Wednesday, June 29, 2005

Random Mutation and Natural Selection

A common argument from the anti-evolution crowd is that random mutation plus natural selection cannot result in the complexity of life we observe on earth. This, of course, ignores all of the other evolutionary forces that work on natural populations and represents a general ignorance of the modern theory of evolution. Furthermore, some people are unclear as to what biologists mean when referring to random mutations. In this post I explain the statistical definition of random, some different classes of mutations, and the random nature of genetic mutations.

1. What it means to be random
In order to understand the statistical meaning of random one must first have some familiarity with probability. Probability is just a mathematical way of describing how likely a certain event will occur relative to all alternative events. For example, there are two possible outcomes when flipping a coin: heads and tails. Assuming the coin is fair (i.e., heads and tails are equally likely), we have a 50% chance of flipping heads and a 50% chance of flipping heads. Another way to describe this is the probability of heads is 0.5 and the probability of tails is 0.5. Notice how the probability of heads plus the probability of tails is equal to one (0.5 + 0.5 = 1); we refer to this as a complete set as it includes all possible outcomes, and the sum of the probability of all those outcomes is equal to one.

The result of a coin flip is random NOT because we have no idea how it will result, but because we cannot say for certain how it will result. We have some idea what will happen – half of time we’ll flip heads, and half of the time we’ll flip tails. The coin flip is said to be random because we cannot say for certain what will happen, but we can determine the probability of each result. Random is another way of saying “not directed” (i.e., there is nothing determining absolutely the result of a particular trial or run).

Now, imagine if the coin is not fair and the probability of heads is 0.6 and the probability of tails is 0.4 (i.e., 60% of the time you will flip heads and 40% of the time you will flip tails). Flipping the coin will still be a random process, but you will flip heads more often than tails. A common misconception is that all results are equally likely in a random process; this is not the case. A random process only implies that every possibly outcome has some assigned probability, and that probability is the only thing that influences whether or not a particular event occurs.

2. Genetic Mutations
Before I get into the random nature of genetic mutations, I think it’s necessary to describe some different types of genetic mutations. Readers familiar with molecular genetics can probably skip this section. If I become unclear at any point, I suggest referring to this excellent summary of mutations.

Your genome is made up of DNA which is composed of four different nucleotides: adenine (A), thymine (T), guanine (G), and cytosine (C). These nucleotides are arrayed in a linear fashion, much like the words on this page. We can write out the order of nucleotides in a gene like we write out letters of a word (e.g., ACGTACCGT). If we change a particular letter to a different letter (an A changing to a T, for example) we say that a “substitution” has occurred.

The adenine (A) molecule is similar in structure to the guanine (G) molecule (they are referred to as purines), and the thymine (T) molecule is similar to the cytosine (C) molecule (T and C are pyrimidines). Purines are more likely to change to another purine (A => G or G => A) than they are to change to a pyrimidine (A => T, A => C, G => T, or G => C). The same is true for pyrimidines – they are more likely to mutate to another pyrimidine than to a purine. Purine to purine (A <=> G) and pyrimidine to pyrimidine (C <=> T) mutations are referred to as transitions, whereas purine to pyrimidine and pyrimidine to pyrimidine mutations are transversions.

Now that I’ve got you totally mixed up with the jargon of substitutions, I’d like to add a couple more types of mutations to your lexicon. We can add or remove a letter or multiple letters from a particular sequence resulting in an insertion or deletion event (indel). These events can be small (only one or a few nucleotides) or fairly large (an entire gene can be duplicated into another part of the genome resulting in an insertion on the order of thousands of nucleotides). Large deletions are thought to be extremely deleterious, but the fitness cost of smaller indels is still unclear and greatly depends on whether or not they are located in coding sequence or noncoding sequence. Gene duplications resulting in large insertions allow for existing biochemical pathways to evolve new functions and for the appearance of new pathways.

