Genetics of Apoptosis

can both induce and inhibit apoptosis in host cells, indicating that parts of the
parasites’ death machinery interacts with the death machinery of their host organisms
(reviewed in (Barcinski and DosReis, 1999; Heussler et al., 2001). It is hard to decide
whether this is evidence for conservation of ancient pathways, or whether those
pathways were acquired later as a result of the development of parasite—host
adaptation.

4.

Conclusions

In conclusion, we want to emphasize three points. First, it is now clear that forms of
programmed cell death involving degradation of nuclear DNA and an organized
elimination of dead cells were present very early in evolution before the development
of multicellular organisms. Although our knowledge of these cell-death events is not
complete, it appears that several apoptotic strategies were developed, some of which
still operate in higher animals. Caspase-dependent apoptosis, however, seems to have
evolved coincident with the development of the Eumetazoa, of which Cnidaria is the
basic phylum.
Second, mitochondria appear to be causally involved in all forms of cell death, not
only in the caspase-dependent pathway but also in caspase-independent pathways,
one of which involves AIF. In the absence of caspases in higher animals, or in simpler
life forms where caspases are not present, cell death can be induced by mitochondrial
release of AIF, as, for example, in Dictyostelium.
Third, programmed cell death is a powerful instrument of ‘social control’ in cell
populations, whether they are part of a colony or an organism. Thus, it remains a
great challenge to understand the evolution of these mechanisms from their very first
appearance to their remarkable refinement in higher animals, including man.

Acknowledgments

We thank our colleagues for permission to cite unpublished results. Dr. Stephanie
Seipp provided the illustrations in Figure 2. Work from our laboratory has been
supported by the DFG.

160 GENETICS OF APOPTOSIS