Figure 1.
A Schematic Representation of E. coli mazEF-Mediated Cell Death
For details, see the text.
Figure 2.
A “Point of No Return” in E. coli after the Induction of the (A) Plasmid Borne or (B) Chromosomally Borne E. coli mazF Gene
(A) E. coli cells growing in minimal medium were cotransformed with two plasmids, one carrying mazE and the other one carrying mazF, each regulated by different promoters: mazF can be induced by arabinose and repressed by glucose, and mazE can be induced by IPTG. At time zero, mazF expression was induced by the addition of arabinose. Samples of the induced culture were withdrawn at various time points and spread on plates containing glucose and IPTG (shown in blue on the graph) or glucose without IPTG (shown in yellow on the graph). Based on data in [54].
(B) E. coli cells growing in minimal medium were transformed with a single plasmid-carrying mazE that can be induced by IPTG. At the logarithmic phase, stress was induced by the addition of a transcription inhibitor. After the cells were incubated at 37 °C for a short period of time, the transcription inhibitor was removed. Samples of the induced culture were withdrawn at various time points and spread on plates containing IPTG (shown in blue on the graph) or without IPTG (shown in yellow on the graph). The percentage of survivors was calculated by comparing the number of colony forming units (CFUs) of the MazF-induced culture to the number of CFUs of the uninduced culture at time zero. Based on data in [55].
Table 1.
The Distribution of MazE and MazF among Various Bacteria
Figure 3.
A Model: How Programmed Cell Death Saves a Bacterial Population from Annihilation by Phage P1 Infection
(A) In wild-type cells, P1 infection triggers the action of mazEF which mediates the death of the infected cells. Because infected cells die before phage can propagate, few phages are released, the titer of the phages is low, and the population survives.
(B) In ΔmazEF cells, nothing interferes with the phage infections: the infected cells lyse, allowing many released particles to spread to the rest of the population. Thus infection by P1 of a ΔmazEF population leads to the death of more cells. Though infection by P1 of wild-type populations leads to the loss of some of the cells, more members of the population survive.
Figure 4.
A Model of Delaying Sporulation by Cell Death
Nutrient limitation activates Spo0A in a subpopulation (Spo0A-ON cells) of the culture of B. subtilis. Spo0A activates the sporulation process, but can delay sporulation by activating two operons, skfA-H and sdpABC. skf is involved in the production of an extracellular killing factor. SkfE and SkfF, which are produced in Spo0A-ON cells, antagonize the lethal action of the killing factor, probably by acting as an export pump that secretes the factor from the cells. sdpC encodes for another killing factor. Two mechanisms are responsible for the resistance of the Spo0A-ON cells to SdpC: i) the three-protein–signaling pathway (SdpC–SdpI–SdpR) (see text); and ii) repression of AbrB synthesis by Spo0A (see text). In Spo0A-OFF cells, the sdpRI operon is repressed by AbrB, leading to sensitivity to SdpC toxin. As a whole, Spo0A-OFF cells are killed and lysed, releasing nutrients to be consumed by the Spo0A-ON cells. Thereby, the process of sporulation of the Spo0A-ON cells can be postponed, a potential benefit should food become available [21,74].