A Database of Drosophila Genes & Genomes

FB2008_07, released August 8, 2008
 

Allele Dmel\Pi3K92EScer\UAS.T:Hsap\MYC

General Information
SymbolDmel\Pi3K92EScer\UAS.T:Hsap\MYCSpeciesD. melanogaster
NameFlyBase IDFBal0058396
Feature typealleleCreated / Updated2006-08-20/2006-08-20
Associated geneDmel\Pi3K92E
Allele class
Mutagenin vitro construct | regulatory fusionin vitro construct | coding region fusion
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Mapped Features and Mutations
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Associated Sequence Data
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DNA sequence
Protein sequence
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UniProtKB/Swiss-Prot
    UniProtKB/TrEMBL
      Progenitor genotype
      Nature of the lesion
      Statement
      Reference
      Construct: Expression of a wild-type cDNA fragment encoding Pi3K92E coding regions tagged at the N-terminus with Myc is influenced by a non-heat shock responsive Hsp70 promoter and five Scer\UAS Scer\GAL4 binding sites.
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      Cytology
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      imaginal disc & cell, with Scer\GAL4Act5C.PP
      cell surface & nurse cell | somatic clone, with Scer\GAL4Act5C.PP
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      Scer\GAL4dpp.blk1 mediated expression caused expansion of the wing margin due to an increase in overall number of cells and their size. Scer\GAL4GMR.PF mediated expression causes enlarged and bulging roughened eyes with fused ommatidia and misplaced or duplicated bristles.
      When expression is driven in imaginal disc cells by Scer\GAL4Act5C.PP the size of the cells is increased (as measured by FSC (forward scatter)). Cells are larger during G1 and the S+G2 phase. Overexpression of Pi3K92EScer\UAS.T:Hsap\MYC is not sufficient to increase cell number. When expression is driven by Scer\GAL4en-e16E, the size of the posterior compartment of the wing disc is significantly increased. There is no comparable effect on the anterior compartment.
      Expression of Pi3K92EScer\UAS.T:Hsap\MYC driven by Scer\GAL4Bx-MS1096 results in an increased wing size.
      When Pi3K92ED954A.Scer\UAS.T:Hsap\MYC is driven by Scer\GAL4ptc-559.1 results in a increase in the distance between the L3 and L4 veins in the wing.
      Clones of cells expressing Pi3K92EScer\UAS.T:Hsap\MYC under the control of Scer\GAL4Act5C.PP in the gut, fat body, Malpighian tubules and epidermis are only slightly larger than control cells at the time of larval hatching. After several days of starvation on 20% sucrose, these cells are much larger than adjacent control cells and have a visibly increased DNA content. Gut and fat body cells expressing Pi3K92EScer\UAS.T:Hsap\MYC under the control of Scer\GAL4Act5C.PP continue to replicate their DNA for at least 2-3 days under starvation conditions. Expression of Pi3K92EScer\UAS.T:Hsap\MYC in third larval instar fat body cells under the control of Scer\GAL4Act5C.PP increases the opacity of the cytoplasm, thus promoting nutrient storage. Expression of Pi3K92EScer\UAS.T:Hsap\MYC under the control of Scer\GAL4Adh.PF in fed animals does not affect survival. In contrast, expression of Pi3K92EScer\UAS.T:Hsap\MYC under the control of Scer\GAL4Adh.PF in starved animals results in first instar larvae dying within 3-4 days of hatching (control animals survive 8-9 days). Expression of Pi3K92EScer\UAS.T:Hsap\MYC under the control of Scer\GAL4en-e16E in starved animals results in them dying within 2-3 days, 4-5 days before controls. Animals expressing Pi3K92EScer\UAS.T:Hsap\MYC under the control of Scer\GAL4Adh.PF feed poorly, often having no food in their gut, and frequently wander away from their food.
