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General Information
Symbol
Dmel\TorΔP
Species
D. melanogaster
Name
FlyBase ID
FBal0120586
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
TorDeltaP, dTorΔP
Key Links
Allele class
Nature of the Allele
Allele class
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Comment:

Mutation is a deletion resulting from imprecise excision of TorEP2353.

Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

Contains a deletion originating from the P{EP}TorEP2353 that extends 3514 bp downstream, removing the Tor translation start site and the amino terminal 902 codons.

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 ( 1 )
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

TorΔP homozygous somatic clones in third instar larval eye discs exhibit a delay in G1/S transition during the second mitotic wave, as mutant cells enter S phase in a more posterior region than control cells.

Electroretinograms (ERGs) recorded from TorΔP/TorΔP full eye clones show significantly reduced amplitudes and off transients compared to controls. TorΔP/TorΔP full eye clones are reduced in size compared to controls. TorΔP/TorΔP mutants exhibit slow growth and developmental delay. TorΔP/TorΔP mutants in egg chamber follicle cells show reduced clone and cell size.

TorΔP larvae show relatively mild dendrite growth defects in the large C4da dendritic arbors.

TorΔP/+ heterozygote adults are significantly lighter compared to wild-type. The females eclose slightly earlier under standard nutrition than wild-type but at the same time as wild-type if nutrition is limited. Adult females have smaller wings as the cells are smaller compared to wild-type but their number is not changed.

TorΔP/+ flies have eyes similar to wild-type.

In TorΔP germline clones, 67% of eight-cell cysts contain pro-oocytes that have prematurely transitioned from the mitotic to the meiotic cycle.

TorΔP MARCM neuroblast clones exhibit developmental axon regrowth defects.

Homozygous dendrite arborization neuron clones show a severe and highly penetrant simplification of the dendritic arbors, with significant reductions in both the number and length of dendritic branches.

In the eye imaginal discs, TorΔP mutant cells proliferate more slowly than their wild-type twin spot control cells.

Cells in homozygous clones in the fat body are 70% smaller than surrounding wild-type cells.

Mosaic TorΔP mutant clones show a nearly complete block of TR-avidin uptake.

BrdU incorporation is normal in somatic clones of TorΔP homozygous cells in the late third instar eye disc.

Loss of Tor activity causes induction of autophagy in normally fed animals. Larvae show reduced size, as do the cells of the fat body. Lethality occurs late in the larval stages.

Clones of TorΔP homozygous wing disc cells show a marked reduction in cell size and an increase in the population of cells in G1 compared to wild-type cells from the same discs.

Homozygotes hatch at normal rates, but grow more slowly than normal and eventually arrest during larval development, reaching only 24% the mass of wild-type controls. The mutants remain viable and active during an extended larval period of about 30 days and eventually die without pupating. Homozygous somatic clones in the adult produces mutant cells markedly reduced in size. Clones in the wing are approximately half the size of controls. When TorΔP clones are compared to wild-type sister clones, in developing imaginal discs, they are similar in size 48 hours after induction, but by 72-96 hours they contain significantly fewer cells. In addition lone twin spots lacking a mutant sister are occasionally observed, indicating that at some frequency TorΔP homozygous cells are eliminated from the disc epithelium. FACS analysis of clones in the developing imaginal discs reveals a decrease in cell size of 30% observed in all phases of the cell cycle. Cell cycle phasing is also considerably different to that of controls, with relatively more cells in G1. and fewer in S and G2 phases. When salivary glands are examined from TorΔP mutant larvae a phenotypes affecting both polytene gland cells and the imaginal ring cells are seen. The endoreplicative cells undergo only four or five rounds of replication before entering quiescence, reaching a ploidy 16 ro 32 C and a size about 10% of wild-type. The imaginal rings of these larvae contain approximately fivefold fewer cells than wild-type. When homozygous mutant clones are examined in the wing imaginal disc, the nucleolar area is approximately half the size seen in wild-type cells. Also the appearance of fat body cells in the larva is changed by an aggregation of lipid vesicles. At 3-4 days after egg deposition (AED), both endoreplicative and mitotic tissues are found to cycle normally in TorΔP homozygotes (as measured by BrDU incorporation). In contrast, by 5-6 days AED all endoreplicative tissues including the gut fat body and salivary glands fail to incorporate BrDU. Whereas neuroblasts continue to cycle. The same is seen at 10d AED.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
NOT Enhanced by
Statement
Reference
Suppressed by
Statement
Reference
NOT suppressed by
Enhancer of
Statement
Reference

