Home » Darwinism, Evolutionary biology, Informatics, Intelligent Design » Responding to Merlin Part III – Merlin’s Delineation Between Darwinian and non-Darwinian Mutations and How It Falls Short

Responding to Merlin Part III – Merlin’s Delineation Between Darwinian and non-Darwinian Mutations and How It Falls Short

This is a multi-part post in response to Merlin’s paper, “Evolutionary Chance Mutation: A Defense of the Modern Synthesis’ Consensus View”. See introduction and table of contents.

Merlin spends a large part of the paper trying to establish what does and does not constitute a directed mutation. Merlin, I think, fails in her attempt to properly differentiate Darwinian and Lamarckian mutations because she has not taken into account the main purpose of Darwinism as described in Part II of this essay. To recap, the entire point of Darwinism was to frame biology as to extricate itself from final causes. Therefore, any mode of genetic adaptation which fails to do so is non-Darwinian.

Explaining Away Apparent Purposefulness

Merlin, it seems, is somewhat aware of this, as she tries to explain away any apparent purposefulness within mutational mechanisms. She says,

the mutator mechanisms themselves, which provoke an increase of mutation rate in response to environmental conditions, can be shown to be an adaptive result of the population’s evolutionary history…This means that the mutator mechanism has some adaptive value for individuals or populations. In a case where a mutator mechanism happens to provoke some favorable mutation, it may be positively selected at the individual level since it may provide an advantage to some lucky individual organism and its offspring (because there is selection for the favorable mutation). But a mutator mechanism could also provide an advantage to populations since it may increase the probability that a population adapts more rapidly than others to their adverse environmental conditions. In both scenarios (i.e., individual selection and group selection), the mutator mechanism is an evolutionary adaptive outcome producing “evolutionary chance” mutations. (pg 15)

This is the classical Darwinian confusion of something being selectable versus something being produceable by natural selection. The fact that a mutator mechanism which is biased towards beneficial mutations is selectable is uncontroversial. The question of whether it could be produced by natural selection is another story. Or whether anything at all worthwhile could be produced in the absences of appropriate mutator mechanisms — that is the entire question between Darwinism and Lamarckianism! You can’t solve it by saying, “I believe it is my way!” The question is, where does the evidence show? It turns out, over and over again, that whenever we find truly beneficial mutations (as opposed to what Behe calls “trench warfare” mutations), we find that there were highly-regulated mechanisms guiding it to its result. That should give people pause, but for some reason, it doesn’t.

So now we will examine Merlin’s demarcation between Darwinian and Lamarckian mutations closer, and see if it holds up. In all cases, we will be comparing biology to the Darwinian guideline of eliminating final causes, and see if the biology supports such a guideline.

Darwinism and Changes in Mutation Rates

Merlin says that Darwinism is compatible with changing mutation rates under stress. I would argue that this is true to some extent, but not quite to the extent that Merlin thinks. It was originally thought that the reason why mutation rates increased under stress was that the cell had less energy to maintain control, and therefore things simply fell apart more quickly. While tumbling out of control, some cells happened upon a mutation that helped it adapt. This is compatible with the Darwinian view – the relationship between beneficial mutations and survival is merely happenstance, due to the inability of the cell to keep it all together in times of crisis.

However, what was later actually found in real biology, was that the increase in mutations under stress is actually an orchestrated increase in mutation rates. In times of stress, bacteria switch DNA polymerases to one which causes mutations, among other activities. In fact, if you disable certain enzymes, the beneficial mutations do not happen at all. So, rather than this happening as the result of a continuing breakup of cell processes that lead to mutations, this is actually an organized response that the cell has to stress, which relies on proper tooling to be effective.

So, while, as a theoretical point, increases in global mutation rates can be compatible with the neo-Darwinian synthesis, I would argue that the specific mechanism by which global mutation rates are actually observed to increase is actually anti-Darwinian. The machinery and orchestration, and the inability to generate proper mutations without the machinery and orchestration, have a distinctive flair of teleology.

