Evolution experiments with microorganisms: the dynamics and genetic bases of adaptation

Elena and Lenski (2003). Nature Reviews Genetics 4: 457-469. Evolution experiments with microorganisms: the dynamics and genetic bases of adaptation

Local optima can hold back a population from doing the best that they could

Local optima can hold back a population from doing the best that they could. From Elena and Lenski (2003).

Will Pearse

Will Pearse

This paper is more than a little beyond what I usually read, but I always enjoy going to bacterial evolution talks, and I enjoyed this. This is such a rapidly-changing field that I’m certain new things have come out – please do chime in!

I was very struck by the discussion of mutators. The idea that individuals with higher rates of mutation can, in some circumstances, be of benefit to the rest of the population is really cool. It also has a lot of implications for the constant arguments I seem to have with people over what ‘evolvability’ is: as far as I’m concerned, if there’s a thing that increases the rate of adaptation of a population, that’s an increase in evolvability, and mutators seem to be that. We talk a lot in large-organism evolutionary biology and biogeography about the importance of historical accident – that fast rates of mutation only sometimes increase the evolvability of a population, and only sometimes do such individuals come to dominate, is an excellent repeatable and predictable example of the problem. It’s nothing short of amazing that we can do accurate back-of-the-envelope calculations and figure out the odds of a particular outcome in a petri dish.

One thing I want to slightly temper some of this with is the importance of natural history in these populations. It’s all very well studying the evolution of bacteria in stationary phase and discussing how this is different from what we normally find in the lab, but stationary phase is not the normal state of affairs for bacteria. In the wild, bacteria are not transferred into new media when there’s too many of them, and the same goes for large-bodied organisms too. If we want to understand natural evolutionary processes, we need more stationary phase experiments (right? Am I being ignorant?). To paraphase someone else, we also spend a lot of time examining bacteria that cause diseases in particular environments (the human gut, for instance), and modelling their evolution in situ. The problem with this is that this isn’t what those species do for their whole natural history – if you don’t consider how those species got into that environment (water, soil, kitchen sink, etc.), or what some might call a ‘fluctuating environment’ then you’re not going to get the complete picture of the evolution of that species.

Lynsey McInnes

Lynsey McInnes

This is a difficult paper to discuss because I feel like I know that there have been many advances since it came out, not least in our capacity to study mutations and their effects right down to the level of single nucleotide polymorphisms and up again to the level of whole genomes. However, my knowledge of this literature is hazy at best (but see Will’s and my first attempt at discussing experimental evolution here). I’m just going to paste in the abstract below so you know what the paper was actually about (seen as my post barely touches on it…).

Microorganisms have been mutating and evolving on Earth for billions of years. Now, a field of research has developed around the idea of using microorganisms to study evolution in action. Controlled and replicated experiments are using viruses, bacteria and yeast to investigate how their genomes and phenotypic properties evolve over hundreds and even thousands of generations. Here, we examine the dynamics of evolutionary adaptation, the genetic bases of adaptation, tradeoffs and the environmental specificity of adaptation, the origin and evolutionary consequences of mutators, and the process of drift decay in very small populations.

What am I going to write about then? Well, I think going off on a tangent seems like the best idea. My background is heavy on macroecology (patterns! scale!) and my current work centres around exploiting neutral genetic variation among populations to infer demographic history (which I am increasingly realising can get quite close to macroecology when it wants to). So I am not accustomed to thinking about mutations that affect function or adaptation in beneficial or a deleterious ways. Selected genes are in fact the bane of my data. Although I remain unconvinced that we are ever confident that a locus is ever completely neutral.

In fact, I am quite jealous of experimental evolutionary biologists. It seems unfair that they are able to watch things (really, anything!) happen in real time whereas macro-scale analyses (macroevolution, macroecology, phylogeography, biogeography) rely on sometimes shaky sets of assumptions, occasional blind leaps of faith and (more often than not) bundling a lot of unexplained variation into historical contingency. I am a big fan of comparative and meta-analytical approaches (which I’ve advocated on many a PEGE post) where generalities can emerge on diverse topics such as prevalence of niche conservatism, latitudinal richness gradients, modes of trait evolution, even of community assembly, but there is always the niggling doubt that contingency gets in the way and overrides any signal. Wouldn’t it be great if we had five Caribbeans and could throw on five identical Anolis clones and watch what happened? Bacterial experiments can do this! So jealous!

