A phenotypic view of evolution Evolution in Structured Populations


IBB, Multilevel Selection and Evolution

I have been meaning to write this, and have resisted because it is (locally) political, and it may be a declaration of the end of the University of Vermont.  

Our university, like many others, has started a budgeting procedure called IBB.  This stands for Irrational Brainless Budgeting, although the administration claims it stands for Incentive Based Budgeting.  In this post I want to explain why it cannot work, and why implementing it may have caused terminal damage to the university, and the 500 million years of data, and 100 years of theory I have to support these claims.

The idea behind IBB is that units (departments, colleges etc.) that produce more revenue should get a bigger budget.  Thus, if a college can grow its revenue by increasing its enrollment it is granted a bigger budget.  On the surface this makes sense.  It takes money to make money, so if a unit is making more revenue it makes sense that they should get more resources.  But this only makes sense on the surface.  The problem is that income tends to be relatively fixed – the number of enrolled students is approximately fixed, as is tuition; grant and contract income is unlikely to increase dramatically.  As a result, the best way to increase a unit’s revenue is to take revenue from other units.  This is exactly what is happening at UVM.  Right now you can take a “biometry” type class in any of four colleges (Arts and Sciences, Agriculture, Medicine, Natural Resources).  The incentives favor this because units gain resources by increasing their revenue, regardless of the cost to other units or the university as a whole.

Animals have been performing this experiment for 500 million years.  The most basal animals (sponges, jellyfish) have an IBB type reproduction.  That is basically any cell can give rise to reproductive cells (the “revenue” of living things).  As animals become more derived (“advanced”) there is a tendency to limit the cells that can become reproductive, until you get to animals such as vertebrates in which the reproductive cells are sequestered very early in development, in fact while development is still under maternal control.  

The importance of this is that the only way a somatic cell (say a liver cell) can increase its fitness is to support the survival of the whole organism and reproduction by the gonads.  That is, by only allowing reproductive cells to reproduce vertebrates have (nearly) eliminated competition within the organism, and provided the strongest incentive possible for cooperation among cells within the organism.

This is exactly the opposite of what IBB does.  IBB encourages self-promotion of units regardless of any effects such self-promotion may have on the soma (i.e., the university).  At this point I should mention that Sears used a similar budgeting procedure.  Sears had other problems, but I am certain that their accounting methods contributed to their demise .

The theory on this is well developed, and dates back to at least the 1960s (Griffing 1977). Selection for populations of interacting genotypes. Proceedings of the International Congress on Quantitative Genetics, August 16-21, 1976).  In recent years there have been major theoretical advances on the importance of group structure in crop improvement (e.g., Wade, Bijma, Ellen, Muir 2010 Group selection and social evolution in domesticated animals. Evolutionary Applications 3: 453-465).  This is an active area of research, and one that has resulted in large increases in agricultural yields.

A conceptual example will illustrate the results nicely.  If you plant 10 1 hectare plots with corn, you can either attempt to increase the yield per hectare by selecting the individual corn plants that produce the greatest yield (bushels of corn) or the hectare plots that produce the greatest yield.  If you select the individual plants with the greatest yield, paradoxically the yield per hectare goes down.  This really happens! (it happened in my thesis, which is how I discovered Griffing).  It happens because the individual selection favors plants that aggressively “steal” resources from their neighbors, resulting in a plot of “mean” plants that fight for resources rather than cooperating to raise overall yield.  On the other hand, selecting at the plot level promotes cooperation and establishes the best compromise between cooperation and aggressive self-interest that maximizes overall yield.

The implications for IBB should be clear.  IBB promotes aggressive self-interest of the colleges and departments within a university.  This will promote duplication of effort in different colleges, “poaching” of revenue resources, and ultimately increase the expenses to the university without increasing its revenue.

Finally, IBB is very much like a carcinogen.  A carcinogen may not cause cancer, but it does promote it.  More importantly, removing the carcinogen does not make the cancer go away.  Similarly, IBB does not cause redundancies, but it does promote it, and the results are long lasting, if not permanent.  In the biometry example at the beginning, IBB provided an incentive to develop redundant courses, which in turn provided incentives to hire faculty and devote resources to teach those courses.  Removing IBB will not make those faculty and resources go away.  Further, colleges and departments are notorious for not easily giving up resources.  For this reason, I fear that the damage done by IBB may be permanent.

On Space Travel

So, one of the things I have been doing with my spare time is thinking about how evolution and the history of life can be used to inform issues that I (and we) think about. One issue that has been around longer than I have is interstellar space travel. Interestingly, evolution has something to say on the topic: Nope, we can’t do it. My reasoning basically comes down to the fact that there is no evidence that anybody or anything has ever done any interstellar travel. Of course, it is hard to prove a negative, and I, not surprisingly, won’t succeed. Nevertheless, I think I can make a strong argument that interstellar space travel won’t happen.

The first thing to point out is that earth is certainly not unique, and that there must be uncountably many planets with life on them. Even if only a tiny subset of those planets have life technologically advanced enough to make space ships, there will still be a huge number of such planets

The second observation is that life, and especially technological life always leaves a trace. There are billion year old fossils, although some are iffy. Importantly, some of our best fossils are waste products. How do we know when photosynthesis evolved? It left behind waste products (oxygen). Caproliths (fossil poop) provide evidence of what animals used to be here, and we have fossil castings of ancient burrowing mammals, not to mention tracks of everything from sea creatures to dinosaurs. Technology only produces more artifacts. My home is stuffed with everything from native American arrow heads and pre-Columbian artifacts (don’t hate me, my father collected most of them in the 1940s, I collected others in the 1960s). Evidence of human activity on earth abounds, most recently being found as patterns that show up on photos taken from space. Importantly, one of the major traces of life is garbage. Thus, there will be evidence that humans went to the moon in the form of footprints, and the base of the lunar lander. It is likely that these traces of space travel will be present for thousands of years at a minimum. The point is that life, and especially technological life leaves traces.

