Friday, 3 March 2017
Saturday, 13 October 2012
6. Embryogenesis defies an evolutionary origin
I apologise to regular readers for the delay in writing again, but I’m reading Jerry Coyne’s Why evolution is true, and I’ll be writing a critique of that as soon as time allows. But first I must finish commenting on Richard Dawkins' book.
As I've mentioned previously, Dawkins recognises that the complexity - and, quite frankly, the stunning achievement - of embryogenesis (embryological development) is a major challenge to the theory of (macro)evolution.
we find it hard to imagine, even in principle, how we might set about writing the instructions for building a body in the way the body is in fact built, namely by what I have just called 'self-assembly', which is related to what computer programmers sometimes call a 'bottom up' as opposed to 'top-down' procedure'. (p217)
He attempts to circumvent the challenge by trying to argue that it is all achieved merely by the operation of 'local rules', i.e. that it wouldn't need an overall plan (and hence no designer). But there are two fundamental issues which cannot be so readily brushed aside:
- To build something as complex as a functioning organism, with many disparate yet interdependent parts, local rules by themselves are insufficient - there has to be some higher level of organisation as well to ensure overall compatibility and function.
- For anything biological to work, implementation of those local rules is carried out by biological macromolecules (mostly proteins and nucleic acids); and, to work, those macromolecules must have closely-defined sequences (of nucleotides or amino acids).
The information required at either of these levels cannot have been generated in an evolutionary manner - by natural selection acting on randomly occurring mutations.
a. Embryogenesis requires higher level organisation
We know from everyday experience that a coherent end-product - one that functions well, or even at all - is not going to emerge from the bottom-up.
To use a simple mechanical example of constructing a car, or even just its engine: There’s no point in e.g. a main bearing of the engine being machined to perfection, unless there is also a matching surface on the crankshaft, and lined up accurately with other bearings, and the crankshaft connected to pistons (with other sets of matching bearings), which fit tightly (via piston rings of appropriate materials and construction) into the correctly orientated cylinders, synchronised with the camshaft etc. - you get the idea.
Put another way: Karl Benz didn’t come up with an automobile by starting with the detail of the engine - he had an overall plan, and he then designed and manufactured the components (which needed to coordinate with each other) in such a way as to implement that plan.
And it’s no different with embryogenesis; in fact there's another reason why overall planning is necessary - because, as Dawkins says, it's all achieved by self-assembly rather than by an external craftsman.
Each organ or tissue requires its specialised cells (e.g. lens, neuron, muscle fibre, erythrocyte) which must be produced only by that organ/tissue; and the organs/tissues must be formed in their right places - they would be useless if not detrimental in the wrong place - and connected appropriately.
How is this done in the course of embryogenesis?
Dawkins outlines the approach by reference to the worm Caernorhabditis elegans which has been studied closely, including its embryological development. He explains that, starting from the initial fertilised egg, at each cell division, each daughter cell is slightly different: each is different in terms of the genes it has switched on or off (gene regulation is much more sophisticated than simply on or off, but that's another story), and progressively the various daughter cells diverge morphologically.
And how is this done? - By a hierarchy or cascade of regulatory genes.
Dawkins is well aware (p358) of the Hox genes which occur in all animals. They play a crucial role in early embryogenesis - organising the overall body plan - for example each controls the development of a particular section (e.g. segment in insects) along the length of an animal's body. They do this initially by turning on the appropriate network or hierarchy of genes that form the organ, and continue to have a role in regulating the action of those genes. Incorrect expression of Hox genes can lead to major disruption of embryogenesis, such as a fully formed organ appearing in the wrong place on the animal's body.
The Hox genes themselves are controlled by a series of 'gap' genes (so called because if one is missing it leaves a gap in the resulting embryo) and pair-rule genes. And these gap and pair-rule genes are themselves controlled by mRNA that comes from the unfertilised egg.
Dawkins is right when he says that development proceeds through asymmetric cell division - i.e. before the cell divides each end is slightly different (e.g. in concentration of a protein or other chemical) and this leads to the differing gene expression in the daughter cells. Is this through the operation of local rules? - Well, yes, but only through a hierarchy of gene regulation which is extremely complex and we're only just beginning to unravel it. In other words, higher level instructions are required to ensure that the lower level development can take place.