Finally, we will consider a few types of large scale chromosomal mutations. These types of mutations affect the structure of a chromosome or the makeup of the genome in a major way. Chromosomal duplications result in the duplication of a single chromosome, whereas genome duplications result in the duplication of an entire genome. Chromosomal inversions result in a large segment of a chromosome reversing in order. Chromosomal fusions occur when two chromosomes join to form a single chromosome, and fissions are when one chromosome splits into two. A fusion event combined with a fission event is referred to as a chromosomal translocation – a large part of a chromosome is removed and attached to another chromosome. Inversions, fusions, fissions, and translocations do not result in any new information in the genome, but they restructure the existing information which could have important evolutionary implications.

3. The Random Nature of Genetic Mutations
Once you are comfortable with random sampling and probability as well as the nature of genetic mutations, it’s clear what biologists mean when they say, “Mutations are random.” We will start by following a single nucleotide from parent to offspring, and then move on to looking at the entire genome.

Let’s assume the probability of a substitution at a particular nucleotide is 10-9 (a very small number). We will only consider two possible outcomes: substitution (mutation) and no mutation. If you’ve followed me up to this point, you can see that this is analogous to the coin flipping example. We do not know if a particular nucleotide will or will not mutate in one generation, but we do know how likely a mutation event is. Whether or not this nucleotide mutates is a random process, with the probability of one in a billion (10-9) that it does mutate. One out of a billion times that nucleotide will mutate in the process of going from parent to offspring.

This line of thinking can be extended to an entire genome, made up of millions of nucleotides. Each nucleotide has the probability of 10-9 that it will undergo a substitution event in one generation. We can also assign probabilities to other mutational events (indels, duplications, inversions, etc) that can be estimated from natural populations or laboratory experiments. We can use these probabilities to calculate the expected number of mutations in the entire genome going from one generation to the next.

It’s important to understand that when biologists say the mutational process is random, we mean that it is not directed. There is nothing determining definitively that a mutation will occur at a particular nucleotide. Mutations provide the raw material on which natural selection acts. Natural selection is a deterministic process; a beneficial mutation will always reach fixation in an ideal population (i.e., natural selection will cause it to replace all the other alleles), and a deleterious mutation will always be lost. We have no way of saying for sure whether or not a particular nucleotide will mutate because mutation is a random process – we can only assign a probability that it will mutate.


At 6:45 PM, Blogger Mark Nutter said...

At the risk of belaboring the obvious, let me also point out that, in the context of natural science, the phrase "not directed" means "not directed by any predictable and verifiable natural force or agent." The question of whether random events are being directed by any metaphysical force or agency (be it fate or deity or what have you) is a question outside the scope of natural science.

I mention this because too many people today hear the phrase "not directed" and immediately leap to the conclusion that science is making dogmatic and religious assertions about God not being in any way involved in the operation of natural forces. In fact, science is not addressing the religious aspects of the question at all, it is speaking only of the natural aspects of the question and whether any natural direction in involved. Being clear about this distinction would help avoid giving creationists the opportunity to accuse science of promoting a religious and anti-Christian agenda.

At 6:25 AM, Anonymous Anonymous said...

"Rather, our analysis support a nonrandom model of chromosome evolution that implicates specific regions within the mammalian genome as HAVING BEEN PREDISPOSED to both recurent small-scale duplication and large-scale evolutionary rearrangements." (Bailey et al, 2004) my emphasis

The above is from my paper "A Prescribed Evolutionary Hypothesis,"
Rivista di Biologia 98(1): 155-166, 2005

In my opinion, one shared by Leo Berg, Pierre Grasse and Reginald C. Punnett, natural selection and allelic mutation never had anything to do with creative evolution and were concerned only with the maintenance of the status quo. The neoDarwinian model is a complete failure and is being replaced by the realities revealed by the quotation with which this post originated.

At 9:44 AM, Blogger Mark Nutter said...

This comment has been removed by a blog administrator.

At 9:53 AM, Blogger Mark Nutter said...

Anonymous, the word "mutation" means "change," the phrase "status quo" means "no change." You're saying the purpose of "change" was to produce "no change"? That can't be what you really meant to say, surely.

