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General Information
Symbol
Dmel\dlg1GD4689
Species
D. melanogaster
Name
FlyBase ID
FBal0209360
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
dlg-IR, UAS-dlgRNAi
Key Links
Allele class
Nature of the Allele
Allele class
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Carried in construct
Cytology
Nature of the lesion
Statement
Reference

UASt regulatory sequences drive expression of an inverted repeat.

Allele components
Product class / Tool use(s)
Encoded product / tool
Associated Sequence Features
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 ( 1 )
Modifiers Based on Experimental Evidence ( 1 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

Expression of dlg1GD4689 (driven by Scer\GAL4Dll-md23) in MARCM clones in the antennal discs in third instar larvae leads to tumorigenic overgrowth, while in the type II neuroblast lineage clones it results in occasional appearance of supernumerary neuroblasts but to overgrowth.

Expression of dlg1GD4689 under the control of Scer\GAL4e22c does not induce formation of syncytia in third instar larval epidermis.

Expression of dlg1GD4689 in all neuroblasts under the control of Scer\GAL4insc-Mz1407 does not cause an obvious change in neuroblast numbers in the larval brain, however it does produce defects in the basal segregation of mira.

The expression of dlg1GD4689 under the control of Scer\GAL4sd-SG29.1 induces wing disc overgrowths.

Expression of dlg1GD4689 (together with UAS-Dicer2 to enhance RNAi efficiency) under the control of Scer\GAL4GMR.PU has no effect on adult eye appearance.

Expression of dlg1GD4689 in a MARCM third instar imaginal disc clone results in small tumours.

Adults expressing dlg1GD4689 under the control of Scer\GAL4elav.PLu (in the presence of Dcr-2Scer\UAS.cDa to increase the efficiency of RNAi) show significantly reduced avoidance of noxious temperature (46[o]C) compared to control flies.

Expression under the control of Scer\GAL4Mef2.PR results in early pupal lethality.

Expression under the control of Scer\GAL4pnr-MD237 results in lethality before the pupal stage.

External Data
Bristle Screen Database (Knoblich Lab) - A database for RNAi phenotypes in bristle and notum development
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Suppressed by
Statement
Reference
NOT suppressed by
Enhancer of
NOT Enhancer of
Other
Phenotype Manifest In
Enhanced by
Suppressed by
Statement
Reference
NOT suppressed by
Statement
Reference
Enhancer of
NOT Enhancer of
Other
Additional Comments
Genetic Interactions
Statement
Reference

Third instar larval eye-antennal imaginal disc clones co-expressing dlg1GD4689 and Ras85DV12.Scer\UAS under the control of Scer\GAL4Act5C.CoinFLP-FRT, in combination with Dicer-2 for efficient RNAi, form invasive tumors and induce autophagosomes in a cell non-autonomous manner in neighboring disc tissue (assessed by a Atg8a fluorescence reporter), as compared to controls; both the tumor formation and the cell non-autonomous autophagosome induction are suppressed by the additional clonal co-expression of either sdJF02514 or ykiHMS00041; the volume of these tumors is also significantly reduced by the co-expression of either slifUY681 or Pi3K92ED954A.Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4Act5C.CoinFLP-FRT; the cell non-autonomous increase in autophagosomes is also suppressed by the clonal co-expression of bskDN.Scer\UAS.cUa, but not of ImpL2dsRNA.Scer\UAS.cUa or Pi3K92ED954A.Scer\UAS.T:Hsap\MYC.

The co-expression of Ras85DV12.UAS and dlg1GD4689 under the control of Scer\GAL4ap-md544 induces wing disc neoplasia which, when transplanted, can form solid tumors in the host; there is amplification of the resident myoblast population, as well as accumulation of circulating hemocytes on the wing disc. Myoblast ablation (by expressing rprlexAop.cSa under the control of Ecol\lexAGMR15B03) does not suppress the tumor-like growth.

The co-expression of Ras85DV12.UAS and dlg1GD4689 under the control of Scer\GAL4hh.PU induces wing disc tumor-like growth, with increased mitotic index.; myoblast ablation (by expressing rprlexAop.cSa under the control of Ecol\lexAGMR15B03) does not suppress the tumor-like growth. Similar tumor induction occurs if expression is induced in wing disc transplants (expression induction is controlled by Gal80[ts] and temperature-shift); hemocyte ablation on the host (by expressing rprUAS.C under the control of Scer\GAL4He.PZ) together with myoblast ablation on the implant (by expressing rprUAS.C under the control of Ecol\lexAGMR15B03) does not suppress the tumor-like growth.

The tumor-like overgrowth of MARCM clones in larval antennal disc expressing dlg1GD4689 under the control of Scer\GAL4Dll-md23 is not significantly worsened by cnoR2 homozygosity but the cellular and tissue morphology and disorganization are exacerbated.

