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General Information
Symbol
Dmel\RafUAS.F179
Species
D. melanogaster
Name
FlyBase ID
FBal0039757
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
UAS-Rafgof, UAS-rafF179, UAS rafGOF, UAS-DrafGOF, UAS-phl.gof, UAS-RafAct
Nature of the Allele
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
A constitutively active form of Raf is expressed under the control of UAS regulatory sequences.
UAS regulatory sequences drive expression of Raf protein in which amino acids 2-431 are deleted.
Allele components
Product class / Tool use(s)
Encoded product / tool
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 )
Disease
Evidence
References
Modifiers Based on Experimental Evidence ( 1 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
mesothoracic tergum & macrochaeta | ectopic, with Scer\GAL4sca-C253
Detailed Description
Statement
Reference
Expression of RafScer\UAS.F179 driven by Scer\GAL4dpp.PU leads to tissue overgrowth in eye-antennal imaginal or wing discs (also in wing discs when driven by Scer\GAL4Bx-MS1096).
The external surface of eyes expressing phlScer\UAS.F179 under the control of Scer\GAL4GMR.PU is disorganised with indistinct facets and a rough exterior retinal surface. Some ommatidia show thin or absent lenses. Rhabdomeres are misoriented and occasionally missing. The rhabdomeres are distinct from wild type appearing more rectangular, especially in R1, R3, R5 and R6. In third instar larvae, expression of phlScer\UAS.F179 leads to disrupted eye disc morphology, with irregular ommatidial spacing and folding of the disc. Neuronal cell fates appear unaffected. By the pupal stages, cell morphologies are profoundly aberrant, with extra and misshapen cone cells and ommatidia misaligned along the D/V axis. Immature cone cell contacts are maintained and secondary pigment cells are absent between some pairs of neighbouring ommatidia. The intracellular pH (pHi) in eye discs expressing phlScer\UAS.F179 under the control of Scer\GAL4GMR.PU is significantly higher than in controls. The pHi remains higher in pupal eyes.
Scer\GAL4btl.PS-mediated expression of phlScer\UAS.F179 causes extra tracheal branching.
Eye-antennal disc clones expressing RafScer\UAS.F179 under the control of Scer\GAL4tub.PU exhibit ectopic differentiation of photoreceptors in and interior to the morphogenetic furrow.
Scer\GAL4bbg-C96-driven phlScer\UAS.F179 expression results in wing notching and truncation of the veins.
Expression of phlScer\UAS.F179 in differentiating eye cells driven by Scer\GAL4GMR.PU causes rough eyes of reduced size.
Expression of phlScer\UAS.F179 in adult Malpighian tubule clones (using the MARCM system, under the control of Scer\GAL80αTub84B.PL and Scer\GAL4Scer\FRT.Act5C) results in renal and nephric stem cell over proliferation, and results in tumorous growth.
Expression of phlScer\UAS.F179 driven by Scer\GAL4esg-NP7397 in adult midgut progenitor cells results in their overproliferation compared with control third instar larval midguts.
Expression of phlScer\UAS.F179 in mushroom bodies under the control of Scer\GAL4c747 does not impair or enhance learning.
Expression of phlScer\UAS.F179 after a 30 minute heat-shock at 37[o]C, under the control of Scer\GAL4hs.PB, results in the formation of ectopic vein cells.
Cells expressing phlScer\UAS.F179 under the control of Scer\GAL4c522 are preferentially located at the front of the cluster during border cell posterior and dorsal migration in mosaic border cell clusters consisting of both wild-type and mutant cells.
Expression of phlScer\UAS.F179, under the control of Scer\GAL4hs.2sev, causes a roughened eye phenotype with extra rhabdomeres in some ommatidia.
Expression of phlScer\UAS.F179, under the control of Scer\GAL4da.G32, causes ectopic eye photoreceptor cell differentiation.
Expression of phlScer\UAS.F179 under the control of Scer\GAL4Ras64B.PW results in adult flies that are smaller than normal at 16</up>oC.
When phlScer\UAS.F179 is driven by Scer\GAL4dpp.blk1 no effect is seen on wing disc growth.
