This is the third and last of a series of posts on the misguided concept of “agency and purpose in biology,” which one can take as the statement that “organisms have goals, and guide their own development and evolution towards those goals”.

In my first post, on December 23, I noted that the John Templeton Foundation (JTF) was spending millions of dollars funding grants on the science of “purpose and agency”. I pointed out one JTF  grant that just ended, which handed out $14.5 million to a consortium of investigators to study this topic.  And the JTF intends to continue funding this area:

Science of purpose. We are looking for experimental and theoretical research projects that will provide insight into the purposive, goal-directed, or agential behaviors that characterize organisms and various components of living systems. Researchers who have familiarity with our ongoing work in this area are especially encouraged to apply.

If you know the JTF, you’ll understand why they keep replenishing a trough full of grant money for such studies, for John Templeton (a mutual-fund billionaire and a believer) funded his Foundation with the intent of showing that science itself gave evidence for “spiritual reality”, aka a god or gods.  Although some of the investigators supping at the trough deny that they’re engaged in teleology, much less giving evidence for divinity, all of their work feeds into the JTF’s mission, and the authors of an article just published online at the Journal of Evolutionary Biology (JEB) agree: the idea of teleology sneaks into many of these papers.

In my second post, on December 26, I analyzed one of the JTF-funded papers often cited to support the idea of agency and purpose in organisms, a paper in BioEssays by Sonia E. Sultan et al. I found it vacuous and intellectually confusing, mistaking “purpose” and “agency” for the results of natural selection and, in the end, making the ID-friendly argument that neo-Darwinism cannot explain the origins of “novel, complex traits”. That assertion alone discredits the paper, for the one paper that actually tried, using conservative assumptions, to mathematically model the origin of a complex trait (the camera eye), did so very successfully. No problems encountered! The purpose-and-agency folks’ view is that “since we don’t fully understand how an eye/wing/brain evolved, there must have been something beyond natural selection involved.”  I suspect you know the fallacy of this argument.

Here are two concepts of agency advanced by Sultan et al and quoted in the paper below:

● “Biological agency—the capacity of living systems […] to participate in their own development, maintenance, and function” (Sultan et al 2022, p. 1);

● “Organisms themselves actively shape their own structure and function” (Sultan et al 2022, p. 4);

Now, a paper by James DiFrisco and Richard Gawne, published in JEB, takes apart the whole misguided notion and program of “agency and purpose” in evolution, and cites a lot of papers that tried to advance misguided ideas similar to those of Sultan et al. The title of the new paper is below, but if you click on it you will go to a truncated version of the article. However, you  can read the entire paper as a pdf file available for free here.

Here are what I take as the paper’s important points:

A.) The idea that organisms direct their own development and evolution through some nebulous, non-neo-Darwinian process is incorrect. Everything touted as “purposeful” and “the results of agency” can be explained by natural selection molding organisms’ responses to a changing environment, both within one lifetime or across generations. As DiFrisco and Gawne say, goal-directedness “is an adaptation due to natural selection.”  In my own example, cats and other mammals often grow longer fur during cold seasons because natural selection has favored genes that give organisms the capacity to put out more fur when their bodies detect cold weather. This is simple natural selection, and there is no “purpose” or “agency” involved.

B.)  Some of the papers on purpose and agency aim to “rescucitate the Aristotelian view of biological purpose and teleology as real rather than merely apparent”, so some authors really do have a teleological bent, one that you can find in some works of the “Extended Evolutionary Synthesis.”

C.) The agency and purpose trope is, in the end, a metaphor that does no explanatory work nor promotes further research. Only the framework of neo-Darwinism can help us understand the origin of adaptations.

D.) The only “true” purpose and agency we see in biology is that which we see in the cognition of organisms capable of responding to environmental challenges by thinking rather than by a mechanical response.  But even the p&a authors are the first to aver that this is not the sense in which they use these terms. In truth, as a hard determinist I see even cognition as a mechanical process and not something different in principle from a bacterium moving towards food, but this is not so important in this debate since the “cognition” view of purpose isn’t the subject of scientific work by the Templeton-funded authors.

