Joe Felsenstein recently posted a rebuttal of a critique of Fisher’s fundamental theorem of natural selection (FTNS). The authors, Basener and Sanford, argue that if new mutation (missing from the original FTNS) is taken into account, the theorem shows that Darwinism is impossible rather than inevitable. I agree with each point of Joe’s rebuttal.
Yet, I think that no discussion of this topic is complete without explaining that Fisher’s view, and more generally the original Modern Synthesis, is inadequate precisely because of the rejection of mutation-limited dynamics.
To begin, I want to introduce a distinction in how scientists invoke “theory” (explained here):
- theoryC (concrete, conjectural): a major conjecture or systematic hypothesis to account for observed phenomena, as in “prion theory of disease” or “Lamarck’s theory of evolution”;
- theoryA (abstract, analytical): the body of abstract principles relevant to some discipline, methodology or problem area, as in “music theory” or “population genetics theory”
A theoryC can be refuted by facts, but the abstract truths or principles in a body of theoryA cannot; a theoryC refers to the actual world, but statements in theoryA may invoke imaginary things like chickens with 3 sexes, or infinite populations.
Fisher was a highly productive theoreticianA who applied his formidable rhetorical skills to promoting a falsifiable theoryC of evolution. This theoryC holds that the population-genetics of natural populations fall into just the right regime to ensure that evolution can be understood as the short-term selective optimization of traits based on shifting the frequencies of available alleles with infinitesimal effects. The details of mutation are canceled out of the evolutionary equation. The researcher who understands this, Fisher (1930) says,
will direct his inquiries confidently toward a study of the selective agencies at work throughout the life history of the group in their native habitats, rather than to speculations on the possible causes which influence their mutations.
Evolutionary research today is not based on this theoryC. Evo-devo rejects Fisher’s position that it is fruitless to study the origin of phenotypic variants. Molecular evolutionists study mechanisms and patterns of mutation precisely because we know this helps us to understand evolution, e.g., Dettman, et al. 2016, Stoltzfus and McCandlish, 2017.
Basener and Sanford say that “we cannot overstate the essential role of new mutations”, but they lack a firm grasp of how our thinking has changed on this issue. This is not addressed by Joe either. To be fair, they are not trying to focus on this issue. They are focused on whether pure mathematical reasoning allows us to conclude in favor of Darwinism or against it, and I’m just trying to point out that we already know that Darwinism in the sense of Fisher’s theoryC is not correct, and we should be adjusting our thinking rather than having an abstruse debate about how far theoryA alone can take us.
But let’s quickly review what Joe is saying. His rebuttal focuses on the claim that theoretical evolutionary genetics is founded on FTNS. We could rebut this logically by showing that the allelic selection model, or the Hardy-Weinberg equilibrium, do not depend on assuming FTNS. Joe makes his argument historically: he lists various key innovations that appeared before the FTNS in 1930.
He states his conclusion in two ways. One statement is that “the literature on the theory of natural selection, of mutation, and of their joint action, did not wait until 1930, and in its 1920s development did not rely at all on the Fundamental Theorem of Natural Selection”. I agree that “did not wait” and “did not rely on” are literally correct and not misleading. The FTNS just is not the basis of evolutionary theory, and it is not even the basis of theoretical population genetics considered narrowly.
However, his other conclusory statement is “the mathematics of mutation and natural selection had been well worked-out before R. A. Fisher published his 1930 book”. This implies that our current understanding of the role of mutation was well worked out before 1930, and this is not correct. All of these early theoreticalA works, and the main works of the Modern Synthesis in the next 4 decades, fail to achieve generality in covering the role of mutation in evolution, because they do not adequately cover the introduction process or provide a theory of mutation-limited dynamics. This lack of generality is not an accident, but a choice: it arises from a deliberate rejection of the non-Darwinian idea that the course of evolution might depend on the timing and character of events of mutation, i.e., the “lucky mutant” view or mutationism.