And - lest any should think (despite my comments below) that it would be relatively easy to add another layer of expression at the bottom of this genetic hierarchy - there is a confounding twist: It will be apparent from what I've said above that the genes that organise development of the gonads (e.g. Hox genes and those 'below' them) are themselves controlled by cells produced within the gonads (via the maternal mRNA). So here is another example of chicken-and-egg scenarios which we find all too often in biological systems (the interdependence of proteins and nucleic acids in the synthesis of each other, is a very obvious one) and which completely defy an evolutionary origin.
b. Embryological development is mediated by very specific macromolecules
So what about implementation of those local rules?
Dawkins should be ashamed of himself for the way he glosses over the biochemical realities - relying on his readers' ignorance of biochemistry to get way with it. Here I can only outline what's involved - for more information you could look at Wikipedia's article on the Regulation of gene expression which includes the following that is particularly relevant here:
Furthermore, in multicellular organisms, gene regulation drives the processes of cellular differentiation and morphogenesis, leading to the creation of different cell types that possess different gene expression profiles, and hence produce different proteins/have different ultrastructures that suit them to their functions (though they all possess the genotype, which follows the same genome sequence).
This article - and others linked to it - gives an indication of the complexity of gene regulation.
But the main point I want to make here is to emphasise the nature of the regulatory proteins.
For example, a Hox gene (a DNA sequence) codes for a Hox protein (a sequence of amino acids) called a transcription factor which selectively binds to a specific regulatory DNA sequence associated with several other completely different genes. (Again, in most cases there are several transcription factors involved in regulating a particular gene, rather than just one.)
In an earlier post Half-truths about proteins I commented on the specificity required of an amino acid sequence just to ensure that it will fold into a 3-dimensional structure - that criterion alone is enough to defeat an evolutionary origin of proteins. Regulatory proteins must not only fold in this way, but part of their outer surface, once folded, must be of the correct shape and chemical composition (derived from its constituent amino acids) to bind to a specific sequence of nucleotides (and, in most cases, interact correctly with other factors involved in regulating that particular gene).
So what would be required for the evolution of just one new protein?
- Obviously, we need a nucleotide sequence to arise by chance that, once translated into an amino acid sequence, will result in a protein that will fold, not only that, but will serve a useful function - one that will benefit the organism. That in itself is so improbable that it should not be taken seriously - but evolutionary texts do or, rather, like Dawkins, they uncritically assume it must be possible, because they aren’t willing to contemplate the alternative of design.
- But that's only the beginning. Because, of course, a random nucleotide sequence will not be used to make a protein - it must also have the nucleotide sequence that means it is recognised as a gene and translated. But if the protein product has no value then there is no reason to recognise it as a gene - so the regulatory sequence must arise (by chance) in close association with, and at about the same time as, the sequence that arises (by chance) to code for a useful protein. Why is it that evolutionary texts never even mention this?
(Evolutionary text books roll out the fairytale of new genes arising by gene duplication - that while one copy retains the original function the other is free to ‘experiment’ to find a new useful function. But what that scenario completely overlooks is that until the duplicate finds a new function there is no reason to produce the protein, so it’s likely the control sequence will degrade, and once that’s happened even if a potentially useful sequence should arise there’ll be no way the organism could ‘know’ it.)
And what if, to realise the potential of the new protein (so that natural selection can act to retain it), just one regulatory protein were also required? What would need to arise (by chance, at more or less the same time) is, as well as the gene (with its regulatory region) for the protein, an independent gene that codes for a protein that selectively binds to the regulatory region of the end-product protein!
It is clear that the hierarchy of gene regulation in embryogenesis involves far more complex arrangements than that, especially when you consider that self-assembly sometimes requires production of additional proteins to transport the end-product proteins (before they can have any use). So it’s not surprising that Dawkins doesn’t want to delve into the details of embryogenesis, and would rather divert readers’ attention with fanciful talk of starlings and origami!
Friday, 7 September 2012
When I learned of Thomas Nagel’s latest book Mind and Cosmos: Why the Materialist Neo-Darwinian Conception of Nature is Almost Certainly False, I looked a little further into what this atheist philosopher has to say. This has led me to make a brief digression from my series of comments on Richard Dawkins' Greatest Show on Earth, as I think it’s worth highlighting some of Nagel's comments.
