National Geographic

Mercenary Ants Protect Farmers With Chemical Weapons

Humans have a long history of bolstering their armies by paying mercenaries to fight on their behalf. Now, Rachelle Adams from the University of Copenhagen has found that some ants do the same.

Some ants defend their colonies with special soldiers, which are bigger and wield more formidable weapons. But others lack a proper army. Sericomyrmex ants, for example, are fungus-farmers. They bring bits of vegetation back to their nests and use these to nourish a fungus, which they then eat. They are poorly defended, and a sitting target for raiders and pirates. That’s why they rely on other ants to fight for them.

Another ant called Megalomyrmex symmetochus forms its own colonies, complete with queen and workers, inside those of Sericomyrmex colonies. This guest is present in over 80 percent of the farmers’ nests and, at first glance, it looks like a parasite. It eats the fungus that the farmers so assiduously grow, without contributing any labour of its own. Worse still, it eats some of the farmers’ larvae and clips the wings of their young queens, so they contribute to the gardening rather than flying off to start their own colonies.

But M.symmetochus doesn’t just freeload off its hosts. In some cases, it can be their salvation.

Megalomyrmex mercenary (top right) defends a fungus garden from a Gnamptogenys raider (bottom). Credit: Rachelle Adams

Megalomyrmex mercenary (top right) defends a fungus garden from a Gnamptogenys raider (bottom). Credit: Anders Illum

Sericomyrmex nests are often attacked by a third ant called Gnamptogenys hartmani—a sort of six-legged pirate. It raids the colonies of farming species, drives them out, usurps their nests and gardens, and eats any remaining larvae.

The farmers can do very little against these raiders, since they lack specialised soldiers and have mostly lost their stings. Their powerful jaws can deliver a strong bite, but at such close quarters, they risk getting stung and bitten themselves. When attacked, they’re much more likely to feign death or flee. That is, unless there’s a M.symmetochus colony living in their nests.

Back in 2011, Adams let some raiders loose upon a colony of Sericomyrmex farmers, which was already being parasitized by M.symmetochus. “To our surprise, the hosts hid and the parasites rose to the top of the garden to confront and kill the invaders,” she says.

Unlike their hosts, the parasitic ants are far from defenceless. They raise their stings and release a powerful venom directly into the air—an airborne chemical weapon that kills the raiders and befuddles any survivors. “Rather than uniting as an efficient infiltration squad they turn on each other and attack, sometimes killing their own kin,” says Adams.

M.symmetochus behaves like a colony of mercenaries. They can cause problems for the farmers during peace-time, but they provide an invaluable defence when an invading force arrives.

By pitting the three types of ants against each other, first in one-to-one battles and then in more realistic groups, Adams’ team showed that the mercenaries are much better at subduing the raiders than the farmers. It takes just two of them to overpower a single raider, while the same task requires at least eight farmers. On average, a pair of raiders can kill 70 percent of farmers in an unprotected nest, but just 10 percent of them if there are six mercenaries around.

And the raiders seem to know it. When the team gave them a choice between two nests, only one of which was defended by mercenaries, they were more likely to attack the unprotected nest. In the experiment, a wire mesh prevented the raiders from actually touching the colonies, so they were probably put off by the smell of the mercenaries’ chemical weapons. Just by living in the same colonies, the mercenaries protect the farmers by cloaking them in a defensive miasma.

The thing that clinches this incredible relationship is probably Megalomyrmex’s life cycle. They form a life-long bond with a single colony of farmers, and won’t leave to seek out a different host. They exploit their hosts but they don’t overexploit them, and if raiders attack, they mount a defence rather than abandoning the farmers to their fates.

Next, the team wants to study how this alliance varies over time and space. For example, it should be easier to find the mercenaries in the farmers’ nests in places where the raiders are more common. Similarly, a different farmer called Trachymyrmex zeteki should be relatively unbothered by raiders, since it also hosts a parasitic mercenary but in fewer than 6 percent of its nests.

For now, they very astutely compare the mercenary ants to a human disease called sickle cell anaemia. It’s an inherited genetic disease that warps the shape of red blood cells and causes a gradual building illness. The mutated gene behind the disease is common in Africa because two copies might cause sickle-cell anaemia, but one copy protects a person against malaria. Similarly, M.symmetochus is like a mild chronic disease that exerts a toll upon its host, while protecting it from an acute and more destructive infection—the Gnamptogenys raiders.

Reference: Adams, Liberti, Illum, Jones, Nasha & Boomsma. 2013. Chemically armed mercenary ants protect fungus-farming societies. PNAS http://dx.doi.org/10.1073/pnas.1311654110

Experimental manipulation of the tendon of the large jumping muscle of one hindleg

There are 32 Comments. Add Yours.