To understand the formal structure of this limitation, consider some statements from eminent evolutionary geneticists, e.g., Yedid and Bell (2002) write:
In the short term, natural selection merely sorts the variation already present in a population, whereas in the longer term genotypes quite different from any that were initially present evolve through the cumulation of new mutations. The first process is described by the mathematical theory of population genetics. However, this theory begins by defining a fixed set of genotypes and cannot provide a satisfactory analysis of the second process because it does not permit any genuinely new type to arise.
Hartl and Taubes (1998) describe inadequacies in previous treatments of mutation, referring to post-1969 (post-Synthesis) neutralist origin-fixation models in the last sentence:
Almost every theoretical model in population genetics can be classified into one of two major types. In one type of model, mutations with stipulated selective effects are assumed to be present in the population as an initial condition . . . The second major type of models does allow mutations to occur at random intervals of time, but the mutations are assumed to be selectively neutral or nearly neutral.
In their treatment of adaptive dynamics, Eshel and Feldman (2001 in Orzack and Sober, Adaptationism and Optimality) stress the distinction between the short-term evolution depicted in classical population genetics (“the dynamics of the relative frequency of a finite, fixed set of geneotypes”) and long-term evolution,
the process, popularly termed “trial and error”, whereby mutation continuously introduces into the population new genotypes that are then subject to the forces of natural selection, sexual selection, recombination, and the like. Each new type may either be eliminated or become established within the population
All of these authors identify a traditional approach in which evolution is equated with sorting out initial variation, without new mutations; the alleles relevant to the outcome of evolution are present initially, and evolution is just a matter of shifting their frequencies.
Does the phrase “evolution is shifting gene frequencies” sound familiar? This is what it means. The original Modern Synthesis (OMS) theoryC held that all of evolution is understandable from the short-term process of shifting gene frequencies, i.e., macroevolution follows from microevolution.
The OMS does not say that new mutations don’t occur, just that that we don’t have to understand their dynamics to understand evolution: we can treat evolution as if the challenge to adapt is always addressed with available variation, on the grounds that natural species have a “gene pool” that “maintains” abundant infinitesimal variation in all traits. When the environment changes, selection crafts an adaptive response from this abundance. Dobzhansky, Stebbins, Mayr and others were so confident about this theoryC that they presented it as an established fact (see the supplement to this piece).
Yet, the OMS quickly proved inadequate. In the 1960s, patterns of molecular evolution demanded theories relating the rate of evolution directly to the rate of mutation. To address this need, origin-fixation models emerged in 1969; subsequently, they have grown into a major branch of theoryA with many applications (McCandlish and Stoltzfus, 2014). This is why I wrote recently that
the development and use of mathematical models reveals unambiguously that the OMS does not suffice to depict evolutionary dynamics, because it fails to cover mutation-driven dynamics. This failure is not a mistake or oversight, but an intentional feature of the OMS reflected in the explicit claims of Mayr, Dobzhansky, Simpson, Stebbins and others that selection uses abundant variation in the “gene pool” and does not wait for new mutations.
That is, we have rejected a major claim of generality from the OMS, a major theoryC. This is precisely what scientific progress is supposed to look like. However, establishing this point (which I’ve been writing about since 2001) has been an uphill battle against the efforts of false conservatives to turn the words “Modern Synthesis” into a moving target. The OMS clearly failed to predict and to explain patterns of molecular evolution uncovered in the 1960s. For 20 years, leading thinkers refused to admit that the theoryC had failed. The most they would admit is that the OMS holds for visible evolution but there may be an invisible “molecular level” where things may look different.
In the 1980s and 1990s, defenses of the “Modern Synthesis” began to shift. Rather than invoking the theoryC of Mayr, et al., or any falsifiable theoryC , defenders now defined the “Modern Synthesis” as an expandable framework of population genetics, or as an evolving research tradition. If Fisher influences Haldane, who influences Kimura, whose work is invoked in contemporary models, we can depict that as the culmination of a continuous research tradition going back to Fisher— without ever pointing out that (for instance) origin-fixation models used in molecular evolution today contradict Fisher’s theoryC.
