A discussion of biochemical evolution with reference to Darwin's Black Box by Michael Behe and to a review of this book by Phillip Johnson.
Behemoth or be he not
He be nothing when I swat
The Review
Judging by the review Phillip Johnson (author of Darwin on Trial) belongs to a plentiful group of people who can't abide the untidiness of evolution- the messiness, the chanciness, the endless blind alleys, the indifference and the mind-boggling multiplicity which we can see as the story of life on earth. The opposition to evolution and to natural selection as its mechanism is to some extent a question of personality. People who seek or need order and purpose find natural selection quite horrible and understandably so. Foremost among these are some physicists quoted by Dawkins in Ch. 3 of his book eg. Darwin's contemporary Herschel who said 'Natural Selection is the law of higgledy piggledy', and later Kelvin and Hoyle. Never mind that concerning the age of the earth, the 'orderly' physicist Kelvin proved to be wrong and the 'messy' biologist Darwin was right. Never mind either that 'higgledy piggledy' is a pretty good description of life as it has developed. Evolution by natural selection has no purpose and confers no rights (how can there be natural rights?) Neither does it reward virtue nor punish transgression. The results of the process are wasteful and cruel, as Darwin said, as often as they are inspiring and beautiful. No wonder many people are not too keen on the idea. Clearly Johnson belongs to this group.
I don't believe there's any evidence that Darwin or any serious scientists of the time thought of the cell as a 'blob of protoplasm' as claimed by Behe- the cell is Darwin's Black Box of the title. Of course they did not know all the wonderful and intricate detail that we know now. There were dramatic discoveries in cell biology going on in Germany notably by Schwann, Schleiden and Virchow. Was Darwin aware of this? Certainly he realised much later in his life that his own theory of pangenesis was incompatible with the new 'cell theory'. Pangenesis was a theory that buds from all the different tissues contributed to the egg cell. The German biologists (cytologists and embryologists) showed that egg cells were derived only from special germline cells laid aside early in development. Darwin struggled all his life with the problems of inheritance without success. But that is not the point. Evolution is something that can be demonstrated at the level of organisms. We do not need to know details of cell structure or biochemistry to sustain the theory any more than a biochemist needs to know about the fundamental particles of physics-leptons, bosons and the like- to describe reactions at the molecular level. It so happens that the discoveries of molecular evolution have supported schemes of evolution at the organism level (i.e.phylogeny) in nearly every respect. The question then is whether the mechanism of evolution proposed by Darwin namely natural selection operates at the cellular and molecular levels or do we need an entirely different theory.
Phillip Johnson is quoted with approval by Behe and it is apparent from the review where he stands. Basically he wishes, like Behe, to entertain the possibility that what looks designed might be designed. This is called the argument from design. It is the same whether it is applied at the macroscopic or microscopic level. The exemplar of the form is William Paley's Natural Theology (1802) which Darwin read when he was considering whether or not to go to Cambridge with the intention of becoming a vicar. (He did go to Cambridge but he did not become a vicar!) The argument from design, following Paley, goes like this: if you find a watch you can infer the existence of a watchmaker and likewise if you find good design in nature you are entitled to infer the existence of a Designer. (Hence the title of Dawkins's book the Blind Watchmaker). Darwin used much of the material that appears in Paley's book while coming to a totally different conclusion as to how the good adaptation, the apparent design, could come about.
Behe's arguments are much the same as Paley's except that instead of talking about organisms he talks about cellular structure or biochemical processes and instead of talking about good design he talks about irreducible complexity and instead of God he postulates a Designer.
Irreducible complexity is a buzz notion at the moment. It describes a phenomenon that is complex and which it is difficult to imagine being derived from simpler processes or structures because if you took away any part of the complex structure or process it would collapse, it would not work.
Of course it is true that cellular processes are extraordinarily complicated, just as the brain, for example, is extraordinarily complicated. One reason the brain is complicated is that in the course of evolution one level of organisation has been superimposed on another. Nerves from a primitive eye connected directly to nerves innervating muscles and the organism moved towards (or away from) light. This is the condition in the flatworm, Planaria. Then came additional neurons to modify this behaviour. Neurons doing the same sort of job collected together in a group called a nucleus (not to be confused with the nucleus of each single cell!) They could interact with other nuclei. In Amphibia vision is 'controlled ' at the level of the optic tectum, in mammals additional pathways sweep up to the cerebrum although the superseded pathways still have an essential part to play. The end result is extremely complicated and we still do not know how it all works. We know (from experience!) that it does work however and it's a pretty safe assumption that it works for the frog and indeed for Planaria each at their different level of complexity.
