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.
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*…
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:
- 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!
- They only have four chromosomes. Their genetic makeup is super simple, but uber useful because their genes are similar to humans.
- 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.
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. Science, 349(6249), 747-750.
Credit to Michael Martin, Reed College, for the wasp video.
Mutant and Wild type Drosophila photograph: http://phys.org/news/2015-08-fruit-flies-sick-offspring-diverse.html