Because of this kind of goal-post-shifting, historians gave up trying to define the Modern Synthesis as a theoryC, e.g., Smocovitis (p 43) writes that
by the late 1980s the notoriety of the evolutionary synthesis was recognized… So notorious did ’the synthesis’ become, that few serious historically minded analysts would touch the subject, let alone know where to begin to sort through the interpretive mess left behind by the numerous critics and commentators.
To summarize,
- The OMS is a theoryC based on extrapolation from (1) microevolution, the kind of short-term process of shifting gene frequencies seen in experimental populations of animals and plants, to (2) macroevolution, i.e., all of evolution.
- By the 1990s, mainstream evolutionary geneticists acknowledged that evolution cannot be understood solely in terms of microevolution as conceived in the OMS, because we have to model the dynamics of new mutations.
- The context to demarcate this major scientific advance is missing, because the OMS has been flushed down the memory hole and replaced with a slippery “Modern Synthesis”
Now, back to the FTNS. Fisher was trying to hit a home-run: to establish a theoryC with pencil and paper, by showing that the gradual increase in fitness is inevitable. The FTNS is only a part of this argument, as is clear from the treatment by Basener and Sanford, who are also trying to hit a home run, playing for the opposing team.
For a theoretician, to succeed at this game— to short-cut empirical science and reach grand conclusions from analytical arguments alone— is to execute a masterstroke. The early 20th century featured a loud and inconclusive debate about the role of different factors in evolution— Lamarckism, continuous shifts vs. discrete mutations, external selection vs. biased variation, and so on. Fisher stepped in and boldly declared that, once Mendelism is accepted, Darwinism is inevitable and all other views must be set aside. The smallest possible changes are the most likely. Internal factors influencing which mutations occur cannot influence the course of evolution because mutation rates are too small, therefore internal tendencies cannot be evolutionary factors.
Fisher’s masterstroke was a great success, giving Darwinism an air of logical inevitability.
Alas, it was wrong. The most likely changes in evolution are not the smallest possible changes, but changes of intermediate size. Biases in variation are a source of evolutionary tendencies.
Fisher was wrong on these points precisely due to his theoryC commitment to rejecting a role for new mutations. The result that intermediate changes are the most likely emerged when Kimura re-considered Fisher’s argument for infinitesimalism (Fisher’s geometric model) within a mutationist framework of evolution as an origin-fixation process (for explanation, see the end of this PDF). Fisher, Haldane and Wright reach the wrong conclusion about the possibility of variation-induced trends (orthogenesis) for the same reason. My colleagues and I have shown that mutational or developmental biases in the introduction of variation can cause evolutionary biases (see a recent blog). However, in a theoretical model where the alleles relevant to the outcome of evolution are assumed to be present initially, there is no introduction process, thus no chance for this kind of causation to operate.
This shows the importance of theoriesC in science. Without them, we can only interpret Fisher’s position as a technical error, which is, in fact, how Fisher’s position is treated today. One author writes that “Fisher erred here and his conclusion (although not his calculation) was flawed. Unfortunately, his error was only detected half a century later, by Motoo Kimura” (source). Yet, it is absurd to suggest that Fisher forgot to compute expectations for the mutationist view of evolution that he ridiculed and despised. Fisher’s original argument is correct and complete, given his theoryC that evolution can be understood adequately as a deterministic process of shifting frequencies of available alleles. The problem is that the theoryC is inadequate.
Excellent OP, Arlin. Thanks.
Very insightful, Arlin.
