6. The distinction between different genes
Let us then take a closer look at an organism’s genes, to see what their ‘adoption-mountains’ look like, and if their structure allows changing to another function.
there are essential genes
Genes can be divided into three groups. There are genes which are so essential to the organism’s development into an adult individual capable of reproducing itself that that gene must not die. If Master Crook Mutation is able to pull such a gene across the border to the Valley of Dead Genes, not only does the gene die, but the carrier of the gene dies. In practice, this means for instance that the embryo does not develop and a spontaneous abortion occurs, or that the individual dies of its genetic defect before it is able to reproduce itself. This kind of genes we will call essential genes, in the sense that they are essential to the viability. An example of such a gene is for instance our Leapfrog protein (in reality it is called Topoisomerase), or Make-A-Model protein and the suchlike. Without proteins like that, an embryo cannot live or develop.
there are ‘tolerant’ genes
On the other hand, there are genes which, when lost or mutated, do not immediately result in the death of the carrier, but do make the individual weaker. There are many examples of this kind. Many hereditary diseases fall into this category, such as hemophilia (blood does not clot after an injury, which can cause the carrier to bleed to death). All the genes needed for sight will be in this group. If they are not functional, the embryo will develop, but the carrier is then blind.
I will call these genes tolerant genes; the organism can tolerate elimination of these genes, but is not ‘happy’ with it, has a (serious) handicap as a result.
There are neutral genes
they are primarily genes which determine hair, colouring, markings, and such appearance-based characteristics, neutral genes.It is especially the turning on or off of the neutral genes, and the combinations there of, which cause the variety from which natural selection can choose, but that is covered extensively in chapter 13.
NOTICE that in this division, we are talking about viability and not about chances of survival. This is about whether or not a gene is necessary at all for an organism to be alive, not about how big its chances of survival are once it is alive. So, in very concrete terms: essential genes are all the genes whose functionality absolutely must be present for an organism to be born alive and be able to reproduce itself. In addition, there are many genes necessary to stay alive and to survive. Insofar as those genes are different from the genes necessary to be born alive and/or reproduce oneself, by definition they do not belong to the genes essential for life. Natural selection can for example easily select for neutral genes, or combinations thereof, which could make them essential to survive, but that is not what I mean here. Even if those neutral genes are essential in order to survive, they are still not essential for viability.
We get the following overview:
||loss of function means
||handicap but vaibility
||no consequenses for the viability
|Table 1, the division of genes into categories|
The line between the different categories will not always be clear in practice, just like any division or categorisation. There will always be borderline cases where the division is less clear, but that does not detract from the usefulness or even necessity of this distinction. It is actually much more dangerous to make no distinction at all, because principles which might apply to neutral genes will then be applied to essential genes without exception.
essential genes cannot evolve
Essential genes cannot evolve! As soon as a mutation in an essential gene is such that its (original) functionality is lost, that means that no viable or even living individual will be born! Perhaps essential genes in certain places which hardly make a significant contribution to the functionality (but maybe only to the structure) do permit mutations; however, as soon as mutations begin to affect the essence of the function, it goes wrong. In other words, essential genes cannot evolve at all! Essential genes are of course surrounded by the cliffs which lead to Dead Gene Valley. As soon as they lose their original function, while they are already mutating towards another function, at a certain point in time life is no longer possible for the embryo.
Take for example hemoglobin, which transports oxygen through the blood. This gene can never ever do anything other than transporting oxygen in the blood, or life cannot continue. The ‘function-acquiring’ mutation is not an option for essential genes.
So, for clarity’s sake I will repeat it:
Essential genes cannot evolve to another functionality.
Perhaps (some) essential genes are susceptible to (multiple) mutations, but that can never go so far that the original function is lost. In this way, (at least) three mutant versions of hemoglobin are known, of which two make no difference and the third causes a serious illness, sickle-cell anemia (which will be discussed in chapter 11).In other words, genes which are essential to life live on the Mount of Isolation no matter what! Perhaps they have some freedom of movement there, but the cliffs are inevitably all around them (see figure 6).
This raises two questions.
1. Then how did these genes originate? Were they at some point in time non-essential genes which became essential genes? Has evolution then in essence, meaning in the essential genes, stopped?
