Scientific Critique of Evolution

8/11/2019 Scientific Critique of Evolution

1/19

Home| Feedback| Links| Books12 September 2009

A Scientific Critique Of EvolutionDr. Lee Spetner

in an exchange with Dr . Edward E. Max

2000 L.M. Spetner. All Rights Reserved.

r. Edward E. Maxposted an essay entitled The Evolution of Improved Fitness by RandomMutation Plus Selectionon http://www.talkorigins.org/faqs/fitness.html. He asked me formy comments and, as a result, I wrote a critique of his essay (of his version updated 12 July

1999) and sent it to him on 2 August 2000. He promised me he would have it posted on thetalkorigins website with a link from his essay. He responded to my critique on 22 August and I

replied to his response on 29 August. I received a reply from him on 25 September that he waslooking forward to responding, but was busy at the time. At the time of this writing (27

November 2000) I have not received any further substantive reply from him, and my commentshave so far not appeared on the above website. I have therefore decided to post here a unifiedversion of the present status of our debate. I have merged my original critique, his response, andmy reply to his response to present our debate in an understandable flow. In my original critique Irefer to Dr. Max in the third person. In my reply to his response, I address him in the second

person.

I recommend you first read his original essay posted at the above-mentioned URL, and then readthe following. I have interspersed Maxs comments into my critique where they are applicable,followed by my response to them.

At the outset, I shall establish an important and necessary guideline in this discussion ofevolution. The word evolutionis generally used in at least two different senses, and thedistinction between them is important. On the one hand, the word evolutionis used to denote thedescent of all life from a putative single primitive source. It is the grand sweep of evolution that issupposed to have led from a simple beginning, something perhaps simpler than a bacterium, to allorganisms living today, including humans. This descent is supposed to have occurred through

purely natural means. Neo-Darwinian theory (NDT), which is the prevailing theory of evolution,teaches that this development occurred through random heritable variations in the organismsfollowed by natural selection. I shall denote the word evolutionused in this sense asEvolution A .When evolution is discussed for popular consumption, it is most often Evolution A.

The second sense in which the word evolutionis used is to denote any kind of change of apopulation. The change can sometimes occur in response to environmental pressure (artificial ornatural selection), and sometimes it can just be random (genetic drift). I shall denote the word

used in this second sense asEvolution B. Evolution B has been observed. Evolution A is aninference, but is not observable. The distinction between these two meanings ofevolution

parallels the distinction between macroevolution and microevolution, but the two pairs of termsare not identical. Evolution A is certainly what is called macroevolution, but what is calledmacroevolution is not identical with Evolution A. In any case, I prefer to use the A and B to avoidhaving to carry whatever baggage might go with the macro/micro distinction.

The distinction between these two meanings ofevolutionis often ignored by the defenders of Neo-Darwinian evolution. But the distinction is critical. The claim is made for Evolution A, but the

proof offered is often limited to Evolution B. The implication is that the observation of EvolutionB is a substantiation of Evolution A. But this is not so. Since Evolution A is not an observable, itcan only be substantiated by circumstantial evidence. This circumstantial evidence is principallythe fossil record, amino-acid-sequence comparisons, and comparative anatomy. Circumstantial

evidence must be accompanied by a theory of how it relates to what is to be proved. NDT isgenerally accepted to be that theory. The strength of the circumstantial evidence for Evolution Acan therefore be no better than the strength of NDT.

The important claim of Neo-Darwinism is that it can account for Evolution A. The public

Page 1 of 19A Scientific Defense of a Creationist Position on Evolution

12/09/2009http://www.trueorigin.org/spetner1.asp
http://www.talkorigins.org/faqs/fitness.htmlhttp://www.talkorigins.org/faqs/fitness.html


2/19

perceives this claim as the core of the controversy over evolution. This claim is also the source ofthe contention by evolutionists that life is the result of purely natural processes, which ensue fromwell-known natural laws. I have examined this claim in my bookNot By Chance!,and havefound it to be empty.

Evolution A is the principle message of evolution, namely that all life descended withmodification from a putative single primitive source. The mechanism offered for the process ofmodification is basically the Darwinian one of a long series of steps of random variation, eachfollowed by natural selection. The variation is generally understood today to be randommutations in the DNA. That primitive source of life is assumed to be sufficiently simple that itcould have arisen from nonliving material by chance. There is no theory today that can accountfor such an event, but I shall refrain from addressing that issue here. That is for another place andanother time. What is relevant to this discussion is that the requirement that life arosespontaneously sets, at the very least, a stringent upper limit on the complexity and informationcontent of the putative first organism that could reproduce itself, and thus serve as a vehicle fromwhich to launch Darwinian evolution. The issue I address here is the alleged development of alllife by the Neo-Darwinian process of random mutation and natural selection, starting from asufficiently simple beginning.

Despite the insistence of evolutionists that evolution is afact,it is really no more than animprobable story. No one has ever shown that the mechanism of NDT can result in Evolution A.

Most evolutionists assumethat long sequences of microevolutionary events can produceEvolution A, but no one has ever shown it to be so. (Those few evolutionists who hold thatmacroevolution is really different from microevolution have changed their story several timessince they first came out with it, and their mechanism is so fuzzy that I have a hard time tellingwhat it is.)

For Evolution A to work, long series of beneficial mutations must be possible, each building onthe previous one and conferring a selective advantage on the organism. The process must be ableto lead not only from one species to another, but to the entire advance of life from a simple

beginning to the full complexity of present-day life. There must be a long series of possiblemutations, each conferring a selective advantage on the organism so that natural selection canenable it to take over the population. Moreover, there must be not just one, but a great manysuch, series.

The chain must be continuous in that at each stage a change of a single base pair somewhere inthe genome can lead to a more adaptive organism in some environmental context. The concept ofthe adaptive landscape is useful here. This concept was first introduced by Sewall Wright[1], butnow nucleotide sequences of the mean population genome have taken the place of Wrights genecombinations. There are a great many adaptive hills of various heights spread over the genomiclandscape. NDT then says that it should be possible to continue to climb an adaptive hill to alarge global maximum (or near-maximum), one base change at a time, without getting hung up ona small local maximum. No one has ever shown this to be possible.

Evolutionists often claim that if the evolutionary process were hung up on a small local adaptivemaximum, a large genetic change like a recombination, or other genetic rearrangement, could

bring it to another hill that has a higher peak, and place it higher up on that hill than it was before.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 itselfimprobable. No one has shown this to be possible either.

Moreover, as I have noted in my book, the large mutations such as recombinations andtranspositions are mediated by special enzymes and are executed with precisionnot the sort ofdoings one would expect of events that were supposed to be the products of chance. Evolutionistschose the mechanism of randomness, by the way, because no one can think of any other way that

beneficial mutations might occur in the absence of a law requiring them to occur. Geneticrearrangements may not be really random at all. They do not seem to qualify as the randommutations Neo-Darwinists can invoke whenever needed for a population to escape from a localsmall adaptive maximum.

Evolutionists can argue, and rightly so, that we have no way of observing long series ofmutations, since our observation time is limited to a relatively short interval. Our genetic

observations over the past 100 years is thought to be more like a snapshot of evolution rather thana representative interval in which we can search for the required long series of changes. But ourinability to observe such series cannot be used as a justification for the assumption that the seriesDarwinian theory requires indeed exist.


http://www.trueorigin.org/spetner1.asphttp://www.trueorigin.org/spetner1.asp


3/19

Max: An equally reasonable conclusion, in my view, would be that our inabilityto observe such series cannot be used as a justification for the assumption thatsuch a series of mutations did NOT occur.