A biologist’s attitude towards Fisher provides a remarkably consistent diagnostic of how that same biologist will see (or understand) evolution. Consider, for instance, the late Soren Lovtrup:
“Fisher’s confidence in the supremacy of mathematics as an infallible guide towards the truth has an interesting consequence: he appears to believe that his mathematical demonstrations constitute empirical evidence. Thus, as far as his theory of evolution is concerned, ‘…he is quite indifferent to the cause of mutations, as long as they are produced somehow…’ It is beyond my comprehension that anybody engaged in the study of evolution can ‘be quite indifferent as to the cause of mutations’.” (S. Lovtrup, Darwinism: The Refutation of a Myth [London, Croom Helm, 1987], p. 293)
Elsewhere — I cannot lay my hands on the article at the moment, but I’ll never forget what he wrote — Lovtrup was more acid about Fisher’s reasoning. “Fisher demonstrated nothing,” he wrote, “he made some calculations.”
Bump
I’ll sticky the OP
Paul A Nelson,
Welcome to TSZ, Paul A Nelson! Just wondering if you are the Doctor Nelson who is a fellow of the Discovery Institute.
Alan Fox,
That’s me, but please don’t call me ‘Doctor.’ In this house, Doctor Nelson is my wife Suzanne, who is a Real Doctor [smiley face here]:
http://www.kidstummydoc.com/about.php
Paul A Nelson,
May I call you Paul, then?
Your most quoted remark (at least attributed to you in a 2004 interview in Touchstone magazine)
struck me as a fair assessment, then. Do you see any progress, since?
ETA you’re => your
Alan Fox,
I’ll always answer to Paul.
Yes — definitely some progress.
Still no general theory, however. Good theories are hard to find, and harder still to make mathematically tractable and analytically rigorous — so that anyone can apply them, without a proponent of the theory standing nearby to guide one’s hand.
Humility is a rarity on TSZ and in many societies today…
I hope it catches on…
Welcome to TSZ Paul! : -)
That’s not an entirely accurate characterization of Basener’s position to say he claims theoretical evolutionary genetics is founded on FTNS. However it is true that FTNS was not foundational in it’s original form as evidenced by this comment by Edwards 2014:
http://onlinelibrary.wiley.com/wol1/doi/10.1111/brv.12047/full
Edwards in that same paper praised Grafen (2003) and I think the more accurate characterization of what Basener said is encapsulated by one quote from Grafen (and Hamilton):
and Hamilton on the dust jacket of the re-printing of Fisher’s book 2000:
The odor of red herring in the morning.
…says J-Mac, the guy who wrote this:
Arlin,
Are you suggesting that population genetics models rely on assumptions known to be false; i.e. not being realistic and therefore not applicable in evolutionary biology?
Arlin,
Great OP.
There are mechanistic issues with mutations. Many are modeled as point mutations with occasionally a small indel. Invasion of new introns in a pre-existing gene are not easily modeled with slow gradual insertions. And conversely, their removal is not well modeled by deletions. Why should an intron gradually grow to great length and then get deleted gradually to nothing. Sure, there may be reverse transcription mechanisms from the mRNA that might effect deletion, but this seems mechanistically difficult to envision, and I’m not sure we’ve had good lab evidence of how this can happen.
So to your point, the mathematically tractable, and simplistic view gets accepted as reality since we would like to believe we’ve figured everything out, when in reality we know very little. The case of intron emergence and deletion, from a mechanistic standpoint is still a deep mystery, and I don’t think Mendelian inheritance or simple stochastic models explain punctuated events.
A Joe Felsenstein pointed out in his book, Inferring Phylogenies, that some of the critics of statistical phylogeny argued much of evolution can’t be captured by simple mathematical theories (Neyman-Pearson statistics). I don’t have the book handy right now, but that expresses my sentiments about some of the features of biology. Simple deterministic and predictable behaviors don’t characterize some major features of biology.
For example, this forgotten paper by Rogozin, Koonin et. al
My intuition is that if ever there is such a theory, it is not going to come from biology but rather from physics, such as quantum physics, which is not an easy task either…
The complexity and the organization of life starts at quantum level or even beyond…
stcordova,
Great points Sal!
To add another layer of problems to the mechanics of mutations, let’s not forget dual coding genes or overlapping genes…remember?
The stochastic nature of mutation. Why not?
