‘Jumping’ mechanisms for the origins of new genes
7. MASTER-CROOK MUTATION'S FAMILY
7.1 Identical-Twin-Brother Mutation Regulator-Gene
7.2 The Uncle of Duplication-to-Divergence
7.3 Uncle Transposon and the ‘jumping genes’
7.4 Uncle Virus Invasion
We have seen that point mutations are insufficient to make new genes or to bring about adoption. Hope now lies in more radical genetic changes, which may be able to do it. It is about time we made acquaintance with Mr. Mutation’s family.
We will start with his twin brother Mutation Regulator-Gene, because he is the most promising: he makes small mutations which effect enormous changes.
7.1 Identical-Twin-Brother Mutation
In Figure 1, there are two depictions of the head of a fruit fly. The photo on the left is normal. There are two antennas between the eyes. In the photo on the right, however, you see that two legs have grown in the place where the antennas would normally be. It seems that a mutation in one gene, Antennapedia, is responsible. At first glance, this is a spectacular example of evolution: very small genetic changes, which result in very big changes in appearance. It has been suggested that the fruit fly’s antennas are developed from what were previously legs mutations in regulator genes result in enormous changes in appearance
|Figure 1 Twin-Brother Mutation Regulator-Gene at work, Genetic analysis pp.747|
It can be even more striking. During the development from an egg cell through the larval stage to an adult fruit fly, the larva divides itself into various segments as can be seen in Figure 2.
|Figure 2.The segments of a fruit fly, |
Genetic analysis pp. 752
The T2 segment usually develops into the part to which the wings are attached; the T3 segment divides the front and back sections of the body from each other and contains the balancing rods that the fruit fly uses to fly straight. Three mutations in regulator genes can cause the T3 segment to develop as a T2 segment, so that a fruit fly comes into existence with four wings (see Figure 3)!
|Figure 3. A fruit fly with four wings,|
Genetic analysis, pp. 767
because of regulator mutations, a ‘wrong turn’ is made during growth
How is this possible? To understand this, it is necessary to understand something of the embryonic development from fertilized egg cell to adult fly. During that development, cells need to specialize. Some will end up in a wing, others will become back hairs, yet others will form the eyes, etc. How do these cells, which are constantly dividing and multiplying, know what they are supposed to become? During the very first cell divisions, all the cells are totipotent, which means that each cell can still grow into anything. As the growth progresses, differentiation arises. Groups of cells split off and such a group is destined to become, for example, segment T2. Within this group, cells split off again, for instance into one group that will make the wings and another that will make a leg. Within a leg, there is another division of labor. Some will make the foot, others the hair on the foot. Once a group of cells is split off, or differentiated, there is no way back, it can no longer do anything else but continue in the direction it is going and continue with the differentiation which belongs to that path.
Cells give each other signals, so that they know what their neighbors are doing. Partly by such means, they determine their position and certain groups of genes are turned on or off. Each cell has all the genetic information within itself (in the form of chromosomes in the cell nucleus) for the growth of the entire organism.
And what happens if a mutation occurs in such a regulator gene? Then a group of cells goes in the wrong direction. The growth plan is muddled. The group of cells that was supposed to make the antennas suddenly goes on with the genetic information for a leg, and they make a leg. Or, the group of cells that is supposed to make segment T3 suddenly thinks it has to make segment T2. Because the cells can communicate with each other, they still make everything fit neatly at the edges, so that it still becomes a living fly.
regulator mutations are changes within the existing genetic material
Twin Brother Mutation Regulator Gene is capable of considerable feats of prowess. He can muddle the entire body blueprint with large changes in appearance, but he is still not capable of going outside the banks of the ‘gene pool’, the existing genetic material which is already present. What Mutation Regulator-Gene does is a form of degeneration, of creating disorder where order used to be. The idea that antennae could have evolved from what previously were legs is absurd. If the genes that make an antenna were not present, they will not appear. If they are present, but are not used due to a mutation, and the genes for legs are used instead, that clearly has nothing to do with evolution or gene growth.
Furthermore, Mutation Regulator-Gene would, under normal circumstances (i.e. outside the laboratory), be deported by Angel Natural Selection immediately. Anyway, fruit flies without antennas or without balancing rods would not survive in nature.
Mutation Regulator-Gene is not responsible for macro-evolution. On the level of variation-within-a-species, Mutation Regulator-Gene could make the occasional change (think about the huge differences in build between kinds of dogs), but he is not married to Aunt Adoption. He does not bring new genes into the pool.
