Programmed cell death (PCD), also called apoptosis, is a necessary part of life for multicellular creatures such as ourselves. Superfluous, sickly or harmful cells must do the right thing and kill themselves before they cause problems for the entire organism. PCD is essential not only for keeping us healthy as adults (think of avoiding cancer), but for our very development from embryos. For example, it’s PCD that removes the webbing in between our fingers at around eight weeks gestation.
It’s harder to see why single-celled prokaryotes would have PCD, but they do. In conditions of extreme stress (lack of nutrients, attack by viruses), greatly reducing the population may allow a few individuals to carry on. Since members of a population of bacteria are likely to be clonally related, this sacrifice actually increases the chances that the microbes’ gene pool will persist, which is after all the ultimate goal of all organisms.
One of the ways prokaryotes control when to off themselves is via ‘toxin-antitoxin’ (TA) systems. The bacteria produce both a toxin and the corresponding antitoxin. However, the antitoxin degrades more quickly than the toxin. Thus, if a microbe sustains damage to its DNA or protein assembly machinery such that it can’t make more antitoxin, the lingering toxin will kill it. Although this seems like a crazy idea, it does ensure that only properly functioning bacteria survive.
Ariel Erental, Idith Sharon and Hanna Engelberg-Kulka from the Hebrew University-Hadassah Medical School have identified a second method of PCD that more closely mimics the system used in eukaryotes. This system is triggered solely by DNA damage and may have originated as part of the DNA repair system.
Taken together, these two pathways of cell death weed out excess or damaged individuals from a cluster of bacteria.