Darwinism and Mutational Hot Spots

Merlin then says that having hot-spots of mutation is compatible with the neo-Darwinian synthesis. Again, as a theoretical point, this is true. We would expect that the physical and chemical properties of DNA would lead some sequences to be more mutable than others. But not only do we have hot-spots for mutations, these hot-spots are right where they need to be for a beneficial mutation to occur. The fact that the observed hot-spots are correlated with potentially beneficial mutations is a giant blow to the neo-Darwinian outlook, because it implies that information already present in the genome, not natural selection, is responsible for the direction of evolutionary change.

Interestingly, this actually leads to a quantitative approach to deciding the question of Darwinism or Lamarckianism. Dembski’s Active Information concept could, at least in theory, be used to determine this. You could set up colonies of bacteria, and give them stressors. In one group, you let their mutational machinery do the work, and in the other, you knock out the mutational machinery, but simulate truly random mutations at the same estimated mutation rate using a source such as radiation. If the natural cells produce adaptive mutations at a significantly better rate than than the radiated cells, then it shows that they have positive Active Information. According to the No Free Lunch theorems, this would indicate final causes, and thus be in violation of Darwinism.

The fact is, modern biology shows that cells are pre-loaded with scads of information about how they can be best mutated. One can deny this if they wish, but they do not do so based on the data we have at hand.

Semi-Directed Mutations

While I can see where the above two categories of mutations might cause some people to not be able to differentiate between the Darwinian and Lamarckian versions of mutation theory, I am completely bewildered when it comes to semi-directed mutations. Semi-directed mutations are mutations which satisfy all of the following criteria:

  • A stress condition increases a cell’s mutation rate
  • The mutation rate is increased in a localized area only
  • The area that the mutation rate is increased in includes the area of the beneficial mutation

Now, I can understand if we only had one or two known mutations that fit this profile, how someone might think they were flukes. If, for most of the time, the localized mutation rate area did not match the location of the likely beneficial mutation, then we would be warranted to think that on rare occasion these might align, and produce what we need. However, what we are seeing is that the cell often times focuses its mutations precisely on the genes, or sets of genes, which need mutating. In bacteria, this is often done by increasing transcription rates using a mutagenic DNA polymerase.

In your immune system this is done, at least in part, by a deaminase attaching to the antibody gene to cause mutations. This deaminase is targeted by a non-coding DNA element, which points it not only to the correct gene, but the correct *part* of the correct gene. It would make no sense to mutate the part of the antibody which attaches to the cell, but only the part which attaches to the antigen. And, in fact, that is precisely the part that gets mutated. The region which attaches to the cells suffers almost no mutations whatsoever.

Merlin’s complaint about this process is that it doesn’t single out a single, specific mutation to accomplish the result. In the case of the immune system, the localization of the mutation rate increases the likelihood that a beneficial mutation will occur by well over 6 orders of magnitude. So how does one reconcile that with the idea of “evolutionary chance” mutations?

So, sure, it doesn’t target the exact mutation. If by “Darwinian” one means “organisms aren’t omniscient”, then, sure. Nobody thought they were. But what the data points to is that the adaptations that organisms undergo are well-regulated. They don’t seem to be accidents for any usable meaning of the word. In fact, they appear to be quite purposeful.

So, if the purpose of keeping the term “Darwinism” or “The Modern Synthesis” is to save face for an idea, then, sure, keep it to keep anyone from getting embarrassed. But one can only call this Darwinian, or non-teleological, by completely removing any real meaning from these concepts. It comes down to, as one commenter put it on this forum, being like redefining the meaning of “is”. Sure, you can do that, but if you do, it isn’t because you are trying to be precise, but rather because you are trying to obfuscate the obvious.

Now, in the next posting, we will dive into a class of mutations which Merlin seems to be unaware of, but which are definitively within her own category of directed mutations.

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