The case of accidental evolution in HeLa

How does one accidentally evolve a population of cells? Quite easily it seems. 

This story begins in 1951, when Henrietta Lacks went to see her doctor at Johns Hopkins Hospital. She had cervical cancer. A biopsy of her tumor was taken, which then fell into the hands of a scientist by the name of George Gey, who was working on trying to culture the first human cells in the lab. Henrietta’s cells, to Gey’s surprise, flourished in the rich environment he had created for them, quickly growing far beyond their original volume. With letters taken from the first and last name of Henrietta Lacks, he called them HeLa.

Meanwhile, as Henrietta’s cancer proceeded, the aggressiveness of the tumor caused it to spread throughout her body, and eventually resulted in her death just a few months later. The cells taken from Henrietta’s tumor grew and grew and grew, now surpassing the weight of the body they were once a part of. They were immortal. HeLa had found a way to cheat death, and divide indefinitely.

The limit to cellular replication is the length of the ends of the chromosomes, termed the telomeres, and through each replication cycle, a small part of the DNA is lost. After many years of replication of chromosomal DNA, the telomeres reach a critically short length and cells essentially give up (senescence). However, the HeLa cells did not give up. Through the random mutations accumulated in cancer, the cells managed to activate a part of the cellular machinery to lengthen the telomeres, an enzyme called telomerase .

Since these cancerous cells had the ability to essentially live forever and survive in a lab, HeLa cells became the perfect tool for medical research. Following their discovery and use by George Gey, over 60,000 papers have been published using HeLa, which of course led to the identification of telomerase in chromosome maintenance, the development of the first polio vaccine, and many more life saving discoveries. However, given the very nature of cancer cells, they can undergo rapid changes through mutations, allowing them to evolve over a very short time period (as what happens in human bodies when cancer progresses).

Therefore, some people began to wonder, are HeLa cells evolving? If they are, what effect does this have on recently made medical discoveries using these cells? Are they even human anymore?

With these questions in mind, an Italian group of researchers sought to find the answers

There is a standard practice when it comes to culturing HeLa cells. A medium was manufactured for their specific growth needs, and virtually all tissue culture labs around the world use these same products. That is what makes the culturing of human cells so relevant in the field of experimental evolution, whether it is on purpose or not.

A not very exciting, but tasteful shot of some standard media that can be used for HeLa in the tissue culture lab upstairs from me.

These researchers knew of other groups in the field that had been culturing the same HeLa cells for 8 and 12 years continuously, potentially accumulating multitudes of differing mutations. Therefore they sought to find out exactly how distinct these cell lines were from the original human genome (since Henrietta never had any normal tissue taken for us to sequence).

To get a general idea for the amount of divergence between the HeLa cell lines and also the normal human genome, the researchers carried out simple karyotyping, basically visualizing and counting chromosomes under the microscope. Now, just to get an idea of a normal set of chromosomes, you need to know that humans usually have a total of 46 chromosomes (23 pairs). The HeLa cells are clearly not “normal”.

Cells that had been continuously cultured for 8 years had chromosome numbers ranging from 71 to 79. Almost double that of a typical human.

And even more shocking, the cells that had been continuously cultured for 12 years had chromosome numbers ranging from 56 all the way to 240!

To further demonstrate the evolution of these HeLa cells from known common HeLa markers, the researchers used Fluorescent In Situ Hybridisation (FISH for short) to “paint” certain chromosomes different colours.

The image above shows chromosomes that contain the DNA of chromosome 5 and chromosome 9, with a myriad of each present.

Just FYI, humans usually have two copies of each chromosome (with my very own chromosomes for reference!).

Clearly, these cells may be a little inaccurate when being used for medical research if some have far more chromosomes than they should.

Now knowing that there were definitely huge differences in chromosome number, the researchers then wanted to know which specific parts of the genome were actually being gained or duplicated. So they showed the sequenced genomes of 2 groups of HeLa cells grown for 8 years (HeLa P and HeLa H derived from the same batch) or 12 years (HeLa V and HeLa SR derived from the same batch) continuously, compared with the human genome.

“The genomic landscape of the 4 HeLa cell lines.” Fig. 1A from Frattini et al. 2015.

The above Circos plot above showed that each HeLa line had a huge proportion of genetic information deleted (in red) or duplicated (in green) from the human genome, but with lines derived from the same batch somewhat similar. This picture illustrates just how different a cancer genome is from normal human cells, and also shows the differing evolution of cancer cell lines grown under very similar conditions over time.


It is obvious, at least to me, that these cells are vastly different from humans. It has actually been proposed that HeLa should be classified as a new species, Helacyton gartleri, but unfortuantely the name just never caught on.

Most scientists that culture cancer cell lines know that the nature of these cells allows for them to accumulate mutations, and eventually become unreliable in terms of testing for real-world medical applications. Therefore, it is standard practice to not continually culture your cells for more than a couple of months (about 50 transfers to new media). But clearly, this message has not reached everyone in the field, and this is a cautionary tale to all those who do not heed the information gathered in this paper.

All of this information together tells us two things.

Firstly, that cancer cells grown in culture can evolve rapidly, analogous to the way in which a benign group of cells can undergo changes to become an aggressive cancer in the human body.

And finally, that you should never let your HeLa cells run rampant for 10 years. 


You can find the aforementioned paper here!
If you want to learn more about HeLa cells and the life of Henrietta Lacks, I would recommend “The Immortal Life of Henrietta Lacks” by Rebecca Skloot.
Posted in Experimental Evolution | Tagged , , , , , , , | 1 Comment

The life of a pea aphid, and why you don’t want to be him

Aphids live pretty simple lives, suck up some plant juices, find a mate, and make some babies…sounds quite chilled, right? Wrong. In fact, the life of a pea aphid or Acyrthosiphon pisum, is a constant battle against predators and parasites. In fact, if you were to compare aphid life to anything, it would be Ridley Scott’s Alien movies. These films were pretty gory (one of the reasons I illustrated this post with the Shrek reference), and I always wondered where he came up with the idea of baby aliens bursting out of people’s chests. Well I can I quit my wondering, because parasitoid wasps or Aphidius ervidid it first.


Aliens bursting out of chests is something you only see in movies, right…?

Now before you join team aphid, you have to realise that aphids are actually pests of multiple crops, and cause problems by spreading devastating plant viruses. And those parasitoid wasps you thought were the bad guys? Farmers actually use them as biological control agents to keep down aphid populations. Isn’t that the plot twist of the 21st century!

