Natural selection is what keeps the gene pool strong and helps keeping the group alive and removing the weaker genes and defective genes and of course mutations.
If there was no natural selection we and all organisms would die off.
Natural selection is what would work against evolution because it would remove mutations that are not solidified in the gene pool.
How could a non-thinking and non-intelligent natural process think and create all the vital organs it would take for an organism to live ?
Micro-adaptations;
Fact #1 produce the same kind of plant or animal because of the DNA code barrier. Never will a cow produce a non-cow.
Micro-adaptations ;
Fact #2 result from the sorting or the loss of genetic information.
Fact # 3 scientist know of no way for nature to add appreciable amounts of new & beneficial genetic information to a gene pool.
Neo-darwinism is based on three false assumptions.
1. Mutations create new & beneficial genetic data.
2. Natural selection lets the mutant gene take over the population.
3. Needs long ages for this to happen millions of years ,given enough time they claim a bacteria cell overcame the law of abiogenesis and all mathematical possibility and came to life and then mutated its way to everything alive now,whew talk about faith. and they say it ended up the thing they call the ultimate mutation,you and I.
Here is a problem for you darwinist.
All observed mutations after millions of observations,mutations are caused by the sorting or loss of pre-existing genetic data. This is Gene Depletion. Gene depletion applies to Micro-adaptations and mutations,so they get weaker and weaker until they're removed by Natural Selection.
NATURAL SELECTION PREVENTS EVOLUTION FROM BEING POSSIBLE.
So you're being taught mutations + Natural Selection leads to Neo-darwinian Evolution.
But real science reveals based on millions of observations; DNA code barrier + Gene depletion + Natural Selection is what prevents Macro-evolution. Macro-evolution is an impossibility.
You make several erroneous assumptions:
The first is that natural selection is directional. It is not. Mutations and novel phenotypes occur that can either be good, bad, or neutral based on the environment. The organ system we have didn't evolve off of a blue print. It might seem like a fully functional system to you, but it has several flaws. Why can't brain tissue regenerate?
Secondly, mutations would not necessarily be "removed" if that were deleterious. Do you know what happens if you have one copy of the sickle cell gene? You are resistant to malaria. Do you know what happens if you have two copies? You have the disease. Your statement is a simplistic way of looking at the process. It's the phenotype, driven by genotype change, that is important for survival. In the absence of a really bad phenotype, the new genetic information in mutations will be passed on and may manifest in different ways in different generations.
Finally, your statements about DNA barriers and "Gene Depletion" are just silly. A mutation doesn't necessitate loss of that genetic information from the genome.
Don't start with more theories about new information arrising from mutations. fellow evolutionist Dr Spetner totally refuted what you're saying. What is your proof that a mutation can take over a gene pool ?
Lee Spetner/Edward Max Dialogue
Dr. Lee Spetner
continuing an exchange with Dr. Edward E. Max
© 2001 L.M. Spetner. All Rights Reserved.
fter I posted my critique of Edward E. MaxÂ’s essay, Max posted our dialogue with additional comments to my responses. The order of topics in his posting does not correspond exactly to the order of my posting, but both postings are fairly accurate representations of our dialogue. The following is my latest response (23 May 2001) in a form that reproduces his posting into which I have inserted my comments. I have identified each of our statements as he has reproduced them by putting our names in boldface followed by a colon. My new comments are inserted into the text in small caps inside square brackets and identified by "LMS".
Introduction
Spetner: I am writing this essay in response to a request from Edward E. Max to comment on his posting The Evolution of Improved Fitness (updated July 12 1999). His essay is an attempt to defend evolutionary theory against attacks by creationists. Although Max scored some points against some alleged creationist arguments, he failed to defend Darwinian evolution against my attack on it in my book Not By Chance. He did not mention my book in his posting, but he referred to my book in his request for my comments. I shall also take this opportunity to clarify some issues in my book about which some readers have written me.
The principle message of evolution is that all life descended with modification from a putative single primitive source. I call this the grand sweep of evolution. The mechanism offered for the process of modification is basically the Darwinian one of a long series of steps of random variation, each followed by natural selection. The variation is generally understood today to be random mutations in the DNA.
