Field of Science

Data from the quorum sensing paper supports diffusion sensing

With the colleague who brought the flawed quorum sensing paper to my attention, I'm writing a 'Commentary' letter to Nature pointing out the paper's glaring flaws. Crafting this letter has been scientifically instructive in two ways.

First, the colleague is a biomathematician who uses bacterial cultures as models of evolutionary and ecological processes. He wasn't familiar with my diffusion sensing hypothesis, but once he read the paper he realized that work he'd been doing about communities containing exploiters (the Snowdrift model) nicely applied to this system. So he's been educating me about his model.

Second, I realized that the flawed paper provides excellent data supporting some assumptions of the diffusion sensing hypothesis. Although the paper's interpretation and conclusions are flawed, the experiments themselves look to have been carefully done and to have produced solid data. In particular, they determined the final cell densities of pure cultures of bacteria growing in rich medium, where protease production is not beneficial.

The diffusion sensing hypothesis assumes (sensibly) that synthesis and secretion of such effector molecules as proteases, antibiotics and siderophores is expensive, but that production and secretion of the autoinducers that regulate the effectors is cheap.

In one of the paper's experiments, cultures of protease-producing cells grew to about 35% lower density than cultures of non-producers. This was very nicely controlled by including cells that did not produce the autoinducer signal that activates protease production. Without activator these cells grew as well as cells that did not produce protease because they couldn't recognize the autoinducer signal, but when activator was provided externally they grew as poorly as wildtype cells.

This tells us two things. First, production of the protease is indeed quite costly - a 35% difference in final cell density means that natural selection will strongly favour cells that don't secrete proteases when they're not needed (confirmed by the paper's competition experiments). Second and more important, secretion of the autoinducer is very cheap. The final cell densities of the cells that didn't produce autoinducer and of the cells that produced it but couldn't respond to it were identical (within the resolution of the figure), so the cost of production must be very low. The cost is unlikely to be zero - this could be tested by competition experiments between the two strains.


  1. I don't know how much the figure in that paper supports the idea that protease production is taxing on growth; after all, the autoinducing system controls the expression of "6-10% of its genome", including biofilm formation, changes in motility, and so on, so there is most likely "something else" involved as well in the growth and competition experiments. Altogether, this may be taxing on the Pseudomonas, but the multitude of downstream functions obfuscates the evolutionary origins of the autoinducing system, since undoubtedly many of these functions were added on later to an already existing regulatory system. So, at least with this paper, the question of the ultimate adaptive origin of autoinduction is left unaddressed.

  2. I am extremely frustrated by the QS literature and I am glad to hear you are picking this up and writing your letter. I believe an important point of your 2002 paper that is widely misunderstood or ignored is the fact that most people studying QS assume the signaling must benefit the group rather than individual even though (at least in the Vibrio literature) there is really no evidence for this being the case.


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