Interbreeding humans: The Sassy Palaeolithic Action

Posted on March 14, 2014 by Danae Dodge

Are you confused about the different types of humans that got it on with each other?
If you are, then in this blog entry, I provide a summary factsheet style of the pairs of hominids that interbred with each other, with evidence for and against it, and the current conclusion. All dates are expressed as years before present, and be aware that in the field of ancient DNA, human contamination is always an issue that can potentially confound the results.

Hominid Action Pair #1:     Neanderthals     +        Humans: Non-Africans
Home-turf:    Europe/Asia                       Global
Lived from:                        400,000 – 30,000             200,000- present
When and where:                     47,000-65,000 Middle East
Evidence for getting it on: If the different colours represent different genetic make-up, then the answer to the question “Where did the modern humans get their genes from?” can only be “from mating with Neanderthals”.

Evidence against getting it on: This model clearly produces the same pattern but without mating.

Current status: The literature arguing against interbreeding has been focused on the pitfalls of the method used. Nevertheless, new methods are now confirming that Neanderthals and humans were up in a tree K.I.S.S.I.N.G. Now, we are starting to identify what genes we got from them.

Hominid Action Pair #2:         Denisovans      +      Humans: Asians/ Oceanians
Home-turf:                       Siberia (Tropics?)                       Oceania
Lived from:                        ? – ~50,000                       200,000- present
When and where:                      S.E Asia and prior to 44,000
Evidence for getting it on: It’s the same case as the evidence for mating between Neanderthals and humans, except here the genes that went into the ancestral populations of the Aboriginal Australians, Near Oceanians, Polynesians, Fijians, East Indonesians, and Philippine Mamanwas and Manobos can only have come from the Denisovans.
Evidence against getting it on: While models are presented in the literature for discussion, they have been argued against. The consequence of which is that the results are described as a best fit to the data.
Current Status: We know that the action took place BUT we don’t know enough about the Denisovans. We only have a tooth and small finger bone from a Siberian cave. Watch this space!

Hominid Action Pair #3:              Denisovans       +         Homo erectus?
Home-turf:                              Siberia (Tropics?)        Africa, China, Indonesia
Lived from:                                 ? – ~50,000               1.9 million years- 150,000
When and where: ? and Asia?
Evidence for getting it on: The Denisovan tooth has some features that you can find in some of the older Homo species, and the DNA appears to also look quite archaic. Homo erectus was widespread across Asia, so it does seem likely that the two hominids crossed paths.
Evidence against getting it on: At the minute, there isn’t any. This model was proposed as the most likely scenario to a result that arose from another study.
Current Status: As already said before, we don’t know that much about the Denisovans. There are still a lot of gaps making this a hypothesis.

Hominid Action Pair #4:             Neanderthals        +       Denisovans
Home-turf:    Europe/Asia              Siberia (Tropics?)
Lived from:                                400,000 – 30,000              ? – ~50,000
When and where:                                    ? and Europe/Asia?
Evidence for getting it on: Evidence against getting it on: Not presented.
Current Status: This has just recently been published, and the amount of DNA material from the Neanderthals into the Denisovans is calculated to have been very small. More analyses will have to be done.

*********************************

Summary
Here is a final tree summarising the relationships between the hominids, and the arrows indicate where interbreeding took place. Adapted from Prufer et al 2014.

While I used a lot of literature to create the above summary, if you are looking for more information then I recommend Veeramah and Hammer 2014, Nature Reviews Genetics 15, 149-162 as it provides an up to date informative review while also including relevant references.

Science on the Origin of Life

Posted on February 5, 2014 by Jenny Ventress

Since the dawn of civilisation and the dreaming up of our early creation myths, the philosophical and scientific debate of the origin of life has enchanted people worldwide. Since the thousands of years when early man prayed to sky gods have we got any closer from determining how life originated on earth? And can we even prove any of the theories through the scientific method?

The most widely held theory is that of abiogenesis. This is the idea that the conditions present on early earth when life was beginning, such as the electrical activity and dense atmosphere, resulted in the spontaneous creation of the building blocks of life. When these early conditions were replicated in the lab, in the iconic Urey-Miller experiment of 1953, some ingredients for life, such as amino acids, were seen.

