As a result, the history of evolution is much more unpredictable than most people realize, especially when coupled with environmental effects. I call this "Evolution by Accident." It's similar to Stephen Jay Gould's idea of contingency.
The idea has been around for a very long time but recently it has become possible to test the idea at the molecular level by looking at actual mutations occurring in evolving populations [Strolling around slopes and valleys in the adaptive landscape]. It's also possible to reverse engineer an ancient gene and then test to see which of the historical mutations were important. This is what Joseph Thornton's group did with vertebrate glucocorticoid receptor (GR) genes. They showed that historical contingency and chance events dominated the evolutionary pathway leading to a cortisol-specific version of these receptors genes (Harms and Thornton, 2014). [see Historical contingency and the evolution of the glucocorticoid receptor].
Now Thornton's group has provided further evidence of historical contingency by looking at the evolution of steroid hormone receptor genes (Starr et al., 2017). Steroid hormone receptor proteins normally don't bind specifically to DNA but in the presence of hormone they form a hormone-protein complex that binds to specific sequences near the promoters of some genes. This promotes transcription of those genes. The receptor proteins are transcription activators in the presence of hormone.
There are two related steroid hormone receptor genes in vertebrates. One of them responds specifically to corticosteroids, androgens, and progesterones by binding to the steroid response element (SRE) with the sequence AGAACA. The other responds to estrogen by binding the estrogen response element (ERE) with the sequence AGGTCA. The genes apparently arose by gene duplication from an ancestral gene. Thornton's group reconstructed the ancestral gene (AncGR1) and showed that it binds to ERE.
Following an ancient gene duplication, one of the duplicated genes shifted function to become responsive to corticosteroids by binding to a different sequence (SRE). The shift in binding specificity is due to three substitutions in the DNA-binding site, or recognition helix (RH). However when these three mutations are added to the hypothetical ancestral protein, they are not sufficient to convert the receptor into a fully functional receptor that recognizes corticosteroids and binds tightly to SRE. Eleven different amino acid substitutions were also required during the evolution of the new receptor protein. These eleven substitutions were "permissive" in the sense they prepared the way for the shift in hormone recognition and DNA binding.
Thus, the evolution of the new receptor gene involved 11 permissive mutations (11P) followed by 3 RH mutations. We want to know how many different pathways could have produced the same result. Is the gene we see today the only possible outcome of millions of years of evolution or is it only one of many possibilities in sequence space?
Starr et al. (2017) began by constructing an ancestral gene containing the eleven permissive mutations (AncGR1 + 11P). They then asked how many pathways could lead to a change in sequence specificity. They answered the question by making mutation in four codons of the recognition helix—the three that were actually observed and one other that was bound to be important. They substituted all 20 amino acids at each of the four sites creating 160,000 combinations. They found 828 new variants that were just as good or better than the current mammalian gene. There were another 500 variants that were functional but not as efficient as the current gene.
What this means is that there are more than one thousand different ways of evolving a new receptor that recognizes the sequence AGAACA instead of AGGTCA. Almost all of the functional variants are accessible by gradual step-wise mutation of the three or four codons without going through a nonfunctional intermediate. The authors conclude that the historical outcome is not unique— it's only one of many possibilities. Some of these possibilities involved shorter paths than the historical outcome.
Taken together, these data indicate that the historical trajectory was not the only path, or even the shortest, from the ancestral RH to a derived protein that is SRE-specific.This is not surprising. There's tons of data pointing to the same conclusion. In addition, evolutionary theory has always assumed that chance and contingency play an important role in the history of life. What's important about this paper is that the authors have quantified functional sequence space by testing all possible outcomes.
The pathway to SRE binding is enhanced by the eleven permissive mutations that preceded the change in binding. There are some pathways to SRE binding that don't require those permissive mutations but most do. The 11P mutations are mostly neutral and they presumably arose by chance during the evolution of these receptor genes. That means there are two different roles for chance and contingency in the evolution of corticosteroid-responsive receptors. Here's how the authors express it ...