Spetner: Thank you for acknowledging that what I said was reasonable. But the two statements,yours and mine, are not symmetrical. I dont have to assume the series did not occur to make acase for the inadequacy of NDT. Those who base a theory of evolution on the occurrence of sucha series are required to show that it exists, or at least that it is likely to exist. They are obliged todemonstrate an existence. I am not obliged to prove a non-existence. NDT has the convenientcharacteristic that the very events that would prove the theory valid are inherently not observable.Pleading that one should be excused from bringing such proofs because they are not observabledoes not help the evolutionists case. If you want to prove the theory, you had better findsomething observable.

Continuing my original critique, I pointed out that the argument against evolution is considerablystronger than merely noting that the evolutionists have not proved their case. It turns out thatthere is evidence that the series of mutations NDT requires do not, in fact, exist. The theoryrequires there be a vast number of possible point mutations which, coupled with natural selection,can generate the evolutionary advances that could produce Evolution A. If there really are a largenumber of potentially qualifying mutations, at least a few of them should have been observed insome 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, alsocontribute to the information, or complexity, increase that surely distinguishes present-day lifefrom the putative primitive organism.

These mutations must have whatever characteristics are necessary for them to serve as elementsof Evolution A. Thus, for a mutation to qualify as a representative member of the requiredmultitude of the long series that are supposed to produce evolution, it must bring new informationnot just to the genome of the organism, but the information must be new to the entire biocosm. [2]The horizontal transfer of a gene from one species to another does not inject new information intothe biocosm. To show evolution in action, one must at least demonstrate examples of a mutationthat can serve as a prototype of those required by the theory. Such a mutation must be one thatcould be a contributing member of a series of mutations that could lead to the vast increase ininformation required by the theory. Thus, for example, a mutation that yields an enzyme new tothe biocosm, or one that makes an enzyme more specific than anything in the biocosm, would be

adding information. On the other hand, a mutation that disables a repressor gene causing aconstitutive synthesis of an enzyme might be advantageous to an organism under specialcircumstances, but the disabling of a gene is not the kind of mutation the theory requires. Once ina while, such a mutation might make an adaptive contribution, but it cannot be typical of themutations required by the theory.

Max devoted a good portion of his essay to challenging what he calls the creationist argumentsagainst evolution. The arguments he challenged include false statements such as: (1) allmutations are harmful; (2) random mutations cannot increase the information content of a system;(3) the proteins had to arise by random trials without the benefit of natural selection. If he foundcreationists that said such things, then I suppose its part of the job he has assumed upon himselfto refute them. His challenges, however, are hardly a telling argument for evolution. (1)Mutations have indeed been observed that confer an adaptive advantage, but that alone does not

qualify them to serve as components of a series of Neo-Darwinian steps. (2) Some special casesof mutations may add information to the genome, but here again, that alone does not qualify themto serve as components of an evolutionary series. (3) Although the creation of proteins byrandom trials is not the thesis of NDT, no one has shown that they can be generated by randommutations and natural selection in the context of evolution. His challenges are valid, but they arefar from sufficient to establish NDT. I shall address these points in what follows.

The following is additional criticism of Maxs original essay that was not included in my originalresponse.

Max challenged point (1) by indicating that beneficial mutations indeed occur. The intention ofhis essay was to argue for Evolution A. Had he limited himself to Evolution B, I would have noquarrel with him. He claimed that a rare beneficial mutation can confer a survival, orreproductive, advantage to the individuals that carry it, thereby leadingover several

generationsto the spread of the mutation throughout a population.

His description is of what is often called a step in the evolutionary process. Max statedcategorically that such a step can occur. Moreover, to support Evolution A, the kind of step he




4/19

described must have happened over and over again, millions upon millions of times. Hepresented no evidence that it has ever happened, but simply tacitly assumed that it could. Can itindeed? I address that question.

One must understand that at the heart of NDT lies chance and randomness. Mutations are randomevents. The occurrence of a beneficial mutation at any given time in any given population isgoverned by chance. Even natural selection, which carries the burden of being the directive force

of evolution, is subject to the laws of chance. Selection coefficients are average values. Whathappens in any particular instance is a random event. A mutation, even one that confers adaptivebenefit on the organism, is likely to be wiped out by chance events (see Chapter 3 of my book).There is a good chance that it will disappear before it can take over the population. The questionis not if it can happen, but, with what probability will it happen?

NDT is a theory that is supposed to account for the natural development of all life from a simplebeginning. I dont know why we need such a theory, because the development of life from asimple beginning is not an observable. The theory is gratuitous; it comes to account forsomething that was never observed.

Actually, evolutionary thinking goes like this.

1. One observes present life.

2. One then assumes that it arose in a natural way.3. One then concocts a theory (e.g., the NDT) to account for the observation, given the

assumption.

I suppose that if the theory were really a good one, and could really explain well how life couldhave developed in a natural way, it would lend some credence to the assumption that life didindeed develop in a natural way. But it is not a good theory, and it does not account for what it issupposed to. Evolutionists, realizing this, have lately been reduced to arguing that if no one has a

better theory that can account for the natural origin of life, then one must accept NDT. As youwill see from some of Maxs comments below, he also adopts this approach. I dont know why

NDT merits the pedestal on which evolutionists have put it.

Now lets get back to the probability of occurrence of one of those evolutionary steps of Maxs.

Since they are chance events, we cannot say with any certainty that they will happen. The best wecan do is to say with what probability such an event will occur. So, evolutionists have offered usa theory (NDT) that postulates a long string of random events to account for the existence of life,assuming it developed in a natural way. If the probability of those events were to turn out to beclose to 1, then one could say that the theory accounts for the observation. On the other hand, if,according to the theory, the probability of those events were very low, one would have to say thatthe theory does not account for the observation. If a theory predicts observed events to be highlyimprobable, then one cannot justifiably say that the theory accounts for those events.

You would think that, since the issue of the probabilities of the evolutionary events is so crucial tothe validity of the theory, the advocates of evolution would have calculated the necessary

probabilities to make their case. But they havent. Since they have not made these calculations,Max is not entitled to assume that evolutionary steps can occur.

There is some difficulty in calculating these probabilities because the values of the relevantparameters are not all known. In my book, I addressed the problem of the probability of gettingenough successful evolutionary steps to account for the evolution of the horse. In spite of thedifficulties I just mentioned, I was able to calculate an important result. I found that either the

probability of the horse evolving was impossibly low, or else convergent evolution cannot occur.This result refutes NDT, and with it Evolution A. Not only is Maxs point here not substantiated,it stands refuted.

Antibiotic Resistance as an Example of Evolution

Continuing his effort to show the evolutionary efficacy of beneficial mutations, Max presented inhis essay the acquisition of antibiotic resistance by microorganisms as an example of evolution.He said one can demonstrate a beneficial mutation with laboratory organisms that multiply

rapidly, and indeed such experiments have shown that rare beneficial mutations can occur. Forinstance, from a single bacterium one can grow a population in the presence of an antibiotic, anddemonstrate that organisms surviving this culture have mutations in genes that confer antibioticresistance. Such an experiment shows that de novo beneficial mutations can arise.




5/19

My response to this is that I have shown in my book that mutations leading to antibiotic resistancefail the test of representing the mutations necessary for evolution. I summarize that argumenthere.

All antibiotics are derived from microorganisms. Recall the story of the serendipitous discoveryof penicillin by Alexander Fleming in 1928, when he noticed that his plate ofStaphylococcus

bacteria was clear in the vicinity of a bread-mold contaminant. The mold was found to produce

something that could lyse and kill the bacteria. That something was a molecule later namedpenicillin. Afterwards, other antibiotics were found to be produced by other microorganisms,such as soil bacteria. Soil has long been recognized in folk medicine as a cure for infections.

