larval optic lobe & glial cell | somatic clone | cell non-autonomous, with Scer\GAL4αTub84B.PP
medulla cortex & glial cell | somatic clone | cell non-autonomous, with Scer\GAL4αTub84B.PP
The wing defects induced by the expression of Ras85DN17.UAS under the control of Scer\GAL4Bx-MS1096 (smaller wing and loss of L3-5 vein material are: fully suppressed by the co-expression of either rlD334N.UAS.cKa or rlR80S.D334N.UAS, even leading to extra vein material (more severe in the latter, with darker pigmentation); partially suppressed by the co-expression of rlR80S.UAS (complete suppression in L3, partial suppression in L4 or L5); not suppressed by the co-expression of rlWT.UAS.
Co-expression of Ras85DN17.Scer\UAS and PvrCA.Scer\UAS under the control of Scer\GAL4esg-NP5130 and Scer\GAL80ts.αTub84B significantly abrogates the PvrCA.Scer\UAS dysplastic phenotype, indicating that Ras85D is a downstream signaling component in the Pvr-dependent regulation of intestinal homeostasis.
Expression of Ras85DN17.Scer\UAS in motor neurons under the control of Scer\GAL4unspecified suppresses the increased synaptic growth and transmitter release observed at the neuromuscular junction in comt6 Ca-P60AKum170 larvae.
Co-expression of Bap170C1.Scer\UAS enhances the loss of wing vein L4 that is seen in flies expressing Ras85DN17.Scer\UAS under the control of Scer\GAL4bi.PU, such that there is a loss of the entire L4 vein distal to the posterior crossvein. The distal end of wing vein L3 is missing in these flies and a reduction in wing surface area and occasional notching of the wing margin is also seen.
Expression of Ras85DN17.Scer\UAS moderately suppresses the glial neoplasia seen in third instar larvae when btl::EgfrScer\UAS.T:λ\cI-DD and Pi3K92EScer\UAS.T:Hsap\MYC,T:Hsap\CAAX are co-expressed under the control of Scer\GAL4repo.PU.
Co-expressing BacA\p35Scer\UAS.cHa with Ras85DN17.Scer\UAS under the control of Scer\GAL4Act5C.PP completely suppresses the Ras85DN17.Scer\UAS cell death phenotype and increases the number of cells per clone. The doubling time defect is only partially rescued. 40 hours after induction, clones in imaginal discs co-expressing Ras85DN17.Scer\UAS and BacA\p35Scer\UAS.cHa under the control of Scer\GAL4Act5C.PP are 23% smaller than clones expressing BacA\p35Scer\UAS.cHa alone under the control of Scer\GAL4Act5C.PP. Clones expressing both dmScer\UAS.cZa and Ras85DN17.Scer\UAS under the control of Scer\GAL4Act5C.PP in clones in the imaginal discs have a similar cell size and cell cycle profiles as those of cells expressing dmScer\UAS.cZa alone under the control of Scer\GAL4Act5C.PP. The elongated doubling time of cells expressing Ras85DN17.Scer\UAS under the control of Scer\GAL4Act5C.PP is partially rescued by co-expression of dmScer\UAS.cZa.