Now for those of you who are still on team aphid (who likes vegetables anyway), fear not, these little guys have someone defending them. Some lucky aphids harbour a symbiont, the Enterobacteriaceae, Hamiltonella defensa. However, unlike the Captain America that I have portrayed them as, these bacteria require something in return (so much for superhero). The aphid provides the bacteria with nutrients, and the bacteria provides toxins which act to prevent the development of parasitoid wasp larvae. Or specifically, the bacteriophage H. defensa harbours produces the toxins. Is three a crowd? Obviously not to the pea aphid!

Now the question that is addressed in the study I’m reviewing for you here is, is it all really worth it? Does harbouring this symbiont really save these pea aphids from the doom of being eaten alive by wasp larvae? Think I’m just being pessimistic? You may just change your mind after reading what they discovered in this article.

In this study, the first experiment they performed determined what level of defence H. defensa provided to the aphids. This involved growing parasitoid wasps on two aphid populations, one harbouring the symbiont, the other not, and counting how many stung aphids survived (ie. didn’t hatching any wasp larvae). They found that:

143/200 aphids harbouring H. defensa survived

33/400 aphids not harbouring H. defensa survived

So that symbiont bacteria really does make a difference to aphid survival! What we can also see from this data is that aphids also have an innate (or natural) immunity, evident from the fact that while 143 of the non-symbiont-harbouring aphids hatched wasp larvae and died, there were still 57 that survived.

The second experiment they performed was an evolution experiment that monitored components of fitness from parasitoids grown on symbiont-harbouring or non-symbiont-harbouring aphids over 10 generations.

Experiment 2

Experiment 2: Measuring fitness components of parasitoid wasps during evolution

Now fitness in the science world doesn’t mean the most muscular or the fastest organism, instead it means ability to survive (guess you can tell your friends you’re fit now). In this experiment, the fitness components measured were; effective parasitism rate (of the number of aphid stung, how many hatched wasp larvae), and the size of the left tibia of the wasps that emerge (used as a determinate of wasp size).

Experiment 2 results

Components of fitness measured from experiment 2. Modified from Dion, Zele, Simon, & Outreman, 2011.

It was found that after just 4 generations, the parasitism rate of wasps grown on the symbiont-harbouring population had increased to equal that of the wasps grown on the non-symbiont-harbouring population. Did H. defensa take a holiday? Nope, that’s the power of evolution kids. Just like you evolved to eating cereal out of a pot because your flat mates never clean the dishes, these parasitoid wasps can evolve against the symbiont-mediated resistance in their aphid prey. Basically, there is massive selection pressure on these wasps, either their young survive, or they don’t. Therefore, only the wasps best adapted that carry the most useful genes (possibly acting to de-toxify that symbiont toxin), will survive to contribute to the next generation.

The other fitness component measured was the left tibia of surviving wasps, which estimates the body size. The researchers wanted to know if the wasps that emerged from the aphids harbouring the symbiont got smaller, suggesting that there had been a trade-off. Essentially, some of the nutrients wasps would normally use for growth are siphoned off (or traded) for the production of proteins that protect the wasp larvae from toxins. And indeed, these results were found in the experiment. After 10 generations, the wasps grown on the symbiont-harbouring population got smaller. Therefore, while these parasitoid wasps are getting the better of the only defence these aphids have, at least they’re looking a little bit starved in the process. Totally makes up for their babies hatching out of aphid larvae and eating them alive…

Interestingly, a further study by these researchers found that a trade-off occurs in the aphids as well, from their symbiont-mediated resistance. Aphids that harboured the symbiont suffered higher predation by ladybugs because they didn’t use as many defensive behaviours (Polin, Simon, Outreman, 2014). The researchers called this an “evolutionary cost”, and suggested that symbiosis might not be as beneficial as it’s talked up to be. Guess that’s even more bad news for the pea aphid!

Experiment 3

Experiment 3: Determining if selection on symbiont-harbouring aphids increases survival rate of wasps

The last experiment they performed really hits hard the shortcomings of H. defensa. For this experiment, they used the same wasp populations that were used in experiment 2 and exposed them to two different H. defensa-harbouring aphid clones (aphids can reproduce asexually essentially cloning themselves, these aphids are the same species but different clones). They then measured the effective parasitism rate (how often a stung aphid hatches wasp larvae), of the two different wasp populations and compared this to the effective parasitism rate they calculated from experiment 1, before evolution. This experiment will determine if selection of symbiont-mediated resistance will help these wasps survive on new symbiont-harbouring aphids.

Experiment 3 results

Effective parasitism rates before and after evolution to the symbiont-harbouring aphid. Modified from Dion, Zele, Simon, & Outreman, 2011.

And would you look at that, in both clones the wasps that had been grown on a symbiont-harbouring aphid population had a higher effective parasitism rate after evolution. Therefore, was it all worth it? Well, carrying the symbiont H. defensa did provide protection to the aphids, however it doesn’t last for long in these laboratory conditions. I did tell you this story doesn’t have a happy ending! However, this study does illustrate the power of evolution and that in nature, there will always be predators and prey, that’s life. No symbiont will offer complete protection, which is good news for farmers (and you if you like vegetables)!

Now you might be wondering what the practical uses of this study are. As I mentioned earlier, farmers are using these wasps to manage aphid populations. When they were first introduced in North America, the native parasitoid wasp populations were displaced and only one remained to compete with A. ervi (Schellhorn, Kuhman, Olson, Ives, 2002). This shows how important it is that we understand the biological systems we are manipulating and the implications that could occur. The use of parasitoid wasps as biological control agents disrupts the ecological system in crops, and the evolution and adaption of these organisms must be studied to anticipate and manage any changes that could occur.

It is becoming ever more prevalent that nature is a complex system and when meddled with, can result in disaster. I’m sure you’ve all heard about “super bugs” that are becoming resistant to every antibiotic, how is this different to pests becoming resistant to their parasitoids? There are also stories about messing with the food chain, such as this interesting story about shark finning. Science and evolution is a way to understand how to manipulate nature to our advantage, while preventing any catastrophes. Essentially, we need to be aware about what could happen if we introduce something new into the ecological system or take something away. Therefore this study is just one small part of the bigger picture, which is to understand and safely manipulate this biological system.

