tag:blogger.com,1999:blog-3381117866759226132024-03-05T04:43:25.194+00:00Evolution under the microscopeDavid Swifthttp://www.blogger.com/profile/15746973752887188780noreply@blogger.comBlogger12125tag:blogger.com,1999:blog-338111786675922613.post-18383019939262517262017-03-03T20:10:00.000+00:002017-03-03T20:10:52.189+00:00An explanation, and an alternative platformI apologise for the inordinate length of time since last posting here. The main reason was simply shortage of time due to other commitments. But I also came to think that a blog isn’t all that suitable for the type of material I write. Some articles are rather long and technical for a blog post; and, because the same issues arise in various contexts, rather than repeating stuff it makes more sense to cross-reference. So I decided to use a new website instead. This I have finally got started, at <a href="http://evolutionunderthemicroscope.com">evolutionunderthemicroscope.com</a>. I hope you will find it of interest, and helpful.
David Swifthttp://www.blogger.com/profile/15746973752887188780noreply@blogger.com0tag:blogger.com,1999:blog-338111786675922613.post-64664953256188454582012-10-13T09:18:00.000+01:002012-10-15T18:29:39.277+01:00A Critique of Richard Dawkins' The Greatest Show on Earth: The evidence for evolution - cont...<h2>6. Embryogenesis defies an evolutionary origin</h2>
<p>I apologise to regular readers for the delay in writing again, but I’m reading Jerry Coyne’s <i>Why evolution is true</i>, and I’ll be writing a critique of that as soon as time allows. But first I must finish commenting on Richard Dawkins' book.<p>
<p>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.<p>
<blockquote>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)</blockquote>
<p>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:</p>
<ul style="list-style-type: lower-alpha;">
<li>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.</li>
<li>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).</li>
</ul>
<p>The information required at either of these levels cannot have been generated in an evolutionary manner - by natural selection acting on randomly occurring mutations.</p>
<h3>a. Embryogenesis requires higher level organisation</h3>
<p>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.</p>
<p>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.</p>
<p>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.</p>
<p>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.</p>
<p>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.</p>
<p>How is this done in the course of embryogenesis?</p>
<p>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.</p>
<p>And how is this done? - By a hierarchy or cascade of regulatory genes.</p>
<p>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.</p>
<p>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.</p>
<p>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.</p>
<p>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.</p>
<h3>b. Embryological development is mediated by very specific macromolecules</h3>
<p>So what about implementation of those local rules?</p>
<p>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 <a href="http://en.wikipedia.org/wiki/Gene_regulation">Regulation of gene expression</a> which includes the following that is particularly relevant here:<p>
<blockquote>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).</blockquote>
<p>This article - and others linked to it - gives an indication of the complexity of gene regulation.</p>
<p>But the main point I want to make here is to emphasise the nature of the regulatory proteins.</p>
<p>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.)</p>
<p>In an earlier post <a href="http://www.evolutionunderthemicroscope.blogspot.co.uk/2012/08/a-critique-of-richard-dawkins-greatest.html">Half-truths about proteins</a> 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).</p>
<p>So what would be required for the evolution of just one new protein?</p>
<ul>
<li>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.</li>
<li>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?</li>
</ul>
<p>(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.)</p>
<p>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!</p>
<p>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!</p>
David Swifthttp://www.blogger.com/profile/15746973752887188780noreply@blogger.com4tag:blogger.com,1999:blog-338111786675922613.post-90452354231491995672012-09-07T23:09:00.000+01:002012-09-07T23:09:40.028+01:00Thomas Nagel: Public Education and Intelligent Design
<p>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.</p>
<p>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.</p>
<p>The main points he makes are:</p>
<ol>
<li>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.</li>
<li>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.</li>
<li>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.</li>
<li>Claims about the certain truth of evolution are exaggerated, not supported by the evidence.</li>