The antibiotics produced by these microorganisms serve them as a defense against attack by othermicroorganisms. Some microorganisms are endowed with genes that grant resistance to theseantibiotics. This resistance can take the form of degrading the antibiotic molecule or of ejecting itfrom the cell. Unfortunately for human health care, the organisms having these genes can transferthem to other bacteria making them resistant as well. Although the resistance mechanisms arespecific to a particular antibiotic, most pathogenic bacteria have, to our misfortune, succeeded inaccumulating several sets of genes granting them resistance to a variety of antibiotics.

The acquisition of antibiotic resistance in this manner qualifies as evolution only in the sense thatit is an adaptive hereditary change. It is an example only of Evolution B. It is not the type of

evolution that can make a baboon out of a bacterium. The genetic change is not the kind that canserve as a prototype for the mutations needed to account for Evolution A. The genetic changesthat could illustrate the theory must not only add information to the bacteriums genome, theymust add new information to the biocosm. The horizontal transfer of genes only spreads aroundgenes that are already in some species.

It turns out, however, that a microorganism can sometimes acquire resistance to an antibioticthrough a random substitution of a single nucleotide, and this is the kind of example Max

presented. Streptomycin,which was discovered by Selman Waksman and Albert Schatz and firstreported in 1944, is an antibiotic against which bacteria can acquire resistance in this way. Butalthough the mutation they undergo in the process is beneficial to the microorganism in the

presence of streptomycin, it cannot serve as a prototype for the kind of mutations needed byNDT. The type of mutation that grants resistance to streptomycin is manifest in the ribosome and

degrades its molecular match with the antibiotic molecule. This change in the surface of themicroorganisms ribosome prevents the streptomycin molecule from attaching and carrying out itsantibiotic function. It turns out that this degradation is a loss of specificity and therefore a loss ofinformation. The main point is that Evolution A cannot be achieved by mutations of this sort, nomatter how many of them there are. Evolution cannot be built by accumulating mutations thatonly degrade specificity.

In the final paragraph of my original critique, I said the following:

The mutations needed for macroevolution have never been observed. No random mutations thatcould represent the mutations required by NDT that have been examined on the molecular levelhave added any information. The question I address is: Are the mutations that have beenobserved the kind the theory needs for support? The answer turns out to be NO! Many have lostinformation. To support NDT one would have to show many examples of random mutations that

add information. Unless the aggregate results of the genetic experiments performed until now is agrossly biased sample, we can safely dismiss Neo-Darwinian theory as an explanation of how lifedeveloped from a single simple source.

Max: I think that the sample of genetic mutations you cite is in fact biased,incorrectly interpreted, and much too small and non-systematic to draw such asweeping conclusion. I will try to explain why I believe this.

Some streptomycin resistance mutations do, as you point out, reflect mutationsof the ribosomal protein S12 which cause loss of binding of this antibiotic, whichyou interpret as loss of information. However, you ignore other mutations ofthis protein that do not lead to loss of antibiotic binding (e.g. Timms et al.,MolGen Genet 232:89, 1992). According to your formulation, these mutations

would not represent a loss of information, yet they are represent naturalmutations that are adaptive under conditions of exposure to streptomycin.Would you accept that this kind of mutation is a good model for an adaptiveevolutionary change consistent with Neo-Darwinian Theory?




6/19

Using your own example of streptomycin resistance, I have pointed out thatsome mutations of the S12 ribosomal protein do not represent a loss ofinformation even by your own questionable criteria.

Spetner: First of all, I would recommend that you not refer to my criteria of information loss asquestionable until you understand them. See below, where I explain your misunderstanding.You let your own tacit assumptions get in the way of understanding my thesis.

Furthermore, you misunderstood the paper by Timms et al.,which you cited. All of the adaptivemutations reported in that paper show reduced binding of the streptomycin molecule. The 12adaptive mutations reported in the S12 protein fall into two categories. There was no example ofwhat you claimed I ignored. Five of those mutants are designated as streptomycin resistant (Smr),and seven are designated as streptomycin dependent (Smd). All 12 of them, in the words of theauthors reduce the affinity of the ribosome for streptomycin. Perhaps you would like to pointout to me where in that paper they mention mutations in S12 do not lead to reduced binding, andwhich you claim I have ignored.

Max: how about the single amino acid substitution in a blowflycarboxylesterase that converts this enzyme into an organophosphorus hydrolaseunder selection by organophosphate insecticides[Newcomb et al.,PNAS 94:464,1997]?

Spetner: In the Newcomb et al.paper that you cited, the experimenters started with 15 existingstrains of blowflies, some of which were resistant to organophosphorus (OP) insecticide and somewere not. No mutations were imposed or observed. The amino-acid differences between the twogroups were only assumed to have arisen by mutation.

The esterase enzyme E3 plays an important role in the operation of the flys nervous system. OPinsecticides kill the insects by interfering with this activity. Newcomb et al.found that theresistant allele of the gene encoding the enzyme E3 and the corresponding susceptible allele differfrom each other in 19 nucleotides. These differences translate into 5 amino-acid differences

between the enzymes. The authors concluded from their study that one of those 5, namely

Gly137 Asp, could account for both a loss of esterase activity and an acquisition of OP hydrolaseactivity.

Although it is not certain that the difference in the activities of this enzyme arose through arandom mutation, let us even suppose it did. If it did, then this mutation is not likely to haveoccurred recently, because much time would be needed to have accumulated all the 19 nucleotidedifferences between these two phenotypes. Both phenotypes have likely been in the populationsof blowflies long before OP insecticides entered the environment. The resistant allele musttherefore have adaptive advantages in addition to OP insecticide resistance.

One can say with a large measure of confidence that the resistant strain did not arise through asingle random mutation and proliferate through natural selection in the presence of OP. This isevident from a close examination of Fig. 2 of the above-cited paper. From what the authors have

shown, if there were such a mutation it would have been the substitution Gly137 Asp. Theauthors created two chimeric alleles of the E3 enzyme. One of these (lets call it the susceptiblechimera) had Gly137, corresponding to the allele susceptible to diazinon insecticide, but had the

other 4 of the 5 discordant amino acids identical with the wild-type allele resistant to diazinon.The other chimera (well call it the resistant chimera) had the opposite; it had Asp137, and theother 4 of the 5 discordant amino acids identical with the susceptible allele. The authorsmeasured the OP hydrolase activity in the wild-type susceptible allele, the susceptible chimera,the wild-type resistant allele, and the resistant chimera. They presented the results of theirmeasurements in Fig. 2 of their paper, which shows the following:

1. There is negligible OP hydrolase activity in the wild-type susceptible allele of E3 and in thesusceptible chimera.

2. There is marked OP hydrolase activity in the wild-type resistant allele of E3 and in theresistant chimera. It is this activity that the authors understand to be responsible for theresistance to OP insecticide.

3. The OP hydrolase activity of the resistant chimera is about two and a half times that of thewild-type resistant allele.

Accepting the authors premise that the OP hydrolase activity is responsible for the resistance, wecan say that a strain of blow fly whose E3 enzyme is identical with that of the wild-typesusceptible, except for the single substitution Asp137, should be even more resistant than the wild-




7/19

type resistant strain. Therefore, if a mutation occurred in the susceptible strain achieving the

substitution Gly137 Asp, it should be more adaptive than the wild-type susceptible strain in thepresence of diazinon insecticide. That being the case, the resistant population of blow flies shouldhave an E3 enzyme with only Asp137differing from that of the wild-type susceptible strain. Sincethat is not the case, one can conclude that the other 4 of the discordant amino acids must havesome overriding adaptive value that trumps the greater OP hydrolase activity of the resistantchimera, even though we dont know what that adaptive value is. In light of these data, one can

conclude that the substitution Gly137

Asp did not arise by random mutation from the susceptiblestrain.