Life Leaves Evidence. (https://geochristian.com/2008/10/28/dinosaur-footprints-part-3/)

The reason that this is relevant is that we have been looking at the heavens for a long time, and around earth even longer. Nevertheless, we have yet to see any evidence of interstellar travel. Some have argued that things like the Nazca lines suggest space travel. I won’t argue that that could be an explanation, only that human ingenuity is at least as plausible and that as a consequence it can’t be used as proof of alien visitors. More importantly, we have never found a piece of broken alien technology, the alien equivalent of the lunar lander base, or anything similar to the middens and garbage dumps that typify human societies.

One mitigating factor is that you could argue that aliens had not visited for a long time (I would argue at least 500 million years) and that the garbage had rusted away. While you would still expect a discarded ray gun or something to appear, maybe we have missed it. However, this brings me to the next point: There is no evidence of space travel.

Consider human travel on earth and in our solar system. We have left a lot of evidence of our travels. First there is the garbage. Our ocean bottoms are littered with ship wrecks, there are airplane and car wrecks everywhere. (I stumbled on one in the Amazon for example). We have left part of the lunar lander on the moon, and various vehicles on Mars and other planets throughout the solar system. Nevertheless, we have never seen an alien space ship or evidence of past space travel by non-humans.

This can be explained because wrecks don’t emit energy and are hard to detect as a result. After all it’s a big deal when a Spanish galleon is found, and because the have gold bullion people are looking for them. What is a problem, however, is that our ports and airports are very easy to detect. Ports have always been harked by sight houses and flags (not to mention flotsam). More importantly, airports are purposely very easy to find. In the western part of the country you will find cement markers pointing towards airports, and airports emit radiation in every part of the spectrum, from long waves to microwaves. Importantly, this is not an accident. This radiation is important for communication (radio), navigation (e.g. Loran), and monitoring air traffic (radar). Of course, airplanes and ships all have transponders and other devices (EPIRBS) that make them easy to detects. The point is that the transportation on earth generally leaves a big signal both historically and in the form of released energy. There is no reason to believe that space travel would be any different, and in fact we would expect it to produce more signals since getting lost in space would be, if anything, more serious than being lost on earth. That said, there is no evidence of any form of radio communication or interstellar navigation aids.

No wonder they were lost in space:  They didn’t have navigation aids. (http://www.peoplequiz.com/trivia-quizzes-1459-Lost_in_Space_60s_Space_Adventure.html)

Putting this all together, I see no evidence that extraterrestrials have ever visited us, or that there is and evidence that there is interstellar space travel in our region of the universe, even though such evidence should exist if space travel did occur. Perhaps I am overlooking something. Perhaps pulsars are navigation aids. Perhaps the Nazca lines were put there by aliens. Perhaps aliens directed human evolution. All that is, of course, possible, but that would require that alien life was entirely different than terrestrial life in that it always cleaned up after itself, and navigated without using energy. A much simpler explanation is that interstellar travel doesn’t happen, and mysteries such as the Nazca line have a mundane explanation instead of being evidence of aliens.


Back from sick leave

Well, I guess I am back blogging. I missed it, but I had a stroke a year ago thanksgiving, and well, unnecessary writing was sort of out of the question. . . As you can imagine it has been something of a struggle to reenter the world of the living, but I am back.

It is worth mentioning some of the details of my stroke, since some of the details are rather interesting.

One of the most interesting was the most likely cause. Of course nobody knows the actual cause, and it almost certainly no one single factor; however, during recovery I was (self) diagnosed with severe sleep apnea, and I suspect this was a (the?) major contributing factor. This is interesting because fixing this problem was key to my recovery, and seems to have fixed a whole host of more minor health issues as well. The other thing that is interesting is the doctors totally missed it until I demanded a test. It has happened on several occasions in the past. The most dramatic of these was a fungal infection I diagnosed treated and had in remission before the test results I demanded came back. What was humorous is that the worlds expert on this disease was in the same building, and was completely panicked that I had this deadly disease, even though it was kind of after the fact.

During my (still ongoing) recovery from the stroke this issue with doctors has continued. One of the features of stroke recovery is a tendency for seizures to occur. I have had two grand mal and one petit mal seizures. I have been unable to convince the doctors that these are a good thing in that each seizure is associated with a major improvement in my symptoms. I can’t really blame them as seizures are dangerous, and the finding that they were part of the healing process presumably wouldn’t change the treatments. Still, I was stunned by there complete lack of interest when I reported that my symptoms had improved.

This le me to wonder: am I just so much smarter than doctors that I am a better diagnostician and more curious about health related issues, or is something else? I wonder if perhaps being a functioning doctor requires shutting down some of the creativity that makes a scientist a scientist. After all treating patients requires following protocols, and creativity is, or should be. Frowned upon. I don’t have an answer, but it is worth pondering. By the way – I am not that smart.

Anyway, other interesting things: My language came through intact. I did have one interesting thing happen. In a conversation I couldn’t come up with the word “bat” (as in the animal that flies). I was abled to get to it by remembering murciélago and fledermaus. More interesting, I have a lot of difficulty reading some thinds, but often science doesn’t give me problems. Interestingly words, letters etc. are easy enough, but stringing it together into a coherent phrase is hard. On the other hand, I have no problem if the computer reads it to me, and I have no problem writing. Go figure.

So, I will resume my blog, but probably not at the pace I maintained in the past.


Of cultural inheritance and cultural evolution

As you may know, I am writing a book on evolution.  Below is modified from a very rough first draft of part of my chapter on cultural inheritance. 

My thinking about culture has change in that I now think more about cultural inheritance than cultural evolution. The reasoning being that evolution is evolution. It is the change in the distribution of a population due to the gain and loss of individuals. Evolution, and especially evolution by natural selection (if we allow that secular environmental change can be a force of evolution, then arguably this evolutionary force does not require heritable variation), requires that at least a portion of the variation be heritable, but makes no claims as to the cause of that heritability. As such, whether a trait is a physiological trait such as body size, or a cultural trait such as some aspect of a person’s language it is still a component of the individuals phenotype, and it is still organic evolution.