Why should it be different at the cellular level? To take one of Behe's examples; the biosynthesis of adenine. (Adenine is one of the organic bases in DNA- one of the four 'letters' of the genetic alphabet). Apparently this is incredibly complicated-as he describes. Does this mean it has always been so? I shouldn't be surprised if sooner or later someone finds a bacterium that makes adenine by some much simpler process just as we find creatures with very simple brains. These things happen, even in biochemistry! Adenine is one of the substances that appears quite readily in 'origin of life' experiments. These are attempts to recreate in the laboratory the conditions on earth when life began. The experiments are bedevilled by the difficulties of knowing what chemicals were available in the early atmosphere- was there ammonia or cyanamide for example. It does seem possible that adenine was quite readily available in the early environment which is why, perhaps, it is found not only in the nucleic acids but also as the core molecule of the universal energy currency ATP (adenosine triphosphate), the intracellular 'messenger ' AMP and the essential metabolic agents FAD, NAD and Coenzyme A. You do not need to know what all these chemicals do- you just need to appreciate that adenine is a very important molecule and therefore it would be most convenient to have a theory explaining its universal presence in living things. It is the universality which makes for the problem- we cannot imagine life without adenine (and a few other related molecules) and it is difficult, but not impossible, to imagine adenine without life.
In the review Phillip Johnson ridicules Dawkins for 'story-telling'. Admittedly story-telling is just what I've been doing when describing complexity in the brain. Of course it would be better if we could describe the origin of complexity in factual detail (though it would make a big book- the book of life in fact). The existence of atoms was a story once. Copernicus told a story about the planets going round the sun (which is quite the opposite of what we observe every day). Mendeleyev told a story when he described elements in his periodic table that hadn't yet been discovered. But when it comes to story-telling these people (Johnson, Behe and the like) take the biscuit. For what could be a more fantastic, amazing and incredible story than theirs: that a designer outside space and time had invented the whole lot- apes, ants, adenine, atoms and all.
In one respect I do agree with Johnson. I do not find Dawkins's computer generated biomorphs very illuminating. I think the intention is to demonstrate that small changes in one or a few genes can lead to considerable differences in phenotype (the observable form of an organism-in this case the observable 2-dimensional form of the biomorph). Does this happen in real life? Definitely. A small change in a single gene might put it out of action entirely or cause it to change function. More subtly a small genetic change might lead to small changes in some less obvious feature such as relative growth rate and this in turn could have dramatic consequences. For example the progressive increase in the size of the chin relative to the face or the size of the brain relative to the body in human evolution. Something similar occurred with the great antlers of the giant elk or the increasing intricacy of ammonite shell sutures. More is emerging about the interaction of genes during development and will help to explain effects of this kind.
Before discussing the book I shall just provide an essential vocabulary; biochemists and other scientifically literate folk can skip this bit. Organic compounds are the compounds of the element carbon. They can be very complicated because they can form chains and rings. Besides carbon they contain other elements notably hydrogen, oxygen, nitrogen, phosphorous and sulphur. They were once thought to be made only by living things but simple ones can be made in the laboratory . Complicated compounds can be made in the laboratory from others that have usually been produced by living things, sometimes in the distant past (coal, oil). Carbon dioxide and Carbonates (eg limestone) count as inorganic substances. polymers are long molecular chains formed by smaller molecules (monomers) joining end to end. Most organic compounds whose names are familiar are polymers eg nylon, rubber, polythene, cellulose. starch is a polymer whose monomers are sugars, proteins are polymers whose constituents are the amino acids (20 of them in a host of different arrangements). The nucleic acids (DNA, RNA) are polymers whose constituents are the nucleotides (4 of them). An enzyme is a protein catalyst that takes part in a chemical reaction without itself being consumed in the process. A gene is a sequence of DNA ( or in some viruses RNA) that has a specific function- often to produce a specific protein. bacteria are a huge collection of titchy organisms usually divided into two groups the archaea and the eubacteria. They are also called collectively the prokaryotes as described later. A mutation is a change in the DNA sequence. There are many ways this can happen. Only one is discussed in this paper- a repeat or duplication of an existing gene.