<li>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.</li>
<li>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.</li>
</ol>
<p>I'll now amplify and illustrate these points.</p>
<h3>1. ID is distinct from creationism, because it is based on scientific observations and inference rather than a religious authority.</h3>
<blockquote>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)</blockquote>
<blockquote>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)</blockquote>
<blockquote>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)</blockquote>
<h3>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.</h3>
<blockquote>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)</blockquote>
<blockquote>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)</blockquote>
<h3>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.</h3>
<p>Immediately following the preceding quote from p189 he says:</p>
<blockquote>[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)</blockquote>
<p>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!</p>
<blockquote>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)</blockquote>
<p>Especially interesting are his comments that the actions of a god could be scientifically detectable:</p>
<blockquote>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)</blockquote>
<p>and</p>
<blockquote>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)</blockquote>
<h3>4. Claims about the certain truth of evolution are exaggerated, not supported by the evidence.</h3>
<p>Referring to the theory of evolution he observes:</p>
<blockquote>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)</blockquote>
<blockquote>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)</blockquote>
<h3>5. The theory of evolution is not immune to scientific challenges, and such challenges should be taken seriously.</h3>
<p>To begin with he reminds us that any scientific theory must at least in principle be falsifiable:</p>
<blockquote>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.</blockquote>
<p>And he recognises that the progress made in biochemistry and genetics opens up the possibility of such scrutiny.</p>
<blockquote>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)</blockquote>
<p>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:</p>
<blockquote>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]
<br />
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)</blockquote>
<p>But he notes that ID arguments are sidestepped rather than refuted or even considered at all:</p>
<blockquote>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)</blockquote>
<h3>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.</h3>
<blockquote>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)</blockquote>
<blockquote>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)</blockquote>
<blockquote>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)</blockquote>
<p>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.</p>
David Swifthttp://www.blogger.com/profile/15746973752887188780noreply@blogger.com0tag:blogger.com,1999:blog-338111786675922613.post-88601485816436304412012-08-14T20:26:00.000+01:002012-10-17T23:12:32.252+01:00A critique of Richard Dawkins’ The Greatest Show on Earth: The evidence for evolution
<h2>5. Smoke and Mirrors - trying to obscure the challenge of embryology</h2>
<p>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.</p>
<h3>Blueprints</h3>
<p>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.</p>
<p>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?</p>
<h3>Starlings</h3>
<p>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.</p>
<p>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.</p>
<p>I shall explain later why his flock analogy falls woefully
short of embryological development anyway.</p>
<h3>Origami</h3>
<p>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.</p>
<p>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.</p>
<p>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.</p>
<p>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.</p>
<p>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.</p>
David Swifthttp://www.blogger.com/profile/15746973752887188780noreply@blogger.com0tag:blogger.com,1999:blog-338111786675922613.post-81132469158416425232012-08-02T23:40:00.001+01:002012-10-17T23:24:37.529+01:00A critique of Richard Dawkins’ The Greatest Show on Earth: The evidence for evolution - cont...<h2>4. Half-truths about proteins</h2>
<p>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 ...</p>
<p>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.</p>
<blockquote>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)</blockquote>
<p>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; <i>J Mol Biol </i>341(5):1295</p>
<p>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.</p>
<p>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.</p>
<p>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.</p>
<ol>