  1. James V. Kohl
    September 9, 2013

    Comparing genetically predisposed nutrient-dependent pheromone-controlled behavioral development in insects to a mutation-caused disease in humans stretches the imagination far beyond any model of genetic or of epigenetic cause and effect. In the ants, food odors and pheromones are responsible for differences in brain development and behavior. In sickle cell, a parasite supposedly causes mutations that are responsible for natural selection of a disease process, not behavior. If the primary consideration in adaptive evolution is epigenetic cause, sensory input from the social environment can be linked to behavior via the effects of olfactory/pheromonal input. If evolution is mutation-driven, a parasite-induced mutation would cause behavioral adaptations, not just simply enable some populations of humans to survive who might otherwise become infected. Therefore, M.symmetochus is NOT “…like a mild chronic disease that exerts a toll upon its host, while protecting it from an acute and more destructive infection… It’s a species that constructs an ecological and social niche to symbiotically exist within the ecological and social niche construction of other species whose adaptive evolution is nutrient-dependent and pheromone-controlled, NOT mutation-driven.

  2. John S
    September 9, 2013

    James:

    I think you are over-analysing the metaphor. Regardless of the actual genetic mechanism at play, the selection pressures are comparable between the malaria/sickle cell anemia and this ant story, as the author rightly points out. If the ants are in a symbiotic, or even mutualist relationship as you claim, then the malaria parasite and humans are as well.

  3. James V. Kohl
    September 9, 2013

    That’s a good point, John S. It helps make it clearer that the underlying conserved molecular mechanisms enable the nutrient-dependent pheromone-controlled reproduction of parasites and hosts sans mutations. Perhaps the metaphor (e.g., something akin to the selfish gene metaphor) should be left to prevail. But that’s not where scientific pursuits are headed. Indeed, many of today’s scientists have actually begun to look for explanatory power in their opinions about cause and effect. They’ve learned that mutation-driven evolution explains nothing.

  4. DrYak
    September 10, 2013

    ” In sickle cell, a parasite supposedly causes mutations that are responsible for natural selection of a disease process, not behavior. ”
    That is the weirdest representation of evolution I’ve come across for a while. Why would the mutations be “parasite-driven”? The mutations are random and the presence of the parasite is a driver of selection pressure. In no way is the malaria parasite a cause of the mutation that leads to SCA but when the SCA mutation is present then heterozygotes for the SCA mutation have a selective advantage.
    The analogy is apt – they have made several testable predictions that are strikingly parallel to the SCA case: 1 – Ants that have low rates of predation have lower rates of this association just as where malaria is not present there are lower rates of SCA. 2 – If the ants have other ways of fighting off pirates (or are capable of doing it themselves) then there will be lower rates of the association just as if there are other ways of combating malaria, etc..

  5. John S
    September 10, 2013

    James:

    I’m not clear what your objection to “mutation driven” explanations is. Behavioural changes are necessarily built on physiologies which are made capable of such changes by their underlying genetics. Different pheromones certainly can elicit different responses in ants, but those responses are mediated by receptors, and interpreted by neural systems that are both, as far as we can tell, products of mutation and natural selection.

  6. James V. Kohl
    September 10, 2013

    John S.
    My objection is based on the fact that the only way the epigenetic landscape clearly becomes the physical landscape of DNA in any organized genome is via de novo creation of olfactory receptor genes. Creation enables all other receptor-mediated interactions, which are required to epigenetically link the sensory environment to genes and behavior and back. Nutrient-uptake is the bottom-up approach to that link: behavior (at the cellular level) is required for nutrient uptake. That nutrient-dependent “behavior” is controlled from the top-down by the metabolism of nutrients to species-specific pheromones that control reproduction.

    Mutation-driven evolution simply does not enter any explanation of cause and effect in the context of the physiology of reproduction, and yet mutations theory continues to show up in metaphors and in misrepresentations of randomly-driven adaptations to predation like the one offered above by DrYak.

    I’ve often wondered if people who tout things like that are familiar with the fact that the pattern of migration in the peppered moth example of industrial melanism was 2 km/night, which precisely matches the distance some male moths will fly to find the female who is producing nutrient-dependent pheromonal signals of reproductive fitness that control reproduction in species from microbes to man. Whenever I ask about that, however, people seem too embarrassed to consider anything else but theory, which is akin to an unending series of books titled “evolution for dummies.”

    Your comments seem more sincere and clearly you wish to bring in the physiology of nutrient-dependent receptor-mediated reproduction. But, as you must intuitively know, reproduction is not controlled by mutations. It’s controlled by the metabolism of nutrients to species-specific pheromones, and that degree of finely-tuned control of conserved molecular mechanisms is the basis for species diversification via ecological, social, neurogenic, and socio-cognitive niche construction.

    Simply put, my objection to “mutation driven” explanations is that they explain nothing about adaptive evolution, since they do not address the physiology of reproduction.