7.2 Uncle Duplication to Divergence
Gene duplication means that a gene is doubled. For instance, during recombination, a mistake is made, which gives one chromosome no gene and the other gets two. If a mutation occurs in one of the two genes, the other gene will still ensure proper functioning. In this way, a gene is, as it were, ‘freed’ in order to do something else. A mutation in this gene will not immediately result in the death of the organism or give it a serious disadvantage in the struggle for existence. It is ‘free’ to adopt a new function, and to be once more, whether subsequently or simultaneously, adopted by the community of genes.
Biologists have discovered ….. that genes may undergo duplication and divergence so tha t an extra copy of a gene arises by a mutational process. This duplicated copy is then free, in a sense, to evolve: while the original diploid set is still present to produce the phenotype and is still influenced by natural selection, the duplicated allele may have an altered base sequence and thus may yield new proteins with novel properties..Biology, pp. 1027
|figure 4, duplication and divergence
Biology, pp. 1027
gene duplication occurs
Let’s take a look at an example of such a gene duplication.
One example of a beneficial mutation comes from the mosquito Culex pipiens. In this organism, a gene that was involved with breaking down organophosphates - common insecticide ingredients -became duplicated. Progeny of the organism with this mutation quickly swept across the worldwide mosquito population. There are numerous examples of insects developing resistance to chemicals, especially DDT which was once heavily used in this country. And, most importantly, even though "good" mutations happen much less frequently than "bad" ones, organisms with "good" mutations thrive while organisms with "bad" ones die out.
Chris Colby, The Talk.Origins Archive, Introduction to evolutionary biology
gene duplication is still not adoption
Gene duplication does occur, at any rate, but does it occur on such a large scale with such regularity that it can be seen as a practical mechanism for macro-evolution? We will leave that for the moment. The question is whether this is an example of adoption? Not really. It is an example of duplication. A lot more than just duplication is necessary for adoption. Besides, as you probably know, bacteria and insects can lose their resistance if the product they are resistant to is no longer used. Why? Because a gene duplication like that is always a deviation from normal. The balance in which the gene in question functions tilts 200% to one side, and this substance is made twice as fast or in twice the quantity. As a result of the high selection pressure which rests on it (every mosquito without this double gene dies!), it appears to bring great benefits, but under normal conditions it is probably a disadvantage (because they break down organic phosphates much faster than normal; the balance is disturbed). So the mosquitoes which survived and did not have that double gene slowly begin to regain the upper hand, which in the long run means that the species loses its resistance. However, such duplication could be permanent if all the other fellow members of the species had died out.
divergence’ does not lead to adoption
Because duplication is absolutely not adoption, the main feature must be in divergence. Divergence literally means ‘to split up’. The duplicated gene mutates away from the original gene. It starts moving away. But where to?
Suppose the entire mosquito community, as a result of the complete extinction of the original mosquitoes, inherits that double gene. On a sunny summer day, a mosquito is sitting on a reed sunbathing and, oops, a mutation happens in a gamete which causes the second gene to change. Offspring come into existence with a duplicated, moving-away, freely-mutating gene. But how can this gene now adopt a new function? As soon as it loses its original function, breaking down organic phosphates, all selection pressure on this second gene disappears (given that they have stopped using the pesticide; by the way, this is also a way in which the mosquitoes lose their resistance again!) If the gene has lost its function, it becomes a dead gene and the mosquitoes are left with a strange piece of DNA in the chromosomes, and Master-Crook Mutation can do nothing further with it, because it has fallen into the hands of King Entropy!
In other words, Uncle Duplication does exist. If Uncle Duplication is done with his work, he sometime gets the nickname Divergence, because it is absolutely conceivable that mutations occur in the duplicated gene. But actually, that divergence is the work of Master-Crook Mutation (they have agreed to co-operate). And Master-Crook Mutation has just been proven powerless to make new complicated protein structures without selection pressure. The Uncle of Duplication-to-Divergence is NOT married to Aunt Adoption, because that divergence immediately involves loss of function, after which the protein is ripped to pieces by King Entropy’s dogs. Aunt Adoption and the Uncle of Duplication-to-Divergence can have no viable children. The Uncle of Duplication-to-Divergence is not capable of explaining structural gene growth and adoption.
7.3 Uncle Transposon and the ‘jumping genes’
In the 50’s, Barbara McClintock discovered the so-called ‘jumping genes’ in corn.