<li> 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 <i style="mso-bidi-font-style: normal;">Protein structure and function</i> 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.</li>
<li>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.</li>
</ol>
<p>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.</p>David Swifthttp://www.blogger.com/profile/15746973752887188780noreply@blogger.com0tag:blogger.com,1999:blog-338111786675922613.post-31975173579801921772012-07-12T21:13:00.000+01:002012-10-17T23:45:14.678+01:00A critique of Richard Dawkins’ The Greatest Show on Earth: The evidence for evolution - cont...<h2>3. The case for ID vindicated</h2>
<p>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.</p>
<h3>The long-term evolution experiment (LTEE)</h3>
<p>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</p>
<p>The LTEE involves propagating 12 lines of <i>E. coli</i> 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.</p>
<p>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<i style="mso-bidi-font-style: normal;"> Evolution under the
microscope</i> pp235-244, where such resistance is generally at the expense of
reduced overall fitness.</p>
<h3>Utilisation of citrate</h3>
<p><i>E. coli</i> 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.</p>
<p>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.</p>
<p>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.</p>
<h3>Advantageous mutations</h3>
<p>A typical mutation rate is approx 10<sup>-9</sup> (1 in 10<sup>9</sup>
per cell per generation) for any particular base in DNA (the authors cite the
slightly lower figure of approx 5 x 10<sup>-10</sup> for <i>E. coli</i>). 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).</p>
<p>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.</p>
<p>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 10<sup>18</sup>), e.g. some resistance to penicillin, bacterial populations
and their reproduction rate are so high that these can occur, albeit at a low
frequency.</p>
<p>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<sup>-13</sup>, which they say indicates the change involves
multiple point mutations or a rarer type of mutation.</p>
<p>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.</p>
<h3>Geological time isn't enough</h3>
<p>In <i>Evolution under
the microscope</i> - 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.</p>
<p>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.</p>
<p>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?</p>
<p>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.</p>
<h3>ID vindicated</h3>
<p>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.</p>
<p>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.</p>
<p>Which is why, yet again, Dawkins misleads his readers by
saying:</p>
<blockquote>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)</blockquote>
<p>because the size of the human population will be so much
smaller than the bacterial populations of the LTEE.</p>
<p>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.</p>
David Swifthttp://www.blogger.com/profile/15746973752887188780noreply@blogger.com0tag:blogger.com,1999:blog-338111786675922613.post-55133718538380904932012-06-23T11:51:00.000+01:002012-10-18T23:29:33.246+01:00A critique of Richard Dawkins’ The Greatest Show on Earth - cont..<h2>2. Macroevolution?</h2>
<p>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.</p>
<p>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).</p>
<p>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:</p>
<blockquote>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)</blockquote>
<p>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:</p>
<blockquote>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.</blockquote>
<p>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):</p>
<blockquote>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.</blockquote>
<p>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!</p>
<p>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.)</p>
<p>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.</p>
<p>It's interesting that in chapter 1 he discusses the dictionary
definition of a fact:</p>
<blockquote>... a particular truth known by actual observation or
authentic testimony, as opposed to what is merely inferred ... (p14)</blockquote>
<p>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):</p>
<blockquote>... I shall show the irrefragable power of the inference
that evolution is a fact. (p16)</blockquote>
<p>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).</p>
<p>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.</p>
David Swifthttp://www.blogger.com/profile/15746973752887188780noreply@blogger.com3tag:blogger.com,1999:blog-338111786675922613.post-35101756382050745982012-06-23T11:44:00.000+01:002012-10-18T23:34:25.739+01:00A critique of Richard Dawkins' The Greatest Show on Earth<h2>1. Looking at the evidence</h2>
<p>Although Richard Dawkins published his The <i>Greatest Show on Earth: The evidence for
evolution</i> in 2009 to celebrate the 150th anniversary of Darwin’s <i>Origin
