Evaluation of Darwin’s Doubt by Stephen C. Meyer, Part 3

This is a continuation of my book review series on Darwin’s Doubt. You can read the first installment HERE and the second HERE. Although this is the third article (of four) in my series, it will focus on “Part II” of the book.

 

Section two of Darwin’s Doubt is entitled, “How to Build an Animal.” Meyer gets a bit more technical at this point. He first explains the specified complexity of DNA coding and the problem this biological information poses for the body-plan explosion of the Cambrian era. The argument is basically that new body plans require an enormous amount of new genetic information, and the Cambrian phenomena shows that this information came about in a geological blink–not nearly enough time for natural selection acting upon random mutations to accomplish the explosion of body-plan diversity.

A key question highlighted by ID theory is detailed in chapter 9: How common are functional protein sequences among all the possible amino-acid combinations? Meyer is quite meticulous here, explaining exactly what the debate is all about. The work of MIT molecular biologist Robert Sauer is described, work which demonstrated the incredible rarity of functional proteins when considered in ratio to the number of total possible amino acid sequences. Sauer found that while it is true that many arrangements of amino acids could produce the same protein structure and function, that number is still minuscule whenever it is considered in context. Chapter 10 greatly enhances the argument by citing the work of Dr. Douglas Axe. What Axe was able to do was estimate the frequency of amino acid chains that are able to create stable protein folds, a necessity of protein functionality. Meyer argues that finding sequences that can produce new stable folds is the key to generating new structures in living organisms. He says:

Building fundamentally new forms of life requires structural innovation. And new protein folds represent the smallest selectable unit of such innovation. Therefore, mutations must generate new protein folds for natural selection to have an opportunity to preserve and accumulate structural innovation.

But the problem is, the odds of unguided mutations stumbling upon a sequence that can produce a novel protein fold are way too far below the threshold of reasonable probability. Meyer goes on to examine the counter-claim that gene duplication coupled with random mutation could simply modify a pre-existing protein fold into a new one. He explains why the extreme rarity of sequences that are capable of forming stable folds still poses too much of a problem for such a scenario. The bottom line being:

The sensitivity of proteins to functional loss, the rarity of proteins within combinatorial sequence space, the need for long proteins to build new cell types and animals, the need for whole new systems of proteins to service new cell types, and the brevity of the Cambrian explosion relative to rates of mutation–all conspire to underscore the immense implausibility of any scenario for the origin of Cambrian genetic information that relies upon random variation alone, unassisted by natural selection. Yet the classical model of gene evolution–which relies on neutral evolution [the accumulation of mutations that neither harm nor benefit an organism]–requires novel genes and proteins to arise, precisely, by random mutation alone. Adaptive advantage accrues after the generation of new functional genes and proteins. Natural selection cannot play a role until new functional information-bearing molecules have independently arisen.

So you see, unguided natural processes face a formidable challenge–making a very large leap through a string of random mutations before any selection can operate to help things along. Axe’s research showed how dire of a situation this is for naturalistic theories.

Lots of great material follows from there, but I’m going to skip ahead from this point to talk about what I find to be the most serious difficulty for any naturalistic account of evolutionary history: the science of epigenetics. Meyer takes up this topic in chapter 14, “The Epigenetic Revolution.”

Epigenetics is the study of non-genetic influences on animal development. Advances in this relatively new area of research seem to be undermining the theory that natural selection acting upon mutations is the engine of evolutionary change. It is now known that many aspects of development aren’t controlled by DNA. Rather, the biological information is stored in actual cell structures. Once DNA has dictated the production of the needed proteins, those proteins must be arranged in higher-level systems of proteins and cell structures, and the properties of proteins themselves don’t fully determine the patterns of organization that are needed. It turns out that the 3-D structure of embryonic cells is crucial to determining body-plan formation. The key, says Meyer is that:

If DNA isn’t wholly responsible for the way an embryo develops…then DNA sequences can mutate indefinitely and still not produce a new body plan, regardless of the amount of time and the number of mutational trials available to the evolutionary process.

What is needed, then? A pre-existing three-dimensional cell structure and organization inherent to embryonic cells that can dictate the development of the organism’s body plan and then pass that type of non-genetic information to the next generation of organisms by way of the mother’s egg cell. It is a classic chicken-and-egg problem. You need pre-existing cell structure and organization to get the cell structure and organization of subsequent cells. Meyer points out:

[R]esearch suggests that protein patterns in the cell membrane are transmitted directly from parent membrane to daughter membrane during cell division rather than as a result of gene expressing in each new generation of cells.

Theories that suggest mutability of epigenetic “information” are problematic, as research shows us that altering those cell structures even slightly very likely results in embryo death or sterile offspring. So, how does one develop brand new body plans, even gradually, if there needs to be change in an organism’s epigenetics in order to make changes leading to new body structures but such change is highly detrimental, or even fatal? How, then, could all of the novel Cambrian body plans have come about?

I must say that this area of research is by far the most compelling to me. At this point, I’m convinced that the “epigenetic revolution” will be the undoing of the neo-Darwinian conception of biological history (blind, unguided processes). Meyer even cites several scientists who have already abandoned the ship of neo-Darwinian orthodoxy in search of an alternative. I love how Jonathan Wells (Ph.D. in developmental biology) answered Meyer whenever Meyer asked him why developmental biology was key to assessing neo-Darwinism. Wells said,

“Because, that’s where the whole theory is going to unravel.”