The one major problem with this theory is that just as in cooking, adding the ingredients together doesn’t automatically make the meal. Life is amazingly complex and intricate. Having the building blocks doesn’t account for how they organised themselves into the patterns that can be call life.
Scientists are working to fill in this gap, producing theories based on the original abiogenesis. These ideas attempt to explain how order was achieved. These include the Deep Sea Vent hypothesis, the Coenzyme and RNA world hypothesis, and the Iron-Sulfur World theory. Other theories stray away from the abiogenesis idea, such as Autocatalysis Clay hypothesis, Gold’s “Deep-Hot Biosphere” model, Lipid world and Polyphosphates, to name a few.

One theory looks beyond the earth for the origin of life. This is known as panspermia, the theory that life originated in space. The main proof behind the theory is the presence of dead microbes and fossils found in debris in the stratosphere. However this evidence has faced harsh criticism from the scientific world.

There are many questions yet to be answered by Panspermia. In the theory, life, in the form of microbes, came to earth piggybacking on meteors and asteroids. How did the microbes survive the harsh conditions of space, and the harsher conditions whilst entering or exiting the atmosphere? Where did they come from? How did they then survive on a barren planet enough to divide and evolve? This theory doesn’t really solve the fundamental question of where life originated, but it does extend the time for which life can form over. In the history of the universe, earth is relatively new.
Science is yet to form a watertight theory on the origin in life, and there is question if it ever will. The many different ideas debate over which is the closest to what events occurred millions of years ago. Without concrete evidence all we can do is continue to develop these ideas based on theories and assumptions.

Neolithic Revolution in the air!

Posted on December 2, 2013 by Danae Dodge

THE NEOLITHIC REVOLUTION WAS A KEY MOMENT IN THE PREHISTORY OF HUMANS. It sparked civilisation as we know it- settlements were established, crops were grown and animals were domesticated transforming the economy of subsistence globally. Beginning in the Levant (Near East) around 12,000 years ago, the Neolithic Revolution spread into Europe 8000 years ago and lasted up until 4000 years ago when the Bronze Age began.

The major question is how did this revolution spread? Did the indigenous hunter gatherers adopt farming solely though cultural transmission? Or did the farmers pass on their practices alongside their genes? These two models (see diagram) – culturally diffused model (CDM) and demic diffused model (DDM) – originally seen as two polar opposites as mechanisms of the spread, have been debated throughout the 20^th century. By identifying the proportion of Mesolithic/ hunter-gatherer and Neolithic/ farmer genes within the current gene pool (see diagram), the correct model could be identified.

Classical genetic markers in present day populations (such as blood groups) appear to lend support to the DDM revealing a genetic cline from the Near East towards the West. But modern genetic markers can reflect population processes that have taken place both before and after the Neolithic spread. Instead ancient DNA (aDNA) provides a unique window of opportunity to look back into the past. Ancient DNA studies do come fraught with difficulties. Over time DNA degrades and fragments into short molecules. Usually this means any contaminating modern DNA is favourably extracted and analysed instead. Nevertheless strict and rigorous protocols exist to minimise contamination and new technology has been optimised for aDNA extraction.

The archaeological record has shown that as farmers migrated across Europe, two different routes were taken as indicated by distinct ceramic styles. One route was through Central Europe, from Hungary to Slovakia, Ukraine and through to Paris, as shown by the Linearbandkeramik (LBK) and Alföldi Vonaldiszes Kerámia (AVK) pottery styles. The other route represented with Impressed Ware/Cardial culture was along the Mediterranean coast. aDNA studies have been conducted on samples from these different sites and cultures, and the picture that emerges is one more complex than just picking one model over the other. It certainly appears that the two routes have their own model: while the Central Europe/ LBK route shows little to no genetic continuity between the Mesolithic hunter-gatherers and the Neolithic farmers, the Mediterranean route tends towards genetic continuity and therefore a level of gene flow between the two populations, a pattern which even seems to lead up into Sweden.

But this most certainly is not the end of the story. For one thing, the genetic studies carried out were analysing the mitochondrial DNA (mtDNA), which is inherited solely down the female line (men inherit their mothers’ mitochondrial DNA but will not pass it on). In one study, it was found that of Spainish Neolithic samples while the mtDNA belonged to hunter gatherer groups from the Palaeolithic, the Y chromosome was shown to be from the Neolithic Near East. This does seem to suggest that the role of men and women during the advance of the Neolithic differed to some extent. Additionally, it also appears that the change to farming practices did not happen as rapidly as expected, and was not as clear cut. In two recent papers (with a particular focus on Germany), it was found that hunter gatherers and farmers lived alongside each other for about 2000 years and, interestingly while the Mesolithic hunter gatherers and the Neolithic farmers had their own distinctive gene pools, at some point in the Neolithic there were intermediary groups with shared ancestry and lifestyle undoubtedly reflecting the transition that was taking place.