Changes to the genome aren't going to maintain the status quo, they're going to produce, well, changes. In a dynamic, competitive, and hostile environment, that's a good thing, an intelligent design, right?

At 9:56 AM, Blogger RPM said...

Mark Nutter,

Thanks for the clarification. I wouldn't want to be charged with supporting some theological viewpoint.


Certain sites are more prone to be rearrangement hotspots than others. Some have suggested that these are fragile sites (Zhou and Mishra 2005, PNAS 102:4051). Others have pointed to the existence of TE at rearrangement breakpoints in humans (Bailey et al 2003, Am J Hum Genet 73:823) and Drosophila (Casals et al 2003, MBE 20:674).

What we do know is that there is a non-random distribution of rearrangement hotspots in any given genome. This does not mean, however, that the mutagenesis process is not random. All it means is that certain parts of the genome have a higher probability of being sites of chromosomal rearrangements than other sites. We can incorperate these different probabilities into our random model.

We also see some sites more prone to small scale mutations compared to other sites. Microsatellites are much more mutable than non-repetitive sequence. This does not mean that the mutagenesis process isn't random, just that our random model must incorperate these different probabilities.

This is like the example of the unfair coin (one side has a higher probability of coming up than the other). The coin flipping process is still random even though the two results have different probabilities of occurring.

At 11:03 AM, Blogger RPM said...

I'd also like to point out that in order to show that the rearrangements are predetermined one must also show that the elements that promote rearrangments (repetitive sequences or fragile sites) were purposely placed at certain locations in the genome in order to induce rearrangements. Just because certain sites are disproportionately associated with rearrangement breakpoints does not mean that they were designed to induce rearrangements.

At 12:44 PM, Blogger skm said...

"whereas purine to pyrimidine and pyrimidine to pyrimidine mutations are transversions."

Not to be picky, but you mean pyrimidine to purine above. Easy typo.

Great post. Failure on the part of scientists (myself included) to communicate our jargon has contributed to the current state of affairs.

At 2:00 PM, Anonymous John A. Davison said...

The clearly demonstrated fact that certain sites are more prone to rearrangements than others can hardly support the idea of randomness. Those observation speak for themselves. Chromosome restructurings are not and have not been random events. If not random they, by definition, became directed events exactly as the authors of that work have stated. Just as all of ontogeny is internally directed so has all of phylogeney been as well. The primary difference is that phylogeny is for all practical purposes finished. Both proceded by the controlled release and expression of latent preformed blocks of specific information in which chance played no role whatever.

At 8:45 PM, Blogger Mark Nutter said...

John, your objection seems to have been already addressed, quite clearly, by point #1 in RPM's post, "What it means to be random." Randomness does not require that all probabilities be equal, it merely requires that the outcome not be predetermined as far as natural science is able to tell. If you step off of a tall building, the direction you will move is not random; it is predetermined by the acceleration of gravity. If you roll a 20-sided die with 19 black faces and 1 white face, the odds of rolling a black face up are disproportionately higher, but it's still a random roll. The fact that you're much more prone to roll a black face than a white one doesn't change the fact that it's still random, as far as natural science can tell.

At 10:49 PM, Blogger Mike the Mad Biologist said...

Great post! (I'm going to link to it). I would emphasize one more way randomness is often used in conjunction with natural selection. With respect to the outcome of natural selection, mutation is random; mutations don't preferentially occur at 'beneficial' sites. This doesn't mean, as one of your commenters claimed, that all sites will experience the same mutational forces.

At 7:20 AM, Anonymous John A. davison said...

Natural selection, the cornerstone of the Darwinian myth, never had anything to do with creative evolution. It served in the past as it does now only to prevent change. That is why every chickadee looks like every other chickadee and why anyone can identify any living thing without question armed with nothing more than a simple binary key or even a photograph.

The prevention of change was a key element in the evolutionary scenario, because it ensured extinction without which progress could never have been made. There is not a single extant diploid organism on this planet that will ever become anything basically different from what it already is. Evolution, a phenomenon of the past, is competely incompatible with sexual reproduction as every experiment has demonstrated.
Evolution WAS emergent, auto-generated, progressive, goal directed and self-terminating exactly as is the development of the individual from a single cell, the fertilized egg. There has been no role for either chance or the environment in directing either ontogeny or phylogeny. Leo Berg realized that in 1922.