However, all this still doesn’t help the poor pea aphids.  At least they helped invent a block buster movie enterprise! Someone should really let them know they aren’t suffering for nothing…



Dion, E., Zele, F., Simon, J., & Outreman, Y. (2011). Rapid evolution of parasitoids when faced with the symbiont-mediated resistance of their hosts. Journal of Evolutionary Biology 24, 741-750. doi: 10.1111/j.1420-9101.2010.02207.x

Polin, S., Simon, J., Outreman, Y. (2014). An ecological cost associated with protective symbionts of aphids. Ecology and Evolution 4(6), 836-840. doi: 10.1002/ece3.991

Schellhorn, N. A., Kuhman, T. R., Olson, A. C., & Ives, A. R. (2002). Competition between Native and Introduced Parasitoids of Aphids: Nontarget Effects and Biological Control. Ecology, 83(10), 2745-2757. doi:10.2307/3072012

Posted in Experimental Evolution | Tagged , , , , , , | 2 Comments

Taking sibling rivalry to a whole new level.

Picture it. You are a larva, freshly hatched from an egg, and squirming around with just one goal. Survive. How best to survive? Well, you need food pronto; you’ve literally never been hungrier in your life!! You survey your options, in addition to the flour surrounding you there are a bunch of lush round eggs, some full siblings, some half siblings, and some of no relation at all. While flour alone may be sufficient for survival, cannibalising some eggs would provide you with an edge over the other larvae.
So now you have to choose. Will you become a cannibal, bettering your chances of survival? Does your relatedness to the egg affect the degree of cannibalism?
Are you… confused?


Adult Confused Flour Beetle.

In 1980, Michael J. Wade decided to study the tendency of larvae from the coolest named beetle, the confused flour beetle (Tribolium confusm), to cannibalise eggs. He used it as a platform to investigate the conditions required for the evolutionary theory of kin selection.

Kin selection is defined as:

“Natural Selection in which an apparently disadvantageous characteristic increases in the population due to increased survival of individuals genetically related to those possessing the characteristic” 

So here, larvae eat eggs due to a genetically inherited behaviour which you think would be bad for the population but since larvae that ate the eggs thrive, the behaviour has stuck around and even increased in the population.

In 1980 this theory was poorly defined, while it was agreed that the relatedness of individuals is important, there were many differing opinions to whether the breeding structure was important leading Wade to his big research question.

However, firstly I had a question of my own: Why bother developing evolutionary theories, they require such specific conditions that it does not seem to be realistic or applicable in nature?

It had really stumped me as it made the whole study of evolution seem rather redundant. Thankfully I have come up with an answer which is actually pretty simple, the experiments we all conduct give information on the present. Organisms in the present time, how they act and react, right at this moment. Developing evolutionary theories and taking the time to carefully refine them is all we have, it is the very best we can do to take what we see happening right now and use it, not only opening up the mystery of what occurred in ancient populations as species fought to survive but to also predict what will happen to populations in the future.

Now sense of importance restored, back to Wade and his big research question!

What is the role of population breeding structure in the evolution of social behaviour?

To test this Wade designed 3 different population structures which tested both the effect of the relatedness of individuals and the breeding structure on the evolution of the egg cannibalism behaviour.


Experimental process of population structure one.

Population Structure One is shown above. 5 larvae from each of the selected 15 mating pairs were put into separate vials; in both groups 45 fully related eggs (R=50) were offered over time and all beetles were allowed to mature then counted to determine the degree of cannibalism. If no cannibalism occurred, you would have 50 adults in each vial (5 larvae + 45 eggs). The mature beetles are then subjected to different breeding structures, either random or within-group mating. Larvae were again collected from 15 mating pairs and the experiment was repeated for 8 generations.
Population Structure Two is the same only half related eggs (R=25) were offered.
Population Structure Three is also the same but with non-related eggs (R=00) offered.

What Wade found…


Raw results with no significant trends. (Wade, 1980)

At first glance the results seemed to be a bust with no trends in the rate of cannibalism for either breeding structure, there are fluctuations, but they are attributed to an uncontrollable aspect of environmental variation.

But don’t despair!


Adjusted results revealing the within-group mating trend. (Wade, 1980)

When Wade plotted the difference between the average cannibalism rate when eggs were related and when the eggs were not related, effectively normalising the results, theoretical expectations as predicted by the kin selection model were met!!

There was a lower cannibalism rate when larvae and egg are closely related, but only in the within-group breeding structure. Population structure did not seem to affect the cannibalism rate when random breeding occurs.

It turns out this all comes down to the variance of the genetic basis for this behaviour within the groups. It is either preserved (within-group mating) or destroyed (random mating).
Variance is essential for the ability of a behaviour to become pronounced, so it is no surprise that when random mating occurs there are no behavioural trends.
Furthermore, he concludes that population genetic models which assume random mating of individuals are inappropriate to the study of evolution of these traits.

To simply answer Wade’s question, population breeding structure DOES plays a critical role in determining how a social behaviour evolve and should be considered when studying the kin selection theory!

Let’s now take a moment to appreciate the irony that clarity is provided by none other than the confused flour beetle!
Maybe, just maybe, this wee beetle is not as confused as first suggested…

To read the full paper by Michael J Wade click here.

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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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One Guppy to Rule Them All.

Trying to find a paper on experimental evolution wasn’t an easy task for me. I found papers that I thought were interesting, but were lacking in experimental evolutionary methods and others that bored me to death. Personally guppies are what come to mind when I think about natural selection and evolution – being pretty and shiny is just an added bonus!

Natural selection: “the process whereby organisms better adapted to their environment tend to survive and produce more offspring. The theory of its action was first fully expounded by Charles Darwin, and it is now regarded as be the main process that brings about evolution” – wikipedia

Endler (1980) used guppies to look at two aspects of natural selection in both natural and artificial environments. He has been quite a prominent fixture in evolutionary mechanisms within guppies and provides an example of natural selection with the simplicity needed to grasp this topic by following colour patterns and spot sizes in these guppy populations. Guppies are common additions to household aquariums, but would generally be overlooked in terms of their importance in understanding evolution.

This experiment, which utilized the vast expanses and populations of guppies found in Northern Trinidad and Venezuela, demonstrates the impact of natural and sexual selection in these guppy populations. Its a simple, yet comprehensive, study that is still relevant today. Some websites have taken the fundamentals from this experiment and delivered in it a way that is fun and easy to understand. With that in mind, lets take a look at what Endler’s (1980) study entailed.

This is an awesome website that summarizes the experiments outlined in this paper!