The primacy of selection in OMS is also problematic on many levels. As Michael Lynch points out, many features of genome architecture require complete dis-engagement of natural selection. Hence, Fisher and others who define evolution in terms of selectionist paradigms cannot account for features that evolve under the dis-engagement of selection except to model them as something to dismiss.
Additionally, Lewontin and to some extent Andreas Wager point out there are conceptual issues with the notion of fitness which underlie selectionist models. Lewontin’s made such a good, albeit unwitting, critique of the notion of fitness that Stanley Salthe abandoned Darwinian ideas after reading it.
So, I’m a little glad to see people like Nei promoting the old school views of Thomas Morgan.
How do we create new donor and acceptor sites at the intron boundary? I don’t know that we’ve even figured out exactly how introns are mechanistically demarcated given that the donor sequence “GT” and acceptor sequence “AG” that demarcate introns aren’t exactly rare with respect to chance! As far as I can tell, efforts to find a consensus sequences that allow navigation to the intron boundaries have met with mixed success. So I don’t think we understand introns that well, much less how they evolved.
There is more evolving intron insertion or intron deletion than just a typical accumulation of random indel mutations.
And this is but one of the evolutionary things not modeled by simple statistics. There other things : for example Evo-Devo was excited about a discovery by John Rinn regarding the HOTAIR lncRNA. It showed how an entire developmental pathway for a cell type can be shut down or activated by a single amino acid modification.
The HOTAIR lncRNA emerges from Chromosome 12, somehow navigates to the Hox gene cluster in Chromosome 2, identifies a specific histone (Histone 3) and then modifies a specific amino acid residue (Lysine 27) on histone 3.
I don’t know how evolution of changes to Hox Regulation can be easily modeled by OMS. The effect of a mutation change in such systems may not be a minor change of fitness that can be modeled in gradualistic terms. A single change to a single amino acid in the Hox Cluster could put an organ in a new location!
This is the machine that HOTAIR docks with at the Hox cluster, btw, the PRC2 complex that modifies the single amino acid residue on a specific histone (histone 3).
What does all that have to do with introns gradually increasing or diminishing in size due to mutation?
OK, so ‘Paul Nelson’ is the Paul Nelson. Is arlin, Arlin Stoltzfuz by chance?
RodW,
I don’t think I’m outing arlin as he’s already linked to his own paper. So, yes it’s Arlin Stoltzfus, research biologist..
First off in relation to the OP, how can population genetics model this.
Next, specifically for an intron, especially since the gene-centrism of OMS is also exon-centric, how is an insertion mutation in an exon distinguished from an insertion mutation that creates an new intron??? This is a basic question. I welcome answers. If we don’t even know, we can’t even model it under “abstruse theorems” (to use Arlin’s phrase). If exeperience is a guide, the reason humans share more introns with a plant like A. Thanliana than they do with animals like fruit flies and nematodes is not by chance. How can this be modeled under “abstruse theorems”.
So after all these years (215 and counting) does anyone have any theory of the cause of mutation?
We had a thread or two on Wagner, and a pretty well established hypothesis about why stochastic mutations can lead to nearly complete replacement of functional sequences, without passing through dead zones.
So does it make any difference whether mutations are anything other than stochastic?
Since mitosis seems to be controlled by quantum coherence, I propose that mutation could be an indirect effect of quantum effects…
https://www.sciencedirect.com/science/article/pii/S0303264704000619
Unless you are Stuart R.Hamerof you don’t “propose” that at all. You just recycled it.
Even if that’s the case in what way does it support your contention that mutations happen under conscious direction?
I don’t see why mutations are so mysterious. Between replication errors, ionizing radiation, and probably some other stuff, it seems that mutations are not much of a mystery. To expect the reproductive process to be perfect is at variance with everything else in nature.
sean s.
Mutation is inevitable. You can’t have sequences that are replicated entirely without error.
While there is a lot of room to ask exactly what causes the errors, saying that there is no explanation of why we have any errors is ridiculous.
How do you know I hadn’t proposed it first?