I’ll quote the authors’ own conception of their aims as given in the JEB paper:

Box 1: The central claims of this paper. 1. An organism’s capacity for goal-directed behavior does not itself explain any biological phenomena. Apparently goal-directed behaviors are, instead, something to be explained as an evolved characteristic of biological systems. 2. The capacity for goal-directed behavior (outside of human cognition, which can set arbitrary, novel goals) is explained by Darwinian natural selection acting in populations of individuals. 3. Notions such as self-determination, or the idea that the whole organism is a cause of its own developmental or physiological processes, are either empirically untestable, or restatements of ordinary questions about which causal mechanisms at which scales influence events. 4. Downward causation and context-dependence are “mechanistic” in the sense relevant to experimental biology. They are not mysterious processes that require adopting the teleological form of investigation provided by an agency perspective. 5. Rejection of molecular reductionism or determinism does not necessitate a commitment to the idea of biological agency. Researchers need not embrace the agency perspective in order to acknowledge the importance of multi-level complexity, emergence, and downward causation. 6. The idea that biological goal-directedness is a product of natural selection rather than the inherent agency of organisms does not require commitment to the idea that all traits are adaptations. It is compatible with genetic drift, mutation, and developmental constraints playing an important role in evolution. 7. Agency is a psychological concept with origins in heuristic ascriptions of intentionality. Accordingly, it is applicable only where psychological explanations are useful—i.e., when explaining the behavior of humans and possibly other neurologically complex organisms such as primates. 8. Agency is not an empirically meaningful property, and incorporating the agency concept into experimental practices will not contribute to progress in biology.

And a few quotes that underline their contentions (indented). First, the important of natural selection in explaining adaptations:

It is important to recognize that the attribution of non-fitness-related goals to an organism can only be empirically grounded in the psychological case, where investigators can ask another human being to report on their internal cognitive states. For systems that lack the capacity to report on such states, the attribution of goals is empirically unmoored and arbitrary (see Fig 1). Is it the goal of a given stem cell to differentiate? (Manicka and Levin 2019; Levin 2021; 2022) Or, if the stem cell fails to differentiate and dies, was that really its goal? In order for goal-attributions to explain anything, goals would need to be linked to some empirically detectable feature of the system other than the actual outcomes of its behavior. Otherwise, these explanations would be circular and uninformative. It is not clear that this can be done without reference to natural selection.

The intellectual and biological vacuity of adding “purpose” to already-existing explanations:

Even if one allows explanations based on agency, it is difficult to see how such explanations could be useful for understanding an ordinary biological process—e.g., wound healing. To explain why a wound heals following injury, the statement that it is because the system possesses agency and pursues the goal of healing wounds is not useful from a scientific point of view. This is because agency is not an experimentally meaningful property that can be subjected to tests as to whether its presence or absence influences wound-healing. The “goal” of wound-healing is not something that can be detected or measured, but would have to be inferred and attributed ex post facto based on the system’s actual behavior (see above, “Agency and goal-directedness”). This procedure cannot predict that wound-healing fails in pathological cases (e.g., tumorigenesis), nor can it explain why such malfunctions do or do not happen. In the context of modern biological research, wound-healing is understood to be explainable in terms of complex positive and negative feedback mechanisms in which a wide array of signaling molecules mediate the progression through cell- and tissue-level processes, from wound detection to hemostasis, inflammation, cell proliferation, re-epithelialization, and tissue remodeling (Singh et al 2017; Rodrigues et al 2019). These feedback mechanisms are tuned to parameter values conducive to survival and reproduction because of natural selection.

Between mechanistic explanations and adaptive ones (Tinbergen 1963; Stearns 1982), there is no obvious role for a distinct form of explanation based on agency.

How could you investigate how wounds heal by even considering the idea of “purpose and agency”?  As the authors note, there is no real “goal” here, but merely the sorting-out of genes that have different effects on wounds, with the genes that contribute to healing leaving more copies (their bearers survive and/or reproduce better).  That’s simply natural selection.  Ergo, there is no scientific benefit of JTF giving lots of dollars to study agency and purpose. They could give money for studying neo-Darwinian explanations, which we know are often the way to go, but doing so would simply justify scientific materialism, something anathema to JTF, as it leaves out god.

