At Last, the Details of How Proteins Evolve?
Cornelius Hunter
How did proteins evolve? It is a difficult question because, setting aside many other problems, the very starting point — the protein-coding gene — is highly complex. A large number of random mutations would seem to be required before you have a functional protein that helps the organism. Too often such problems are solved with vague accounts of “adaptations” and “selection pressure” doing the job.
Cornelius Hunter
How did proteins evolve? It is a difficult question because, setting aside many other problems, the very starting point — the protein-coding gene — is highly complex. A large number of random mutations would seem to be required before you have a functional protein that helps the organism. Too often such problems are solved with vague accounts of “adaptations” and “selection pressure” doing the job.
But this week researchers at the University of Illinois announced ground-breaking research that provides a step-by-step, detailed, description of the evolution of a new protein-coding gene and associated regulatory DNA sequences. The protein in question is a so-called “antifreeze” protein that keeps the blood of Arctic codfish from freezing, and the new research provides the specific sequence of mutations, leading to the new gene.
It would be difficult to underestimate the importance of this research. It finally provides scientific details answering the age-old question of how nature’s massive complexity could have arisen. As the paper triumphantly declares, “Here, we report clear evidence and a detailed molecular mechanism for the de novo formation of the northern gadid (codfish) antifreeze glycoprotein (AFGP) gene from a minimal noncoding sequence.” Or as lead researcher, professor Christina Cheng, explained, “This paper explains how the antifreeze protein in the northern codfish evolved.”
Just One Problem
This is a monumental finding. Having the scientific details, down to the level of specific mutations, of how a new protein-coding gene evolved — not from a related gene but from non-coding DNA — is something evolutionists could only dream of only a few short years ago. There’s only one problem: it is all junk science.
The first difficulty is that this new “research” is, in actuality, a just-so story. As Wikipedia defines it:
In science and philosophy, a just-so story is an unverifiable narrative explanation for a cultural practice, a biological trait, or behavior of humans or other animals. The pejorative nature of the expression is an implicit criticism that reminds the hearer of the essentially fictional and unprovable nature of such an explanation. Such tales are common in folklore and mythology.
For example, the antifreeze protein is of relatively low complexity chiefly consisting of a repeating sequence of three amino acids (threonine-alanine-alanine), and the evolutionists claim that these repeating sequences “strongly suggest” that the protein-coding gene “evolved from repeated duplications of an ancestral 9-nucleotide threonine-alanine-alanine-coding element.”
Why is that true? Why does a repeating genetic sequence “strongly suggest” that it “evolved from repeated duplications?” What experiment revealed this truth? What evidence gives us this profound principle? The answer, of course, is that there is none. Nowhere do the evolutionists justify this claim because there is no empirical justification.
There is no scientific evidence for it. Zero.
More Non-Empirical Claims
The paper continues with yet more non-empirical claims. Those nine nucleotides “likely originated within a pair of conserved 27-nucleotide” segments that flank each side of the repetitive region. And these four 27-nucleotide segments are similar to each other, “indicating they resulted from the duplication of an initial copy.” As the paper concludes, “chance duplications” of an ancestral 27-nucleotide segment “produced four tandem copies.”
But why are those claims true? Why do such similarities imply an origin via evolutionary mechanisms? The problem is, they don’t. There is no empirical evidence for any of this. This is completely evidence-free.
The evolutionists next explain that the 9-nucleotide segment duplicated a large number of times because it worked well:
We hypothesize that, upon the onset of selective pressure from cold polar marine conditions, duplications of a 9-nt ancestral element in the midst of the four GCA-rich duplicates occurred.
The above quote is an example of the non-empirical teleology that pervades evolutionary thought. It was upon the onset of cold conditions that the needed genetic duplications occurred. This is not empirical; this is story-telling.
The paper continues with a series of one-time, contingent events crucial to their story and non-empirical claims. The genetic sequence “was appropriately delimited by an existing in-frame termination codon.” Appropriately delimited?
The presence of a region in two of the species “indicates that it existed in the gadid ancestor before the emergence of the AFGP.” The absence of a thymine nucleotide at a location in some of the species “very likely resulted from a deletion event,” causing a fortuitous frameshift which supplied the crucial signal peptide segment, telling cellular machinery that the protein should be secreted to the bloodstream. As the paper concludes, “the emerging AFGP gene was thus endowed with the necessary secretory signal.”
Endowed with the necessary signal? There is no empirical evidence for any of this.
Substantial Serendipity
Another problem with this just-so account is the substantial level of serendipity required. The new antifreeze protein did not arise from some random DNA sequence, but rather from crucial, preexisting segments of DNA that just happened to be lying around. In other words, the fish were facing a colder environment, they needed some antifreeze in their blood, and the pieces needed for such an antifreeze gene were fortuitously available.
The authors hint at this serendipity when they conclude that their story of how this protein evolved is an example of “evolutionary ingenuity.” Evolutionary ingenuity?
The press release is even more revealing. Cheng admits that the evolution of this gene “occurred as a result of a series of seemingly improbable, serendipitous events.” For “not just any random DNA sequence can produce a viable protein.” Furthermore, in addition to the gene itself, “several other serendipitous events occurred.”
The DNA was “edited in just the right way,” and “somehow, the gene also obtained the proper control sequence that would allow the new gene to be transcribed into RNA.”
Even the evolutionists admit to the rampant serendipity. Nonetheless they are triumphant, for “the findings offer fresh insights into how a cell can invent ‘a new, functional gene from scratch.’”
In actuality the findings arose from a series of non-empirical claims. Fresh insights? Not so much.
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