Following the Dover trial in the USA, he wrote a paper 'Public Education and Intelligent Design' which was published in Philosophy & Public Affairs, 36(2), p187-205, in which he discusses the issues in the context of the Establishment Clause of the US Constitution. In the course of doing this he makes many perceptive observations regarding the debate about evolution and intelligent design (ID). When I read the paper I highlighted a lot of it, but clearly must be very selective about what I quote here. I encourage readers who are interested in these issues to read the whole of Nagel's paper.
The main points he makes are:
- ID is distinct from creationism, because it is based on scientific observations and inference rather than a religious authority, and it is open to scientific scrutiny.
- Because the basis for ID is scientific, it cannot simply be dismissed from consideration as non-science - to do so is just a feeble excuse or ruse to try to avoid facing up to the legitimate questions it raises.
- Neither can the possibility of a supernatural designer - a god - be summarily dismissed; it is a legitimate a priori worldview. Not only that, but the actions of such a being may be scientifically detectable.
- Claims about the certain truth of evolution are exaggerated, not supported by the evidence.
- The theory of evolution is not immune to scientific challenges - though many of its proponents speak as if it were - and such challenges should be taken seriously.
- The exaggerated claims for evolution and illegitimate refusal to take seriously any challenges to it, is leading to evolution being taught in a less than academically responsible way.
I'll now amplify and illustrate these points.
1. ID is distinct from creationism, because it is based on scientific observations and inference rather than a religious authority.
ID is very different from creation science. To an outsider, at least, it does not seem to depend on massive distortion of the evidence and hopeless incoherencies in its interpretation. Nor does it depend, like biblical literalism, on the assumption that the truth of ID is immune to empirical evidence to the contrary. What it does depend on is the assumption that the hypothesis of a designer makes sense and cannot be ruled out as impossible or assigned a vanishingly small probability in advance. Once it is assigned a significant prior probability, it becomes a serious candidate for support by empirical evidence, in particular empirical evidence against the sufficiency of standard evolutionary theory to account for the observational data. Critics take issue with the claims made by defenders of ID about what standard evolutionary mechanisms can accomplish, and argue that they depend on faulty assumptions. Whatever the merits, however, that is clearly a scientific disagreement, not a disagreement between science and something else. (pp196-7)
ID is a different story. Its defense requires only that design be admitted as a possibility, not that it be regarded as empirically unassailable. It would be difficult to argue that the admission of that possibility is inconsistent with the standards of scientific rationality. (p199)
Those who offer empirical evidence for ID do not have to argue that a completely nonpurposive explanation is impossible, only that it is very unlikely, given the evidence available. That is a scientific claim, though a contestable one. (p199-200)
2. Because the case for ID is essentially a scientific enterprise, it cannot simply be dismissed from consideration as non-science - to try do so is just a feeble excuse or ruse to try to avoid facing up to the legitimate questions it raises.
No one suggests that the theory [of evolution] is not science, even though the historical process it describes cannot be directly observed, but must be inferred from currently available data. It is therefore puzzling that the denial of this inference, i.e., the claim that the evidence offered for the theory does not support the kind of explanation it proposes, and that the purposive alternative has not been displaced, should be dismissed as not science. The contention seems to be that, although science can demonstrate the falsehood of the design hypothesis, no evidence against that demonstration can be regarded as scientific support for the hypothesis. (p188-9)
The conceivability of the design alternative is part of the background for understanding evolutionary theory. To make the assumption of its falsehood a condition of scientific rationality seems almost incoherent. (p201)
3. The possibility of a supernatural designer - a god - cannot be summarily dismissed - it is a legitimate a priori worldview. Not only that, but the actions of such a being may be scientifically detectable.
Immediately following the preceding quote from p189 he says:
[The contention seems to be ...] Something about the nature of the conclusion, that it involves the purposes of a supernatural being, rules it out as science. (p189)
And this is the crux of the anti-ID argument. It’s not that the arguments themselves are unsound, only that the conclusion is unacceptable - even if true!