There is a level of difficulty when studying the past; we cannot always state processes or cause and effects with a perfect degree of certainty, but we can say what the evidence appears to suggest, and in this case it appears to suggest a high a degree of complexity as the Neolithic Revolution took hold. There is never just any one specific model that can answer our questions, and there will always be other lines of evidence to explore. To answer the original question how the Neolithic Revolution spread cannot be placated with just one simple answer. It is never that easy. But as aDNA analyses show, we can still get one step closer to that very complicated answer.

More information:

Bollongino et al 2013 Science 342 (6157) 479-481

Brandt et al 2013 Science 342 (6155) 257-261

Gamba et al 2011 Molecular Ecology 21 (1) 45-56

Haak et al 2005 Science 310 (5750) 1016-1018

Lacan et al 2011 PNAS 108 (45) 18255–18259

Pinhasi et al 2012 Trends in Genetics 28 (10) 496-505

Skoglund et al 2012 Science 336 (6080) 466-469

Reproduction Revamp: Stick Insects and Going It Alone.

Posted on November 21, 2013 by Marni Brennan

125227306.pX5ldchw

Timema cristinae: making a lack of a love life cool.

Love can be tough. If you wish awkward dates and trawling through match.com were a thing of the past, you could take a leaf out of this stick insect’s book. Tanja Schwander (University of Lausanne) studies how Timema stick insects are changing the dating game. Rather than reproducing with a partner, female Timema have developed the ability to produce offspring individually. There could be a number of causes for this bizarre transition from sexual to non-sexual offspring production, so read on for a how-to guide in ditching dating.

Conversion to non-sexual reproduction may occur genetically. When female Timema are prevented from mating, some eggs that haven’t been fertilised by sperm hatch and develop. Could this virgin birth scenario, reminiscent of biblical times, replace sexual reproduction in Timema? Or are virgin births merely a strategy to ensure female stick insects can carry on their line when opportunities to mate are thin on the ground?

Alternatively, a type of bacterial infection may stimulate non-sexual reproduction. Infecting bacteria are only transmitted through the female sex cell, the egg, and so males slow the spread of the bacteria. In light of this, the bacteria devised a cunning strategy to eliminate males: inducing a kind of non-sexual reproduction that produces only female offspring. Could bacterial infection be the instigator of non-sexual reproduction?

Schwander’s studies of genetic data reveal the virgin birth scenario cannot explain the change in Timema reproduction. Conversion to non-sexual reproduction may occur genetically, but not via virgin births. To determine if bacterial infection causes the stick insect’s lack of libido, Schwander cured the infection. This restored sexual reproduction and production of male offspring, proving bacterial infection can result in non-sexual reproduction. Watch this space; could Boots’ next bestseller be bacteria to eliminate human males?

The rise and fall of the slasher dinosaur

Posted on November 18, 2013 by Jenny Ventress

Almost every child goes through a dinosaur phase. In some cases, it’s a frenzied week of roaring and leaving spiky plastic models all over the floor, before a combination of sore feet and a sore throat drive you onto the next stage of development. In my case, it lasted about 5 years. I owned sacks of dinosaur toys, a library’s worth of dinosaur books, and irritated my friends by criticising the accuracy of their dinosaur games (You can’t play with a dinosaur from the Creataceous and a dinosaur from the Jurassic at the same time. You just cannot.) Eventually, peer pressure made me decide that dinosaurs were for little kids, and I forgot about them for a decade or so.

But last year, I took a module in Palaeobiology– the study of extinct organisms– as part of my degree. I was back in the realm of dinosaurs– older, wiser but still embarrassingly excited. Then as I delved deeper into my external reading, I found some papers that shook my world, shattered my dreams, and generally slapped my childhood in the face. My dinosaur books had been lying to me about my favourite dinosaur of all time: Deinonychus.

Deinonychus (pronounced Die-NON-ik-uss) was a mean guy. Resembling its smaller, superstar cousin the Velociraptor, Deinonychus nonetheless has its own claims to fame.

