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Evolution in Structured Populations

Genetic distance and FST

Posted: December 17th, 2014 by Charles Goodnight

First off, I did a search for papers that used contextual analysis in some form or another to analyze experimental data. This is the list I came up with. It seems pretty pitiful for a statistical method that (1) works and (2) with the exception of Heisler and Damuth using a very small data set to demonstrate the technique, has been wildly successful at detecting multilevel selection. I am hoping that I missed some important references. If you know of any that I missed, please let me know! If I didn’t miss anything, well, it looks like it is time for us to get to work!

Aspi, J., A. Jåkålåniemi, J. Tuomi and P. Siikamåki (2003). “Multilevel phenotypic selection on morphological characters in a metapopulation of Silene tatarica.” Evolution 57: 509-517.

Donohue, K. (2003). “The Influence of Neighbor Relatedness on Multilevel Selection in the Great Lakes Sea Rocket.” American Naturalist 162(1): 77-92.

Donohue, K. (2004). “Density-dependent multilevel selection in the great lakes sea rocket.” Ecology 85: 180-191.

Eldakar, O. T., D. S. Wilson, M. J. Dlugos and J. W. Pepper (2010). “The role of multilevel seleciton in the evolution of sexual conflict in the water strider Aquarius remigis.” Evolution 64(11): 3183-3189.

Heisler, L. and J. D. Damuth (1987). “A method for analyzing selection in hierarchically structured populations.” American Naturalist 130: 582-602.

Herbers, J. M. and V. S. Banschbach (1999). “Plasticity of social organization in a forest ant species.” Behavioral Ecology and Sociobiology 45: 451-465.

Laiolo, P. and J. R. Obeso (2012). “Multilevel Selection and Neighbourhood Effects from Individual to Metapopulation in a Wild Passerine.” PLoS ONE 7(6): e38526.

Moorad, J. A. (2013). “Multi-level sexual selection.” Individual and Family-level selection for mating success in a historical human population 67(6): 1635-1648.

Pruitt, J. N. and C. J. Goodnight (2014). “Site-specific group selection drives locally adapted group compositions.” Nature 514: 359-362.

Stevens, L., C. J. Goodnight and S. Kalisz (1995). “Multi–Level Selection in Natural Populations of Impatiens capensis.” American Naturalist 145: 513-526.

Tsuji, K. (1995). “Reproductive conflicts and levels of seleciton in the ant pristomyrmex pungens: contextual analysis and partitioning of covariance.” American Naturalist 146: 587-607.

Weinig, C., J. Johnston, C. G. Willis and J. N. Maloof (2007). “Antagonistic multilevel selection on size and architecture in variable density settings.” Evolution 61: 58-67.

The second thing I wanted to talk about was that I was asked about the relationship between inbreeding coefficients and genetic distance. I thought I would share my answer, in part to be told where I was wrong. My disclaimer is that all I know about genetic distance, is that it is something I rarely care about. . .

Consider a metapopulation with M alleles, with the mth allele having a frequency of pm in the overall metapopulation. We would like to calculate d, which from I got a formula cited by Smouse and Peakall (1999, Heredity 561-573) to be:

Screen Shot 2014-12-17 at 11.43.46 AM

Here the summation is over the M possible alleles, and yijm is the number of alleles of type m in individual i in the jth deme. This takes on a value of 0, 1, or 2.

If we are interested in the average genetic distance between deme j and deme l then we would calculate this as:

Screen Shot 2014-12-17 at 11.44.02 AM

We can now define dmax to be the maximum value that can take on. This will occur when the FST = 1. In an infinite metapopulation this means that every population will be fixed for an allele, and pm of the populations will be fixed for the mth allele.

If demes j and l are fixed for the same allele the genetic distance is 0. For allele m this occurs with probability (pm)2. If deme j and l are fixed for different alleles the genetic distance is:

Screen Shot 2014-12-17 at 11.44.11 AM

For alleles m and n this occurs with probability pmpn, thus:

Screen Shot 2014-12-17 at 11.44.20 AM

We want a measure that is a function of FIT and FST (I just figured out that I have never talked about FIS,  FST and FITTry this) that goes from zero to 1. When FST = 0, dij,kl = 0, and when FST = 1 dij,kl =1.

Working this out (the excel worksheet is available here: genetic distance work sheet)

Screen Shot 2014-12-17 at 11.44.34 AM

If we assume random mating within demes then FIT = FIS.

Screen Shot 2014-12-17 at 11.44.44 AM


Note that when FST=0, d = 0, and when FST=1, d = 4. The problem, of course is that we want to multiply this by dmax. For this to work we need the equation to go from 0 to 1. Thus, we divide by 4:

Screen Shot 2014-12-17 at 11.44.54 AM


Screen Shot 2014-12-17 at 11.45.03 AM

OK, A lot of algebraic noise. What this is telling us is that using Smouse and Peakall’s formula, there is a fairly direct relationship between FST and Screen Shot 2014-12-17 at 11.45.14 AM. Basically the difference is that genetic distance is based on identity by state, whereas F is based on identity by descent. If, at the start, every allele is unique then Screen Shot 2014-12-17 at 11.45.23 AM. If not, then dmax will be some number smaller than 4, and Screen Shot 2014-12-17 at 11.45.32 AM. If you care here is a graph of my equation:

Screen Shot 2014-12-17 at 11.47.04 AM

Genetic distance standardized to a maximum value of one as a function of FST.  If mating is non-random then  FIT will not equal FST and the results will be somewhat different.

Finally, I was asked about our fly collecting trip. Well do to a whole bunch of odd events we are understaffed to take care of a new batch of flies, so the trip has been postponed until January. The other question was about how I was going about bringing flies back to the US. The answer is I am not. I strongly recommend doing research in Brazil, but if you do get a Brazilian collaborator, and do your experimental work in Brazil, and leave your samples there. The reason is simple. We, as in the US and other first world countries, have been pillaging countries like Brazil for too long, and they are, unsurprisingly, sensitive about this. Doing research in Brazil is dead easy IF you have a Brazilian collaborator and you do the work in Brazil.

OH, and yes, I am slowing down my posts for a while, but I will still be occasionally posting as the occasion arises.

Hiatus announcement and group selection 1 and 2.