Our results shed light on the roles of determinism and chance in protein evolution. The primary deterministic force is natural selection, which drives the evolution of forms that optimize fitness. Chance appears in two non-exclusive ways: as historical contingency, when the accessibility of some outcome depends on prior events that cannot be driven by selection for that outcome; and as stochasticity, when there are paths to numerous possible genotypes of similar function, and which one is realized is random.Keep in mind that we are dealing with the evolution of a corticosteroid-responsive receptor. There's no particular reason why this particular receptor evolved as opposed to one that responded to other chemicals in the body and there's no particular reason why the new receptor had to bind to AGAACA as opposed to some other sequence variant. Therefore, the possible pathways to evolution of a new functional gene are many times greater than this result indicates.
Harms, M.J., and Thornton, J.W. (2014) Historical contingency and its biophysical basis in glucocorticoid receptor evolution. Nature, 512:203. [doi: 10.1038/nature13410]
Starr, T.N., Picton, L.K., and Thornton, J.W. (2017) Alternative evolutionary histories in the sequence space of an ancient protein. Nature, 549:409-413. [doi: 10.1038/nature23902]
32 comments :
There's no particular reason why this particular receptor evolved as opposed to one that responded to other chemicals in the body and there's no particular reason why the new receptor had to bind to AGAACA as opposed to some other sequence variant. Therefore, the possible pathways to evolution of a new functional gene are many times greater than this result indicates.
Life can walk, swim or fly; breathe oxygen, carbon dioxide or hydrogen sulfide.... So it shouldn't be surprising that it's "turtles all the way down" (I mean that in a good way).
The fact that there is such a diversity of life "out there" (hundreds of thousands of species of beetles alone) is evidence of the many possible evolutionary trajectories. And given the still limited time that life has existed on this planet, there is probably even more unsampled but possible variation in forms.
Any particular system or molecule we see is likely to be just one among basically countless possible, but coincidentally never sampled and therefore unrealized biochemical pathways.
Two points.
First having evolution by random fixing of all alleles , and that by chance, surely makes evolution too chancy as a option for biology origins.
Selection on a mutation is bad enough. BUT mutations affecting a population without selection is a dramatic OTHER OPTION as proposed by darwin.
Something wrong here.
second point.
Is it being said here a population will evolve without selection going on?
That alleles will go through a population, just random, and change body plans?
Recently i was shocked to hear professional evolutionist say populations are always evolving.
The whole point of puncuiated equilbrium was that THEY DIDN'T evolve. instead only segregated pairs, geographically probably, evolved quickly and then they replaced the parent population by them going extinct or somehow.
PE means populations don't evolve, and the fossil record proves they didn't, by the whole group. Is random alleles trying to reject PE?
Anyways it must be people/animals today are not evolving.
If so how??
@Mikkel
The fact that there is such a diversity of life "out there" (hundreds of thousands of species of beetles alone) is evidence of the many possible evolutionary trajectories
Beetles are still beetles...just as homo sapience are still homosapience...billions of variations...
Would it be kind of boring in everyone man on earth looked like you? And every women would look like your wife? That is if you have one... ;-)
I wonder whether Larry is not giving the wrong impression by the title of this post. He is, I think, not saying that natural selection plays no role in the outcome, only that "chance" initial steps, the first mutations, can lead to process to follow different paths.
But most of the movement along those paths leads to adaptation, owing to natural selection.
Or do I misunderstand?
You seem to have missed the point, which is just that there are many different ways evolution could have turned out, but didn't, in large part due to historical chance events.
Whether something is "boring" is not a valid excuse for accepting or rejecting it's possibility. The facts of the matter are not determined by how they feel to you.
Joe, I thought the part of Larry's post I quoted above, and this quote from the paper, lay out the fact that those "'chance' initial steps" can be quite a substantial part of the total path (recall the 11 "permissive" steps, before we even think of Larry's final point that evolution of a corticosteroid-responsive receptor, as opposed to one responsive to another chemical, was contingent in itself):
Chance appears in two non-exclusive ways: as historical contingency, when the accessibility of some outcome depends on prior events that cannot be driven by selection for that outcome; and as stochasticity, when there are paths to numerous possible genotypes of similar function, and which one is realized is random.