When we are talking about organic evolution we think of individuals (frequently the organism, or the organism and its microbiome), and how the distribution of these individuals change over time. Thus, the population is a set of individuated entities with a phenotype with measurable traits that may change as the individual develops. Because it is the individual living entity (e.g., organism) we can call it biological or organic evolution. In real systems individuals will occupy physical space, and when that space is filled, or the organism is otherwise constrained, and the population can no longer grow it is said to be at its carrying capacity.

However, we would like to have a concept of cultural evolution. Fortunately, the beauty of the concept of evolution is that it can be applied to any system as long as we can identify the individuals and the population. This is what needs to be done to have a useful concept of cultural evolution.

To develop a concept of cultural evolution we first need to identify the individual. We have to remember that ideas or concepts are not fixed entities. In some cases this is almost trivial. It would surprise no one if my interpretation of a poem or song were different than your interpretation. Nor is it surprising that people miss-hear lyrics of songs, such as the miss-hearing of Credence Clear Water Revival’s lyric “there’s a bad moon on the rise” as “there’s a bathroom on the right”. However, there is no reason to believe that my interpretation of the letter A or the wavelength we agree to call the color blue is the same as your interpretation. As long as we agree on the name for the symbol or object we are able to communicate. What this means is that the Dawkins concept of meme is quite meaningless. There is no object that can be identified clearly as a meme. I think the better concept of individual for cultural evolution is the idea as it exists in a person’s mind. Thus, my understanding of the concept of the color blue and your understanding of the concept of the color blue are two different but very similar concepts. Our different understandings of the concept are individuals, and they, along with everybody else’s understanding of the concept of the color blue are analogous to a “species”. The formal definition of evolution I gave is change in the distribution of a set due to the gain or loss of elements of that set. Using this we can define cultural evolution to be change in the distribution of a concept due to the gain and loss of individual understandings of that concept.

Interestingly, the internet the term meme, or internet meme, which needs to be distinguished from the Dawkins meme, appears to be directly analogous to the collection of individual concepts that are closely related. Thus, I would suggest that we use internet meme, or just meme, to describe a set of similar individual concepts that are held by individual humans. That is, meme is analogous to population, and could potentially be substituted for “concept” in the definition above.


Grumpy cat is a classic internet meme.  My understanding of the grumpy cat meme is different from yours or anybody else’s. (from https://jasoninwv.wordpress.com/tag/grumpy-cat/)

In this conception of cultural evolution an individual is a person’s understanding of a concept. Thus, each person is effectively a territory for the concept, and the “population size” of the concept is the number of people in the population. A new individual concept is “born” when a person is exposed to the concept, and dies when the person forgets the concept or dies. Once a concept has been introduced (“born”) it can change within that person over time, however, this is development in the same way that changes in an individual are development when speaking of biological evolution.   An individual concept in a person can change due to simply the person thinking about it, or due to discussions with others. Much of the process of teaching thus, can be seen as introducing heritable changes in the concept a person holds. Importantly, this phenotypic approach allows us to recognize that what we do in learning is to gather information either by observation or being taught and building our own understanding of a concept. That understanding is not transferred as an intact object. Rather the teacher presents their understanding of the concept and the student takes that presentation and makes a similar, but not identical, understanding.

Another recurring theme in this blog is that changes that occur are independent of the name we give it. Thus, if we assign fitness at the level of the organism changes below that level must be analyzed as development, or a related term. In a similar vein, if somewhat orthogonally, if we are interested in the evolution of culture we can treat humans as the “environment” in which cultural concepts “live”, or, if we are interested in biological evolution we can treat the understanding of a concept held by an individual as part of their phenotype, and study the evolution of the human phenotype. The point being that acquisition of a new understanding of a concept by an individual changes both the individual phenotype which can be either development or biological evolution depending on the circumstances, and it changes the distribution of the concept. Thus a cultural change can be studied both as biological evolution and as cultural evolution, the difference being whether the focus is on changes in the organism, or changes in the concept.

The details of the expression and inheritance of a concept will be very different than those of traits and phenotypes in biological systems, thus we can expect the details of cultural evolution to be quite different than those of biological evolution. Nevertheless we can still talk of concepts as having phenotypes or something analogous to phenotypes, and we can talk of a transition equation that describes the process by which a the understanding of a concept in one person gets transmitted to become a new understanding of that concept in a different person. Thus, in broad strokes cultural evolution will be conceptually similar to biological evolution.

There are two areas where the two forms of evolution differ. First is defining the individual.   In biological evolution we defined the individual as the level at which we assign fitness. A similar approach should work for cultural concepts.   But, at least to me as a biologist, identifying a cultural concept where it makes sense to assign fitness seems problematical. There is also the question of how “large” can a cultural concept logically be? As with biological evolution we can assign fitness at any of a number of different levels. One presumes that for cultural concepts a similar set of nested levels could be identified, and logically appropriate levels identified. In any case, whether the appropriate unit for study is classic internet “memes”, smaller units such as the concept of the color blue, or much larger concepts such as the concept of relativity is a question I am not prepared to answer.


Which box is a different color?  The Himba have no problem with this test. (from http://www.iflscience.com/brain/when-did-humans-start-see-color-blue)

The second major difference is in the transition equation.   In biological systems a large portion, and probably in most cases the dominant portion, of the heritable aspects of the phenotype will be due to genetic and cytoplasmic effects. These enter into the system at conception, remain unaltered throughout life, and in many cases will follow discrete Mendelian inheritance rules. In contrast, one suspects that a new understanding of a concept in a person would first occur as a poorly formed understanding, and then develop into a more detailed understanding as the person acquired more information on the topic. Thus, in cultural evolution it seems reasonable to imagine that much of the heritable components of the transition equation will enter well after the understanding of the concept is first formed. Also, unlike biological evolution, it is likely that discrete elements in the transition equation will be rare if they exist at all.