Finally, one more quote, as you can read the paper yourself (it’s written very clearly and should be accessible to those with a smidgen of biology knowledge):

An initial difficulty with the notion of self-determination centers on the self. It is not clear how to interpret expressions such as “the capacity of living systems […] to participate in their own development.” Development is the process of an organism going through the stages of its life cycle. It is not something separate from the organism. So how can an organism fail to participate in its development? If we suppose that the development of a given organism is fully determined by a set of underlying molecular factors, it is still the development of that particular organism rather than of another entity. It is also difficult to interpret the statement that “typical descriptions […] treat organisms [as] separate from and passive to the conditions under which they develop and evolve” (Nadolski and Moczek 2023, p. 3). If this refers to environmental conditions, it is an ordinary question of the relative causal importance of internal versus external factors. If it refers to internal conditions, however, the statement veers into obscurity. How can an organism be or separate from, or passive to, a process of development of itself?

This quote—and indeed, the whole paper—shows that the “purpose-and-agency” school is either engaged in a semantic rather than a biological argument, they are simply unable to grasp evolution, or they wish to make a name by couching neo-Darwinian mechanisms in “I-have-a-new-paradigm” language. .  Indeed, epigenetics (at least some forms) were not part of the modern synthesis, but neither do they play into notions of agency and purpose. Epigenetic modifications can be evolved features of organisms that are ultimately coded in the genome, or they can be environmentally-induced modifications of DNA that are rarely adaptive and, at any rate, usually disappear in two or three generations at most, making them useless to explain the evolution of adaptations.

The lesson is twofold. Beware when you see biologists banging on about agency and purpose, and think about natural selection instead. Second, the JTF is throwing away its money on misguided projects. I’d like to ask them to give money to fund real biology, as they have over a billion dollars in endowment, but funding real biology would not advance the JTF’s purpose of finding the numinous using science.

On December 23rd, I called attention to the huge amount of money that the John Templeton Foundation (JTF) was throwing at biology projects giving evidence of “purpose and agency” in organisms. For example, one grant given to a group of investigators, titled “Agency, directionality, and foundations for a science of purpose,” handed out more than $14.6 million! And one of the few areas in biology they’re funding again next year is, yes, projects on the “science of purpose”, to wit:

Science of purpose. We are looking for experimental and theoretical research projects that will provide insight into the purposive, goal-directed, or agential behaviors that characterize organisms and various components of living systems. Researchers who have familiarity with our ongoing work in this area are especially encouraged to apply.

Now you can easily see how this fits into the JTF’s original aim, which was to find evidence for divinity and spirituality in science. And indeed, I’m sure that’s why they’re funding this area.  But I’ve already argued that the only kind of “purpose” found in organismal behavior is that involved in conscious cogitation, which is present in only a few organisms.  Yes, some behaviors look “purposeful,” as when a bacterium moves toward or away from light, but that’s a purely mechanical response—not the kind that, say, humans have when they decide, “I’m going out for pizza.” And of course there is no goal-directedness or purpose in evolution, which simply sorts out genetic variation based on whether genes leave more or fewer copies of themselves, often leaving more when they adapt their carrier better to the environment.

However, the biologists who get funded for work on “agency” and “purpose” will be the first to tell you that they are not really imputing to organisms the kind of mental “purpose” that some organisms have, nor are they looking for anything numinous or supernatural. Rather, they seem to be whipping up a bunch of word salad that makes it seem that they are overthrowing the neo-Darwinian view that adaptations arise from genetic variants sorted out by their relative contribution to the genes of descendants.  Such researchers pretend that they are making profound new statements about biology and evolution, but when you look at the papers carefully, as I did with one of the influential papers (below) that Templeton funded in its “purpose and agency” program, you find nothing new. In this case, a whole paper touting “purpose” is merely re-describing something known for a long time: organisms can evolve “norms”of reaction”. These are simply the plastic developmental programs that organisms evolve to respond to environmental changes, so that behavior, physiology, and appearance can change when conditions change. That superficially may look like “agency”, but there’s no “will” involved, and nothing beyond genes responding to environments.