 Greenhouse Experiment


Artificial pools for greenhouse experiment

Ten artificial pools were set up that mimicked natural guppy environments. Two control
pools with no predators, 4 pools with the weak predators (Rivulus hartii) and 4 pools
with the dangerous predators (Crenichichla atla) were used for these experiments. For full details of the methods used in this study have a look at the paper by Endler (1980)


Timeline for greenhouse experiments

Endler (1978)  had previously observed that predators influence male
color patterns
 and with this knowledge was able to predict the results from this experiment. Dangerous predators (Crenichichla) result in guppies with dull colors and smaller spots while weak predators (Rivulus hartii) result in guppies with brighter colour patterns and larger spots (Endler, 1978). Only male guppies exhibit these elaborate colour patterns –  indicating an element of sexual selection, more on this later.

The figures that follow (Endler, 1980) support these previous observations (Endler, 197
8) and demonstrate the impact predation has on natural selection.

Figure 1

Endler, 1980

Figure 2

Endler, 1980

Figure 3

Endler, 1980

The colour pattern and spot sizes increased in the presence of weaker predators and decreased in the presence of dangerous predators (Fig. 1-3). Blue and iridescent (shiny) spots were seen to almost diminish in the presence of dangerous predators (Fig. 2 & 3). It was later suggested that blue and iridescent spots were highly reflective and eye catching to predators, so a decrease in the presence of dangerous predators is concurrent with this view as something yummy and shiny is easier to see when you’re looking for it, similar to spotting a donut with sprinkles as you walk past a bakery window.

With these findings in mind they then compared the results they obtained from the field experiments to see if similar results were drawn.

Field Experiment


Aripo Introduction site for natural experimental population

The field experiment used an isolated portion of a stream (Aripo I), with only the presence of the weak predator (Rivulus hartii), to relocate guppies from a high predation area (c) to a low predation area (x). In this experiment they expected to see a shift in colouration and spot size from that seen in high predation environments (dull colours and small spots) to low predation environments (colourful guppies with large spots). After two years the guppies in the Aripo Introduced population had phenotypes similar to that of guppies found in low predation environments (r), more colourful and displaying larger spots. This deviates from the high predation phenotype that was initially exhibited prior to translocation indicating natural selection within this population.

Figure 4

Endler, 1980

Habitual Background

The second parameter considered in this study was the influence gravel colour and size had on colour patterns and spot sizes in the guppies. If you think about it, for guppies in the presence of dangerous predators the better you are at blending into your surroundings the more likely you are to evade the lunch menu. With this in mind, colour patterns and spot sizes were observed and scored to see what influence this had on natural selection. It was observed that the overall body sizes were proportionate to the gravel backgrounds they inhabited and the colour proportions in the gravel background. This was more obvious in the greenhouse pools as the artificial gravel colours were brighter in some pools than others and this reflected in the results (Fig. 2-4).

Sexual Selection

Sexual selection is a concept that is prevalent in any social standing. People (and animals) choose a mate based on their ideal preferences. Generally, it can be considered what society deems as an appropriate fit but this ingrained preference goes a little deeper than that, even if we aren’t consciously aware of it. A study by Godin and Dugatkin (1996) looked at female mating preferences in guppies and identified their tendencies to mate with brightly coloured males. Surely this isnt based entirely on aesthetically pleasing characteristics? Godin and Dugatkin (1996) identified that males with brighter colours were more likely to approach predators in both the absence and presence of females. This resonates in many social situation where a male tries to portray his masculinity by challenging someone larger than him in order to woo a mate. This boldness ultimately leads to these characteristics  being passed onto their sons and thus increasing genetic fitness of both parents. The protective element is always desirable as males exhibiting these characteristics are able to fend for and protect their families from danger and thus contribute, genetically, to the next generation.

I enjoyed looking at this paper again. I was first introduced to Endler and his guppies in my undergrad degree, where we were given a computer simulation that was based on this experiment. At the time I didn’t appreciate the intricacies of it, clicking aimlessly until it was time for lunch, but the concept stuck with me. It’s quite a cool concept to consider when you’re thinking about natural selection, as it is not only the predation element that is operating in this study but also sexual selection.

I had been watching a program on tv about fertility issues some couples face and later discussed this with my husband. With the addition of modern medicine and the ability to over come issues that would have initially stalled reproduction in some individuals, will this ultimately lead to an increase in the susceptibility of future generations? This can be applied to many evolutionary concepts where adaptation culls the weak and selects for the strong. If we are able to alter this selection process, what does that mean for the future? Will we see increasing amounts of people succumbing to illness? Is this changing the natural course of evolution? These are questions that I often think about and by looking at the current population its easy to see the shift. This is a deviation from what guppies can tell us at this point in time but simply put, only the strongest survive.



  1. Godin, J.-G.J. & L.A. Dugatkin, Female Mating Preference for Bold Males in the Guppy, Poecilia reticulata. Proceedings of the National Academy of Sciences of the United States of America, 1996. 93(19): p. 10262-10267.
  2. Endler, J.A., A Predator’s View of Animal Color Patterns, in Evolutionary Biology, M.K. Hecht, W.C. Steere, and B. Wallace, Editors. 1978, Springer US: Boston, MA. p. 319-364.
  3. Endler, J.A., Natural Selection on Color Patterns in Poecilia reticulata. Evolution, 1980. 34(1): p. 76-91.
  4. Amy E. Deacon, Hideyasu Shimadzu, Maria Dornelas, Indar W. Ramnarine & Anne E. Magurran. From species to communities: the signature of recreational use on a tropical river ecosystem, 2015. Ecology and Evolution 5 (23): 5561–5572. DOI:10.1002/ece3.1800. (Feature Image).
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Sorry for killing you, I thought you were someone else.

Legionella pneumophila is the bacteria behind legionnaires disease, a severe disease with high mortality rates, but it infects you accidentally… But what do they mean when they say “accidental”? Is it like when I accidentally ate that whole pack of biscuits, or is it actually sincere? Well it turns out that L. pneumophila is a pathogen of single cell organisms named protozoa but when it is inhaled into the lungs it spots an immune cell called a macrophage. Now normally the bacteria wouldn’t infect the macrophage but just like gingernut biscuits, if there are no better options you have to settle for it. But now I bet you’re thinking “what do the bacteria do when they’re only given macrophages to survive in”? Well luckily for you a paper published in 2012 will answer all of your questions using experimental evolution methodology and I will try to make it a bit easier to understand.

So let’s start with what we already know. Within the vacuole of the mouse macrophage, which is where the bacteria replicate, lysine is present. It just so happens that most L. pneumophila can synthesize lysine and those which don’t have trouble replicating in lysine devoid environments (1). We also know that whilst the bacteria has many protozoan targets (~15) there are no natural mammalian reservoirs in which they replicate (2).