2. Are the genes which fill the same functions in non-related species the same or different? If they are the same, there is no problem. Then all life must have received these genes from each other in some way. If they differ from each other and cannot be derived from each other, then there can have been no evolution between them.
In order to answer question 1, first an example is given in point 7 of a protein which cannot possibly have descended from predecessors. Next, in point 8, is a search to see whether or not more proteins like that exist. Question 2 is finally answered in point 9.
7.The Leapfrog protein is an essential protein which could not have evolved
The Leapfrog protein (see paragraph 6.3) is a concrete example of an essential robot-protein, which cannot possibly originate from predecessors of that protein by ‘function-acquiring mutations’. It is an essential gene – without it there will be no viable individuals – which means that it lives on the Mount of Isolation and is surrounded by the sheer drop of non-functionality. And it cannot have originated from a non-essential predecessor. It is the Lone Ranger we seek…
The Leapfrog protein is so specialised and dedicated to its task that it must fulfil several functions to be functional at all. These are those minimal functions:
1. It needs to attach itself to a strand of DNA on two sides.
2. It needs to be capable of cutting through that strand of DNA.
3. It needs to be able to hinge after cutting.
4. It needs to allow a second DNA strand inside or even to go and get it.
5. It needs to recognise that a strand of DNA is encircled.
6. In reaction to that recognition, it needs to be able to close.
7. It then needs to be able to glue the cut DNA back together again.
8. After that, it needs to be able to open without cutting the cut DNA again.
9. It needs to release or even remove the second strand of DNA.
10. It needs to recognise when the second DNA strand has disappeared.
11. It needs to release the first DNA strand.
The Leapfrog protein needs to be able to fulfil each of these functions. If one of them is missing, it means that it does not function at all. Each of these functions needs to be present from the beginning. Almost every one of these functions is a biochemical reaction which costs energy. For each of these functions, a specific combination of amino acids is required which is capable of fulfilling this function. If these combinations are not in very specific places in the protein, of course the protein also cannot function.
The Leapfrog protein is a hugely complex, specialised, dedicated, precise, integrated, adjusted robot-protein, with more than ten specific functions, all of which it must fulfil in order to be functional at all.
However, beyond this specialisation, there is another simple fact which shows that the Leapfrog protein could not have had predecessors: it needs to be at least big enough to encircle a strand of DNA! A hypothetical predecessor of the Leapfrog protein that was not capable of encircling a DNA strand would certainly not have that function at all, 100%! Even if many forms of the Leapfrog protein were to exist which could have been derived from each other by mutations, not a one would be able to function if it were not at least capable of encircling a strand of DNA. If that were not possible, it would have to release the cut strand of DNA in order to allow another DNA strand to pass through. That means that it is very much in doubt whether it can find that end that it released or that then any other loose end could be attached to it (there are always more than one of the same kind of protein active at the same time). Considering the loss of information, this can never be permitted. Thousands of mistakes would be made with every cell division, which simply means that no cell division is possible. Natural selection would send an organism which handles the DNA in such a destructive way directly to hell!
Graph 4 shows that the functionality (or complexity) is null up to the point in time that a strand of DNA can be encircled; from that point onwards. the functionality/complexity could (theoretically) increase.
Whichever way you look at it, the Leapfrog protein has no beginning. It has to be present all at once or it does not work. Because the Leapfrog protein is such a large protein, it has to be made up of many hundreds to even thousands of amino acids (I could not find the exact number anywhere). This ‘beginning’ could therefore also not possibly have originated ‘coincidentally’.
the Leapfrog protein cannot have originated by ‘function-acquiring mutation’ (compare graphs at point 5)
In short, the Leapfrog protein did not evolve. The Leapfrog protein is our Lone Ranger. The Leapfrog protein shows that Darwin’s idea of evolution is a genetic impossibility:
If it could be demonstrated that any complex organ ( or gene! PMS) existed, which could not possibly have been formed by numerous, successive, slight modifications, my theory would absolutely break down.Charles Darwin, The Origin of Species
point mutations cannot elongate proteins
The above example, by the way, shows a serious lack in mutation in a surprising way: it actually cannot make proteins any longer than they already are!
The Leapfrog protein (or a possible predecessor) can never have received its complex, specialised function all at once by sheer coincidence. The only alternative (apart from the problems discussed before) would be a step-by-step increase in the length of the arms. A too sudden arbitrary change would mean loss of function and condemnation by the Angel of Natural Selection.