The evolution of norms of reaction is not hard to understand. Take one familiar plastic response: mammals like cats that grow longer fur in the winter.  This is due simply to natural selection acting on the DNA to respond to cold temperature by growing thicker fur. And, of course, as we know from all the varieties of dogs and cats with more or less fur, artificial selection can do that, too. We needn’t think about “purpose” or “agency” when we see this, nor need we say, “one purpose of this trait is to keep the cat warm” or “the cat has agency to grow longer fur to keep in warm in winter.”  That kind of talk about “purpose” is only confusing, hiding what really happened during evolution: natural selection for flexible forms of development.

And there are gazillions of traits that you could say look as if organisms have such agency or purpose, but they are all the result of natural selection. If a goat loses its front legs in an accident, it may well eventually walk on its hind legs. To do that, a number of their bones, tendons, and muscles have to be reconfigured to allow adaptive locomotion. But this, too, is a result of evolved plasticity: in the past, injuries may have been common, and those individuals with genes that allowed their development to compensate for those injuries, thus allowing the sufferer to survive and reproduce, outcompeted individuals lacking genes giving their bodies the ability to cope with injuries.

This is nothing new in evolution; people have talked about plasticity and “norms of reaction” (how organisms change to cope with changes in the environment”) for ages, and there are even experiments showing that such coping is due to natural selection.  But authors like those of the paper below, funded by the JTF, gussy up an old concept by calling it “biological agency”, enabling them to get a ton of cash from the JTF.

I see the effort as intellectually confusing and, indeed, hubristic, because surely the authors know what they’re doing. In the next and final installment of this “agency” mishigass, I’ll highlight a paper that calls this kind of effort to task, showing that it really doesn’t show anything new. Yes, I get excited when new concepts and findings appear in biology and especially evolution, but this ain’t one of them.

Click on the headline below to read the paper, which is free (there’s a pdf here):

The Sultan et al. paper is poorly written, full of big words that are supposed to constitute their idea of agency. But let’s see first how they define agency. Excerpts from the paper are indented.

What is agency? Sultan et al. assure us that it isn’t anything supernatural, but what it really is comes down to “self-regulation” that, in the end, simply amounts to the norms of reaction of an organism.

Living systems have evolved to be robust, responsive, flexible, self-synthesizing and self-regulating. This dynamic flexibility is manifest across diverse levels of biological organization, from cells, to tissues, to entire organisms, to reproductive lineages, to social colonies, and throughout a variety of organismal activities—from molecular signaling pathways to morphogenetic, metabolic, immune, endocrine, and behavioral systems. We use the term biological agency to refer to this suite of robust processes that is constitutive of living systems (See Box 1). Biological agency, in this sense, is the capacity of a system to participate in its own persistence, maintenance, and function by regulating its own structures and activities in response to the conditions it encounters.^[69] Attributing agency to a biological system is based on natural, empirically determined processes and connotes neither consciousness nor deliberate intention.

or

Agency is a dynamical property of a system.^[162] It consists in the system’s capacity to transduce, configure, and respond to the conditions it encounters. Crucially, agential systems are capable of maintaining functional stability in response to conditions that would otherwise compromise their viability.

Try as I might, I cannot see a distinction between this farrago of fancy words and good old “norms of reaction”.  “Self regulation” is simply the end result of natural selection acting on organisms so that when the environment changes, they respond through their evolved developmental systems in an adaptive way. Note that the authors explicitly rule out “purpose” of “deliberate intention” in the “consciousness” sense here.  Ergo, “maintaining functional stability in response to conditions that would otherwise compromise their viability” is just like a cat growing longer fur in the winter, but it sure is a fancy way of saying it.