Expression of phlScer\UAS.F179, driven by Scer\GAL4sca-C253, leads to expression of ectopic bristles on the notum.
Clones of eye imaginal discs that express phlScer\UAS.F179 autonomously (under the control of Scer\GAL4Act5C.PI) develop into vigorously proliferating tissue during larval stages and ultimately overgrow much of the adult eye. The overgrowth is not invasive and the animals survive until pharate adult stages, with rare adult escapers.
Expression of phlScer\UAS.F179 under the control of Scer\GAL4Cg.PA results in a massive increase in hemocyte number in larvae compared to wild type.
Expression of phlScer\UAS.F179, under the control of Scer\GAL4C380 results in a dramatic increase in bouton number, comparable to that found in Ras85DV12.Scer\UAS or Ras85DV12.S35.Scer\UAS mutants.
Expression of phlScer\UAS.F179 under the control of Scer\GAL4Act5C.PP in wing disc cells results in an increase in cell size and an increase in clone area compared to controls. The proportion of cells in G1 is decreased compared to controls. Clones expressing phlScer\UAS.F179 under the control of Scer\GAL4Act5C.PP are significantly more round than control clones.
Expression of phlScer\UAS.F179 under the control of Scer\GAL4slbo.2.6 has no effect on border cell migration.
The ventralised phenotype of eggs derived from females expressing kek1Scer\UAS.cGa under the control of Scer\GAL4T155 is overridden if the females are also coexpressing phlScer\UAS.F179; the resulting eggs are dorsalised.
Scer\GAL4c532-mediated expression causes 90% of mature eggs to have no dorsal appendages.
Scer\GAL4sli.PS-mediated expression causes ectopic midline glial cells.
Scer\GAL4 activation of phl in the follicle cells is sufficient to dorsalise the egg. Of the fertilised eggs only 25% give rise to dorsalised embryos, in the severe cases embryos are twisted and lack nearly all ventral structures.
External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
NOT Enhanced by
Suppressed by
Statement
Reference
NOT suppressed by
Enhancer of
NOT Enhancer of
Suppressor of
NOT Suppressor of
Other
Phenotype Manifest In
Enhanced by
NOT Enhanced by
Suppressed by
Statement
Reference
NOT suppressed by
Statement
Reference
Enhancer of
Suppressor of
Other
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference
Co-expression of Dis3KK101473 significantly enhances tissue overgrowth in eye-antennal imaginal or wing discs with expression of RafScer\UAS.F179 driven by Scer\GAL4dpp.PU (or in wing discs driven by Scer\GAL4Bx-MS1096).
Expression of phlScer\UAS.F179 under the control of Scer\GAL4GMR.PU in a Nhe2null mutant background results in synthetic cell lethality. Externally, the adult eye phenotype is identical to expression of phlScer\UAS.F179 alone, except that eye colour is lighter, but internally there is loss of tissue architecture and cell structure with coagulative necrosis, including loss of rhabdomere morphology, absence of distinct cell membranes and diffusion of pigment granules. Nhe2null suppresses the tissue morphology defects and hyperproliferation seen in third instar larval eye disc when phlScer\UAS.F179 is expressed under the control of Scer\GAL4GMR.PU. Neuronal cell fates appear unaffected. Nhe2null enhances the morphological defects seen in the retina of pupal expressing phlScer\UAS.F179 under the control of Scer\GAL4GMR.PU. All cell types appear smaller and more cells have abnormal morphologies. More ommatidia have extra cone cells. Cell death is seen that is not detected in either mutant alone. In contrast to either mutant alone, the intracellular pH (pHi) in eye discs expressing phlScer\UAS.F179 under the control of Scer\GAL4GMR.PU in a Nhe2null mutant background is similar to wild type. However, the pHi is reduced compared to wild type by the pupal stages.
Expression of FakScer\UAS.T:Ivir\HA1 does not suppress the eye phenotypes seen when phlScer\UAS.F179 is expressed under the control of Scer\GAL4sev.PU.
