Cell death, also known as apoptosis, is a significant part of normal animal development. However, the question arises whether bacteria, similar to higher organisms, have a built-in mechanism that determines when the cells die.

Researchers at the Hadassah Medical School of the Hebrew University in Jerusalem, Israel have for the first time described a unique cell death pathway in bacteria, which is comparable to apoptosis in higher organisms. The study published in the March 6 issue of the online, open-access journal PLoS Biology, shows that this newly described apoptotic-like death (ALD) pathway was prevented by another non-apoptotic programmed cell death (PCD) pathway that was mediated through the mazEF toxin-antitoxin system.

To their surprise, leading researcher Hanna Engelberg-Kulka, and her team discovered two very different death pathways in E. coli. Given that the bacterial cell death system they just discovered shared multiple characteristics with apoptosis in multicellular eukaryotes, they decided to call it Apoptotic-Like Death (ALD).

By marking the cell with a fluorescent dye, they observed that the cellular DNA became fragmented and the cell membrane depolarized, particularly in both eukaryotic apoptosis and in ALD. Furthermore, they discovered that a severely damaged cellular DNA causes the PCD pathway, which is mediated by the mazEF system of E. coli to block the newly described ALD pathway.

Further studies are needed to shed more light on the similarities between eukaryotic and bacterial apoptosis, as well as on the evolutionary origin of apoptotic death. It seems that ALD is a non-altruistic back-up death pathway for the traditional mazEF altruistic death pathway insofar, and if one of the components of the mazEF pathway should be inactivated, bacterial death would occur through ALD.

In answer to the question why it matters how a bacterium dies, the team states that the answer may affect the evolution of altruism. They discovered that the mazEF system relies on cell-density and that it controls during a crisis that sufficient bacteria die off to ensure sufficient bacterial raw materials are available in the environment for those that survive. Unlike the mazEF, the ALD pathway has no density dependence and could therefore function as a backup system in case the mazEF system fails.

The researchers state that future experiments will shed more light on the underlying molecular mechanisms for ALD, and whether this system really does affect a “good-for-the-community” population response.

Written by Petra Rattue