The issue is whether the function is the accidental result of random wandering in protein space to an arbitrary place. Or is the wandering biased by natural selection toward regions having some function? Many readers who see the phrase "determined by chance events" will take it to mean the former.
It seems to me the specific function is not the only outcome being investigated here. It is also the particular protein that performs that function. If more than one protein can perform the same function more or less equivalently, then even if the function was an inevitable outcome of evolution, the specific protein that arises would not be.
I thought the point of this and other work was that relatively small changes can predispose a lineage to take a certain evolutionary path. A small change in sex-determination in an ancestral solitary insect species can lead them on the inevitable path to becoming social - ants and bees. Some minor non-selected change in ATPase or some other protein billions of years ago that was on a path to allow ATP being produced from mechanical work would have led to an utterly different biosphere today.
Right, even if "prior events...cannot be driven by selection for that outcome," this doesn't necessarily mean they weren't "biased by natural selection toward regions having some function."
I'm certainly not equipped to deal with such a question on a general basis, so I'll ask specifically with regard to the steps that were outlined in this paper: Is it at all possible to know (or at least to arrive at a reasonable surmise) which of these were "biased by natural selection toward regions having some function"?
It can't merely be PREDISPOSE. Evolutionism was based on populations changing because they had tpo TO survive.
selection must mean something and have selected some gain to survival/fitness.
it can't be gradual changes without a selective advantage.
This undercuts the whole evolutionary claim surely.
A lineage/population will only have new body plans and these change and change, as evolutionism needs, if the need is great.
Populations di not evolve as a natural thing.
People are not evolving today.
Evolutionists should be clear about this.
I wish that we could (1) translate this into causal language and (2) get the history right. "Chance" and "contingency" (and "constraints") are not causes. These are explanatory devices, whose meaning depends on the counterfactual idea of evolution without chance or contingency. Rather than making positive claim about causation, they refer back to an ideal. This is why it is so jarring to say that the course of evolution is "determined" by chance. Can we have a different theory of evolution, instead of Darwinism-plus-excuses-for-its-failure-to-apply?
The claim that "evolutionary theory has always assumed that chance and contingency play an important role in the history of life" is dubious. Our thinking has changed so much since the molecular revolution that people forget the pre-molecular view in which evolution was a deterministic process of shifting gene frequencies to a new optimum determined by the environment.
In his 1975 book, Maynard Smith gives a very close retelling of King's 1971 argument that the correlation of amino acid frequencies with codon numbers (in the genetic code) can be reconciled with selective allele fixations, and does not require neutrality, as argued earlier by King and Jukes in 1969. King was thinking in the new way, invoking mutation-driven evolution. Maynard Smith concludes by saying:
"Hence the correlation does not enable us to decide between the two. However, it is worth remembering that if we accept the selectionist view that most substitutions are selective, we cannot at the same time assume that there is a unique deterministic course for evolution. Instead, we must assume that there are alternative ways in which a protein can evolve, the actual path taken depending on chance events. This seems to be the minimum concession the selectionists will have to make to the neutralists; they may have to concede much more."
"Evolutionism is based on populations change because they had to TO survive." Well, not really. Populations change. If they have traits that fit their environment well, they survive. If they don't, they die out. Extinction is always an option.
Evolution doesn't "need" anything.
It does need something. Evolution is a process, your side claims, changing body plans. So small matter.
The environment must FIRST change and some of the parent population, to survive in the new one, must have NEW traits that allow it to survive and so a new population THAT HAS EVOLVED.
Populations going from a fish to a rhino need good reasons for body plan changes.
Science fiction is wrong. people are not evolving right now in any direction to bigger heads etc. we are in stasis. As PE would preach it.
storytelling at The Sandwalk???.....well I neeeeeevvvvvaaa!!!
Since life is a system that tends toward dynamic equilibrium, it follows that the history of life would be the history of a system that tends toward dynamic equilibrium.
It follows the history of life would be one determined by ‘chance’ events because that is the nature of any system that tends toward dynamic equilibrium.