That primitive source of life is assumed to be sufficiently simple that it could have arisen from nonliving material by chance. There is no theory today that can account for such an event, but I shall not address that issue here. That is for another place and another time. What is relevant to this discussion is that the requirement that life arose spontaneously sets, at the very least, a stringent upper limit on the complexity and information content of the putative first organism that could reproduce itself, and thus serve as a vehicle from which to launch Darwinian evolution. The issue I address here is the alleged development of all life by the Neo-Darwinian process of random mutation and natural selection, starting from a sufficiently simple beginning.
Despite the insistence of evolutionists that evolution is a fact, it is really no more than an improbable story. No one has ever shown that macroevolution can work. Most evolutionists assume that macroevolution is just a long sequence of microevolutionary events, but no one has ever shown it to be so. (Those few evolutionists who hold that macroevolution is really different from microevolution have changed their story several times since they first came out with it, and their mechanism is so fuzzy that I cannot tell what it is. John Maynard Smith seems to be of a similar opinion.)
For the grand process of evolution to work, long sequences of “beneficial” mutations must be possible, each building on the previous one and conferring a selective advantage on the organism. The process must be able to lead not only from one species to another, but to the entire advance of life from a simple beginning to the full complexity of life today. There must be a long series of possible mutations, each of which conferring a selective advantage on the organism so that natural selection can make it take over the population. Moreover, there must be not just one, but a great many such series.
The chain must be continuous in that at each stage a change of a single base pair somewhere in the genome can lead to a more adaptive organism in some environmental context. That is, it should be possible to continue to climb an “adaptive” hill, one base change after another, without getting hung up on a local adaptive maximum. No one has ever shown this to be possible.
Now one might say that if evolution were hung up on a local Maximum, a large genetic change like a recombination or a transposition could bring it to another higher peak. Large adaptive changes are, however, highly improbable. They are orders of magnitude less probable than getting an adaptive change with a single nucleotide substitution, which is itself improbable. No one has shown this to be possible either.
Moreover, as I have noted in my book, the large mutations such as recombinations and transpositions are mediated by special enzymes and are executed with precision - not the sort of doings one would expect of events that were supposed to be the products of chance. Evolutionists chose the mechanism of randomness, by the way, because we canÂ’t think of any other way beneficial mutations might occur in the absence of a law that might govern them. Genetic rearrangements may not be really random at all. They do not seem to qualify as the random mutations Neo-Darwinists can invoke whenever needed to escape from a local adaptive Maximum.
Evolutionists can argue, and rightly so, that we have no way of observing long series of mutations, since our observation time is limited to a relatively short interval. Our genetic observations over the past 100 years are more like a snapshot of evolution rather than a representative interval in which we can search for the required long series of changes. But our inability to observe such series cannot be used as a justification for the assumption that the series Darwinian theory requires indeed exist.
Max: I agree that there are no definitive examples where a macroevolutionary change (such as the development of cetaceans from terrestrial mammals) has been shown to result from a specific chain of mutations. And I agree with your further comment that “we have no way of observing a long series of mutations.” But you go on to say that “our inability to observe such series cannot be used as a justification for the assumption that the series Darwinian theory requires indeed exist.” An equally reasonable conclusion, in my view, would be that our inability to observe such series cannot be used as a justification for the assumption that such a series of mutations did NOT occur.
Spetner: Now Ed, thatÂ’s ridiculous! Those two statements are not symmetrical. I donÂ’t have to assume the series did not occur to make a case for the inadequacy of NDT. You, who are basing your theory of evolution on the occurrence of such a series, are required to show that it exists, or at least that it is likely to exist. You are obliged to show an existence. I am not obliged to prove a non-existence.
[LMS: IN MAXÂ’S POSTING HE MOVED THIS REMARK OF MINE TO A LATER POINT IN THE DIALOGUE. I ORIGINALLY HAD IT HERE, AND HERE IS WHERE IT BELONGS.]
