Why make it when you can take it?

I don’t know about you, but when I think of evolution I think of gaining the ability to do something. Just look at humans who live at high altitudes; they make a massive amount of red blood cells (among other things) so that they can breathe when the air is thinner. Sure the ability to breathe may not necessarily seem like a whole lot, we can all do it after all, but put a person who has adapted this ability at an altitude where the air is “normal” and step back and watch the magic. They don’t fatigue like the rest of us. Any aerobic athlete would KILL for this ability – look at Lance Armstrong, he ruined his reputation and cost himself 10 million dollars for the chance to exchange oxygen as efficiently as a Tibetan native. But what if adapting to a certain environment involves the loss of an ability? Not necessarily because the adaption is harmful, but because it is simply unnecessary. Athletes who train at high altitudes for just two weeks begin to adapt to life at low oxygen levels very quickly. Among these adaptions, the elusive increase in red blood cell count. Take these freshly adapted humans, put them back in life at sea level and there you have it, a super human ability for oxygen transport. But there’s a catch: these changes aren’t permanent. Want to maintain this wonderful ability to breathe super well? Back up the mountain you go! 

If you’re anything like me, you’re probably wondering why this happens. It seems to me that this specific adaption is really, really helpful. So why would we lose the ability to keep an abnormally high red blood cell count when it so clearly increases our fitness (both literally and evolutionarily). For this I have one simple answer: it’s just not an ability we need to have. The average human doesn’t have an evolutionary need to run a fast 10K, we just need to be able to be fit to survive long enough to reproduce. And the effort it takes our body’s to make these extra cells isn’t worth the benefit that we get from it. Evolution isn’t about being exceptionally good at living – it’s just about being able to survive. 

Personally, this came as a bit of a surprise to me. We are so used to associating evolution with natural selection and then in turn associating natural selection with the idea of the “survival of the fittest”. So what exactly is natural selection? How does it work and why have we not ended up with a super human population? 

Essentially the theory of natural selection is as follows:

  1. Traits, or characteristics are heritable. This means we get things from our parents. Eye colour, nose size, beak shape, short temper – all thanks to mum and dad.
  2. In any population (human, elephant, bacterial) certain individuals will inherit traits that make them better at reproducing and surviving than the rest of the population. These guys go on to have the most offspring.
  3. Because these good traits are heritable, they will pass them onto their children and because these traits allow them to have the most children, eventually these traits will become more common.
  4. Over generations, the original population will become adapted to its environment.

So basically natural selection doesn’t give us the fittest possible population available, it gives us the fittest population FOR THAT ENVIRONMENT. Rather than survival of the fittest we get survival of the least likely to die.

Let’s look at an example:

So if natural selection works to make sure that beneficial traits are passed on, we can assume that every trait we inherit from our parents is beneficial, right? Not quite. Natural selection isn’t the only evolutionary force in action, in fact some evolution happens purely by random chance. Now this may be a bit confusing seeing as I’ve just been going on about evolution ensuring that good traits get passed on and bad ones don’t. But there’s one little thing I didn’t mention about natural selection – it’s only really effective when we’re talking about large populations. Occasionally, a population can suddenly decrease in size. This can happen for a number of reasons: maybe a handful of individuals decide to move away from the rest to make their own new population, a predator might come in and eat all but a few or perhaps a natural disaster strikes. Either way, populations can suddenly go from huge to small, and when this sudden size decrease happens the individuals that remain are there purely by chance. This chance survival can mean that we end with a lot of individuals within this left over population that have traits we don’t necessarily want. And this random change in the prevalence of a certain trait in the population, due to “random population sampling” (i.e. taking only a small portion of the population) is called genetic drift.

If we refer back to the beetle colour example, natural selection would ensure that the population ends up being mostly green because the green beetles are the ones who are most likely to survive. But suppose one day massive rain fall caused a flood that killed 75% of the beetle population, with the remaining 25% surviving by chance and chance alone. The random survival of these individuals could mean that we end up with most of these surviving individuals being black rather than green, even though green is more advantageous. Then when these individuals reproduce, they will pass their colour trait down to their offspring and the population will remain mostly black in colour. So here we’ve ended up with a population that is mostly black, despite the fact that being black is actually a disadvantage. 

So how can we tell if a trait is present because it’s beneficial or because of random chance? This is where a little something called experimental evolution comes in. Experimental evolution allows scientist to use lab experiments or controlled field environments to explore the dynamics of evolution. This particular question was asked by a couple of scientists ( Glen D’Souza and Christian Kost) who noticed that bacteria sometimes lose the ability to make some nutrients and/or molecules that they need to survive. Bacteria are known for their ever-changing genome (think of a genome as a genetic blue print), so the loss and gain of genetic information is not a new thing for bacteria. But it does seem odd that they would lose the ability to carry out a task as important as making a molecule essential for their survival. So the question was asked: is the loss of this ability favoured by natural selection or does it occur as a result of random genetic drift?

D’Souza and Kost set out to answer this question by performing experimental evolution on a type of bacteria calledE.coli. Personally I think E.coli are underappreciate and misunderstood. Yea sure if the wrong strain populates your insides in the wrong place then they could kill you. But they’re not all out to get you, in fact we all contain a population ofE. coli in our gut that helps us break down and digest the food we eat. If that isn’t enough to change your mind then go and look at a video of them growing under a microscope – adorable. Plus, on top of all of that, their tiny genomes, super-fast reproductive rate and the fact that they’re super easy to manipulate make them the perfect model organism to perform evolutionary experiments on. 