I never knew that "life is a system that tends toward dynamic equilibrium". And here I've been working on the theoretical aspects of evolutionary biology all these years. Silly me.
To allow me to re-educate myself and possibly redeem my reputation, can you provide a reference for that statement, as a starting place for me to re-do my understanding of evolution?
Joe, I remember you once discussing how small a selection coefficient could be yet still achieve an allele's eventual fixation in a population. If I remember, the number was so small that, for all intents and purposes there existed scenarios where the coefficient could not be measured.
Joe-
Here is one reference-
http://www.cbhs.k12.nf.ca/stephenwhalen/circulatorynotes.pdf
Homeostasis is dynamic equilibrium at the cellular level- predator-prey relations would be an example at a higher level of organization.
The rough rule is that when 4Ns < 1 then the effect of the selection will be swamped by genetic drift. s in that case is the absolute value of the selection coefficient, and N is the effective population size.
One-generation experiments cannot detect selection coefficients that small but comparisons of at the population level and between species may be able to. Basically, nature can do a much larger experiment than we can, and for far longer.
Right, so if I plant a dandelion seed in our back yard, it will just molder and decay away, and I don't have to worry about it growing into a troublesome weed, and those weeds spreading all over the yard? Because growing into lots of weeds would be a very non-chance thing to do. So I'm safe -- weeds can't grow?
I think you are misunderstanding what I'm saying-
I don’t know why anyone would have to change his thinking on evolution given what I wrote about life being a system tending toward dynamic equilibrium.
A system in dynamic equilibrium will tend to wander around a mean.
I think of ladybugs and aphids.
In order to change the mean significantly, something from outside the current system has to effect the system.
In terms of living systems we could have a new creature enter the system, we could have climate changes, we could have mutations (new genes= new traits entering the system)…
Those changes will be ‘random with respect the system’ because they have to come from outside the current system to alter a system in dynamic equilibrium sufficiently to alter the ‘mean’ it wanders around.
What we call ‘natural selection’ will be ‘random with respect the system’ being selected from—
Sometimes ‘getting bigger’ is an advantage, sometimes it will be a disadvantage.
In general what causes the trait to be tried (mutations) will be random with respect to the system (the mutation won’t know if ‘getting bigger’ will help or not).
And your dandelion won't grow without water and sun to alter the 'dynamic equilibrium' state of dormancy.
Hi again Joe
Thank you for replying, yet I remain confused. I thank you in advance for your patience.
I remember you once saying: …in addition to natural selection, neutral mutation has caused a lot of molecular differences within and between species
I really am unclear how this is supposed to be different than boilerplate textbook reiteration of one of Darwin’s five principles; i.e. variation exists between offspring
http://www.sketchplanations.com/post/81722763064/darwins-5-principles-of-natural-selection
When (as you suggest) we compare differences within and between species, but from an ecological POV, these taxa all demonstrate VARIOUS adaptations to their environment… and these VARIATIONS occurred at a molecular level by random happenchance.
The observation that no population ever attains their adaptive peaks and that much variation is non-adaptive, i.e “is just there”, to my jaundiced eye is reiterating exactly what Darwin set out to explain, at the outset.
Offspring demonstrate variation – PERIOD! Variation provides grist for Evolution’s Mill. Of course, variation is of necessity random and happenchance and only a subset of variation is actually subject to Natural Selection. Of course, that must be true, in Darwinian terms! Otherwise, teleological processes would be occurring, and any such teleology was anathema to Darwin.
So reading and rereading your cryptic and inscrutable summary:
Basically, nature can do a much larger experiment than we can, and for far longer.
… am I to understand that the New Synthesis remains standing? Or as you also once opined: … that if there is no natural selection you will not get (or maintain) adaptations.
What am I missing here? Could it be as simple as an empirical version of the fable of the blind men and the elephant? When looking at variation from a molecular POV, a different perspective is attained than from an ecological POV?
@Tom: Whether we call the current theory the Modern Synthesis, or something else, is primarily a matter of semantics. Everyone seems to want naming rights, and credit for being the one that overthrew the Modern Synthesis.