    I noticed the mention recently, however, of “epistatic mutations” that obviously must somewhat simultaneously occur. This indicates to me that virtually no scientific progress has been made since the statistical bastardization of Darwin’s theory. Now, instead of mutation-driven evolution, we have “mutation(s)-driven” evolution, where one deleterious mutation leads to another mutation and the combination results in a beneficial mutation. Yet, people like DrYak will continue to say to me: “That is the weirdest representation of evolution I’ve come across for a while.”

    I’ve seen misrepresentations of evolution that are much weirder. In the context of sickle cell, for example see: “Epistasis Among Adaptive Mutations in Deer Mouse Hemoglobin” [subscription required] and my comment on the article.

  7. David Bump
    September 10, 2013

    Fascinating study, curious analogy, intriguing discussion. It seems to me the disagreement(s?) is/are due to several factors. For one thing, analogies are almost always imprecise and prone to misunderstanding, depending on how close a fit was intended and how much play others will allow for a valid analogy. Another difficulty here is our lack of knowledge, especially in the case of the ants, versus the human propensity for jumping to conclusions and the desire to tie up loose ends. Too much of science (or reporting of science) today seems to be coming up with a plausible explanation and then taking that as the truth simply because it’s plausible, consistent, and nobody has proposed one that’s more popular … yet. As I commented in the story on Science History the Second Time Around (?), between accepting as “science” things which haven’t been repeatedly observed or clearly demonstrated (in the real world, not computer simulations) to be possible, and pressures from academic reviews, the media, and funding sources, it’s all to easy for scientists to make pronouncements that there’s a good chance they’ll have to retract later.

  8. James v. Kohl
    September 10, 2013

    Thanks David. The problem is the popularity of mutations theory, and as you said, “…pressures from academic reviews, the media, and funding sources…” It’s long past time for pronouncements about mutation-driven evolution to be retracted, but there is no pressure being placed on academics or journalists to move forward with what is known about ‘conditions of life’ and convergent evolution. Both are obviously nutrient-dependent and pheromone-controlled.

    The idea of “epistatic mutations” can only have come from those who are thoroughly trained to think as their professors were trained to think, and so they report on mutations to journalists who include mutations theory in the context of evolved behaviors in ants.

    Even if Ed Yong knew better, he might not want to enter a battle over cause and effect in a simple report like this one, or his editor(s) may not give him license to do anything except stick with the pack. But sooner or later everyone is going to need to deal with accurate representations of “Biological Information” in the context of the “Physiology of Reproduction,” all of which refutes mutation-driven evolution and the “Just-So” stories of theorists.

    My specific complaint is derived from our section on molecular epigenetics in a 1996 Hormones and Behavior review article I co-authored. The mammalian model of hormone-organized and hormone-activated behavior was subsequently extended to invertebrates (e.g., including eusocial ants and honeybees). Sixteen years later, we still have reports on mutations in the context of insect behavior when there has never been any evidence that mutation-caused alternative splicings are adaptive, or that they could possibly lead to epistasis. For contrast, everything about adaptive evolution tells us that the alternative splicings are nutrient-dependent and pheromone-controlled.

    Academics can continue to ignore the associated biological facts, which include what’s known about the epigenetic effects of food odors and human pheromones, but the biological facts are not going to simply go away. And neither are the misrepresentations of biological facts in this article.

  9. Lucas
    September 10, 2013

    James, your preoccupation with pheromones is perhaps understandable, considering your occupation. However, as John pointed out, regardless of the mechanism, there is a clear analogy in the selection pressures between the ant system and sickle cell anemia, which is the point made in the article.

  10. John S
    September 10, 2013

    James said: “It’s long past time for pronouncements about mutation-driven evolution to be retracted, but there is no pressure being placed on academics or journalists to move forward with what is known about ‘conditions of life’ and convergent evolution. Both are obviously nutrient-dependent and pheromone-controlled”

    You are right I think, the ants are responding to signals such as you mentioned, and an “enabling” mutation may not be present. Looking for such a mutation was not the subject of Ed’s article, or of the paper it was based on, so I’m a little mystified why this most vehemently voiced objection was raised.

    However, the receptors, signalling networks and physiology are genome-dependent, and in order for an ant to respond in the way described in the article it must be in a fitness landscape that allows it to be possible. In addition, in order for it to persist it must be beneficial. The fitness landscape is of course entirely contextual; environmental conditions can and do alter it, but it is always in the context of the genome, which is altered by mutations. What other mechanism do you propose?

    • James V. Kohl
      September 10, 2013

      Thanks for asking, John S.

      1) Finding a mutation that might be involved in adaptive evolution has never been the subject of anyone’s article. That’s my objection. Ed Young connected the adaptive evolution of behavior in the ants to a mutation in humans. That’s why I wrote: Comparing genetically predisposed nutrient-dependent pheromone-controlled behavioral development in insects to a mutation-caused disease in humans stretches the imagination far beyond any model of genetic or of epigenetic cause and effect.

