A Database of Drosophila Genes & Genomes

FB2008_07, released August 8, 2008
 

Allele Dmel\Ptendj189

General Information
SymbolDmel\Ptendj189SpeciesD. melanogaster
NameFlyBase IDFBal0117670
Feature typealleleCreated / Updated2006-05-15/2006-05-15
Associated geneDmel\Pten
Allele class
Mutagen
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Allele class
Mutagen
Mapped Features and Mutations
Type
Symbol & Location
Additional Notes
References
 
 
 
 
Associated Sequence Data
DDBJ /
EMBL /
GenBank
DNA sequence
Protein sequence
Name
 
UniProtKB/Swiss-Prot
    UniProtKB/TrEMBL
      Progenitor genotype
      Nature of the lesion
      Statement
      Reference
      The F-element is within a coding exon at the 5' end of the Pten gene.
      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.
      Assay mode
      Caused by insertion
      Cytology
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      hide Phenotype Manifest In
      nurse cell & actin cytoskeleton | germ-line clone
      nurse cell & nucleus | germ-line clone
      hide Detailed Description
      Statement
      Reference
      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.
      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.
      Pten[dj189] mutants show no defects in opsin regulation.
      hide Interactions
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      hideNOT Enhanced by
      Statement
      Reference
      hideSuppressed by
      Statement
      Reference
      hideNOT suppressed by
      Statement
      Reference
      Ptendj189 has increased cell size phenotype, non-suppressible by Tap42Δ305b
      hideNOT Enhancer of
      Statement
      Reference
      hideNOT Suppressor of
      Statement
      Reference
      Ptendj189 is a non-suppressor of reduced cell size | somatic clone phenotype of TorΔP
      hideOther
      Statement
      Reference
      hide Phenotype Manifest In
      hideNOT Enhanced by
      Statement
      Reference
      hideSuppressed by
      Statement
      Reference
      hideNOT suppressed by
      Statement
      Reference
      hideNOT Enhancer of
      Statement
      Reference
      Ptendj189 is a non-enhancer of cell cycle | somatic clone phenotype of TorΔP
      hideNOT Suppressor of
      Statement
      Reference
      Ptendj189 is a non-suppressor of cell cycle | somatic clone phenotype of TorΔP
      hideOther
      Statement
      Reference
      Akt11/Akt13, Ptendj189/Pten117 has lipid particle & nurse cell phenotype
      hide Additional Comments
      hide Genetic Interactions
      Statement
      Reference
      The addition of Ptendj189 to TorΔP mutant clones shows no effect on the TorΔP phenotype.
      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.
      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.
      Pten[dj189] does not protect Df(1)su(s)R194/+ clones in the eye; Df(1)su(s)R194/+ ; Pten[dj189] 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, Pten[dj189] does not prevent apoptosis of Df(1)su(s)R194/+ cells in the wing.
      The nurse cells of Pten[dj189]/Pten[117]; Akt1[3]/Akt1[1] viable females show normal lipid storage, while clones of Pten alleles show formation of large lipid droplets.
      hide Xenogenetic Interactions
      Statement
      Reference
      hide Complementation & Rescue Data
      Fails to complement
      Comments
      hide Stocks ( 0 )
      hide Notes on Origin
      Discoverer
      hide Comments
      Identified during a FRT/FLP recombination screen for mutations affecting the development of adult cuticular structures. Mutagen not stated.
      hide Synonyms & Secondary IDs ( 8 )
      Reported As
      Symbol Synonym
      dPTENDJ189
      PTENDJ1
      Name Synonym
      Secondary FlyBase IDs
        hide References ( 14 )
        Research paper
        Tyler et al., 2007, Genetics 175(2): 643--657
        Genes affecting cell competition in Drosophila. [FBrf0192304]
        Vereshchagina and Wilson, 2006, Development 133(23): 4731--4735
        Cytoplasmic activated protein kinase Akt regulates lipid-droplet accumulation in Drosophila nurse cells. [FBrf0193043]
        Coelho et al., 2005, Genetics 171(2): 597--614
        A genetic screen for dominant modifiers of a small-wing phenotype in Drosophila melanogaster identifies proteins involved in splicing and translation. [FBrf0190712]
        Cygnar, 2005, Genetics 170(2): 733--740
        The phosphatase subunit tap42 functions independently of target of rapamycin to regulate cell division and survival in Drosophila. [FBrf0188576]
        Mikeladze-Dvali et al., 2005, Cell 122(5): 775--787
        The growth regulators warts/lats and melted interact in a bistable loop to specify opposite fates in Drosophila R8 photoreceptors. [FBrf0187233]
        von Stein et al., 2005, Development 132(7): 1675--1686
        Direct association of Bazooka/PAR-3 with the lipid phosphatase PTEN reveals a link between the PAR/aPKC complex and phosphoinositide signaling. [FBrf0183928]
        Reiling and Hafen, 2004, Genes Dev. 18(23): 2879--2892
        The hypoxia-induced paralogs Scylla and Charybdis inhibit growth by down-regulating S6K activity upstream of TSC in Drosophila. [FBrf0180258]
        Stocker et al., 2002, Science 295(5562): 2088--2091
        Living with lethal PIP3 levels: viability of flies lacking PTEN restored by a PH domain mutation in Akt/PKB. [FBrf0151483]
        Gao and Pan, 2001, Genes Dev. 15(11): 1383--1392
        TSC1 and TSC2 tumor suppressors antagonize insulin signaling in cell growth. [FBrf0136941]
        Rintelen et al., 2001, Proc. Natl. Acad. Sci. USA 98(26): 15020--15025
        PDK1 regulates growth through Akt and S6K in Drosophila. [FBrf0141724]
        Gao et al., 2000, Dev. Biol. 221(2): 404--418
        Drosophila PTEN regulates cell growth and proliferation through PI3K-dependent and -independent pathways. [FBrf0127089]
        Zhang et al., 2000, Genes Dev. 14(21): 2712--2724
        Regulation of cellular growth by the Drosophila target of rapamycin dTOR. [FBrf0131434]
        Personal communication to FlyBase
        Neufeld, 2001.1.11, PTEN-MGH1.
        PTEN-MGH1. [FBrf0133211]
        Pan and Levis, 2001.9.10, Tsc1<up>12</up>, Tsc1<up>+t4.7</up>, and Pten<up>dj189</up>.
        Tsc1<up>12</up>, Tsc1<up>+t4.7</up>, and Pten<up>dj189</up>. [FBrf0137847]