Thursday, May 21, 2009

Evolution and the Individual

(After yesterday's tour de force, this post's going to be a lot lighter, especially on the references.)

Let's start by defining the individual. Are two human identical twins separate individuals? Of course. We humans have an ability to develop independent personalities, so our definition of "individual" is based on that. Even if you started with a hundred identical human clones, and raised them in a hundred similar environments/families, they'd develop separate personalities. Very similar, perhaps, they might all e.g. have a liking for dipping their buttered toast in their coffee, but still separate.

But that's not true in an evolutionary sense. Natural selection works, ultimately, on the genome.A1 And, for all intents and purposes, the genome of identical twins, and other types of clones, are identical. For purposes of natural selection, it makes no difference whether a person sacrifices his/her life for his/her own children or that of his/her identical twins. Similar applies to other sacrifices or benefits.

What we often don't realize is how the whole idea of reproduction as we usually think of it is at odds with this fact. We talk about single-celled creatures "reproducing" when they undergo mitosis, even though the result is two cells with identical genomes.

Most Eukaryotes have a time in their life cycle when they undergo sexual reproduction, with re-shuffling of the genome and creation of new ones. This is also seen as reproduction, and the distinction is often lost.

I'd like to propose a new paradigm here: let's not call mitosis "reproduction", but consider all the cells with identical genomes created through mitosis as parts of a single multi-celled creature, despite the fact that the cells are independently free-living. Thus mitosis creates "growth" rather than "reproduction" just as it does in multi-celled creatures.

Why? Because how we think about these things affects what questions we ask, and that affects what we find out through research. Consider a population of amoebae growing in a well-fed environment. These free-living cells may well consist of a small number of competing genomes, each present in many copies. The could well have the ability to recognise other cells with an identical genome, perhaps by means of a number of "identity" proteins on their outer surfaces, with enough different proteins that there would be many on each chromosome. Of course, there might be a little mis-recognition in cases of recombination (crossover), but in general they could distinguish self from non-self.

Not only that, but they could well leave very complex messages for members of their own genome. It's been demonstrated that mammalian cells are capable of sending packages of cytochrome full of protein and RNA messengers to one another,1, 2 and it's hard to believe that this capability isn't present in "single-celled" creatures as well. These packages are called exosomes, or microvesicles, and are probably large enough to contain a full set of recognition proteins on their outer surface. This means that an individual consisting of a large number of free-living amoeboid cells with identical genomes could keep its cells in touch, and coordinate its activities, at least to some extent.

The same logic applies to multicellular clones, for instance in the case of Cnidaria, where clonal populations "can form distinctive anemone-free zones, several centimetres across", due to hostile interactions between different individuals of the same species.3 Indeed, clones of the same genome can differentiate into various types depending on need, in a way similar to how cells differentiate during development of multi-celled creatures. We should not assume that individual cells are less capable of this sort of behavior, the cell is actually pretty smart.

All in all, we should probably assume that many "single celled" creatures are likely to be multi-celled, just not with their cells hooked together.

Hunter, M., Ismail, N., Zhang, X., Aguda, B., Lee, E., Yu, L., Xiao, T., Schafer, J., Lee, M., Schmittgen, T., Nana-Sinkam, S., Jarjoura, D., & Marsh, C. (2008). Detection of microRNA Expression in Human Peripheral Blood Microvesicles PLoS ONE, 3 (11) DOI: 10.1371/journal.pone.0003694


Appendix 1. "Evolution works, ultimately, on the genome."

Only ultimately. It works directly on the expressed phenotype, as modified by various epigenetic and other forms of information transmission. See Evolution in Four Dimensions for an extended discussion.


1. Membrane-derived microvesicles: important and underappreciated mediators of cell-to-cell communication by Hadi Valadi, Karin Ekström, Apostolos Bossios, Margareta Sjöstrand, James J. Lee, and Jan O. Lötvall

2. Detection of microRNA Expression in Human Peripheral Blood Microvesicles by Melissa Piper Hunter, Noura Ismail1, Xiaoli Zhang, Baltazar D. Aguda, Eun Joo Lee, Lianbo Yu, Tao Xiao, Jeffrey Schafer, Mei-Ling Ting Lee, Thomas D. Schmittgen, S. Patrick Nana-Sinkam, David Jarjoura, and Clay B. Marsh

3. Behind anemone lines: factors affecting division of labour in the social cnidarian Anthopleura elegantissima by Ayre, DJ and Grosberg, RK


  1. Yeah!

    The same reasoning is likely to apply to cancer cells in many circumstances, as well.