of Species</i>, it’s only recently that I’ve got around to reading it. He’s right
that nature is indeed the greatest show on earth, and his book includes good
descriptions and photographs of some of the wonders of biology.</p>
<p>His aim in this book is, of course, to present the
evidence for evolution, mistakenly thinking (or, at least, implying) that this
proves the overall theory of (macro)evolution must be true (p9).</p>
<blockquote>Evolution is fact ... no unbiased reader will close the
book doubting it.</blockquote>
<p>What he fails to take on board - though it is well known
in the philosophy of science, so surely he is aware of it - is that no amount
of supporting evidence can prove a theory true; what matters is whether there
is contrary evidence that shows it to be false - Karl Popper’s falsifiability,
which I’ve dealt with previously, so I won’t dwell on it here. I realise that
some may think I am just raising this as a sort of smoke screen to try to avoid
considering the supporting evidence. But this is not so, and you can judge for
yourself from my subsequent comments whether this is the case. I will show (a) that
the evidence presented by Dawkins (and others) is not as convincing as he would
have you believe, and (b) there is substantial contrary evidence that shows the
theory to be false.</p>
<p>One final introductory comment: It is a travesty that he lumps
together those, such as myself, who have exclusively scientific objections to
the theory of (macro)evolution, with those who reject evolution primarily for
religious reasons; and it is utterly ridiculous that he then labels such as ‘history
deniers’ and compares them with those who deny the holocaust - this does him no
credit at all. I wonder if the main reason he does this is to fabricate an
excuse to avoid taking seriously the scientific arguments against (macro)evolution,
because he has no answer to them.</p>
David Swifthttp://www.blogger.com/profile/15746973752887188780noreply@blogger.com0tag:blogger.com,1999:blog-338111786675922613.post-89513805708566863222011-02-07T20:19:00.000+00:002012-10-19T22:02:04.083+01:00Homology refutes evolution<p>Homology is commonly cited as demonstrating, or even proving, common descent and evolution. But there is substantial evidence showing that supposedly homologous structures in fact are not; and in doing so this provides compelling evidence against both common descent and macroevolution. Let me explain:</p/>
<h3>Homology - what is it?</h3>
<p>Historically, homology is simply similarities of biological structure. Probably the most widely-used example to illustrate this is the skeleton of vertebrates, especially the forelimb of tetrapods (vertebrates with four limbs): despite the substantial differences in overall appearance of e.g. a horse’s foreleg, human arm, bird’s wing and whale’s flipper - the underlying bone arrangement is remarkably similar.</p>
<p>The theory of evolution seems to provide an elegant explanation for these similarities. It proposes that the tetrapod leg, from its first appearance with the early amphibians, as their descendants diversified, was itself progressively modified to adapt to differing uses. Similarly, the supposed evolution of tetrapods from fish is supported by the similarities of skeleton of all vertebrates. This evolutionary explanation has become so widely accepted that it now defines homology as referring to those organs which have been derived from the same structure in a common ancestor.</p>
<p>That is, over the course of evolution, modifications of the embryological developmental processes have resulted in divergence from the common embryological source to give the range of modern day organs. And with this evolutionary account of homology, embryology acquired an important role in identifying and interpreting homologies. The point being that, even if adult structures look rather different (wing, flipper, arm), if they are homologous then they will be derived from equivalent embryological sources.</p>
<p>Conversely, even if structures from different species look similar, if they have developed from different embryological tissues then they would not be regarded as homologous, but due to convergent evolution. A good example of this is the vertebrate eye and that of the cuttlefish (a mollusc related to squid). In overall structure they closely resemble each other, notably in having a lens and iris, are equally specialised and with comparable performance. But they are not considered to be homologous, as there is no doubt they have arisen quite independently in separate phyla (chordates and molluscs) which have completely different body plans. And there was no common primitive eye from which they have both evolved.</p>
<h3>Homology - the inconvenient truth</h3>