What I’d like to see is more engagement between experimental evolutionary biologists and macro-people. How close can we get to equivalent situations? Can we apply our macro approaches to bacterial setups and see what we find? What is and is not transferable? How much does asexuality mess things up? How much does single cellularity mess things up? I am quite sure that there must be some theoretical exploration of these ideas, but I’d like to see more cross-talk among empiricists. Especially now that we can sequence anything (especially easily bacteria), let’s find out more about how comparable these systems are and what the next stage might be?


Parallel Evolutionary Dynamics of Adaptive Diversification in Escherichia coli

Matthew D. Herron and Michael Doebeli. PLoS Biology 11(2): e1001490. DOI:10.1371/journal.pbio.1001490. Parallel evolutionary dynamics of adaptive diversification in Escherichia coli.

Below, we give our first impressions of this article. Please comment below, or tweet Will or Lynsey (maybe use #pegejc). Think of this as a journal club discussion group!

Will Pearse

Will Pearse

This is another article that pushed me outside of my comfort zone; I know nothing about bacterial ecology, and probably even less about bacterial evolution. However, this is a very neat demonstration of how bacterial approaches can shed light on questions biologists have been asking for decades: what would happen if we turned back the clock and started evolution afresh?

According to this paper, very similar things. The authors find that bacteria exposed to the same conditions evolved the same kinds of responses, and split into the same kinds of species. Us big-bodied ecologists know that things like this can happen in species like Anolis lizards, but we don’t have the ability to turn back the clock, do the whole thing again, and sequence the genomes of everything while it’s happening. Indeed, while Anolis lizards have radiated into similar niches, I’m not sure there’s evidence that they underwent mutations at exactly the same loci. To be precise, these mutations happened in the same genes, and in the same order, but were not at the exact same points in the genes. This is still amazing, and I guess makes it less likely that we’re just picking up mutations that were previously at too low a frequency to be sequenced.

I wonder what effect gene transfer has on all of this. I’m happy to admit that these are distinct ecotypes, but I’d be surprised if the bacteria weren’t able to share genes. Thus it seems that this is the perfect example of reinforcement driving the generation of these ecotypes – becoming half of one ecotype and half of the other must be maladaptive, and this is something that could be experimentally tested. Thus despite the ability to rapidly ‘hybridise’ and share genes, the bacteria don’t, or rather those that do die out. I imagine it’s the frequency-dependent ‘clonal niche construction’ mechanisms the authors discuss that help this get going to begin with – otherwise the first variant to evolve would dominate the entire assemblage. I wonder to what extent such dynamics are a consequence of constant environmental conditions that allow these biotic interactions to play out.

Lynsey McInnes

Lynsey McInnes

I have a soft spot for experimental evolution. I think it’s because I know, and like, simulation studies and experimental evolution seems like the elusive next step. Elegant, tractable and yet also more ‘valid’ than the clinical world of simulations where, some might say, you get out what you put in. One day, perhaps, I’ll have the guts to team up with these people and step out of my simulated world.

The beauty in these setups include the opportunity to have multiple replicate ‘runs’, for evolution to occur relatively fast and with the possibility to take samples during the run to monitor the trajectory of diversification, to manipulate the ‘environment’ of each run while minimising variation from the outside the system. Mmmm…

Anyways, I digress.

This paper builds on previous work from the Doebeli lab and I think provides a neat addition, capitalizing on advances in sequencing technology to really get at how parallel the dynamics of adaptive diversification can be. I found the conclusions – that the dynamics of diversification follow the same trajectory across populations and that this sometimes involves parallel mutations, sometimes not, really quite cool. That different mutations at the genetic level can lead to the same derived phenotype was also a very neat finding. The authors also make a convincing case that the patterns observed are due to frequency-dependent ecological interactions rather than genetic drift or clonal interference.

The introduction touches upon sympatric speciation and how frequency-dependent selection can cause it; the authors seem to shy away from this still controversial topic in their discussion. This is perhaps fair enough, they make their case briefly and then stick to the study in hand, although the implicit message throughout is that this study is providing further evidence for the feasibility of sympatric diversification.

My following of the literature on sympatric speciation is a bit patchy (although I know Doebeli has made some major contributions) although I have had countless relatively uninformed discussions on its prevalence in macroscopic speciation, me spouting that there is probably some kind of microallopatry going on, my opponent countering that such a setup might still be considered sympatric. Anyways, this paper was one of the first to effectively explain how frequency-dependent selection might lead to ‘sympatric’ speciation. My mind is now whirring as to how this mechanism translates up out of this microcosm setup.

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