The denier that ID is science faces the following dilemma. Either he admits that the intervention of such a designer is possible, or he does not. If he does not, he must explain why that belief is more scientific than the belief that a designer is possible. If on the other hand he believes that a designer is possible, then he can argue that the evidence is overwhelmingly against the actions of such a designer, but he cannot say that someone who offers evidence on the other side is doing something of a fundamentally different kind. All he can say about that person is that he is scientifically mistaken. (p195)
Especially interesting are his comments that the actions of a god could be scientifically detectable:
So the purposes and intentions of God, if there is a god, and the nature of his will, are not possible subjects of a scientific theory or scientific explanation. But that does not imply that there cannot be scientific evidence for or against the intervention of such a non-law-governed cause in the natural order. (p189)
I suspect that the assumption that science can never provide evidence for the occurrence of something that cannot be scientifically explained is the principal reason for the belief that ID cannot be science; but so far as I can see, that assumption is without merit. (p190)
4. Claims about the certain truth of evolution are exaggerated, not supported by the evidence.
Referring to the theory of evolution he observes:
To rule it out decisively would require that the sufficiency of standard evolutionary mechanisms to account for the entire evolution of life should have been clearly established by presently available evidence. So far as I can tell, in spite of the rhetoric to the contrary, nothing close to this has been done. (p199)
A great deal depends on the likelihood that the complex chemical systems we observe arose through a sufficiently long sequence of random mutations in DNA, each of which enhanced fitness. It is difficult to find in the accessible literature the grounds for evolutionary biologists’ confidence about this. (p199)
5. The theory of evolution is not immune to scientific challenges, and such challenges should be taken seriously.
To begin with he reminds us that any scientific theory must at least in principle be falsifiable:
I assume it will be granted by everyone that, even though the past cannot be directly observed, a scientific argument against the Darwinian theory of evolution is not impossible. If it were impossible, that would cast doubt on whether the theory is itself science.
And he recognises that the progress made in biochemistry and genetics opens up the possibility of such scrutiny.
For example, as we learn more about the behavior of the genetic material, and more about how the properties of organisms depend on it, it will be possible to give more precise answers to questions about the rate at which viable mutations can occur randomly as a result of physical accident, the kinds of phenotypic changes they can generate, and the number of generations within which specific changes would have had to occur to make the theory fit the development of organisms as we know them. Together with calculations of the numbers of individual organisms that have been involved in the major transitions in evolution, this should make it possible to evaluate the theory mathematically. (p190)
This of course is a key aspect of the ID challenge to the theory of evolution. And Nagel thinks that Michael Behe makes a valid point when he says:
alterations to DNA over the course of the history of life on earth must have included many changes that we have no statistical right to expect, ones that were beneficial beyond the wildest reach of probability. [from Edge of Evolution]
Like Kauffman, he believes that random mutation is not sufficient to explain the range of variation on which natural selection must have acted to yield the history of life: some of the variation was not due to chance. This seems on the face of it to be a scientific claim, about what the evidence suggests, and one that is not self-evidently absurd. (p192)
But he notes that ID arguments are sidestepped rather than refuted or even considered at all:
That [‘ID is hopelessly bad science’] would be true if ID, like young earth creationism, can be refuted by the empirical evidence even if one starts by assuming that the possibility of a god who could intervene cannot be ruled out in advance. So far as I can tell, however, no such refutation has even been offered, let alone established. What have been offered instead are necessarily speculative proposals about how the problems posed by Behe might be handled by evolutionary theory, declarations that no hypothesis involving divine intervention counts as science, and assurances that evolutionary theory is not inconsistent with the existence of God. (p202)
6. The exaggerated claims for evolution and illegitimate refusal to take seriously any challenges to it, is leading to evolution being taught in a less than academic way.
The political urge to defend science education against the threats of religious orthodoxy, understandable though it is, has resulted in a counterorthodoxy, supported by bad arguments, and a tendency to overstate the legitimate scientific claims of evolutionary theory. (p187)
It would be unfortunate if the Establishment Clause made it unconstitutional to allude to these questions in a public school biology class, for that would mean that evolutionary theory cannot be taught in an intellectually responsible way. (p188)
One of the disturbing things about the public debate is that scientists engaged in it sometimes write as if the idea of fundamental problems with the theory (as opposed to problems of detail in its application) were unthinkable, and that to entertain such doubts is like wondering whether the earth is flat. (p190-1)
Evolutionists often complain that questioning evolution undermines scientific progress. But it's exactly the opposite: it is the blinkered refusal by proponents of evolution to allow the theory to be subjected to scrutiny that is inhibiting scientific enquiry.