Posted: December 4th, 2014 by Charles Goodnight

The main piece of sad news this week is that I am just simply overwhelmed, and I am going to have to take a hiatus from writing. I will try to post occasionally, but look for once or twice a month rather than weekly. The reason is that I signed a book contract. I need to get writing on that, but before I do I have a chapter to complete, and I need to keep my research going – we are off to collect Flies in Southern Brazil next week. In some sense, it is good that I am slowing down. The logical progression of the blog would start to lead me into unpublished territory. The phenotypic approach has a lot to say about the evolution of sex, and the origin of life, for example. I think it makes sense to keep these a bit under my hat until they can get out in a citable peer reviewed format. The reason it is perhaps not so good is that there are a lot of ideas tearing at me that really do belong in the blog. Some subjects I should write about: It dawned on me that there is a difference between the contextual traits of contextual analysis on the one hand and indirect genetic effects on the other; I am once again confronted with philosophers of science talking about “group selection 1” and “group selection 2”, which are terms that I think confuse the issue and interfere with a nuanced understanding of multilevel selection. These are just issues that came up in the last week. Thus, I am not ready to abandon the blog yet, but I do think I need to slow down.

The book contract mentioned above is to write a book on exactly the topic of the blog, and as a result hopefully put it in a more permanent and citable form. The target date for a draft is a year from January, so it will be occupying a lot of my time for the next year.

So to rather randomly choose one of these topics. Lets talk about group selection 1 and group selection 2. This concept was introduced by Heisler and Damuth (1987, Am Nat 130:582), and recently popularized by Okasha (2006) (http://www.amazon.com/Evolution-Levels-Selection-Samir-Okasha/dp/0199556717/). The basic idea is that when you have individuals, or particles, you can do a multilevel analysis of selection on particles and selection on the collective, or you can just do an analysis of collective. Group selection 1 is an analysis in which fitness is measured at the particle level, and contextual effects of higher levels of organization are included. In other words, group selection 1 is what we think of when we think of group and individual selection acting simultaneously. In contrast, in group selection 2 we ignore the particles and focus on the collective. Thus, we might look at the fitness of bacterial colonies even though we know full well that these colonies are made up of individual cells.

This concept has gotten good traction in the philosophy world, and I will agree that it raises an important point. That is, it makes clear that results change depending on your point of reference. In the past there has been a lot of useless ink wasted when people were arguing about things like whether species selection was just the summed effects of individual selection, when in fact, they might be the same thing. That is, from a group selection 1 perspective in which the individual organisms are included in the analysis, it could indeed be that species selection is just the cumulative effects of selection on individuals. Even if this is true, however, if we take a group selection 2 perspective then indeed it is species selection, since we are only looking at the collective, or species.

So, this all sounds very positive, so what’s the problem? The problem is that every system is always group selection 1 and group selection 2 at the same time. Cells are made up of subcellular components, organisms are made of cells, groups are made of organisms. The levels need not be strictly hierarchical. For example, I “belong” to a number of different groups: My family, my department, the Evolution society, the blogosphere. These groups are in no sense hierarchical, and yet the do overlap to some extent. The group selection 1/2 perspective implies that there are really only two such levels, and basically enforces a false dichotomy. Question: are you working on particles or collectives? Answer: Yes.

So, rather than be destructionist I would like to offer a much better alternative. Let us clearly identify the level at which we assign fitness. This is Okasha’s particle, and my individual. Let me repeat that: The level at which we assign fitness is the individual. Then, rather than having the ambiguities of what exactly the levels are when we talk about group selection 1 and 2, we can instead clearly say that in this study the individual is the cell, whereas in that study the individual is the organism. The conclusions will, of course be different, but we don’t have to argue about them. We will know why they are different. They are different because they have different perspectives, they assign fitness at different levels.

Again, I apologize for taking a hiatus on my blogging. Hopefully I will be able to put up posts at a lower rate, and still keep this blog alive. One reason I will not be blogging next week is that we are going fly collecting. This will be an adventure, so don’t feel sorry for me!

Screen Shot 2014-12-04 at 1.59.48 PM


We will be driving south into wine country to sample Tephritid flies.  There are a number of interesting species complexes here.  Hopefully we will be able collect some of interesting species.


Variance in a structured world

Posted: November 19th, 2014 by Charles Goodnight

So far I have been writing about things that in some sense I fancy I know something about the answer. Today, all I have is conundrum. The conundrum I have is this: one of the unspoken themes of this blog is that the “mean field approximation” is inadequate, and yet I am failing to provide an alternative.   Sadly, this is the comment from my physicist friend for which I had no answer.

Consider one of the most basic mean field statistics, variance. Variance is fundamental to our understanding of selection. For example, the selection vector, S, is the covariance between a trait and relative fitness, which in turn is a product of the standard deviations of the trait, relative fitness, and the correlation between the two:

Variance eq 5

Now, lets think about what this means. As far as selection is concerned it means that we are effectively lining everybody up, and choosing those with the most favorable value of the trait, and discarding those that don’t measure up.   In effect this is very much like the start of a race: Everybody lines up at the start line, the gun goes off, and the runners can be ranked based on the time it takes them to cross the finish line.

Race start

The start of a race is a situation in which the variance in a trait, such as muscle mass, can be used with some confidence to predict the outcome the race. The important point is that all are competing equally at the same time and under the same conditions. (http://www.dailymail.co.uk/travel/article-2176034/London-2012-Olympics-Things-London-Olympics.html)

Unfortunately, most of the world is not like this. Even in the world of sports it becomes more complicated. Consider the NCAA basketball tournament. In this contest only pairwise contests are possible. Thus, a team is never competing against the entire field, but is instead competing against a single competitor. This means that for any given contest the performance of teams not in the contest are (at least for the moment) irrelevant. Thus, a measure of the variance in some trait, say team mean free-throw percentage, is irrelevant, whereas the difference in the means of the trait between the two teams is highly relevant. This has some interesting consequences. For example, it is not unusual for a low ranked team to put everything it has into the opening game and defeat a top ranked team only to get trounced in the next game because they don’t have the depth to continue at that level of play.


The results of the 2014 NCAA basketball tournament. Note that the championship was played between 7th ranked Connecticut and 8th ranked Kentucky. Also there are a number of interesting upsets, such as 3rd ranked Duke being defeated by 14th ranked Mercer. These anomylies indicate that summary statistics, such as variance, are not always predictive of the final results. (http://www.printyourbrackets.com/ncaa-march-madness-results-2014.html)

Turning to nature, it is the same thing. As far as our favorite gazelle is concerned it doesn’t matter how fast cheetahs run on average, or how fast the fastest cheetah runs. What matters is how fast the cheetah that is chasing it can run. In a large panmictic population with random interactions mean field summary statistics such as variance are indeed appropriate for predicting the response to selection it is very much like the race example I started with, and we are justified in calculating S as the covariance between relative fitness and the trait value. But what do we do when selection is taking the form of a tournament or interactions are local?