Max: In the absence of conclusive data defining such a series, if we want to distinguish between various hypotheses to explain the origin of species we must rely on other data, such as from various laboratory model systems that show adaptations in short enough timeframes that we can observe them. Then we must extrapolate as best we can the information learned from these model systems to the questions of species origins. This extrapolation from laboratory model systems to systems unobservable in the laboratory is the method of science common to medicine, astronomy, chemistry, meteorology, physics, etc.
I think there is some semantic confusion here about the word “justification” in Spetner’s sentence “But our inability to observe such series cannot be used as a justification for the assumption that the series Darwinian theory requires indeed exist.” He is correct that acceptance of the NDT implies the belief that a series of successive mutations (including duplications and translocations) occurred in the evolution of an ancient primitive genome into the complex genome of a modern species. Because we can access only genomes of modern (or very recent) species, we can never obtain the direct evidence—i.e., a complete list of those mutations—that some anti-evolutionists (e.g. Behe) seem to think would be necessary to support NDT.
[LMS: MAX’S STATEMENT HERE IS A DISTORTION OF MY ARGUMENT INTO AN EXTREME POSITION. I NEITHER SAID NOR IMPLIED THAT EVOLUTIONISTS MUST “OBTAIN...A COMPLETE LIST OF THOSE MUTATIONS” REQUIRED FOR NDT. I DO MAINTAIN, HOWEVER, THAT THEY SHOULD AT LEAST ACCEPT THE RESPONSIBILITY OF SHOWING THAT NDT IS REASONABLY SUPPORTED BY EVIDENCE. THEY HAVE NOT DONE THAT. THE MECHANISM OF NDT CONSISTS OF TWO BASIC STEPS. AN ADAPTIVE MUTATION MUST BE ACHIEVED, AND THEN NATURAL SELECTION MUST OPERATE TO ENABLE IT TO TAKE OVER THE POPULATION. EVOLUTIONISTS ARE OBLIGATED TO SHOW THAT BOTH THESE STEPS ARE REASONABLY SUPPORTED BY EVIDENCE IF THEY ARE TO MAKE A CASE FOR NDT. MOST OF THEIR EFFORTS ALONG THESE LINES HAVE BEEN LIMITED TO ARGUING FOR NATURAL SELECTION. THEY USUALLY DO NOT DEAL WITH THE PROBABILITY OF ACHIEVING AN ADAPTIVE MUTATION. THEY MERELY ASSUME ONE WILL BE AVAILABLE WHENEVER IT IS NEEDED.]
In the absence of such direct evidence, it seems pointless to argue which side is “obliged” to provide what indirect evidence; certainly neither side can hope for anything close to “proof.” Although Spetner denies that he is “obliged to prove a non-existence” of such a chain of mutations, his whole effort in the correspondence seems to be directed to just that aim. Evolutionists have the job of defending the reasonableness of such a series of mutations. I believe that Spetner would agree with this.
[LMS: RIGHT. EVOLUTIONISTS DO HAVE THAT JOB AS AN OBLIGATION, AND THEY HAVE FAILED TO FULFILL IT. I AM NOT OBLIGED TO PROVE A NON-EXISTENCE. BUT IN MY BOOK, I HAVE MADE A GOOD CASE FOR THE UNREASONABLENESS OF THE EVOLUTIONISTSÂ’ TACIT ASSUMPTIONS OF THE UNIVERSAL AVAILABILITY OF ADAPTIVE MUTATIONS, AND I HAVE GIVEN SOME OF THOSE ARGUMENTS IN THIS DIALOGUE.]
Spetner: But the argument against Darwinian theory is considerably stronger than that. The theory requires there be a vast number of possible point mutations which, coupled with natural selection, can produce the evolutionary advances that could produce the grand sweep of evolution. Because there must be a large number of qualifying mutations, at least a few of them should have been observed in some of the many genetics laboratories around the world. All the mutations in these long series must not only confer selective advantage on the organism but they must, on the average, also contribute to the information, or complexity, increase that surely distinguishes present-day life from the putative primitive organism.
