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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

“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.

HornbillMycorhizza 

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

“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

“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.
 
A picture of a cleaner fish Some Bees
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?

“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.

 

Heathland Restoration

Go back 250 years and beautiful heaths and remote moors covered much of Britain. Visited by characters from many well loved classics, such as The Hound of the Baskervilles, Pride and Prejudice and Tess of the d’Ubervilles, these atmospheric, but highly diverse habitats are an important part of British heritage and culture. On top of this, heaths are popular leisure areas for hikers, bikers and grouse shooters, who bring money into the local area. However, many heaths are being lost by increasing demands for new farmland. Professor Jane Memmott, leader of a team researching heathland restoration at the University of Bristol gave a seminar to the Animal and Plant sciences department in Sheffield discussing new approaches to combating damage to heathlands.
Memmott argued that an ecosystem such as a heathland is like a machine, with many working parts that do different jobs. Animal and plant species, the birds, the bees and the buttercups, are the cogs and gears of the machine, each with its own role to play. Exhaust pipes remove fumes while axles let car wheels turn. On a heath, bees pollinate flowers, buttercups turn sunlight into food and nightjars eat insects which would otherwise swarm everywhere.
Attempts to restore animals and plants that have dissappeared from heaths have begun, despite the problems caused by continuing demands for farmland. The restoration of habitats is a difficult prospect but Memmott’s team are leading the way in developing new tools for applied ecologists. The most important of these tools is the food web. Food webs have many invaluable applications, such as being able to predict the effects of removing a pest species.
The challenges facing heathland restoration are threefold. Firstly, the ‘fuzzy target problem’ is that we have limited knowledge of which animals and plants lived on a heath before it was turned into farmland. If we do not know what it is we are restoring, how can we know if we are succeeding? Secondly, the ‘moving target problem’ is that heaths are constantly changing, and so even if we knew what a heath was like before farming, how can we know what it would be like now had it not been damaged? Finally, the ‘experimental design problem’ is that every area of heath is different, even if they are quite nearby. In more extreme cases such as tropical rainforests, each tree has its own set of insect species! How can we do proper scientific experiments, and thus backup any claims of successful restoration, in a world where each area is unique? These are some of the problems being tackled by Memmott’s team, especially in their restoration research in the Dorset heathlands. A large focus of this work is the utility of food webs for practical ecologist.
What to restore?
One way of dealing with the problems caused by the the ‘fuzzy target problem’ may be to define our targets (what we hope to be left with after restoration) in a different, more flexible way. Instead of focusing on the individual animal and plant species, argues Memmott, we should aim to restore the roles (such as pollination or herbivory) that they played  in the heathland ‘machine’. This avoids the fuzzy target problem by creating a new target that is common to many areas of heathland. If a car engine needs to be replaced, it doesn’t matter if the new engine is exactly the same, as long as it turns the wheels. Memmott claimed that getting the car running is the most important task.
Using food webs and focusing on the roles played by plants and animals also tackles the ‘moving target problem’. The plants and animals that live on a heathland are always changing as a plant or animal might become locally extinct and will be replaced by a new, invading species. However, a herbivore will be replaced by a new herbivore and a parasite replaced by another parasite and the heath will remain healthy. Beause of this, all we can aim for is the restoration of the various roles in the machine, as we can never really know whether or not the individual species would have dissappeared from the heath even if it had not been turned into farmland. If we were to restore the Titanic, you wouldn’t hope to have exactly the same chairs as the original. As long as the chairs looked about the same, the restoration would count as a success.
This more abstract approach is the beginning of a new way of looking at restoration. However, being new it is lacking many of the tools needed for it to work efficiently. Memmott claims that food webs, including plant-pollinator webs are one major tool that are not yet exploited fully, especially in terms of studying interactions other than predation and herbivory. Memmott and her team has  ”made the first ever plant-pollinator network.”  This network can be seen below and shows which insects (top) pollinate which plants (bottom). If an insect often pollinates a particular plant, they are linked with a thicker line. These food webs allows ecologists to visualise and record who’s doing what on a heath, define targets for restoration, and finally to predict the effects of adding or removing a species. “Although removing an alien species could help rare species in the area, it may also make them even rarer by decreasing pollinator numbers.” explains Memmott.
Looking Ahead
The restoration of habitats such as heathlands is a daunting task and the development of practical tools to aid field ecologists is vital. This work is in its fledgling stages, but is being advanced by the hard work of scientists such as Memmott and her team. All this however is only one part of the challenge of restoration. A larger and harder problem still lies with the difficulties presented by development, human population increase and an increasing demand for farmland. Field ecologists can have a box full of useful tools and all the good will in the world, but it is all in vain if their work is stopped by farmers and other people who want to keep changing heaths into farmland.