Co-expression of Rho1GD4726, zipGD1566 or RokGD1522 fails to suppress the ectopic differentiation of seen in eye-antennal disc clones expressing RafScer\UAS.F179 under the control of Scer\GAL4tub.PU. Co-expression of RafScer\UAS.F179 enhances the decreased photoreceptor differentiation seen in eye-antennal disc clones expressing RhoGEF2RE.Scer\UAS under the control of Scer\GAL4tub.PU. These clones show overgrowth, similar to those expressing only RhoGEF2RE.Scer\UAS, but also show large undifferentiated clonal masses in the basal regions of the posterior region of the eye disc. Larvae containing clones expressing both RhoGEF2RE.Scer\UAS and RafScer\UAS.F179 under the control of Scer\GAL4tub.PU exhibit an extended larval period, as compared with controls. Co-expression of LIMK1GD9586 fails to suppress the reduction of differentiation seen in eye-antennal disc clones expressing both RhoGEF2RE.Scer\UAS and RafScer\UAS.F179 under the control of Scer\GAL4tub.PU, and also fails to suppress the developmental delay shown by larvae containing these clones. Co-expression of Rho1GD4726, zipGD1566 or RokGD1522 suppresses the formation of undifferentiated clonal masses and partially suppresses the reduction of differentiation seen in eye-antennal disc clones expressing both RhoGEF2RE.Scer\UAS and RafScer\UAS.F179 under the control of Scer\GAL4tub.PU, and also suppresses the developmental delay shown by larvae containing these clones.
Expression of phlScer\UAS.F179 induces cell polarity changes in Apc2g10 ApcQ8 mutant intestinal stem cell clones.
Flies that co-express phlScer\UAS.F179 and PlzfScer\UAS.cMa under the control of Scer\GAL4Bx-MS1096 die at the pupal stage due to wing malformation.
Co-expression of gemininScer\UAS.cQa with phlScer\UAS.F179 via Scer\GAL4bbg-C96 does not significantly affect the notched wing phenotype resulting from the expression of phlScer\UAS.F179 alone. Co-expression of brmK804R.Scer\UAS.T:Ivir\HA1 with phlScer\UAS.F179 via Scer\GAL4bbg-C96 does not significantly affect the notched wing phenotype resulting from the expression of phlScer\UAS.F179 alone. Co-expression of both brmK804R.Scer\UAS.T:Ivir\HA1 and gemininScer\UAS.cQa with phlScer\UAS.F179 via Scer\GAL4bbg-C96 results in a significant suppression of the notched wing phenotype resulting from the expression of phlScer\UAS.F179 alone. brm2/+ significantly suppresses the notched wing phenotype resulting from the expression of phlScer\UAS.F179 via Scer\GAL4bbg-C96. geminink03202b/+ causes a significant worsening of the notched wing phenotype resulting from the expression of phlScer\UAS.F179 via Scer\GAL4bbg-C96. geminink14019/+ causes a significant worsening of the notched wing phenotype resulting from the expression of phlScer\UAS.F179 via Scer\GAL4bbg-C96.
The supernumerary spectrosome-containing cell phenotype of stet1A3 mutants is partially suppressed by phlScer\UAS.F179 expression driven by Scer\GAL4C587.
Co-expression of Rabex-5VDRC.cUa fails to enhance the eye phenotypes resulting from the overexpression of phlScer\UAS.F179 driven by Scer\GAL4GMR.PU. Co-expression of Rabex-5Scer\UAS.T:Hsap\MYC driven by Scer\GAL4GMR.PU does not suppress the appearance of black tissue in phlScer\UAS.F179-expressing eyes.
Expression of phlScer\UAS.F179 alone, or combined with the Scer\GAL4c747 driver but kept silent by Scer\GAL80ts.αTub84B does not suppress the learning deficit of drkΔP24/+ animals. Conditional expression of phlScer\UAS.F179 in adult mushroom bodies reverse the learning deficit of drkΔP24 heterozygotes. Expression of phlScer\UAS.F179 under the control of Scer\GAL4c747 does not rescue 90 minute memory in drkΔP24/+ animals. Expression of phlScer\UAS.F179 under the control of Scer\GAL4c747 results in full reversal of the learning deficit of drke0A heterozygotes.