Behe's book is very easy to read, full of colourful analogies, the biochemical episodes are accurate and readable but you can miss them out if you want to. The case made is not new. It is this: practically every biochemical process in the cell involves many stages and each stage requires a different enzyme. Furthermore some of the products of the intermediate stages have no function in the cell other than as precursors for the next stage. So how can the whole process have arisen step by step as required by gradual evolution? It certainly is impossible to believe that these complex sequential processes arose all at once. So we must look for a different format. For a start we must assume that there was a more direct method of synthesis available at one stage indeed that a more direct process might still be available in some creature yet to be investigated (as I have suggested in the case of adenine). Then we must go on to surmise that the intermediate stages are refinements interpolated subsequently. The idea of interpolation is the important one here. In other words we do not have to prove that a series of chemical reactions appeared in the course of evolution in the same order that they occur in biosynthesis by cells today.
When Darwin was challenged on this sort of problem he would look for living forms that exhibited intermediate conditions. Not because they might be ancestral for it is most unlikely that a living species could be the ancestor of another quite different from itself. For example a tapir could not be the ancestor of a horse or chimpanzees of humans. If it were possible it would imply, as Darwin said, that one branch had remained unchanged for millions of years while the other had altered beyond all recognition. In the human example the original 'apeish' population was split into two by the geological events creating the great rift valley with the chimps subsequently evolving in the damp, forested west and the hominids in the savannah to the east. This is the usual pattern of evolutionary divergence. To return to intermediates: the idea is that living intermediates might yield a clue or two as to the properties of an ancestor. Thus Darwin dealt with, for example, the origin of eyes and social behaviour in bees.
Behe sets up a very good example of the method with regard to the Bombardier beetle. This creature has an unusual defence system- it ejects a mixture of hydrogen peroxide and hydroquinone which in the presence of the enzyme catalase react together to generate heat. The hot liquid hurtles outwards roughly in the direction of the 'enemy'. How do we suppose such a bizarre procedure could have arisen? Well- hydrogen peroxide and catalase have been around for a long time probably ever since oxygen came to be produced in any quantity (by photosynthesising bacteria). As Behe tells us, many beetles produce noxious quinones if only to give themselves a bad taste (excuse the apparent suggestion of purpose here- it's just a manner of speaking!) and thus deter predators. Many beetles, Behe tells us, have pygidial glands with muscles to expel noxious contents. Some species of Bombardier, he goes on, have 'bombs' that are less hot and therefore less dangerous to the exit channel presumably because there is less catalase available and so on. From these intermediate conditions we can construct a 'story' to describe the evolution of the Bombardier beetle. Yes, he's practically done it- he's set up a scenario like the very best evolutionist in the pattern of Darwin- whereby we can imagine how this strange defence system could have arisen step by step. But he's set it up only to knock it down. He rejects it on the grounds that we don't have enough detail to fill in the gaps.
Notwithstanding Behe's objections, finding intermediates is a great help even with the major transitions. Thus Peripatus helps us to see how arthropods are related to annelids. Likewise Amphioxus clarifies the transition from invertebrates to vertebrates, the coelacanth, Latimeria, illuminates its fossil relatives that gave rise to land vertebrates. True we have to fill in the gaps with a 'story'. As Darwin said: 'show me the intermediates between a bulldog and a greyhound'. [At this point you should go and see the Evolution display on the first floor of the Natural History museum]. Behe rejects the evolutionary 'story' only to replace it with one a lot more incredible- the designer.