Clearly, much needs to be done to develop the concepts underlying cultural evolution. Just as clearly, a biologist such as myself is not the person to do it.


On Kinship

On Facebook one of my friends posted that they were attending a conference on reconceptualizing kinship, and of course, I responded that it was tempting to put in my two cents worth on the subject. To my shock another commenter asked me to do just that. SO, given that I have been absolutely swamped since getting back from sabbatical, I figure I ought to at least pretend to have a blog (I actually have a couple of other issues that really need to be addressed. Maybe in a few weeks). In any case, here goes.

Of course, kinship means many things in different contexts. Colloquially kin can mean relatives, as in my cousin is kin. From a genetic perspective, the classic use of kinship is in inbreeding coefficients, and thus it is the probability that two individuals share common genes. Finally, kinship was coopted by Maynard-Smith to describe the “r” term of Hamilton’s rule.

Colloquially we can use kinship in a more general sense. Thus, a person might describe themselves as having kinship with others of a similar political view, or a group fighting for a cause may consider their fellow members as kin.


Sisterhood: 1) A bond between two or more girls or women not necessarily related by blood. 2) An association, society, or community of women linked by a common interest, religion, or trade. (Image from http://www.thismorleylife.com/wp-content/uploads/2013/09/25473872sisterhood.jpg, definition from Google.com, and Urban dictionary.com)

Of particular importance here from a genetic perspective is that the inbreeding coefficient definition of kinship is very consistent with the colloquial definition of kinship as relatives. This is not true of Maynard-Smith’s definition of kinship as the r term in Hamilton’s rule. In fact, Maynard-Smith’s definition comes much closer to the social extension of kinship as two individuals that share a common bond, regardless of the cause of that bond. I would suggest that Maynard-Smith made a mistake here. In common culture we make a distinction between kin as in relatives and kin as in shared interest. For example, we have no problem referring to relatives strictly as “kin”, but for those with a shared interest we are likely to put in a modifier – brother in arms, brother from another mother, BFF. I would argue that Hamilton’s r is actually a combination of these two colloquial concepts of kinship. Sharing of genes in an additive sense, and other forms of sharing of phenotypes.

The reason I say this comes from contextual analysis. First, in one of my papers (Goodnight 2013, Evolution 67:1539) I show that the mathematics of kin selection can be directly translated into the mathematics of contextual analysis. The basic process is that Hamilton’s inclusive fitness can be translated into the direct, or neighborhood fitness approach (Taylor and Frank 1996 JTB180:27 for the neighborhood fitness approach, Taylor, Wild and Gardner 2007 J. Evol. Biol. 20301 for the equivalence of inclusive fitness and direct fitness). The neighborhood fitness approach in turn is based on EXACTLY the same equation as inclusive fitness (fun fact: Contextual analysis predates neighborhood fitness by a lot. It has precedence, and I think a strong argument could be made that the neighborhood fitness approach should be re-named contextual analysis).

It is worth emphasizing that there are significant differences between kin selection and multilevel selection, and these are the basis for my reasoning behind why I don’t like kin selection. However, given the close mathematical association between contextual analysis and neighborhood fitness it is hardly surprising that it is possible to derive Hamilton’s rule using contextual analysis (Goodnight Schwartz and Stevens 1992.  American Naturalist 140:743) :

Hamiltons rule

This formulation differs from the classic kin selection version in several important regards. The first, a bit irrelevant, but something I personally can’t ignore, is that CA is treating Hamilton’s rule as a competing rates problem. That is, altruism will evolve when group selection is stronger than individual selection, and this can happen either due to differences in the intensity of selection (measured in genetic standard deviations at the two levels), or in the relative magnitudes of the variances in the group and individual trait (measured as the proportion of variance that is among groups).  In contrast, neighborhood fitness is providing the optimality solution.  This difference rather fades away when applied to contextual analysis, but it is a big difference in philosophy.

Much more important, however, is that using contextual analysis it is clear that Hamilton’s “r” is the fraction of the total variance that is among groups. This is an important point.   In an additive world where nobody interacts with anybody kinship, as measured by Wright’s FST, is exactly equal to the variance among groups. However, in a world in which interactions occur this will no longer be the case. Consider:

If there is epistasis is gene interation: For epistasis, the variance among groups will roughly be proportional to FSTN, where N is the order of the interaction. For example if there is two-locus epistasis the fraction of variance among groups will go up roughly as FST2. This is really only strictly true for additive by additive epistasis, nevertheless it makes the point that relatedness and variance among groups are not necessarily the same thing.

If there are interactions among individuals: This can be indirect genetic effects, but it can also be non-genetic effects. One of the very common features of social groups is some form of policing behavior. For example, in bees workers typically destroy worker laid eggs. Thus, even if there is genetic variation among workers in their propensity to lay eggs, it doesn’t matter since all of this variation is suppressed by the policing behavior. On an emphatically non-genetic scale, musical bands work together to enforce a steady rhythm on the band members. This rhythm produces a product (music) that is appealing, and, if the stories about rock bands are correct, has a definite effect on fitness. Similar stories can be made about everything from sports teams to military organizations. These interactions affect the heritable variation among groups, but have no effect on the heritable variation within groups. They simply are not in kin selection models, and as such they represent a complete wild card that will nearly always make altruism easier to evolve.

The point is Hamilton was thinking about a linear additive world when he was talking about the r term in his rule. This was perfectly reasonable in 1964 when he published his work. That was before the days of computers, before any math around gene interactions had been developed, and before there was any data to suggest that group selection could act on interactions among individuals. It was also over 50 years ago. I think it is probably time we considered moving on!

So, what should we do: Recognize that Maynard-Smith was incorrect to call Hamilton’s rule it kin selection. Hamilton’s r DOES NOT refer to kinship, or at least not kinship in the narrow genetic sense. Rather it refers to the ratio of the variance among groups to the total phenotypic variance. Given what we know about gene interactions and social interactions we are long past the time when we should have abandoned Hamilton’s simplistic view of the cause of the variance among groups. I leave it to the reader to decide whether kinship applies to individuals related by social interactions. Maybe we should have a “grouphood of the interacting genes”?