TorΔP is an enhancer of lethal | pupal stage phenotype of Atg1Δ3D

Suppressor of
NOT Suppressor of
Statement
Reference

Tor[+]/TorΔP is a non-suppressor of lethal | larval stage phenotype of Tor+t9.4, gig193/gig109

Tor[+]/TorΔP is a non-suppressor | partially of lethal | larval stage phenotype of gig193/gig109

Other
Phenotype Manifest In
Enhanced by
Statement
Reference
NOT Enhanced by
Statement
Reference

TorΔP has cell cycle | somatic clone phenotype, non-enhanceable by Ptendj189

Suppressed by
Statement
Reference

TorΔP has cell cycle phenotype, suppressible by CycEhs.PR

NOT suppressed by
Statement
Reference
Enhancer of
Statement
Reference

Tor[+]/TorΔP is an enhancer of eye phenotype of EBV\BZLF1GMR.PA

TorΔP is an enhancer of eye phenotype of EBV\BZLF1GMR.PA

NOT Enhancer of
Statement
Reference

Tor[+]/TorΔP is a non-enhancer of wing phenotype of pydtam/pydex147

Suppressor of
Other
Additional Comments
Genetic Interactions
Statement
Reference

The delay in G1/S transition during the second mitotic wave in third instar larval eye discs displayed by TorΔP homozygous somatic clones is not suppressed by additional clonal homozygosity for Thork13517.

The level of non-contacting dendrite crossing in class IV dendrite arborizing larval neurons is significantly increased in TorΔP;Df(2R)Sema-2b-C4 double mutants compared to either TorΔP/+ or Df(2R)Sema-2b-C4/+ heterozygotes.

TorΔP/+ suppresses the increase in excitatory junction current amplitude and quantal content seen in larvae NMJs expressing LrrkScer\UAS.cIa under the control of Scer\GAL4Mhc.PW.

Wings from pydex147/pydtam flies are broader compared to control wings, and this phenotype is not modified in a TorΔP/+ background.

The body weight of TorΔP/+ flies is increased by the presence of fkh1/+.

The dendritic branches of ddaC neurons in TorΔP/+ ; S6kl-1/+ double heterozygous larvae have fewer branch points than wild-type controls.

The dendritic branches of ddaC neurons in TorΔP/+ ; Sin1e03756/+ and in TorΔP/+ ; rictorΔ2/+ double heterozygous larvae show increased crossing over of each other, indicating a tiling defect.

Class IV da neurons of TorΔP/+ ; trc1/+ double heterozygous larvae show defects in dendritic tiling, with a significantly higher number of dendritic branches crossing one another compared to wild type.

Expression of Atg1Scer\UAS.cSa under the control of Scer\GAL4Act5C.PP in TorΔP clones in the fat body results in a further decrease in cells size compared to TorΔP single mutant clones.

Around 60% of gig109/gig193; TorΔP/+ flies survive to the pupal, but not the adult stage. However, one copy of the Tor+t9.4 transgene blocks the ability of TorΔP/+ to rescue gig109/gig193 flies to pupal viability.

Expression of Atg5dsRNA.Scer\UAS catastrophically arrests development of TorΔP; larvae are 6-fold smaller than TorΔP mutants alone. Fat body cell size is reduced a further 2-fold. Atg1Δ3D,TorΔP double mutants show lethality at the embryonic stage.

The small size and increase in proportion of cells in G1 seen in cell from TorΔP homozygous wing disc clones, is unafected by the expression of RhebScer\UAS.cSa in the clone cells (driven by Scer\GAL4αTub84B.PL when Scer\GAL80αTub84B.PL is removed in the same mitotic recombination event that creates the TorΔP homozygous clone.)

The small size and increase in the proportion of cells in G1 seen in cells from TorΔP homozygous wing disc clones, is unaffected by the expression of RhebScer\UAS.cSa in the clone cells (driven by Scer\GAL4αTub84B.PL when Scer\GAL80αTub84B.PL is removed in the same mitotic recombination event that creates the TorΔP homozygous clone).

The addition of Ptendj189 to TorΔP mutant clones shows no effect on the TorΔP phenotype. The addition of CycEhs.PR bypasses the cell cycle arrest seen in TorΔP larvae.

Xenogenetic Interactions
Statement
Reference

TorΔP/+ partially suppresses the eye-phenotype associated with EBV\BRLF1GMR.PA-expression.

TorΔP/+ partially enhances the eye-phenotype associated with EBV\BRLF1GMR.PA-expression.

Complementation and Rescue Data
Rescued by
Comments
Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (9)
References (43)