When it comes to biochemical processes we are a bit pushed to find intermediates. Behe knows this. It is his trump card. That's why he's discussing biochemistry and not whole organisms where so many intermediates have been found. The biochemical intermediates may be found in the future as the vast array of archaea and eubacteria are surveyed. Meanwhile we have got something that Darwin never dreamed of - considerable knowledge of how molecules and genes themselves evolve. Take one of Behe's examples -the clotting system. This is complex all right but irreducible? I'm not so sure. The basic reaction is between fibrin monomers that spontaneously react to form an insoluble mesh. The fibrin is released from a longer protein (fibrinogen) by the enzyme thrombin. All the rest is refinement - improved modulation and regulation that could have been added or interpolated in the sequence one process at a time. It clearly was an advantage to have the fibrin contained within a larger molecule or there'd be clots all over the place. The larger molecule could arise by internal duplication within a fibrin gene. Much the same is true of many other active peptides which have to be released by proteolytic enzymes (enzymes that break up protein) from larger molecules. Where did the thrombin come from? Well- it is closely related to the digestive enzyme trypsin (another proteolytic enzyme)- indeed most of the enzymes in the clotting cascade are structurally related. It is very likely the genes for many of the proteolytic enzymes are derived, by small changes (i.e. evolution), from one ancestral gene. One way that this might happen is described in the next paragraph.
We know that strips of DNA of a length which may or may not constitute a whole gene occur as repeats or duplicates within a chromosome. One way this may happen is by a process called unequal crossing over whereby one chromosome comes to have two copies of a strip of DNA while its partner is missing that particular sequence. Sometimes the duplicate genes are similar and permit a great increase in the quantity of the gene product where a lot is needed- ribosomal RNA for example (oops- did a hint of purposefulness slip in there? What I mean is that 'the advantage to the cell ' for those cells that inherit the altered chromosome might be that a greater quantity of gene product is obtained). In other cases the duplicate gene or genes may accumulate deleterious mutations and become inactive(nontranscribing). In yet other cases, rarer no doubt, the 'spare' gene may mutate and take on new functions as outlined for the clotting case in the previous paragraph. We have here the most marvellous mechanism for evolution- a novelty that could be 'selectively neutral', need not disturb the function of the parent gene but is 'available' to introduce new features.
I can illustrate using another of Behe's pet bogeys- the chemistry of vision. Here again we can see how very complicated biochemistry might arise from a simpler system which had different functions. As described by Behe the chemistry of vision sounds so complicated as to be inherently highly improbable. But he is describing mammalian vision. Here's a brief summary: the outer segment of photoreceptive cells in the retina is formed from cilia (see below) by extremely numerous infoldings of the plasma membrane (the outer layer of the cell) forming a stack of discs. Embedded in the membrane of the discs is rhodopsin -one of a family of transmembrane proteins. Associated with it is retinal and the protein transducin which belongs to the family of G-proteins. When light falls on these cells some of it is absorbed by the rhodopsin and its associated molecules causing the protein to change shape- this is how many proteins work. The change of shape restrains entry of sodium ions (sodium atoms carrying a positive charge) changing the electrical properties of the cell, this in turn excites neighbouring nerve cells.
It may sound very complicated - in fact the full story is a good deal worse! But as in case of the Bombardier beetle what was required in the first place was the association of two proteins that already had other functions together with the substance retinal which is closely related to and derived from carotene. Carotene is a pigment plants use in photosynthesis. Carotene, Vitamin A and retinal are all interconvertible. Retinal has also been found in the light absorbing pigment of archaebacteria where it is involved in ion transport and response to light as well as photosynthesis. So this is an ancient and widespread substance with a number of functions. Its salient property is its ability to absorb light. The light energy can then be used in cellular processes usually by way of a change of shape of its 'host' protein.
Rhodopsin is a transmembrane protein, in other words a molecule that straddles the cell membrane with parts hanging outside, a substantial part lying within the membrane and a further part within the cell. (Remember that in the rod cell of the eye the inside of the disks is equivalent to the outside of a simpler cell). Now in other cells transmembrane proteins in the cell membrane act as receptors (molecular docking proteins) for hormones- adrenaline for instance. A G-protein is associated with the transmembrane receptor and together they initiate the response of the cell to the presence of the outside 'stimulus' (in the case of adrenaline the 'stimulus' is a chemical one). Recently it has been shown that plant hormones also use the mechanism of receptor protein and G-proteins in the same manner. Evidently the mechanism is commonly involved in communication between a cell and its environment. The coupling of these two types of protein is therefore likely to be very ancient. Transducin in rods and cones has a structural relationship to the other G-proteins. In short these proteins, and retinal too, have an ancient lineage and their close association may be ancient as well.
