A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Allele Dmel\Pten1

General Information
SymbolDmel\Pten1SpeciesD. melanogaster
NameFlyBase IDFBal0104064
Feature typealleleAssociated geneDmel\Pten
Also Known AsDPTEN1
Allele class
Mutagenethyl methanesulfonate
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Description
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FB2013_03
FB2013_02
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Allele class
Mutagen
Mutations Mapped to the Genome
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Location
Additional Notes
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Associated Sequence Data
DDBJ /
EMBL /
GenBank
DNA sequence
Protein sequence
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Nature of the lesion
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Cytology
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lipid particle & nurse cell | somatic clone
wing & cell | somatic clone
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Statement
Reference
Pten[1] mutant somatic clones generated in the eye display highly disorganised ommatidia with compromised apical membranes. There is a failure of rhabdomere morphogenesis, and most photoreceptors display abnormally elongated, deformed, or split rhabdomeres. These defects are evident from mid-pupal development onwards. There is no evidence of photoreceptor degeneration in retinas from a series of aged adult flies.
Nurse cells in 90% of Akt11 mutant clones show cell-autonomous formation of large aggregated droplets and a corresponding reduction in small perinuclear droplets compared to wild-type nurse cells.
Mutant clones in the adult eye produce large cells and misrotated ommatidia. Cells in mutant clones in the eye disc show precocious differentiation several rows ahead of wild-type cells. In addition, ommatidia within clones in the eye disc initiate rotation before wild-type ommatidia.
Mosaic animals in which the eye is largely homozygous for Pten1 (generated using the "eyFLP" system) have larger eyes than normal. The eyes contain about 12% more ommatidia than wild-type eyes and individual ommatidia are 78% larger in surface area.
Hemizygotes die as late embryos or early first instar larvae. Homozygous mutant clones in the eye bulge out from the eye surface. Ommatidia sometimes fuse interommatidial bristles are abnormal, particularly (but not exclusively) in the dorsal half of the eye. Mutant clones typically contain at least twice as many ommatidia as their wild type twin spots. The largest clones can form a hyperplastic tumor-like overgrowth, though this phenotype is less severe than for tumor suppressor mutations. Within each ommatidium cell type specification seems normal. Cell bodies of mutant photoreceptors are enlarged compared to wild type neighbors, and the rhabdomeres are misshapen. The cell size and rhabdomeric phenotypes are cell autonomous. Homozygous mutant clones in the wing reveal an increase in cell size. Wing hairs are occasionally duplicated and crossvein formation is abnormal. Occasional extra wing vein material develops. Longitudinal veins are rarely affected.
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Statement
Reference
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Statement
Reference
Pten1/Pten[+] is a non-suppressor of large body phenotype of Scer\GAL429BD, dallysec.Scer\UAS.T:Hsap\MYC
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Statement
Reference
Pten1/Pten[+] is a non-suppressor of pupa phenotype of Scer\GAL429BD, dallysec.Scer\UAS.T:Hsap\MYC
Pten1/Pten[+] is a non-suppressor of wing phenotype of Scer\GAL429BD, dallysec.Scer\UAS.T:Hsap\MYC
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Statement
Reference
Pten1/+; dallysec.Scer\UAS.T:Hsap\MYC/Scer\GAL429BD pupae show the same large pupae and disordered wing patterning phenotype as wild-type animals expressing dallysec.Scer\UAS.T:Hsap\MYC under the control of Scer\GAL429BD.
Mosaic animals in which the eye is largely homozygous for both Pten1 and chicoflp147E (generated using the "eyFLP" system) have greatly enlarged eyes. The eyes contain about the same number of ommatidia as wild type, but the ommatidia are larger in surface area than normal.
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Fails to complement
Rescued by
Partially rescued by
Comments
Expression of Pten[2.Scer\UAS.T:Avic\GFP] under the control of Scer\GAL4[GMR.PF] is able to suppress all rhabdomeric phenotypes in Pten[1] mutant eyes. Expression of Pten[3.Scer\UAS.T:Avic\GFP] under the control of Scer\GAL4[GMR.PF] is able to suppress most of the mutant Pten[1] eye phenotype, but some split and misshapen rhabdomeres are still evident.
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hide References ( 9 )
Research paper
Vereshchagina et al., 2008, J. Cell Sci. 121(20): 3383--3392
The protein phosphatase PP2A-B' subunit Widerborst is a negative regulator of cytoplasmic activated Akt and lipid metabolism in Drosophila. [FBrf0206002]
Betschinger et al., 2006, Cell 124(6): 1241--1253
Asymmetric segregation of the tumor suppressor brat regulates self-renewal in Drosophila neural stem cells. [FBrf0189901]
Pinal et al., 2006, Curr. Biol. 16(2): 140--149
Regulated and polarized PtdIns(3,4,5)P3 accumulation is essential for apical membrane morphogenesis in photoreceptor epithelial cells. [FBrf0190038]
Vereshchagina and Wilson, 2006, Development 133(23): 4731--4735
Cytoplasmic activated protein kinase Akt regulates lipid-droplet accumulation in Drosophila nurse cells. [FBrf0193043]
Takeo et al., 2005, Dev. Biol. 284(1): 204--218
Expression of a secreted form of Dally, a Drosophila glypican, induces overgrowth phenotype by affecting action range of Hedgehog. [FBrf0187400]
Bateman and McNeill, 2004, Cell 119(1): 87--96
Temporal control of differentiation by the insulin receptor/tor pathway in Drosophila. [FBrf0180028]
Lu et al., 2004, EMBO J. 23(5): 1089--1100
Localization of Tec29 to ring canals is mediated by Src64 and PtdIns(3,4,5)P(3)-dependent mechanisms. [FBrf0174599]
Goberdhan and Wilson, 2002, Dev. Genes Evol. 212(4): 196--202
Insulin receptor-mediated organ overgrowth in Drosophila is not restricted by body size. [FBrf0148955]
Goberdhan et al., 1999, Genes Dev. 13(24): 3244--3258
Drosophila tumor suppressor PTEN controls cell size and number by antagonizing the Chico/PI3-kinase signaling pathway. [FBrf0123020]