Since the mechanism of apoptosis has been conserved in evolution from worms to insects to man, knowledge gained from studying cell death in Drosophila is likely to apply to mammalian systems as well. In order to test this directly, we are studying the activity of Drosophila cell death genes and their mouse or human homologs in cultured mammalian cells. In Drosophila , the size of the optic ganglia, the visual centers of the brain, is always perfectly matched to the variable size of the eye. We have previously shown that this matching in the number of cells is accomplished by adjusting both the rate of cell death and cell proliferation through competitive interactions between retina and optic ganglia. This situation is reminiscent of trophic interactions that have been widely described in vertebrates.
Neurons also die in response to various insults and external stress.
We have studied a neurodegenerative disease model in Drosophila , the late-onset retinal degeneration that is observed in certain phototransduction. We have found that retinal degeneration due to mutations in either rhodopsin or a phospholipase C gene occurs by apoptosis and can be blocked by cystein protease inhibitors. Significantly, this suppression of apoptosis restors visual function to otherwise blind flies. These findings demonstrate that stressed or damaged cells that are rescued from death can serve a useful purpose for the organism. During Drosophila development, large numbers of cells undergo natural cell death.