The information in the previous paragraph suggests that rhodopsin and transducin might have evolved while retaining an association already established by their ancestor proteins. There are striking parallels to be found at the macroscopic level. For example: two of the tiny bones in the middle ear of mammals have evolved from bones that are part of the jaw in other vertebrates. Not only have the bones evolved but they've done so while preserving the articulation between the two bones. To be precise: the articulation between the hammer and the anvil of the middle ear is derived from the jaw articulation between the articular bone of the lower jaw and the quadrate of the skull. What was once used for munching we now use for hearing. Who, confronting the anatomy for the first time, would believe such a 'story'? Yet we know it to be true because a whole array of intermediates (fossils this time) show how this transformation took place. Doubters please note: there's no evidence of purpose here. The jaw bones were not released 'in order that' mammals might have a good sense of hearing! The improvement of the munching apparatus was the advantage selected for during most of this transition and the trend is apparent in several fossil lines that did not achieve mammalhood. (Mammals, by definition, have the new jaw articulation between dentary and squamosal). Unfortunately for our vision 'story' we don't have much fossil biochemistry! Nonetheless the evolution of the proteins of vision from ancestral proteins previously engaged in other activities is no more extraordinary than that of the bones. Anyone prepared to accept that evolution has occurred and natural selection has been operating in the one case should feel able to accept that they also work for the other.
Families of proteins are called families for the same reason that related groups of organisms are called families. So what is the reason? it is because their structural similarities suggests a common origin and what does that mean if not evolution? The association of the key molecules concerned with vision in the distant past may have been improbable but certainly not inconceivably so, and once having arisen (by one or more favourable mutations) it has proved remarkably robust. Eyes have developed in the course of evolution perhaps 40 times (see the Dawkins book for a review of this). The eyes of arthropods (eg crustacea, insects), molluscs ( eg. snails, squids ) and vertebrates are quite different in structure and embryology and yet, interestingly enough, the chemistry is remarkably similar. Has the chemistry arisen more than once in the course of evolution? If so then it's not quite as improbable as it appeared! Alternatively the chemistry was already present in the last common ancestor of these three major phyla in which case it is even more robust (in terms of longevity and resistance to disruption) than we could have imagined. The present evidence suggests that the second alternative is correct and that all photosensitivity is based on variants of the rhodopsin-carotene-transducin story. The variants are in some ways the interesting bit since they are all based on small changes leading to adaptation in different environments- well surprise!- evolution.
There is an additional titbit to this story though it is a bit difficult so miss it out if you want to. Retinal associated with rhodopsin has an absorption spectrum peaking at 500nm. The photoreceptor proteins of cones have the same overall configuration as rhodopsin but are sufficiently different to give rise to different absorption spectra accounting for our three-colour vision. These three pigments are located in the cone cells blue-, green- and red- absorbing. The genes for these 4 variants (rhodopsin and the 3 cone opsins) must have evolved from a common ancestral gene by the processes of gene duplication and subsequent divergence described above. New world monkeys have only two cone pigments, a blue-sensitive one and a long wavelength one. In other words the duplication of the gene for the long wavelength pigment has not taken place as it has in the old world monkeys and apes. We have caught this gene in the process of evolving. The red and green pigments differ by only 15 out of 348 amino acids. Their genes lie close together on the X chromosome and colour blind males may lack one or the other or have a hybrid form yielding a pigment with intermediate spectrum. There are also people having 2 or 3 tandem repeats. They have a spare gene which might continue to evolve. This means that their distant progeny, millions of years from now, might have 4 colour vision!
The other biochemical processes Behe describes all raise similar problems- how complicated processes and structures could have arisen by stages. There are many others he could have chosen. Just look at any biochemistry book! So the last topic I'm going to discuss are the cilia (singular cilium)- the hairlike projections of cells which move fluid along like oars in a boat. Ciliated cells line our air passages, oviducts and brain ventricles. Sperm move with flagella. A vast array of unicellular creatures use cilia(short) or flagella(long) to move around. The cilium described by Behe is the eukaryote cilium and not, as Phillip Johnson (no biologist he) leads us to believe, the bacterial flagellum which is totally different. There'll be a short digression now to explain about eukaryotes
The eukaryote (meaning proper nucleus) cell is so called because it has most of its DNA bundled up inside a little bag made of a double membrane with pores in. A large array of unicellular organisms and all multicellular organisms are made of eukaryote cells. The archaea and eubacteria are called prokaryotes because they don't have a discernible nucleus. They do have DNA I hasten to say! The prokaryotes have been around for about 3 1/2 billion years whereas the earliest eukaryote probably arrived around a billion years ago. Of course the prokaryotes have been evolving all that time and not surprisingly they have the edge on the rest of us so far as biochemical diversity is concerned. On the other hand they're a bit limited when it comes to size and shape!