The easy solution that I have used is to assume that the population is structured using an island model of migration. This is a metapopulation in which each subpopulation has random mating and random interactions. In addition, migration among subpopulations is random, with no effect of distance on probability of migration. This is in effect a two level mean field approximation in which we can use variances to describe selection among individuals within subpopulations, and another set of variances to describe selection among subpopulations within the metapopulation. This is fine, and probably often a good approximation, but it is at least conceptually unsatisfying in continuous populations with localized interactions.

Another solution is to use the recently very popular network approach. I am honestly not sure how this works, so I will leave it to others rather than embarrassing myself. That said, I have concerns about this approach in the practical world of measuring plants and animals in natural populations where measuring connections may be difficult or impossible.

So, what is the answer here? The simple truth is that I don’t have one, but I do have some ideas. My thought is that we do something along the lines of a weighted mean and variance, and that we weight the variance by the probability that the interaction will occur. For example, if we have a continuous population the standard manner for calculating the variance in a particular trait in the population would be:

Variance eq 4

Two things to note: (1) yup, I am using the MLE formulation of variance, not the BLUE (Best Linear Unbiased Estimator) one. It may be biased, but from a theoretical perspective it is cleaner. And (2) pi can be thought of as the frequency of the ith type. My thought is that the pi can be any number, as long as it sums to one. Thus, we can replace pi with another value, say qi as long as it also sums to one. I suggest that we define a number, say kji = the probability that individual j interacts with individual i, and:

Variance eq 3

Thus, for each individual we would get a separate “local” mean and variance:

Variance eq 1


Variance eq 2

I will admit at this point I am stuck and running out of space, however, my thought is that we could similarly calculate a local variance for relative fitness and a local covariance between local relative fitness and local phenotype. Summing across individuals (S Zj) may well give a more meaningful estimate of the selection differential in the population. Estimating kji might be difficult, but perhaps reasonable estimates could be obtained using home range distributions, or other behavioral measures.

Actually, there are people who are much more adept at such things than I am so I am sure there is a better solution, but I just don’t know what it is.



On partitioning fitness

Posted: November 6th, 2014 by Charles Goodnight

I realized last week that I should probably explain more clearly what I meant by temporal components of fitness. As a result, a discussion of variance will have to wait until next week (I actually am flying to California for a National Academies Keck Futures Initiative meeting next week, so the next update may be two weeks).

What I am using is Arnold and Wade’s (1984, Evolution 38:709) episodes of selection paper. In this paper they partition episodes of selection using a very simple idea. They start with the multivariate breeders equation, but in reality there is no need for that. Lets forgo the opportunity to be cool and use matrices, and instead use the simple univariate breeders equation:

Screen Shot 2014-11-06 at 6.01.31 PM

Where (Yea, you know the drill): z̄’ is the mean phenotype between generations, VA is the additive genetic variance, VP is the phenotypic variance, and z̄* is the mean phenotype within generations due to selection.

Another point (yea, I know: boring) but one that bears repeating, is that z̄ etc. are real quantities with units attached to them. For example, the average weight of men in the United States is z̄ = 195.5 pounds. It is important to remember that, all equations aside, we really are talking about the real world!

From our perspective the important part of this equation is the selection differential S:

Screen Shot 2014-11-06 at 6.02.43 PM

What Arnold and Wade pointed out was that you could easily divide this selection vector into multiple episodes of selection by simply adding and subtracting the mean phenotype at various moments in the history of the organism:

Screen Shot 2014-11-06 at 6.02.53 PM

In other words, it is quite easy to divide an overall selection differential into multiple episodes of selection. So, that tells us about selection, but does not tell us about fitness. However, that is easy if we further expand our equation. In particular, the mean of the population after selection, but before reproduction, is found by taking the fitness-weighted sum of the traits:

Screen Shot 2014-11-06 at 6.03.04 PM

What can be seen from this is that indeed each episode of selection is associated with an episode specific relative fitness.

It is a bit involved, but Arnold and Wade show that absolute fitness can be partitioned easily as long as the absolute fitnesses are multiplicative. That is:

Screen Shot 2014-11-06 at 6.03.16 PM

where capital Wi etc. is the absolute fitness of the ith individual. Absolute fitness is the fitness of an individual on an arbitrary scale – for example, it might be the number of eggs a frog lays ranging from zero to the maximum clutch size possible – whereas the breeders equation uses relative fitness, which has a mean of one. For each episode of selection the relative fitness must be calculated as Screen Shot 2014-11-06 at 6.03.25 PM .

What it means for fitnesses to be multiplicative is that they need to be conditioned on previous events. Examples of appropriate conditional fitnesses would be:

W1 = the probability of being born alive

W2 = the probability of surviving to adulthood given that the individual was born alive

W3 = the probability of successfully mating given that the individual survived to adulthood.

W4 = the number of eggs the individual lays given it successfully mated

Note that in each case the fitness is a function of previous events. Thus, survival to adulthood is only measured on those individuals that are born alive, etc.

The beauty of this is that as I pointed out last week it is probably impossible to measure true fitness. What this paper tells us is that even if we can’t actually measure total fitness, as long as we are honest about what temporal component we measure, and the temporal component of fitness is multiplicative (e.g., we measure survival to adulthood only on live born individuals) we are safe. We simply need to make sure that we are aware that other episodes of selection, and other temporal fitness components affect the evolution of the trait. For example, Arnold and Wade measured selection for mating success in male frogs. They found that mating selection favored larger males. One could immediately ask why frogs aren’t huge. A reasonable answer would be that there are selection episodes other than mating that keeps the males size in check.

The net result is that we can define “fitness” in conceptual terms that cannot be realistically measured, and then when we actually need a definition that can be used in actual research or modeling just use a valid temporal fitness component and call it good. Last week I defined fitness as the probability of founding a lineage that persists until some arbitrary point (such as a speciation event) in the distant future. First off, there is an obvious problem with this definition for sexual species, so that was definitely not the last word in fitness definitions. But for the purposes of this discussion it is also a useless definition from a practical perspective. However, using this idea of partitioning fitness it is easy to see we can have this useless conceptual definition, and at the same time use a temporal component of fitness that Can be measured. For example, to the list above we can add an additional component of fitness:

W5 = the probability an egg gives rise to a lineage that survives to the arbitrary point in the future times the number of eggs laid.

Now we have our unworkable conceptual definition of fitness, and we can still, say focus on sexual selection and W3, the probability of successfully mating given that the individual survived to adulthood. In short, we can have our cake and eat it too. We can (although apparently I can’t) develop a comprehensive definition of fitness that will satisfy the most demanding critic, and still develop a temporal component of fitness that is usable in experimental settings.

