A new study adds fuel to the controversy over whether yeast cells undergo programmed cell death by suggesting that it occurs for the good of the species.

Death spares no one, not even yeast cells. But the how and why of death in Saccharomyces cerevisiae is dividing the community. In a recent paper, Paola Fabrizio and colleagues propose that the death of older yeast cells occurs to allow younger cells to thrive — in essence, therefore, they suggest that apoptosis occurs in yeast as an adaptive process that benefits other members of the group. This conclusion is controversial for two reasons — first, because it presupposes that death is actually programmed in yeast and that it occurs by apoptosis, and second, because it invokes the maligned theory of 'group selection', which runs counter to the well-established idea that selection occurs at the level of the individual.

Fabrizio and colleagues first addressed how cell death occurs. The ageing yeast cells they studied showed many features of mammalian apoptosis, including chromatin condensation and acidification of the cytosol. Also consistent with programmed ageing in yeast was the cellular pathway used to bring about death: the authors found that ageing and dying yeast cells downregulate an inhibitor of superoxide ( SOD2 , a superoxide dismutase) and become sensitive to superoxide, both of which mediate cell death in higher eukaryotes. Indeed, mutant yeast colonies in which SOD genes are upregulated live longer.

To see whether this programmed death had an adaptive purpose, the authors assayed the ability of various yeast strains of varying longevity to repopulate a yeast colony after a substantial proportion of the colony had died. This phenomenon, called adaptive regrowth, occurs normally in wild type strains — however, the longer-lived strains, which overexpress SOD enzymes, could not repopulate the colony in the long term, and eventually died out. So, although longevity might confer an immediate advantage, it is detrimental to the species as a whole. Short-lived strains that lack the superoxide inhibitors were even better than the wild type at adaptive regrowth; the authors show that the ability of superoxide to promote adaptive regrowth depends on its ability to release nutrients from dying cells into the growth media, which in turn would allow younger cells to thrive and reproduce. In addition, because superoxide induces DNA mutations, its presence favours the selection and growth of mutants that are better adapted to the environment.

The results were not peculiar to laboratory strains, as the same phenomena occurred in three strains newly collected from the wild. Computational simulations tell a similar story — that a population that undergoes premature death and has a high mutation frequency is more likely to adapt to a changing environment.

So in yeast, at least, apoptosis is an altruistic act, as not dying damages the chances of survival of the whole group. If the theory stands up to scrutiny then what consequences does it have for humans? Should we thwart any attempt to extend our lives for the sake of our species? Whatever the eventual answer, this is a debate that isn't being laid to rest.