The point now is this: How can a protein become longer? Not by inserting base pairs, because in an insertion one base pair is added, which makes that entire code move over one base pair, and all information is lost (see chapter 4.4). And insertions do not happen in groups of three! Insertions, just like deletions of course, drop out.
A point mutation, however, changes only an existing amino acid. The only way in which a protein would be able to grow longer is therefore by a few point mutations on a multiple of three base pairs, after the stop sign, which causes a new stop sign to arise. Afterwards, the original stop sign must change into an amino acid by mutation.
There are a few problems with this:
- There is another reason to understand that the Leapfrog protein could not have originated from more simple predecessors.
- Master-Crook Mutation needs to be written off as a mechanism for gene growth. Because of his volatile disposition, he cannot usefully elongate proteins. Once two functional parts are definitely established on a location about, say, 30 amino acids apart, he can no longer possibly put anything in between. The longer the arbitrary piece is that he sticks in somewhere by changing the stop codon, the more nonsense it will contain, and the greater the chance that it will become a useless protein. The smaller the piece he sticks in, the less probable it is that it occurs regularly (one arbitrary mutation is possible, but to have it repeatedly three or four times at specific locations with specific results is too much to ask).
8. The greater part of the genes does not vary at all!
The important question now is whether Lone Ranger Leapfrog protein is a lonely exception, or whether there are more of that kind of genes, which are surrounded by precipices, genes to which no paths lead?
The answer is yes. Far from all genetic information is known even about humans, but there are probably many examples of this kind of protein to be found, which will be found in the coming years. That can be derived from an interesting fact from population genetics.
Considerable variation is present in natural populations. At 45 percent of loci in plants there is more than one allele in the gene pool. [allele: alternate version of a gene (created by mutation)] Any given plant is likely to be heterozygous at about 15 percent of its loci. Levels of genetic variation in animals range from roughly 15% of loci having more than one allele (polymorphic) in birds, to over 50% of loci being polymorphic in insects. Mammals and reptiles are polymorphic at about 20% of their loci - - amphibians and fish are polymorphic at around 30% of their loci. In most populations, there are enough loci and enough different alleles that every individual, identical twins excepted, has a unique combination of alleles.Chris Colby, The Talk.Origins Archive, Introduction to evolutionary biology.
About one-third of structural-gene loci are polymorfhic, and the average heterozygostity in a population over all loci sampled is about 10 percent. This means that scanning the genome in virtually any species would show that about 1 in every 10 loci is in heterozygous condition and that about one-third of all loci have two or more alleles segregating in any population.Genetic analysis, pp. 784.
In populations of the fruit fly Drosophila, the gene pool typically has two or more alleles for about 30% of the loci examined, and each fly is heterozygous at about 12% of its loci…
The extent of genetic variation in human populations, is comparable.Biology, Campbell, pp. 426.
No variation has been discovered in mammals in at least 67% (80% for Chris Colby, and 70% for Campbell) of the genes. I repeat: in mammals, in any case more than 65% of the genes show no variation. That is unbelievable! How is that possible?
|Figure 10. The biggest part of the genoom of each |
There are species which, according to scientists, have not changed at all in millions of years, such as for instance sharks. In those millions of years, a mutation has occurred often enough on every location in the genome. Humans, for instance, have 3 billion base pairs and there are 6 billion people, and on average there is probably 1 mutation in each person. Over a period of millions of years, that means that mutations have simply happened everywhere. But then why are two-thirds of the genes still the same? The answer is, of course: by selection! One amino acids sequence was chosen above another, was ‘more suitable’. Then, by selection, that sequence of amino acids was maintained. If mutations recurred that had the same effect, that was also so disadvantageous that either the individual could not live, or it could not survive.
But what does that tell us about the functioning of the proteins that belong to those two-thirds of the genes?
That one single change in amino acids can have such far-reaching effects on the functioning of that protein that selection can take place for it. Once more, but slightly differently: one change in an amino acid already changes the functioning of that gene in such a drastic way that it can no longer fulfil its original function at all, or at the very least more than insufficiently. If a change in amino acids should almost not or barely influence the functioning of the protein, no selection could take place for it and then one amino acid sequence would not be chosen over another. Now that that does happen, that simply means that these genes do not permit any change at all. Their functioning is so specialised, so critical, so dependent on the exact sequence of amino acids, that they permit no change at all, because that would mean the loss of the entire function to such an extent that the carrier of the mutated gene cannot live or cannot survive.