      2) Creation of olfactory receptor genes is experience-dependent, and de novo creation occurs with exposure to potential nutrient sources that may become the ecological niches that precede the social, neurogenic, and socio-cognitive niche construction required for adaptive evolution sans mutations. Thus, the receptors, signalling networks and physiology are genetically predisposed but clearly experience dependent.

      There is no model and no model organism that suggests a genome altered by experience-dependent mutations would lead to adaptive evolution, which is nutrient-dependent and pheromone-controlled in species from microbes to man. Granted, there must be a cell with a genome that can adaptively evolve, but as I said everything about adaptive evolution tells us that the required alternative splicings are nutrient-dependent and pheromone-controlled. We now know that the microRNA/messenger RNA balance drives alternative splicings, and that balance appears to be nutrient-dependent and pheromone-controlled. Mutations may alter the balance, but they’re not likely to cause anything related to adaptive evolution, which is the only type of evolution there is in my model.

  11. James V. Kohl
    September 10, 2013

    I just read in “ScienceShot” that “The scientists compare Megalomyrmex to the mercenaries who protected a medieval city during conflicts but drained its resources in times of peace.” Ed Yong may want to comment about the difference in his representation, and how much confusion it could cause if he agrees it is a misrepresentation. For all we know, he made his representation as part of an “evolution for dummies” scenario and
    Kelly Servick (of ScienceShot) did not want to do that.

    Also, in a Facebook post, Carl Zimmer just admitted he apparently was wrong to say “newborns are sterile” in an article he published two years ago. So, I mentioned that “In the mouse model, the diet of the mice determines their nutrient-dependent pheromone production and social interactions with other mice.”

    If, as is now suspected in humans, the colonization of the newborn gut occurs, in part before birth, the genetic predisposition and in utero experience with nutrients and their metabolism in the gut would predispose their preferences for olfactory/pheromonal input from a species-specific mammalian mother. And that would be consistent with my model of nutrient-dependent pheromone-controlled adaptive evolution, which includes transgenerational epigentic inheritance, but not mutation-driven evolution.

    Does everyone agree that responsible journalism might make a difference in what people believe about cause and effect?

  12. lkr
    September 10, 2013

    Occurs to me that the sickle-cell comparison is just confusing — “seven samurai”-like mercenary comparison is clear enough without worrying about the genetic bases for this relationship in each of the players. But hardly irresponsible journalism!

  13. John S
    September 11, 2013

    James, thanks for your answers. I am beginning to grasp that you are advocating a systems-level approach to explain behaviour as an emergent phenomenon, as opposed to the more reductionist approach of trying to identify the specific genetic changes which are responsible. I can’t say that I disagree, but surely you can’t have one without the other. For example, in your first point you said that:

    “… genetically predisposed nutrient-dependent pheromone-controlled behavioral development in insects…”

    should not be compared to “…a mutation-caused disease in humans..”

    What is “genetic predisposition” except for accumulated mutations? What is a “mutation caused disease” except for the final pathological step in a series of thus far innocuous mutations amounting to a genetic predisposition for contraction or development of that disease?

    In a comparison between closely related (for example) ant species where significant behavioural differences are seen, the explanation must have two layers; the genome and the environment (and by environment I include physiology). The exact contribution of each layer may vary from comparison to comparison, but consideration of one shouldn’t be done in isolation of the other.

  14. John S
    September 11, 2013

    James, thanks for your answers. I am beginning to grasp that you are advocating a systems-level approach to explain behaviour as an emergent phenomenon, as opposed to the more reductionist approach of trying to identify the specific genetic changes which are responsible. I can’t say that I disagree, but surely you can’t have one without the other. For example, in your first point you said that:

    “… genetically predisposed nutrient-dependent pheromone-controlled behavioral development in insects…”

    should not be compared to “…a mutation-caused disease in humans..”

    What is “genetic predisposition” except for accumulated mutations? What is a “mutation caused disease” except for the final pathological step in a series of thus far innocuous mutations amounting to a genetic predisposition for contraction or development of that disease?

    In a comparison between closely related (for example) ant species where significant behavioural differences are seen, the explanation must have two layers; the genome and the environment (and by environment I include physiology). The exact contribution of each layer may vary from comparison to comparison, but consideration of one shouldn’t be done in isolation of the other.

  15. DrYak
    September 11, 2013

    James Kohl.
    I say a misrepresentation based on your statement (repeated twice) that, quoting directly from you, ” a parasite supposedly causes mutations that are responsible for natural selection”. Here you are conflating two different processes, that of random mutation, which produces variation, and natural selection that leads to differential reproduction of those variants. These two processes are both critical for evolution via natural selection but are not the same thing. Thus to say that ” a parasite supposedly causes mutations” is simply false.