"Neither in the one nor in the other is there room for chance."
Nomogenesis, page 134

Some are slow learners. I am not one of them.

At 11:38 AM, Blogger Mark Nutter said...

The flaw in your theory is that natural selection operates outside the organism and its DNA--it has no way of knowing what the "correct" species is. Worse, the external environment does change, sometimes dramatically, which means the natural selective pressures change as well. Natural selection is not going to be a conservative force. It has no detailed information-storage mechanism or error-correction protocol. It's a source of change, not a mechanism for preventing change.

At 4:21 PM, Anonymous John A. Davison said...

All I can say is that you do not agree with St George Jackson Mivart, Henry Fairfield Osborn, Leo Berg, Reginald C. Punnett, Pierre Grasse, Otto Schindewolf and myself all of whom have identified natural selection as a conservative rather than a creative element. Accumulated mutations, virtually all of which are deficiences, have been a primary cause of extinction. The sole role of natural selection was to eliminate as many of these as possible, a process it has been able to carry out only with limited success. The result has been ultimate extinction for the vast majority of all the organisms that ever existed. To claim that mutation and natural selection were creative elements in the evolutionary scenario is unfounded. Now as in the past their function remains entirely conservative. How anyone can continue to claim otherwise escapes me. When the most intensive of natural selection has still not been demonstrated to produce a new species even in the same genus, it is time to come to grips with the reality that it is quite impossible. The last serious attempt was made by Dobzhansky with Drosophila and it is to his credit that he admitted defeat.

At 6:16 PM, Blogger Mark Nutter said...

So you are claiming that a significant change in environmental conditions, which selectively gives a significant survival advantage to characteristics that previously were not advantageous, and/or makes other characteristics disadvantageous in the same regard, is somehow a mechanism for preserving a species unchanged? What, precisely, are the mechanics by which this particular conservation works?

At 8:04 PM, Blogger Mark Nutter said...

Just to clarify, I meant a significant survival/reproductive advantage, not just a significant survival advantage.

At 7:02 AM, Anonymous John A. Davison said...


What I am saying is that allelic mutations are either deleterious or neutral and have little or nothing to offer in the way of advantage to the organism. More inportant, the experimental attempts to demonstrate speciation through selection for such changes have failed. I also do not regard prokaryotes as models for eukaryote evolution. Neither Lamarckian nor Darwinian models have received laboratory support and neither can be reconciled with the fossil record. Those are the considerations that have led me to the Prescribed Evolutionary Hypothesis. The elimination of alternative hypotheses is a perfectly sound basis for presenting a new one. The PEH is little more than an extension and integration of the evolutionary conclusions of William Bateson, Leo Berg, Robert Broom, Pierre Grasse, Reginald C. Punnett and Richard B. Goldscmidt. I am confident that if they were still alive they would give it serious consideration. I owe them a great debt and in my opinion we all do.

"No sadder proof can be given by a man of his own littleness than disbelief in great men."
Thomas Carlyle

At 9:23 AM, Blogger RPM said...

When the most intensive of natural selection has still not been demonstrated to produce a new species even in the same genus, it is time to come to grips with the reality that it is quite impossible. The last serious attempt was made by Dobzhansky with Drosophila and it is to his credit that he admitted defeat.

Check out the work of Coyne and Orr. Selection plays a major role in speciation. See HMR (Barbash et al 2004), which is a speciation gene between Dmel and Dsim and shows strong evidence for a recent selective sweep.

Also, Dobzhansky's favorite study species (Dpseudobscura and its sister species Dpersimilis) shows evidence for selection driving speciation. It also provides a nice model for how genome rearrangements can encourage sympatric/parapatric/reinforcement speciation (see the work of Noor and Navarro). All of the data points to an important role for nat seln in speciation.