Tuesday, 14 August 2012
5. Smoke and Mirrors - trying to obscure the challenge of embryology
As I said previously, it's evident that Dawkins realises the complexity of embryological development presents an insuperable challenge to an evolutionary origin; but, being committed to the evolutionary cause, he tries various diversionary tactics to dumb down that complexity.
First he goes to considerable lengths to argue that the popular portrayal of DNA being a blueprint is wrong. For example he says that, although a house can be built from a blueprint and a blueprint drawn from the house, it's not possible to deduce the DNA sequence from the form of the host body. Of course no-one is suggesting that DNA is a graphical representation, even in coded form, of the developed body; and this is so obvious that one might wonder why Dawkins takes the trouble to make the point. His reason is that, because it's obvious a blueprint must have a designer, he seems to think that by showing that DNA is not a blueprint he is showing that there is no need for its having a designer. As if the only way the input of a designer might be inferred is if they leave some sort of blueprint - which is obviously not the case.
DNA may not be comparable with a blueprint, but certainly it contains the information for developing an organism; so, quite apart from how that information is encoded, the important question is, How did that information originate?
He then turns to starlings to try to support his premiss that biology does not have a designer. Starling flocks may appear to act as a whole - perhaps resembling a troupe of ballet dancers; but, he emphasises, in the case of starlings there is no choreographer - each bird is merely acting individually (not independently, as it responds to those nearby). And so he extrapolates from this that there is no director behind the embryological development of organisms - he argues that each cell is merely following local rules.
To try to reinforce his argument, he describes how the behaviour of birds in a flock can be modelled mathematically, just by building in local rules for each bird to follow. But actually this serves to reinforce the point that, even with something like a flock of birds (whose behaviour is so much simpler than that of cells in a developing body) at bottom it rests on rules. Rules which, even in the case of his simple model, must but be conceived and formulated, coded into a computer programme, and then fed into a complex machine that can apply the rules for all the individuals - each stage requiring intelligence.
I shall explain later why his flock analogy falls woefully short of embryological development anyway.
This is taken even further with his other ‘analogy for development’ - origami. Dawkins accepts that, even though not a blueprint, DNA does contain the instructions for growing an organism. And, because embryological development includes (among many other things) the folding of tissues, he compares this with origami - using the well-known construction of a junk as an example.
Even at a very superficial level, this analogy falls well short of illustrating his evolutionary premiss, because he would have to assume that an origami junk had arisen simply through random foldings of randomly shaped pieces of paper - which of course is totally wrong. On the contrary, an artisan will first have conceived of the end product and then devised a way of constructing it - with the desired object in mind as he does so.
But the really amazing thing about embryological development is the way in which all of the development takes place internally - there is no external agent doing the folding etc. Dawkins acknowledges the importance of self-assembly, but yet again thinks that by modelling the process with a computer he is explaining it away.
He wrongly says that the scientists in question have ‘deciphered’ the embryological process whereby tissues can fold (p229). They have not done this at all; all they have done is mimicked one aspect - and that in only two dimensions rather than three. But the key point, yet again, is that, even with this considerably simplified system, it requires formulation and programming of the rules, and then using a computer to implement them.
It’s all very well for Dawkins to argue that development proceeds through the implementation of local rules (and does not require a grand plan, but I will contest that next); but even the implantation of local rules requires considerable input of information. And none of his examples even attempts to explain whence or how that information is derived.
Thursday, 2 August 2012
4. Half-truths about proteins
It is clear Richard Dawkins realises that the complexity of embryological development poses a serious challenge to the theory of evolution, so he goes out of his way to gloss over the realities. The cornerstone of his approach is to try to argue that embryological development proceeds simply through the natural operation of local rules i.e. without an overall plan that would need a designer. I will explain subsequently how his attempted sleight of hand doesn’t work. Meantime ...
Unfortunately (for him), he tries to build up his case with reference to the structure of proteins; but it is his undoing because exposing his half-truths here makes it all the easier to explain the fallacy of trying to apply a similar approach to embryological development. As he says, proteins comprise linear sequences of amino acids, which fold up into a 3-dimensional structure which is essential for their biological function.