Is a Grouphood of traveling genes a form of kinship? (http://trailers.apple.com/trailers/wb/thesisterhoodofthetravelingpants/images/sisterhood_01.jpg)

Population structure and recombination

One of the joys of a genic view is the apparent constancy of things. One of the big ones is that a gene has an effect that can in some sense be considered a constant that can be written down and stored on a piece of paper in a mayonnaise jar on Funk and Wagnall’s front porch (that is a Carnac the Magnificent reference for those less than a million years old). As I have pointed out before, the way we measure the effect of an allele is to use a defined, usually homozygous, background and ask what the “mutant” and “wild type” alleles do to the phenotype (yes, I know the reality is more sophisticated than that, but really not by much!). The point is that the effect of the gene is only constant in the context of the simplified genetic background in which it is measured.


CARNAC THE MAGNIFICENT (Johnny Carson): Supercalifragilisticexpialodocious and constant gene action. ED MCMAHON (reading question): Name two phrases that have no meaning. CARNAC: May the fleas of a thousand camels infest your armpits.

I got to thinking about this and realized that there are other genetic parameters that we take as constants, that are actually functions of the context in which they are measured. The one I want to talk about today is recombination rate. Typically recombination rate is simply the map distance between two genes measured by the frequency of crossovers in a dihybrid cross.


A dihybrid cross tells us the recombination rate for a pair of loci. In this case the loci are linked with a recombination rate of 0.17 (From https://www.studyblue.com/notes/note/n/lecture-exam-2/deck/8120019)

This is all well and good, until you get to population genetics textbooks. They will then tell you about linkage disequilibrium (or gametic disequilibrium if you prefer). First a few fun asides. Linkage disequilibrium is actually the covariance between the allele state of two loci. To see this imagine we have an A locus with alleles A1 (value 1) and A2 (value 0), and a B locus with B1 (value 1) and B2 (value 0). The four haplotypes have frequencies of p11 (A1B1), p12 (A1B2), p21 (A2B1), and p22 (A2B2). Then the covariance is:

Equation 1

Second fun aside: D is the determinant a matrix of the frequencies of the gamete types in a population.

Equation 2

What that all means I am not sure. That is other than demonstrating the obvious fact that all of nature is embodied in covariances and linear algebra.

At this point your population genetics textbook will go on to tell you about the decay of linkage disequilibrium based on the recombination rate. It doesn’t take a lot of algebra to show that linkage disequilibrium decays as a function of the recombination rate. For example:

Equation 3

where the prime mark indicates the next generation and

Equation 4

At first blush this is beautiful. It demonstrates that simply by knowing the map distance between two loci we know the recombination rate, and with it the rate of decay of linkage disequilibrium. In other words, we assume that this classic measure of association is a property solely of the genome, and thus only the genome is responsible for the behavior of the genes.

Sadly, as is so often the case with the genic view, there is a hidden assumption that has been hidden for so long that it is even lost from our intuition. This hidden assumption, of course, is the assumption that the population is unstructured. The important point to realize is that the only time that recombination has any effect is in the double heterozygote. If either locus is homozygous then a crossover event produces exactly the same gametes as are produced in the absence of crossing over. The problem comes that population structure tends to reduce the frequency of heterozygotes. As a consequence, in a classically inbred population the rate of decay for linkage disequilibrium is affected by a factor of (1-f)2, where f is Wright’s the inbreeding coefficient. The easy way to think about it is (1-f) is the probability that two alleles are not correlated, usually because they are identical by descent (IBD). If the alleles in an individual are IBD that individual is by definition homozygous at that locus and crossing over will have no effect. The quantity is squared because homozygosity at either locus negates the effects of crossing over. Thus we can re-write the above equations as:

equation 5


equation 6

In other words we can think of the “effective” recombination rate as r(1-f)2.

This seemingly trivial point is actually quite important. It emphasizes that population genetic parameters are a function both of the genes and the population in which they are measured. Even something as seemingly constant as recombination rate can be changed simply by changing the population structure, and the degree of mating among relatives.

It also has some fun adaptive story telling implications. There is a battle between sex as a source of variation, and sex as breaking up well adapted genotypes. This little exercise suggests that there is a middle ground: sex with relatives. Population structure limits the field of recombination, and has the effect of reducing the recombination rate among loci. One can imagine population structure evolving as a means of preserving local adaptations and reducing the effective recombination rate. Of course this would come at a cost of decreased heterozygosity, so perhaps that would be a different battle.

Finally, I should mention that in many mammals fIS is often negative. This should have the effect of increasing the recombination rate. I leave it to you to make up adaptive stories for that one. . .


A quick review of the phenotypic perspective, pt 2

Continuing on with my brief reprise of the tenets of this blog:

Individuals are the level at which we assign fitness.

First a parable. If we go back to Mayr, he thought that the species was the only natural unit of organization, and argued that the biological species concept (BSC) was the correct definition of species. Since then we have realized that species are perhaps not that monolithic. There is gene flow between species, and it is not always clear whether two different populations are the same or different species.

I argue that the same is true of individuals. (part 1, part 2, part 3)(Not so long ago it was easy to argue that individuals were “organisms”, and that they were a natural unit. The problem, as always, comes when we look too close. Just like the BSC works until we look to closely, this classic definition of individual breaks down when we look closely. Evolution is always defined in a way that precludes changes within an individual, usually called development. Thus, evolutionary biologists are adamant that the change in an individual as it grows from zygote to adult is not evolution. On the other hand we would like to study distinctly cellular level processes, such as cancer development, as evolution. Similar problems come when we study proto-multicellular organisms like volvox, or organisms that grow clonally, such as Aspen. On the one hand a clean definition of “individual” as organism works fine when we are talking about vertebrates and not looking too closely, ignoring that the vertebrate organism is a multispecies entity. However, on the other hand, such a narrow definition results in our narrowing our definition of evolution to changes at or above the organismic level. Something has to give, and I would argue that the correct thing to do is to allow flexibility on what we call an individual.