Darwin knew a lot about variation, but nothing about genetics. Mendel was around, but even if they had met, Darwin would not have understood what were the implications of these funny ratios that this seemingly mad monk from Brünn was talking about. After the rediscovery of Mendelian genetics and the working out of the implications of it in populations, we now have a much clearer understanding, and can make distinctions between the standing variation and the variation due to new mutations. We can predict the rate of loss of genetic variance from genetic drift. We understand why differences between offspring of one pair of parents are not entirely due to new mutations in that generation, but have a lot to do with genetic segregation. We can make the distinction between direct environmental effects that go away immediately, and selection due to environmental causes. We understand how quickly epigenetic effects go away.
We're way ahead of Darwin in all these areas, thanks to the rediscovery of Mendel and the century of work on genetics since.
@Joe
"We can predict the rate of loss of genetic variance from genetic drift."
I thought that you, Larry and the most of the Darwin's faithful, have agreed that genetic drift is the long-ignored , driving force of evolution, that was going to defeat the 3rd Way evolutionary heresy?
Joe,
The way we identify modern evolutionary theory is not a question of "semantics." It's a matter of definitions.
I prefer to define the "Modern Synthesis" as that version of evolutionary theory that was promoted by Julian Huxley and Ernst Mayr—the version that was popular in the 1950s and 1960s. That version no longer corresponds to the evolutionary theory found in today's textbooks.
You, on the other hand, prefer to keep the term "Modern Synthesis" as the way to describe the most up-to-date view of evolutionary theory. That's okay as long as you make it clear that the 21st century version is very different from what Huxley described in his 1942 book.
Hi Joe & Larry
I fear we are rehashing
http://sandwalk.blogspot.com/2014/10/nature-criticizes-science-hyperbole-and.html?showComment=1417808999992#c4727783262835368592
http://sandwalk.blogspot.com/2014/10/nature-criticizes-science-hyperbole-and.html?showComment=1417689326456#c5162259549721915404
http://sandwalk.blogspot.com/2014/12/how-to-think-about-evolution.html?showComment=1419796938669#c2892502125609596176
I really do not understand how “… the "Modern Synthesis" as that version of evolutionary theory that was promoted by Julian Huxley and Ernst Mayr—the version that was popular in the 1950s and 1960s…no longer corresponds to the evolutionary theory found in today's textbooks.”
As Joe explains: Darwin did not know about Mendelian Genetics, not to mention Julian Huxley and Ernst Mayr did not enjoy the insights of Modern Molecular Biology.
That said, even Darwin acknowledged that much Evolution was not driven by Natural Selection. He even wrote a book on that: The Descent of Man
https://upload.wikimedia.org/wikipedia/commons/thumb/e/ec/Darwin_sexual_caricature.gif/170px-Darwin_sexual_caricature.gif
Darwin even speculated that many traits just happened – by happenchance.
This brings me back to what is probably a simplistic contention. Yes of course, much variation is not subject to Natural Selection and many traits were fixed by processes other than Natural Selection.
But if I understand correctly, even Darwin himself (not to mention Husley, Mayr and Dobzhansky) said as much! (and again, I repeat myself)
And to repeat myself again: Offspring demonstrate variation – PERIOD! Variation provides grist for Evolution’s Mill. Of course, variation is of necessity random and happenchance and only a subset of variation is actually subject to Natural Selection. Of course, that must be true, in Darwinian terms! Otherwise, teleological processes would be occurring, and any such teleology was anathema to Darwin.
So what am I missing?
My last kick at this can of worms:
Is it fair to say we can walk away from this on the understanding Joe is a "lumper" and Larry is a "splitter"?
https://en.wikipedia.org/wiki/Lumpers_and_splitters
@Tom: Yes. I just don't want the name of the theory to change every few years.
I have made 2 claims-
1) biological systems tend toward a 'dynamic equilibrium'
https://biologydictionary.net/dynamic-equilibrium/
2) this feature of biological systems explains why the 'history of life' looks like it does.
Is there any hope for this argument?
I remain in debt to you both!
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