Protein molecules, simply by following the laws of chemistry and thermodynamics, spontaneously and automatically twist themselves into precisely shaped three-dimensional configurations. ... Any given sequence of amino acids dictates a particular folding pattern. (p236)
What he fails to say is that, simply because of the laws of chemistry and thermodynamics (his local rules), the vast majority of amino acid sequences will not fold at all. By not acknowledging this, he gives the false impression (false, but no doubt deliberate, as he must surely know this) that most amino acid sequences will fold in this way. Whereas in fact very few do - Douglas Axe estimated that only about 1 in 10^77 sequences have the potential to fold (Estimating the prevalence of protein sequences adopting functional enzyme folds; J Mol Biol 341(5):1295
Dawkins mentions only the specificity of proteins in terms of their ability to selectively bind their substrates (compounds they act on). What he ignores is their active sites - the parts of the proteins that have just the right chemical groups (derived from the right amino acids) in just the right places in relation to the bound substrates so as to catalyse reaction between them. Needless to say, taking these features on board as well, further compounds the specificity required of the amino acid sequence for e.g. an enzyme, and hence reinforces the prohibitive improbability against their arising by chance.
Dawkins comments that at present we are able to predict how some amino acid sequences will fold; and quite likely we will be able to do this for all before too long. But that’s only one side of the coin. What’s required is to identify an amino acid sequence that will fold, and once folded will perform a required biological function. Thanks to increased computing power and some ingenious programming, I expect that one day we will be able to design proteins to fold in a particular way, and maybe perform a particular function. But that will serve only to reinforce the case that functional proteins require a designer.
The nonsense that proponents of evolution would have us believe is that biologically active proteins, with their highly specific and hence improbable sequences, could arise by chance. Dawkins of course rolls out the usual evolutionary article of faith that complex proteins evolved from shorter/simpler precursors. But, as discussed more fully in my book, there are substantial objections to such a scenario.
- First is the question of folding. The forces between the packed amino acids (Dawkins’ local rules) that hold a protein in its folded state are so weak that there needs to be many amino acids involved, typically requiring a protein to be at least 70 amino acids long (see Protein structure and function by Jack Kyte) So it’s utter nonsense to suggest as some textbooks do, and Dawkins would have us believe, that proteins could have started off with just a handful of amino acids.
- Second is that key amino acids, such as those contributing to the active site, are generally scattered throughout the linear sequence of the protein, and are brought together only once the protein is folded. If proteins had evolved from short sequences, one would have thought that at least these critical amino acids (which necessarily would need to have been close together in a short protein) would still be grouped together; because to disperse them during the course of subsequent evolution would require constant restructuring of the protein.
It’s all very well for Dawkins to argue that proteins fold merely through the operation of local rules / natural forces. But what he fails to acknowledge is that operation of those rules results in something useful only if the underlying components are right - so far as proteins are concerned, that they have the right amino acid sequence. And the evidence clearly shows that natural selection acting on random mutations could not generate such sequences. Evolutionists merely cling to this hope as a drowning man clings to a straw.
Thursday, 12 July 2012
3. The case for ID vindicated
In chapter 5 Dawkins describes various examples of natural selection of which, as I said in the preceding post, all but one are comparable with artificial selection: all that's happening is selection from an existing gene pool; there's no production of new or altered genes. The exception is a long-term experiment using bacteria (by Lenski et al. at Michigan State University) specifically designed to investigate the evolution of new characteristics.
The long-term evolution experiment (LTEE)
For more information about the overall long-term evolution experiment see myxo.css.msu.edu/ecoli/, and for the emergence of the ability to utilise citrate it’s useful to read their paper which is available from www.pnas.org/content/105/23/7899.abstract
The LTEE involves propagating 12 lines of E. coli bacteria, all initially identical (except that 6 had a genetic marker), but then each strain allowed to develop independently. They were grown in a glucose-limiting medium, and initially the experiment was designed to see how their growth adapted to this. The experiment has run since 1988, now exceeding 50,000 bacterial generations.
All strains improved their ability to utilise glucose, evidenced by increased initial rate of consumption, this effect reaching a plateau after about 20,000 generations (typical of selection from a gene pool). On the other hand, all showed reduced ability to utilise other sources of carbon such as maltose or lactose. This is similar to most instances of the acquisition of resistance to antibiotics, discussed in Evolution under the microscope pp235-244, where such resistance is generally at the expense of reduced overall fitness.