These mutations must have whatever characteristics are necessary for them to serve as elements of the grand sweep of evolution. Thus, for a mutation to qualify as a representative member of the required multitude of long series that are supposed to produce evolution, it must bring new information not just to the genome of the organism, but the information must be new to the entire biocosm. The horizontal transfer of a gene from one species to another is not information new to the biocosm. To show evolution in action, one must at least demonstrate examples of a mutation that can serve as a prototype of those required by the theory. Such a mutation must be one that could be a contributing member of a series of mutations that could lead to the vast increase in information required by the theory. Thus, for example, a mutation that disables a repressor gene causing a constitutive synthesis of an enzyme might be advantageous to an organism under special circumstances, but the disabling of a gene does not represent the mutations required by the theory.
Max devotes a good portion of his essay to refuting what he calls the “creationist” argument against evolution. Although some opponents of evolutionary theory may have advanced the arguments he attacks, those arguments are in large measure straw men that Max busies himself with refuting. If some creationists have claimed that all mutations are harmful, they would be wrong, but Max’s observation that there are mutations that are beneficial, while true, is hardly a telling argument for evolution.
The B-Cell Hypermutation Model
Max: The next major point of discussion in the correspondence has been about how well the model of immunoglobulin gene somatic hypermutation in B cells serves as an analog to genomic mutation in evolution. The following section contains the salient points of our exchange about this question, beginning with SpetnerÂ’s initial response to my essay on Talk.Origins.
Spetner: Max’s pièce de résistance was the somatic mutations in B lymphocytes (B cells) of the vertebrate immune system as examples of random mutations that add information. He implied that Evolution could follow this method to achieve baboons from bacteria. I agree with him that these mutations add information to the B-cell genome. I also agree that they are random, but they are random only in the base changes they make; they are not random in where in the genome they can occur. More important, I do not agree that the grand sweep of evolution could be achieved through such mutations.
Although the somatic mutations to which Max referred are point mutations that do indeed add information to the genome of the B cells, they cannot be applied to Darwinian evolution. These are not the kind of mutations that can operate as the random mutations required by NDT that can, through chance errors, build information one base change at a time.
For one thing, the rate of the somatic mutations in the immune system is extremely high - more than a million times normal mutation rates. For this reason they are called hypermutations. If an organism had a mutation rate that was even a small fraction of this rate it could not survive. For a second thing, the hypermutations in the B cells are restricted to a specific tiny portion of the genome, where they can do no harm but only good. The entire genome of the B cell could not mutate at this rate; the hypermutation must be restricted only to the portion that encodes selected portions of the variable part of the antibody.
The mutation rate of the hypermutating part of the B cellÂ’s genome is about one per thousand base pairs per replication (Darnell et al., 1986, Molecular Cell Biology, Scientific American Books, p. 1116.), and it can be as high as one in 500 base pairs per replication (Shen, 1998 Science 280: 1750). These rates are incompatible with Darwinian evolution. If an organismÂ’s genome were to mutate at this rate, there would be, on the average, about one mutation in every gene, with a high probability that many of them would be fatal for the organism. No, Darwinian evolution could not occur with such rates.
These high rates are essential for the working of the immune system. In each replication of a B cell, about 30 of the 300 or so gene regions encoding the CDRÂ’s will have a mutation. A lower mutation rate would make for a less efficient immune system. The high mutation rates, so necessary for the immune system, if applied to an entire organism for evolutionary purposes, would be fatal many times over.
Note that these hypermutations are limited to a restricted portion of the genome. Moreover, the hypermutations are mediated by special enzymes. Thus, although the hypermutations are random in the changes they make in the bases of the genome, they are not random in the positions in which they occur. They occur only in the small region in which they are needed, and occur there through enzymes that apparently play only that role. Furthermore, they occur only when they are switched on by the controlling mechanism of B-cell maturation. Thus it is clear that the hypermutations in B cells cannot serve as a prototype for the random mutations required for NDT.
