Reviewing Darwin’s Doubt Chapter 10

© Can Stock Photo Inc. / kgtoh

© Can Stock Photo Inc. / kgtoh

As I work my way through Darwin’s Doubt, by Stephen C. Meyer, the pace slows as we go from basic information, concepts and analyses  to complex ones. In my first article, I covered four chapters dealing with the fossil record,  the Cambrian explosion and addressing some conclusory solutions to the problem it poses to the theory of evolution. In my next two articles, I took on chapters 5 & 6 and chapters  7 & 8 dealing with more complex solutions that, in turn, expose more problems.

Over the course of those chapters, we traversed the fossil record and got progressively deeper into molecular and biological minutia. In Chapter 9, we stood back and looked at the forest in mathematical and probabilistic terms. The problems that we encountered at the microscopic level reveal problems of cosmic proportions as we examined the complexity of DNA and the plausibility of random mutations leading to functional results on which natural selection could work among the dizzying number of possible outcomes. In Chapter 10, we go back in to the deeper evaluation looking at genes and proteins.

This is where we encounter Douglas Axe, a Ph.D student in chemical engineering who read Richard Dawkins. Axe was enamored with Dawkin’s clarity of thought, but he was not convinced of Dawkin’s thesis of the creative power of natural selection on random mutations. One thing he noticed is that Dawkins repeatedly smuggled in the very principal that he claimed natural selection precluded: “the guiding hand of an intelligent agent.” (p. 185) The “intelligent agent” was Dawkins, who manipulated the data and processes to achieve his desired result.

Axe wondered if there were other ways to assess the creative power of natural selection on random mutations by focusing on process control and genetic regulation. Axe recognized that new organisms would require new proteins and new genetic material.  Given the complexity of DNA, and the cosmic number of possible mutations that could occur, most of which would lead to loss of function, Axe began looking for evidence that the process might be short cut.

Since DNA is made up of coded information in required sequences, the potential number of outcomes from mutations are astronomical. There would have to be a short cut for evolution to have enough time to work within the history of life because it was mathematically implausible without such a short cut.

Robert Sauer, an MIT molecular biologist, began using technology that allowed for the manipulation of DNA to measure how many sequences, as a percentage of the total, produced some functional form of the proteins being studied. Initial results showed that proteins could, in fact, tolerate a variety of amino-acid substitutions along the protein chain, but the analysis also showed that occurrence of functional proteins might still be “incredibly rare.” p 180) The problem to be addressed is like typographical errors in a text. A single typographical error may not destroy the meaning, but ongoing typographical errors that accumulate will destroy the meaning (the equivalent of function in DNA) over time

Axe took up where Sauer left off as the Director of Protein Engineering at Cambridge University.  Axe knew that the many new life forms appearing in the Cambrian era had new organs and new cell types which also required new proteins. Because protein folds are the smallest “selective unit” of structural innovation in life forms, and new life forms need structural innovation, Axe realized that new protein folds were necessary for macro-evolution.

Axe experimented with amino-acid changes in combination with protein folds and the other structural elements of proteins, and Meyer details the results which highlight the problem of functional loss. The rate of functional loss to functional gain is exponentially high, making “protein-to-protein (or functional gene-to-functional gene) evolution … a no go where the mutation and selection mechanism must produce a new protein fold….”, and for Axe “the gradual transformation of one functional fold into another was a complete nonstarter”. (p. 196-97)

Axe and other evolutionary biologists, have believed that, if the necessary protein folds could not be expected to emerge from the functional regions of a genome, then maybe they could arise from the nonfunctional regions. The thought was that new genetic material (“text”) could arise freely where loss of function would not degrade the organism. This “classical model” of gene evolution became Axe’s focus, but an overriding problem lingered.

The work Axe did previously exposed a serious problem: “functional sequences of amino-acids are … exceedingly rare in sequence space.” (p.199) Recall that natural selection does not generate anything new; it does not create new folded functional sequences; it can only operate on functional sequences after they have arisen. Random mutations are the process by which new functional sequences must arise, and such new functional sequences are exceedingly rare “within the vast sea of combinatorial possibilities.” (Id.) For example, one experiment demonstrated that the number of 150-amino-acid-long sequences capable of function compared to the total set of possible amino-acid sequences of the same length is “vanishingly small” (1 in 1077). (p. 200)

The chance of random mutation creating a functional fold is one chance in one hundred thousand, trillion, trillion, trillion, trillion, trillion, trillion. Since the first appearance of life on earth about 3.8 million years ago, scientists estimate that the total number of organisms that have lived on the earth is about 1040, which is a fraction of 1077 (1 trillion, trillion, trillion of 1077). After explaining “conditional probability”, Meyer concludes that the conditional probability that random mutation would create a new protein fold, given those figures, is still only 1037, and if each organism since the dawn of time generated one new relevant base sequence, that would amount to only one 10 trillion, trillion, trillionth of the of the possible sequences in the relevant sequence space.

Axe concluded that the classical model is so vastly more likely to be false than true that a reasonable person should reject it. Meyer summed it up this way: “[I]n the classical model of of gene mutation, random mutations must thrash about aimlessly in immense combinatorial space, a space that could not be explored by this means in the entire history of life on earth, let alone in the few million years of the Cambrian explosion.” (p. 204)

But Meyer says this is “only a hint at the full problem” because “building new animal forms requires generating far more than just one protein of modest length.” (p. 205) New cell types require many more than one or two new proteins; they require coordinated systems of proteins. Yet, “the smallest increment of structural innovation in the history of life – a new protein fold – itself presents a formidable Mount Improbable [using imagery from Dawkins].” (p. 207)

“If only one out of every 1077 of the alternate sequences are functional, an evolving gene will inevitably wander down an evolutionary dead-end long before it can ever become a gene capable of producing a new protein fold.” (Id.)

As we progress through Darwin’s Doubt, searching deep and wide for solutions to the problem that the Cambrian explosion creates for evolutionary theory, the gap seems to yawn wider and wider as we go. Yet, most scientists have remained steadfastly true to Darwinism as it has evolved into Neo-Darwinist form. Whether that continues to remain true will explored further to the end of the book in subsequent articles.

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