Utilisation of citrate
E. coli cannot normally utilise citrate under aerobic conditions, and a surprising discovery was that one strain evolved the ability to do this (citrate was present in the growth medium, and the ability to utilise it resulted in a marked increase in the bacteria’s growth), emerging after about 30,000 generations. Further investigation showed that this development was contingent on an earlier mutation, arising in this strain after about 20,000 generations.
The mutations have yet to be characterised. The authors suggest several possibilities, including enabling the expression of a carrier protein to enable citrate to pass through the cell membrane; as it is transport into the cell that normally limits its use - once inside the cell it is readily metabolised.
Because this evolution required at least two distinct mutations, Dawkins vaunts it as disproving the intelligent design concept of irreducible complexity. But that is merely his spin on the facts; a closer look shows that the results from the experiment actually support the ID case.
A typical mutation rate is approx 10-9 (1 in 109 per cell per generation) for any particular base in DNA (the authors cite the slightly lower figure of approx 5 x 10-10 for E. coli). As they say, despite this low rate, given the high numbers of bacteria and generations it can confidently be assumed that during the course of the experiment all possible single point mutations in the bacterial genome will have occurred, probably many times. Of course, as they comment, only a small number of these will become ‘fixed’ in the genome - even advantageous ones will not be fixed automatically but have only a small chance of spreading throughout the population (contrary to many of Dawkins’ comments, for an explanation see a text-book on population genetics).
It is therefore not surprising that not only have the same genes been affected in several of the strains, but that in some cases the same point mutations have been fixed, especially those that improved the ability to metabolise glucose. This too is analogous to the emergence of some antibiotic (and insecticide) resistance where the same point mutation has arisen independently.
Even where two mutations are required (i.e. neither alone confers resistance, so both must arise together, with a probability of doing so of just 1 in 1018), e.g. some resistance to penicillin, bacterial populations and their reproduction rate are so high that these can occur, albeit at a low frequency.
In a similar way, even after the potentiating mutation, the probability of the citrate-enabling mutation was estimated by the authors at about only 10-13, which they say indicates the change involves multiple point mutations or a rarer type of mutation.
And the preceding potentiating mutation also had a very low incidence - occurring in only one strain, even after efforts by the researchers to reproduce it. They suggest it may be a neutral mutation, which would have been be fixed only by genetic drift.
Geological time isn't enough
In Evolution under the microscope - based on the rate of occurrence of point mutations, the size of bacterial populations and their rate of reproduction, and supported by the observed instances of resistance - I suggest that the upper limit for multiple dependent mutations that could arise in the course of a year is likely to be 3 or maybe 4. And I went on to point out that, given the mutation rate is about 1 in a billion, this implies that the upper limit for mutually dependent mutations arising throughout the whole of geological time (e.g. a billion years) is only 4 or 5.
So, although it may be possible to switch a gene on or off with just a few point mutations, or modify its performance, this cannot be extrapolated to producing genes in the first place, as typically they require hundreds of specific base pairs e.g. to code for the many essential amino acids in the protein product.
In discussing the possible nature of the citrate-enabling mutation(s) the authors consider reactivation of a cryptic transporter, but think this unlikely because they would expect such a cryptic gene to have been degraded beyond recovery after millions of years of disuse. It begs the question - if they consider it so likely that the effect of random mutation is to degrade genes, how do they think useful genes arose in the first place?
Dawkins frequently emphasises the immense length of geological time, suggesting that this is more than enough to overcome the improbability of advantageous mutations. It is time he did a few simple calculations and started to look at geological time objectively. If he did so, he would realise that it is not the answer to evolution's problems that he makes it out to be.
And this is why, as I indicated above, far from defeating the case for intelligent design based on irreducible complexity, the LTEE results actually support it - because they demonstrate how limited is the ability of random mutations to generate useful sequences. And - unfortunately it needs to be repeated often - natural selection is dependent on being fed the right raw material on which it can work.
Further, it should be noted that the above-mentioned rate of finding useful mutation combinations applies to such as bacteria which have very large population sizes (at least billions) and high rates of reproduction (more than one generation per day). In organisms with smaller populations and slower reproduction rates, what can be achieved will be so much less.