Max: You agreed with me that the model system of random somatic mutations and selection that occurs in immunoglobulin genes in B lymphocytes can “add information to the B-cell genome.” I am glad that you accept the idea that random mutation and selection can lead to an increase in information, since this idea directly refutes the notion of Dembski and others who believe that there is some theoretical bar that would prevent achieving what they call “complex specified information” through random mutation and selection. (Incidentally, I don’t think they would appreciate your characterization of them as “straw men.") However, you then go on to declare that the B cell example is a poor model for what happens in “Darwinian” evolution, and you cite two reasons: (1) the mutation rate in this model is much higher than what is seen in non-immunoglobulin genes and in non-B-cells; and (2) these “hypermutations” are mediated by “special enzymes.” With regard to your first point, I agree that the mutation rate is higher in the B cell example than in evolution, but I fail to see why that fact weakens the usefulness of the example as a model for evolution. If adaptive mutations that increase information in the genome of a B lymphocyte population can occur over one week given a high mutation rate, what theoretical argument would lead you to reject the idea that adaptive mutations that increase information in the genome of a germ cell population could occur over many millions of years given a much lower mutation rate?
Spetner: [LMS: IN HIS POSTING, MAX MOVED MY ANSWER FROM HERE TO A LATER POINT IN THE DIALOGUE, BUT THIS IS WHERE I ORIGINALLY PUT IT, AND THIS IS WHERE IT BELONGS.]
The theoretical argument is the following. Evolution requires a long series of steps each consisting of an adaptive mutation followed by natural selection. In this series, each mutation must have a higher selective value than the previous. Thus, the evolving population moves across the adaptive landscape always rising toward higher adaptivity. It is generally accepted that the adaptive landscape is not just one big smooth hill with a single Maximum, but it is many hills of many different heights. Most likely, the population is on a hill that is not the highest in the landscape. It will then get stuck on a local Maximum of adaptivity and will not be able to move from it. This is particularly likely because the steps it takes are very small - only one nucleotide change at a time. The problem is compounded by the lack of freedom of a single nucleotide substitution to cause a change in the encoded amino acid. A single nucleotide substitution does not have the potential to change an amino acid to any one of the other 19. In general, its potential for change is limited to only 5 or 6 others. To evolve off the “dead point” of adaptivity, a larger step, such as the simultaneous change of more than one nucleotide, is required. Moreover, the probability is close to 1 that a single mutation in a population, even though it is adaptive, will disappear without taking over the population (see my book, Chapter 3). Therefore, many adaptive mutations must occur at each step.
The hypermutation in the B cells does this. It achieves all possible single, double, and triple mutations for the immune system, which allows them to obtain the information necessary to match a new antigen. Ordinary mutations, at the normal low rate, cannot add this information - even over long times. I shall explain why. Consider a population of antigen-activated B cells of, say, a billion individuals. In two weeks, there will be about 30 generations. LetÂ’s say the population size will remain stable, so in two weeks there will be a total of 30 billion replications. With a mutation rate of 1 per 1000 nucleotides per replication, there will be an average of 30 million changes in any particular nucleotide during a two-week period. The probability of getting two particular nucleotides to change is one per million replications. Thus in two weeks, there will be an average of 30 thousand changes in any two particular nucleotides. There will be an average of 30 changes in any three particular nucleotides.
How many generations, and how long, would it take to get a particular multiple nucleotide change in a germ cell to have an effect on Neo-Darwinian evolution? Here, the mutation rate is about one per billion nucleotides per replication. LetÂ’s suppose we're doing this experiment with a population of a billion bacteria. Then, in one generation, there will be an average of one change in a particular base. A particular double base change has a probability of one per quintillion, or 10-18. To get one of these would take a billion generations, or about 100,000 years. To get a triple change would take 1014, or a hundred trillion, years. That is why a long waiting time cannot compensate for a low mutation rate. I've given numbers here for a laboratory experiment with bacteria. Many more mutations would be expected world-wide. But the same kind of thing has to happen under NDT with multicelled animals as well. With vertebrates, for example, the breeding populations seldom exceed a few thousand. Multicelled animals would have many fewer mutations than those cited above for bacteria.
Max: Your second objection to the somatic mutation model in B-cells, that “special enzymes” are involved, is unsupportable.
[LMS: ON THE CONTRARY, I HAVE SHOWN IT IS WELL SUPPORTED (SEE BELOW).]
