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Darwin the Newtonian. Part V. A spectrum, not a dogma

Our previous installments on genetic drift (a form of chance) vs natural selection (a deterministic force-like phenomenon) and the degree to which evolution is due to each (part 1 here) lead to a few questions that we thought we'd address to end this series.

First, there is no sense in which we are suggesting that complex traits arise out of nowhere, by 'chance' alone.  There is no sense in which we are suggesting that screening for viability or utility does not occur as a regular part of evolution.  But we are asking what the nature of that screening is, and what a basically deterministic, Newtonian view of natural selection, that is we believe widely if often tacitly held, implies and how accurate it may be.

It's also important here to point out something that is obvious.  The dynamics of evolution from both trait and genome level comprise a spectrum of processes, not a single one that should be taken as dogma.  A spectrum means that there is a range of relative roles of what can be viewed as determinism and chance that the two are not as distinct as may seem, and that even identifying, much less proving what is going on in a given situation is often dicey.  Some instances of strong selection, like some of chance seem reasonably clear and those concepts are apt.  But much, perhaps most, of evolution is a more subtle mix of phenomena and that is what we are concerned with.

Secondly, we have discussed our view of natural selection before, in various ways.  In particular, we cite our series on what we called the 'mythology' of selection, a term we used to be provocative in the sense of hopefully stimulating readers to think about what many seem to take for granted.  Yes, we're repeating ourselves some, but think the issues are important and our ideas haven't been refuted in any serious way so we think they're worth repeating.

A friend and former collaborator took exception to our assumption that people still believe that what we see today is what was the case in the past.  He felt we were setting up a straw man. The answer is somewhat subjective, but we believe that if you read many, many descriptions of current function and their evolution, you'll see that they are often if not usually just equated de facto with being 'adaptations', and that means that doing what they do now came about because it was favored by the force of selection in the past.  We think it's not a straw man at all, but a description of what is being said by many people much of the time: very superficial, dogmatic assumptions both of determinative selection and that we can infer the functional reason.

Of course everyone acknowledges that earlier states had their own functions and today's came from earlier, and that functions change (bat wings used to be forelegs, e.g.), but the idea is that bat flight is here because the way bats fly was selected for.  One common metaphor going back to an article by Lewontin and Gould is that evolution works via 'spandrels', traits evolved for one purpose or incidentally part of some adaptation, that are then usable by evolution to serve some new function. Yes, evolution works through changing traits, but how often are they 'steps' in this sense or is the process more like a rather erratic escalator, if we need a metaphor?

There are ways for adaptive traits to arise that have nothing to do with Darwinian competition for limited resources, and are perfectly compatible with a materialist view.  Organismal selection occurs when organisms who 'like' a particular part of their environment, tend to hang out there.  They'll meet and mate with others who are there as well.  If the choice has to do with their traits--ability to function at high altitude, or whatever--then over time this trait will become more common in this niche compared to their peers elsewhere, and eventually mating barriers may arise, and a new species with what appears to be a selected adaptation. But no differential reproduction is required--no natural selection.  It's natural assortment instead.

All aspects of our structure and function depend on interaction among molecules.  If two molecules must interact for some function to occur, then mutant versions may not serve that purpose and the organism may perish. This would seem most important during embryonic development.  An individual with incompatible molecular interactions (due to genetic mutation) would simply not survive.  This leaves the population with those whose molecules do interact, but there is no competition involved--no natural selection.  It's natural screening instead.

Natural selection of the good ol' Darwinian kind can occur, leading to complex adaptations in just the way Darwin said 150+ years ago.  But if the trait is the result of very many genes, the individual variants that contribute may be invisible to selection, and hence come and go essentially by chance. This is what we have called phenogenetic drift.  Do you doubt that?  If so, then why is it that most complex traits that are mapped can take on similar values in individuals with very different genotypes?  This is, if anything, the main bottom line finding of countless very large and extensive mapping studies, in humans and even bacteria.  This is basically what Andreas Wagner's work, that we referred to earlier in the series, is about.   It rather obviously implies that which of equivalent variants proliferates is the result of chance.  There's nothing non-Darwinian about this.  It's just what you'd expect instead.

We'd expect this because the many factors with which any species must deal will challenge each of its biological systems. That means many screening factors (better we think than calling them selection 'pressures' as would usually be done).  Most of these are affected by multiple genes.  Genes vary within a population.  If any given factor's effects were too strong, it would threaten the species' existence.  At least, most must be relatively weak at any given time, even if persisting over very long time periods.  Multiple traits, multiple contributing genes in this situation means that relative to any one trait or gene, the screening must be rather weak.  That in turn means that chance affects which variant proliferates.  There's nothing non-Darwinian about this.  It's essentially why he stressed the glacial slowness of evolution.

There is, however, the obvious fact that known functional parts of DNA are far less variable than regions with no known function.  This can be, and usually is assumed to be, the expected evidence of Darwinian natural selection.  But factors like organismal dispersion or functional (embryonic) adequacy can account for at least some of this.  Longer-standing genes and genetic systems would be expected to be more entrenched because they can acquire fewer differences before they won't work with other elements in the organism.  This is at least compatible with the view we've expressed, and there could be some ways of testing the explanation.