Methods and Results

In order to select for adaptions to improved survival and growth in a mammalian environment the researchers used mouse macrophages in minimal media as growth conditions and used genome sequencing to identify any mutations in the DNA that these adaptions may be attributed to.


Figure 1: Growth conditions for the four bacterial lineages of L. pneumophila in bone marrow-derived macrophages. Bacteria were extracted and used to infect new macrophages in three day intervals at an MOI of 0.05. Insertion of a lux operon allowed for cell counts using luminescence experiments  (1).

Through whole genome sequencing the researchers were able identify the where the mutations were in the bacterial genome (figure 2). Multiple different mutations occurred in the genome and persistence of these mutations occurs due to a selective advantage or chance, so those mutations which decreased back to 0% of the population genotype after reaching relatively high levels such as lpg0981 likely had a negligible effect on cell growth or had a deleterious effect when coupled with another mutation. There are a few common pathways or structures which these mutations appeared to effect including flagellar structure (used for mobility in bacteria) and also in lysine synthesis.


Figure 2: Mutations present and population genotype in the four L. pneumophila lineages identified using illumine sequencing (1).

Interestingly enough we can also see that many of the mutant strains were able to out-compete the wild type strain (no mutations) in competition experiments. Competition experiments were conducted by infecting macrophages with equal amounts of wild type and a mutant and looking at the ratio after one growth cycle (3 days). If the mutant scores above one on the competitive index we can say that it had a selective advantage, or was able to infect and replicate at a higher rate than the wild type.


Figure 3: Competition experiments between wild type and mutants synthesized in the experiments (1).

Furthermore, when single mutant strains are used to infect protozoa they appeared to have a slower replication rate than that of the wild type (figure 4). In particular, we can see the lysine mutants in Figure 4 d, e and f have a very low growth rate in comparison to the wild type and falls well below one on the competitive index.


Figure 4: Comparative growth in single mutant strains compared to wild type in a variety of protozoa (1).

Additionally, whilst single mutations appeared to slightly increase the ability of L. pneumophila to survive an accumulation of those same mutation resulted in a far higher score on the competitive index, indicating the mutations have a synergistic effect with each other (figure 5a). These mutations may have resulted in some L. pneumophila strains which were grown in the experiment to become lysine auxotroph, which require lysine within the environment to grow (figure 5b).


Figure 5: (A) Accumulation of mutations appears to correlate with a higher competitive index than when the mutations are present alone. (B) Mutation in the macrophage experiments led to what appears to be lysine auxotrophy (reliant on the presence of lysine to grow) in L. pneumophila (1).


Well I guess that means L. pneumophila can adapt to have preferential growth in mammalian macrophages in a year. These experiments have shown that these clonal strains have a superior ability to grow in mammalian macrophages in comparison to wild type as well as a decrease in its competitive index score when growing in protozoa. This may be due to a loss of lysine synthesis as there is already lysine present in the vacuoles of mouse macrophage in addition to changes in flagellar genes. Overall it appears that wild type L. pneumophila isn’t directly targeting mammalian macrophage as a host, however we can see that given the have no other choice they will readily adapt.



  1. Ensminger AW, Yassin Y, Miron A, & Isberg RR (2012) Experimental Evolution of Legionella pneumophila in Mouse Macrophages Leads to Strains with Altered Determinants of Environmental Survival. PLoS Pathog. 8(5):12.
  2. Fields BS (1996) The molecular ecology of legionellae. Trends Microbiol. 4(7):286-290.


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The Red Queen, Evolution, and Sex!

The “Red Queen” hypothesis. Hands down, the coolest name ever for an evolutionary theory! As an avid fan of Disney since forever, I was immediately hooked.

Have you ever wondered: Why does the ability of species to survive NOT increase over time? We have a common misconception of evolution – that evolution is progressive; that organisms are always getting better through evolution. But if organisms are constantly adapting and evolving, surely, they’ll get better at surviving over time? Nope, they don’t. Evidence doesn’t show that they do. And actually, if you think about mutations, they are often more harmful than beneficial. For example, if we get overloaded with radiation, we’ll probably die of radiation poisoning or cancer, not suddenly become Hulk or a Ninja Turtle, nor gain any cool superpowers. What about natural selection? Well, natural selection doesn’t produce perfect organisms – it’s not really “survival of the fittest” because a range of variant organisms go on to reproduce; they just have to be good enough to survive. And since the environment is changing all the time, organisms with traits that help them in one set of conditions, may suck at surviving when these conditions change.

KH red queen drawing

The Red Queen hypothesis addresses this phenomenon. In Lewis Carroll’s “Through the Looking-Glass” (the less-familiar sequel to Alice’s Adventures in Wonderland), the Red Queen says something to explain Looking-Glass land to Alice:

“Now, here, you see, it takes all the running you can do, to keep in the same place”

Leigh Van Valen cleverly used this idea to explain the Law of Extinction. Extinction patterns show that the probability of populations surviving remains constant, despite our misconception that evolution means progress; that species are gradually getting better at adapting and surviving. Sure, they are “evolving”, but they’re not getting any better at surviving. The Red Queen hypothesis states that organisms must constantly adapt and evolve (keep running) just to keep up with other evolving species in the environment. Since every living thing shares its habitat with other living things, the species they interact with must also evolve; otherwise they would lose the competition with other species that DO continue to change. This is called co-evolution: evolving together, affecting each other’s evolution. This is like an evolutionary arms race, because it’s a constant warfare between organisms evolving in an antagonistic co-evolutionary way, such as the relationship between parasite and host. The only way that a parasite can compensate for better defence by the host (that it attacks), is by developing a better offense. Being more strongly attacked then triggers another defence by the host, and so on, so forth. So this interaction; this ‘co-evolution’ means, no matter how much they both try to outcompete each other, neither is able to gain an ‘advantage’. Neither side can quit this arms race, because if they stop, they will no longer be able to exist. As long as they exist, they must keep evolving, or “running” to simply avoid extinction. They must run as FAST as they can, just to keep in the very same place.

How do we know this Red Queen hypothesis is true? Well, as with all theories and hypotheses in science, we can’t be 100% certain that anything is absolutely true. But with more observations and evidence, we can support it to be true with more confidence.

Why is the Red Queen hypothesis important? Besides trying to explain constant extinction rates, the Red Queen hypothesis can provide an answer to another fundamental question: why most organisms reproduce sexually. The evolution of sex! In eukaryotes, sex and recombination (mixing up of genes) is so common, but why this is so, remains poorly understood. Recombination is the re-arrangement of genetic material, and this happens when parents make sex cells which contain half the genetic material that any normal cell would have, so that when two sex cells (gametes) come together (egg and sperm), they make one normal cell: the first cell of their offspring. This is why you get half your genetic material from mum, and the other half from dad. The cool thing that happens in the process of making sex cells is ‘recombination’. Chromosomes can cross over and mix up the genes when the sex cells are being made.