<p>Although most evolutionary texts convey a consistent and hence persuasive picture of homology, there are in fact many substantial anomalies. In particular, as we discover more of how tissues are formed embryologically, increasing doubt is being cast on much of the homology that has been perceived for so long at the morphological level.<br />Notably, in view of the importance attached to the apparent homology of the vertebrate skeleton, and the weight given to embryology for identifying homology, it is especially relevant that vertebrae – a major component of the vertebrate skeleton – form embryologically in significantly different ways for different classes of vertebrate (such as mammals, birds, amphibians and fish), and even from different groups of early embryonic cells. (For example, see Vertebrates: Comparative anatomy, function, evolution by K. Kardong.) This clearly shows that the vertebrae of these different vertebrate classes are not, in fact, homologous - and hence that these different groups of vertebrate do not in fact share a common vertebrate ancestor, despite their superficial similar appearance and contrary to the commonly held view.</p>
<p>Taking this further, in the course of embryological development the members of different classes of vertebrate pass through a similar-looking stage (called the phylotypic stage), which is seen as clear evidence of their common ancestry. However, what is confounding (from an evolutionary perspective) is that even though the phylotypic stage looks similar, and we would have expected it to be formed from a fertilised egg in substantially the same way, there is, in fact, remarkable diversity, including some fundamental anomalies. The fact that the phylotypic stages are formed in different ways prima facie at least undermines, if not completely negates, the notion that they are derived from a common ancestor. And there are similar anomalies in other phyla, not only the vertebrates.</p>
<p>This is not just putting an anti-evolutionary spin on the facts. Here’s what evolutionary biologist Rudolf Raff had to say:</p>
<blockquote>The process of early development from the egg to the phylotypic stage should be at least as conserved as the pattern of the phylotypic stage. One might reasonably expect mechanisms of early development to be especially resistant to modification because all subsequent development derives from early processes.</blockquote>
<h3>Homology - why the evidence is important - and hence ignored!</h3>
<p>The evidence from homology - or, rather, the lack of it - is very important. Although some people try to dismiss the ‘intelligent design’ case against evolution as a ‘gap’ argument, this excuse is not available over homology. The fact that apparently homologous organs such as the vertebrae in fact have proved not to be, not only removes circumstantial evidence in support of evolution - it constitutes clear counter-evidence against the organisms concerned having evolved from e.g. a common vertebrate ancestor. This evidence unequivocally refutes the theory of evolution.</p>
<p>And this no doubt is why so few, including professional biologists, know about these anomalies - they are kept safely out of the limelight so as not to upset the applecart. As mentioned above, textbooks on evolution only cite the evidence that supports evolution. How many who are reading this article knew previously about the anomalies of so-called homology?</p>David Swifthttp://www.blogger.com/profile/15746973752887188780noreply@blogger.com4tag:blogger.com,1999:blog-338111786675922613.post-62364122920609184382010-04-03T19:43:00.000+01:002012-10-22T19:42:23.108+01:00Peer Review<p>In the preceding post (below) I mentioned what I think is a key failing of evolutionary scenarios, such as that of the eye by Nilsson & Pelger - they completely ignore what we now know of the genetic and molecular mechanisms that are essential for forming biological tissues. And along with this they ignore the fact that the evolution of substantially new biological structures, such as eyes and feathers, would require new genes to arise.</p>
<p>And my point here is this: this knowledge has been well known for at least a generation; yet, not only did N&P (and authors of comparable scenarios for other organs) feel free to ignore this, but presumably the reviewers of their paper were happy to overlook this oversight too. And, we should note, it wasn’t published in some minor or obscure journal, but in the prestigious Proceedings of the Royal Society of London.</p>
<p>Before I comment further on peer review, let me also mention another serious flaw in the authors’ rationale. Their aim was not only to show what they considered to be a plausible scenario for the evolution of an eye, but also to estimate how long it would take - to show that there was plenty of geological time for it to happen. But their method was seriously flawed: their calculations used an equation (in Falconer’s Introduction to Quantitative Genetics) formulated to estimate the time to effect change through domestic breeding.</p>
<p>First of all, this reinforces the point I made previously - that their model for the evolution of an eye is based on selection from an already existing gene pool - completely ignoring the fact that a new organ such as an eye will require very many new genes (which are prohibitively improbable to arise - a central theme of my book).</p>
