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General Information
Symbol
Dmel\Ptendj189
Species
D. melanogaster
Name
FlyBase ID
FBal0117670
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
dPTENdj189
Key Links
Allele class
Mutagen
    Nature of the Allele
    Allele class
    Mutagen
    Mutations Mapped to the Genome
     
    Type
    Location
    Additional Notes
    References
    Associated Sequence Data
    DNA sequence
    Protein sequence
     
     
    Progenitor genotype
    Cytology
    Nature of the lesion
    Statement
    Reference

    The insertion site of the F-element is between position 3987 (a T) and 3988 (a C) as numbered for the rescue fragment in Pten+t6.

    The F-element is within a coding exon at the 5' end of the Pten gene.

    Insertion components
    F{}Ptendj189
    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

    Pten5/Ptendj189 flies exhibit a highly penetrant, but mild, disorganised eye phenotype at the posterior edge in the midline.

    Pten5/Ptendj189 mutant males show significantly increase susceptibility to oxidative stress by paraquat, inhibition of mitochondrial complex by rotenone, osmotic stress by NaCl, and water-only starvation compared with wild-type controls.

    The size of the wings is increased in Ptendj189 heterozygotes compared with wild-type.

    Expression of PtendsRNA.Exel.Scer\UAS under the control of Scer\GAL4C57 in the muscles in a Ptendj189/+ background results in a significant decrease in the number of synaptic boutons at the larval neuromuscular junction.

    Larvae expressing PtendsRNA.Exel.Scer\UAS under the control of Scer\GAL4C57 in the muscles in a Ptendj189/+ background show no increase in evoked excitatory junctional potential (EJP) amplitude compared to controls, although the amplitude and frequency of miniature EJPs is increased in these animals compared to wild type.

    Ptendj189 mutants show no defects in opsin regulation.

    Homozygous embryos derived from homozygous female germline clones show severe abnormalities even in freshly laid eggs; the eggs are generally smaller and more roundish than wild type and many do not show any development. In those embryos that do initiate development, formation of pole cells is rarely seen, and where they do form, they are typically only 2 or 3 in number (compared to an average of 35 in wild type). In those homozygous embryos derived from homozygous female germline clones that do show development, axial expansion (the spreading out of nuclei along the long axis of the embryo in cycles 4-7) does not occur, resulting in a spherical rather than ellipsoid arrangement of nuclei prior to cortical migration and an abnormally low nuclear density in the posterior region of the embryo at the syncytial blastoderm stage. The synchrony of the cell cycle during cleavage divisions is lost (the pattern of mitoses is not completely randomised, but occurs in waves that always start at the posterior of the embryo). This results in blastoderm nuclei with different morphology and different condensation states of chromatin in distinct regions of the embryo at the beginning of cellularisation. The cellularisation front advances much more rapidly in the anterior of the mutant embryo compared to the posterior, and the delay in cellularisation at the posterior pole is often accompanied by severe defects in gastrulation, which often results in the rapid degeneration of the mutant embryo shortly after the onset of gastrulation. However, some mutant embryos recover well from the early developmental defects and complete embryogenesis without any gross morphological abnormalities. Survival beyond gastrulation is independent of whether the embryos receive a wild-type paternal copy of Pten. Stage 10 egg chambers in females containing homozygous germline clones have a very disorganised actin cytoskeleton which fills the nurse cell cytoplasm instead of localising to the cell borders. Fusion of nurse cells is often seen, as are mispositioned nurse cell nuclei that appear to have moved into the oocyte.

    Homozygous mutant clones of Ptendj189 in the eye produce ommatidia that are larger than wild-type and often bulge out of the eye. Eye bristles are also larger. Mutant photoreceptors are increased in area by about 140% compared to wild-type. Quantitative examination reveals that homozygous Ptendj189 clones contain on average 3.2 times as many cells as their twin spot controls. The intervening non neuronal cells in these clones are probably increased in size. In clones that included the whole eye, the number of ommatidia increases from about 750 (in wild-type) to about 1075, the area of the eye increases by at least 55%. Clones in the wing margin leads to a smaller number of larger bristles along the margin. In embryos produced from germ-line clones of homozygous Ptendj189 no increase in apoptosis is seen.

