Allele Dmel\Ptendj189
| General Information | |||
|---|---|---|---|
| Symbol | Dmel\Ptendj189 | Species | D. melanogaster |
| Name | FlyBase ID | FBal0117670 | |
| Feature type | allele | Created / Updated | 2006-05-15/2006-05-15 |
| Associated gene | Dmel\Pten | ||
| Allele class | |||
| Mutagen | |||
Nature of the Allele
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| Allele class | |||
| Mutagen | |||
| Mapped Features and Mutations | |||
Type Symbol & Location Additional Notes References | |||
| Associated Sequence Data | |||
| DDBJ
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EMBL / GenBank | DNA sequence Protein sequence Name | ||
| UniProtKB/Swiss-Prot | |||
| UniProtKB/TrEMBL | |||
| Progenitor genotype | |||
| Nature of the lesion | Statement Reference | ||
| Assay mode | |||
| Caused by insertion | |||
| Cytology | |||
Phenotypic Data
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Phenotypic Class
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Phenotype Manifest In
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nurse cell & actin cytoskeleton | germ-line clone nurse cell & nucleus | germ-line clone | |||
Detailed Description
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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. | |||
Interactions
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Phenotypic Class
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NOT Enhanced by | |||
Statement Reference Ptendj189 has increased cell size | somatic clone phenotype, non-enhanceable by Scer\GAL4Bx-MS1096/Pi3K92EScer\UAS.T:Hsap\MYC | |||
Suppressed by | |||
Statement Reference Ptendj189 has increased cell number | somatic clone phenotype, suppressible | partially by eIF-4a1069 Ptendj189 has increased cell size | somatic clone phenotype, suppressible | partially by Pi3K92ED954A.Scer\UAS.T:Hsap\MYC/Scer\GAL4Bx-MS1096 | |||
NOT suppressed by | |||
Statement Reference Ptendj189 has increased cell size | somatic clone phenotype, non-suppressible by Scer\GAL4Bx-MS1096/Pi3K92EScer\UAS.T:Hsap\MYC | |||
NOT Enhancer of | |||
Statement Reference | |||
NOT Suppressor of | |||
Statement Reference | |||
Other | |||
Statement Reference | |||
Phenotype Manifest In
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NOT Enhanced by | |||
Statement Reference Ptendj189 has wing margin bristle phenotype, non-enhanceable by Scer\GAL4Bx-MS1096/Pi3K92EScer\UAS.T:Hsap\MYC | |||
Suppressed by | |||
Statement Reference | |||
NOT suppressed by | |||
Statement Reference | |||
NOT Enhancer of | |||
Statement Reference | |||
NOT Suppressor of | |||
Statement Reference | |||
Other | |||
Statement Reference | |||
Additional Comments
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Genetic Interactions
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Statement Reference 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. | |||
Xenogenetic Interactions
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Statement Reference | |||
Complementation & Rescue Data
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| Fails to complement | |||
| Comments | |||
Stocks
( 0 ) | |||
Notes on Origin
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| Discoverer | |||
Comments
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Identified during a FRT/FLP recombination screen for mutations affecting the development of adult cuticular structures. Mutagen not stated. | |||
Synonyms & Secondary IDs
( 8 ) | |||
| Reported As | |||
| Symbol Synonym | dPTENdj189 dPTENDJ189 PTENDJ1 Ptendj189 PtenDJ189 PTENdj189 PTENDJ189 PTEN-DJ1 | ||
| Name Synonym | |||
| Secondary FlyBase IDs | |||
References
( 14 ) | |||
| Research paper |
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| Personal communication to FlyBase |
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Nature of the Allele