      Expression of Pi3K92EScer\UAS.T:Hsap\MYC under the control of Scer\GAL4Act5C.PP in wing disc cells results in an increase in cell size compared to controls. The proportion of cells in G1 is decreased compared to controls. Clones expressing Pi3K92EScer\UAS.T:Hsap\MYC under the control of Scer\GAL4Act5C.PP are not visibly round, do not generate ectopic folds and do not bulge out of the epithelium.
      Clones of cells expressing Pi3K92EScer\UAS.T:Hsap\MYC under the control of Scer\GAL4Act5C.PP are 28% larger than control cells.
      Expression of Pi3K92EScer\UAS.T:Hsap\MYC under the control of Scer\GAL4Bx-MS1096 results in a slight increase in wing size and in males the wings show a downward curvature.
      Expression of Pi3K92EScer\UAS.T:Hsap\MYC under the control of Scer\GAL4dpp.blk1 results in enlargement of the region encompassed by wing veins 3 and 4, the anterior crossvein and the wing margin.
      Animals expressing Pi3K92EScer\UAS.T:Hsap\MYC under the control of Scer\GAL4GMR.PF have a significantly larger eye than normal, due to an increase in ommatidia size. Expression of Pi3K92EScer\UAS.T:Hsap\MYC under the control of Scer\GAL4ap-md544 results in dramatic overgrowth of the wing, inhibiting wing unfolding. Expression of Pi3K92EScer\UAS.T:Hsap\MYC under the control of Scer\GAL4Bx-MS1096 causes the wing to bend downwards slightly.
      Caspase activation in cells posterior to the furrow in eye discs is unaffected by Pi3K92EScer\UAS.T:Hsap\MYC; Scer\GAL4GMR.PF.
      Pi3K92EScer\UAS.T:Hsap\MYC; Scer\GAL4en-e16E animals are hyper-sensitive to starvation.
      Pi3K92EScer\UAS.T:Hsap\MYC driven by Scer\GAL4HLHmδ has no effect on ommatidial rotation.
      Somatic clones expressing dmScer\UAS.cZa (driven by Scer\GAL4αTub84B.PC, in the wing disc) are significantly larger than controls. Sibling clones next to these clones are similar in size to controls elsewhere. When Pi3K92EScer\UAS.T:Hsap\MYC is driven by Scer\GAL4dpp.blk1 or Scer\GAL4αTub84B.PC lead to wings that are significantly larger than controls.
      Expression of Pi3K92EScer\UAS.T:Hsap\MYC under the control of Scer\GAL4Act5C.PP in clones in the eye disc results in enlarged cells with rotation defects. Precocious differentiation of cells in the eye disc is also seen.
      Expression driven by Scer\GAL4Act5C.PP in clones in the fat body suppresses starvation-induced autophagy, but not the autophagy induced by TorΔP loss of function.
      When expression is governed by Scer\GAL4Lsp2.PH there is a noticeable lack of large autolysosomes. In state similar to when ecdysone signalling is blocked the cytoplasm contains small autophagosomes and autolysosomes. Glycogen accumulates, probably due to a failure of autophagy to degrade glycogen. Autophagic area decreased compared to wild type.
      Overexpression of Pi3K92EScer\UAS.T:Hsap\MYC under the regulation of Scer\GAL4dpp.blk1 does not appreciably alter nucleolar size.
      Expression of Pi3K92EScer\UAS.T:Hsap\MYC, under the control of Scer\GAL429BD, causes overgrown salivary glands and wing discs in third instar larvae.
      Fasted third instar larvae expressing Pi3K92EScer\UAS.T:Hsap\MYC under the control of Scer\GAL4NPFR1.6.6 display an attenuated feeding response to solid food. These third instar larvae do not exhibit significant changes in the intake rate of the richer liquid food, relative to controls.
      Expression of Pi3K92EScer\UAS.T:Hsap\MYC using Scer\GAL4P0206 induces autonomous growth in the ring gland, especially in the prothoracic gland. The whole adults show reduced growth at all stages of development and emerging adults with reduced size and body weight. This decrease was attributable to an decrease in cell number in the wing and a decrease in cell number in eye. The timing of embryonic and larval development in these mutants is comparable to controls. The duration of pupal development is delayed by less than four hours.