Here some examples the authors adduce for “agency”:

Polypterus fish reared in a terrestrialized environment in which fish are forced to walk on their pectoral fins rather than swim, adjust—within a lifetime—not just their behavior, gait and posture but also their skeletal features, in ways that parallel the fossil record of tetrapods’ ascendance onto land.^[136] Tadpoles exemplifying the ancestral detrivorous life style and associated gut morphology will adjust the latter if forced to consume a carnivorous diet, in ways that partly parallel evolved changes in specialized carnivorous lineages.^[137] Examples such as these suggest that interactions between developmental systems and environmental circumstance may bias the production of phenotypic variation in the face of novel or stressful environments toward functional, integrated, and possibly adaptive variants.

No, the phenotypic direction isn’t “biased” by anything but natural selection. Polypterus fish live in shallow water and have lungs, and it’s possible that their ancestors evolved to walk on their fins to get around in that shallow water or even to leave the water for brief periods of time if their ponds are drying up and they need to get to another pool of water.  Or, it’s even possible that this norm of reaction isn’t evolved at all, but simply the result of an organism struggling to move when that’s the only alternative it has. Here’s what it looks like:

Try that with a goldfish! Why do Polypterus show “agency” in this way but not goldfish? Probably because of the evolutionary background of this species, which is sometimes regarded as an example of the kind of fish that evolved into terrestrial teterapods. But what “agency” are they showing? Likewise, it’s easy to see how tadpoles could occasionally encounter a situation in which there is more “meat” (other organisms or their remains) to eat than there is non-animal detritus. In that case, tadpoles able to evolve a way to change their digestion in such a circumstance would leave more offspring than those that couldn’t. Of course for this system to work, the environment would occasionally have to change in a way that would give organisms like this an advantage (it doesn’t have ot change every generation).  If organisms evolved a developmental system to adapt to environmental changes that couldn’t conceivably have occurred, then we’d have something to talk about! But I know of no such cases.

To justify their “new” approach, the authors give examples of three phenomena that, they say, can’t be explained by conventional neo-Darwinism:

1). Genome-wide association studies (GWAS), in which genes for traits are identified by looking at which genetic variation in an entire genome is correlated with variation in a trait, often reveal “too few genes”.  For example:

In the case of body weight, for example—a biomedically critical trait in the context of obesity, insulin resistance and type 2 diabetes—115 genetic loci that showed significant statistical association with body mass index (BMI) collectively explained less than 3% of the variation among adults,^[8] and a meta-analysis based on an enormous sample of 700,000 individuals (conferring great statistical power) still explained only 6% of BMI variation^[9] despite using a high-dimensional correlation matrix that is known to inflate these estimates.^[10] While such extremely large studies may incrementally add to the variance explained by identifying additional loci of small effect through sheer statistical force, over 90% of (a) phenotypic variation for BMI and (b) risk of type 2 diabetes remains unaccounted for,^[11, 12] pointing to a more fundamental issue.

And yet heritability studies, involving simple correlation of BMI between relatives is measured, show that between 40% and 70% of the variation of that trait among individuals is due to variation in genes. We can find only 6% of those genes, so where are the rest?  One explanation is that there are many genes affecting BMI whose effects are too small to be measured by GWAS, which requires pretty big effects to find a genetic region affecting a trait. Further, GWAS analyses rely entirely on SNPs (single nucleotide polymorphisms in DNA sequence), and are unable to detect duplications and deletions, which we know make a contribution to human trait variation (see references here, here, and here). Finally, GWAS is unable, except in vary large samples, to detect rare genes, and yet given the size of the genome, everyone has quite a few “rare” genes.  When you use large samples, as they have done for human height, the missing heritability diminishes to almost zero: the genetic variation detected by GWAS gives predictions that are almost the same as that based on standard heritability studies.