    External Data
    Interactions
    Show genetic interaction network for Enhancers & Suppressors
    Phenotypic Class
    NOT Enhanced by
    Suppressed by
    NOT suppressed by
    NOT Enhancer of
    Statement
    Reference
    NOT Suppressor of
    Statement
    Reference
    Other
    Phenotype Manifest In
    NOT Enhanced by
    Statement
    Reference
    Suppressed by
    Statement
    Reference

    Ptendj189/Pten117 has eye phenotype, suppressible by Akt1/Akt3

    Ptendj189/Pten117 has rhabdomere phenotype, suppressible by Akt1/Akt3

    NOT suppressed by
    Statement
    Reference
    NOT Enhancer of
    Statement
    Reference

    Ptendj189/Pten[+] is a non-enhancer of wing phenotype of pydtam/pydex147

    Ptendj189 is a non-enhancer of cell cycle | somatic clone phenotype of TorΔP

    NOT Suppressor of
    Statement
    Reference

    Ptendj189 is a non-suppressor of cell cycle | somatic clone phenotype of TorΔP

    Other
    Additional Comments
    Genetic Interactions
    Statement
    Reference

    Wings from pydex147/pydtam flies are broader compared to control wings, and this phenotype is not modified in a Ptendj189/+ background.

    Overexpression of IdeKO under the control of Scer\GAL4sd-SG29.1 has no effect on the large wing phenotype of Ptendj189 heterozygotes.

    Ptendj189/+ baz815-8/+ double heterozygous larvae have a significant reduction in the number of synaptic boutons at the neuromuscular junction compared to wild type.

    Ptendj189 does not protect Df(1)su(s)R194/+ clones in the eye; Df(1)su(s)R194/+ ; Ptendj189 clones are not recovered in the adult eye in animals with mosaic eyes containing two genotypes of cells with respect to RpL36; cells which are Df(1)su(s)R194/+ and cells in which the haplo-insufficiency of Df(1)su(s)R194/+ for RpL36 has been rescued by RpL36+t4 (in a wild-type background the Df(1)su(s)R194/+ clones are eliminated by cell competition and are not seen in the adult eye in these animals). Also, Ptendj189 does not prevent apoptosis of Df(1)su(s)R194/+ cells in the wing.

    The rhabdomere defects seen in Pten117/Ptendj189 mutant fly eyes are rescued in a Akt11/Akt13 mutant background. In these animals photoreceptor cell morphology is close to wild-type and eyes display a low frequency of deformed rhabdomeres.

    The nurse cells of Ptendj189/Pten117; Akt13/Akt11 viable females show normal lipid storage, while clones of Pten alleles show formation of large lipid droplets.

    Clones of Ptendj189 Tap42Δ305b double mutant cells (homozygous for Ptendj189 and Df(2L)Tap42Δ305b and with the lack of Nnp-1 and CG6523 function caused by Df(2L)Tap42Δ305b rescued using the P{Nnp-1t5.1} transgene) show the characteristic increase in cell size and S/G2 content of Ptendj189 single mutants.

    Ptendj189, Tsc129 double mutant somatic clones show an additive cell size increase phenotype.

    Ptendj189/Ptenc494 ; Pk61C4/Pk61C5 animals can survive to adulthood, although the abdomen is unproportionally reduced in size and leg structures are deformed.

    The addition of Ptendj189 to TorΔP mutant clones shows no effect on the TorΔP phenotype.

    Xenogenetic Interactions
    Statement
    Reference
    Complementation and Rescue Data
    Fails to complement
    Partially rescued by

    Ptendj189/Pten5 is partially rescued by Pten+t6

    Comments
    Images (0)
    Mutant
    Wild-type
    Stocks (0)
    Notes on Origin
    Discoverer
    Comments
    Comments

    Identified during a FRT/FLP recombination screen for mutations affecting the development of adult cuticular structures. Mutagen not stated.

    External Crossreferences and Linkouts ( 0 )
    Synonyms and Secondary IDs (11)
    References (21)