Control of cannibalism in Bacillus subtilis.

摘要

The Gram-positive bacterium Bacillus subtilis initiates the process of endospore formation in response to conditions of limited nutrient availability. Endospore formation is a dramatic undertaking for a bacterium requiring the activation of approximately 500 genes over the course of six hours. A bacterium becomes irreversibly committed to completing the process of endospore formation relatively soon after its initiation, so it is not surprising that B. subtilis tightly controls the activation of Spo0A.;B. subtilis employs a cannibalistic behavior to forestall committing to the process of endospore formation. Sporulating cells secrete two toxins that kill non-sporulating cells within the population. Lysis of the non-sporulating cells releases nutrients into the extracellular milieu. The sporulating cells metabolize these nutrients and consequently are able to postpone making the commitment to endospore formation.;A simple signal transduction pathway activates immunity to one of these cannibalism toxins. The pathway consists of three components: the toxin, an immunity protein, and an autorepressor which is encoded in the same operon as the immunity protein. When the toxin binds to the surface of a sporulating cell, it is neutralized as it forms a complex with the immunity protein. The immunity protein also serves as the receptor for the toxin/ligand, and in the presence of the toxin, the immunity protein induces its own synthesis by sequestering and inactivating the autorepressor at the cell membrane.;Endospore formation is triggered by the activation of a set of kinases. These kinases phosphorylate the master regulator for sporulation, Spo0A, bringing about its activation as a transcription factor. One kinase, KinA, is primarily responsible for allowing endospore formation to occur efficiently; however, an accessory kinase, KinC, is required for the maximal expression of the genes that mediate cannibalism.;Spo0A indirectly activates the expression of the genes involved in cannibalism by inactivating the transcription of a global repressor. The immunity gene becomes activated at a lower level of Spo0A activity as compared to the toxin genes. We postulate that this is because the global repressor exhibits a lower affinity for the immunity gene's promoter as compared to the promoters for the toxin genes.