Eukaryote cells have other characteristics besides their defined nucleus: they have internal structures and organelles which are difficult to make out with a light microscope but can be seen clearly with the electron microscope. There are internal membranes (endoplasmic reticulum), mitochondria (source of the energy packet ATP), various vesicles and, if they are plants, chloroplasts. They are a lot bigger than prokaryote cells (1000 or more times larger by volume). There's enough in common when it comes to the basic biochemistry however for us to be sure that eukaryotes have evolved from prokaryote forbears.
How could this come about? For one thing it's believed that the mitochondria and the chloroplasts and possibly the peroxisomes are descended from free-living prokaryotes which either became symbionts of the primitive eukaryote cell or were engulfed by it. (Symbiosis is the living together of two or more organisms to their mutual satisfaction. Green algae that live in corals are a well known example). That eukaryote organelles might be descended from prokaryotes was an idea promoted by Lynn Margulis in the sixties (to incredulity) and now widely supported following analysis of the residual DNA in these organelles. But several evolutionary events must have happened first. A convincing scenario has been developed by Christian de Duve (see Scientific American, April 1996) and others. To become an incipient eukaryote cell a hypothetical prokaryote ancestor must first lose its cell wall and grow. The cell membrane ( not the same thing as a cell wall which is outside the membrane) invaginates with vesicles capturing external fluid and other bacteria. The invaginating membrane forms the endoplasmic reticulum and the nuclear membrane and so on. At the end of the process (which could have been as gradual as you like) the cell- let's call it 'my cell'- would have become a large phagocytic cell (like the ones that scavenge around in our own tissues and in all multicellular animals). In the course of time the cells would invent ( by successive mutations) a whole array of new proteins including those responsible for the new cells' internal support and their new methods of moving about: actin, myosin, tubulin, dynein and more. As well as all this there will have to be a new method of cell division. It's quite some transition but it must have happened. At every stage new genes that caused the new products to be made would be retained if they proved advantageous and unfavourable changes would fall by the wayside in their myriads. This is natural selection. Of course natural selection must operate at the biochemical level but equally the new products available will be constrained by what was there before.
To return to cilia. The structure of cilia is so exact and their activity so precise that they represent a veritable paradigm of the sort of process that it's difficult for evolutionists to account for. They have 9 pairs of microtubules round the circumference and one more pair in the middle. The protein dynein causes the microtubules to slide past each other except that they are restrained by another protein which allows them to go only so far. The result is a bend and the general effect is a rowing motion. They are self-contained. Cilia detached from a cell can still beat. Many other proteins and a great many genes are involved. One rare mutation in humans is known which causes malfunction of the dynein, disrupting the structure of the cilia and preventing them from beating. The sufferers have chronic lung problems and males are infertile because the flagella of the sperm don't work.
It is certainly difficult to devise a good 'story' for the evolution of cilia. But we have to remember that most of the ingredients (so to speak) were already there in the ancestral phagocytes. To that extent the story is like that of the Bombardier beetle or vision which I have described above. The ancestral proteins have to be reorganised to serve a new purpose. 'My cell' would first have moved like an amoeba (remember O-level biology?) as most cells do during some stage of their lives using their microtubules and their contractile microfilaments (principally actin). Microtubules are used as a pathway in internal transport too including down the long axons of neurons. Most importantly microtubules attach to chromosomes during cell division and ensure that each daughter cell gets its complete set. Microtubules polymerise from tubulin and depolymerise depending on the stresses to which they are exposed and on the calcium ion concentration. They are organised from a small structure called a centriole- a mini-pack of microtubules. A very similar structure, the kinetosome, is found at the base of each cilium organising the microtubules there too. We know that cilia vary in length. Maybe they were just small protuberances at first helping the creature to lie in a surface film (change of function is something we evolutionists frequently resort to). The self assembly (polymerisation) of microtubules and other proteins is not so different from the way inorganic molecules form crystals- snowflakes for example. The main difference is that these proteins interact with each other in an energy-consuming way. Let's remember too that those other proteins actin and myosin which form the basis of muscle action behave in a similar way to tubulin and dynein in cilia. They too can line up in an orderly fashion. It is a property of these proteins that they can aggregate and line up in an orderly way in certain conditions provided by the cell.