This particular specimen is a bit of a deviant, judging by his facial expression and his public nudity (we now know that Deinonychus probably had feathers)

This guy has a far more modern dress-sense

Before the 1960s, scientists took a pretty dim view of dinosaurs. The consensus was that they were all stupid, sluggish and cold-blooded, and probably died out because they couldn’t cope with the same challenges that we sleek, sexy mammals can. But that view started to fall apart when John Ostrom took a closer look at Deinonychus. He suggested that these animals were speedy, intelligent pack-hunters who worked together to bring down large prey, using the fearsome sickle-shaped claw on each foot to disembowel their victims. Like wolves. Slashy Captain Hook wolves. This image of Deinonychus helped create a revolution in the way that we think about dinosaurs, and it was still championed in all my dinosaur books. As the sort of child who didn’t bat an eyelid at the bloodiest scenes of Watership Down, it inspired me. Over several years, I built up a portfolio of really creepy drawings of dinosaurs killing each other, made with nothing but a pencil and a red felt-tip pen, and ravaging packs of Deinonychus featured heavily in my “art”. On reflection, I feel lucky that my parents didn’t refer me to a child psychologist.

But in 2006, long after I’d abandoned dinosaurs in favour of blushing at teenage boys, some scientists decided to test out the theories about those fearsome feet. Phillip Manning and his team built an accurate hydraulic model of a Deinonychus leg, complete with terror-claw, and made it kick a pig carcass that had kindly volunteered to play the part of an herbivorous dinosaur. Yet far from slicing the carcass into ribbons of sandwich ham, the claws were AWFUL at doing any sort of tearing damage. Instead, they created small shallow puncture wounds that did very little to the surrounding tissue, let alone the internal organs. Not so much a river of blood and gore, then: if Deinonychus behaved like my books said, then the herbivores probably walked away with mildly painful wounds that cleared up in a week. Something else was going on with these bizarre claws. Stumped, Manning suggested that Deinonychus could have used its claws like crampons, allowing it to climb onto the backs of large prey and attack from there. So my vision of dramatic battles between massive herbivores and a fearsome pack of predators wasn’t totally shattered… yet.

It was thanks to a guy called Denver Fowler that my artwork really faded into fantasy. He noticed that modern eagles and hawks—known as raptors—also have one claw bigger than the other on their feet. However, you’ll never see a pack of eagles descending onto a cow in a field and slashing it to death, neither do they need climbing aids. These birds hunt by swooping onto smaller animals, then pick them to bits with their beaks, often while the prey is still alive. A struggling animal could be very dangerous to a bird of prey, potentially breaking its fragile bones, so it’s vital for the raptor to keep it pinned down firmly. This is where that claw comes in. By clamping down with their powerful modified talon, raptors immobilise their prey, allowing them to concentrate on their (very fresh) meal without distraction. Fowler compared the feet of raptors with those of their ancient cousin, Deinonychus, and found many similarities in their anatomy. The flexibility of the toe bearing that large claw may have come in handy not for delivering slashes… but for swivelling down into a death grip on small prey. That’s right—small prey. Those epic clashes I’d envisioned between huge herbivores and fierce little predators seemed less and less feasible.

So how did Deinonychus ACTUALLY live? Fowler envisions a solitary predator that pursued animals smaller or similar to its own size at high speed. It would then pounce on top of its victim and press it firmly to the ground, channelling its bodyweight through the tip of the powerful sickle-claws to prevent escape. Then it would have leaned forward and proceeded to rip its squirming dinner into bitesize chunks—gory, but not quite the image I’d held. Fowler hadn’t gone as far as to demonstrate that my favourite dinosaur was a peaceful vegetarian, but I have to admit—he’d stolen just a little bit of its badassery. This doesn’t mean Deinonychus stops being cool, though. In fact, it could teach us a lot about the early days of its modern relatives: the birds.

Fowler compared modern raptors with Deinonychus once more, and noticed how, when perching on struggling prey, raptors often beat their wings vigorously. This keeps the bird in a prime position on top of the prey, making sure its victim stays pressed to the ground. We’ve known for a while that many predatory dinosaurs like Deinonychus had feathers on their skin– perhaps the first chink to appear in their armour of terror. But scientists have long argued about how the particular lineage of feathery dinosaurs that evolved into birds first developed the “flight stroke”—the special high-powered downbeat of the wings that creates lift. Looking at Deinonychus inspired Fowler to come up with a new theory. If dinosaurs also stability-flapped their feathered arms when making a kill, over the generations, it could have selected for greater upper body strength and the ability to beat the arms hard and fast– features that would later come in very useful when their descendants took to the air. Although Deinonychus was not a direct ancestor of birds—it appeared long after the first flying dinosaurs—it was closely related to them, so it’s likely that they shared similar behaviour. So by looking at how Deinonychus might have hunted, we can take steps in unravelling one of the biggest, most controversial mysteries in all of Palaeobiology.

