FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\Ptendj189
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General Information
Symbol
Dmel\Ptendj189
Species
D. melanogaster
Name
FlyBase ID
FBal0117670
Feature type
allele
Associated gene
Dmel\Pten
Associated Insertion(s)
F{}Ptendj189
Carried in Construct
Also Known As
dPTENdj189
Key Links
Genomic Maps

Allele class
Mutagen
    Nature of the Allele
    Allele class
    Mutagen
    Progenitor genotype
    Associated Insertion(s)
    F{}Ptendj189
    Cytology
    Description

    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.

    (Pan and Levis, 2001.9.10)

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

    (Gao et al., 2000)
    Mutations Mapped to the Genome
    Curation Data
    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

        Ptendj189 somatic cyst stem clones in the testis are progressively lost from day 2 to day 7 post clone induction

        (Yuen et al., 2021)

        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.

        (Mensah et al., 2015)

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

        (Tsuda et al., 2010)

        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.

        (Ramachandran et al., 2009)

        Ptendj189 mutants show no defects in opsin regulation.

        (Mikeladze-Dvali et al., 2005)

        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.

        (von Stein et al., 2005)

        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.

        (Gao et al., 2000)
        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

        Ptendj189 is a non-enhancer of decreased cell size | somatic clone phenotype of mTorΔP

        (Zhang et al., 2000)
        NOT Suppressor of
        Statement
        Reference

        Ptendj189 is a non-suppressor of decreased cell size | somatic clone phenotype of mTorΔP

        (Zhang et al., 2000)
        Other
        Phenotype Manifest In
        NOT Enhanced by
        Statement
        Reference

        Ptendj189 has wing margin bristle phenotype, non-enhanceable by Scer\GAL4Bx-MS1096/Pi3K92EUAS.Tag:MYC

        (Gao et al., 2000)
        Suppressed by
        NOT suppressed by
        Statement
        Reference

        Ptendj189 has wing phenotype, non-suppressible by Scer\GAL4sd-SG29.1/IdeUAS.cTa

        (Tsuda et al., 2010)

        Ptendj189 has wing margin bristle | somatic clone phenotype, non-suppressible by InR35/InR05545

        (Gao et al., 2000)
        NOT Enhancer of
        Statement
        Reference

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

        (Djiane et al., 2011)

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

        (Zhang et al., 2000)
        NOT Suppressor of
        Statement
        Reference

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

        (Zhang et al., 2000)
        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.

        (Djiane et al., 2011)

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

        (Tsuda et al., 2010)

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

        (Ramachandran et al., 2009)

        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.

        (Tyler et al., 2007)

        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.

        (Pinal et al., 2006)

        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.

        (Vereshchagina and Wilson, 2006)

        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.

        (Cygnar et al., 2005)

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

        (Gao and Pan, 2001)

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

        (Rintelen et al., 2001)

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

        (Zhang et al., 2000)
        Xenogenetic Interactions
        Statement
        Reference
        Complementation and Rescue Data
        Fails to complement

        PtenMGH1

        (Neufeld, 2001.1.11)
        Partially rescued by

        Ptendj189/Pten5 is partially rescued by Pten+t6

        (Mensah et al., 2015)
        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.

        (Gao et al., 2000)
        External Crossreferences and Linkouts ( 0 )
        Synonyms and Secondary IDs (11)
        References (24)