Moreover, to tell if the substitution, Gly137 Asp, even if it did arise by a random mutation,represents an addition or a loss of information, we must know more about how the mutationaffects the enzymes hydrolase activity on more than just the one substrate. As in the example Ishowed in my book (and described briefly below), what looked like an enhancement of activity onone substrate, coupled with a degradation of activity on another, turned out to be nothing morethan a simple reduction of specificity of the enzyme over wider a set of substrates. As I wrote inmy original comments (see below) on your posting, one must be careful about jumping toconclusions about what constitutes an information increase. This is not a weasel statement. Onecan know when one has enough data to make a judgment. If the activity profile of the mutantenzyme over several different substrates sharpens by increasing the activity on one substrate andconcomitantly decreasing the activity on other substrates, there is an increase in selectivity and

hence an increase in information. If, on the other hand, the activity profile of the mutant enzymeover a set of substrates is flatter than that that of the wild type, then information has been lost.One just needs enough data to be able to see an activity profile over several substrates for both themutant and the wild type.

Max: Certainly you are not correct when you say all known examples of thesemutations lose information rather than gain it.

Spetner: Since you have not shown any valid counterexamples, my statement still stands, andyour statement falls. None of the examples you gave qualifies as a random mutation in the germline that could be typical of those required for Evolution A. The context in which I made theabove statement was that of random mutations in the germ line that, according to NDT, arecapable of producing Evolution A.

You must admit that the most widely used examples by evolutionists to show evolution in actiondo in fact lose information. You have used such an example yourself in your posted essaytheevolution of antibiotic resistance in microorganisms. These so-called best examples are poorand do not demonstrate, nor even indicate a typical contribution to, Evolution A.

You failed in your attempt to rebut my statement that all known examples of random mutationsthat could play a role in Evolution A lose information rather than gain it.

Evolution and the Increase of Information

In my critique, I included for pedagogical purposes the following short explanation of theinformation in enzymatic activity and its measurement:

I shall emphasize again: There is no theorem requiring mutations to lose information. I caneasily imagine mutations that gain information. The simplest example is what is known as a backmutation. A back mutation undoes the effect of a previous mutation. If the change of a single

base pair in the genome were to change to another and lose information, then a subsequentmutation back to the previous condition would regain the lost information. Since these mutationsare known to occur, they form a counterexample to any conjecture that random mutations mustlose information. An important point I make in my book, and which I emphasize here, is that, asfar as I know, no mutations observed so far qualify as examples of the kind of mutations requiredfor Evolution A.

In discussing mutations in my book I noted in each case in which the molecular change wasknown, that it could not serve as a prototype for the mutations required by NDT. In all the cases Idiscussed, it was the loss of information that prevented the mutation from serving as a prototype

of those required by NDT. The back mutation likewise cannot serve as a prototype of the NDT-required mutations. Here, the reason is not that it loses informationit actually gainsinformation. But the information it gains is already in the biocosm and the mutation contributesnothing new. Evolution is not accounted for if the only information gain was by back mutations.




8/19

In my book, I did not quantify the information gain or loss in a mutation. I left it out mainlybecause I was reluctant to introduce equations and scare off the average reader. And anyway, Ithought it rather obvious that a mutation that destroys the functionality of a gene (such as arepressor gene) is a loss of information. I also thought it rather obvious that a mutation thatreduces the specificity of an enzyme is also a loss of information. But I shall take this opportunityto quantify the information difference before and after mutation in an important special case,which I described in my book.

The information content of the genome is difficult to evaluate with any precision. Fortunately, formy purposes, I need only consider the change in the information in an enzyme caused by amutation. The information content of an enzyme is the sum of many parts, among which are:

Level of catalytic activity Specificity with respect to the substrate Strength of binding to cell structure Specificity of binding to cell structure Specificity of the amino-acid sequence devoted to specifying the enzyme for degradation

These are all difficult to evaluate, but the easiest to get a handle on is the information in thesubstrate specificity.

To estimate the information in an enzyme I shall assume that the information content of theenzyme itself is at least the maximum information gained in transforming the substratedistribution into the product distribution. (I think this assumption is reasonable, but to be rigorousit should really be proved.)

We can think of the substrate specificity of the enzyme as a kind of filter. The entropy of theensemble of substances separated after filtration is less than the entropy of the original ensembleof the mixture. We can therefore say that the filtration process results in an information gainequal to the decrease in entropy. Lets imagine a uniform distribution of substrates presented tomany copies of an enzyme. I choose a uniform distribution of substrates because that will permitthe enzyme to express its maximum information gain. The substrates considered here arerestricted to a set of similar molecules on which the enzyme has the same metabolic effect. Thisrestriction not only simplifies our exercise but it applies to the case I discussed in my book.

The products of a substrate on which the enzyme has a higher activity will be more numerousthan those of a substrate on which the enzyme has a lower activity. Because of the filtering, thedistribution of concentrations of products will have a lower entropy than that of substrates. Notethat we are neglecting whatever entropy change stems from the chemical changes of the substratesinto products, and we are focusing on the entropy change reflected in the distributions of the

products of the substrates acted upon by the enzyme.

The entropy of an ensemble ofnelements with fractional concentrationsf1,,f

nis given by

and if the base of the logarithm is 2, the units of entropy are bits.

As a first illustration of this formula let us take the extreme case where there are n possible

substrates, and the enzyme has a nonzero activity on only one of them. This is perfect filtering.The input entropy for a uniform distribution of n elements is, from (1), given by

since thefisare each 1/n. The entropy of the output is zero,

because all the concentrations except one are zero, and the concentration of that one is 1. Thenthe decrease in entropy brought about by the selectivity of the enzyme is then the difference

between (2) and (3), or

Another example is the other extreme case in which the enzyme does not discriminate at allamong the nsubstrates. In this case the input and output entropies are the same, namely

Therefore, the information gain, which is the difference betweenHO andHI, in this case is zero,

We normalize the activities of the enzyme on the various substrates and these normalizedactivities will then be the fractional concentrations of the products. This normalization will

(1)

(2)

(3)

(4)

(5)




9/19

eliminate from our consideration the effect of the absolute activity level on the informationcontent, leaving us with only the effect of the selectivity.

Although these simplifications prevent us from calculating the total entropy decrease achieved byaction of the enzyme, we are able to calculate the entropy change due to enzyme specificity alone.

The Dangers of Conclusion Jumping

As a final example let me take part of a series of experiments I discussed in my book, whichdemonstrate the dangers of conclusion jumping. This subject bears emphasis becauseevolutionists from Darwin on have been guilty of jumping to unwarranted conclusions frominadequate data. I shall here take only a portion of the discussion in my book, namely, what Itook from a paper by Burleigh et al.[3]to illustrate my point.

Ribitol is a naturally occurring sugar that some soilbacteria can normally metabolize, and ribitoldehydrogenase is the enzyme that catalyzes the first stepin its metabolism. Xylitol is a sugar very similar instructure to ribitol, but does not occur in nature. Bacteriacannot normally live on xylitol, but when a large

population of them were cultured on only xylitol,

mutants appeared that were able to metabolize it. Thewild-type enzyme was found to have a small activity onxylitol, but not large enough for the bacteria to live onxylitol alone. The mutant enzyme had an activity largeenough to permit the bacterium to live on xylitol alone.

