Editors' ChoiceMicrobiology

The Circuit Controlling Bacterial Cannibalism

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Science's STKE  21 Feb 2006:
Vol. 2006, Issue 323, pp. tw67
DOI: 10.1126/stke.3232006tw67

When conditions get really rough and food supplies become dangerously low, spore-forming bacteria take a drastic step and form dormant cells or spores that can survive environmental extremes, but the process is expensive in terms of time and energy and is not immediately reversible. Ellermeier et al. describe the ingenious signaling mechanisms that enable a fraction of the bacteria in a population to cannibalize other bacterial cells in the population and use them as a food source to delay commitment to sporulation. About half the starved cells activate a master regulator called SpoOA, which in turn increases transcription from a multigene operon known as sdpABC. One gene encodes a toxin (SdpC*). The excreted toxin kills cells, but to benefit from this, the toxin-producing cell needs to be toxin-resistant. Genetic analyses showed that the SdpC toxin served two functions. It killed target cells but also functioned as a ligand to activate a membrane receptor protein called Sdpl in protected cells. Sdpl also appeared to serve two functions, which were separable in mutation analysis. On the one hand, it provided cells with immunity to the toxin, and on the other, it sequestered an autorepressor protein at the membrane (thus relieving the repressor's action at the nucleus). Closing the regulatory loop, this repressor controlled an "immunity operon" that includes its own gene as well as that encoding the receptor, Sdpl. The authors propose that this feedback system allows surviving cells to produce just enough of the immunity protein Sdpl as they need. Cells unlucky enough not to have activated the SpoOA master regulator in response to a lack of nutrients do not get the benefit of this system because, without SpoOA, the repressor keeps the immunity operon inactive.

C. D. Ellermeier, E. C. Hobbs, J. E. Gonzalez-Pastor, R. Losick, A three-protein signaling pathway governing immunity to a bacterial cannibalism toxin. Cell 124, 549-559 (2006). [PubMed]

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