Volvox: what is the individual? (http://www.dr-ralf-wagner.de/Bilder/Volvox-aureus-DF.jpg)

Allowing a flexible definition of individual has huge advantages. We can study evolution at any level. That is it IS legitimate to study cancer as an evolutionary process. It IS legitimate to study “species selection” in the fossil record even though you do not have access to the fitness of the underlying organisms. And, when we discover that the microbiome was not something that could be simply ignored we don’t have to through out all of the evolutionary studies that have been done previously. This last point is an important one. Our understanding of biology is expanding rapidly. We need concepts and models that can incorporate these new findings naturally without having to re-do our entire conceptual system. The classic concept of individual as a colony of genetically identical cells of the same species physically separated from other colonies (I made that definition up) is simply too rigid, and cannot be adapted to our expanding understanding of living systems.

The down side is also analogous to issues with species concepts. It is now understood that, in order to avoid confusion, when you talk about species and speciation you need to explicitly state what you mean by species. As with species concepts, our understanding of what is and is not evolution changes dramatically depending on the level at which we define fitness. Everything that is at or above the level of the individual can be studied as evolution. Everything below the level of the individual has to be studied as some form of development. This means that when Gardner argues that cancer cannot be studied as evolution (Gardner’s paper; My critique of Gardner; Gardner’s critique of me) and I argue that it can we are both right. In his view the individual is rigidly defined as the organism, and as such cancer must be treated as changes occurring within the organism. He can call it development, disease, what ever, but he cannot call it evolution. I, on the other hand, by embracing a more flexible definition of the individual, CAN call it evolution. What I am doing is defining the cell to be the individual, then the faster cell division of cancer cells is selection. This is opposed by “group” selection in that, with a few notable exceptions, the spread of a cancer is ultimately stopped by the death of the organism.

cancer and selection

Cancer as an evolutionary process (from http://www.nature.com/nature/journal/v481/n7381/full/nature10762.html)

Multilevel selection:

Viewed from the perspective of a flexible definition of the individual, depending on the level at which you assign fitness potentially ALL selection is multilevel selection. Classic “individual selection” is selection on organisms, which is a group of cells, and actually on a community of cells. It is group selection if we assign fitness at the level of the cell, it is individual selection if we assign fitness at the level of the organism. Given that genic view “individual” selection is actually group selection, and is nearly ubiquitous, is it really surprising that “group selection” works at other levels as well?

This raises a second point. The phenotypic approach follows the lead of quantitative genetics, and makes a sharp distinction between selection and the response to selection. Selection is the ecological process by which some entities leave more offspring than other entities. The response to selection is the evolutionary consequences of that. Organismal selection is the differential survival and reproduction of individuals. The evolutionary consequence is a difference in the distribution of offspring that is due to that differential survival and reproduction of the parents. The point is, regardless of the consequences, the level of selection is the level at which selection acts. Thus, if both individual selection and group selection cause exactly the same change in gene frequency, they are still different things, because they are different ecological processes. If I dye a shirt red it may be the same color as if I wove it out of red thread, but nobody would pretend that dying fabric and weaving fabric are the same thing, even if the outcome was the same. Of course, as with dying versus weaving fabric, selection at different levels has qualitatively different consequences. The result is that we do our understanding of evolution a huge disservice when we decide to dismiss levels of selection a priori. This is especially true when we realize that whether or not selection is acting at a particular level is an empirical question, and that we have the tools we need to answer that question.


Dyed or woven, you’re still dead. (from http://anartistcalledred.deviantart.com/art/Curse-of-the-RedShirt-173225300)


A quick review of the phenotypic perspective, pt 1

Some of the recent comments I have received have made me realize that maybe I should re-emphasize some of the very early points I made on this blog. The point of this blog is to blatantly promote a phenotypic view of evolution, and do try to dislodge the dominant paradigm of the gene as the center of evolution. In the discussion that follows it is convenient to use Dawkins as a straw man. My own feeling, based on no evidence, is that most evolutionary biologists accept Fisher as a brilliant founder of modern genetics, and accept his as a very genic view of evolution. Interestingly, Dawkins perspective, working through the lens of Williams, is the logical outcome of taking Fisher’s work to its extremes. So, just as I feel most evolutionary biologists accept Fisher, I feel that that they are deeply uncomfortable with Dawkins, but most of these biologists would have trouble articulating exactly why Dawkins is wrong. Somewhere between Fisher’s deeply mathematical prose and Dawkins polemics something has gone awry. My feelings are that where Dawkins goes astray is very fundamental, and goes all the way back to Fisher. Basically Fisher imagined a genetical world that was a reasonable abstraction for a world in which we had no idea what a gene was, we were at the very beginnings of our understanding of inheritance, and we lacked the computational machinery to do anything more than relatively simple analytical models.

Another reading of Fisher, however, is that quantitative genetics is fundamentally a phenotypic model. The average offspring is the mean of the parents, but the loss of variation due to averaging is recovered in the form of within family variation. We can interpret Fisher’s book is an example of the phenotypic view of evolution that is illustrated using a simple Mendelian model of genetics, but which can be expanded as necessary and as computational power allows. Viewed in this way the phenotypic perspective I am advocating may be more of a descendent of Fisher’s legacy than the more classical genic view.

