Fight not flight: parasites drive the bacterial evolution of resistance, not avoidance

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In the face of ubiquitous threats from parasites, hosts often evolve strategies to resist infection or to altogether avoid contact with parasites. At the microbial scale, bacteria frequently encounter viral parasites, bacteriophages. While bacteria are known to utilize a number of strategies to resist infection by phages, and can physically navigate their environment using complex motility behaviors, it is unknown whether bacteria evolve avoidance of phages. In order to answer this question, we combined experimental evolution and mathematical modeling. Experimental evolution of the bacterium Pseudomonas fluorescens in environments with differing spatial distributions of the phage Phi2 revealed that the host bacteria evolved resistance depending on parasite distribution and infectivity, but did not evolve dispersal to avoid parasite infection. Simulations using parameterized mathematical models of bacterial growth and swimming motility showed that this is a general finding: while increased dispersal is adaptive in the absence of parasites, in the presence of parasites that fitness benefit disappears and resistance becomes adaptive, regardless of the spatial distribution of parasites. Together, these experiments suggest that parasites should rarely, if ever, drive the evolution of bacterial avoidance via dispersal.

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  1. We do have some expectation that evolving motility is harder than evolving phage resistance. That said, we don't think this fully explains our results. First, we see that all of our evolved bacterial populations have increased dispersal (Fig 4), so clearly there is sufficient variation in dispersal for selection to act upon, it's just that phages don't seem to alter that selection in any way. And second, in our simulations (Fig 6) we see that phage presence doesn't just strengthen selection for resistance, but it actually weakens selection for dispersal. So even if there's variation in motility, phage presence eliminates the selection for increased motility.

    As far as sensing the phages and activating motility, that would have been a really cool result! It's plausible some sort of mechanism like that could evolve, given that bacteria can sense phages and can plastically activate motility based on extracellular signals, but who knows whether it actually exists or not.

  2. We definitely considered sequencing the evolved isolates, but decided that it wasn't worth it for this study.

    Phi2 (the phage used in these experiments) putatively binds LPS, so we'd expect resistance mutations to be involved in the LPS synthesis pathway. It would be really interesting to see if there are different mutations between the local and global treatments, although we don't have much of a prior expectation that they would be

  3. Also, this is assuming that evolution of dispersal would be through evolution of motility mechanisms, but could it also be through evolution of 'phage' sensing and then activation of motility? And would that also take more mutation and selection versus a resistance mechanism?

  4. that bacterial avoidance of parasites may only rarely, if ever, be selected for

    Depending on the motility mechanism (flagellum, versus gliding etc...) of the bacteria, I am wondering if this is easier/faster to evolve resistance (for instance mutation of the phage receptor) versus improving motility through modification of the motility apparatus? Would it take more mutations do evolve better motility? Have the authors any thoughts on this, or idea whether this could be a potential explanation?

  5. solated five evolved bacterial clones

    Have the authors considered doing whole genome sequencing of these 5 isolates to narrow down the mutations associated with these evolved lineages? Or based on the observed evolved phenotypes, can the authors thing of potential gene candidates to investigate mutations associated with the observed resistance. I am wondering if, even if you only see evolution of resistance and not of dispersal activity, this would be associated with similar mutations regardless of the experimental setup or whether we could expect a different mechanism of resistance between local and global phage distribution.

  6. .

    Very simple question: does the 5X on Figure 1 means each experiment has been performed in 5 replicates? Also, during the propagation, was each plate propagated to a single plate?