These genes have natural variation because the Angel of Natural Selection is unfeeling. It pushes the protein off the cliff after one mutation that makes a difference. The protein dies immediately after one single alteration. The protein loses its entire functionality. And with the dead protein, the organism itself also dies before it is capable of passing on the mutated genes to the offspring. And that is why variation does not occur in those genes (as far as the amino acid sequence of the protein).
And guys, we are not talking about one single gene here, about a lone exception. No, 67%. More than half! The greater part! Bingo!
|Figure 11, Adoptive landscape of essential genes|
Those proteins are prisoners of the Angel of Natural Selection. They have absolutely no freedom of movement. They are sitting on lonely, towering peaks without any connection to anywhere at all. Below the peak wait the dogs of King Entropy, and on top, the Angel of Natural Selection keeps them in seclusion. No variation. Not a step to the left or the right, or any of the hundred possible directions. No hidden path through a few fog banks. Not a single minimal infinitesimal change. They are grounded. They have to stay where they are. Master-Crook Mutation can do nothing. Every action he makes is immediately punished. His back is to the wall. In these non-variable genes, he apparently has no right to speak at all! This means that these gees could not have originated by a gradual accumulation of function changes. Or, in proper English: they cannot evolve and they did not evolve. They did not originate through evolution. Two-thirds of the genes do not evolve.
Hey, Charles. Two-thirds of the genes do not evolve!
If there is no other mechanism for the sudden origin of genes, this in itself is sufficient to conclude that macro-evolution is a genetic impossibility. Molecular evolution concerns at most the rest of the genes, for which some things may be possible.
we have been misled by Master-Crook Mutation
It seems that Master-Crook Mutation has pulled the wool over our eyes! Not that he does not exist! Not that he is not ca[able of anything! But he has managed to sketch for us a friendly image of the protein landscape where everyone likes everyone and where proteins, already mutating, visit each other and change function and form, where a protein does get lost every once in a while, but is then kindly taken away by the Angel of Natural Selection to have tea with King Entropy. The harsh reality is evidently completely different. We will bring another charge against Master-Crook Mutation!
there is still an alternative explanation
There is still an alternative explanation for the non-variability of most gene, which, however, testifies just as strongly against the macro-evolution idea as the previous one. That alternative is that they do permit mutations, but that there simply has not been enough time for that to happen. Or in other words, in humanity’s case: the total human population descended fairly recently (say a few thousand years ago) from a human Adam and Eve, from whom we have thus received exact copies of their original genes. In that relatively short period of time, all the possible neutral mutations have not yet been able to spread throughout the entire world population.
Still, in my opinion, this could only account for a part of the non-variability. Even in ten thousand years, mutations could occur in all locations over the whole genome. Perhaps these mutations did not spread throughout the entire world population, but if you looked around a bit, you should be able to find them all. That is apparently not the case. 80% of genes in humans are required to be the same.
At the moment that it is evident that all the gene that are now non-variable do permit mutation to some degree, the fact that it is now not the case is, of course, just as final an argument against an evolution millions of years in length, as when it is evident that these genes do indeed not permit one single change in amino acid. For instance, sharks have been supposed not to have changed at all over millions of years. In that time, all the possible changes that make little to no difference should be criss-crossing the shark population, because one will never be selected over the other. Naturally, a certain gene can, by coincidence, disappear from the population entirely with a neutral mutation (because it is not passed on), but that cannot work for two-thirds of the genes after a few million years, because mutations occur again and again, at the same locations.
There are therefore two possibilities:
- The proteins turn out to permit changes in amino acids. Then the species (and all life therefore) just has not existed as long as has been assumed.
- The proteins do not permit changes in amino acids, because one single change means the loss of the entire function. In that case, they could not have originated by ‘functional change’. They are surrounded on all sides by the precipices of loss of function.
In practice, both will probably turn out to be true. The relationship between the two dos not matter. In one case, evolution did not happen. In the other case, evolution could not have happened! In the rest of this chapter, I will assume that neither one of the two possibilities is solely responsible for the non-variability of most genes, and that there are thus many genes which do not permit any change at all.