A conversation with a physicist: Some thoughts on fitness

Posted: October 29th, 2014 by Charles Goodnight

This past week I went over to the university at a nearby city, and talked to some physicists interested in complex systems, and among other things, biology. As seems to be the nature of physicists turned biologists, I was impressed with some of their ideas, but also impressed with their lack of knowledge of biology, and, to be blunt, their view that biologists were basically inept when it came to theoretical issues. Perhaps the most impressive simple example was one (note no names, but an American, not a Brazilian) wanted to publish a paper showing that the Fisher’s fundamental theorem was not universal. Now that is a paper that would be met with a large yawn. Aside: I find FFT to be a fun mathematical truism, given a set of assumptions, but I seriously doubt anybody has taken its universality seriously in a very long time.

FFT equation 7

Fisher’s fundamental theorem is a mathematical truism, but only if the underlying assumptions are met. It is well known that these assumptions will only rarely be exactly met in real systems, and that this theorem should be used to guide intuition, rather than to make quantitative predictions.

However, there were two issues that came up that I want to cover more seriously. Today I will talk about fitness, and next week I will talk about variance in evolution.

I was telling this physicist about some of my ideas, and in the process talking about “fitness”. In the course of this discussion I was repeatedly told that unless we really understood terms we couldn’t proceed. So as a result I kept being more and more specific, sadly, about everything but fitness. It was only later that it dawned on me that he didn’t think I knew what I meant by fitness. I actually think that this is one of the problems that physicists have with biologists. They tend to come up with wacky examples of where a naïve concept they attribute to biologists doesn’t apply, and then say that because this definition does not apply in this case we have no idea what we are talking about. This is, of course, a bit disturbing for somebody who has published models in which naïve definitions of fitness don’t apply (e.g., Goodnight et al. 2008. Complexity 13(5): 23-44). In short, I think I have a pretty danged good idea of what I mean by fitness.


I might just know something about fitness!      bankai.    (from http://pt.wikipedia.org/wiki/Ichigo_Kurosaki)

What this physicist was missing is that when I talk about “fitness” it is in fact shorthand for “temporal component of fitness”. Please bear with me on this, since I have never attempted to define fitness in a way that I would apply to all situations. But if I were to attempt to define fitness it would define it to be something along the lines of:

Fitness is the probability that an organism will start a lineage that will persist for an arbitrary period into the future.

I think a good boundary would be speciation, thus, I might narrow the definition of fitness to be:

Fitness is the probability that an organism will start a lineage that will eventually participate in the founding of a new species.

Obviously, this is an unworkable definition, but still, there are reasons why a truly general definition would need to be something along these lines. For example in the paper cited above (Goodnight et al. 2008. Complexity 13(5): 23-44) we examined the dynamics of a predator that was subject to mutations with how aggressive it was. What we found was that the optimal aggressiveness was a balance between growing quickly, but not so quickly that a lineage exhausted its prey and went extinct. The interesting thing was that in the short term these “optimal” lineages were always invasible by a more aggressive mutation, but in the long term these more aggressive lineages always went extinct. The point is that very aggressive lineages had an apparent high fitness over the course of a few generations, but a low fitness over a longer term. A true definition of fitness would have to incorporate this.


long term pred prey study

τ is a measure of aggressiveness, or how quickly the predator consumes the prey. Note that in this example a highly aggressive (cyan and dark blue) predator appears, but eventually burns out and goes extinct. (Figure from Goodnight et al. 2008. Complexity 13(5): 23-44.)

So, how do we deal with this obviously unworkable definition of fitness? The answer that my colleague did not understand is that we work with components of fitness. As Arnold and Wade (1984. Evolution 38: 709-718)pointed out so long ago, as long as episodes of selection are described in a multiplicative manner (that is conditional probabilities) it is valid to study a component of selection. In the predator prey example, it is perfectly valid to define a component of fitness that is lifetime reproductive success. If you did this you would discover that for this fitness component, the “fitness” of an aggressive mutant was very high. A biologist who chose their words very carefully would acknowledge that there may well be other later selective events that would counter the effects of this fitness component, but that would not invalidate conclusions about differences within lifetime fitnesses.

Since we are being careful, there are caveats even here. That is, technically the selection events have to be independent, and that will often not be the case. I think that this is another issue between biologists and physicists, however. That is, that in theoretical physics there is this concept of an exact solution. I seriously doubt that any theoretical biologist believes that we could develop a model that gave an exact solution in a living system. It is simply too complicated. Thus, as long as different episodes of selection, and thus temporal components of fitness, are not too highly correlated the assumption of independence will not hurt the ears of biologists too badly.


Unless you are really sensitive, a small amount of non-independence among selection episodes should not hurt your ears. (http://factsaboutbirds.blogspot.com.br/2010/08/desert-animals-list.html)

So, in sum, is life time reproductive success “fitness”? The answer is clearly no, since multigenerational processes can also enter into the equation. Instead, we need to think of it as a temporal fitness component. Am I apologetic about frequently referring to life time reproductive success as fitness, even though I know it is technically incorrect? No, I am not. Referring to it as something else is cumbersome, and honestly, in nearly every experimental system I am aware of, it is the major component of true fitness. It is basically a convenient shorthand and something that is usually pretty close to the truth.


In “truth” as in horseshoes sometimes close is good enough.  (http://lrossentertainment.wordpress.com/tag/outdoor-games-wedding-ideas/ photo credit, Sam Beebe, Ecotrust)

Spider Group Selection

Posted: October 22nd, 2014 by Charles Goodnight

I could keep going on what an individual is, but at least at this point I have put out the main points I have been thinking about. It may be a subject we will return to in the future. What I really should talk about a bit is our recent paper, “Site-specific group selection drives locally adapted group compositions” (Pruitt and Goodnight, Nature 514:359–362).

I am actually a bit surprised that it has gotten so much positive press with so little backlash. But with a very few exceptions we are not being dismissed. I guess times have changed. I am actually not so much going to describe the study so much as talk about what we demonstrated and why it is in actuality a fairly small step.

First a disclaimer: This is John Pruitt’s project. I was honored when he asked me to participate in the analysis of the data, and sometimes I am not sure I did a lot more than provide cover so that he could talk about multilevel selection.

As with all science, this study is but a small step in a long line of studies.


