The comparatively weak tumor induction observed in clones expressing Ras85D^V12.Scer\UAS under the control of Scer\GAL4^{Scer\FRT.Act5C} induced in eye-antennal discs in third instar larvae is strongly enhanced when the clones are also homozygous mutant for fmt¹. With continuous tumor progression almost half of the larvae show invasion of the tumor tissue into the ventral nerve cord at 11 days after egg laying (AEL). Number of mitotic cells is also highly increased compared to either of the single mutant clones, but no increase in the level of apoptosis is observed. The strong tumorigenic activity of Scer\GAL4^{Scer\FRT.Act5C}>Ras85D^V12.Scer\UAS;fmt¹/fmt¹ MARCM clones in third instar larval eye-antennal discs is strongly impeded and their invasive capacity abolished by co-expression of either bsk^DN.Scer\UAS or Tak1^{K46R.Scer\UAS} in the clones.

Co-expression of Ras85D^V12.Scer\UAS and PpV^GD7532 in somatic clones in the eye-antennal disc under the control of Scer\GAL4^Act5C.PI results in mild tumorous overgrowth which is further enhanced by fmt¹ heterozygosity.

The small rough eye phenotype characteristic for adult flies expressing egr^Scer\UAS.cIa under the control of Scer\GAL4^GMR.PU is enhanced by combination with a single copy of fmt¹ or PpV^Δ1, when combined with one copy of both fmt¹ and PpV^Δ1 the eye is almost completely lost.