Saturday, 13 October 2012

A Critique of Richard Dawkins' The Greatest Show on Earth: The evidence for evolution - cont...

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!

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