Two very apt adages “the cutting edge of science is dull” and more positively “if I can see so far it is because I stand on the shoulders of giants.” I have also heard this second being “if I can see so far it is because I stand on a mound of midgets”. It seems to me that all three are apt. The first because science proceeds in small steps. The giant and midget analogies are correct because there are giants (Darwin, Fisher Wright and the like) but advancing science also depends on midgets like you and I. (left: http://www.telegraph.co.uk/travel/travelnews/10088510/Bland-reaches-out-to-Dull-and-Boring.html, right: http://www.stellabooks.com/articles/dr_seuss.php )

The reason for that long-winded preamble is that in reality we did a relatively small thing. First some history. It has long been demonstrated that there were serious flaws in the reasoning of theoreticians dismissing group selection (Wade 1978, Quart. Rev. Biol. 53:101-114 – this paper is remarkable in how prescient it is given that it was published nearly 40 years ago). At the same time Wade was also doing the first studies showing that group selection worked in the lab (Wade 1977 Evolution 31:134-153). Later studies would demonstrate that indeed Wade had been correct in his quarterly review article: group selection could act on interactions among individuals in a way that simply was not available to individual selection (see Goodnight and Stevens 1997 Amer. Natur. 150:S59-S79), and a series of selection experiments led to the wide-spread adoption of group selection as a means of live stock improvement (e.g., Muir 1996 75:447-458). Thus, by this time we really have answered the early questions: In the lab group selection works, and it works so well because it can act on interactions among individuals. The next question was whether group selection IS acting in nature. The methodology for this was brilliantly provided by Heisler and Damuth (1987 Amer. Natur. 130:582-602), and promptly ignored. Fortunately, in recent years this method has been rehabilitated, and shown to work both in theory and in action. The results of these efforts is that, although not enough cases have been examined, it is pretty clear that group selection is at least not uncommon. To give you some idea about how common it might be, (1) recognize that theoretically we can show that soft selection is a mixture of group and individual selection (Goodnight, Schwartz and Stevens 1992, Amer. Natur. 140:743-761), (2) the constant yield law (Weiner and Freckleton 2010 Ann. Rev. Ecol. Evol., & Syst. 41:173-192) is almost universal in plants and (3) the constant yield law is a form of soft selection. Thus, group selection may indeed be extremely common in nature.

So, in some sense the main questions are answered: The models were wrong, group selection works, and it may be very common in nature. What was missing is that up to this point we did not actually have an example of an adaptation that was unequivocally a result of group selection. That is what Pruitt and Goodnight provided. This is no small feat. Consider how many solid examples we have of adaptation due to individual selection. There are a lot of traits that almost certainly are, but have never been demonstrated to be individual level adaptations. Examples of these are things like our hearts. Clearly an adaptation, but has it ever REALLY been demonstrated to be so? The examples we do have are few and far between, and all represent a huge amount of work on somebodies part. I am thinking of examples like the evolution of lead tolerance in grasses (Antonovics and Bradshaw 1970 Heredity 25:349-362) peppered moths (Kettlewell and later Majerus), and beak size in Galapagos finches (Peter and Rosemary Grant).


Social spiders have a group level adaptation that is the proportion of the colony that is aggressive vs. the proportion that is more docile. Populations have evolved to display a mix of these two proportions that is apparently optimal for their local environment. When the distribution is experimentally adjusted it always returns to the evolved ratio regardless of the environment in which they are raised. By the way, this strikes me as grasshopper hell. (From http://www.readcube.com/articles/10.1038/nature13755 — this is a nice writeup by Tim Linksvayer. I recommend it if you have not already seen it.)

Notice that in the cases where we have good evidence of evolution by natural selection there is environmental variation. In the case of lead tolerance there are mine tailings such that soils with high lead content are adjacent to pristine land lacking the metal. In the case of the moths and birds there is sufficient data over a long enough period of time that we can see adaptation occurring as the environment changes. Pruitt’s spiders were closer to the mine tailings scenario. That is there were different local environments that had different optimal mixtures of spider behaviors, and we were able to show that the spiders are locally adapted, and regardless of the environment we placed them in, they always adjusted their colony to reflect the adaptive mixture of behaviors in the environment they evolved in. Thus, Antonovics and Bradshaw were able to show that “normal” plants were unable to grow well in lead poisoned soil, we showed that spiders are unable to adjust their mix of behaviors when placed in the “wrong” local environment.

In reality, then, that is all we really did. We showed that these spiders have a group level adaptation to local conditions. Since it is a property of the group that cannot be meaningfully measured on individuals, it really is a group level adaptation, and since it is non-plastic it is a heritable change. This is the last of the qualitative issues to be addressed about group selection. Group selection works in theory, group selection works in the lab and in agriculture, we see group selection in nature, and now we know that group selection leads to adaptive change in nature. What is left is to work out the quantitative questions, such as how common is group selection relative to lower levels of selection, under what circumstances is it sufficiently powerful (and traits sufficiently heritable) that it leads to adaptations that can be attributed to evolution by group selection.

Individuals as Multispecies Entities

Posted: October 15th, 2014 by Charles Goodnight

I am feeling a bit schizophrenic these days, splitting my time between developing models of species differentiation, experimental design to measure the genetics of species differentiation – yes, it can be done, and blogging. The last is a bit confusing because it starts me wondering, when did I become a philosopher.   And lets just say, there is a reason that they give PhDs for philosophy, and a reason I don’t have one.

Any way on the philosophy issue, today I want to clean up and finish up my discussion of individuality. Hopefully this will be short and sweet.

Here is the issue: I have defined individuality in terms of selection and evolution. I stand by those definitions, but it occurs to me that this does not fit well with our concept of organism. Consider the point I raised before which is that if we choose selection as defining the individual, in many, if not most cases, we will logically assign fitness at what we commonly call the organism. However, what we colloquially call organisms, it is now becoming apparent, are not a single species.



Revisiting an issue raised a few weeks ago, when studying selection on running speed in cheetahs it makes sense to assign fitness at the level of the organism. In this case the “organism” is a multispecies assembly. (http://theruniverse.com/2012/07/running-tips-from-cheetahs/)

It may be that there are a bunch of commensals and parasites inside that organism, but it is still the cheetah that eats or doesn’t eat, and reproduces or doesn’t reproduce. For the rest of this post I will use commensals to mean all of the species associated with a metazoan, including parasites and symbionts.  Remember, selection is blind as to the causes of the phenotype.   If our cheetah cannot run fast because it has a bad mix of gut bacteria (and a belly ache?) it still doesn’t get to eat, and it still starves. Thus, our selection definition of fitness is in this case identifying the assembly of species that is a cheetah as the “individual”.