This view means we need not worry about whether a variant is 'truly' neutral in the face of environmental screening.  We could even agree that there's no testable sense in which a variant evolves by 'pure' chance. Even very tiny differences in real function can evolve in a way that is statistically 'neutral'.  Again, this can be the case even if the trait to which such variants contribute is subject to clear natural or other forms of selection.

This view is also wholly compatible with the findings of GWAS, the evidence that every trait is affected by genetic variation to some extent, the fact that organisms are adapted to their environment in many ways and the fact that prediction based on genotyping is often a problematic false promise.  And because this is a spectrum, randomly generated by mutation, some variants and or traits they affect will be very harmful or helpful--and will look like strong, force-like natural selection.  These variants and traits led to Mendel, and led to the default if often tacit assumption that natural selection is the force that explains everything in life.

Further, it is important for all the same sorts of reasons that the shape of the spectrum--the relative amount of a given level of complexity--is not based on any distribution we know of and hence is not predictable, generally because it is the result of a long history of random and local context and contingencies, of various unknown strength and frequency (about the past, we can estimate a distribution but that doesn't mean we understand any real underlying probabilistic process that caused what we see).  This is interesting, because many aspects of genetic variation (and of the tree of life) can be fitted to a reasonable extent to various probability distributions (see Gene Koonin's paper or his book The Logic of Chance).  But these really aren't causal parametric 'laws' in the usual sense, but descriptions after the fact without rigorous causal characteristics.  Generally, prediction of the future will be weak and problematic.

In the view of life we've presented, evolution will have characteristics that are weak or unpredictable directional tendencies, and the same for genetic specificities (and hence predictive power). It is the trait that is in a sense predictable, not the effects of individual genes.

We think this view of evolution is compatible with the observed facts but not with many of the simplified ideas that are driving life sciences at present.

Our viewpoint is that the swarm of factors environmental and genomic means that chance is a major component even of functional adaptations, in the biodesic paths of life.

Darwin the Newtonian. Part II. Is life really 'Newtonian'?

In yesterday's post I suggested that Darwin had a Newtonian view of the world, that is, he repeatedly and clearly described the organisms and diversity of life as the product of evolution, due to natural selection viewed as a force, which in an implicit way he likened to gravity.  At the same time, he knew that there was widespread evidence of various kinds for long-term evolutionary stasis, which a prominent geologist has recently called  "Darwin's null hypothesis of evolution," the idea that evolution does not occur if the environment stays the same.

That suggests that a changing environment leads to a changing mix of organisms that live in the environment, including of their genotypes.  It makes evolutionary sense, of course, because environments screen organisms for 'fitness'.  However, its negative--no change in the environment implies no evolution-- doesn't make sense and badly misrepresents what is widely assumed that we know about evolution. Even if we define evolution, as often done in textbooks, as 'change in gene frequencies' such change clearly occurs even in stable environments.  Mutations always arise, and selectively neutral variants, that is, that don't affect the fitness of their bearers, change in frequency by chance alone, not by natural selection, which means that at the genomic level evolution still occurs. It's curious that not only can organisms stay very similar in what seem like static environments, but also can be similar even in changing environments.

The idea of dual environmental-genetic stasis is an inference made from species that seem to stay similar for long time periods in environments that also appear similar--but how similar are they really?

Indeed, there are several problems with the widely if often implicitly assumed 'null hypothesis':

  1.  It is a very narrow assumption of the meaning of 'evolution', implicitly implying that it refers only to functionally important traits or their underlying genotypes. As we will see, there are ways for genetic change (and even trait change) to occur even in static environments, so that an unchanging environment doesn't imply no biological change.
  2.  It implies that 'the environment' actually stays the same, although 'environment' is hard to define.
  3.  It implies a tight essentially one-to-one fit between genotype and adaptive traits, so that in unchanging environments there will not be any functional genomic change.

All of these assumptions are wrong.  In essence, there cannot be 'the', or even 'a' null hypothesis for evolution.   Sexual reproduction, horizontal transfer, and recombination occur even without new sequence mutation.  To ignore that along with assuming a stationary environment, and adopt a null hypothesis that had anything like mathematical or Aristotelian rigor would be to reduce evolution's basis to something like this not-very-profound tautology:  Everything stays the same, if everything stays the same.

So let's look at this a little more closely
From the fossil record, we infer that some species stay the 'same' for eons, sometimes millions of years.  Then they change.  Gould and Eldridge called this 'punctuated equilibrium' and it was taken as a kind of up-dated version of Darwinism--mistakenly, because Darwin recognized it very clearly at least by the 6th edition of his Origin.  And while some aspects of animals and plants can hardly change in appearance for long time periods, close inspection shows that only some aspects of what can be preserved in fossils stays similar; other aspects typically change.  Also, speciation events occur and some descendants of an early form do change in form, even if the older species seems not to change. So we should be very careful even to suggest that environments or species really are not changing.