Could these proteins be derived from those in bacteria? I have described a possible common ancestor for the eukaryotes. Genes can be identified that go way back in eukaryote history. We can follow how they've evolved, diverged and changed. It's a little more difficult to bridge the gap (going backwards) to the prokaryotes but there are certain domains of eukaryote proteins that closely resemble domains of bacterial proteins. A domain is a part of a protein that folds up in a constant manner and may have a particular function such as binding to another molecule. A domain may occur in several different proteins. We suspect that one way proteins evolve is by a certain amount of mixing and matching (due to what's called exon shuffling). No doubt a lot more will be learned about this and we shall be able to trace the pedigrees of more and more proteins further and further back. One thing's for sure. Those that are maintained in a population will be there because they confer some advantage on the organisms that possess them. We know very much more about the sources of variation and about the way genes spread in a population than Darwin did but natural selection still operates whether it is the cilium or the feather.
Now lets look at the scenario offered by Behe on p.227 of his book: 'The designer made the first cell' 4 billion years ago 'already containing all of the irreducibly complex biochemical systems' including 'designs for systems that were to be used later, such as blood clotting.....' What sort of a cell was this!? 4 billion years ago it certainly was not a eukaryote cell and 'my cell' (described above) contains antecedent prokaryote cells so my cell was not a 'first' cell. If Behe's cell contained designs for all subsequent biochemistry how come we Eukaryotes can't do all those clever things bacteria can do like 'fixing' Nitrogen or living off sulphur or crude oil? Perhaps the designer made a different cell for the bacteria or have we just failed to 'turn on' these systems!?
As for the clotting mechanism- I'm afraid my cell is not up to scratch there. My cell would have contained a gene for a proteolytic enzyme certainly- probably more than one, derived from a single ancestral gene, (different proteases clip proteins in different places so it's handy to have several) but they'd have a lot more evolving to do before they could be deployed as clotting system enzymes! But then Behe's cell would have a great advantage over mine- it popped into existence at the behest of the designer. My cell has to come from another cell or, conceivably, from a bacterial colony. Its genes must come from other genes, its proteins must be related to other proteins previously existing- in short I have to explain how they all got there.
One of the troubles for dedicated evolutionists is precisely that: in the end we come to the crunch question- how did it all start? Do we get back to some inorganic, replicating template molecule- a crystalline structure? Or can we find some credible way of providing the 'first' ribonucleotides? We have to wait and see. Meanwhile do we need some other hypothesis to cover our ignorance?
It seems to me that a thoroughgoing evolutionist has to believe in the inorganic origin of life i.e. the first organic molecules would have been assembled from the supply of inorganic substances in air, water and earth namely carbon dioxide, nitrogen (or ammonia if that was around) iron, silica etc. probably with sunlight as the energy source. What is the alternative? Organic molecules from outer space? A freak shot of lightning? A miracle? None of these explanations is very satisfactory and especially not the last one because if we allow that some 'divine spark' was available to start things off then equally we have to allow that he, she or it (the designer) might intervene at any other stage- even to make Behe's ludicrous cell.
Evolution- leaving aside mechanism for the
moment- is a matter of observation not of belief. Can
anyone go to the zoo, look an orangutan in the face and not say
to her/himself 'we're related!' or go to the natural history
museum, look at the 7 neck vertebrae of a dolphin squashed up
flat like dinner plates and the 7 neck vertebrae of the giraffe
elongated like posts and not say ' Aha! evolution ' or more
long-windedly 'yes, they're related by descent from a common
ancestor '. In this paper I have tried to show very briefly that
it is possible to have the same sort of reaction when studying
processes, microstructures, genes and proteins. There's plenty
still to elucidate at macro and micro level. Above all
until we've cracked the problem of the origin of life there will
always be a platform for Behe and his like.
Oh let us never, never doubt
what nobody is sure about.
May 1998
Please send any comments to: Clare Stevens