Mutations should not happen..
In a sense, it is a destructive force, making random changes in the genetic material. In any highly adapted organism such changes are overwhelmingly likely to be detrimental. The usual analogies we make in such cases involve making random adjustments in a finely constructed watch, or making random alterations of a carefully-written poem. While one will occasionally improve the timing of the watch or the effectiveness of the poem by random changes, with much greater probability one will make things worse.
I agree…So, the real question should be ‘why we have replication errors’ leading to mutations? Right Joe?
The OP ends with “The problem is that the theory(sub c) is inadequate.”
(I don’t know how to insert a subscript, but that is unimportant.)
If this theory is inadequate, that only means there’s still work to do, things to discover. that’s good news to scientists.
sean s.
There are many causes: atoms are not static objects, they are dynamic, vibrating quantum mechanisms. Expecting them to combine perfectly every time is unreasonable. If the real question is “why replication errors” then there’s no real question.
sean s.
But they do, so some of your underlying assumptions are obviously wrong.
sean s.
Ho Boy!!! Mark Twain once remarked: History may not repeat itself, but it sure does rhyme!!”
Let’s examine the historical context wherein Fisher operated:
“Blending Inheritance” was antithetical to Natural Selection. Mendel’s “particulate inheritance” appeared to represent an even greater contradiction of Neo-Darwinism as first expounded by August Weisman.
Let’s set the stage. Mendel himself never used the word “gene” and Darwin never referred to the fundamental unit of inheritance as a “pangene” when expanding his mistaken theory of Pangenesis. The word “pangene” was invented (in deference) to Darwin) by Hugo DeVries; who came up with a new version of evolutionary theory after rediscovering of Mendel’s laws. In an ironic twist of fate, De Vries became aware of Mendel’s thirty year old publication before publishing his own results and even changed some of his vocabulary according to Mendel’s. De Vries then attempted to publish without giving Mendel any credit, but was called out by two Biologists who had known about Mendel all along even though they never had understood his importance. Carl Correns and Erich von Tschermak now (undeservedly?) share credit with De Vries for the rediscovery of Mendel’s Laws.
De Vries’ next series of experiments constituted a major setback for neo-Dawinism. As bizarre coincidence would have it, De Vries had stumbled across a variety of evening primrose growing wild in a meadow called Oenothera lamarckiana (how ironic is that!). It gets better: it turns out the variant was an unstable polyploid that produced many new varieties in his experimental gardens that appeared very dissimilar to parental strains. De Vries invented the term “mutation” for these suddenly appearing variations, which he considered new species. These new species subsequently remained stable, allowing De Vries to postulate the first version of “Punctuated Equilibrium” as theory. These findings contradicted Darwin who (like Lamarck) was a “gradualist” believing that evolution occurred by the accumulation of gradual change. Darwin often cited “Natura non facit saltum”. (“Nature never makes jumps”) http://www.macroevolution.net/hugo-de-vries.html
De Vries’ new theory of Evolution was called “Mutationism”; a version of “Saltationism” (“saltus-saltum”-“saltation” – get it?). Many Naturalists of the day were already avowed “Saltationists” and seized upon De Vries’ data to explain apparent gaps in the fossil record in order to justify their opposition to Darwin’s version of events. Given De Vries’ earlier success in rediscovering Mendel’s Laws, “Mendelism” and “Saltationism” were considered now a “package deal” and co-opted by politically liberal scientists. To be fair, “Hard Heredity” and “Soft Heredity” need not be mutually exclusive. Perhaps there was more than one mechanism of inheritance. Sadly, hard-held political beliefs prevented any possibility of conciliatory compromise. http://www.macroevolution.net/saltation.html
Small Denmark had just lost territory to Germany and shared Belgium’s general antipathy to Germany’s new-found political and military might on a rapidly changing political chessboard. It was no small coincidence that a Danish Botanist named Wilhelm Johannsen supported De Vries’ line of reasoning in opposing Germany’s preferred neo-Darwinist version of Evolution.