9.Essential genes can differ greatly between non-related species
One important question, which has been posed before, is this: do the genes differ (significantly) between non-related species. That question is important, because if the genes that do not allow any change at all are the same in non-related species, then that means that evolution between non-related species is possible after all.But, unfortunately, that is not the case. The genes are different. There are of course many genes which are not different, but it can be clear that a jellyfish does not have the genes that a human has, even though a number will correspond (both are made up of cells and have DNA, just to name a few).
An extremely interesting group of very essential genes, which will permit no or little change, but do differ greatly and cannot have been derived from each other, are the gender-determining genes. These genes are surrounded on all sides by the precipices of non-functionality, because they are essential in their own way: without them there is no gender (or at the most one, which is then usually not fertile) and therefore no reproduction. Then they have influence over tens or hundreds of other genes which determine the difference in gender. If the gender-determining gene has changed, all those other genes must change simultaneously, which is genetically impossible. Therefore, in practice they will permit very little change. And they differ between non-related species. The gender-determining gene in fruit flies is a so-called RNA-binding-cutting protein, and in humans it is a DNA-binding-translating protein. In chapter 15, I give an extensive description of these genes and of other gender-determining systems.
non-related species are not descended from each other
The fact that essential genes cannot really change, combined with the fact that most genes do not permit any change at all, shows that in essence, in other words in those non-variable and essential genes, a species does not change. That means that it stays the same type. (Within that type, very diverse variation is possible and new variation can arise. See part II, chapters 13, 14, and 15.)
On the other hand, genes can differ greatly between non-related species, such as the gender-determining genes. These three facts thus show that non-related species are not descended from common ancestors:
Proteins can differ greatly between non-related species.There are therefore two possibilities:
- Essential genes cannot evolve past their own functionality
- Many (essential) protein do not vary at all.
- The proteins turn out to permit changes in amino acids.
|Figure 12.Each animal has (among other kinds) essential genes, which do not permit mutations (green), tolerant genes which result in a hereditary disease or handicap when lost or damaged (brown), and neutral genes which are by their very nature cause variation (red).|
|Cytochrome c differs between non-related species|
In 38 species, research has been done on cytochrome c, and it turns out that each species has a different version of that protein. With humans and Rhesus monkeys, it is a difference of one amino acid, with horses twelve, kangaroos ten and baking yeast forty-five. Cytochrome c is a small protein of 104 amino acids, which plays a part in electron transport in mitochondria and can therefore be called essential: without it, the carrier cannot live. An interesting question is now: is cytochrome c one of the proteins which permits no change at all? The only way to find out 100% for sure would be to test each possibility within every species. That confronts practical problems. What can be said about cytochrome c, however, is that (even if one single change in amino acid might be possible) it cannot have evolved right through all the species and left each species with its ‘own’ version. And that is because of the teamwork of the genes.
We have already discussed the fact that a protein often needs a key to function, or a keyhole and/or a kind of ID. Such a ‘password’ has to link up precisely with other proteins with which it works. One mutation in cytochrome c (to the extent that it does not immediately incapacitate the protein) means that simultaneously, various other protein must mutate in such a way that all the keys and locks still fit! Or, in other words, the entire metabolic pathway in which cytochrome c functions has to be reprogrammed by simultaneous, arbitrary mutations, which are attuned to each other! Donald Voet writes in Biochemistry:Cytochrome c is a rather small protein that, in carrying out its biological function, must interact with large protein complexes over much of its surface area. Any mutational change to cytoscrome c will, most likely, affect these interactions unless, of course, the complexes simultaneously mutate to accommodate the change, a very unlikely occurrence. (Italics by PMS) Biochemistry, pp. 128.
If you then take the frequency of mutation which follows from that into account, it follows that, in the arbitrary practice of life, that is impossible. In humans, each gene has a chance of mutation somewhere between 10-4 and 10-9. The chance that two mutations happen simultaneously, one in cytochrome c and the other in the larger protein complex with which it has to react is an average of 10-4 x 10-9 = 10-13.The fact that a protein like cytochrome c differs between non-related species, but is the same within one species, shows that the non-related species do not have a common ancestry. The point of the different versions of cytochrome c is that they all do the same thing: transport electrons. Natural selection can thus never choose one version over another, because they all do exactly the same thing. A term has also been thought up for that: neutral drift. But it is then strange that different versions of cytochrome c are not also found within the same species (such as perhaps the sharks, which have not changed in millions of years)! It could be called extraordinarily coincidental, if not to say miraculous, that these neutral changes always and only take place around the diverging of two species. What does that indicate? Either the non-related species have no common ancestry and each species received their own variant of cytochrome c, which then theoretically (or by genetic manipulation) could change. Or cytochrome c, in combination with the protein with which it reacts, does not permit any mutations, which means that the non-related species do not have a common ancestry. (This was concluded earlier, but now we see it confirmed in practice.)