A pair of genes along the ninth chromosome, the Ac (activator) gene and the Ds (dissociation) gene (XXX), act in concert to turn on and off the genes that control color in the kernels. A signal from the Ac gene causes the Ds gene to jump to new positions along the chromosome, thus inactivating neighboring genes. This, in turn, causes abrupt changes in kernel pigmentation once the ears of corn develop.Biology, pp. 299.
This is surprising news. Genes which move around and turn other genes on and off. Are these Aunt Adoption’s children? How do these jumping genes work?
jumping genes are pieces of DNA which move themselves
The kernels of corn in Figure 5 show the results of these jumping genes. It appears to be a transposon, which is inserted into a gene which makes anthocyanine. This causes the kernel of corn to lose its original color and become yellow. During the development of the seeds, however, it can happen that the transposon disappears from the gene again (indicated by Ac), which allows anthocyanine to be produced again. Further growth of the kernel through cell division causes all the cells which come out of this cell with the good gene to get their color back. This results in the appearance of a pattern of speckles on the kernel of corn.
The three rows show kernels in which the transposon disappeared from the gene early (top), late (bottom) and somewhere in between (middle).
Figure 5. Uncle transposon at work in corn,
Cenetic analysis pp. 660
But what is a transposon? The name transposon comes from transposable or movable element.
Each transposon codes for the enzymes that specifically insert into the recipient DNA. This process has been described as illegitimate recombination because it requires no homology between donor and recipient DNAs. In contrast to general recombination, however, transpoition is a highly inefficient process: It occurs at a rate of only 10-7 to 10-4 events per generation. Biochemistry, pp. 1060.
A transposon is a specific piece of DNA that can be between 800 and 5,000 base pairs long. On the piece of DNA is a gene that codes for a protein which makes it possible for the transposon to settle elsewhere in the DNA. Nothing in DNA-country happens on its own. Everything is arranged by proteins (except for mutations). If a transposon wants to add itself to an existing piece of DNA, a protein is needed which cuts the host DNA and pastes the transposon in between and glues the edges neatly together again. Therefore, in a transposon, there is a gene that codes for that protein. The transposon also has a left and a right ‘hand’, two opposing pieces of DNA somewhere between 15 and 50 base pairs in length, which assist in copying and inserting the transposon. One mutation in these ‘hands’ causes the transposon to cease working. The place in the host DNA also has to have a certain sequence of bases if the transposon is going to be able to insert itself. Afterwards, a transposon also needs to do something more than just copy itself and place itself in another piece of DNA. It thus contains code for one or more genes.
A transposon is a highly specialized piece of DNA with at least the codes for two complete proteins 
jumping genes are genetic viruses from another species
What must have happened in the corn is that (by a virus from an aphid, or by one of its own regulation mechanisms gone awry?) it was infected by a transposon, which has nested in chromosome 9. It is not capable of doing much else than producing the protein, which arranges its own shifting of place, which does occasionally happen. The (most likely) mutilated piece of transposon, which however does still have intact ‘hands’, can end up in a few specific places in the chromosome, with exactly that sequence of bases which the Shifting protein needs. In the kernels of corn, you then see a certain ‘new’ characteristic never seen before. But the basis of this ‘new’ characteristic is not a ‘new’ improved protein. It is only a variation on what was already present. The corn has gotten a gene in its DNA -- it is a special uncle of Master-Crook Mutation – but it cannot do anything with it. It creates a controlled form of destruction! Uncle Transposon is a White-Collar Criminal! Because Uncle Transposon has, in this case, been kind enough to carry out his actions only in non-essential genes, the damage he causes remains limited. He is not married to Aunt Adoption. What Uncle Transposon does is a form of degeneration of the corn genome.
Controlling elements (or transposons, PMS) in corn can inactivate a gene in which they reside, cause chromosome breaks (!!, PMS) and transpose to new locations within the genome.
Genetic Analysis, pp. 660
The similar base sequences of many eukaryotic (plant- or animalcells, PMS) transposons, as yeast, corn, and fruit flies, and retroviral genomes (and their dissimilarity to bacterial transposons) suggest that these transposons are degenerate retroviruses….A retrotransposon may therefore be considered an “internal virus”.Biochemistry, pp. 1064, 1065
Because people are interested in just this kind of thing, they look for this, and such corn is artificially cultivated further. In free nature, where the Angel of Natural Selection rules, this corn would not survive. Humans, on the other hand, are capable of breaking loose from the strict laws of the Angel of Natural Selection, and applying un-natural selection.
jumping genes do not cause gene growth
Someone may say, But the corn ‘adopted’ these two genes. Still, that is in no way the kind of adoption which is meant, or is necessary for macro-evolution. In the first place, the corn has no use for a protein which constantly shifts pieces of its DNA, and that shifted piece is probably a dead gene, which can now only be shifted. This is not functional adoption, this is not a protein which takes the corn ‘leaps’ forward in its evolution. In which metabolic process is the protein adopted, other than that the Shifting gene is parasitic on the available means which are present (such as the Make-A-Copy protein which translates the gene)? Could this be the way in which one of the genes which is necessary for Darwin’s most primitive eye can be adopted? Are the genes which make a cell light-sensitive transported from one organism to another in this way? Of course not. This kind of transposon only codes for its own selfish functions.