Fig. 1 shows the activity of the wild-type enzyme andthe mutant enzyme on both ribitol and xylitol. Note thatthe mutant enzyme has a lower activity on ribitol and ahigher activity on xylitol than does the wild-type enzyme. An evolutionist would be tempted tosee here the beginning of a trend. He might be inclined to jump to the conclusion that with aseries of many mutations of this kind, one after another, evolution could produce an enzyme thatwould have a high activity on xylitol and a low, or zero, activity on ribitol. Now wouldnt that bea useful thing for a bacterium that had only xylitol available and no ribitol? Such a series would

produce the kind of evolutionary change NDT calls for. It would be an example of the kind ofseries that would support NDT. The series would have to consist of mutations that would, step bystep, lower the activity of the enzyme on the first substrate while increasing it on the second.

But Fig. 1 is misleading in this regard becauseit provides only a restricted view of the story.Burleigh and his colleagues also measured theactivities of the two enzymes on anothersimilar sugar, L-arabitol, and the results ofthese measurements are shown in Fig. 2.With the additional data on L-arabitol, adifferent picture emerges. No longer do wesee the mutation just swinging the activity

away from ribitol and toward xylitol. We seeinstead a general lowering of the selectivity ofthe enzyme over the set of substrates. Theactivity profiles in Fig. 2 show that the wild-type enzyme is more selective than is themutant enzyme.

In Fig. 1 alone, there appears to be a trendevolving an enzyme with a high activity onxylitol and a low activity on ribitol. But Fig. 2 shows that such an extrapolation is unwarranted.It shows instead a much different trend. An extrapolation of the trend that appears in Fig. 2 wouldindicate that a series of such mutations could result in an enzyme that had no selectivity at all, butexhibited the same low activity on a wide set of substrates.

The point to be made from this example is that conclusion jumping from the observation of anapparent trend is a risky business. From a little data, the mutation appears to add information tothe enzyme. From a little more data, the mutation appears to be degrading the enzymesspecificity and losing information.




10/19

Just as we calculated information in the two special cases above, we can calculate the informationin the enzyme acting on a uniform mixture of the three substrates for both the wild type and themutant enzyme. Using the measured activity values reported by Burleigh et al.we find theinformation in the specificities of the two enzymes to be 0.74 and 0.38 bits respectively. Theinformation in the wild-type enzyme then turns out to be about twice that of the mutant.

The evolutionist community, from Darwin to today, has based its major claims on unwarranted

conclusion jumping. Darwin saw that pigeon breeders could achieve a wide variety of forms intheir pigeons by selection, and he assumed that the reach of selection was unlimited.Evolutionists, who have seen crops and farm animals bred to have many commercially desirablefeatures, have jumped to the conclusion that natural selection, in the course of millions of years,could achieve many-fold greater adaptive changes than artificial selection has achieved in onlytens of years. I have shown in my book that such extrapolations are ill founded because breedingexperiments, such as those giving wheat greater protein content or vegetables greater size, resultfrom mutations that disable repressor genes. The conclusions jumped to were false because theywere based on data that could not be extrapolated to long sequences. One cannot gaininformation from a long sequence of steps that all lose information. As I noted in my book, thatwould be like the merchant who lost a little money on each sale, but thought he could make it upon volume.

Max: I want to make it clear that I dont buy your interpretation of certain

specific mutations as reflecting a loss of information. You state that theinformation content of an enzyme is the sum of many parts, among which are:level of catalytic activity, specificity with respect to the substrate, strength [andspecificity] of binding to cell structure, [and] specificity of the amino-acidsequence devoted to specifying the enzyme for degradation. This formulation isvague, non-quantitative, not supported by clear logic, not accepted in thescientific literature (to the best of my knowledge; please educate me if I amwrong), and in my view not useful.

Spetner: Ed, the level of your argument here is quite low. You have seen this entire section(above), and you took from the introduction my list of what characteristics can contribute to theinformation content of an enzyme and criticized it for being non-quantitative (followed by other

pejorative epithets). Is that supposed to be some sort of debating tactic? In any case, the tactic is

out of place in this discussion. From the context of what I wrote, it should have been clear to youthat this partial list of characteristics that can contribute to the information in an enzyme was anintroduction to my quantitativeestimate of one of the characteristics of specificity of an enzyme.After I showed how one might calculate the information related to a type of specificity, I showedhow a mutation that appeared to enhance activity on a new substrate actually reduced theinformation by about 50%.

It is elementary that specificity translates into information and vice versa. Have you ever played20 questions? With the YES/NO answers to 20 judicious questions, one can discover a

previously-chosen number between 1 and a million. If the questions are well chosen, thoseYES/NO answers can be worth one bit of information each, and 20 bits can specify one object outof a million. Twenty bits of information translates to specificity of one part in a million. Ten

bitsto one part in a thousand.

The Zip codes in the US also demonstrate that specificity and information are two sides of thesame coin and go hand in hand. An address in the United States can be completely specified bythe nine-digit zip code. One digit of information will narrow down the address from beinganywhere in the United States to being in just a few states. Thus if the first digit is a 6, theaddress is located somewhere in Illinois, Missouri, Kansas, or Nebraska.

A second digit of information will add specificity by narrowing down the address further. A 3, 4,or 5 in the second digit puts the address in Missouri. A 3 in the second digit puts it in the eastern

portion of the state. Two digits of information are more specific than one.

A third digit of information is still more specific, narrowing down the address even more, makingit still more specific. If the third digit is a 1, the address is specific to St. Louis and its suburbs.The next two digits of information pin down the address to within a few blocks. The last 4 digits

of information can locate a specific building. Thus, it is clear that the information contained inthe digits of the zip code translate into specificity.

There is no question about it: SPECIFICITY = INFORMATION.




11/19

Max: there are several other ways of considering how mutations affectinformation. In my view, even if all S12 mutations that caused streptomycinresistance abolished antibiotic binding, a reasonable argument could still bemade that such mutations represent a gain of information rather than a loss. Inthe universe of all the possible S12 amino acid sequences that can function in theribosome, essentially all S12 proteins found in wild-type bacteria (i.e., thosegrown in the absence of streptomycin) bind to this antibiotic. The S12 sequencesthat allow bacterial growth in the presence of streptomycin represent a small

subset of the universe of observed functional S12 sequences. Therefore bygrowing bacteria in streptomycin we select for a specific and small subset ofpossible S12 sequences; thus it might be argued that we have forced a smallincrease the information content of the genome by narrowing the choice of S12sequences.

Spetner: I cannot agree with what you wrote here. The wild-type S12 proteins that bind to thestreptomycin molecule also form a subset of the universe of all possible S12 proteins. The set ofS12 proteins that allow bacterial growth in streptomycin (i.e. that do not bind to the antibiotic)form a disparate subset of the universe of S12 proteins. My intuition tells me that the set that

binds (the susceptible set) is smaller, and therefore has a smaller entropy, than the set that doesnot bind (the resistant set). Mutations that appear in the presence of the antibiotic convert onesubset to the other. A mutation that transfers the enzyme from a low-entropy set to a higher-

entropy set loses information; it does not gain it.

Max: Alternatively, it could just as well be argued that in all cases of singleamino acid replacements there has been no change in information content at all,in that any given amino acid sequence is equally improbable compared withany other amino acid sequence of the same length.

Spetner: This is not a useful concept. It is like the pleading of the poker player who had a busthand. When it came to the call, his opponent showed four aces. He pleaded that his bust handwas just as improbable, and therefore worth as much, as the four-aces, and suggested they splitthe pot. Hes right about the probabilities of the two hands, but in the context of poker, four aceswin and the bust hand loses. Although in the context of the organisms survival in streptomycin,the degraded specificity of the S12 protein is beneficial, in the context of evolution, it is a deadend and it loses.