As far as I can tell from my reading of the literature, the mechanism of somatic hypermutation in B-cells is not currently known.
[LMS: TO WHAT EXTENT THE MECHANISM IS KNOWN IS IRRELEVANT TO THIS DISCUSSION. THE POINT IS THAT THE CONSENSUS AMONG EXPERTS IS THAT SUCH A MECHANISM EXISTS FOR B-CELL MUTATION, AND DOES NOT EXIST FOR GERMLINE MUTATION.]
The mechanism could perhaps involve “special” enzymes that create mutations, but an alternative possibility is that the high rate of accumulation of mutations simply reflects selective inhibition of normal proof-reading mechanisms. But again, I fail to see why the source of the random mutations should influence the general validity of the conclusion that random mutations and selection can increase genomic information, or why you feel that these mutations cannot serve as a model for evolutionary adaptations.
Indeed, both the rate and predominant mechanism of mutation may be different in different species of organisms, depending on whether they have more or less exposure to cosmic rays and other environmental mutagens, and depending on the nature and robustness of their genomic error-correction mechanisms. Therefore, if we accept your argument against extrapolation from B cell adaptation to species adaptation, should we reject the extrapolation of any information learned from studying one organism to understand adaptations in a second organism, unless it is shown that both the rate and mechanism of mutation are the same in both organisms?
[LMS: HERE AGAIN, MAX DISTORTS MY ARGUMENT INTO AN EXTREME POSITION AND THEN RESPONDS TO THAT EXTREME POSITION.]
In my view this would be like refusing to use the gravitational constant determined in laboratories on earth to analyze stellar physics. Such a reluctance to extrapolate would certainly prevent the use of modern organisms as a basis for understanding evolutionary events that occurred millions of years ago (which may be precisely your intent). I sometimes hear arguments like yours from creationists who are demanding rigorous “proof” of evolution. These creationists do not seem to understand the distinction between mathematics, where a rigorous proof is expected, versus most experimental and observational science, where all we are seeking is the best theory that explains observed data. Of course it is possible to extrapolate unreasonably, but I do not see that you have shown how evolutionary theory (or my essay) does this.
Spetner: Extrapolations made in astrophysics and cosmology may not be entirely valid, but at least they are reasonable based on everything we know. The extrapolation you propose from B-cell hypermutation to Neo-Darwinian evolution is unreasonable based on present knowledge, and it is therefore unjustified.
[LMS: THIS ANSWER OF MINE SOMEHOW GOT MOVED AWAY FROM THIS PLACE WHERE IT BELONGS.]
Yes, Ed, the hypermutation in the B cells cannot be a prototype of the kind of mutation required by NDT for Evolution A for the two reasons I gave. You question both those reasons, so I shall elaborate to explain to you why they are valid reasons for rejecting your example of B-cell hypermutation as support for NDT.
One of my arguments to invalidate hypermutation as a model for NDT is that this kind of mutation requires “special enzymes", and is not the kind of mutations held to be responsible for the variation required in NDT. You rejected that argument as unsupportable, but that rejection is unjustified. These mutations, unlike ordinary errors in DNA replication in the germline, are turned on precisely when they are needed and turned off when they have done their job. They are accurately targeted to the very small regions of the genome where they can provide variability to the CDR’s, which form the antibody binding site. Although the mechanism of this precisely targeted phenomenon is not yet known in complete detail, enough is known to say that there has to be a “mechanism” - it doesn’t just happen by chance.
Max: {At this point Spetner quotes a number of speculative statements in the scientific literature, to the effect that B cell somatic hypermutation involves a “special mechanism.”