Much has been published on Natural selection, evolution, and speciation since the modern synthesis. I suggest you check it out before arguing against nat seln. And the work out of Evan Eichler's lab (the Bailey paper you cited) doesn't support your hypothesis, JAD.

At 9:36 AM, Blogger Mark Nutter said...

So according to your theory, it ought to be impossible for bacteria to evolve a beneficial mutation that would improve its resistance to a new antibiotic, correct?

At 10:51 AM, Blogger Mark Nutter said...

(My last comment was addressed to John, btw, in case that wasn't obvious.)

At 1:00 PM, Anonymous John A. Davison said...

I have presented my hypothesis and published it. If you choose, as you obviously do, to dismiss it with the same old Darwinian unsubstantiated claims, there is little I can do here to dissuade you as you have every right to continue to adhere to a myth. Even should the PEH be proven wrong, and I am confident it won't be, it will in no detract from the total failure of the Darwinian fairy tale to explain anything in evolution beyond the production of varieties and subspecies. For many life forms even that is quite impossible. There is obviously little more I can accomplish here. Groupthinks are like that.

At 5:07 PM, Blogger Mark Nutter said...

I'm not dismissing it, I'm just asking how it would apply here so that I can understand it better. Does your theory predict that bacteria should be unable to produce beneficial mutations enabling them to become more resistant to new antibiotics or not?

At 5:17 PM, Blogger Mark Nutter said...

Sorry, I don't mean to badger you. I am curious about your theory, and I thought you wanted to talk about it, but if that's not the case, don't let me pressure you.

At 7:05 PM, Anonymous John A. Davison said...

Prokaryotes are not models for eukaryotic evolution. I hope that answers your question. Furthermore, there is not a shred of evidence that any prokaryote ever evolved into anything but the same species and certainly not into any eukaryote. All real tangible evidence remains entirely compatible with an internally driven, auto-regulated phylogeny comparable to what we already know about ontogeny. Phulogeny and ontogeny are part of the same continuum. The only fundamental difference seems to be that phylogeny is finished.

At 8:49 PM, Blogger Mark Nutter said...

So it sounds like you saying that beneficial mutations do occur in bacteria, but you deny that this has any implications for eukaryotic organisms, correct?

At 6:53 AM, Anonymous John A. Davison said...

I see no evidence for beneficial mutations occurring in diploid organisms: certainly nothing that could lead to speciation or any of the higher categories. The only beneficial mutations are the reverse ones that return the genome to its wild-type status. Others may at best fine tune the genome to a certain extent although even that is difficult to demonstrate.

At 2:50 PM, Blogger Mark Nutter said...

Let us suppose, then, that diploid organisms do not experience beneficial mutations. They do, of course, experience mutations. And we know that the mechanisms by which mutations occur, in general, are not different between bacteria and diploid organisms, as documented in the original post above. (That is, a point mutation is a point mutation, whether it occurs in a bacteria or a baseball player; an inversion is an inversion, a retrotransposition is a retrotransposition, and so on.)

So what this suggests, if beneficial mutations do occur in bacteria and do not occur in diploid organisms, is that there must be some molecular mechanism in the diploids which is able to recognize beneficial mutations and suppress them. This must be a very sophisticated mechanism, however, because "beneficial" can depend a great deal on context, which is where natural selection comes in. Hollow bones are beneficial for a bird because it makes flying easier, for instance, but thick bones are beneficial for creatures that have to endure hard physical contact while fighting for food, mates, or survival. So "beneficial" is not an easily or permanently defined quality.

Logically, then, we should be asking, do we have any evidence that diploid organisms possess a mechanism for selectively identifying and suppressing beneficial mutations, and if so, why on earth would they have such a mechanism?

Alternately, if no such mechanism exists, then perhaps the problem is not a lack of beneficial mutations, but a certain difficulty in detecting the ones that do occur. If beneficial mutations did occur, how would we know it?

At 4:27 PM, Blogger RPM said...

Furthermore, there is not a shred of evidence that any prokaryote ever evolved into anything but the same species and certainly not into any eukaryote.

