The dendritic field coverage defects and loss of terminal branches observed in class IV dendritic arborizing neurons of third instar larvae expressing nosdsRNA.Scer\UAS.WIZ under the control of Scer\GAL4477 is suppressed by co-expression of Diap1Scer\UAS.cHa.
The dendritic field coverage and branching defects observed in class IV dendritic arborizing neurons of third instar larvae expressing pumHMS01685 under the control of Scer\GAL4477 is suppressed by co-expression of Diap1Scer\UAS.cHa.
Expression of Diap1Scer\UAS.cHa under the control of Scer\GAL4bun-GSG5961 and Scer\GAL4GSG5966 (along with RU486 to induce expression via the GeneSwitch system) in the gut fully restores growth of wild type clones in the presence of ApcQ8/ApcQ8, Apc2g10/Apc2g10 mutant clones in the posterior midgut, and suppresses the growth of ApcQ8/ApcQ8, Apc2g10/Apc2g10 mutant clones; however, ApcQ8/ApcQ8, Apc2g10/Apc2g10 mutant clones expressing Diap1Scer\UAS.cHa under the control of Scer\GAL4tub.PU do not have suppressed growth.
Inhibition of apoptosis using (Diap1Scer\UAS.cHa under the control of Scer\GAL4αTub84B.PBb) suppresses the contact-dependent delamination seen in wild type 'loser' cells when cell competition is induced in the pupal notum through generation of wild type clones in super-competitive MycαTub84B.PBb-expressing tissue. Inhibiting apoptosis does not suppress the increase in clone splitting (used as a readout for winner-loser cell mixing) or reduction in clone compactness seen in wild type 'loser' clones in the wing disc.
The increased level of cell death (detected by Casp3 antibody staining) observed in wing discs of third instar larvae expressing REGKK102083 RNAi under the control of Scer\GAL4ap.PU is suppressed by co-expression of Diap1Scer\UAS.cHa.
The reduced size of the third larval instar imaginal wing disc characteristic for pcm14 homozygotes is strongly rescued by expression of Diap1Scer\UAS.cHa under the control of Scer\GAL469B (using tub-Gal80[ts] to limit the time of expression) in the mutant background. The resulting disc size is intermediate between that of pcm14 alone and that of Diap1Scer\UAS.cHa-expressing discs (which are bigger than wild-type) and smaller than wild-type.
Expression of thScer\UAS.cHa enhances the eye phenotype seen when Sin3AKK100700 is expressed under the control of Scer\GAL4GMR.PF; approximately a third of all adults examined show enhanced overgrowth and secondary tumors that grow stably at distant sites.
Expression of Diap1Scer\UAS.cHa suppresses the reduction in CCAP/bursicon neuron number seen in newly eclosed flies expressing TBPHScer\UAS.T:Zzzz\FLAG under the control of Scer\GAL4CCAP.PP. The wing inflation defects are also rescued.
Co-expression of thScer\UAS.cHa completely suppresses the lethality caused by expression of scnyGS13668 under the control of Scer\GAL4GMR.PF at 25[o]C, and partially suppresses the mutant eye phenotype.
Co-expression of thScer\UAS.cHa with both lkb1Scer\UAS.cLa and SlnEP2245 considerably suppresses the apoptotic cell death induced by lkb1Scer\UAS.cLa and SlnEP2245 co-expression in the eye (all under the control of Scer\GAL4GMR.PF).
The border follicle cell migration defects that are seen in flies co-expressing both PvrDN.Scer\UAS and hepAct.Scer\UAS under the control of Scer\GAL4slbo.2.6 are partially suppressed by the co-expression of thScer\UAS.cHa.
Vps25N55/thScer\UAS.cHa mosaics exhibit non-autonomous cell proliferation. Eye-antennal discs of Vps25N55/thScer\UAS.cHa mosaics are extremely overgrown and can be 5-times as large as wild-type discs. Cell death is completely blocked in Vps25N55/thScer\UAS.cHa mosaics. Vps25N55/thScer\UAS.cHa clones occupy a large fraction of the eye discs, suggesting that these clones have no intrinsic growth disadvantage over wild-type tissue if cell death is blocked. Thus, inhibiting cell death in Vps25N55 clones can give rise to an even stronger overgrowth phenotype.
lkb1Scer\UAS.cLa-induced apoptosis is completely suppressed by expression of thScer\UAS.cHa, both under the control of Scer\GAL4GMR.PF. Interestingly, even when lkb1-indueced apoptosis is completely blocked by th, the BrdU and His3 staining patterns do not deviate from the wild-type patterns.
Expression of thScer\UAS.cHa, under the control of Scer\GAL4tub, in ykiΔ.w mutant clones generated in the wing disc, rescues the survival of these clones but results in clones that are smaller than those generated in wild-type controls.
Clones in the wing disc that express hpoScer\UAS.cUa, under the control of Scer\GAL4tub, (rescued for apoptosis by expression of thScer\UAS.cHa) cause nuclei to move basally, inducing cells to change shape and causing a basally-directed folding of the epithelium.
The eye degeneration and the associated rough eye appearance, ommatidial fusion and pigmentation loss characteristic for adult flies expressing Hsap\FUSScer\UAS.cIa under the control of Scer\GAL4GMR.PS cannot be rescued by co-expression of Diap1Scer\UAS.cHa.