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.
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.
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.
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.
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 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.