    In systems like that, "proliferation" is the word of choice for when cells sub-clone themselves. Perhaps that could be used when referring to unicellular organisms as well?

  2. I suppose so. I wonder if cancers ever act as a parasitic individual, that is cells cooperating with one another in their invasion of the parent/host? I wonder if anybody has ever done any research looking for that? (I know that cancer cells can recruit blood vessels through release of the appropriate hormones.)

    My main point, however, is that a population of cloned cells might act as a coherent individual even it they're independent, free-living cells. I can visualize a population of amoeba clones spread out over a surface scrounging bacteria and detritus, communicating with one another by dissolved signals, pheromone trails on the substrate, the exchange of packages of cytoplasm, and actual membrane contact (using surface signaling molecules). In fact, acting much like any other multi-celled individual, except that they're not physically connected (except perhaps intermittently).

  3. I agree very much with your main point, which is supported by concepts such as quorum sensing in bacteria of the gut.

    In cancer, very similar evolutionary pressures arise, but are able to act only over short time-spans. It's well known that cancers often have subpopulations of cells that contribute in various ways to the growth of the whole tumour. For example, in breast cancer it is often just a relatively small subpopulation that secretes angiogenic factors enabling blood supply for all the tnmour cells. In other cases, a subpopulation may secrete a growth-stimulating hormone that influences the whole tumour. So they do cooperate, although haphazardly, and likely with an unstable evolutionary equilibrium leading to the emergence of "defecting" cell phenotypes that parasitise on the cooperative behaviour of the original tumour cells.

  4. Thanks, evolvingideas.

    "It's well known that cancers often have subpopulations of cells that contribute in various ways to the growth of the whole tumour."

    It hadn't been well-known to me, I'm glad to know that. A thought I've been playing around with: is it possible that somatic "failures" such as cancer are part of an evolutionary process at the group level? Cancers remove individuals who have become anti-selective for the group, thus they can "evolve" through positive selection for the genetic features that promote them through selective enhancement of the group.

    I'll admit it's far-fetched, too much so for its own post, even. But I've seen references to cancer responding to hormones (and, perhaps, neuromones), so it may be that pre-cancer cells are partly encouraged to evade apoptosis by the specific hormone (and neuromone) balance in the body.

    Something I'm a lot more sure of is that the hormone balance in the body reflects (in some ways) the social status of the individual. I can't point to any proof yet, having done no literature searches (that's for sometime after I've finished ranting about holistic biology), but with primates having specialized as social mammals for 60-90MYears, it's hard to believe that interactions haven't risen between social status and the hormone system.

    Come to think of it, I recall a mention Molecules of emotion By Candace B. Pert of AIDS viruses preferentially attacking receptors depending on emotional state. I'm going to have to re-read it (and chase ref's) before I'm sure what it's about, but it's a start.

  5. Hi AK! Didn't mean to drop out of the discussion, but I've been offline over the week-end.

    The idea that cancer might develop more easily in people who do not contribute to group fitness is very interesting! The effect must in that case be mediated by the emotional state, as you write.

    It's not entirely far-fetched that this could be the case, but most speculations in that vein have looked at the immune system rather than the balance of hormones.

    Assuming that the loss of one's contribution to group fitness correlates to depression, I think there's a strong rational. Take a look, if you want, at this paper for the evo-psych and this paper for the cancer link.

    When it comes to hormone-sensitivity in tumours, that's usually most prominent in sex-specific tissues where the proliferation of the normal cells is controlled by sex hormones. The main examles are probably breast, prostate, and endometrium. Of course, testosterone will probably decrease in men who lose social status/become depressed, which ought to work against prostate cancer development. In principle, there could be an effect on cancer risk mediated by other hormones even without the link through the immune system, but I'm not aware of any examples that lend themselves to speculation in that vein.

    It's a fun discussion!

  6. That's OK, I've been offline until now. Going to miss a few posts behind this weekend as well.

    I couldn't get to more than the abstract of your first link, and the second link also claimed a paywall, but I found a way around here.