Fine, you may argue, but it is the cheetah that survives and reproduces, and as such we ignore the rest as environment. The philosophical problem with this is that it is exactly the same issue with the gene-centered view. The gut bacteria may be along for the ride, but they are there. To ignore them is the same as in the gene-centered view ignoring other loci even though they are interacting with the locus you are focusing on. We know that doesn’t work. I would argue that the reason we know the reductionism to only the colony of “cheetah” cells doesn’t work is because nobody has ever bothered to ask the question.

There is, however, another issue. I would also argue that many of these commensals ARE heritable. Remember using the phenotypic view I consider “heritability” referring only to genes to be far too narrow. Basically many of the commensals ARE heritable. At one extreme, we can consider mitochondria to be “commensals”. The only reason that we normally don’t is that they are strictly vertically transmitted, and they have coevolved with their host cells to the point that neither can survive without the other (except, the case of chloroplasts and nudibranchs )


The emerald green sea slug, Elysia chlorotica, isolates cholorplasts from algae and incorporates them into their own cells, using them for photosynthesis. (from http://scienceblogs.com/notrocketscience/2008/12/28/solarpowered-green-sea-slug-steals-ability-to-photosynthesis/)

The case of mitochondria is not really so different from that of Wolbachia, except that insects cured of Wolbachia typically survive, whereas “curing” animals of mitochondria is probably not a good idea! (OK, our cheetah neither uses chloroplasts, nor has a wolbachia infection, hopefully you get the point).

Other commensals have a looser association, nevertheless, in the context of the phenotypic approach they have to be considered heritable. For example, an old study (Bettelheim, Breadon, Fairs, O’Farell and Shooter 1974, J. Hyg. Camb 72:67) found that in most cases mothers and their babies had the same serotypes of E. coli. One can imagine similar “inheritance” of even ectoparasites such as fleas (mother cheetahs infecting their offspring). Thus, yes, many of these commensals WILL be part of the patterning node. Others will be more opportunistic infections and thus nonheritable, but that does not negate the fact that many are indeed heritable.

So, that leaves us with the reality that in many cases “individuals” will be multispecies entities. You are not just you, you are you and your pets. Lest this bother you, please remember that commensals CAN affect your behavior. I have a friend that swears that an amoeba infection he got caused him to become depressed, and toxoplasmosis can apparently make people more reckless (and make the cat litter box less offensive). So, yes, parasites do affect the way you think, and no, even your behavior is not just your own.

So, here is my proposal. I think we do need a name for a colony of cells of the same species. I suggest we define “organism” as a colony of cells derived from a single cell and physically connected to each other.   In this view the cheetah “organism” would be the set of cells derived from the fertilized egg from the mother cheetah. On the other hand, the cheetah “individual” would be the actual creature that includes the organism and its commensals. I am not sure that this will ultimately end up being a good idea, but hopefully it is a good place to get the discussion started.


No, not that cheetah, I am talking about the one that can run fast. (from http://www.lavantis.com/2011/12/cheetah-chimp-of-tarzan-dies-at-80/)

Heritability and the individual

Posted: October 9th, 2014 by Charles Goodnight

First off, an ad from a former graduate student I used to work with. Josh Payne, who was an author on the speciation in continuous populations paper I discussed some time ago , is looking for students and a postdoc to study evolution and robustness. Check out his ad if you are interested.

To summarize to this point, I first defined an individual as that which you define to be an individual, or more specifically, the level at which you assign fitness. This definition makes sense since there may be constraints on what can be measured. There are a trillion some odd cells in our bodies. Assigning fitness at the level of the cell would be a huge chore unless there was some compelling reason to do otherwise. On the other end, a paleontologist may have access to presence or absence data for species in a fossil assemblage, but no way of assigning fitness to individual organisms, or even knowing how many individuals there are in the population. Thus, they may forced to assign fitness at the level of the species. This first definition is entirely consistent with the pragmatic needs of research.

At this point an admonition to paleontologists: Do not apologize for studying “species selection”. In your world species ARE individuals. From this perspective, the waxing and waning of the range of a species, or anagenesis of the species is simply “species development”. It may well be that if we had a time machine, and ear tagged all of the mastodons, and measured traits and their reproductive success we would discover that the change in their distribution was due to selection at the level of the organism, but we can’t and because we can’t we cannot study it as evolution, and we need to let go of that and be happy with the evolution we can study. By the way, this also means that two investigators could choose to assign fitness at different levels, and as a result come to very different conclusions about how evolution works. It being the nature of biologists, they will almost certainly argue about which one is “right” when in fact, since they are using different definitions of what the individual is, they can both be correct.

My second definition is that the individual is the level at which selection is acting. I like this definition a lot since it is logically appealing that selection should define the individual. It also suggests that metazoans are metazoans because groups of cells have higher fitness than individual cells. Following this through, it logically also suggests that under some circumstances groups of organisms have higher fitness than individual organisms. We actually see that eusocial organisms often exploit environments and resources that solitary organisms can’t. Thus, naked mole rats can live in an environment that is too harsh for other rodents.   Social wasps can have open nests even though their larvae are extremely attractive food sources.   And ants have virtually taken over the world. It also suggests that there are times when social living may not improve an organism’s fitness. Just as there are environments where naked mole rats out compete all other rodents, there are many other environments where naked mole rats cannot compete. Presumably, in these richer environments the strength of group selection is lower and individual selection higher and as a result the naked mole rat cannot compete with its solitary brethren.

naked mole rats

Naked mole rats live in a harsh environment where other rodents cannot survive, but have not spread into more benign environments. Presumably this is because the balance of selection tips towards group selection in harsh environments. (http://adarwinstudygroup.org/illustrations/#img-01-2402 )

There is one last concept of individuality that needs to be discussed. This is the classic one that is the subject of books such as Maynard-Smith’s book supporting group selection (he said laughing in his hat five ways*), “The Major Transitions in Evolution“. That is the observation that selection at the group level can overwhelm individual selection, and effectively suppress evolution at the lower level.

The interesting thing about metazoans is that they rather famously start from a single fertilized egg, and eventually divide into trillions of cells. Importantly, the cell division is via mitosis, which has almost unbelievable fidelity. Thus, all of the cells are genetically virtually identical. From the perspective of individuality, what this does is that it lowers the heritability at the cellular level to nearly zero. To remind you, the breeder’s equation is:

R = h2S

Which basically means that if we are going to get evolution by natural selection we need both selection and heritability. In my second definition I identified the individual as the level at which selection is acting. Lowering the heritability has exactly the same effect. Thus a reasonable definition of individuality is the lowest level at which there is heritable variation for a trait under selection acting at that level.