In asexual organisms, offspring are mostly identical or very similar to the one parent, and differences only happen rarely by chance – by random mutation. But sexually reproducing organisms don’t have to wait for slow random mutations to build up because of this recombination. Logically, we would think that when a parasite is trying to feed off a victimized host organism, sexual reproduction and recombination in the host would make offspring more genetically different and unique, so they may have a better chance to survive the parasite attack. However logical this may seem, no experimental evidence has been described in animals… until NOW! (Click here for the paper)

Nadia Singh and her people at the Singh Lab used a very clever and easy way to identify how often recombination happens, and looked into whether this recombination frequency changes when the same host is under parasitic attack. Recently published in Science, this great experimental evolution approach gives support to the Red Queen hypothesis, by using… *drum roll*…

Fruit flies!

Those pesky little critters that hang around bananas and beat you to the fruit bowl are fruit flies. Scientists call them: Drosophila melanogaster. Normally, I’d be asking my best friend, Google, for tips on mass-murdering these tiny bastards. But I’ve learned they are actually pretty useful for scientific experiments that help us understand some of the neat stuff happening in the world we live in – including the Red Queen phenomenon!

Fruit flies are called the “Cinderella of modern genetics”. They’re super easy to work with in labs because:

  1. Mega short generation time. They are animals that only take 10 days at room temperature to go from eggs to adults. Their entire life cycle is just 12 days!
  2. They only have four chromosomes. Their genetic makeup is super simple, but uber useful because their genes are similar to humans.
  3. They are easy to mutate. Since many genes are essential, mutations in these genes kill the animal. But scientists have figured out how to trick the fruit fly by removing gene function within some particular parts, such as the eye. By removing different groups of cells within a fly, they’ve created a whole library of different mutant fruit flies! These are really easy to identify – because you can just see the mutations with the naked eye. Here’s a few that I’ve attempted to draw…


In Singh’s experiment, they wanted to see if the recombination frequency of offspring would increase when host fruit flies are infected with parasites, as the Red Queen hypothesis would dictate. Do infected fruit flies respond to parasite attack by producing offspring with more genetic variation? If they did, then it could give their babies more chance of survival from the same parasite, directly supporting the Red Queen hypothesis that argues sex is favoured in antagonistic relationships between co-evolving organisms. To do this, they used two mutant fruit flies (*): ebony (e) and rough eyes (r). These mutant phenotypes (appearances) are recessive traits, which mean they are only seen in offspring that have mutant (recessive) genes from both parents. Here are what the mutant (left) and normal (wild type on the right) flies actually look like:

To understand their clever approach, we first have to understand how they measured recombination frequency. They created double heterozygote mother fruit flies. These are female fruit flies that carry exactly one mutant and one wild type gene for each of the two traits – body colour, and eyes. Remember here that the normal wild type fruit fly has brown body and normal eyes, whereas the recessive mutant has rough eyes (r) and a black/ebony body colour (e). So a “double heterozygote” would look normal, because they must have two mutant genes to show the visible mutant phenotype, and since they still carry one normal dominant gene, this masks the other mutation genes from showing up. A double heterozygote can be easily made by mating a normal wild type with a double mutant:




Then female double heterozygotes were infected with one of three different parasites (two bacteria and one parasitic wasp). The mama fruit flies that survived the infection made babies, with mutant males, that were more diverse. This increase in recombination frequency could easily visibly be seen, because offspring carrying recombinant maternal genetic material only has ONE visible mutation (either ebony or rough) but NOT the other. Under normal conditions, 50% of offspring are expected to be recombinant…

But under parasitic attack, the infection-surviving mama fruit flies must have shuffled their offsprings’ DNA more frequently in response, because the visible recombination frequency increased! There were more occurrences of offspring showing one visible mutation only.


The results:


Figure 2, Singh et al. 2015

Firstly, they infected four different strains of Drosophila melanogaster (fruit flies) with Serratia marcescens (S. marscescens) bacterium. The “wounded” group is a control, because instead of bacteria (infected), they did the same thing with sterile media (wounded). This shows that more of the offspring from infection-recovered mother fruit flies were recombinants, in comparison to the control.



Figure 3B, Singh et al. 2015

They then did exactly the same thing, but with a second parasite Providencia rettgeri (P. rettgeri), and again observed an increase in recombination in the offspring!



Figure 4, Singh et al. 2015

To engrave their point in stone, they repeated the experiment with a third parasite. But this time, instead of bacteria, they infected fruit flies with Leptopilina clavipes – a parasitic wasp (click here to watch them in action). These wasps are super gross because they lay a single egg in the bodies of flies when they are just larvae. When the wasp egg hatches, the wasp baby eats the fly from the inside out! So mama double heterozygote fruit flies used here were those that had fought off the wasp infection when they were just larvae. These were also visibly identifiable because a black capsule can still be seen in their abdomen. And these infection-surviving heterozygotes then went on to produce offspring with higher recombination frequencies.

The results of this paper indicates that sex is favoured in the face of dynamic (ever-changing) selection pressures – in this case, the antagonistic interactions with co-evolving organisms (parasite & host). Sex and recombination results in greater diversity in their offspring. If they stop “running”, parasites will exploit their static genotype → EXTINCTION.

So to round it all up, mama fruit flies, when whacked with bacterial parasites or a parasitic wasp, purposefully shuffle the genetic makeup of their offspring in response! Isn’t it cool how parents can influence the potential fitness of their babies? Is this happening in US HUMANS as well?


Question:Why shuffle beneficial combinations of alleles that so far have allowed them to survive and reproduce?

Answer:Evolution of SEX!


This blog was based on the following paper:

Singh, N. D., Criscoe, D. R., Skolfield, S., Kohl, K. P., Keebaugh, E. S., & Schlenke, T. A. (2015). Fruit flies diversify their offspring in response to parasite infection. Science349(6249), 747-750.

Credit to Michael Martin, Reed College, for the wasp video.

Mutant and Wild type Drosophila photograph:

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Altruism, does it exist?