    You then go on to say that “the fact that the only way the epigenetic landscape clearly becomes the physical landscape of DNA in any organized genome is via de novo creation of olfactory receptor genes.” This is also not true. There are many ways for these sorts of changes to come about that do not require “de novo creation of olfactory receptor genes”, changes in gene regulation, i.e. where, when or in what combinations a gene is expressed – these are probably much more common – even in cases where a change in coding sequence is required a point mutation can often change ligand binding characteristics. Even “de novo” creation by gene duplication followed by drift is not uncommon – there are many cases described in the literature.
    With respect to mutation driven changes in olfaction I point you to the recent paper in science (http://www.sciencemag.org/content/340/6135/972.short) about the evolution of glucose avoidance in cockroaches.
    While you might baldly state that “But, as you must intuitively know, reproduction is not controlled by mutations.” the rest of us look at the literature in both the field of reproductive biology and speciation for example on the evolution of reproductive isolation and follow the data rather than intuition.
    Could you please define what you mean by epigenetic? This is a concept that has been made to mean so many things recently that we could be flailing in the dark unless we clearly state what we mean by it.
    Yours,
    Dave

  16. James V. Kohl
    September 11, 2013

    DrYak wrote:”…the rest of us look at the literature in both the field of reproductive biology and speciation for example on the evolution of reproductive isolation and follow the data rather than intuition.”

    No biologically based data link mutations to selection, which must be involved in adaptive evolution. What you have been following is nonsensical theory, which is a common problem known to physiologists. For example, in 2011 Denis Noble wrote: “If you learnt evolutionary biology and genetics a decade or more ago you need to be aware that those debates have moved on very considerably, as has the experimental and field work on which they are based.”

    Earlier this year I wrote: Epigenetics: “An essential mechanism for pruning down the wide range of possible behaviors permitted by genes, selecting those that fit an individual’s environment (Berreby, 2011).” Excerpted from Nutrient-dependent/pheromone-controlled adaptive evolution: a model (http://www.socioaffectiveneuroscipsychol.net/index.php/snp/article/view/20553/27989).

    Recently, David Eagleman wrote: 3. Stem the flow of bad information (http://eagleman.com/blog/item/59-public-science), which is precisely what I am trying to do here.

    Clearly, one of the biggest problems I will continue to encounter in attempts to stem the flow of bad information disseminated via mention of mutations in articles like the one we are discussing is that there is no such thing as mutation-driven evolution. In fact, given the context of what is currently known about systems biology (e.g., yes, John S, I am one of “them”) mutation-driven evolution cannot be considered as anything significant except an example of nonsense.

    Reproductive isolation is nutrient-driven and pheromone-controlled, which is how you get the diversification (e.g., since the last ice age) in marine stickleback fish and the obvious diversification in species from microbes to man via conserved molecular mechanisms, not via mutation-driven evolution.

    Apparently, like many others, you need to “…look at the [CURRENT] literature in both the field of reproductive biology and speciation.” I’ve been publishing and presenting on that for more than 2 decades. But thanks for your comments and questions. Scientific progress isn’t possible without them (i.e., all we would have is theory).

  17. James V. Kohl
    September 12, 2013

    My response to John S. and DrYak has been on hold for more than 24 hours, with only this notation to me: “Your comment is awaiting moderation.”

  18. Happy
    September 12, 2013

    Cool!

  19. Flower
    September 12, 2013

    Isn’t that awesome!!!!!!!!!!!!! I love nat geo

  20. James V. Kohl
    September 12, 2013

    John S. asked: What is “genetic predisposition” except for accumulated mutations?

    Thanks for asking. Genetic predisposition is determined by ‘conditions of life’ that are nutrient-dependent and pheromone-controlled in species from microbes to man. That is, unicellular and multicellular organisms have genetic predispositions.

    Attributing “genetic predisposition” to accumulated mutations does not address how the mutations are controlled in any species, or how they would be beneficial without being controlled. My model of systems biology includes pheromone-controlled reproduction, which controls the accumulation of mutations that you say results in genetic predispositions.

  21. Bill
    September 13, 2013

    Sorry but I don’t see why there should be a big discussion about all this.

    The authors (if you read the paper) do make both comparisons with human mercenary troups and also sickle cell anemia…
    when they talk about sickle cell anemia they are not comparing the genetic mechanisms behind, they are not saying that the same genetic principle is at work or that the parasites impose mutations and so on. The parallel is at the ecological level, at the geographic scale and on the parasitism-mutualism continuum. Sickle cell anemia confers protection against malaria, so that if you have the burden of having this disease but you live in an area where you would have very likely died of malaria, you might have a net fitness benefit. This is exactly what might happen in this ant system. If you have the guest-ant it is surely a burden and you might not be able to grow big colonies or produce many sexuals… but if you happen to live in a place where Gnamptogenys would have likely exterminated your colony… oh well, it’s good to pay the cost of the guest-ant…
    Nothing more that this simple parallel. Any discussion on genes and pheromones and so on is surely interesting, but it is off topic…

  22. Sury
    September 13, 2013

    Fascinating debate,,
    The data is not too bad itself.

