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Abstract
Bacillus subtilis is used as a model organism for studying cellular differentiation because, under conditions of nutritional starvation, it undertakes a dramatic process to form a resistant spore. Before this differentiation takes place, however the bacterium must first detect the change in its environment and signal the process to initiate.
Upon entry into stationary phase, a subset of a population of B. subtilis will activate the response regulator protein Spo0A. In addition to regulating numerous stationary phase responses, like competence, motility and antibiotic production, Spo0A also acts as the major regulator for sporulation, activating transcription of a majority of the early sporulation gene products, particularly the transcription of the primary mother cell and forespore-specific alternative sigma factors (σE and σ F, respectively). The formation of a spore is a time- and energy-consuming process that cannot be reversed after the formation of the asymmetric septum. If the cells that have activated Spo0A progress immediately into sporulation only to have the signal that activated them turn out to be transient, then they would be at a disadvantage to those cells that had remained in a vegetative state. Additionally, the conditions required for the spore to germinate are much more stringent than those required for active (albeit slowed) growth. Because of this, B. subtilis has evolved a mechanism to delay commitment to sporulation by killing its siblings. Upon their death these sibling cells lyse, where upon the cannibals are then able to feed on the nutrients released. The locus responsible for this cannibalism behavior, skf, has recently been reported to be activated under low-phosphate conditions by the PhoP response regulator. We investigated the mechanism by which Spo0A and PhoP activate the skf promoter under both sporulation and low-phosphate conditions. Through the use of base substitution to critical binding site residues, transcription behavior in strains harboring deletions of the regulators and mobility shift assays we propose mechanisms by which skf is activated under these nutritional starvation conditions. Additionally, we speculate on the possibility that the skf response is primarily a predation response and that the cannibalistic behavior is a fortuitous side effect of the manner by which it is activated.