Recently I was reading a paper by  Kuzdzal-Fick et al. about my all time favourite social amoeba Dictyostelium discoideum, or as I like to call them, dictys, and it got me thinking: is altruism a real thing among non-sentient beings? Altruism, as Wikipedia defines it, is “the principle or practice of concern for the welfare of others”. In biological organisms, it can be defined as “an individual performing an action which is at a cost to


The lifecycle of Dictyostelium discoideum Credit: Kessin, 2009

themselves”. Now, a little a bit of background for those of you who are not familiar with these social amoebas: dictys are a species of single-celled eukaryotes that primarily live in soil and can be found just about anywhere. When dictys favourite food source, bacteria, are readily available, they live happily as individual amoeba, but when this food source becomes scarce they send out signals to each other and begin to aggregate together. Once aggregated, they form a slug that is able to move around as one multicellular organism and then form a fruiting body. Here’s a link to a cool little video of this occurring: Dicty Lifecycle.

The fruiting body formed is composed of 80% fertile spores and 20% sterile stalk. Here is where my question about altruism comes into play. Do the 20% of dictys that become the sterile stalk sacrifice themselves to save the other 80%? Altruism is often driven by culture and religion, or by high relatedness. In this paper, the experimenters were trying to discover if high-relatedness (having a common origin) could stop so-called ‘cheaters’ from destroying multicellular populations. These cheaters work by forming disproportionately more spores, while forcing others to form more than their share of the sterile stalk, but are unable to form fruiting bodies on their own. To test this question, two experimental evolution experiments were undertaken to measure the ‘cheating ability’ of evolved lines in social competition with their ancestors. One line was constructed to have low relatedness and the other high relatedness. The results showed populations with low-relatedness had a higher proportion of cheaters than populations with high-relatedness. They also showed if a single-cell bottleneck occurred every 100 generations, cheaters that could eliminate cooperation were unable to spread.

Graph Evo

Cheating differences among low-relatedness lines & high-relatendess line  Credit: Adapted from Kuzdal-Fick et al, 2011

Does this cheating occur because dictys work in an altruistic manner or could there be another explanation? After doing some digging around in the literature I came across this interesting paper: here. This paper explained if dicty cells were lacking the copine A (cpnA) gene they were unable to form fruiting bodies as this gene is necessary in pre-stalk cells (cells that will become the stalk). This explanation that ‘cheaters’ are missing necessary genes, which results in them being unable to become pre-stalk cells, and therefore unable to form fruiting bodies, makes a lot more sense.

It is a hard to imagine these tiny single-celled amoeba are working for the ‘greater good’, but a mutation that causes them to ‘cheat’ is something I can comprehend. What are your thoughts on altruism? Do you believe dictys could be ‘performing the ultimate sacrifice which is at a cost to themselves’?

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Down the memory lane of a fruit fly

Pineapple medium or orange medium, which medium do I choose? Both of it were her favourite, zooming past the other flies, flapping her wings vigorously, Mrs. Drosophila landed on the pineapple medium. She was soon followed by Mr. Drosophila. Little did they both know that the pineapple haven which they chose to breed on had something totally amiss and that they were going to learn and remember this flavour for long time, and also pass on the experience of an bitter episode to their kids in the near future .In this blog post I have made an earnest attempt to understand views, experimental data involved in the Experimental Evolution of learning ability in fruit flies, a study conducted by Frederic Mery and Tadeusz J. Kawecki.

Learning rate and memory are two important aspects very much vital for survival and being part of an environment which is constantly at change it is necessary for any system to learn, adapt, remember and finally pass on the information to successive generations. Here in today’s post let’s discuss about the improved learning ability and better memory seen in Drosophila melanogaster when exposed to favor associative learning with regard to oviposition substrate choice. In short the experiment consisted of three phases; phase 1 known as the training period, phase2&3 called the test period respectively. Each phase was of a 3 hr duration wherein the flies were offered choice between an orange medium and a pineapple medium. The experimental population flies were supplied with both mediums, one of which contained the chemical cue quinine hydrochloride in addition to the tasty fruit pulp. From the beginning it was seen that the experimental population flies strongly avoided the quinine medium and showed drastic decrease in egg laying. The training period was meant for the flies to associate with the medium containing quinine in it and hence to learn and remember to avoid it from next generations. The 2&3rd phase known as test period was where there was no chemical cue added to either of the medium, this phase was just to determine the level of conditioning that had occurred in phase 1. For further studies, next generation population was bred from eggs laid in period 3 on the medium that had not contained the chemical cue, it was made sure that the larvae was always reared on the same medium, which precluded any kind of preference induced by larval medium. The control flies on the other hand were treated equally except they were never given quinine containing medium.

o-p medium

Fig1:Design of the experimental evolution:selection Regime in the experimental lines at even and odd numbered generations. Only eggs laid in medium 3 on one medium, i.e., orange in odd and Pineapple in even were used to breed next generation.

The experimental flies from period 1, which had tasted the bitter medium would have to learn to remember and thus avoid choosing the same medium without the chemical cue in period 3.  Within 20 generations of selection, there was significant evolutionary changes, wherein the flies evolved and learnt to avoid the medium with quinine.

Resting cycles

Fig 2: ‘‘Conditioned to avoid pineapple”means that quinine was present in the pineapple                  medium offered in period 1. The proportion of eggs laid on the orange medium was                 averaged over  period 2 and 3.

eggs laid

Fig3: Comparison of rate of learning. The response of experimental and control populations to conditioning time. Solid lines, flies conditioned to avoid orange, dashed lines, flies conditioned to avoid pineapple.

The improvement in the flies with regard to avoiding the quinine containing medium, was attributed towards faster learning and longer memory. To test the decay of the conditioning response, i.e., to test the memory of the flies, the authors also conducted an Decay of conditioned Response test wherein they observed the decline of the effect of conditioning on oviposition as the time elapsed. With respect to experimental flies it was observed that the flies laid a smaller proportion of eggs than the control flies on the medium they were conditioned to avoid.

With this study the authors concluded that the flies were able to learn and avoid the bitter medium with the chemical cue and it also commented on their memory playing vital role.

In another study conducted by the same team of researchers, Olfactory Memory in the flies was investigated, wherein the flies were conditioned with an airborne odour with mechanical shock and then tested for odour choice.  With olfactory shock task, it was pointed that a genetic variation was present which underlined the experimental evolution of learning performance which affected several phases of memory formation in olfactory aversive learning. Another aspect to look into was, which form of memory is involved in course of the experimental evolution. It has already been demonstrated that Drosophila’s memory works basically, with four distinct forms of olfactory memory. They are Short term memory (STM) which forms within seconds and decays within less than an hour, Middle term memory (MTM) which arises within minutes, reaches a peak at about an hour, and decays within several hours. Anesthesia-resistant memory (ARM) begins to form within 30min and can last for 24 hours and finally Long term memory (LTM) lasts for several days.