  23. James V. Kohl
    September 13, 2013

    Thanks Bill. I attempted to address Ed Yong’s representation of cause and effect, which was perhaps inadvertently attributed to a mutated gene: “The mutated gene behind the disease is common in Africa because two copies might cause sickle-cell anaemia, but one copy protects a person against malaria.” No one else has addressed how a mutated gene (or accumulated mutations) might enable what are obviously nutrient-dependent pheromone-controlled activities among species that co-exist.

    If there are parallels between those found to be predisposed at the ecological level and those to be found along the parasitism-mutualism continuum, they will be found — as they repeatedly have been — to reflect on aspects of nutrient stress and social stress that alter the immune system. Those stressors may result in mutations that alter the course of adaptive evolution, but they’re not likely to result in beneficial mutations or in mutualism attibuted to mutations. The mutualism is nutrient-dependent and pheromone-controlled, which is why I started this discussion and have continued to participate in it.

    What you think is off topic has quite naturally become a topic because of its relevance to what Ed Yong represented. How else might we get to discussion of genes and pheromones if misrepresentations of cause and effect are not addressed?

  24. James V. Kohl
    September 13, 2013

    This just published: “An experimental test on the probability of extinction of new genetic variants”

    Quote: “In conclusion, classical theory in population genetics is confirmed, but natural selection might not be of invariable magnitude and sign. Our findings thus set the stage for the development of more general theoretical models explaining the fate of new alleles across long evolutionary timescales.

    Comment: My model is not theoretical, it integrates biological facts across species from microbes to man. Species incompatibilities in nematodes are associated with cysteine-to-alanine substitutions (Wilson et al., 2011), which may alter nutrient-dependent pheromone production and fixation.

    I was alerted to the latest report about genetic variants and the BIG BUT about their natural selection, by mention of it here: Fate of New Genes Cannot Be Predicted. The problem with prediction is that alleles initially are not fixed. And there is no way to predict which alleles are nutrient-dependent and pheromone-controlled until after they are fixed. After new alleles are fixed, it becomes clear that their benefit to species survival was directly linked from nutrient uptake to the metabolism of novel nutrients to pheromones that control reproduction , which is how pheromones control fixation of “bottom-up” nutrient-dependent ” alleles from the top down.

    However, fixation obviously must incorporate the degree of plasticity that enables adaptations to changes in the availability of nutrients, or changes in the amount of nutrients required to maintain behavioral development across life cycles in different organisms. This is where the examples from model organisms become essential to establishing a model that can be compared to misrepresentations of mutation-driven evolution (e.g., in sickle-cell disease), which have never explained mutation fixation or anything else about fixation and are still unable to do so. The BIG BUT of theory is “…natural selection might not be of invariable magnitude and sign.” So much for use of the sickle cell “mutation” in disease to exemplify ecological and social niche construction that is nutrient-dependent and pheromone-controlled in the example of mutualism here.

  25. John S
    September 15, 2013

    James, I’m very sorry to burst your bubble a bit, but all models are theoretical; at least, the good ones are. Incoporation of biological facts makes yours robust, but still theoretical.

    Although I can see the thrust of your argument, and agree up to a point, I can’t help but feel that you are arguing in circles. Claiming that genetic predisposition is “misrepresented” by describing it in terms of mutations, but perfectly accurate if described without considering the genetics! I’ll say it again; genetic presdisposition requires genetic factors, which includes mutations of all kinds. Because we are dealing with phenotypes (as always) and not naked genotypes we of course must take the environment into account, otherwise genotype is meaningless. Similarly, attempting to remove genetic considerations seems like an exercise in futility, and leaves you with only half the story. The paper you quoted found that it was indeed genetic changes which set the stage for the physiology/behavioural changes. I think you are wrong to dismiss this (ie Ed’s) article as “misrepresentation”. Perhaps a more nuanced view is appropriate, it is after all a complicated situation that has yet to be completely covered accurately by a single model.

    • James V. Kohl
      September 15, 2013

      John S.
      I’ve exemplified my “model” in the context of “model” organisms in species from microbes to man. Your regurgitation of what I’ve written: “Claiming that genetic predisposition is “misrepresented” by describing it in terms of mutations, but perfectly accurate if described without considering the genetics!” is ridiculous outside the context of mutation-driven evolution, which is now a thoroughly refuted theory.