The decreased size of neuroblasts in the cnoR2 type II neuroblast lineage MARCM clones is not affected by expression of dlg1GD4689 (driven by Scer\GAL4Dll-md23) in the clones.

Eye discs co-expressing dlg1GD4689 and Ras85DV12.Scer\UAS in clones show tumour-like overgrowth and metastasis.

Transplanted tissue fragments of Ras85DV12.Scer\UAS donors also expressing dlg1GD4689 under the control of Scer\GAL4ey.PU cause non-autonomous wasting.

Expression of ImpL2GD6004 within the tumors of Scer\GAL4ey.PU>Ras85DV12.Scer\UAS,dlg1GD4689 origin significantly ameliorates the peripheral tissue wasting phenotypes. Hosts bearing dlg1GD4689, Ras85DV12.Scer\UAS, ImpL2GD6004 tumors show increased abdominal fat body mass. Muscle function assays further reveal improvements in both climbing ability and speed. There is a significant rescue of ovariole health, leading to restoration of egg production.

Co-expression of wakeGD12087 and dlg1GD4689 in all neuroblasts under the control of Scer\GAL4insc-Mz1407 causes massive overproliferation of neuroblasts, accompanied by increased mitotic activity.

Expression of Ras85DV12.Scer\UAS and dlg1GD4689 in MARCM third instar imaginal disc clones results in a neoplastic phenotype.

Co-expression of Pi3K92EGD11228 suppresses tumour growth in dlg1GD4689 MARCM third instar imaginal disc clones, although this suppression is weaker than that seen upon expression of Pi3K92EGD11228 in Ras85DV12.Scer\UAS-dlg1GD4689 MARCM third instar imaginal disc clones.

Knockdown of either Pi3K92E or Akt1 in Ras85DV12.Scer\UAS-dlg1GD4689 cells, through expression of either Pi3K92EGD11228 or Akt1GD1361, causes a complete suppression of neoplastic growth and even causes a near-complete absence of mutant eye cells. Only small structures, which contain few cells, remain.

MARCM Ras85DV12.Scer\UAS-dlg1GD4689 expressing clones are dramatically smaller in a Pi3K92E1C1 homozygous mutant than in a wild-type background, indicating that a loss of Pi3K92E signaling interferes with Ras85DV12.Scer\UAS-dlg1GD4689 tumour growth.

Depletion of InR, through expression of InRGD104, slightly reduces tumour size in Ras85DV12.Scer\UAS-dlg1GD4689 MARCM clones.

Depletion of S6k, through expression of S6kGD6646, slightly reduces tumour size in Ras85DV12.Scer\UAS-dlg1GD4689 MARCM clones.

Depletion of Rheb, through expression of RhebNIG.1081R, strongly reduces tumour size in Ras85DV12.Scer\UAS-dlg1GD4689 MARCM clones.

Depletion of Tor, through expression of TorNIG.5092R, strongly reduces tumour size in Ras85DV12.Scer\UAS-dlg1GD4689 MARCM clones.

Depletion of Pten, through expression of PtenKK109278, increases tumour size in Ras85DV12.Scer\UAS-dlg1GD4689 MARCM clones.

Overexpression of ykiScer\UAS.cHa in dlg1GD4689 MARCM clones generates larger tumorigenic overgrowths than in either single mutant clone.

Expression of Ras85DV12.Scer\UAS and dlg1GD4689 in the posterior compartment of wing discs, under the control of Scer\GAL4en.PU results in an enlarged posterior wing disc compartment. These wing discs exhibit high levels of cell proliferation.

Co-expression of Pi3K92EGD11228 together with Ras85DV12.Scer\UAS and dlg1GD4689, under the control of Scer\GAL4en.PU, strongly reduces the size of the Ras85DV12.Scer\UAS-dlg1GD4689 tumours in the posterior wing disc compartment. There is an almost complete absence of cellular proliferation in this compartment.

Wing disc compartments expressing Ras85DV12.Scer\UAS, dlg1GD4689, Pi3K92EGD11228, together with CycEScer\UAS.cRa and stghs.PE2 show a rescue in compartment size and high levels of His3-positive cells.

Xenogenetic Interactions
Statement
Reference

The moderate rough eye phenotype and reduced adult eye size characteristic for flies expressing Scer\GAL4GMR.PU under the control of Hsap\MAPTV337M.Scer\UAS is significantly worsened by co-expression of dlg1GD4689 (together with UAS-Dicer2 to enhance RNAi efficiency), exacerbating the rough appearance.

Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 1 )
Crossreferences
Bristle Screen Database (Knoblich Lab) - A database for RNAi phenotypes in bristle and notum development
Synonyms and Secondary IDs (4)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (24)