Matt Foley

Just a bit of self promotion, and maybe a bit of motivational speaking (http://gallery4share.com/c/chris-farley-snl-matt-foley.html)

So here are some of the relevant points:

1) Phenotypes create new phenotypes: At first blush this is just a change in perspective. At the risk of setting up a Dawkinsonian straw man, the classic genic view is that genes make copies of themselves, and use phenotypes as a mechanism to protect themselves, and help them survive to the next generation. This is why Dawkins refers to DNA as “immortal coils”. In the phenotypic perspective parent phenotypes create offspring phenotypes using “transition equations”. These transition equations are accepted to be impossibly complex, and so we accept at the outset that the best we can do are approximations. The simplest approximation to a transition equation is probably the heritability of quantitative genetics, or the simple Mendelian math of a Punnett square, however, in many situations it will be useful to add complications ranging from maternal inheritance and indirect genetic effects, to epigenetic effects, and all the way up to cultural effects.

What this change of perspective buys us is that genes are no longer the center of evolution. There are no such things as vehicles and replicators. These are the construct of a fevered mind that deeply misunderstands evolution. Instead, genes are relegated to being a prominent, but certainly not the only, contributor to the transition equation. This leaves the transition equation as an open ended construct that can incorporate new scientific findings. Rather than having to totally reconstruct our understanding of evolution every time we come up with a new mode of inheritance, we simply need to recognize that the transition equation was more complex than we had originally thought, and we need to modify that equation appropriately.

2) Some aspects of our understanding of evolution change with a shift to a phenotypic perspective, but our basic understanding remains remarkably similar. There have been many definitions of evolution, some of which have relied on a genic view. For example, a classic definition is that evolution is change in gene frequency. Re-framing our understanding to a phenotypic perspective demands a careful rethinking of what we mean by evolution. My own definition is evolution is the change in the distribution of phenotypes in a population due to the gain or loss of individuals. This definition is consistent with phenotypically oriented classic definitions, but ends up being more specific in many ways.

Classically there have been four forces of evolution  that have been identified: mutation, migration, selection and drift. These have mostly been defined in genetic terms. Thus, drift is often called “genetic drift”, mutation is discussed in terms of change in DNA structure.   However, these terms can be defined and discussed in phenotypic terms without reference to the specifics of the underlying mechanisms of inheritance. Clearly migration and selection do not need reference to genes, and our understanding of them really does not need to change at all. From a phenotypic perspective “mutation” need not be genetic change. It can be any change that randomly alters the phenotype of an individual, and that does not correlate with fitness. There is the interesting caveat here, however, that based on our definition of evolution, such random changes do not become “evolution” until they are passed on to offspring. Similarly, drift can be viewed as a change in phenotype frequencies due to the random gain or loss of individuals. With the phenotypic perspective, however, a fifth force must be recognized. This force is easily ignored in the genic world, but cannot be ignored in the phenotypic perspective. This is force is secular environmental change. A lasting change in the environment, such as global warming, can change the distribution of phenotypes directly, and in at least some cases it will be an intergenerational event. For example, global warming is changing sex ratios in some reptiles. If we assume an individuals sex is fixed at hatching, then indeed this change in the distribution of males and females is an evolutionary change by our definition.

I seem to have run into my self imposed thousand word limit, so I will continue this review next week.


Down the rabbit hole: More on multispecies organisms

I just tripped and fell down another rabbit hole. I was going to skip this week, but I would love input on this issue, so here it is. Earlier I argued that the organism was a multispecies entity. This makes perfect sense if we consider mitochondria to be symbiotic bacteria in a host cell, and we talk about the microbiome. Now here is the question: If you catch the flu, or get a bacterial infection (to keep it cellular), is that disease part of you as an organism?


Dang another rabbit hole.

There are two important points to remember. First, in the phenotypic view I am advocating considering the phenotype to be a vector through time, with every trait (a measured aspect of the phenotype) having a time element. Thus, it is not my weight, but my weight when I am 19001055824 seconds old (that is approximately how old I am while writing this). This means that even very temporary things such as whether you are inhaling or exhaling is technically a valid trait. Thus, if you have a fever of 104 degrees on a Saturday morning, that is the value of the trait “body temperature”  at that particular moment. The question is, do we make a distinction because that temperature is “caused” by a flu virus? The truth is I am beginning to believe we cannot make that distinction.

Taking a clearer example. Consider a person who chooses to dye their hair purple. This color comes out of a bottle, and it is no sense genetic or otherwise heritable (well, maybe in some odd cultural sense). That said, it is part of the phenotype. If you were to categorize people by the trait “hair color”. this person would go into the “purple”. Thus, it is a valid trait, and a valid part of their phenotype. How do we deal with this? I would argue that the best way would to consider the bottle of hair color to be a non-heritable or environmental influence on the phenotype. By analogy, I think it is perfectly reasonable to suggest your 104-degree fever is also part of your phenotype.

purple hair

This woman has a purple hair. It is certainly part of her phenotype, but probably not heritable.   (from http://darkuro.tumblr.com/)

So, your fever is part of your phenotype, but is the virus part of you as an organism? Certainly, we would not consider the bottle of hair color to be part of an organism. It is an external aspect of the environment that changes your hair color. Cold air temperatures may cause you to put on a coat (the coat wearing trait?), but it is certainly not part of your body. However, the virus differs here. It is IN your body, and in fact it is in your cells.

Consider our microbiome. There certainly are aspects of the microbiome that are acquired from our parents, either at birth, or because we live next to them as infants, and many of these we will pass on to our children.   Thus, they are heritable from the phenotypic perspective. However, others are picked up late in life, perhaps when we temporarily change our diet, and then lost again, perhaps when we revert to our old diet, and are not heritable. I think a strong argument can be made that this microbiome should be considered part of the multispecies organism: Selection acts on the whole organism; outside of perhaps prokaryotes, single species organisms don’t exist; as far as I know, animals cannot survive without their symbionts. From an experimental perspective, it is difficult or impossible to separate symbionts that are heritable from those that are non-heritable, and perhaps more important both can have significant effects on our phenotypes in ways that can affect our fitness. Thus, I think it can be argued that all aspects of the microbiome, whether heritable or not, should be considered part of the organism. Nor does it makes sense to me to argue that there is a minimum residence time before a symbiont or disease should be considered part of the organism. Such a waiting time is necessarily arbitrary, and as a result there will always be situations that are ambiguous.

