A comfort zone is a beautiful place, but nothing ever grows there

Experimental evolution is not a subject that I would describe as being within my comfort zone. This may explain the interesting experience I have had with this topic and why my appreciation for experimental evolution has grown considerably.

In many ways, lack of growth within one’s comfort zone is a nice analogy for the evolutionary process. Changes in environment push populations outside of their comfort zones creating the selection pressure required to drive the evolutionary process. Take the highly diverse beak shapes of Darwin’s finches for example, changes in the environment altered food availability. This pushed some members of the population outside of their comfort zone, increasing selection pressure which drives evolution.


Different beak shapes in finches are specialized for different types of food. Changes in food availability can push birds with the wrong beak shape out of their comfort zone and drive selection towards the best suited beak shape for the available food.

The concept of evolution as proposed by Darwin, first shook the world over 150 years ago, since then science and technology advancements have continued to drastically change the world we live in. Despite this our understanding of evolution remains incomplete, we are constantly revealing new insights into the evolutionary processes which have happened and which are continuing to happen around us. Interestingly it is now possible to observe evolution in real time, and in real organisms through studies designed with microbes and specific environmental parameters. This field of research has been dubbed “Experimental Evolution” and the findings being produced are both interesting and relevant to a wide range of biological fields.

A recent paper in this field which really sparked my interest was the article by Vogwill et al on population bottlenecks released earlier this year.

A population bottleneck is the biological term used to describe a dramatic reduction in population size. Bottlenecks occur frequently, and in a variety of situations both biological and in the physical world around us. For example, a bottleneck occurs when traffic builds around areas where many cars from many roads are trying to move onto the same road. All cars are used for transport, but they vary greatly in shape, size and colour.  If at any one time only 5 cars were able to enter the road and all 5 of them were vans, we would suddenly have a “population” of cars which was all vans. When a species experiences a population bottleneck a similar situation to the 5 cars occurs. Only a few members of the species survive the bottleneck and the genetic composition of the future population is derived only from the surviving member’s genes.


Bottlenecks can occur in a variety of settings. As described above we can now see a “population” of 5 vans. 

The study by Vogwill et al set out to investigate the effects of population bottlenecks on the rate and mechanisms of adaptation to the environmental conditions.

Using a simple experimental design, of artificially bottlenecking a Pseudomonas fluorescens Pf0-1 bacterial population each day, the group was able to study the effect of different bottleneck intensities on the bacteria’s ability to adapt. In order to produce a selection pressure, the bacteria were exposed to antibiotics at a constant concentration throughout the experiment. Each day the researches took a small proportion of the bacterial population and transferred them to a “fresh” environment consisting of fresh, plentiful nutrient supply, oxygen and the antibiotic selection pressure. After 110 total generations of bacterial growth, genetic analysis was carried out on members of the surviving populations to determine which genes were being modified and how.  They found that in the Pseudomonas strains mutations which allowed survival arose most often in two specific genes (rpoB and cpxA).  Both genes are known to be involved in the acquisition of antibiotic resistance, but rpoB is more specific to the antibiotics used in this study than cpxA. Further to this, of the three different bottleneck intensities (weak, medium and strong) used in this study, rpoB was mutated at higher frequencies in both the weak and strong bottleneck conditions. The intermediate bottleneck condition lead to the most variation in gene mutation with both genes being favoured.  The researchers explained this finding by looking at the effect mutations in each gene had on the absolute fitness of the population. They suggested that under strong bottleneck conditions the higher fitness caused by the rpoB mutations was necessary to survive. However in the weak bottleneck populations both  rpoB and cpxA mutations competed with each other and the greater fitness of rpoB lead to the observed increase in frequency. This study wasn’t perfect for a range of reasons, and the authors outlined a variety of ways in which their work could be improved and built upon. They did however highlight some interesting observations on the trends evolution seems to follow when experiencing a bottleneck.


Experimental design used in this study to investigate the effects of three different population bottleneck intensities.

Despite this the paper got me thinking about how we can use experimental evolution studies to further understand not only how bacteria evolve in laboratory conditions but how diseases evolve and mutate.

My first and true love when it comes to genetics is cancer, I never cease to be amazed at the mechanisms the disease develops for surviving despite natural and medical attempts to remove it. Cancer can be described as “the uncontrollable growth of cells within the body”, basically cells are being rapidly replicated, not unlike the bacteria in the bottleneck study.

Perhaps then information from studies like this can provide insight into the patterns of genetic changes seen in cancer cells during treatment. The drugs used to treat cancer can create a bottleneck for the disease, most of the cancer cells are die but those that survive will be the few cells that are best able to adapt and respond to changing environments. So while it sounds great to hear that 90% of the tumor is gone, knowing that the 10% that survived are the sneakiest, most adaptable cells of the cancer isn’t exactly the kind of news most patients are hoping to hear. Experimental evolution studies may hold the key to understanding and ultimately treating the sneaky, adaptable cancer cells causing painful and expensive treatments to continue and in some cases relapse.

Despite the validity of some of the results from the bottleneck study being a little bit questionable, this paper definitely succeed in expanding my comfort zone and making a fan of experimental evolution out of me!

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3 Responses to A comfort zone is a beautiful place, but nothing ever grows there

  1. danielle8601 says:

    Very interesting concept linking this back to cancer. I loved the video defining evolutionary bottlenecks! It’s quite a convincing and scary thought, to think in trying to irradiate cancer we are actually selecting for the worst and hardest to target cancer cells.

  2. kellysyh says:

    Love how you can make a not-so-fantastic paper become very interesting! *hi5* cancer-mon 🙂

  3. weisup says:

    I loved the way you wrote this. It is so relatable to so many different people. Definitely the best explanation of a bottleneck I have seen so far, and the pen and paper drawings were a really nice touch!

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