<p>Second, their model assumes that only those organisms having a variation that confers at least a 1% improvement in vision will contribute to the next generation. This is the sort of thing a breeder can put into practice, but totally unrealistic to think that natural selection (which of course is what the evolution of the eye would have had to rely on) will operate this way - most of the mature individuals (even those with reduced visual acuity) in a population will have some offspring.</p>
<p>So these criticisms completely undermine their claim that their calculations are a ‘pessimistic’ estimate of the time for an eye to evolve. Quite the opposite!</p>
<p>This also gives some insight into peer review: Presumably the reviewers were so happy with the overall message of the paper that either (a) they didn’t examine it too closely, and/or (b) they were aware of its serious shortcomings but chose not to stand in the way of a paper which said what they want to hear. At very least It shows that ‘peer review’ is not the independent objective assessment it’s claimed to be.</p>
<p>And its not just the reviewers who are at fault. This paper is referred to widely to support the notion that eyes could have evolved readily. Have none of these bothered to take a careful look at what N&P actually proposed?</p>David Swifthttp://www.blogger.com/profile/15746973752887188780noreply@blogger.com3tag:blogger.com,1999:blog-338111786675922613.post-38724600174242600952010-04-03T19:29:00.000+01:002012-10-27T00:26:13.415+01:00Eye Evolution<p>A good example of where belief in evolution is maintained because people aren’t prepared to look at the detail is in the supposed evolution of new organs such as the eye.</p>
<p>The eye is the classic example of a highly specialised organ, considered by many pre-Darwinian scientists such as John Ray as incontrovertible evidence of design in biology. Even Darwin recognised that the eye was a challenge to his theory, but in the <i>Origin</i> speculated how it might have arisen progressively from a simple light-sensitive tissue through a series of variations.</p>
<p>In the 1990s a couple of Swedish scientists, Dan-E Nilsson and Susanne Pelger (Proceedings of the Royal Society of London Series B - Biological Sciences, 256:53-9), expanded on this sort of scenario, illustrated as follows:</p>
<img id="BLOGGER_PHOTO_ID_5455981974353912690" style="DISPLAY: block; MARGIN: 0px auto 10px; WIDTH: 415px; CURSOR: hand; HEIGHT: 221px; TEXT-ALIGN: center" alt="" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgq4VWkqurkGRq43MSRs3Sn7cNFxStSybfGcM_mEe1REnlqIxJGGGDBl_utLopN-Qygt6CkdUx3geSti_Aen5xwKehrossch5KF1smA8RqJEF_f5woYuW9CnHTcQ2zW3aeSG2OEPPqK0Gg/s320/eye+evolution.gif" border="0" />
<p>Starting from a patch of light-sensitive cells (which is a huge presumption in itself, though I can’t expand on that here) it is envisaged that an eye evolves by a flat patch of cells becoming a depression, which gradually deepens into a small pit (a to c), the neck of which then narrows (d). Each of these stages, taking place over several generations, is driven by the advantage of increased optical acuity (better resolution). When this stage has been reached, further improvement can be achieved only by addition of a lens (e), and the authors boldly assert that ‘Even the weakest lens is better than no lens at all, so we can be confident that selection for increased resolution will favour such a development all the way from no lens at all to a lens powerful enough to focus a sharp image on the retina.’</p>
<p>The totally unjustified assumption in this scenario is that if a variation will offer some advantage, then we can be sure that it will arise. No thought whatsoever is given to the crucial question of how those variations will arise. I think this blind spot (!) has arisen for two reasons.</p>
<p>First, before we knew about genetic and molecular mechanisms, it was thought that biological tissues were innately plastic in the sense that variations would arise spontaneously, and favourable ones could then be passed on. However, we now know that the formation of morphological structures – whether it be an eye, feather or leaf – is not by some sort of vague plasticity, but through the closely orchestrated action of many genes. So new structures need new genes. But in the above scenario, all that we have learned in the last 50 years about the biochemistry of tissues and the molecular mechanisms involved in forming tissues is totally ignored.</p>
<p>The second reason arises from the fact that much variation is possible through the mixing of genes that are already available. For example, it’s been known since well before Darwin that domestic varieties of crops and animals can be developed by breeding selectively from those individuals which have the desired variations (which have arisen naturally). But it was also well-known that there are limits to the amount of change that can be achieved this way. Which is why, although artificial selection could validly help to illustrate natural selection, Darwin’s contemporaries also knew that domestic breeding could not support changes such as the evolution of new organs. We now know why: new organs need new genes and molecular mechanisms to construct them - which are not available in the genomes of the original parents.</p>