The chance that the mutation in cytochrome c (104 amino acids in humans) is on the location where the interaction with the larger protein is, say, 1 in 10; in the larger protein, say, 2,000 amino acids, it is 1 in 200. This makes the total chance approximately 1 in 1017.
If a third mutation is necessary to let the keys fit, the total chance is about 1 in 1026. So many living creatures have not even existed in 5 billion years!
A contradiction for this could be this: you should not calculate the chance of a certain coincidental occurrence afterwards. If you were to throw a series of 100 dice, the chance afterwards if have thrown it is always 6100, but that particular series still resulted. Such a ‘calculation of chances’ therefore no longer matters.
Still, it does matter. In the series of dice, every possibility is good. If only half of the possibilities were good and you throw a good series, the chance of that was 50%. If only one combination was good and you throw that, the chances were, even afterwards, 6100. In this case (and in all other cases in which proteins react with each other, in other words most of the time!) only one, maybe two, maybe three specific countermutations are possible at the exact moment that the other mutations also happen, because otherwise the keys would no longer fit. Even now, beforehand, the chance that three simultaneous mutations in cytochrome c & co. happen in such a way that the keys continue to fit is 1 in 1026, or if there are perhaps ten or one hundred possibilities for permanent keys that fit, 1 in 1024. The precisely attuned teamwork of the genes requires that an entire, specific, non-damaging path is travelled. If evolutionists claim that such paths have been travelled, it is quite possible to ask yourself ‘afterwards’ if that was actually possible.
10.The Evolution Mountain Range
In the immeasurable plains of non-functional protein country, there is a mountain range with all sorts of peaks and paths and plains and everything we would want it to have. There, Master-Crook Mutation can do what he wants to. There he works together with the Angel of Natural Selection to create the most beautiful, well-formed proteins. Above the mist which divides the peaks of those mountains, called the Evolution Mountain Range, from the realm of the dead, the sun shines, the grass is green, it is lovely to linger. And yet, inevitably, the distance to another mountain is immeasurably great. If you don’t think about those other lonely peaks, you can dream that the life of the proteins is like this everywhere, like here on the Evolution Mountain Range, where the Angel of Natural Selection has built its castle. He even gives guided tours to tourists and Master-Crook Mutation assures everyone that it is like this everywhere and that there is a path from the Evolution Mountain Range to every other protein and that there are so many proteins that they cannot see all the paths anyway and that the mist which hangs around the border with the kingdom of the dead hides secret passageways and underground tunnels, along which mutating proteins can go to avoid the inexorable clutches of King Entropy. And he says to the visitors, “That can’t be true, can it? That there are no paths anywhere? Look, here one is, right in front of me! Did you see it?’, and everyone laughs.
Because Master-Crook Mutation is so good at his trade and because the reality of proteins is so complex and therefore he probably knows what he’s doing, and... because we want it to be true, that’s why we believe him.
11. A bone to pick with E. coli.
We still have a bone to pick with E. coli. (see the beginning of paragraph 6.4.2), concerning the function-altering mutation. I will line up why it is not a case of adoption.
a) It is a case of mild functional change, not of adoption of a new function, or in other words, this is at most some manoeuvring on a remote plateau.
b) A cross-section of the adoptive landscape of the protein looks like this:
|Figure 13. mutation sensitivity for the ebg gene of E. coli(a cross-section of the adoptive mountain)|
c) There were three non-arbitrary (because they were carried out by B. Hall) mutations necessary to bring about the change in the protein. If this were to happen in nature, the protein would be a dead protein after one change and the selection pressure would have disappeared. But it is possible that Fool Coincidence could have managed to fool King Entropy...
d) Because no clear function was known for that gene, could it have been a duplicated lac-gene that was already dead?