In future, then, perhaps we’ll look back on Deinonychus as triggering a second revolution in how we see the dinosaurs. If I told that to my 7-year-old self, I hope she’d have been consoled. Deinonychus… you might not be the psycho-killer of my imagination, but you’re still cool to me.

Originally posted at http://notazookeeper.blogspot.co.uk/

Image credits:
Naked creepy Deinonychus: By Mistvan (Own work) [GFDL (http://www.gnu.org/copyleft/fdl.html) via Wikimedia Commons

Fluffy Deinonychus: By Peng 6 July 2005 16:32 (UTC) (selbst gemacht –Peng 6 July 2005 16:32 (UTC)) [GFDL (http://www.gnu.org/copyleft/fdl.html) via Wikimedia Commons

Twitter

Posted on March 17, 2010 by admin

I am on twitter. @timcdlucas. I will try and let people know on twitter when I write a new post. Might be easier than RSS for some people. Who knows.

Science Brainwaves are also on twitter. @SciBrainwaves. They are doing good regular updates of interesting bits of science news.

The Evolution of Cooperation 3: Mutualism

Posted on March 16, 2010 by admin

“By virtue of exchange, one man’s prosperity is beneficial to all others.”
Frederic Bastiat

Mutualism is quite an alien concept to us humans. In evolutionary terms it is not a good-for-group idea. Nor is it a “scratch my back and I’ll scratch yours” arrangement (I will discuss this in the next post). Surprisingly, it is also completely selfish.

Mutualism is any process or behaviour where both parties make gains which immediately outweigh the costs. Sometimes this is because the costs are virtually nothing. I am struggling to think of more than one example of mutualism in human society, but it is in fact so common it is hard to see it in this light. Trade in humans is nearly always mutualistic. If it is not mutualistic we think of it as either a con or charity, depending on who benefits. So, how is trade mutualistic? The fact that both parties benefit instantly means they must have different needs and assign different value to whatever service or good is being traded. So, a shopkeeper buys chocolate bars in bulk. Lets say they cost £10 for 100 at a cash-and-carry, bulk buy type place. So the bars cost 10p each and the shop keeper sells them for 50p. As the consumer, 50p isn’t much to pay for a chocolate bar. You want a snack and it would be more expensive to buy 100 bars from the cash-and-carry even though they are cheaper per bar. So you are getting a good deal, you would probably pay 60p for the chocolate bar, but it is only 50p. The shopkeeper paid 10p for the chocolate bar so is also getting a good deal. For both parties the benefits (50p to the shopkeeper or a chocolate bar to the consumer) immediately outweigh the costs (10p to the shopkeeper or 50p to the consumer). This then is a true mutualism.

Mutualism then is actually an extremely simple idea. Both parties benefit instantly. Easy. However, the situations in which it occur are harder to understand. There are other mutualisms in human society. When bands play together, especially at smaller gigs, often a out of town headliner will play with a local support band. The support band get to play with a more famous band and get more exposure in their own town. The headliner gets a guaranteed crowd due to the fans of the local band. Everyone wins.

Hornbill Mycorhizza

Above: (left) A hornbill eating some fruit and so dispersing the seeds. (right) Mycorhizzal fungi on a plant root.

What about the natural world then? There are many, many examples of mutualisms in the natural world. Humans generally need the same things. Food, money, a house. As organisms are all so different, with different food sources and different needs, mutualism is more common. For example, plants need their seeds to be dispersed (but often have plenty of food, as they make it from carbon dioxide and sunlight). Animals on the other hand often need food. So plants and animals have a form of mutualistic trade. Plants produce fruit, a good food supply for animals. When the animal eats the fruit the seeds get carried around and dispersed. Plants have plenty of food and animals move around anyway, so the costs are minimal. The benefits to both (food for the animal and seed dispersal for the plant) are enough to instantly outweigh the costs.

