FB2024_03 , released June 25, 2024
Allele: Dmel\Pi3K59FΔm22
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General Information
Symbol
Dmel\Pi3K59FΔm22
Species
D. melanogaster
Name
FlyBase ID
FBal0243862
Feature type
allele
Associated gene
Dmel\Pi3K59F
Associated Insertion(s)
Carried in Construct
Also Known As
vps34Δm22, Vps34m22
Key Links
Allele class
Mutagen
Nature of the Allele
Allele class
Mutagen
P-element activity
(Juhász et al., 2008)
Progenitor genotype
P{GawB}Pi3K59FNP1626
(Juhász et al., 2008)
Cytology
Description

Imprecise excision of the progenitor insertion resulting in a deletion extending 3349 bp downstream of the insertion site. The entire Pi3K59F coding region is removed.

(Juhász et al., 2008)
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

      Pi3K59FΔm22 somatic clones in the follicular epithelium exhibit dysplasia-like defects, namely a high frequency of epithelium multilayering and mild cell polarity defects (i.e. abnormal expression of the adherent junction components Arm and E-cad, and occasional overlap between the apical marker aPKC and the basolateral marker Dlg), with cells occasionally invading between germline cells, as compared to controls.

      (O'Farrell et al., 2017)

      Homozygous adult mushroom body gamma neuron clones show an axon pruning defect.

      (Issman-Zecharya and Schuldiner, 2014)

      Expression of Pi3K59FΔm22 using Scer\GAL4Act5C.PP results in basal autophagy defects in larval fat body cell somatic clones.

      Pi3K59FΔm22 mutants display basal autophagy defects in larval fat body cells.

      (Pircs et al., 2012)

      Females carrying homozygous germline clones have a significant increase in the number of stage 14 egg chambers that have persisting TUNEL-negative nurse cell nuclei compared to wild-type egg chambers at the same stage, in which nurse cell nuclei are rarely detected (and those that are detected are all TUNEL positive). The persisting nurse cell nuclei show condensed nuclear staining.

      (Nezis et al., 2010)

      Starvation-induced expansion of the lysosomal system is blocked in Pi3K59FΔm22 mutant fat-body cells. Autophagosome and autolysosome formation is disrupted in these animals. Fat-body cell size is normal.

      Pi3K59FΔm22 mutant fat-body and garland cells show disruptions in endocytosis.

      In the eye imaginal disc, Pi3K59FΔm22 mutant cells proliferate at a rate similar to that of twin spot control cells. No accumulation of autophagosomes is observed in mutant eye disc cells.

      (Juhász et al., 2008)
      External Data
      Interactions
      Show genetic interaction network for Enhancers & Suppressors
      Phenotypic Class
      Phenotype Manifest In
      Additional Comments
      Genetic Interactions
      Statement
      Reference

      The frequent follicular epithelium multi-layering and the mis-localization of cell polarity markers presented by Pi3K59FΔm22 homozygous follicle cell clones is strongly suppressed by the clonal expression of Lkb1HMS01351 under the control of Scer\GAL4tub.PU.

      Both the frequent follicular epithelium multi-layering and the occasional invasion of germline cells by follicle cells exhibited by Pi3K59FΔm22 homozygous follicle cell clones is strongly suppressed by the clonal expression of bskDN.Scer\UAS.cUa under the control of Scer\GAL4tub.PU.

      (O'Farrell et al., 2017)

      The lack of F-actin rich radial protrusions seen in primary hemocytes derived from mtmΔ77/mtmz2-4747 larvae is not rescued if the larvae also carry Pi3K59FΔm22/Pi3K59FΔm22.

      (Velichkova et al., 2010)

      Expression of Tsc1Scer\UAS.cTa and gigScer\UAS.cTa under the control of Scer\GAL4Act5C.PP results in a significant reduction in fat-body cell size in a Pi3K59FΔm22 background, and the formation of autolysosomes is disrupted.

      Pi3K59FΔm22 and Vps25A3 double mutant fat-body cells show disruptions in endocytosis.

      Vps25A3 and Pi3K59FΔm22 double mutant clones generated in the fat-body or eye-disc show accumulation of autophagosomes under fed conditions, compared to none observed in Pi3K59FΔm22 single mutant clones.

      Vps28k16503 and Pi3K59FΔm22 double mutant clones generated in the fat-body show accumulation of autophagosomes under fed conditions, compared to none observed in Pi3K59FΔm22 single mutant clones.

      (Juhász et al., 2008)
      Xenogenetic Interactions
      Statement
      Reference
      Complementation and Rescue Data
      Partially rescued by

      Pi3K59FΔm22 is partially rescued by Scer\GAL4Tub.PU/Pi3K59FUAS.cJa

      (O'Farrell et al., 2017)
      Comments

      The follicular epithelium multi-layering exhibited by Pi3K59FΔm22 homozygous somatic clones is almost fully rescued by the expression of Pi3K59FScer\UAS.cJa under the control of Scer\GAL4tub.PU.

      (O'Farrell et al., 2017)
      Images (0)
      Mutant
      Wild-type
      Stocks (0)
      Notes on Origin
      Discoverer
      External Crossreferences and Linkouts ( 0 )
      Synonyms and Secondary IDs (6)
      References (14)