visible phenotype, enhanceable by Df(1)N-54l9/+

      (Ye and Fortini, 1999)
      Suppressed by
      Enhancer of
      Phenotype Manifest In
      Enhanced by
      Suppressed by
      Enhancer of
      Suppressor of
      Additional Comments
      Genetic Interactions
      Statement
      Reference

      Co-expression of UbqnScer\UAS.cLa with Psn+14.Scer\UAS in the developing eye under the control of Scer\GAL4GMR.PF leads to an increase in eye size compared to Psn+14.Scer\UAS single mutants. In addition, the irregular ommatidial packing and fusion are reduced and the number of ommatidia returns nearly to normal. Most strikingly, the 'bubble-bristle' phenotype is completely rescued. However, tufting is observed in many facets of the eye, where duplicated or triplicated bristles are found in single interommatidial regions.

      Silencing of Ubqn through co-expression of UbqndsRNA.Ex2.Scer\UAS with Psn+14.Scer\UAS in the developing eye under the control of Scer\GAL4GMR.PF enhances the Psn+14.Scer\UAS-induced rough eye phenotype, leading to an even smaller and rougher eye than that observed with Psn+14.Scer\UAS expression alone. Double mutants exhibit a loss of eye pigmentation, suggesting the loss of pigment cells. RNAi silencing of Ubqn in addition to Psn+14.Scer\UAS overexpression results in a much more severe degenerative phenotype than Psn+14.Scer\UAS single mutants, as evidenced by numerous visible holes (2-5υm in diameter) on a small, rough eye. In addition, the ommatidia are very irregular and mostly fused with very few bristles.

      (Li et al., 2007)

      Coexpression of ApplScer\UAS.cTa and Psn+14.Scer\UAS under the control of Scer\GAL4Act5C.PI does not cause lethality or affect wing patterning.

      (Greeve et al., 2004)

      The rough eye phenotype caused by expression of two copies of Psn+14.Scer\UAS under the control of Scer\GAL4GMR.PF is largely suppressed by thGMR.PH or BacA\p35GMR.PH and is strongly enhanced by one copy of Df(1)N-54l9. The level of apoptosis in eye discs of animals carrying two copies of Psn+14.Scer\UAS expressed under the control of Scer\GAL4GMR.PF is strongly reduced by the expression of Nact.sev. Enhances the eye phenotype of flies expressing rprGMR.PH when expressed under the control of Scer\GAL4GMR.PF.

      (Ye and Fortini, 1999)
      Xenogenetic Interactions
      Statement
      Reference

      The survival rates and wing patterns are not affected when flies coexpress Psn+14.Scer\UAS and Hsap\BACE1Scer\UAS.cGa under the control of Scer\GAL4Act5C.PI.

      Flies that coexpress Hsap\APP695.Scer\UAS and Hsap\BACE1Scer\UAS.cGa under the control of Scer\GAL4Act5C.PI exhibit ectopic wing veins. This phenotype is enhanced in flies that express Psn+14.Scer\UAS in addition to Hsap\APP695.Scer\UAS and Hsap\BACE1Scer\UAS.cGa under the control of Scer\GAL4Act5C.PI.

      (Greeve et al., 2004)
      Complementation and Rescue Data
      Partially rescues

      Scer\GAL4elav-C155/Psn+14.UAS partially rescues PsnRNAi.UAS.2

      (Kang et al., 2017)
      Comments

      The pupal lethality in males and the semi-lethality in females observed upon the expression of PsndsRNA.shRNA.Scer\UAS.2 under the control of Scer\GAL4elav-C155 are partially suppressed by the co-expression of Psn+14.Scer\UAS; while the rough eye and wrinkled wing phenotypes in adults females are partially rescued by the Psn+14.Scer\UAS expression, the rescued adult males now present both these phenotypes, as compared to controls.

      (Kang et al., 2017)
      Images (0)
      Mutant
      Wild-type
      Stocks (2)
      Notes on Origin
      Discoverer
      Comments
      Comments

      Carried in a plasmid and transfected into S2 cells to study the effect of Psn protein on N protein processing.

      (Ye and Fortini, 1999)
      External Crossreferences and Linkouts ( 0 )
      Synonyms and Secondary IDs (2)
      Reported As
      Symbol Synonym
      Psn+14.Scer\UAS
      Psn+14.UAS
      Name Synonyms
      Secondary FlyBase IDs
        References (11)