[LMS: MAX DID NOT REPRODUCE HERE THE REFERENCES I CITED. I WON’T REPEAT THEM HERE, BUT THEY CAN BE SEEN IN MY PREVIOUS POSTING. MAX CALLS MY CITED REFERENCES “SPECULATIVE", AND THAT MIGHT CREATE THE IMPRESSION THAT THEY ARE NOT REPRESENTATIVE OF RELIABLE SCIENTIFIC OPINION. THAT IMPRESSION IS FALSE. THE REFERENCES ARE FROM MAINSTREAM EXPERTS IN THE FIELD, ALL AGREEING THAT THERE IS A SPECIAL MECHANISM FOR HYPERMUTATIONS THAT IS NOT AVAILABLE TO GERMLINE MUTATIONS. THEY ARE “SPECULATIVE” ONLY IN THE SENSE THAT THESE PAPERS WERE SPECULATING ABOUT WHAT THE MECHANISM COULD BE. BUT THERE IS NO SPECULATION ABOUT THE EXISTENCE OF THE MECHANISM. ALL AGREED TO THAT, WHICH IS THE ONLY POINT I INTENDED, AND NEED, TO MAKE.]
The enzymes involved in somatic hypermutation in B cells remain unknown, so if Spetner is correct that “special enzymes” is supportable, he is correct only in the sense that the idea of “special enzymes” is supported by speculation in the literature. It is unsupported by any evidence, which is what I meant by “unsupportable.”
[LMS: MAX IS WRONG. THE EXISTENCE OF A MECHANISM IS SUPPORTED BY A LOT OF EVIDENCE, AS REFERRED TO IN THE PAPERS I CITED.]
To be fair I should note that an enzyme known as Activation Induced Deaminase (AID), reported after my initial comments to Spetner, has been shown necessary for somatic hypermutation to occur, but it is not clear whether this enzyme participates directly in the introduction of mutations. Indeed, since absence of AID also blocks isotype switch recombination, a phenomenon not obviously related to hypermutation, and also leads to enlarged germinal centers, it is possible that this enzyme is required for a step in B cell developmental maturation that triggers both hypermutation and switch recombination, and that the enzyme plays no direct role in mutating DNA. In any case, I never have questioned the idea that somatic hypermutation in B cells involves a “special mechanism"; the question of whether unique enzymes are directly involved in creating the mutations seems to me rather tangential to the present discussion, but it is accurate to say that this question has not been settled as of yet.}
[LMS: SINCE MAX HERE ACKNOWLEDGES THAT HYPERMUTATIONS MAKE USE OF A “SPECIAL MECHANISM” NOT AVAILABLE TO GERMLINE MUTATION, HE IS LOGICALLY OBLIGATED TO CONCEDE TO ME THAT HIS EXAMPLE OF HYPERMUTATIONS CREATING INFORMATION IN THE B-CELL GENOME BY RANDOM MUTATIONS AND SELECTION CANNOT BE USED TO DEMONSTRATE THE POSSIBILITY THAT RANDOM MUTATIONS IN THE GERMLINE CAN CREATE INFORMATION FOR EVOLUTION. THIS CONCESSION ON HIS PART SHOULD LOGICALLY END OUR DEBATE. THE PRECISE NATURE OF THE MECHANISM OF HYPERMUTATION IS NOT SETTLED, BUT THE EXISTENCE OF SUCH A MECHANISM IS A CONSENSUS AMONG THE EXPERTS. FURTHERMORE, THE EXISTENCE OF A SPECIAL MECHANISM WITH ITS SPECIAL ENZYMES THAT PERMITS THE HYPERMUTATIONS TO DO THEIR JOB IN THE IMMUNE SYSTEM IS NOT TANGENTIAL TO OUR DISCUSSION. THE MECHANISM, WHATEVER ITS NATURE, IS WHAT PERMITS HYPERMUTATIONS CREATE INFORMATION FOR THE IMMUNE SYSTEM. SUCH A MECHANISM IS NOT AVAILABLE FOR GERM LINE MUTATIONS TO MAKE EVOLUTION POSSIBLE, AND THEREFORE MAX’S EXAMPLE OF B-CELL HYPERMUTATION TO SHOW THAT INFORMATION CAN BE GENERATED IN EVOLUTION IS INVALID.]
Spetner: It thus seems quite clear to me that informed opinion in this field supports my contention and rejects your suggestion that “an alternative possibility is that the high rate of accumulation of mutations simply reflects selective inhibition of normal proof-reading mechanisms". Please let me know if you agree or disagree.
