In Vps25N55/Vps25K2 mosaic eyes, in a WGMR.PG background, the rescued tissue is genetically wild-type or heterozygous, suggesting that Vps25N55 and Vps25K2 mutant tissue does not contribute to the suppression of WGMR.PG.
Vps25N55/NDN.Scer\UAS mutants (using the MARCM technique) exhibit reduced or absent Stat92E activity. Cell proliferation is not significantly increased in Vps25N55/NDN.Scer\UAS mutants, with eye imaginal discs appearing normal in shape and size. These Vps25N55/NDN.Scer\UAS double mutant clones exhibit the same level of apoptosis as Vps25N55 single mutant clones.
Vps25N55/thScer\UAS.cHa mosaics exhibit non-autonomous cell proliferation, as do Vps25N55/ArkH16 mutants. 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/ArkH16 cells undergo apoptosis. Vps25N55/ArkH16 clones cannot be recovered in the adult eye. Vps25N55/thScer\UAS.cHa and Vps25N55/ArkH16 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. The adult eye of Vps25N55/ArkH16 mosaics is severely overgrown and folded. Thus, inhibiting cell death in Vps25N55 clones can give rise to an even stronger overgrowth phenotype.