AS if it’s not hard enough at the bottom of the food chain, being cannibalised by your own bottom-dwelling compatriots must add insult to injury. The soil dwelling Gram-positive bacterium Bacillus subtilis is fully equipped to take appropriate action when faced with food shortages; a sub-population of cells initiate a process of dormancy by turning themselves into hardy, robust spores. In this form the bacteria are capable of enduring temporary, or prolonged, harsh environmental conditions.
However, this is not a process entered into without some careful deliberation. Sporulation, the act of forming a spore, is an energy intensive process that results in the formation of the essentially inactive spore, and the death of the ‘mother’ cell producing it. It comes as no surprise, therefore, to discover that B. subtilis has evolved a means of delaying sporulation as long as possible.
In an alternative strategy, a sub-population have a genetic pre-disposition to become cannibals.
With the onset of nutrient poor conditions, cannibal cells secrete two toxins that kill some of their ‘sensitive’ siblings, whilst the toxin-producing cells themselves are protected by simultaneous production of ‘immunity machinery’. The nutrients released by the killed cells then feed the community and delay the onset of sporulation.
An additional general strategy for eking out an existence in a potentially harsh environment is to encapsulate the population of cells in a viscous ‘slime’, biofilm, that acts as a barrier to the external environment (which may include antibiotic molecules or immune cells). The biofilm is formed by a sub-population of cells that produce the extracellular matrix, so-called matrix producers.
The three pathways, sporulation, cannibalism and matrix production, are known to be controlled by a master regulator protein, spoOA; however the degree to which each pathway is controlled differs depending on the state of spoOA itself. The key has been to determine the environmental cues that differentially activate spoOA and how this in turn triggers one or more of the three pathways.
Daniel López, a postdoc working in the Kolter lab at the Harvard Medical School, has previously reported1 a ‘quorum-sensing’ peptide molecule called surfactin, produced by B. subtilis, which stimulates a cascade that results in the activation of spoOA and the triggering of biofilm matrix formation. Quorum sensing molecules are a means by which a cell population can monitor the density of cells in a given area, with high cell densities – and thus the potential for food competition – resulting in a high concentration of quorum sensing molecules. Such signals therefore trigger the population to take action.
López et al. now report2 that surfactin stimulates both cannibalism and matrix formation in the same sub-population of cells. Thus an alternative role of cannibalism may be to promote growth of the matrix producer cells, and thus the amount of encapsulating biofilm, at the cost of toxin-sensitive sibling cells. This approach therefore provides a temporary reprieve against sporulation.
As if that wasn’t enough excitement from one bug, in an upcoming paper in PNAS3 a member of the Weitz lab at Harvard University, Thomas Angelini, reports on how the B. subtilis can spread by ‘surfing on a wave of surfactant’. This form of ‘cooperative spreading’ is enabled by surfactin-producing cells and thus may allude to a strategy wherein cells stave off sporulation, survive on the sacrifices of cannibalised sibling cells and seek a means of spreading to a more favourable environment.
Interestingly, within the spreading wave of cells, the facilitating surfactin-producers only reside at the ‘centre’ of the spreading wave. These central cells therefore don’t benefit from food resources that wave initiation provides for those cells on the outer wave of spreading, and thus raises another complicated question of cell co-operativity and pseudo-altruism that is worthy of a ResearchBlog in its own right.
Indeed, a question that arises from the above papers is how the balance between cannibal cells and sensitive cells is maintained in the face of such selection favouring cannibal-matrix producing cells? How does a population ensure that, upon initiation of a new colony, there are sufficient ‘sensitive’ cells to enable such an alternative to sporulation? Do all cells have equal potential to become cannibals or remain sensitive? Or, as in the case of some slime moulds, do homogeneous populations of ‘cheaters’ realise that if no cell is willing to sacrifice itself, they’re all doomed, thus revert to co-operativity?
1. Lopez, D., Fischbach, M., Chu, F., Losick, R., & Kolter, R. (2008). Structurally diverse natural products that cause potassium leakage trigger multicellularity in Bacillus subtilis Proceedings of the National Academy of Sciences, 106 (1), 280-285 DOI: 10.1073/pnas.0810940106
2. López, D., Vlamakis, H., Losick, R., & Kolter, R. (2009). Cannibalism enhances biofilm development in Bacillus subtilis Molecular Microbiology, 74 (3), 609-618 DOI: 10.1111/j.1365-2958.2009.06882.x
3. Angelini, T., Roper, M., Kolter, R., Weitz, D., & Brenner, M. (2009). Bacillus subtilis spreads by surfing on waves of surfactant Proceedings of the National Academy of Sciences DOI: 10.1073/pnas.0905890106
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4 thoughts on “Bug eat bug…”
Your final Q’s sound like just the job for some cellular automata modelling.
Well the 3rd reference seems to be heading off in that direction. They’ve been doing some interesting stuff.
Thanks for the RT btw 😉
Wow…I was aware of the behaviors, but I didn’t know they shared control mechanisms. I would love to work with b. subtilis sometime, they sound fascinating.
Thanks for the heads up about Seed! That was amazing 🙂