Max: {As indicated above, I disagree.}
[LMS: MAX IS, OF COURSE, WRONG IN DISAGREEING, AS EXPLAINED ABOVE]
Spetner: You ask, why does the existence of a special mechanism for the hypermutation in B cells preclude the example from being a model of mutations for NDT? The simple answer is that if you really want to suggest that mutations for NDT are capable of hypermutations as are the B cells, you have to show two things. First you have to show that such a highly complex system with its requisite enzymes actually exists in germ cells, where they can play a role in evolution. As far as I know, there is no such mechanism in germ cells. If you know of anything like this please let me know.
Max: {I have pointed out that the enzymatic mechanisms creating somatic mutations in B cells is not known. I have never claimed that it is the same mechanism as causes mutations in germ cells where they play a role in phylogenetic evolution, so I am not obligated to show what Spetner says I am.}
[LMS: THIS IS ANOTHER EXAMPLE OF DISTORTING THE ARGUMENT. IF MAX WANTS TO USE B-CELL HYPERMUTATIONS AS A DEMONSTRATION OF THE CAPABILITY OF GERMLINE MUTATIONS TO GENERATE THE INFORMATION REQUIRED FOR EVOLUTION (WHICH WAS THE MAIN PURPOSE OF HIS ESSAY) THEN HE IS OBLIGATED TO SHOW THAT GERMLINE MUTATION HAS THE SAME CAPABILITY AS B-CELL MUTATION. THAT IS NOT TO SAY THAT IT HAS THE SAME MECHANISM, BUT IT MUST HAVE A COMPARABLE MECHANISM. SINCE NO SUCH MECHANISM IS KNOWN FOR GERMLINE MUTATIONS, THE MAIN THESIS OF MAXÂ’S ESSAY FALLS.]
Spetner: Furthermore, according to the evolutionary paradigm, you must account for the origin and development of such a mechanism in the germline, or at the very least, you must suggest how such a development could reasonably occur. You are obligated to do this because you hold that all characteristics of life have evolved through random variation and natural selection.
Max: {Here Spetner, like Behe, seems to demand that I provide an “origin and development” scenario that he knows he will be able to disparage as another “just-so story.”
[LMS: I HAVE ASKED HIM TO BRING AN ARGUMENT. I DIDN’T ASK FOR A “SCENARIO". HIS PROBLEM, BUT NOT MY PROBLEM, IS THAT A FICTIONAL SCENARIO IS THE ONLY KIND OF ARGUMENT HE HAS, AND IT’S NOT SCIENTIFIC.]
Furthermore, the question of how somatic hypermutation evolved is totally irrelevant to the question of whether it is a good model for the efficacy of random mutation and selection in promoting “increased fitness,” which is the subject of my Talk.Origins essay.}
[LMS: THIS IS AN OTHER DISTORTION OF MY STATEMENT ABOVE. I DID NOT ASK FOR A DESCRIPTION OF HOW HYPERMUTATION EVOLVED. I ASKED FOR ONE ABOUT HOW A COMPARABLE MECHANISM IN THE GERMLINE COULD EVOLVE. ITÂ’S NOT IRRELEVANT BECAUSE IF ONE IS TRYING TO JUSTIFY NEO-DARWINIAN THEORY (NDT), THEN ONE WOULD BE ON SHAKY GROUND TO SUGGEST IT DEPENDS ON THE EXISTENCE OF A MECHANISM WHOSE OWN ORIGIN CANNOT BE ACCOUNTED FOR BY NDT]
Spetner: You are not entitled to postulate a mechanism that could not have evolved. Such a mechanism of germline mutation would have to produce accurately targeted mutations that could play a role in evolution. For such a system to develop by Neo-Darwinian evolution, a long series of evolutionary steps in ordinary evolution would have to play the role of a single step in the evolution of this mechanism, because selection here is based on successful evolution of the ordinary kind. Thus if a million generations are necessary for the evolution and perfection of a new phenotypic character, then a million times that, or a trillion generations, would be required for the evolution and perfection of this mechanism.
Dr. Lee Spetner's continued exchange with Dr. Edward E. Max