Coexpression of phlScer\UAS.F179 with putDeltaI.Scer\UAS after a 20 minute heat-shock at 37[o]C at 18h APF, under the control of Scer\GAL4hs.PB, not only fails to induce ectopic vein cells, but also inhibits endogenous vein formation.
The roughened eye and increased rhabdomere phenotype seen when phlScer\UAS.F179 is expressed under the control of Scer\GAL4hs.2sev is enhanced in a S6kIID1/+ or S6kIID1/Y background. These eye phenotypes are suppressed when either S6kIIScer\UAS.T:Hsap\MYC or S6kIIK231R.Scer\UAS.T:Hsap\MYC is coexpressed with phlScer\UAS.F179 (all under the control of Scer\GAL4hs.2sev).
When phlScer\UAS.F179 is expressed under the control of Scer\GAL4da.G32 in ave108V mutant clones, ectopic photoreceptor cells are induced and the ave108V phenotype is suppressed.
When phlScer\UAS.F179 is driven by Scer\GAL4dpp.blk1 in a ftG-rv background a significant enhancement is seen in the ftG-rv overgrowth phenotype, throughout the whole imaginal disc. When phlScer\UAS.F179 is driven by Scer\GAL4ey.PH in ftG-rv mutant eyes, significantly enlarged eyes are seen.
Expression of hepAct.Scer\UAS in eye imaginal disc clones that express RafScer\UAS.F179 (both under the control of Scer\GAL4Act5C.PI) suppresses the aggressive tissue expansion, resulting in clones of this genotype remaining much smaller than RafScer\UAS.F179 (under the control of Scer\GAL4Act5C.PI) clones. hepAct.Scer\UAS expression can elevate the occurence of apoptosis among RafScer\UAS.F179 expressing cells (from 6.0% to 17.3%). However, a significant fraction of hepAct.Scer\UAS RafScer\UAS.F179 (both under the control of Scer\GAL4Act5C.PI) clones survive (6.4%). Clones of eye imaginal discs that express RafScer\UAS.F179 autonomously (under the control of Scer\GAL4Act5C.PI) in scrib1 clones grow into massive and invasive tumours during larval stages, resulting in 80% of animals not pupating and dying as giant larvae. Expression of hepAct.Scer\UAS in eye imaginal disc clones that express RafScer\UAS.F179 (under the control of Scer\GAL4Act5C.PI) results in adult eyes with massive overgrowth. The heads are significantly bigger and the retina of these mutants are dramatically larger than that of a wild-type eye. In many cases, the retina is folded and bunched to accommodate the surfeit of tissue. These severely hyperplastic eye structures are well patterned and show a distinctive ommatidial organisation. The tumourous overgrowth is induced non-autonomously in the wild-type cells surrounding the clones. The same phenotype tumorogenic phnotype occurs in flies that express both RafScer\UAS.F179 and hepAct.Scer\UAS, under the control of Scer\GAL4Act5C.PI, in a scrib1 background.
When phlScer\UAS.F179 and pntP2.Scer\UAS are coexpressed in the embryo under the control of Scer\GAL4en-e16E, the number of scolopidia in the lch5 organs is reduced from the normal number of 5 to 3 or 4 in 71% of hemisegments. When phlScer\UAS.F179 and pntP2.Scer\UAS are coexpressed under the control of Scer\GAL4GMR.PY in cells posterior to the morphogenetic furrow, most ommatidial clusters in the early stages of ommatidial assembly contain fewer than the normal number of neurons, with the specification of R3, R4, R1 and R6 being severely disrupted.
Lethality of phlScer\UAS.F179, Scer\GAL471B is rescued by styScer\UAS.cHa. Wings of phlScer\UAS.F179, styScer\UAS.cHa, Scer\GAL471B mutants are largely devoid of wing vein.
Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Fails to rescue
Comments
Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (7)
Reported As
Symbol Synonym
RafScer\UAS.F179
RafUAS.F179
phlScer\UAS.F179
phlUAS.F179
Name Synonyms
Secondary FlyBase IDs
    References (52)