e) There was absolutely no question of metabolic adoption, because the regulator gene was emphatically eliminated. For metabolic adoption (which means: not eliminated, but regulation attuned to the new function), many subsequent mutations would be necessary, all without selection pressure, and therefore, the gene would be under the power of King Entropy.
f) Such a suspicious way of ‘changing function’ cannot be representative of the large-scale structural changes necessary for macro-evolution or gene growth. This is ‘messing about in the genetic margins’ of a species. This is not a mechanism by which the genes for Darwin’s most primitive eye will originate.
g) Because bacteria and moulds are exceptionally simple organisms, the possibilities for the origins of derivative proteins are greater than in higher plants and animals.
It could be possible that, in living nature, a gene with a derivative function does originate in this way, which has survival chance under high selection pressure. Still, this cannot explain the origins of dedicated, specialised, precisely regulated (groups of) genes working together.
6.4.3 Metabolic adoption
So far, we have only discussed functional adoption through gradual change, which means the origin of some genes and protein improvement. We have seen that, in some cases, a mild functional change is possible, but that protein specialisation in many cases means that there is no path at all that they can walk to have descended from predecessors, or to ‘grow’ to another function. Metabolic adoption actually comes right on top of functional adoption. If functional change takes place, metabolic change must take place simultaneously. A multiple of functional adoption is necessary for metabolic adoption, because this always involves several genes. If functional adoption is not possible, metabolic adoption, the origins of new groups of co-operating genes which are dependent on each other, a complete impossibility! The twelve genes which are necessary to make a cell light-sensitive in Darwin’s most primitive eye are an example of that. The ‘leap’ to the function of a single protein has already been proven to be too big in a number of cases, let alone the jump to twelve co-operating genes.
there is a certain tolerance
enes permit mutations which influence their function, or in other words that there is a plateau on which they can move around, shows that there is not only a refined degree of attunement between all genes, but also a certain tolerance. The problem with evolutionists is that they raise this kind of exceptions to the level of a rule of the vehicle that brought evolution in our country.
All the parts in the engine of my automobile together form just such a refined mechanism, in tune with each other, as gene teamwork. Small alterations in the functioning of engine parts do not necessarily have to mean that the engine no longer runs at all, although it is possible. That depends on how important that part is and how drastic the alteration is. However, if the alterations accumulate, in the long run the engine will perform less well, until at a certain point in time it no longer works. Small alterations which do not immediately immobilise the entire functioning exist by the grace of an already working, well-tuned whole.
Now an engine is not a living organism and is made up not of twenty but of many more parts (a protein is not actually alive either, it is only a molecule). But this is about understanding the comparison with the term tolerance. However, if the small alterations accumulate, in the long run, such a ‘worn-out’, no longer well-tuned whole that it is question of a degenerated species!
However, it can be clear meanwhile that this kind of ‘fraud’ in the DNA by mutations is absolutely insufficient to explain structural gene growth, adoption and evolution.
To propose and argue that mutations even in tandem with ‘natural selection’ are the root-causes for 6,000,000 viable, enormously complex species, is to mock logic, deny the weight of evidence, and reject the fundamentals of mathematical probability.I.L. Cohen, Darwin was wrong: A study in probabilities, pp. 81.(quoted from Acces Research Netwerk at www.arn.org)
another amino letter game
A parallel or comparison which goes very well with base pair and amino acid changes is our amino letter game. There are also about 20 letters and the relation between useful and useless combinations is very much to the benefit of the amino letters. In order to approach reality more closely, we will make it more difficult. This is the sentence:
But now, on the basis of the table in chapter 4.4 with the ‘genetic’ code, we get a nice strand of DNA:
[ATG TAC TGG GCG TGG GGC CGC ACA ACG GGG CAT TCC CTT TTT GAA
CGA AGA TCT CGG AGT ATT AGG AAA CGG GTG GGC CAT ACG CGG GGT
TCT ACT TGG GCG GCC TGG TCA GGC AGA TAC GTG AGG TGG TTA CGA
GAG AGG GTT GGG CAT AAT CGC ATA CTT ATG TTT AAA CGT ATT ACA
ACA GCT ATG AGG TCT GTT CGC CCT ATA AGA TCT AAT CGT AGC GCT
TAC GTT ATC CGG TAT CCT GGT GAG GAG CGA CCT AGG GAG TAC AAA