D’Souza and Kost’s particular question of interest was to see whether or not E. coli would evolve to stop making amino acids (think of amino acids as the building blocks used to make proteins, and thus VERY essential) when they were provided by the environment. Firstly they looked at whether or not bacteria grow faster in an environment that lacks amino acids, compared to an environment that contains amino acids. They found that E.coli grown in the presence of amino acids reached a much greater cell density, or population size, than those that weren’t (figure 1A.). Remember how natural selection needs big populations to work? A larger population means it’s more likely that natural selection is actually happening and that any adaptions and mutations that happen are likely to be beneficial. 

So then the next question was – do these populations grow larger because of the increase in available nutrients? To determine this they subtracted the growth rate of populations in the presence of environmental amino acids from the growth rate of populations not in the presence of environmental amino acids and calculate the difference. If this number was a negative value it showed better growth in the presence of amino acids but if this number was positive it showed better growth in the absence of amino acids. If you look at the figure 1B you can see how these values over time. Initially the presence of amino acids was not the cause of increased growth rate, but over time that reversed. So by the time 2000 generations had passed, the E. coli grew far better when amino acids were available to them from the environment. So what does that mean? It means that over time the bacteria in this population have become dependent on the environmental amino acids for growth. 

A possible answer for this dependence is that the bacteria evolved amino acid auxotrophies. This means that they lost the ability to make these amino acids themselves and now rely on the environment to provide them. To confirm this, the genomes of 1000 bacterial colonies were analysed. The results were converted into a heat map (figure 2.) which shows the percentage of the population that had developed an amino acid auxotrophy along with how many generations it took them to obtain that auxotrophic mutation. Any square that is black shows no auxotrophies, any square that is pink or darker indicates auxotrophies. If you look at figure 2, you can see A and B – A shows populations grown in the presence of amino acids, B shows populations grown in the absence of amino acids. Both of these heat maps show pink squares – indicating auxotrophies evolve when grown in either environment (although more when amino acids were provided). Coupled with the large population sizes, these results suggest that the development of auxotrophs are in fact evolutionarily advantageous. 

So how can we confirm that having these auxotrophic mutations are advantageous? Well we can compare the fitness of the cells that don’t have them with the cells that do have them, which is exactly what D’Souza and Kost did. This figure below may look a little bit confusing, but essentially it shows the fitness of one strain compared to another in either of the two possible environments. The red boxes are auxotrophs, the bacteria that can no longer make certain amino acids, and the green boxes are bacteria that can make all of the amino acids themselves (these guys are called prototrophs). If the box sits higher up on the graph it has a greater fitness. So now looking at this figure we can see that when grown in the presence of amino acids, the auxotrophs have a greater fitness than the prototrophs, but when grown in the absence of amino acids this is reversed. The fitness of the phototrophs doesn’t really change at all. And this pattern was seen regardless of whether the strains evolved in the presence (A) or absence (B) of amino acids. 

It seems odd that these bacteria would evolve to lose the ability to make amino acids, even when there are no amino acids available from the environment right? Absolutely! But the thing is, the environment doesn’t just mean the physical place in which the bacteria grow. The fact that there was the development of auxotrophs when amino acids weren’t provided in the growth liquid shows that these bacteria were able to get the amino acids they needed from somewhere else. But where? Well not all the bacteria in these populations evolved into auxotrophs, some still retained the ability to make all the amino acids they needed on their own (prototrophs). So even when there are no amino acids obviously available in the growth liquid, the prototrophic cells that evolved with them provide a source of amino acids to the cells that need them. This is evident when looking at the how the fitness of the auxotrophs changes when they are assessed with the prototrophs.

So now we know that:

  1. Bacterial populations grow faster and when grown in a liquid media that contains extra nutrients (like amino acids)
  2. Over time bacteria evolve to become reliant on the nutrients provided by the environment
  3. This reliance is due to a loss in the ability to make the nutrients on their own (auxotrophs).
  4. When auxotrophs are grown in an environment that provides the nutrients they have a higher fitness levels than the cells that make all of these themselves.
  5. Auxotrophs can get the nutrients they need not only from the liquid their grown in but from the cells that can still make all the nutrients required.

There is one more important take away from this paper, and it involves something called negative frequency dependent selection. Sounds fancy and complicated right? It’s actually pretty simple. Basically it means that a certain trait is maintained at a low frequency because the more common it becomes in a population, the more its fitness decreases. So basically the trait is only beneficial when it’s not very common. It was determined that this is the case with these auxotrophic bacteria found in the population – they only had an increased fitness when they were present in low amounts. Why? Because the more auxotrophic bacteria there are in the population, the more the whole population relies on the environment to provide what they need. Think of the environment like a grocery store – the more people that need to buy groceries, the less there are available for everyone.  But if 75% of the population can grow their own vegetables at home then only 25% of the population needs to buy them. The less people that buy, the longer the stock lasts.

So there you have it, sometimes losing the ability to do something can actually increase the fitness of an individual. Yea sure making an essential nutrient is a good thing, but why make it when you can just take it?  

This blog was based on the following paper:

D’Souza, G., & Kost, C. (2016). Experimental evolution of metabolic dependency in bacteria. PLoS genetics12(11), e1006364.

Find it here: https://journals.plos.org/plosgenetics/articleid=10.1371/journal.pgen.1006364

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