Max: Certainly you have provided no theoretical justification for using yourarbitrary criteria such as specificity of binding to assess information content;indeed, you fail to provide any quantitative theory of how all the criteria you list(level of catalytic activity, specificity with respect to substrate, . . etc) would beintegrated into a quantitative information measure.

Spetner: On the contrary, I have provided substantial theoretical justification for equatinginformation to specificity. You just chose to ignore what I wrote.

Max: In general, if a protein has evolved under selection for a specific function,changes in the structure of that protein to meet some new criterion can beexpected to adversely affect the original function. This is true in ribosomal S12

proteins that have become streptomycin resistant (they are less efficient inproof-reading) and is clear in the example of the carboxylesterase, which losesthis activity essentially completely when mutated to become anorganophosphorus hydrolase. The structure of any proteinlike the product ofengineering designinvolves trade-offs between various opposing optimizationgoals. Thus it is likely that intense selection for resistance to a lethal agentexactly the kind of quick experimental protocol useful for laboratory models ofadaptive evolutionary changewill lead to mutations that involve what mightbe construed by you as a loss of information something is always likely to belost when a modified, mutated protein becomes prevalent in the face of a newselective pressure. This fact explains, I believe, why such genetic experimentsmay in fact be grossly biased in the way that led you to inappropriately dismissNeo-Darwinian theory.

Spetner: You show here that you misunderstand what I mean by a mutation losing information.If a mutation in an enzyme were to lose its specificity to one substrate and gain specificity toanother substrate, I would credit the mutation with againof information and I would notconstrue it as a loss. But I will not credit it with a gain if the enzyme increased its activity to




12/19

another substrate merely by becoming less specific, as in the example I gave above with ribitoland xylitol.

What you have presented is not so much a case for bias as it is a pleading that any modification toa protein mustcause some degradation, and therefore you want to be excused from having toshow a case where information is increased. But you have overplayed your hand. You seem to

be saying in effect that because proteins have evolved so well, anychange will degrade them. (Ifthat were so, it would be a good argument for Creation.)

Suppose a mutation causes a protein to become more adaptive in a particular environment. Thenby your thesis, it is already so well evolved that something is always likely to be lost when amodified, mutated protein becomes prevalent in the face of a new selective pressure. You implythat the loss is one of information, because thats the context of this discussion. But then,according to you, after that modification, it is again well evolved, so the next time it undergoes anadaptive mutation, it must again lose something. Continuing the process you have described, the

protein will continue to lose something. You have just consigned the evolutionary process to adead end!

Max: But consider this: If blowflies happened to have duplicated theircarboxyhydrolase gene before they were exposed to organophosphates, and ifthey mutated one of their two copies to organophosphate hydrolase, we would

have a clear example of an increase in genetic information: creation of a newfunctional gene without any loss of information since the original sequencewould be intact in the unaltered copy.

Spetner: I have already shown above that the organophosphorus hydrolase activity did notnecessarily come from a single point mutation. I have also noted that we dont have enoughinformation to know if the acquisition of this activity is a loss or a gain of information.Furthermore, you dont have to keep bringing up the necessity of gene duplication. If an enzymelost its old activity to gain a new specificity, I would credit it with a gain of information withoutregard to the loss of the old activity. I have always assumed that gene duplication is available toevolution.

Max: Now, gene duplications are rather rare events, and favorable mutationsare also rare; so the combined frequencies of these two events are so rare that

they are not likely to be observable in a laboratory experiment. But if we look atmany gene systems in modern animals we can see how they might have beencaused by duplication followed by mutation to a new, or at least slightlydifferent, function.

Spetner: As I said above, I grant the possibility of gene duplication, so you neednt throw that into make the probability low. If I saw the gain of specificity through a random mutation, I wouldcredit the mutation with an increase of information without deducting for the loss of the oldactivity. A single point mutation (which is all that NDT requires at each step) is not very rareconsidering all the genetic experiments that have been performed throughout the world. If therereally are as many adaptive, information-adding mutations as NDT needs, we should expect tohave seen many of them.

Max: As an example of such a system, lets consider a gene locus that I havestudied in my lab: the human immunoglobulin heavy chain (or IgH) locus. Inthe human locus one sees evidence of a large DNA duplication that created twocopies that are highly similar in both coding and non-coding flanking regions.One duplicate includes constant region sequences known as gamma3, gamma1,pseudo-epsilon and alpha1, while the second copy contains gamma2, gamma4,epsilon and alpha2. More primitive primates like the New World monkeysappear to have a single copy of this locus and a single gamma gene. The fourhuman gamma chain genes are thus thought to have derived from a singleancestral gamma chain gene in a primate ancestor by a series of duplicationsand mutations. In the ancestral primate we had one non-specialized genewhereas in modern humans we have four specialized genes. This is exactly thesort of genetic change that would be consistent with Neo-Darwinian evolutionleading to an increase in complexity.

Spetner: Yes, information would have been increased if what you speculate had indeedhappened. The proof would only lie in showing that it has indeed happened through randommutations and natural selection. Let us not lose sight of the requirement of Neo-Darwinian




13/19

evolution for long series of single-nucleotide substitutions, where each mutation makes thephenotype sufficiently more adaptive than it was to permit the mutated phenotype to take over thepopulation through natural selection with a high probability. It is far from clear that theindividual mutations you suggest will each be adaptive and selected at each step. You cannotshow thisyou merely assume it. You are postulating an historical event that cannot possibly beverified. It seems that all of your arguments are based on postulating events that are inherentlynot observable. That should make one a little suspicious of the theory, shouldnt it?

Max: I realize that the above model for the human IgH locus is hypotheticaland assumes that the evolutionary triad of duplication, random mutation andselection is a reasonable naturalistic explanation for the four human gammagenes. We cannot verify this explanation since we can never know theproperties of the primordial ancestral gamma immunoglobulin, or know theseries of mutations that occurred in the various duplicate gamma genes duringour evolution from that primordial ancestor. What I am asking is: is thereanything so implausible in this model to justify your suggestion that we shoulddismiss Neo-Darwinian theory as an explanation for this example?

Spetner: Yes, it is implausible because you are postulating a series of events of a type for whichthere is evidence that they have not occurred. If they had occurred to produce Evolution A, thereshould have been a vast number of them, and there arent. Had there been the required large

number of them, we should have seen some of them in all the genetic experiments performed inall the laboratories of the world. And we havent, to my knowledge, seen a single one.

Max: Or more to the point, exactly what alternative explanation for the originof the four human gamma genes do you propose that is more plausible than theone I offered?

Spetner: How does Creation grab you? You probably are reluctant to admit that possibility, butyou can think of it as a default position. It cannot be demonstrated scientifically, not because ofany philosophical defect in the proposition, but because of the limitations of Science. BecauseScience is incapable of dealing with it does not mean it hasnt happened. There are, after all,some truths in the physical world that cannot be reached by Science, just as there aremathematical truths that cannot be reached by mathematical proof. [4] If we dont have ascientifically viable theory to account for the origin of the four human gamma genes, or for the

origin of life itself, we neednt despair. Not every mystery necessarily has a scientific solution. Ido not mean to say that one should not look for a scientific solution. One should. But not havingsuch a solution is not a license to make up stories and pass them off to a gullible public asScience. Because I dont have a (scientifically) plausible explanation of the origin of life, doesnot mean that your improbable stories are correct and should be foisted on the public under theguise of scientific truth.

Max: This is important, because considering the weaknesses I have pointed outin your arguments, you are far from having definitively ruled out the Neo-Darwinian evolutionary triad as the correct explanation for what you call thegrand sweep of evolution[I am now calling this Evolution A (LMS)].