We have evidence for common descent of prokaryotes and eukaryotes based on gene homology. We also have evidence for the prokaryotic origin of eukaryotic organelles based homology.

At 4:42 PM, Anonymous John A. Davison said...

I have great difficulty applying logic to evolutionary matters. The major weakness in the Darwinian scheme is the fact that superficially it seems very logical. That does not make it correct. As someone put it:

"Hypotheses have to be reasonable - facts don't."

Boris Ephrussi who proved that mitochondria are self replicating entities, put it this way:

"An hypothesis does not cease to be an hypothesis when a lot of people believe it."

There is not a shred of evidence implicating allelic mutation in the origin of any plant or animal species or any of the higher categories. Indeed there is no direct evidence that the environment was implicated in any way in such origins which certainly did take place in the past but seem no longer to be occurring. Chance, in my carefully considered opinion, had absolutely nothing to do with creative evolution, a phenomenon no longer in progress. Such a view is hardly mine alone as it was proposed independently in roughly chronological order by Mivart, Bateson, Osborn, Berg, Broom, Goldschmidt, Schindewolf and Grasse, a list to which I am happy to append my name. Evolution has indeed been a "Nomogenesis or Evolution According to Law," the complete title of Leo Berg's remarkable book. In my opinion it is the most significant single volume addressing the great mystery of organic evolution, a phenomenon which remains without a solution but not for much longer.

At 7:45 PM, Blogger Mark Nutter said...

I take it then that there is no evidence of any mechanism operating within the cells of diploid organisms, that would be capable of recognizing and suppressing any beneficial mutations that might occur in diploid organisms as they do in bacterial organisms, is that correct?

At 7:15 AM, Anonymous John A. Davison said...


Cells recognize and neutralize all sorts of mutations as you well know. The only cells that matter in the evolutionary scheme are those in the reproductive lineage. I know of no random events that have produced progress in a past evolution. As I and others have claimed, creative evolution is no longer in progress, while degenerative evolution most obviously is. In my opinion that has been the most important factor in extinction, now as in the past. In the long run natural selection not only is incapable of producing progress but typically fails even to maintain the status quo as deleterious mutations overwhelm its limited capacities. This is especially true for large organisms which typically leave few descendents.

Of course these are only my opinions but I feel they realistically represent the facts.
A major error was made at the onset when it was assumed that evolution was driven by the environment. I know of not a single example supporting that notion in any higher organism. What an organism can or cannot do is determined entirely by its intrinsic makeup. Some forms are more labile than others and accordingly less prone to extinction. I realize this does not resonate with the Darwinian perspective but it represents my position nevertheless.

"Here I stand. I can do no otherwise."
Martin Luther

At 8:03 AM, Blogger RPM said...

I know of no random events that have produced progress in a past evolution.

Evolution does not result in "progress." Evolution is merely change. I'm assuming you mean "adaptation." In that case, Natural selection results in adaptation. Natural Selection is not random -- it's deterministic.

At 11:34 AM, Blogger Mark Nutter said...

John, the question is not whether cells selectively neutralize harmful mutations, the question is whether there exists a mechanism which selectively identifies only the beneficial mutations and eliminates them. Is there any evidence that such a mechanism exists in diploid organisms, and what would be the purpose of evolving such a self-detrimental mechanism?

I am not dismissing your theory that more complex organisms have some factor that ensures that ensures that their mutations will never be beneficial, I'm simply inquiring as to why this situation would be the case, and whether there is any evidence suggesting that cells have the necessary infrastructure to support such a purposeful and selective mutational mechanism.

At 4:21 PM, Anonymous John A. davison said...

You seem to believe that there are beneficial mutations in diploid organisms. I know only of deleterious or neutral ones. If there are such beneficial mutations they will never result in speciation, of that I am quite certain. Accordingly they have little or no significance with respect to a progressive evolution which I believe is finished anyway.

Please do not bring up sickle cell or industrial melanism because they have no evolutionary application whatsoever and do not even have an implication for subspeciation. In short, I have, with Pierre Grasse, rejected all allelic changes as having evolutionary significance. They are just errors on what Grasse described as the magnetic tape on which species information is inscribed. They are important for extinction but not for evolution.