CGC CGG CCC AAT AGG GAA CGT TCA CGG AGT TGG AAT CTC CGT TCC
CTT TCA TGG ACC TGG GCT GCA TCC TGA AGC TAG CGC CTC AGA CTG
CCA TCG GTA GTC GGG CAC CTA CGG CTC AAA GAA CTA ACG TTC GCG
CCA GTG GAT GCA GTC AAC AGC ACA CTC TGA CGG GTG GGG CTA
According to the principle of arbitrary-mutations-plus-non-arbitrary-selection, one base pair can be changed each time. (One base pair can also be removed or added, but that will definitely not result in anything.) If that change results in a ‘good’ English sentence, which my publisher would not correct if I had written it here (imagining the spaces), then that means that the sentence is still ‘functional’ and can be selected. In this way, a ‘path’ needs to be created from this sentence (or ‘peak’) to an arbitrary different sentence (or ‘peak’) which has a totally different ‘function’, so it says something completely different than what it now says. That sentence must be specialised in the same way and as dedicated as this first sentence right up to the period: every word has to contribute to the meaning of the sentence. Other than that, the s can be used for the z and the v for the w (because there are only 20 letters; this only gives more possibilities to find a path) and we will not be too picky about spelling.
The reader will discover that such a ‘protein’ is not very tolerant of ‘mutations’, or in other words: there is not much to select.
That doesn’t make this game much fun, so let’s just assume that this protein is not essential and that is does not work precisely with other genes and therefore can contain as many grammar mistakes as is possible! However, with this qualification: my publisher has to be able to read the sentence and correct every grammar mistake so that he ‘understands’ what it says (in the co-operation of proteins, they also have to ‘understand’ each other or they cannot work together).
The reader will notice that there may be some variation possible now, but that changing it into another functional sentence does not work. And that while there are hundreds or thousands of possible sentences with about one hundred letters, many more than there are useful proteins with 100 amino acids! How is that possible? Because the number of useless combinations of letters is infinitely greater than the useful ones, so that the above sentence is ‘surrounded’ by precipices of uselessness and ‘dead sentences’, into which it falls one a few ‘mutations’ accumulate.
Master-Crook Mutation is not capable of causing the structural gene growth and adoption necessary for macro-evolution. Perhaps his family is capable of it, or that he can make beautiful new robot-proteins in co-operation with his family. That is also the subject of the next chapter.
List of difficult words:
A gene that codes for a protein.
A gene that regulates a structural gene, turns it on and off.
A gene that no longer codes for a protein or fulfils a useful function.
The sequence of amino acids in a certain protein.
the biochemical process in which proteins and other molecules work on and with each other.
Taking up or adopting new genes into the genome of an organism or even a species, which essentially contributes to the functioning of the organism, so that gene growth and an increase in complexity is possible.
The adoption by a structural gene of a new function, different from the old, by any mechanism. In practice, this means a change in the DNA code for the protein.
Taking up or adopting a structural gene that has undergone functional adoption, including the whole gamut of regulating genes, into the gene teamwork. Regulator genes, promotors and repressors can be involved in that, as can necessary changes further up the metabolic ladder.
Functional and/or metabolic adoption by means of accumulative mutations which continually minimally changed the original function. By gradual adoption, a gene grows, as it were, to a new function it did not have at first.
Adoption in one generation of one or more genes with new function.
Schematic representation of the lower boundary at which a protein has lost its functionality completely, becomes a dead gene, and/or has a connection above the selection border to another functional protein.
The border at which a protein becomes a dead protein, which means that there is no longer (indirect) selection pressure on the protein sequence.
There are multiple alleles of one gene in a population.
The exact location of a gene on a chromosome.
Micromutations do occur, but the theory that these alone can account for evolutionary change is either falsified, or else it is an unfalsifiable, hence metaphysical theory. I suppose that nobody will deny that it is a great misfortune if an entire branch of science becomes addicted to a false theory.But this is what has happened in biology; ...I believe that one day the Darwinian myth will be ranked the greatest deceit in the history of science. When this happens many people will pose the question: How did this ever happen? …S.Lovtrup, Darwinism: The refutation of a myth, pp. 422.
(quoted from Acces Research Netwerk at www.arn.org)