It is important to recognize that mitosis is but one way that heritability can be minimized. In social insects you get the same minimization of heritability through “policing” behaviors. For example, in worker bees there is variation in their propensity to lay eggs (all haploid male eggs, of course); however, because workers eat eggs laid by other workers, this variation does not translate into reproductive success, and there is no variation among workers in offspring produced. Other mechanisms for reducing variation that have evolved are things such as having a single reproductive in a colony. Such reproductive behaviors increase relatedness within groups, having the effect of reducing heritability, and decreasing the response to selection.


A bee killing a worker laid egg. This policing effectively eliminates the heritability of fertility among worker bees. (from http://www.nature.com/news/2002/020425/full/news020422-16.html)

An interesting anecdote on this is that as good as mitosis is at making exact copies, there are mistakes. As a consequence there IS heritable variation among cells in metazoans. This would suggest that there should be strong selection, but low heritability, for cells becoming reproductive cells. So, why hasn’t your liver evolved to become a gonad? Obviously, part of this is the fidelity of mitosis, but another part is that the reproductive cells are isolated very early in development, and actually while development is still under maternal control. What I mean by that is that early cell division in vertebrates occurs far faster than is apparently possible based on normal rates of protein synthesis. The way this can occur is that the mother “packs” the cells with RNA and proteins before fertilization. Thus, the early cell division is under maternal control but after a few divisions the zygote derived gene products take over control of cell division. It turns out that in Drosophila for at least one important gene product, notch, isolation of the germ line occurs immediately before the shift from maternally derived notch to zygotically derived notch occurs. Of course I have no real idea, but as an adaptive story it is tempting to suggest that the maternal control of germ line segregation is similar to policing in social insects. (don’t ask me for references on this. Years ago I wrote a grant for this with somebody. We got the grant, but my collaborator left and I never saw the money or did the research. Also, this idea can be traced to Leo Buss [http://www.amazon.com/The-Evolution-Individuality-Leo-Buss/dp/0691084696], so I take no credit.)

Thus, the three definitions of individuality, and particularly, the second and third are really cut from the same cloth. An individual is an evolving unit. At the simplest, it is that which we recognize as an individual. Given that humans are good at recognizing patterns, it is hardly unreasonable that we intuitively identify “individuals” more or less correctly. The second and third are more formal definitions in the sense that we are saying that individuals are units of adaptation. They can be units of adaptation either because of the patterns of selection, or because of the patterns of heritability, or both.

* 10 points if you can identify that reference! The actual quote is “One little sniffer with his eyes half shut and a mitten on his nose, laughed in his hat five ways and said, ‘They are going to the moon and when they get there they will find everything is the same as it always was.’ ” And by the grace of the cosmos Disney never laid waste to those stories.

Selection and Individuality

Posted: October 1st, 2014 by Charles Goodnight

Apparently I have shifted to an every other week post. It is not that I am lazy, just that my life is a bit chaotic. A week ago Saturday my daughter got married, and this week I am flying back to Brazil. Somewhere in the haze last weeks post simply didn’t happen.


blame the lack of post last week on the haze of getting out of town for a year. Besides, how else am I going to work Jimi Hendrix into a post? (from http://markmywordssite.com/2011/05/05/purple-haze-all-in-my-brain/)

In any case, I felt that I left you last time with a rather unsatisfying answer: An individual is that which you define to be an individual. This week I want to argue that some designations of “individual” are better than others. To see this we need to continue to work with contextual analysis.

To start, lets imagine we assign fitness at the lowest possible level, that is the cell. Ten points if you can tell me why it is NOT the gene! Twenty points if you can tell me why the lowest level might be the organism! – hint: What is an orgamism?. In that case we are calling the cell the “individual”.


Selection at the level of the Gene (Simmons) makes no sense. (from http://musicrowgirl.com/tag/gene-simmons/)

First lets look at cancer. If we imagine that fitness is just the rate at which cells divide (and ignoring organismal mortality for the moment) then cancer cells have a higher fitness than “normal” cells because they divide more rapidly. Thus in contextual analysis we can imagine a case of pure cellular (individual) selection then:

sel and ind eq 1

Here is the kicker: If we assume that there is ONLY cellular selection and we do a bit of math I prefer not to show you then we quickly discover that:

sel and ind eq 2


sel and ind eq 3

what this tells us is that, because we assumed it to be that way, there is selection at the level of the Individual cell, but no selection at the level of the organism. Thus, in this simple case the qualitative result is that selection is acting at the cell level.

If we assign fitness at the level of the organism then we are de facto defining the organism to be an individual. Here we get a very different answer. In particular, since there is no assignment of fitness at the cell levelsel and ind eq 4 and sel and ind eq 5are undefined. Similarly we cannot do the partial regression sel and ind eq 6, and can only do the simple regression, sel and ind eq 7, which emphatically does not equal zero, and in fact had we measured it, sel and ind eq 8.

Whether we assign fitness at the level of the cell or the level of the organism, we still measure evolution by natural selection; however, what happens is that our interpretation of how selection is acting qualitatively changes as we move between levels.

Now, lets consider selection on a second trait. In this case it is something that only acts at the organismal level, nevertheless we will assign fitness at the level of the cell. Because, by assumption, selection is only acting at the whole organismal level

sel and ind eq 9

On the other hand

sel and ind eq 10

Again, because we considered only a situation with selection at the organismal level, contextual analysis says there is group (organismal) selection, but no individual (cellular) selection.

Now, if we were to assign fitness a the level of the organism instead of the cell we would discover that sel and ind eq 7 had not changed, and that we still detected exactly the same strength of selection at the organismal level as we did when we assigned fitness at the level of the cell. In other words, in this second case when we changed levels at which we assigned fitness we got no qualitative change in our interpretation of how selection was acting.

So, what does this have to do with individuality? I would defend the statement I made in the last post that the individual is at some level arbitrary, and it is the level at which you assign fitness, however I would argue that some choices are better than others. In particular, if we imagine that we assign fitness at the lowest conceivable level, for selection on most traits we would find some higher level at which “contextual” selection is acting. If we assign fitness at the level of the cell we would find that for a large number of traits there is a strong contextual component of fitness that is at the level of the organism. I would argue that for selection on any given trait the logical level at which to assign individuality is the level at which there is a strong contextual component to fitness.

