page 711, Váchová and Palková report evidence that ammonia signaling triggers death in specific areas within aging colonies. Colonies that lack the ability for such signaling have widespread cell death and die off sooner.
Recent years have seen an increase in the study of yeast colonies to see how yeast cells may or may not cooperate in nature. For example, ammonia signaling is now known to trigger metabolic changes in yeast as the colony ages.Now, Váchová and Palková find that cell growth and death occur in a predictable but uneven manner in a colony. By picking cells from the center and periphery of colonies at set time points, they find that cells proliferate and die in both the center and at the periphery in young colonies. But in older colonies, death is concentrated in the middle and proliferation at the outer edges. Sok2p mutants that lack ammonia signaling show death throughout the colony at all ages and the colony lifetime is reduced.
For those who argue that yeast undergo apoptosis, the observation that the community suffers without regulated death is key—at least if apoptosis is thought of as a mechanism that protects the community at the expense of the individual. However, that point may be balanced out by the team's observation that deletion of either of the two putative homologues of mammalian apoptosis proteins, Mca1p and Aif1p, does not disrupt the position-specific death in colonies. That leaves the score sheet on apoptosis in yeast tied, but one point up in the regulated cell death column.