Johannsen was the first (some credit Bateson) to coin the term “gene’ (a contraction of De Vries’ “pangene” but intentionally implying a contradiction of neo-Darwinism). The expressions “phenotype”, “genotype” and “pure line” were also invented by Johannsen to explain the experimental results of seed size variation in his bean plants. Johannsen observed that pure-line bean plants produced seeds of various sizes that exhibited a bell curve typical of normal distribution. Johannsen then subjected the variants to artificial selection (today called directional, stabilizing and disruptive) but was unable to shift the bell curve in subsequent generations. Johannsen interpreted these results along the same lines as De Vries before. Neo-Darwinists considered normally distributed trait variation in populations as proof positive of previous selection and the basis for future selection. Johannsen’s results of pure line “bell curves” unresponsive to selection seemed to indicate otherwise. http://instruct.uwo.ca/biology/Zoo441a/hist1.html
An unfortunate and totally unnecessary shouting match between Gradualists and Saltationists ensued. Éminences grises like August Weismann refused to implicate themselves in the imbroglio.
If much of the debate outline above sounds ultimately sounds like quibbles about semantics – that conclusion would be correct.
Enter Stage Right Fisher, who attempted to cut through this Gordian Knot.
OK. Why is it unreasonable to expect the perfections from this process?
What would you change to make it perfect? No errors..
OK, but in a sense, mutations are a destructive force, wouldn’t you agree Joe? Making random changes in the genetic material is bullocks…
How about in any highly adapted organism?
Could such changes be overwhelmingly likely to be detrimental or even lethal?- I’d presume….
Were the usual analogies made in such cases involving making the random adjustments? Could they be applied to the real life scenario,one would ask..?
Yikes! I hesitate because the question sounds naive. Scientists use models that are unrealistic all the time, because they seem to be useful. Can you be more specific?
OK – that last post was too long. http://theskepticalzone.com/wp/getting-beyond-abstruse-theorems-to-science/comment-page-1/#comment-211757
But necessary. I will attempt to make this one shorter.
Julian Huxley introduced the phrase “modern synthesis” in 1942 to describe the resurrection of Darwin as viewed through the lens of Mendelian genetics and codified by Fisher (1918) and J. B. S. Haldane and Sewall Wright (later).
The next VERY important event was the The Luria & Delbruck Fluctuation Test in 1943 which addressed the question whether, genetic mutations arise in the absence of selection, rather than being a response to selection? No teleology or orthogenesis to see… move along.
Again NeoDarwinism was vindicated. No surprises really.
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.
Yes of course, in addition to natural selection, neutral mutation has caused a lot of molecular differences within and between species. How this is supposed to be different than boilerplate textbook reiteration of one of Darwin’s five principles?
When comparing differences within and between species, but from an ecological POV, VARIOUS taxa all demonstrate adaptations to their environment… and the VARIATIONS which generated these variations originated at a molecular level by random happenchance and ongoing mutation. Fer crying out loud – don’t forget every round of DNA replication and/or repair generates mutation.
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.
Even Darwin acknowledged that much Evolution was not driven by Natural Selection. He even wrote a book on that: The Descent of Man
So is there anything new under the sun? Do Pigliucci or Koonin really have anything new to offer? So how are these different syntheses “new and improved”?
Gainsayers could highlight Fisher’ genetic naiveté inhis description of continuous variation resulting from a number of discrete genetic loci. But Fisher, still even in 1918, understood that traits are determined by many loci. He understood all traits are multigenic and all genes are pleiotropic. Meanwhile, wasn’t it Mayr himself who coined the term “beanbag genetics”?
OK… what about:
Deep homologies and EvoDevo? Darwin thought it first. Just read his observations on snake embryology, for example.
Deep homologies? Darwin
Or multilevel selection? Just read Bateson’s racist rants to confirm the earliest Neo-Darwinists were already thinking on those lines.
How about Niche Construction? Darwin again… remember his preoccupation with Earthworms.