Logically, how do we find this “natural” level of individuality? The easy way is simply to do the contextual analysis and find the level at which contextual selection is acting. A corollary to this is that when you move through that level at which contextual analysis is acting you will see a qualitative change in your interpretation of how selection is acting. In the example above when selection was acting at the cell level, assigning selection at a higher level qualitatively changed our interpretation. That is when we assigned fitness a the level of the organism what had formerly been interpreted as cellular level selection becomes organismal level selection. Importantly, when we had a situation in which selection was acting at the organismal level then moving up the level of individuality from the cell to the organism does not qualitatively alter our interpretation of how selection is acting, and we see that in this later case the cell is not the natural individual, whereas the organism is.

This actually has some important philosophical implications. First, it appears that selection in some sense defines individuality. Since selection acts on traits that means that these selection defined individuals will be trait dependent. Thus, the selection defined individual for cancer or differential cell proliferation will in most cases be the cell, whereas selection on running speed will most likely end with defining the individual as an organism. Now we ask the musical question of whether a bee colony is an individual. From a selection standpoint the answer is it depends. For the probability of a worker producing an egg we might decide the bee (the organism) is the individual, whereas for a trait such as the probability of the colony surviving the winter we may well decide that the colony is the individual.


Japanese honey bees mob and “cook” an Asian hornet. The Asian hornet hunts honey bees, however if the colony detects one they will mob it, surrounding the hornet and raising its body temperature until it dies. European honey bees do not have this behavior. For this trait the hive is the individual. (http://www.nbcnews.com/id/20823983/ns/technology_and_science-science/t/surprise-strategy-bees-smother-enemies/#.VCw2n-dfnzg)

The final question is why is multilevel selection a better term than say, “group selection”. The answer, of course, is that selection is acting at only one level then that level is the selection defined individual. In the simplistic world of selection acting at only one level there is only individual selection, but sometimes the “individual” will be a group. The only time it makes sense to talk about group selection in this view is when selection is acting at more than one level. In this case the lowest level at which selection is acting would be “individual selection”, and selection on contexts larger than the individual would be “group selection”.


What is an individual (Part 2): An arbitrary definition

Posted: September 17th, 2014 by Charles Goodnight

Last week I discussed why defining the individual is so difficult. Having put you in an existential crisis over whether or not you are an individual, it is time to pick up the pieces and see if we can come up with a useful phenotypically based definition of an individual. At the very least perhaps I can help you decide whether or not you need to buy an extra bus ticket, one for you one for your symbionts, or whether one bus ticket is enough.

jadzia of deep space 9

Does Jadzia Dax of Deep Space 9 need one ticket or two when she takes the megabus to Leran Manev (the capital city of Trill)? (https://mycrazylosttheory.wordpress.com/tag/trills/)

So, what is an individual? It turns out that a big hint comes from contextual analysis. Who would have thought that a statistical technique that is frankly just multiple regression could provide answers to philosophical questions! To remind you, contextual analysis is a method of analyzing multilevel selection. Using this method the fitness of an individual is measured, as well as a set of traits measured on the individual and on the group (or neighborhood, or kin group etc) that they belong to. A multiple regression is then done, and if there is a significant partial regression of individual fitness on a group level trait we say that group selection is acting. This makes sense because a significant regression implies (taking all of the appropriate caveats into account) that the fitness of an individual is a function of the group to which they belong.

Here is point number 1: in contextual analysis fitness can only be assigned at one level. It is measured by the investigator, and the level at which they measure fitness is a function of what is possible, and on the investigator’s understanding of biology. Thus, if you want to see if there is selection for running speed in cheetahs it makes sense to measure and assign fitness at the level of the whole organism. You could assign it at the level of the cell, but it would be a waste of time (who wants to measure the fitness of a trillion cells?). On the other hand, you could measure it at the level of the population of cheetahs, but from our understanding of biology, we would be inclined to decide that this would not be terribly helpful. Thus, logically, it makes sense to assign fitness at the level of the organism. I will make the interesting point that in this case the “organism” is actually a multi-species assemblage that collectively hurtles through space trying to catch gazelles.


When studying selection on running speed in cheetahs it makes sense to assign fitness at the level of the organism. Interestingly, in this case the “organism” is a multispecies assembly. As an aside, this stretched out all legs off the ground position is the one part of the cheetah gate that is found in very few if any other animals. (http://theruniverse.com/2012/07/running-tips-from-cheetahs/)

Point number 2: Nature changes as nature changes. That is, change in groups occurs at all levels at all times. Cells in our bodies are produced by mitosis, and lost through cell death, organisms live and die, populations are founded and go extinct, as do communities, species, ecosystems, and presumably planets. Every one of these may cause a change in the distribution of their appropriate population. That is, if you drink a lot of alcohol perhaps some liver cells die. This is a change in the distribution of cell types in your body. If some cheetahs run to slow perhaps they starve, this can result in a change in the distribution of running speed in the cheetah population. In the first situation case we are inclined to call the decrease in the proportion of liver cells as development (or perhaps stupidity), in the second situation we would be inclined to call the change in running speed evolution. I would argue that both cases are qualitatively similar, however the difference is that we intuitively assign fitness at the level of the organism. Because we assign fitness at that level there can be variation among organisms in fitness, and since there is variation in fitness among organisms and we can speak of changes in running speed in terms of evolution. In contrast, in the case of the case of the liver cells, since we intuitively assign fitness at the level of the organism speaking of the fitness of cells within that organism makes no sense. Thus, we have to call differential death and proliferation of cells by another name, such a “development”.

The point is that there is no qualitative difference from nature’s perspective between these two scenarios, but there IS a qualitative difference in our interpretation of these two scenarios. The difference is that in the case of the liver cells we are speaking of a process taking place at a level below that which we assign fitness, and thus call it development, whereas in the second it is above the level at which we assign fitness, and thus we an call it evolution.

So, this gives us a very simple and unsatisfying definition of what an individual is: An individual is the level at which we assign fitness.

So, to consider the examples I talked about last week. For an aspen stand, is the individual the clone or the tree? For identical twins are they one or two individuals? Based on my argument, the answer is you decide.

There are a couple of interesting points about this idea. The first is that this explains why we have so much trouble defining the individual. The definition I gave suggests that from a very fundamental perspective what an individual is is an arbitrary construct of how we view nature. It is not a natural unit any more than any other part of nature is (remember Mayr arguing that the species is the only natural unit in phylogenetics?). The more interesting point is that in almost every case, probably every case for metazoans, what we call an “individual” is typically a multi-species assemblage. In other words, not only is the individual an arbitrary construct, it is not even a single organism, if you define “organism” as a colony of cells derived from a single fertilized egg.

Next week I will expand on this definition of the individual, and hopefully make it a little less arbitrary. Nevertheless, I do stand by this as a perfectly valid definition of the individual, oh and Jadzia Dax should be fine buying only one bus ticket.

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