Many plants have mycorrhizal fungi attached to their roots. Again, plants have plenty of food because they make it themselves. The fungi are particularly good at absorbing water. Plant growth is often limited by the amount of water they can get while fungi are often limted by the amount of sugar. So they trade. The fungi live on the plant roots and give up some of the water that they absorb. In return they get some of the sugar that the plant makes. The cost of water is low to a fungus and high to a plant while the cost of sugar is low to a plant and high to fungus. Because they have different needs, the trade is beneficial to both parties.

We humans also have mutualisms. The bacteria in our gut (the ones that yoghurt adverts insist on calling “friendly bacteria”… pah!) can digest cellulose. Cellulose is the carbohydrate that makes up most of the structure of plants and human cells can’t digest it. We provide the bacteria with a warm, wet place to live. In return the bacteria digest our cellulose for us. Once again, everyone wins.

So that is mutualism. I’ve said that science is made interesting by paradoxes. Mutualism is not a paradox, and so is not the most exciting thing in the world. It is however all around us and some of the most important groups of organism have got where they are due to mutualisms. Animals and bacteria, plants and fungus, termites and digestive fungus, coral and algae. Wherever you look mutualisms abound. However, in the next post I will discuss another paradox. How does evolution evolve when the benefits don’t immediately outweigh the costs, when some individuals can cheat or when the quest for quick gains disrupts long term cooperation.

The Evolution of Cooperation 2: Group Selection

Posted on March 12, 2010 by admin

“Do you live for the good of the tribe, Stilgar?”
“There is no other way.”
“And for the good of the tribe would you let me stab this knife into your heart?”

Frank Herbert – Dune
Normally I wouldn’t bother writing about group selection because as an idea it is dead and gone as far as I, and most evolutionary biologists are concerned. However, I started reading this blog about group selection. I thought I would write about group selection for a few reasons. Firstly, it’s on my mind at the moment so hopefully the post will be quite good. Secondly, the link provides a good “other side of the story”, so hopefully a couple of readers might immerse themselves in the debate. Finally, many members of the public might intuitively see group selection as plausible. This is not something to be ashamed of. A certain Charles Darwin thought it was the best explanation for some social behaviour. Do a biology degree however, and group selection is blasphemy. Because of this it is easy for biologists to lose sight of what an intuitive idea it is.

Two groups of people go into two shops. One of the groups are well versed in the wonderful British institution that is queuing. People politely accept their position in the queue for the tills and everyone gets served quickly and efficiently. In the other shop it is a free-for-all (you might have experienced this in France/Italy. It is very disconcerting.) and because of all the scrummage everyone actually takes longer to pay. However, if anyone in the free-for-all shop tried to form a queue, they would be the last to pay. In the polite shop, if someone skipped the queue they would get their goods quicker than if they joined the queue, but this would increase the time it takes for everyone else to do their shopping. This is the crux of group selection. Group selection says that a group with a behaviour that is for the common good will reproduce faster than those without this behaviour. As long as the selection between groups is stronger than the selection within groups the cooperative behaviour will spread through the population, even though anyone who behaves selfishly will do better than the rest of their group.

The great, British queue

The counter argument is that whenever an individual is selfish in a non-selfish group (pushing to the front of the queue), this selfish behaviour will spread through the group. Soon there will be no cooperative groups to even compete with the selfish groups. The selection within groups is stronger than the selection between groups.

Despite what some might say, there is an issue of semantics now. Originally, group selection was supposed to work in the same way as individual selection. Instead of the best individuals surviving and reproducing, the best groups survived and reproduced. Now however, the thinking goes that genes are the unit of selection but if group living allows a social behaviour to evolve, this is also group selection. In other words, group selection can only work when gene level selection says it can work anyway. Some say this is group selection and a highly useful scientific advance. Others say, whats the point in worrying about group selection when gene level selection tells you exactly the same thing? The important addition to this is that gene level selection will never give you the wrong answer. If you make a model and gene level selection says something can evolve, it can evolve. With group level selection however, a model might give you the wrong answer. The only times it will give the right answer in fact, is when you arrive at the gene level selection model, but from a different standpoint.