<p>This oversight is illustrated by the fact that the above-mentioned authors’ calculation of the rate of eye evolution is based on <em>selection from an existing pool of genes</em>. Whereas there can be no doubt at all that the evolution of an eye would require very many <em>new</em> genes – for several proteins used exclusively in the eye, and for the molecular mechanisms that construct the eye in the course of embryological development. So their comment about a lens arising simply because it would be advantageous to do so is just ignorant wishful thinking - scarcely science at all.</p>
<p>There are so many speculative scenarios for the evolution of new structures - whether they be for eye, wing, feather, limb or whatever - but they are no better than those available in the 19th century - because they are based on the assumption that biological tissues are plastic, and completely ignore the genetic and molecular implications. If proponents of evolution want their scenarios to be taken seriously then they really do need to take on board the genetic and molecular detail.</p>David Swifthttp://www.blogger.com/profile/15746973752887188780noreply@blogger.com9tag:blogger.com,1999:blog-338111786675922613.post-22202356964210462752008-02-08T11:53:00.000+00:002012-10-27T00:31:32.807+01:00Design or Apparent Design?<p>It’s my intention to debate the issues, not personalities; but as Richard Dawkins is such a popular advocate of evolution, I’m going to start by referring to some of the things he says; partly, because I agree with some of them.</p>
<p>In particular, I agree with him that the biological world looks designed, but that the subjective perception of design in itself is not conclusive. In <i>The Blind Watchmaker</i> (Ch.2) he calls this the Argument from Personal Incredulity - e.g. ‘I don’t see how something as beautiful / complicated or whatever as ... could have evolved’. As he says, there’s not much point in saying that something-or-other could not have arisen by chance, because no-one is seriously suggesting that a mammal, flower, or even bacterium has arisen spontaneously by chance.</p>
<p>We need to fully take on board the non-chance process of natural selection and its potential for producing a very unlikely end-product through a long series of small stages where each offers a small advantage over its predecessor. As he puts it in God Delusion (p 121, my emphasis) :</p>
<blockquote>What is it that makes natural selection succeed as a solution to the problem of improbability, where chance and design both fail at the starting gate? The answer is that natural selection is a cumulative process, which breaks the improbability up into small pieces. <em>Each of the small pieces is slightly improbable, but not prohibitively so.</em></blockquote>
<p>But it seems to me that he is so taken with the elegance of the idea of evolution that he assumes it must be true and does not actually expose it to scrutiny. That last sentence which I emphasised is merely asserted, never substantiated or even scrutinised. He says we should examine the issue objectively, but doesn’t practise what he preaches!</p>
<p>I have also read Dawkins’ <i>The Blind Watchmaker</i> and <i>Climbing Mount Improbable</i>, both of which extol the power of cumulative natural selection, yet neither examines the crucial issue of the likelihood of occurrence of the variations on which natural selection can act. Despite his comments about breaking down immense improbabilities into smaller steps, nowhere is there any attempt to quantify the probability of those steps. In discussing the possible evolution of the eye (<i>Watchmaker</i>, Ch 4) he assumes that it can be broken down into infinitesimally small steps (in order to improve their probability); but this is not correct because of the discrete nature of genes.</p>
<p>Bertrand Russell said:</p>
<blockquote>This [design] argument has no formal logical defect; its premises are empirical and its conclusion professes to be reached in accordance with the usual canons of empirical inference. The question whether it is to be accepted or not turns, therefore, not on general metaphysical questions, but on comparatively detailed considerations.</blockquote>
<p>I agree, and I sought to examine the theory of evolution in the necessary detail in my <i>Evolution under the microscope</i>. But Dawkins never examines it in detail; he merely relies on the elegance of the theory, and polemic (and, sadly, ridicule).</p>
<p>Design or Apparent Design? - the answer is in the detail.</p>David Swifthttp://www.blogger.com/profile/15746973752887188780noreply@blogger.com5