A phenotypic view of evolution Evolution in Structured Populations

Individuals as Multispecies Entities

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/)

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  1. Directly applicable to Conservation Biology, although I do not expect CBs to pay any attention to the idea of multispecies entities; they are still laboring under the fallacy that mutation rates in DNA are random, which is entirely false. The question of “units of conservation interest” has become much more complex with your construct, and I am including your construct in my discussions of conservation.

  2. Yes, I have been thinking about these issues too. They have huge implications for evolutionary psychology and such questions as the evolution of altruism and so on. With commensals affecting our behavior and being transmitted vertically, many we recently learned are transmitted before birth by the mother even, do we have an R of 1 to ourselves? Are we not a type of group selection as individuals? It is easy to say that altruism is not in the interest of an individual, but what if we are host to an organism or organisms who alter our behavior to make us altruists because that is in their best interests? What if our group social behavior or other critical evolved predispositions are the result of co-evolution not just with culture but with commensals? It seems to get quite complicated quite rapidly, and it was complicated enough for my tastes already.

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