The authors add this:

Biomedical researchers concerned about the limits of the GWAS approach are therefore increasingly calling for conceptually broader studies directly addressing processing pathways that modulate gene function and hence phenotypic outcomes in individuals via complex gene-environment interactions,^[18] environmentally-mediated epigenetic modifications,^[19, 20] and physiological and developmental feedback systems such as microbiome composition, which changes dynamically in response to the individual’s diet, behavior, and social environment.^[21]

Yes, perhaps there are some differences in microbiomes that are responsible here, but there are many traits where there are “missing genes” that cannot be imputed to microbiome inheritance. As for epigenetic modifications and the like beyond bacteria in the gut, those would also show up in GWAS studies, and so can’t constitute “missing genes” (an epigenetic modification occurs at a given site in the DNA, involves a modified base, and is supposedly inherited over at least one generation).

But much of the above is simply gobbledygook: how can “dynamic changes in response to diet, behavior, and social environment” account for missing genetic variation that shows up in heritability studies but not GWAS studies? This could occur only in species in which cultural, nongenetic factors are inherited, like the tendency to eat fatty foods. But these factors are usually ruled out in most heritability (e,g., in flies) and those studies still show a substantial genetic contribution to variation in a phenotype. What the authors consider “agency” here is not clear, but they are doing a service by highlighting a problem that has yet to be solved: “dark heritability.” We don’t know the answer yet, but we have some clues, and time will tell.

2). The authors drag in epigenetics to explain the missing heritability. This second problem is really the same as the first: we have a mismatch between results revealed by GWAS analysis and simple studies of heritability via correlation between relatives.  But this doesn’t solve the problem: it compounds it for two reasons. First, epigenetic modifications of DNA will show up in GWAS and heritability studies, and so don’t constitute “dark genetic variation”. Further, non-coding RNAs, which the authors further use to explain missing variation, are also inherited.  Finally, and most important, epigenetic modifications of DNA resulting solely from the environment (and not coded for themselves in the genome) almost never persist for more than two or three generations, and thus can’t explain a persistent appearance of “adaptive change” over evolution. Nor are epigenetic modifications usually adaptive, and they can be maladaptive (as in the “Dutch famine trauma”), because they are not evolved but simply the effect of the environment on a genome not adapted to changes in that environment.

Here is one example the authors use to show agency via purported epigenetic change:

An experimental example using isogenic plants points to part of what may be missing. In one series of experiments with the common herb Polygonum, parent plants of the same genetic line were either drought-stressed or given ample water. When their offspring were grown in identical, dry, conditions, they developed differently: the offspring of drought-stressed parents produced significantly larger and more rapidly-extending root systems than those of the moist-grown parents, an inherited phenotypic effect that resulted not from a genetic difference but in response to parental conditions.

“Isogenic” means that all the plants were genetically identical. And yes, it’s hard to imagine that offspring have a way of genetically “knowing” whether their parents experienced drought, though there could be cytoplasmic effects.  So this looks like agency, and may be due to adaptive epigenetic modification.  But this is the exception, rather than the rule.

3.) This is the kicker: neo-Darwinism cannot, say the authors, explain the origins of “novel, complex traits”. Here we have one of the assertions of intelligent design, but although there’s no designer, the authors’ claim about the impotence of neo-Darwinism in producing complex adaptations is simply wrong (they are implying, I think, that organisms are somehow using their AGENCY to develop those complex traits. Here’s the assertion:

The origin of novel complex traits constitutes a central yet largely unresolved challenge in evolutionary biology.^[61] Ever since the founding of evolutionary biology one of the discipline’s core motivations has been to understand such elaborate innovations as the vertebrate eye, the insect wing, or the mammalian placenta, traits whose origins transformed the diversity of life on earth. Yet conventional approaches to understanding evolutionary change have provided few opportunities to make significant headway.^[62] Of the four evolutionary processes conventionally recognized—natural selection, genetic drift, migration, and mutation, the first three can only sort among existing variants and their distribution within and among populations, but by themselves cannot bring about novel features.^[63] This privilege is instead restricted to mutation, yet all attempts to explain the evolution of novel complex traits solely via the coincident origin, spread, and fixation of one beneficial mutation at a time have failed.