      I am attempting to clarify the fact that mutations must become fixed in the organized genome of any species for them to become important to evolution, and the article I provided the link to clearly states the mutations are not fixed. That does not remove genetic considerations, it simply places them into the context of the epigenetic effects that make genetic factors important considerations because they are not important in the context of mutation-driven evolution. Indeed, we now know there is no such thing as mutation-driven evolution because there is no evidence that alleles resulting from mutations are fixed in sufficient numbers for them to cause anything at all (except diseases and disorders).

      Back to the ants. There is no accurately detailed link between mutations and their nutrient-driven pheromone-controlled behavior, which is because there is no connection between nutrient-dependent species-specific signals that control reproduction and mutation-driven evolution.

      For contrast, you wrote: “The paper you quoted found that it was indeed genetic changes which set the stage for the physiology/behavioural changes.” It did not! It found that mutated genes did nothing because the new alleles are not fixed in the organized genome. If they are not fixed, they can’t cause adaptive evolution via physiological/behavioral changes. Can they?

  26. John S
    September 15, 2013

    James;
    After a closer reading of the just-published paper you mentioned, I remain of the same mind, as it in no way supports this idea that mutations have no bearing on evolution. I bemusedly note the very first line of the first paragraph of the introduction:

    “When a new allele appears by mutation or recombination, it will be represented in very low numbers and it can be lost even when it is adaptive.”

    The authors went on to show exactly that, which is hardly new theory, though quite beautifully shown in this case. They also showed that even when an allele is adaptive in one condition, it is not necessarily adaptive in another. This is of course the contextual fitness I mentioned earlier, and still isn’t new theory. These data did not show, nor did the authors claim, that selection is not “mutation driven”. What is does clearly indicate is that the situation during selection is more complicated than a simple allele=bad/good, which is in line with fitness-landscape modelling studies I’ve seen. To quote directly from the paper:

    “Interactions among fitness components are nevertheless complex, and only a comprehensive characterization of several life-history traits would allow a full understanding of the possible mechanisms underlying the observed frequency dependence, an endeavour that is beyond the scope of the present study.”

    The authors even go on to say that beneficial alleles might not be fixed due to changes in fitness due to frequency-dependent effects, and the same for deleterious alleles. This applies directly to the malaria/sickle cell anemia situation, and supports the comparison made by Ed in this article. Note that in these cases, fixation was not required for a trait to survive.

    Despite your obvious strong feelings about what you see as misrepresentation, the fact remains that selection based on physiology is selection of phenotype, which is influenced by genotype. There is no way that you can dismiss that link, even while insisting that adaptation by mutation and natural selection has been refuted. It has not. The C. elegans paper is all about selection from two heterogeneous populations, not two homogenous populations.

    That doesn’t mean that your favourite model is incorrect, or even inaccurate! I can easily envision selection and adaptation using contextual environmental factors without a proximate beneficial allele. But it does suggest that you are being too dismissive, insultingly so. The language you are using is too strong, bordering on the hyperbolic, and, dare I say it, misrepresents the facts.

    • James V. Kohl
      September 16, 2013

      Thanks JohnS. Perhaps you should read at least one of my published review articles and consider the evidence from molecular epigenetics of olfactory/pheromonal cause and effect. That evidence also refutes mutation-driven evolution in species from microbes to man.

      However, I note that you now infer I am indicating that “mutations have no bearing on evolution” which is a trick others have used. I’m clearly saying that –without fixation– mutations cannot have an impact on adaptive evolution, which is what the most recent published paper — that refutes mutation-driven evolution — also says.

      In addition, it mentions “…a comprehensive characterization of several life-history traits…” which is the clearest indicator that the characterization would include nutrient-dependent pheromone-controlled molecular mechanisms since they are the most important of all life-history traits in the context of adaptive evolution. In 2005, our 1996 mammalian model of hormone-organized and hormone-activated behavior was extended to life-history traits in the honeybee model organism, for example.

      Earlier this year I wrote, in Socioaffective Neuroscience & Psychology that: “Clearly, however, the epigenetic effects of food odors and pheromones are involved in neurogenic niche construction as exemplified in nematodes (Bumbarger, Riebesell, Rödelsperger, & Sommer, 2013), and in flies (Swarup et al., 2013).” Later, I added: Differences in the behavior of nematodes are determined by nutrient-dependent rewiring of their primitive nervous system (Bumbarger et al., 2013). “Species incompatibilities in nematodes are associated with cysteine-to-alanine substitutions (Wilson et al., 2011), which may alter nutrient-dependent pheromone production.”

      Nutrient-dependent pheromone-controlled amino acid substitutions in species from microbes to man enable fixation of new alleles. Clinging to mutations theory without any information whatsoever on how the new alleles become fixed in an organized genome of any species leaves you grasping at straws.

      Denis Noble has addressed that fact in the context of what you just wrote: “selection based on physiology is selection of phenotype, which is influenced by genotype.” For example, see “Physiology is rocking the foundations of evolutionary biology.” Selection is based on conserved molecular mechanisms that are the determinants of genetically predisposed phenotypes, and the conserved molecular mechanisms are epigenetically effected.The epigenetic effects of olfactory/pheromonal input, for example, allow for the fixation of new alleles that is not enabled in the context of mutation-driven evolution.