      When Pi3K92EScer\UAS.T:Hsap\MYC is driven by Scer\GAL4Aug21 no effect on adult size is observed. Expression of Pi3K92EScer\UAS.T:Hsap\MYC in the ring gland using Scer\GAL4P0206 induces autonomous growth.
      Flies overexpressing Pi3K92EScer\UAS.T:Hsap\MYC in dopaminergic neurons (through Scer\GAL4ple.PF) exhibit basal levels of reactive oxygen species (ROS), as in wild-type.
      Expression of Pi3K92EScer\UAS.T:Hsap\MYC in the prothoracic gland, driven by Scer\GAL4phm.PO, causes enlarged prothoracic gland cells during all feeding stages. Scer\GAL4phm.PO>Pi3K92EScer\UAS.T:Hsap\MYC pharate adults are 73% (females) and 80% (males) the weight of controls. This phenotype is enhanced when larvae are reared under constant light (LL) as pharate adults are then 51% the weight of controls and pupariate ~4 hours earlier than controls reared under 14 hours light:10 hours dark. Scer\GAL4phm.PO>Pi3K92EScer\UAS.T:Hsap\MYC flies are the same size as controls at hatching, but grow more slowly than controls during L1 and L2. However, when Scer\GAL4phm.PO>Pi3K92EScer\UAS.T:Hsap\MYC larvae are reared under LL on a yeast-supplemented diet they grow at the same rate as controls. Scer\GAL4phm.PO>Pi3K92EScer\UAS.T:Hsap\MYC larvae overestimate their size so that they initiate metamorphosis before reaching the minimal viable weight necessary to survive pupation; 50% of Scer\GAL4phm.PO>Pi3K92EScer\UAS.T:Hsap\MYC larvae are able to pupariate after starvation at 2.6 hr after L3 ecdysis (AL3E) when they are only 0.36mg, instead of pupariating at 11.4 hours at a weight of 0.86mg like controls. While control larvae do not pupariate under starvation conditions unless they have been fed for at least 10 hours AL3E, Scer\GAL4phm.PO>Pi3K92EScer\UAS.T:Hsap\MYC larvae can pupariate at 0 hour starvation. This results in the formation of partial puparia that are tanned but have failed to contract properly, although they are competent to undergo some of the earliest metamorphic processes such as eversion and elongation. However, such puparia are non-viable and any larvae that fail to pupariate at this time die. When Scer\GAL4phm.PO>Pi3K92EScer\UAS.T:Hsap\MYC are starved after 4 hours AL3E, 73% form normal puparia, 13% form partial puparia, and the remaining larvae die. These animals exhibit molting defects in the prepupal stages. Scer\GAL4phm.PO>Pi3K92EScer\UAS.T:Hsap\MYC flies starved at 8 hours AL3E form normal puparia and do not exhibit molting defects. Expression of Pi3K92EScer\UAS.T:Hsap\MYC, under the control of either Scer\GAL4P0206 or Scer\GAL4Aug21, does not affect body size. However, Scer\GAL4P0206>Pi3K92EScer\UAS.T:Hsap\MYC pharate adults reared under constant light (LL) are 80% the size of control pharate adults grown under the same conditions.
      80% of pupae expressing Pi3K92E[Scer\UAS.T:Hsap\MYC] under the control of Scer\GAL4[hs.PB] (using a 30 minute heat shock at 9 hours after puparium formation) still possess intact salivary glands at 20 hours after puparium formation (this is approximately 6 hours after the glands are normally destroyed in wild-type animals).
      Nurse cell clones that express Pi3K92E[Scer\UAS.T:Hsap\MYC] under the control of Scer\GAL4[Act5C.PP] show a normal distribution of lipid droplets. However, 16% of egg chambers with these clones exhibit elongated cell surface lipid droplet-type structures in nurse cells at the periphery of the egg chamber, which are not seen in wild-type egg chambers.