But mutations certainly occur and that means that even for a set of fossils that look the same, the genomes of the individuals would have varied, at least in non-functional sequence elements.  That itself is 'evolution', and it is misleading to restrict the term only to visible functional change.  But genetic drift is just the tip of the molecular evolution iceberg.  It is now very clear that there are many ways for an organism to produce what appears to be the same trait--and this is true both at the molecular and morphological levels.  That is, even a trait that 'looks' the same can be produced by different genotypes.  I wrote about this long ago in a rather simple vein, calling it phenogenetic drift, and Andreas Wagner in particular has written extensively about it, with sophisticated technical detail, in his book The Origin of Evolutionary Innovation, and this paper.  (The images are of my general paper and Wagner's book given just to break up the monotony of long text! ; he has written a more popular-level book as well called Arrival of the Fittest, which is a very good introduction to these ideas).

Recent exploration, with great detail



A modest statement of principl


Wagner explores this in many ways and among his views is that the ability of organisms to evolve innovative traits is based on the huge number of overlapping, essentially similar ways it can carry out its various functions, which allows mutations to add new function without jeopardizing the current one. Redundancy is protective against environmental changes as well as enabling new traits to arise.

This is in a sense no news at all. It was implicit in the very foundational concept of 'polygenic' control-- the determination of a trait by independent, or semi-independent of many different genes.  The way complex traits are thus constructed was clear to various biologists more than a century ago, even if the specific genes could not be identified (and the nature of a 'gene' was unknown).  A fundamental implication of the idea for our current purposes is that each individual with a given trait value (say, two people with the same height or blood pressure) can have its own underlying multi-locus genotype, which can vary among them.  Genotypes may predict phenotypes, but a phenotype does not accurately predict the underlying genotype (a deep lesson that many who promote simplistic models of causation in biomedical contexts should have learned in school).

And of course that does not even consider environmental effects, even though we know very well that for most characters of interest, normal or pathological, 'genetic' factors account only for a modest fraction of their variation. And, of course, if it's hard to identify contributing genetic variants, it's at least as difficult to identify the complex environmental contributors who make inference of phenotype from genotype so problematic. That is, neither does genotype reliably predict phenotype, nor does phenotype reliably predict genotype and the idea that they do so with 'precision' (to use todays' fashionable branding phrase) is very misleading.

In turn, these considerations imply that even if we accepted the idea of natural selection as a Newtonian deterministic force, it works at the level of the achieved trait, and can ignore (actually, is blinded to) the underlying causal genetic mechanism.  There can be extensive variation within populations in the latter, and change over time.  Just because two individuals now or in the past have a similar trait does not imply they have the same underlying genotype and hence does not imply there's been no 'evolution' even in that stable trait!

In this sense, evolution could be Newtonian, driven by force-like selection, and still not be genetically static.  But there's more.  How can there actually be stasis in a local environment?  If organisms adapt to conditions, then that in itself changes those conditions.  Even within a species, as more and more of its members take on some adaptive response to the environment, they change their own relative fitness by changing the mix of genotypes in their population, and that in turn will affect their predators and prey, their mate selection, and the various ways that the mix of resources are used in the local ecology.  If, say, the members of a species become bigger, or faster, or better at smelling prey, then the distribution of energy and species size must also change.  That is, the 'environment' cannot really remain the same.  That ecosystems are fundamentally dynamic has long been a core aspect of population ecology.

In a nutshell, it must be true that if genotypes change, that changes the local environment because my genotype is part of everybody else's 'environment'. In that sense, only if no mutations are possible can there be no 'evolution'. Even if one wants to argue that all mutations that arise are purged in order to keep the species the 'same', there will still be a dynamic mix of mutational variants over time and place.

One could even assert that an essence of Darwinism, literally interpreted, is that environments cannot be the same because the adaptation of one species affects others, even were new mutations not arising, because it affects the fitness of others. That is what his idea of the relentless struggle for existence among species meant, so stasis did cause him a bit of a problem, which he recognized in the later edition of the Origin.

I think that in essence Darwin viewed natural selection as being basically a deterministic force, like gravity, corresponding to Newton's second law of motion. And the idea of stasis corresponds to Newton's first law, of inertia. Today even many knowledgeable biologists seem to think in that way (for example, invoking drift only as a minor source of 'noise' in otherwise force-like adaptive evolution). Selective explanations are offered routinely as true, and the word 'force' routinely is used to explain how traits got here.
But there are deep problems even if we accept this view as correct.  Among other things, even if natural selection is really force-like, or if genetic drift exists as a moderating factor, then these factors should have some properties that we could test, at least in principle.  But as we'll see next time, it's not at all clear that that is the case.

Rare Disease Day and the promises of personalized medicine

O ur daughter Ellen wrote the post that I republish below 3 years ago, and we've reposted it in commemoration of Rare Disease Day, Febru...