Spetner: As you can see from my above remarks, you have not succeeded in pointing out any

weakness in my arguments. What you call the Darwinian evolutionary triad is no more than abig bluff. It has great theoretical and empirical difficulties, which neither you nor anyone else hassucceeded in overcoming.

Mutations in the Immune System

Maxs field of expertise is the immune system. This is the field in which he does research and inwhich he has published. In his original posting, hispice de rsistancewas the presentation ofsomatic mutations in B lymphocytes (B cells) of the vertebrate immune system as examples ofrandom mutations that add information. He implied that Evolution A could follow this method toachieve baboons from bacteria. I agree with him that these mutations add information to the B-cell genome. I also agree that they are random. They are random, however, only in the basechanges they make; they are not random in where in the genome they can occur. More important,I do not agree that the Evolution A could be achieved through such mutations, and I shall show

why.

Although the somatic mutations to which Max referred are point mutations that do indeed addinformation to the genome of the B cells, they cannot be applied to Darwinian evolution. These




14/19

are not the kind of mutations that can operate as the random mutations required by NDT, whichallegedly 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 highmorethan a million times normal germ-line mutation rates. For this reason they are calledhypermutations. If an organism had a germline mutation rate that was even a small fraction ofthis rate it could not survive. For a second thing, the hypermutations in the B cells are restrictedto a specific tiny portion of the genome, where they can do no harm but only good. The entiregenome of the B cell could not mutate at this rate; the hypermutation must be restricted only tothe region encoding selected portions of the variable part of the antibody.

The mutation rate of the hypermutating part of the B cells genome is usually about 10-3per basepair per replication[5], and it can be as high as 10-2per base pair per replication[6]. These ratescannot produce Darwinian evolution. If a genome were to mutate at this rate, there would be, onthe average, several mutations in every gene, with a high probability that many of them would befatal for the organism. Darwinian evolution could not occur with such rates.

These high rates are essential for the working of the immune system. In eachreplication of a Bcell, about 30 of the 300 or so gene regions encoding the CDRs (complementarity-determiningregions) will have a mutation. A lower mutation rate would make for a less efficient immunesystem. 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, thehypermutations are mediated by special enzymes. Although the hypermutations are random in thechanges they make in the bases of the genome, they are not random in the positions in which theyoccur. They occur only in the small region in which they are needed, and occur there throughenzymes that apparently play only that role. Furthermore, they occur only when they areswitched on by the controlling mechanism of B-cell maturation. Thus, it is clear that thehypermutations in B cells cannot serve as a prototype for the random mutations required for NDT.

Max: You declare that the B cell example is a poor model for what happensin Darwinian evolution, and you cite two reasons: (1) the mutation rate in thismodel is much higher than what is seen in non-immunoglobulin genes and innon-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 Bcell example than in evolution, but I fail to see why that fact weakens theusefulness of the example as a model for evolution. If adaptive mutations thatincrease information in the genome of a B lymphocyte population can occurover one week given a high mutation rate, what theoretical argument would leadyou to reject the idea that adaptive mutations that increase information in thegenome of a germ cell population could occur over many millions of years givena much lower mutation rate?

Spetner: The theoretical argument hinges on the fact that the benefit that accrues to the immunesystem is a nonlinear function of the mutation rate. Evolution requires a long series of steps eachconsisting of an adaptive mutation followed by natural selection. In this series, each mutationmust have a higher selective value than the previous [7]. Thus, the evolving population moves

across the adaptive landscape always rising toward higher adaptivity. It is generally accepted thatthe adaptive landscape is not just one big smooth hill with a single maximum, but it is many hillsof many different heights. Most likely, the population is on a hill that is one of the many lowestand not on one of the few highest in the landscape. It will then get stuck on a low local maximumof adaptivity and will not be able to move from it. That is particularly likely because the steps ittakes are very smallonly one nucleotide change at a time. The problem is compounded by thelack 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 ofthe other 19. In general, its potential for change is limited to only 5 or 6 others. To evolve off thedead point of adaptivity, a larger step, such as the simultaneous change of more than onenucleotide, is required[8]. 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 mybook, Chapter 3). Therefore, several adaptive mutations must occur independently and randomlyat each step.

Hypermutation in the B cells does this. It quickly achieves all possible single, double, and triplemutations for the immune system, which allows them to obtain the information necessary tomatch a new antigen. Ordinary mutations, at the normal low rate, cannot add this information




15/19

even over long times. I shall explain why. The effects of mutation rate are nonlinear. Consider apopulation of antigen-activated B cells of, say, a billion individuals, which is smaller than thetypical number. In two weeks, there will be about 30 generations. Lets say the population size isstable, 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 independent changesin any particular nucleotideduring a two-week period. The probability of getting twoparticularnucleotides to change is one per million replications. Thus in two weeks, there will be an averageof 30 thousand changes in any two particular nucleotides. There will be an average of 30 changes

in any three particular nucleotides. If the mutation rate is 1 per 100, these numbers would becorrespondingly larger.

How many generations, and how long, would it take to get a particular multiple-nucleotide changein a germ cell to have an effect on Neo-Darwinian evolution? Here, the mutation rate is about one

per billion nucleotides per replication. Lets suppose were doing this experiment with apopulation of a billion bacteria. Then, in one generation, there will be an average of one changein any particular base in some one individual. A particular double-base change has a probabilityof one per quintillion, or 10-18. To get one of these would take a billion generations, or about100,000 years. To get a triple change would take 1014, or a hundred trillion, years. That is why along waiting time cannot compensate for a low mutation rate. Ive given numbers here for alaboratory experiment with bacteria. Many more mutations would be expected world wide. Butthe 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. Multicelledanimals would have many fewer mutations than those cited above for bacteria.

Max: Your second objection to the somatic mutation model in B-cells, thatspecial enzymes are involved, is unsupportable. As far as I can tell from myreading of the literature, the mechanism of somatic hypermutation in B-cells isnot currently known.

Spetner: On the contrary, my objection is well supported in the professional literature. Thesomatic hypermutations you cite do indeed require special enzymes, and is not the kind ofmutations held to be responsible for the variation required in NDT. These mutations, unlikeordinary errors in DNA replication in the germline, are under precise control in the cell. They areturned on exactly when they are needed, and they are 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 CDRs, which form the antibody-binding site. They do not occur at any otherplace in the genome. Although the mechanism of this precisely targeted phenomenon is not yetknown in complete detail, enough is known to say that there has to be a mechanismhypermutation does not happen by chance. Thus, even 14 years ago, a popular textbook in cell

biology said[9], There must exist mechanisms that direct mutational activity to variable-regionsequences. How this might occur is not known; possibly some sequence in the area of thevariable region directs aspecial enzyme system to carry out point replacements of nucleotidesindependent of template specification. (my emphasis)

Informed current opinion on the subject of somatic hypermutations is overwhelmingly (andperhaps even unanimously) in favor of the suggestion that they are produced by a specialmechanism requiring special enzymes that are unlike the spontaneous germline mutationsassumed to be responsible for evolution. Experts in this field are very clear on this point. Let me

just bring you a few quotes from a recent paper by Robert Blanden and his colleagues[10]

, in whichthey describe important characteristics of somatic mutations, and note how they differ fromgermline mutations [all emphases are mine (LMS)]:

The accumulated findings strongly suggest a complex mechanism [forhypermutation], which is unlikely to employ simple error-prone DNA repair

processes involving DNA template directed DNA synthesis.

there should logically be a mechanismto ensure that when successful mutationhas taken place, there is no further mutation which may destroy successful V(D)Jsequences.