Furthermore, the “group” is a very fuzzy concept. Since the 60s the idea of an individual has been very carefully scrutinised to the point where an individual or even a cell counts as group. What used to be a group is now a lose nit group. Bigger units, all the way up to the entire earth, can be considered losely bound groups. Everything down to chromosomes can also be considered a group, albeit a tightly nit one. The gene on the other hand has a quite precise, consistant definition. This just leads to more mistakes and fuzzy thinking. Most group selection models consider selection between groups and compare it to selection between individuals. If selection between groups is stronger than selection between individuals group selection can occur. But individuals are now another type of group. So we need to consider individuals as groups as well as our original group (as kin selection essentially does). Eventually you end up considering genes to be “individuals” and everything else a group. Then you have a gene level selection model, albeit in an interesting social setting. Why not start with the gene level model? The maths ends up being easier and you can’t make mistakes.

I intend to write more on the definition of an individual soon. Until then I hope you read DS Wilsons blog and see what you think. The section on Dawkins is an interesting insight into the slightly more personal side of science.

The Evolution of Cooperation 1: Selfish genes and helpful family

Posted on March 9, 2010 by admin

“I, I, I is the refrain of my whole life, which could be heard in everything I said.”

Albert Camus – The Fall

This is the first instalment in what will hopefully become a series of blogs (six or so) about the evolution of cooperation. I mentioned before that science is made more interesting by paradoxes. Cooperation is the ultimate paradox of evolution. How does “survival of the fittest” end up with people helping each other? And we do see cooperation in nature. Below are two examples. The first is a moray eel allowing a cleaner fish to eat the debris from its mouth. In the second picture are the extremely cooperative bees. A worker bee will sacrifice its life for the hive, and nearly all worker bees sacrifice all opportunities for reproduction for the good of the hive.

Natural selection favours genes that make more copies of themselves than other genes do. This gene level view of evolution is commonly known as the Selfish Gene Theory and is the cause of more misunderstandings than nearly any other biological concept. In this post I will try and debunk a couple of myths about The Selfish Gene Theory and then let it shine as a theory that explains things that are hard to understand without it.

Surprisingly, the Selfish Gene Theory is not particularly about genes being selfish. The main idea of the Selfish Gene Theory is that evolution acts at the level of genes and not the level of the individual or the group. What this means is that a gene will only become more common if the function of the gene increases the average number of copies of that gene. If a gene increases the success of the body that holds it, at the expense of the genes own interest, it will rapidly disappear from the population. The Selfish Gene Theory is about the level of selection (as genes are the level of selection, only they can be said to be truly selfish). It is not about genes wanting to be selfish or being able to make conscious ethical decisions. I will often use phrases like “genes want to make copies of themselves”. This is not true as genes don’t ‘want’ anything. They are molecules without the ability to think. However, it makes for easier reading if I talk about what genes ‘want’ rather than the passive act of genes spreading. Genes don’t ‘want’ to make copies of themselves, the genes that do make copies of themselves will become more common. Selfish Gene Theory is also not about people being selfish or suggesting that people should be selfish. In fact, it provides one of the best explanations as to why humans or any other organism may not be selfish.

The purpose of a scientific theory is to explain how the world works. The Selfish Gene Theory helps us understand why organisms are often not selfish. That sounds backwards but it is true. Only when we really accept that genes are selfish can we understand why individuals may not be selfish. A gene does not really care if the body it is in lives or dies. As long as it creates more copies of itself it will become more common. Therefore, if a gene makes the organism it is in help organisms with that same gene, this gene may well become more common. This is called kin selection and is an example of selfish genes creating unselfish individuals.

A sibling falls into a river. You know you can save them, but at the cost of your own life. There are clearly ethical discussions either way, but in terms of creating the most copies of your genes what should you do? Put another way, will a gene that makes you more likely to dive in to the river become more common? On average, you share half your genes with your siblings. So if you save your sibling, there is a 50% chance that you have saved a copy of the “save your siblings” gene. Your death comes at a cost of 1 copy of the “save your siblings” gene but saves on average 0.5 copies of the gene. This gene will be removed from the population fairly rapidly as it is running on a loss. If you buy 50p for a pound, it doesn’t take long to run out of money.

What if 3 siblings fall into a river? You can save them all, but at the cost of your own life. The gene for this behaviour will become more common. You save 1.5 copies of the gene (on average 0.5 copies in each sibling), and only lose 1 copy (like buying £1.50 for £1). This is kin selection and it means the gene will spread. If a behaviour increases the number of copies of itself by helping relatives (who may well have that gene) it will spread, even if this is bad for the body that the gene is sitting in.