It was established by F. Mery and T.J. Kawecki and the team, that fruit flies have ability to learn, remember and transmit the acquired knowledge to the next generation when faced with variations, be it in any context, such as a particular stimuli as in orange and pineapple medium or particular context as in oviposition in cages or particular behaviour as in oviposition. This experiment established the fact that learning and memory gives rise to change, which in turn results in improvement and is beneficial to the species, all of these ultimately gives way to Evolution.

‘’Change is inevitable’’ every system strives for its own growth and development. The demonstration by the fruit fly to adapt and memorise opened up new prospects in the field of experimental Biology, putting the modest fruit fly on an apostle, making it an intelligent star in the insect world, and further pulling it up on top of the model organism chart. Three cheers for our dear fruit fly…




  1. Mery F. and T.J. Kawecki. 2002. Experimental evolution of learning ability in fruit flies. Proc Natl Acad Sci USA 99: 14274–14279
  2. Mery F. and T.J. Kawecki. 2003. A fitness cost of learning ability in Drosophila melanogaster. Proc R Soc B 270:2465–2469.
  3. Mery F. and T.J. Kawecki. 2005. A cost of long-term memory in Drosophila. Sci-ence 308:1148.


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Evolution in our backyard

Evolution. A quick Google search will tell you evolution is “the process by which different kinds of living organism are believed to have developed from earlier forms during the history of the earth”. That answers the what. But who is actually evolving, and when, and why?

Evolution is not about the individual, but about populations and their ability to survive and adapt to changing environmental situations. In order to survive, individuals of that population must reproduce, and in doing so pass on genetic information to their offspring. Evolution is constant, though one of the reasons it has taken so long to become a (more or less) accepted idea in society is because it is also a slow, hard-to-observe process. However, with the constantly evolving field of genetics there is now plenty of evidence to support the theory of evolution. I have recently come across a study of freshwater snails in New Zealand by Britt Koskella and Curtis Lively which provides convincing evidence that evolution, in particular co-evolution, is still occuring.

Co-evolution is a form of evolution, involving more than one species evolving together. Most often this particular evolutionary process is seen in the form of host-parasite interactions. Which is exactly what is going on here. The players in this evolutionary game of cat and mouse are tiny native freshwater snails, Potamopyrgus antipodarum, and even smaller parasitic sterilising trematodes or flukes from the Microphallus species.

The parasitic eggs are present in many of the lakes where the snails live. During feeding the snail may ingest an egg which is then able to infect and reproduce in the snails tissues, forming cysts. These cysts can replace the snails sexual organs, thereby reducing reproductive success. But it doesn’t end there. To complete the parasitic lifecyle the unsuspecting snail is eaten by waterfowl, the final host. The parasitic eggs will then go back into the water when the bird defacates, starting a new cycle.


Credit: Clipart Kid, 2016

Koskella and Lively seek “To determine whether parasite populations are able to adapt to infect common host genotypes, and whether this selection pressure on host populations is sufficient to significantly alter the frequencies of different host genotypes in the experimental population”. In plain English, the study wants to test whether evolution is demonstrated through adaptations in the parasite and the host. Because the study focuses on snail populations, this can be tested and demonstrated over a relatively quick period.

At a genetic level all snails are different. But genetics can also be used to determine which snails are the most similar. This is done through the method of genotyping. A genotype is a set of genes that are responsible for a particular trait, for example; eye colour. Check out the personal genetics education project website for more information. In this case genotyping was used to identify snails that belong to distinct clonal lineages. This has allowed researchers to determine if the genetic makeup of a snail population changed over time (i.e., whether it evolved), something which cannot be visually identified.


Experimental design

Snails were collected from Lake Alexandrina in the South Island and put in 12 different tanks. Some of these tanks were treated with parasites (recycled), and others were not (control). In order to reinfect the parasite treated snail tanks, snails were collected and analysed to determine infection status. Infected snails were then fed to mice (the final host), and the mice droppings used to reinfect the tanks with the parasite eggs. At generation zero (when the snails were collected from the lake) a subsample was taken for genotyping. Genotyping was also carried after three and six generations.


Credit: Google maps, 2016




Koskella and Lively, 2009

These graphs compare the results of the parasite treated snail tanks with the control snail tanks that had no parasites at the end of generation six. The various symbols represent different genotypes that were found, where “C” stands for genotypes that were found at a high frequency in the population at generation zero (the initial frequency), and “R” indicates genotypes that were initially rare in the population. (Red circle, C1; Purple square, R1; Yellow diamond, R2; Green triangle, R3; Orange inverted triangle, R4). Each individual symbol represents the results from one tank (population).

Based on this we can see that in the recycled population C1 was present at a frequency of 0.32 at generation zero. Over the course of the experiment this frequency decreased by at least 0.1 in most populations. In contrast the R1 genotype was not detected in the population at generation zero (initial frequency). But by generation six it had increased in frequency in all recycled populations except one.

The slope of the line in the recycled population is much steeper than that of the control, which is almost horizontal. This suggests that there has been a greater change in the frequency of genotypes in the population of experimental snails compared to the control. Indeed statistical analysis concluded there was significant negative frequency-dependent selection ocurring in the parasite infected population and that there was no significant selection process ocurring in the control tanks. This means that the most common genotypes were being selected against in the recycled populations.

This study shows that the most common snail genotype (C1) was being targeted by the parasites as the change in frequency of C1 in most recycled populations was negative. This then allowed other rarer genotypes (such as R1) to become more common in the population, as seen by the mostly positive change in frequency for initially rare genotypes in the recycled population. Though the experiment did not continue past the sixth generation we can speculate that the parasites would eventually begin to target the new common genotype (R1), this would then allow another genotype to become more prevalent in the population. Thereby continuing the cycle.

But this doesn’t just happen in a controlled lab environment. The researchers went back to Lake Alexandrina towards the end of the experiment and collected another set of snails from the same site for genotyping. Genotype C1 was significantly less common in the newly collected field snails compared to the control experiment snails, but there was no significant difference in the frequency of C1 between the parasite infected experimental snails and the freshly collected field snails. This suggests that the field population may be evolving in a similar way (C1 becoming less common) to the lab populations, but at a slower rate.

For further details and more information on the other experiments performed, check out the paper; Evidence for negative frequency-dependent selection during experimental coevolution of a freshwater snail and a sterilizing trematode, by Britt Koskella and Curtis Lively, 2009.


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