Let me also bring you a few quotes from another recent paper by David Winter & PatriciaGearhart (whom you may even know) on the subject of somatic hypermutations [11]:

The pattern of somatic mutations in rearranged variable (V) genes differs from thepattern of meiotic mutations, indicating that a different mechanismgenerateshypermutations than generates spontaneous mutation.




16/19


17/19

Spetner: And I have shown above the errors of your argument. Your use of pejorativeadjectives cannot make up for the weakness of your case.

Max: (2) I have argued that your information criteria (for deciding whethergenes gain or lose information after specific mutations) are vague, non-quantitative, not supported by any logic, not accepted in the scientific literatureand not demonstrably superior to other ways of judging the effects of mutationon genomic information.

Spetner:Not only have I made it clear above that my criterion for gain/loss of information isquantitative, and supported by logic and the conventional understanding of these notions ininformation theory, I included that section in my first critique of your posting. You chose not torelate to it at all, and instead you made up the above criticism out of thin air.

Max: (3) I have discussed why examples of adaptive mutations in non-duplicated genes might appear to show some loss of one type of function (if notloss of information) as they gain a new function under selection by a novelenvironmental stress, and thus exhibit a kind of bias that might have misleadyou into making your rather risky extrapolations about the role of randommutations in evolution.(4) I have explained why an example of a gene duplication followed by

differentiation of the two gene copies to enlarge genomic information might behard to observe in the laboratory, contributing to the bias mentioned above inthe set of mutations that we do observe in the laboratory.

Spetner: And I have shown above that what you call a possible bias in our observations ofmutations stems from your lack of understanding of my arguments. You have shown no validreason why there is any bias in the set of all mutations that have been observed in all the geneticlaboratories in the world.

Max: (5) I have provided an example of duplicated and differentiatedimmunoglobulin gamma genes that can plausibly be interpreted by theevolutionary triad of mechanisms (gene duplication, random mutation andnatural selection) each of which has been demonstrated individually as naturalmechanism in appropriate laboratory experiments; and I have challenged you to

provide an alternative more plausible explanation for the origin of these fourgamma genes.

Spetner: And I have shown above that your laboratory experiments are not applicable toEvolution A. I have also pointed out that there is no obligation to provide a natural explanation oforigins. There may not be one. But I encourage you to keep looking. But please remember thatthe solution to the problem of the origin of proteins, or the origin of life, may not be where youare looking.

Max: (6) Finally, I have asked you to explain why hypermutation and selectionof immunoglobulin genes in B cells should not serve as an instructive prototypedemonstrating the potential of mutation and selection to improve function ofproteins in evolution; specifically, I have asked why either the faster mutation

rate in the B cell model or the unknown mechanisms of the mutations arerelevant to the question of whether random mutation and natural selection canlead to increased fitness of proteins in evolution.

Spetner: And I have explained all that above and showed you why the somatic hypermutationsdo not qualify as examples that could pertain to the germ-line mutations required for evolution.

Summary

I have shown here, with references to my book, that the examples most often cited byevolutionists as evidence for evolution occurring now are not evidence at all for the grand sweepof evolution, which I have called here Evolution A. For an example of evolution happening nowto have any relevance to Evolution A, it must be based on a mutation that could be typical ofthose alleged to be in the long series of steps that lead from a bacterium to a baboon. Themutation must at least be one that when repeated again and again will build up enoughinformation to turn a bacterium into a baboon. The favorite example cited for evolution isantibiotic resistance. I have shown that the mutations leading to antibiotic resistance do not addany information to the biocosm. In some cases, they actually lose information. I have shown an




18/19

example of a mutation that can easily be misconstrued to demonstrate the addition of informationto the genome. Upon the gathering of further data, this example turned out to be a demonstrationof information loss and not gain. Conclusion jumping is always risky, because we seldom haveenough data. Yet, the evolutionist community has persisted in making the shakiest ofextrapolations.

Max has tried to argue that his triad of gene duplication, random mutation, and natural selection,

can add information to the collective genome of the biocosm.

I have exposed his argument as being nothing more that offering possible scenariosit isargument by just-so-stories. But the argument against NDT does not stop with the failure of itssupporters to show proper theoretical or empirical evidence for it. The telling blow against NDTis that examples of information addition have never been exhibited. The absence of suchexamples is more than just the absence of evidence for evolution. It is actually evidence againstevolution because if NDT were correct, there should be millions of such examples and in all thegenetic experiments performed until now we should have seen many.

Finally, the example of mutations in the B cells of the immune system carries no weight as anexample of a mutation that adds information. Although these mutations do add information to theB-cell genome, they cannot be applied to evolution for the reasons I laid out above.

Dr. Edward E. Max made a valiant attempt to present a case for evolution in his posting on theURL cited above. That he failed is not because of any defect in the author. Dr. Max is anintelligent, competent, and articulate scientist. He has a PhD and an MD, and for many years hasdone research and published on the genetics of the immune system, and he has made importantcontributions to our knowledge in this field. If he could not make a good case for evolution, theremust be something woefully wrong with evolution.

Dr. Lee M. Spetner

Endnotes

[1] Wright, Sewall, (1932). The roles of mutation, inbreeding, crossbreeding and selection inevolution,Proceedings 6th Intnational Congress of Genetics, 1: 356-366. [RETURN TO TEXT]

[2] biocosmis a word I have coined to denote the totality of life on our planet. [RETURN TO TEXT]

[3] Burleigh, B. D., P. W. J. Rigby, & B. S. Hartley, (1974). A comparison of wild-type and mutantribitol dehydrogenase fromKlebsiella aerogenes.Biochem. J., 143: 341-352.. [RETURN TO TEXT]

[4] G

del, Kurt On Formally Undecidable Propositions of Principia Mathematica and Related Systems.(1962) Translated from the German by B. Meltzer and R. B.Braithwaite. London: Oliver &Boyd. [RETURN TO TEXT]

[5] Darnell et al.(1986),Molecular Cell Biology, Scientific American Books, p.1116. [RETURN TO TEXT]

[6] Winter, D. B. & P. J. Gearhart (1998) Dual enigma of somatic hypermutation of immunoglobulinvariable genes: targeting and mechanism.Immunological Reviews 162: 89-96. [RETURN TO TEXT]

[7] For simplicity in explanation I am assuming here that the environment does not change. The sameargument holds when the environment changes, with a slight alteration of thelanguage. [RETURN TO TEXT]

[8] Evolutionists often glibly argue that a recombination in the chromosomes can provide the largechange to throw the genome off the small adaptive hill it is on and provide the opportunity for it toland on another adaptive hill. But it is highly improbable that it will land at a higher adaptiveelevation. This argument abandons the Darwinian premise of small, and not unlikely, changes drivingevolution. [RETURN TO TEXT]

[9] Darnell, J., H. Lodish, & D. Baltimore (1986),Molecular Cell Biology , Scientific AmericanBooks, New York: Freeman. p. 1116. [RETURN TO TEXT]

[10] Blanden, R. V., H. S. Rothenfluh, P. Zylstra, G. F. Weiller, & E. J. Steele, (1998). The signatureof somatic hypermutation appears to be written into the germline IgV segment repertoire.

Immunological Reviews 162: 117-132. [RETURN TO TEXT]




19/19

[11] Winter, D. B. & P. J. Gearhart (1998). Dual enigma of somatic hypermutation of immunoglobulinvariable genes: targeting and mechanism.Immunological Reviews 162: 89-96. [RETURN TO TEXT]

Home| Feedback| Links| Books| Donate| Back to Top

TrueOrigin Archive. All Rights Reserved.

powered by Lone Star Web Works

Web TrueOrigin Archive


Scientific Critique of Evolution

Documents