      Expression of Pi3K92E[Scer\UAS.T:Hsap\MYC] under the control of Scer\GAL4[nub-AC-62] results in tissue overgrowth in the larval salivary glands.
      The salivary glands of animals expressing Pi3K92E[Scer\UAS.T:Hsap\MYC] under the control of Scer\GAL4[fkh.PH] are greatly increased in area compared to controls at 13.5 hours after puparium formation (APF). At 24 hours APF, animals expressing Pi3K92E[Scer\UAS.T:Hsap\MYC] under the control of Scer\GAL4[fkh.PH] still contain salivary gland tissue, in contrast to wild-type animals, where the salivary glands have completely degraded by this stage. The salivary glands in the mutant animals are always present at 24 hours APF, but are partly degraded. The induction of autophagy that is seen in wild-type salivary glands at 13.5 hours APF is not seen in animals expressing Pi3K92E[Scer\UAS.T:Hsap\MYC] under the control of Scer\GAL4[fkh.PH]. DNA fragmentation is detected by TUNEL in salivary glands of animals expressing Pi3K92E[Scer\UAS.T:Hsap\MYC] under the control of Scer\GAL4[fkh.PH] at 13.5 hours after puparium formation, as occurs in control salivary glands at this stage.
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      Suppresses the eye phenotype caused by PtenScer\UAS.cHa, when co-expressed using Scer\GAL4ey.PH.
      Flies expressing Pi3K92ED954A.Scer\UAS.T:Hsap\MYC and PtenScer\UAS.cGb under the control of Scer\GAL4Bx-MS1096 have wings even smaller than flies expressing Pi3K92ED954A.Scer\UAS.T:Hsap\MYC or PtenScer\UAS.cGb alone.
      Coexpression of TorWT.Scer\UAS.T:Zzzz\FLAG and Pi3K92EScer\UAS.T:Hsap\MYC under the control of Scer\GAL4Bx-MS1096 results in a severe reduction in wing size.
      Co-expression of S6kScer\UAS.cMa does not result in any further increase in eye size in animals expressing Pi3K92EScer\UAS.T:Hsap\MYC under the control of Scer\GAL4GMR.PF. Co-expression of Akt1Scer\UAS.cRa results in a clear increase the size of the eye and individual ommatidia in animals expressing Pi3K92EScer\UAS.T:Hsap\MYC under the control of Scer\GAL4GMR.PF. Co-expression of S6kScer\UAS.cMa does not modify the bent wing phenotype caused by expression of Pi3K92EScer\UAS.T:Hsap\MYC under the control of Scer\GAL4Bx-MS1096. Co-expression of Akt1Scer\UAS.cRa in animals expressing Pi3K92EScer\UAS.T:Hsap\MYC under the control of Scer\GAL4Bx-MS1096 causes the wing to bend strongly downwards. The enlarged eye and ommatidia phenotype caused by expression of Pi3K92EScer\UAS.T:Hsap\MYC under the control of Scer\GAL4GMR.PF is not affected if the flies are also homozygous for S6kl-1. The enlarged eye and ommatidia phenotype caused by expression of Pi3K92EScer\UAS.T:Hsap\MYC under the control of Scer\GAL4GMR.PF is completely suppressed in a Akt11/Akt13 background.
      Co-expression of Pi3K92EScer\UAS.T:Hsap\MYC almost completely rescues the eye phenotype caused by expression of foxoScer\UAS.cKa under the control of Scer\GAL4GMR.PF; the ommatidia and nearly all of the mechanosensory bristles are restored. Co-expression of Pi3K92EScer\UAS.T:Hsap\MYC partially rescues the eye phenotype caused by expression of Mmus\Foxo1AA.Scer\UAS under the control of Scer\GAL4GMR.PF; a lack of ommatidia and mechanosensory bristles is still seen.
      The hyper-sensitivity of Pi3K92EScer\UAS.T:Hsap\MYC; Scer\GAL4en-e16E animals to starvation is partially suppressed by RhebPΔ1/+ or