Now comes the question: Should we make the distinction between the bacteria that we picked up on vacation that makes it easier to digest shrimp from another bacteria that gives us diarrhea? I cannot think of a criterion that does not require special pleading that incorporates the former, but not the latter into the organism.

One final caveat is that it is important to remember that the most appropriate unit to assign fitness depends on the trait being investigated. Thus, the colony might be the appropriate unit if we are examining colony defense, the organism if we are examining foraging behavior, and the cell if we are examining cancer. Perhaps the organism is best thought of as being equally fluid. A flu infection is an assault on our bodies, thus if our trait is immune response, maybe the organism is everything but the flu virus, whereas if we are looking at body temperature the organism is everything including the flu virus. This is a bit of a conundrum for me, and I am happy to get any feedback that anybody else may have.


Some thoughts on aging and the phenotype

I have been gone a while. Something of a creative meltdown after the Evolution meetings. Perhaps one to many Caparinha, at what might have been the best party ever at an Evolution meeting. Leave it to the Brazilians to throw a party with enough food and liquor and the wackiest live music ever. In any case, I am back in Vermont, eating kale and other healthy things that us aging hippies do, and thinking about the pain of having to ply my profession as a teacher. Time to get back to work.


Admittedly a terrible picture, but the party was one of the best.   If you missed the Evolution meetings this year you made a mistake.

Jake Moorad started a discussion with me about how aging affects individuality. My first thought was that I have no idea. As usual, such an answer means that it is a really interesting question. After giving it more thought I have come to realize that it has no effect at all. After all, an individual is the level at which we assign fitness, which is potentially quite arbitrary. In most cases the “individual” will be an organism and its associated symbionts. Thus, despite the fact that an individual changes as it ages, I think it should have little influence on what we call an individual. What it does change, however, is it complicates what we think of as the phenotype. The fact that the phenotype changes over time is not a trivial issue, and it is one that needs to be given some attention.

How to view the phenotype as a vector through time is a topic I have discussed before, and one that is a general issue for the phenotypic view of evolution. My solution is to treat the phenotype of an individual as a vector through time that begins at formation of the individual, and ends at their dissolution. There are a couple of interesting things in that sentence. Note that I am specifying the “individual”. It seems to me that, although perhaps not essential, it makes sense to assign phenotypes at the same level at which we assign fitness. I could be argued out of that, but for the moment it seems right (which is not terribly convincing to me, let alone anybody else). Second, I speak of the “formation of the individual” and “dissolution” of the individual. If we assign fitness at the level of the organism, this will be at conception or birth, depending on your perspective, and ends when the organism dies. But remember two things: First, if we assign fitness at a level other than the organism, “birth” and death may not be an appropriate terms. However formation and dissolution will always be appropriate, since our definition of evolution involves the gain and loss of evolution, individuals must of necessity have a beginning and an ending if they are to be considered to evolve.

If we take a classic genic perspective of the individual as a single species organism it is easy to ignore the time dependent aspects of the phenotype. Most importantly under a genic perspective genes are the only important heritable effects on the phenotype. These all enter at the time of formation (birth) and are unchanging through time (this last ignores somatic mutations of course).   This is not true from a phenotypic perspective. Culture is a prime example. The language you speak whether you are most comfortable with a fork and knife or with chopsticks are all heritable aspects of phenotype that are added after birth. Similarly, your cultural parents will not necessarily be the same as your genetic parents. Children learn their earliest language from their parents, but the vast majority of their language comes from peers and children that are slightly older than they are. This acquisition of heritable elements is not limited to culture, of course. We acquire much of our microbiome from our parents, and other individuals with which we live, and in many social insects, such as termites, trophallaxis is essential for their survival.

Screen Shot 2015-04-20 at 12.25.47 PM

The phenotype as a vector through time. Effects entering from the top are possibly heritable inputs, effects leaving below the lines are products of the phenotype. Note that the phenotype ends at death. This is why products such as beaver dams and human produced things like books are part of the phenotype, and not part of the distended (or is it extended, I always get it wrong) phenotype.

However, it is not just the acquisition of heritable elements that affect the need to consider the time element in the phenotype. Traits also change over time.   At a simple level every trait will have a time element. One way that this is handled is to simply to measure traits at a time when they are stabilized. For example, most vertebrates have targeted growth. Thus, there is a period between when adulthood is reached, and before senescent decline that traits are stable enough that we can effectively ignore the time element. In reality, of course, we should always include the age component, thus, it should be considered weight at age X, not adult body weight. However, speculating about how things ought to be done is different than doing things, and well, I for one will not be angry at people who simply measure adult body weight.

This does raise one additional interesting point. That is we can measure the time element of a trait to whatever precision we choose. Thus, in principle we could measure a trait such as whether an animal is inhaling or exhaling, or whether their heart is in systole or diastole. From an evolutionary perspective it would be silly to measure such highly time dependent transient traits, nevertheless it emphasizes the point that traits are aspects of the phenotype we choose to measure, and as such can be measured to whatever precision is appropriate.

More interesting, however, is the expression of traits with non-genetic inheritance. In some instances traits might not be expressed at all until the causal elements are acquired. For example, the trait of speaking a language cannot be expressed until the language is learned. Language is not acquired at birth, and if it is not the mother tongue, it may be acquired quite late in life. Further, if this person goes on to teach others their newly acquired language we can say that they have a heritable trait (the language understanding) that they acquired late in life.

Finally, some traits we may be interested in might be rate of change over time. Such traits might be the slope of the decline in fertility with age since puberty. To be honest I am not sure of the language to use to describe such traits, since such traits are explicitly incorporating the time element, and do not fit well with my phenotype as vector metaphor. If anybody has any ideas I would be pleased to hear them.

The point of this is that the evolution of aging remains an important issue. However, I am inclined to think it will have at most a small effect on our understanding of individuality. Where I think it will have its big impact will be on how we think about the phenotype, and the necessity to think of traits as being age dependent.



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