Wednesday, May 11, 2016

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.


KD said...

If I understand your argument, conserved functional DNA should tolerate more "neutral" variation, not less. So in the following:

"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"

shouldn't "fewer" be "more"?


Ken Weiss said...

Blog posts are I guess always written in haste....and not reviewed! So thanks for any questions about errors or clarity. Mutations in a region of functional DNA are more likely to affect or interrupt function than if they occur in 'functionless' DNA (to the extent the latter truly exists). So a stretch of functional DNA (a coding region, for example), will manifest less variation. In that sense, a higher fraction of mutations will alter function. It is correct in a sense (see the earlier post's reference to phenogenetic drift and in particular to Andreas Wagner's work) that if there is conserved function but many genes to serve it, with overlapping actions, they can acquire variation. The basic point was that known functional regions vary less than suspectedly neutral regions because selection or malfunction removes variation in these regions; in a really nonfunctional region there's nothing for mutations to interrupt and so they're more tolerated.

But overall, the variation that is in clearly functional reagions will be in less critical sites (generally, say, introns vs exons, codon 3rd positions). So I think my sentence was basically right....unless I'm not understanding you.