      What happens when I say there has never been any scientific support for the concept of mutation-driven evolution is different than when the president of the International Union of Physiological Sciences says it. But he and I are saying the same thing.

      Although neither of us could expect that an actual experiment would refute the concept of mutation-driven evolution, since no one had ever done such an experiment to support the concept (since 1927), now that the results from the experiment are available, hanging on to the refuted theory is the last thing I would want to be caught doing. But I wouldn’t want to be caught arguing with Denis Noble, either.

      Your claims that I am being too dismissive, using language that is too strong or misrepresenting the facts can be examined in the context of “Biological Information: New Perspectives” For example: John C. Sanford writes: “The neo-Darwinian paradigm literally saturates the content of most biological journals. In fact any deviation from this view is generally regarded as academic treason — often being characterized as a threat to science itself. Yet in this section of our proceedings (Biological Information and Genetic Theory), we will show that there are huge genetic problems which bring this reigning paradigm into serious question.”

      Not only have the huge genetic problems with mutation-driven evolution now been addressed in an experiment, it’s long past time to move forward and it may take some strong language with accurate representations of biological facts to make people move. Mutation-driven evolution has no biologically based scientific support, and it never had any.

  27. John S
    September 17, 2013

    Ah, I just found pheromones.com.

    This intransigence over non-existent inappropriate comparisons and insistence in the incredible power of semiochemicals now makes sense in light of an obvious commercial bias; James is selling human “pheromones” to the public, to make you sexier, or something. So much for the rigors and requirements of evidence.

    James, I read your 2012 review in SNP, as well as some others elsewhere regarding human pheromones, and the consensus on the science of epigenetics vs mutation evolution isn’t as clear cut as you are making out here.

    SNP itself is a pretty all-round unimpressive journal, with only 15 or so total articles in its archive since beginning in 2011, two of which list you as the sole author. It is also not indexed by any of the services I frequent and has no listed impact factor I can find. An unimpressive journal (thought I did actually like the review you wrote) and a commercial bias = I’ve had to resist dismissing what you say out of hand. Leaving the putative implications for different models of evolution aside for a moment, the over-arching notion of pheromonally (or food odor) induced epigenetic changes is fascinating, and I look forward to seeing what contribution the still-maturing field of epigenetics makes to the science of evolution, without resorting to the kind of dismissive hyperbole that I have encountered in your posts on this other websites.

    • James V. Kohl
      September 17, 2013

      Thanks JohnS. You just dismissed the entirety of my published works on molecular epigenetics beginning with co-authorship of a 1996 review in Hormones and Behavior. That review led to extension of our model of hormone-organized and hormone-activated mammalian behavior to invertebrates, which makes the consensus on epigenetics perfectly clear via the honeybee model organism (see anything written in the past decade, for example). Food odors and pheromones epigenetically effect genes linked to behavior and back.

      In my SNP review I included other model organisms like: microbes, nematodes, other insects, other mammals, and a human population in what is now central China. So what are you telling others about the supposed “intransigence over non-existent inappropriate comparisons and insistence in the incredible power of semiochemicals?” I think that your focus on my commercial interests says it all. You’re saying ignore the biological facts. Continue promoting a ridiculous theory, instead!

      For comparison, a colleague said this: ” James Kohl, an independent researcher who also markets “human pheromones” to the general public, believes that pheromones may have a primary influence in setting up a person’s basic sexual orientation. Other, more consciously perceived aspects of attractiveness, such as facial appearance, are attached to a person’s basic orientation through a process of association during early postnatal life, according to Kohl. 35″

      This model is attractive in that it solves the “binding problem” of sexual attraction. By that I mean the problem of why all the different features of men or women (visual appearance and feel of face, body, and genitals; voice quality, smell; personality and behavior, etc.) attract people as a more or less coherent package representing one sex, rather than as an arbitrary collage of male and female characteristics. If all these characteristics come to be attractive because they were experienced in association with a male- or female-specific pheromone, then they will naturally go together even in the absence of complex genetically coded instructions.” p. 210 Gay, Straight, and the Reason Why: The Science of Sexual Orientation by Simon LeVay.

      Given your opposition to my model, are you willing to say that homosexual orientation is the result of mutations? If so, you and LeVay should discuss that ridiculous theory in the context of my model and my commercial interests. If you want to discuss facts, don’t insult me with the inference that my commercial interests trump my scientific representation of biological fact in published works. Attack those representations so that they can be compared to the ridiculous mutations theory of evolution (of sexual orientation, for example).

  28. William Holz
    September 23, 2013

    I’m just going to add the cheerful observation that I think it’s delightful that they have a confuse attack!

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