The addition of E2f276Q1/E2f2p111-5 to homozygous E2fsu89 leads to lethality in the majority of mutants - 75% of the mutants die during the larvae stage, 24% during the pupal stage, with only 1% surviving to adulthood. Larval development is asynchronous: while most larvae are smaller, some healthy larvae can reach sizes similar to wild-type, and their development is only delayed about a day. The surviving adults do not show gross defects in their adult structures, though 88% display extremely short macrochaetae on the notum. These macrochaetae form the proper structure but fail to grow to its normal size. This seems to be a result of a defect in endoreplication in those cells. Mutants also exhibit defects in maintaining cell cycle arrest in the scutella. Third instar larval salivary glands are also smaller in these animals. The number of cells is wild-type, but the DNA content of those cells is about 40% of wild-type, probably due to fewer rounds of endocycles. The length of each endocycle is correspondingly longer due to an increased length of the gap phase. The addition of CycEAR95 to E2f276Q1/E2f2p111-5, E2fsu89, partially suppresses the salivary gland endoreplication defect. Salivary gland nuclei in these animals have about 70% of the DNA content of wild-type. The lethality is also partially suppressed - 52% of animals survive to the pupal stage (compared to 25%). Finally the macrochaetae phenotype is strongly suppressed. - 99% of flies show normal macrochaetae (as opposed to 12%).
The addition of E2f276Q1/Df(2L)G5.1 to E2f91/E2frM729 flies almost completely suppresses the E2f91/E2frM729 phenotypes - mutants develop normally without any significant delay in larval growth, reach pupal stage and finally die as mid- or late pupae. The pattern of DNA synthesis in eye discs is largely normal. The pattern of DNA synthesis in eye discs is largely normal.