7.4 Uncle Virus Invasion
What follows is the story of the P elements in fruit flies, possibly once inserted by a virus:
Gene flow between more distantly related species occurs infrequently. This is called horizontal transfer. One interesting case of this involves genetic elements called P elements. Margaret Kidwell found that P elements were transferred from some species in the Drosophila willistoni group to Drosophila melanogaster. These two species of fruit flies are distantly related and hybrids do not form. Their ranges do, however, overlap. The P elements were vectored into D. melanogaster via a parasitic mite that targets both these species. This mite punctures the exoskeleton of the flies and feeds on the "juices". Material, including DNA, from one fly can be transferred to another when the mite feeds. Since P elements actively move in the genome (they are themselves parasites of DNA), one incorporated itself into the genome of a melanogaster fly and subsequently spread through the species. Laboratory stocks of melanogaster caught prior to the 1940's lack of P elements. All natural populations today harbor them.  Chris Colby, The Talk.Origins Archive, Introduction to evolutionary biology
no new genes originate by virus invasions
After the story about the corn, this story speaks for itself, but it still surprises me. How is it that right-minded people come up with something like horizontal gene transfer? But then to also see that as a serious mechanism for the much-needed evolutionary variation across the borders of species?
I can find only one explanation for this: insufficient realization of the complex and specialized reality of proteins, insufficient realization that adoption, which is the ‘loving’ reception of a gene into the community of genes and the accompanying exact coding of the DNA, does not belong to the reality of proteins. If this is difficult to understand, think of Darwin’s most primitive eye, the Leapfrog protein, or the twelve genes for ‘light-sensitivity’: can transposons insert the genes for this eye? So that the infected organism would suddenly be able to see? Through mites and viruses? And if that absurdity were true, that still says absolutely nothing about how those genes originated (which is what this is all about), but only about how they were shifted.
Uncle Virus Invasion is the twin brother of Uncle Transposon, and Aunt Adoption is also not married to Uncle Virus Invasion. Aunt Adoption is a widow. Or is Aunt Adoption still a virgin? No, Aunt Adoption is a widow. She was married to the Uncle of Duplication-to-Divergence, but because they could not have viable children together, they got divorced. Uncle Transposon, together with Uncle Virus Invasion, raped her. Her genome has been violated. Both of these uncles have left her with a bastard child that she did not conceive herself, the transposon, which is a cuckoo’s egg: it kicks the other genes out of the nest.
And now? Aunt Adoption is bitter and disappointed. She was a nice woman. She dearly wanted children. But that did not happen. She had herself checked to see how that happened. And the results were surprising: it was genetically determined!
We have taken a look at the state of affairs in the evolutionary theory. Their proponents have been allowed to speak for themselves to indicate where we need to look. In the preceding material, I have named and gone over every (!) example from reality which they used and which I could find in the sources I had. If you think about the gigantic, complex genetic task which is necessary for Evolution to happen, the distinctly disappointing results of these examples, and the impossibility for proteins to take on the new specialized functions which are necessary for macro-evolution, only one conclusion remains: there is no macro-evolution. The Mutation family is capable of only two things, causing variation-on-the-same-genetic-theme and degeneration.
- Mutations in regulator genes cause great differences in external appearances which can bring about enormous variation within the existing genetic material and thus within the type. They do not add new information.
- The proposed mechanisms for punctuated macro-evolution cannot make adoption possible in any way, because they have no pre-prepared genes to insert which are neatly regulated and integrated into the rest of the genome. They only insert genetic material that comes from another species.
- The only way in which these genes from another species could then take on a function within this species is by accumulative gradual mutation, which has been shown (in the previous chapter) not to be able to cause adoption.
- There is therefore not one single concrete example of punctuated functional adoption known for new genes.
- The only correct conclusion is that adoption does not take place at all, with the possible exception of minimal functional alteration.
- Functional alteration is a form of degeneration.
- If adoption is structurally impossible, macro-evolution is not possible.