So, kin selection is an explanation for why family members may help each other, even at their own expense. It relies on the fact that as long as a gene makes more copies of itself it will spread. It doesn’t matter if the copies are in the same body or in different bodies. Finally, I will add that Richard Dawkins did not suggest the Selfish Gene Theory (as he always makes sure to point out). It was developed by some of the great biologists of the 20th century, W.D. Hamilton, John Maynard-Smith, George C. Williams (probably the best beard in biology) and others. This is then my little dedication to some of the scientists that have inspired me and enriched my life so much.

Why do diseases make us ill?

Posted on March 7, 2010 by admin

“And I will smite the inhabitants of this city, both man and beast: they shall die of a great pestilence.”

Jeremiah 21:6

Why do diseases make us ill? Why do some diseases kill us outright? As with many biological questions this is really two questions. Firstly, “What chemical and biological processes are happeningin our body that makes us feel ill?” Secondly, “What evolutionary gains does a disease get by making us ill?” These two questions are asking about different things known as the proximate and ultimate answer. The proximate question is looking for the mechanism that makes something happen. The ultimate question is asking why that mechanism has evolved in the firstplace.

Why are humans so intelligent? Here again we have a proximate and ultimate question. Proximately, humans are intelligent because we have large brains. Our brains fold in a way that allows more connections to be made and this also increases our intelligence. You can find the answer to this proximate question by finding a willing volunteer, cutting their head open and having a look inside (or maybe looking in a text book). For the ultimate question, we have to look into our past and try to understand whether higher intelligence perhaps allowed humans to hunt and forage better? Or maybe it helped us live in groups, which meant we could fight rival groups better? The point is, there are often two questions hidden in a single biological question.

So then, why do diseases make us ill? I am most interested in the ultimate question here because it is a paradox, and that’s when science gets exciting. It is a paradox because diseases are spread by their human host. If the human dies, or sits in bed with a lemsip, they are not out and about spreading the disease to new hosts. If a new disease arrives in a country, infects one person and promptly kills them, that is the end of the disease. If instead the disease arrives in a country and keeps the one host alive, the infected person wanders around, sneezing near people, kissing their partner(s), shaking hands with work associates etc. etc. The disease spreads.

Only diseases that keep their hosts alive will spread. All the diseases that have ever infected just one person are gone and forgotten. So, this is the paradox. We see many diseases that kill their host quite quickly, and a few that kill their host very quickly. The best thing a disease can do however, is never kill its host (this is called low virulence). So what’s going on?

The classical answer for this problem is that highly virulent diseases are just less evolved. Diseases like colds that do not kill their host have had a long time to evolve so they have evolved low virulence. More deadly diseases such as malaria must therefore have starting infecting humans much more recently. However, the very high speed of disease evolution makes this theory quite unlikely. However, slightly turned on its head, this theory becomes useful. Maybe diseases aren’t adapted to living in humans at all. It seems likely that many diseases that kill humans are not really ‘human diseases’. The Ebola virus is a good example. In humans it is fatal. However, it is likely that it is not a human disease at all, but a bat disease. It is not lethal to bats, and so is a successful disease. On occasions however, it gets spread to humans. It is not adapted to living in humans and so ‘accidentally’ kills its host.

Another theory comes from the idea of trade-offs. Trade-offs are very common and very important in biology for much the same reason as they are important to humans; we have limited resources. I like reading, but I also like walking in the Peak District. However, I have limited time. Going for a walk indirectly reduces the amount of reading I can do. So I try to find the right balance. I still don’t read as much as I would like, or do as much walking as I would like, but I do the best I can. What then are the trade-offs that affects virulence?

Transmission is how well a disease can spreaditself to other hosts. It depends on many things such as how many copies a disease makes of itself in its host. The more malaria bacteria in the blood,the more likely it will be picked up and spread by a mosquito. However, these bacteria need nutrition, and so the more bacteria, the more of the bodies resources they use and the more ill the host becomes. Here then is a trade-off between transmission and virulence. The balance found by diseases depends on many things such as how densely populated the area is and whether the disease is spread by contact, by animal vectors or some other means of transmission.

This then explains why some diseases are quite fatal, whereas others are benign. It is an ultimate explanation. I don’t know much about the specifics of how malaria kills people or how the common cold avoids killing its host, but I know that they are both struggling with a trade-off between transmission and virulence. This trade-off is (ultimately) why some diseases make us slightly ill and some diseases kill us very rapidly.