Sorry, but this resembles what comes out of the south end of a cow looking north. There is no conceptual reason that sorting out existing and new genetic variants via conventional natural selection is impotent to produce complex traits. The problem is that we simply weren’t there when many complex traits evolved, and so don’t know the genes involved, the selection pressures involved, or even the developmental pathways involved in producing the traits.

I know of only one attempt to get at this problem, and that involved the evolution of the camera eye. This was the work of Nilsson and Pelger summarized in a delightful summary by Richard Dawkins called “The eye in a twinkling“.  Using conservative (“pessimistic”) assumptions about mutation rates, heritabilities, and the number of developmental steps required to transform a light-sensitive spot into a complex “camera eye” with a lens, retina, and cornea (viz., what we and some cephalopoods have), Nilsson and Pelger found out that the evolution of this assuredly complex trait took around 400,000 generations. As Dawkins noted:

Assuming typical generation times of one year for small animals, the time needed for the evolution of the eye, far from stretching credulity with its vastness, turns out to be too short for geologists to measure. It is a geological blink.

And so it might be with other traits, like wings or placentas. The problem is making an appropriate model, and that is hard or impossible without knowing how the trait evolved (we have some idea with the eye, as Dawkins notes, hearkening back to Darwin, who first raised the “eye problem”.) But without such models, it’s almost deceitful to say that we need a new paradigm to explain the evolution of complex traits. (In fact, we can see the evolution of complex traits—like whales evolving from land ungulates in a mere 10,000 years. And that is surely due to selection, though we can’t say with assuredness that conventional neo-Darwinism was involved. But our ignorance does not justify us trying to depose a well-established paradigm, and one that works very quickly in the case of artificial selection (genetic analysis of adaptations invariably shows that changes in the DNA are involved).  Are dog breeds all due to epigenetic modifications of DNA or “agency” in the ancestral wolf? I don’t think so!)

I’ve already gone on too long, but if this paper is typical of the kind of research the JTF is funding as evidence for agency and purpose, it’s throwing its money down the toilet,.

Oh, and one last beef. When I saw this claim in the Sultan et al. paper, I was astonished:

In Maize, for instance, the “profound” architectural and reproductive changes that distinguish cultivated Maize from its wild progenitor, Teosinte, resulted not from novel mutants but from the response of a complex epistatic network to the atmospheric CO₂ and crowded planting conditions encountered during the species’ early cultivation.^[155]

What? This change, from the grass teosinte on the left to modern corn on the right (hybrid is in the middle) has nothing to do with novel mutations?

I looked up reference 155 and found this:

For example, genetic research shows that once-emphasized conventional assumptions about morphological change—e.g., that the change was driven mainly by human selection for rare mutants of a few single genes that were deleterious in wild plants and favorable in field environments or by selection for new, advantageous mutations that appeared postcultivation—have, for some major traits, been supplanted by different and/or more complex processes. These processes include (i) regulatory changes that targeted diverse developmental pathways and led to changes in gene expression (e.g., how, when, and to what degree existing genes are expressed through changes in the amount of mRNA during transcription); (ii) extensive rewiring of transcriptomic and coexpression networks; (iii) in an increasing number of wild progenitors, the presence and availability to the first cultivators of preexisting, nondeleterious genetic components for major domestication traits (known as “cryptic genetic variation”) that induce trait variation only under specific environmental or genetic conditions; and (iv) deviations from simple Mendelian expectations.

Every change mentioned involves mutations, whether they be structural, regulatory, or “cryptic” (genes showing their effects only under limited conditions). There is nothing new here, merely an explication of how artificial selection on teosinte involved a variety genetic changes.  There is NO AGENCY in teosinte, not even construed as broadly as Sultan et al. do.

In the end, the paper seems to be much ado about nothing, which, in the last chapter (maybe tomorrow) another author will analyze critically, showing that there’s no “there” there.

I know many people won’t be interested in this analysis, but I wanted to get it on the record because so many people are hearing that not only is neo-Darwinism a pretty useless paradigm for understanding adaptation, but now are hearing as well that some nebulous “purpose” and “agency” are involved. As usual, Templeton’s money has only muddied the water.

 

h/t: Luana for her explanations of GWAS.