At 8:57 PM, Blogger Mark Nutter said...

I'm just interested in your theory that even though diploid organisms have the same mutational mechanisms as bacteria (which you implicitly concede do have beneficial mutations), there is some factor which prevents these same mutational mechanisms from producing advantageous mutations in diploid organisms. That would seem to be a difficult thing for a mutational mechanism or cellular filter to achieve, considering the extent to which environmental factors can determine whether a change is in fact beneficial or not. I would also like to hear you explain why more complex organisms would develop a mechanism designed to prevent them from experiencing the benefits of beneficial mutations, while retaining the potential negative consequences of neutral and deleterious mutations, when simpler organisms like bacteria enjoy the "good" mutations along with the bad. It's easy to understand why an organism would evolve mechanisms for filtering out harmful mutations, but it's much less clear to me why a species would evolve a mechanism designed to prevent beneficial mutations, or why, if it did manage to do so, this system would become so widespread as to become dominant among all the more complex species.

At 7:10 AM, Anonymous John A. Davison said...


You have asked the question WHY. That is a nono. The scientist is supposed only to ask the question HOW.

All I can say is that I see no evidence for beneficial mutations in diploid organisms and even if there were some, which I cannot disprove, I cannot conceive of a role they might have played in creative evolution. The only mutations which we can directly implicate as of progressive evolutionary significance involved the restructuring of existing information by alterations of chromosome structure. Such changes do not require a change in existing genetic information, only an alteration through gene silencing and gene activation of preexisting genetic potentialities. That is why I now regard much of evolution as what can be described in simple terms as "position effect."

I do not mean to suggest that all chromosomal restructurings are going to result in speciation as we know that is not the case. But that some have been involved (past tense) seems to me to be undeniable.

I hope this serves to explain my position and to offer an explanation for why I have proposed the Prescribed Evolutionary Hypothesis.

At 11:11 AM, Blogger Mark Nutter said...

So, then, your theory does not rule out the possibility of beneficial mutations in diploid organisms after all. It's just that you haven't observed any. That's fine, that's all I wanted to know.

At 11:11 PM, Anonymous John A. Davison said...

Sure Mark
I don't have a theory of evolution however, just another hypothesis. Theories, sensu strictu, are hypotheses that have received some concrete support. To date there is still no sound theory of organic evolution beyond the undeniable fact that it occurred. The mechanism or mechanisms still remain unproven or at least that is my contention.

Of course I still have great confidence in the PEH or I wouldn't have published it.

At 8:51 AM, Anonymous G Lynn said...

John A. davison said...
1. 2 Prokaryotes are not models for eukaryotic evolution. 2
What evidence is there for this ?
2. " The clearly demonstrated fact that certain sites are more prone to rearrangements than others can hardly support the idea of randomness."
Why not ?
3. " Chromosome restructurings are not and have not been random events. "
What evidence supports this ?
4. " Evolution, a phenomenon of the past, is competely incompatible with sexual reproduction as every experiment has demonstrated. "
What experiments are these.
Surely evolution at its most basic simply states that the offspring are not completely identical to the parents. Do you not consider this to be so ?

I would be grateful if you could clarify the above points :

At 7:44 AM, Anonymous John A. Davison said...

There is no need for me to clarify anything as my work is published and a touch of your mouse away. Now close this one down too you pathetic creatures you. That way, sooner or later, I will be able to shut down your whole precious, idiotic little blog. I recommend lifetime banishment as the "final solution to the Davison problem." Got that? Write that down.

At 10:31 PM, Blogger Doug said...

Is it true that mutations never
increase the amino acid sequence on a dna chain? ie they either keep the same number or decrease it.

Cheers Doug

At 7:30 AM, Blogger RPM said...

Insertions in a protein coding sequence will increase the length of an amino acid sequence. Deletions will decrease the length. Because the genetic code is composed of codons (groups of three nucleotides that encode an amino acid), insertions and deletions within a protein coding sequence usually need to be in multiples of three.


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