    Regarding hormone sensitivity, I'm personally convinced there are lots of hormones still to be discovered, although I can't prove it. (Heh! how could I?) I'm thinking partly of depression, but also potentially of mechanisms that would kill off a highly successful individual under conditions where his (or perhaps "her", but the odds are "his") success detracts from the group fitness. An example that comes immediately to mind (contradicting my pronoun comment) is the case the chimp Passion and her daughter Pom who killed at least three infants of other females in the troop, and attempted more. Quoting:

    "Passion and Pom began their killing spree just as Pom was reaching adolescence and establishing her feeding range [ref]."

    Since chimps generally practice female migration, helping to establish Pom as a stable member of a group containing her father might threaten the long-term genetic diversity of the troop. A mechanism that made her more susceptible to cancer might provide for the long-term welfare of the troop despite her high personal status.

    I don't know if anybody's come up with a study of relative cancer frequency among psychopaths and/or sociopaths (assuming there's actually a consistent definition of those terms), but I can see how a mechanism that preferentially killed such individuals could benefit the group.

    Another point to consider is that whatever mechanism(s) might exist would have been adapted to the long-term conditions of social primates, overlaid by those of the great apes. A million years of human evolution (since H. erectus and kin) could easily have been enough to randomize the mechanism, while 10,000 years of agriculture might well be totally different from the conditions originally adapted for.

  7. Yes...

    In a game-theoretical perspective, I think the sociopaths are the defectors that arise in response to our generally cooperative attitudes in human society. The most obvious counter-strategy is to ostracise them. However, I can't see why a trait possibly favouring the group (cancer) should arise in conjunction with a trait that builds on parasitising on the group.

    You are right of course in that we must consider the evolutionary pressures of the past, pre-agricultural societies in these discussions.

    Sorry about the paywall, not much I can do there I'm afraid... (except publishing my own papers with open access...)

  8. Thank you for your continued comments, evolvingideas. First, your main point:

    "I can't see why a trait possibly favouring the group (cancer) should arise in conjunction with a trait that builds on parasitising on the group."

    Actually, I was thinking more of the trait arising to respond to a specific emotional state in the parasitizing individual: one consistent with parasitizing the group as a result of any number of traits.

    This, in turn, would probably require a more sophisticated definition of "emotional state" than we normally recognize. This is consistent with my belief that we haven't yet discovered the majority of hormones involved in human state.

    Suppose we start with the idea that the total hormone state represents an n-dimensional vector (with n the number of hormones), and assume that the (blood) concentration of each hormone is a function of various aspects of state: physical, social, self-referential, etc. The receptors for these hormones are potentially present on any cell that needs to respond to that aspect of state.

    We know that some emotional signals are carried by nerves, but except for those aspects of state that need to be communicated within a few seconds, hormones (especially low-concentration hormones) are actually a better system because their message can be recovered by any (type of) cell in the body just by tying the expression of their genes to the appropriate markers for the cell's type. Note that a mutation can tie any cellular mechanism to emotional state just by expressing the right combination of receptors and internal links. This especially applies to the neurons that (potentially) vary their calculating activity in response to different emotional states.

    Now, I'd propose that we define any dimension of this hormonal system as "emotional": that is rather than trying to define "emotion" in traditional terms, we simply assume that "emotion" represents the total hormonal state (plus whatever neural signals have to be included).

    Since the expression and secretion of any hormone can be influenced by neural calculations, anything the individual is aware of, even subliminally, can become an input to the total emotional state. (Similarly, every hormonal dimension of the total emotional state can potentially become an input to the calculations of any neuron/synapse.)

    So, suppose we assume there's a difference in total emotional state between individual success that clearly benefits the group, and individual success that clearly parasitizes the group. It doesn't matter how that state is implemented, but I'll mention that a number of animals (besides primates) have been shown to be very good at estimating their own and others' economic cost/benefit positions. It's hard to believe that a primate would lack the ability to know its position relative to the group advantage.

    Given that difference in emotional state, all it would take is a cancer mutation that makes an individual in such a state more vulnerable to cancer. Those with the mutation who didn't parasitize the group would not be damaged by the mutation, but by carrying it and passing it on to (part of) their descendants, they would benefit the group and therefor their own descendants as a group, even if it ended up killing a few who were parasites.

    Of course, I'll grant that a similar mutation for defects in the immune system would be more strongly selected by the same mechanism, since one immune defect could result in death from any number of causes, but the benefit would still be there in reduced form for other types of mutation.

    As for the paywall, I wasn't complaining, just mentioning why I wouldn't be able to discuss it. I'm all for open access, I try very hard not to use papers that aren't as references in my posts.