OK – maybe Darwin never considered transgenerational epigenetic inheritance?
So what? Maybe important to Developmental Biologists – sure. But probably irrelevant to changes over geological time in evolutionary terms
Somebody enlighten me.
Aren’t we witnessing another Bataille Royale, tap-dancing about inconsequential semantics no differently than the one I just described earlier along similar lines 100 years ago between the Gradualists and Saltationists?
Is there really anything new? … or is all evolutionary theory just a footnote to Darwin where the FTNS provided the first foundations for Neo-Darwinism as a first chapter for the Summa Theologica of the OMS
ETA
This is way less mysterious than you are making it out to be. For the case of nucleotide mutations, consider the review by Maki, 2002. The three main sources of nucleotide mutations are replication errors, incorporation of damaged pre-cursors (e.g., 8-oxo-G), and error-prone repair of damage (e.g., from free radicals).
Quantum uncertainty clearly affects the latter two pathways, but this is a tiny part of the story. If an energetic particle is heading toward a cell, with the potential to cause a reactive oxygen species, which may then diffuse to DNA and damage it, or damage a nucleotide precursors, then this is clearly subject to quantum uncertainty in the path of the particle.
But that is only one step in the formation of a mutation. Most damage does not lead to mutation, e.g., if you stick your finger out into the sun, the genome in every skin cell is getting damaged thousands of times per minute (subject to quantum fluctuations) and repaired thousands of times per minute by highly efficient enzymes.
Mutation does not seem like a big mystery to me, but I was addressing the ID community (since 1802). Do they have a theory that explains how just the right mutations occur?
This is a restatement of the directed/undirected debate.
Of course! So how do you move from the unrealistic model to the reality of science using the experimental proof in this particular case, so that your answer doesn’t sound as naïve as my question, or even more?
You must realize that speculative talk is as good as it deserves, even if it is clocked as science…
For the record – this OP thesis has been addressed earlier on sandwalk.blogspot
http://sandwalk.blogspot.ca/2014/02/on-difference-between-neutral-theory.html
My favorite citation:
There are only ever models….
Publish or perish.
I used to be an expert on intron evolution, 10 years ago. My knowledge is a bit out of date. So far as I know, there is some evidence for a duplication-mediated mechanism of intron gain first proposed by Dibb and Newman. Imagine duplication mutations happening by some model of choosing endpoints. Occasionally one of them includes an AGGT site, and voila, if it looks enough like an intron to get processed, it’s an intron.
Introns in humans often grow by addition of Alu elements, for instance.
There is evidence for reverse-transcription-mediated intron loss. An extreme example would be processed pseudogenes (pseudogenes appear that are missing all of the introns of the parent gene, indicating an mRNA intermediate). But there is also systematic evidence that intron loss in functional genes is correlated with reverse-transcriptase activity (Cohen, et al. 2012)
You lost me there.
You just can’t quite bring yourself to complete the thought can you?
So, yes, all of that. And then what?
The designer steps in and makes the right mutation happen at the right time? Or is it all on a downward trend from the original perfection from the garden of eden? It’s like you’ve never even thought about your own position, you’ve concentrated so hard on attacking something you’ve never understoof.
Also, can you think of a way that a random change in the genetic material that is highly detrimental to the organism, perhaps even fatal, that might limit the spread of that mutation in the gene pool?
J-Mac? Or is yours, J-Mac, a purely negative argument?
You’re missing quite a lot here. With respect to the inadequacy of Fisher’s view on infinitesimalism, we already have alternatives with experimental support. For instance, Kimura’s revision, which completely changes Fisher’s model, is the basis for the current literature on “Fisher’s geometric model”, and this literature includes a number of empirical studies on the distribution of sizes of fitness effects in evolution. With respect to the inadequacy of the Fisher-Haldane-Wright argument against the possibility of variation-induced tendencies, I proposed an alternative theory 20 years ago and the paper by Stoltzfus and McCandlish, 2017 is an example of evidence of the predicted effect of mutation biases on adaptation.