Which is why, yet again, Dawkins misleads his readers by saying:
So whatever evolutionary change Lenski may have clocked up in the equivalent of a million years of bacterial generations, think how much more evolution might happen in say 100 million years of mammalian evolution (p119)
because the size of the human population will be so much smaller than the bacterial populations of the LTEE.
The ID argument is not that an advantageous mutation cannot occur, or even that a few mutually dependent ones cannot - but that the complexity and specificity of molecular biology would require so many mutually dependent ones that it is not credible they could have occurred.
Saturday, 23 June 2012
Darwin used the artificial selection of domestic breeding to introduce the concept of natural selection. Dawkins follows this, in particular using the breeding of the various types of dog from the wolf to illustrate the range of characteristics that can be achieved. Indeed, he points out that with almost any plant or animal we can breed for almost any trait we wish, such as maize for high or low oil content (p67) or rats for low or high susceptibility to tooth decay (p68). He also observes that in all such cases, though rapid change can be achieved in the first few generations, before long it tails off - not just because e.g. low oil content trends to zero, and you can't get any lower than that, but also the cultivation for high oil content tends to plateau.
Dawkins recognises that domestic breeding is through losing or subtracting genes, comparing it with removing pieces of stone in making a sculpture (p37). And this, of course, is why there is a limit to the degree of change achievable - because once all of the genes available in the original species that favour the desired trait are retained, and all those that detract from the trait are bred out, then no further change is possible through conventional breeding (ignoring genetic engineering which is now available).
So he is completely unjustified to extrapolate from the changes possible through domestic breeding (which involves the loss of genetic information) to macroevolution (which would require the emergence of new genes), yet this is how he tries to mislead his readers:
If so much evolutionary change [referring to dog breeding] can be achieved in just a few centuries or even decades, just think what might be achieved in ten or a hundred million years. (p37)
And this isn’t just a momentary oversight or over-enthusiasm on his part, for he repeats this false extrapolation at the end of chapter 3:
if so much difference can be achieved in breeding such different breeds of dogs in just a few centuries, think how much can be achieved over geological time.
From what he has written in these first chapters he must surely be aware that this is a misleading comparison. Of course, he says that the gene pool is added to by mutation (p37); but this is merely the evolutionary dogma. It is clear that he does not see this as taking place in the course of domestic breeding (certainly not to the extent of producing new characteristics), because he recognises (p56):
Domestically bred songs are longer, louder and more frequent than the wild ancestral type. But all these highly prized songs are made up of elements that occur in wild canaries, just as the habits and tricks of various dogs come from elements found in the behavioural repertoire of wolves.
He claims to be a science educator and is not slow to berate creationists for any misrepresentation of scientific facts - yet this is exactly what he's doing here!
The title of his chapter 3 is 'The primrose path to macroevolution'; but it's nothing of the sort - all but one of his examples of natural selection are comparable with the changes achievable through domestic breeding - i.e. merely through selection from an existing gene pool - whereas macroevolution would require new genes to arise. (The exception relates to bacteria, which I will discuss subsequently.)
Unfortunately this is typical not only of Dawkins, but of many evolutionary writers: the unsupported presumptions required to support the overall (macro)evolutionary theory (notably that new useful genes arise through mutation) are tucked away among the facts of microevolution (that substantial morphological change can be achieved merely using existing genes) - no doubt to give the impression that the unsupported assumptions are valid too.
It's interesting that in chapter 1 he discusses the dictionary definition of a fact:
... a particular truth known by actual observation or authentic testimony, as opposed to what is merely inferred ... (p14)
and he takes issue with 'inferred', arguing that although the overall theory of evolution is inferred from limited observations, the inference is as sound as any observed fact (p16):
... I shall show the irrefragable power of the inference that evolution is a fact. (p16)
But I think the definition is right, and particularly apposite here: it highlights the fact that the whole theory of (macro)evolution (which would require new genetic information) is an inference from the observed facts of microevolution (which merely involves the use of existing genetic information).
Evolutionists are keen to promote the notion that macroevolution is nothing more than accumulated microevolution. But this is wrong. There is a fundamental distinction that microevolution is based merely on existing genes (even though sometimes this may result in large morphological changes, such as the different dog breeds) and macroevolution which would require new genes.