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Finally, the Details of How Proteins Evolve


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.” 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. Read more

Thanks Bill. I read what Dr. Behe had to say and Art's panicked response. Art has been told many times that he is not justified in calling recombination a blind and mindless process. ET
ET February 19, 2019 at 12:39 pm Hi Bill, When you contact Dr. behe can you please ask him what he thinks of the Dr. Spetner quote I posted in comment 7. I can tell you now that he would have no problem with that idea based on a discussion we had on one of Art Hunts claims that a corn plant developed a new gene sequence due to recombination. Mike is as pure an empiricist as gpuccio. bill cole
Bill Cole: Great, thank you! :) gpuccio
Hi Bill, When you contact Dr. behe can you please ask him what he thinks of the Dr. Spetner quote I posted in comment 7. ET
gpuccio I should receive it on my Kindle on Febriary 26, and I will try to read it immediately, and probably give some feedback here! Thats great I will incorporate it into my feedback to Mike. You guys along with Kirk are doing very interesting empirical work that is validating our thesis. My email is colewd@aol.com. bill cole
Bill Cole: I should receive it on my Kindle on Febriary 26, and I will try to read it immediately, and probably give some feedback here! :) gpuccio
Bill Cole:
No, not personally. But I am a great admirer of his work!
Are you planning to read his latest book soon? I think his work in his latest book and yours regarding information infusion are highly complementary. I plan to send him feedback in the next 30 days or so and would like your view if possible. bill cole
He [the Creator] indeed seems to have "carefully crafted" information in His species giving them the ability to respond to environmental stimuli to alter their own genome to adapt to new environments. He then evidently let them wander where they will with the ability to adapt.- Dr. Lee Spetner "the Evolution Revolution" p 108
The antifreeze gene is an excellent example of this. ET
Bill Cole: No, not personally. But I am a great admirer of his work! :) gpuccio
Gpuccio Have you had any conversations with Mike Behe? bill cole
Interesting paper. Two simple thoughts: 1) The antifreeze proteins are really "simple" from the point of view of functional complexity, because they are highly repetitive. Behe already made that point a lot of time ago. Therefore, they are not the best candidates to infer design (even if they are probably designed too!). Other proteins, almost all of them indeed, are definitely more functionally complex. 2) The abstract states:
We experimentally proved that all genic components of the extant gadid AFGP originated from entirely nongenic DNA. The gadid AFGP evolutionary process also represents a rare example of the proto-ORF model of de novo gene birth where a fully formed ORF existed before the regulatory element to activate transcription was acquired.
That's really interesting. The model according to which functional proteins arise from non coding DNA, and are functionalized only at the last step, when they are transformed into an ORF and transcribed, is really a design model. Indeed, this model excludes any intervention of NS in the shaping of the functional sequence, because the sequence is not translated until it becomes an ORF and transcription is activated. Therefore, the origin of the sequence can be attributed only to either RV or design. So, if this model is correct for a number of proteins (and I think there is strong evidence of that), the design inference is extremely easy: if the functional complexity is big enough, the evidence of design is overwhelming. No help from NS here. Now, maybe the antifreeze proteins are not the best case for a design inference: as already said, their functional complexity is relatively "low" (but still significant, IMO). However, the fact remains that any moderately complex protein that arises in this way (IOWs, from a non coding sequence which, at the last step, becomes an ORF), is certainly designed. gpuccio
OK, but these guys all got PAID, and I bet the ultimate source of the MONEY was Tax Dollars. Is there any way to shut this waste down? vmahuna
Dr. Hunter quotes the 'more revealing' press release:
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.’” Fresh insights? In actuality the findings arose from a series of non-empirical claims.
Non-empirical just so story telling of the step-by-step process by which a single protein could have possibly evolved? In short, imagination apparently IS the empirical evidence that Darwinists offer as proof that proteins can randomly evolve. To try to claim that this is even in the realm of empirical science is pathetic! Real empirical evidence, as opposed to their imaginary empirical evidence, is not so kind to their dream world of empirical science where imagination apparently takes the place of actual testing.
Here Are Those Two Protein Evolution Falsifications That Have Evolutionists Rewriting Their Script - Cornelius Hunter - March 2012 Excerpt: Several different studies indicate that, at a minimum, about 10^70 (a one followed by 70 zeros) evolutionary experiments would be needed to get close enough to a workable protein design before evolutionary mechanisms could take over and establish the protein in a population. For instance, one study concluded that 10^63 attempts would be required for a relatively short protein. And a similar result (10^65 attempts required) was obtained by comparing protein sequences. Another study found that 10^64 to 10^77 attempts are required, and another study concluded that 10^70 attempts would be required. This requirement for 10^70 evolutionary experiments is far greater than what evolution could accomplish. Even evolutionists have had to admit that evolution could only have a maximum of 10^43 such experiments. It is important to understand how tiny this number is compared to 10^70. 10^43 is not more than half of 10^70. It is not even close to half. 10^43 is an astronomically tiny sliver of 10^70. Furthermore, the estimate of 10^43 is, itself, entirely unrealistic. For instance, it assumes the entire history of the Earth is available, rather than the limited time window that evolution actually would have had. Even more importantly, it assumes the pre existence of bacteria and, yes, proteins. http://darwins-god.blogspot.com/2012/03/here-are-those-two-protein-evolution.html The Case Against a Darwinian Origin of Protein Folds - Douglas Axe - 2010 Excerpt Pg. 11: "Based on analysis of the genomes of 447 bacterial species, the projected number of different domain structures per species averages 991. Comparing this to the number of pathways by which metabolic processes are carried out, which is around 263 for E. coli, provides a rough figure of three or four new domain folds being needed, on average, for every new metabolic pathway. In order to accomplish this successfully, an evolutionary search would need to be capable of locating sequences that amount to anything from one in 10^159 to one in 10^308 possibilities, something the neo-Darwinian model falls short of by a very wide margin." http://bio-complexity.org/ojs/index.php/main/article/view/BIO-C.2010.1 Quantum criticality in a wide range of important biomolecules - March 2015 Excerpt: “Most of the molecules taking part actively in biochemical processes are tuned exactly to the transition point and are critical conductors,” they say. That’s a discovery that is as important as it is unexpected. “These findings suggest an entirely new and universal mechanism of conductance in biology very different from the one used in electrical circuits.” The permutations of possible energy levels of biomolecules is huge so the possibility of finding even one that is in the quantum critical state by accident is mind-bogglingly small and, to all intents and purposes, impossible.,, of the order of 10^-50 of possible small biomolecules and even less for proteins,”,,, “what exactly is the advantage that criticality confers?” https://medium.com/the-physics-arxiv-blog/the-origin-of-life-and-the-hidden-role-of-quantum-criticality-ca4707924552 Probability Of A Single Protein Forming By Chance - video https://uncommondesc.wpengine.com/origin-of-life/probability-of-a-single-protein-forming-by-chance/ etc.. etc.. etc..
Moreover, even though this was an evidence-free imaginary just-so story, it is interesting to note that it was still just a just-so story for only one single protein of a single function, i.e. a antifreeze protein. I seriously wonder if even the fevered imagination of Darwinists can possibly concoct a half-way believable imaginary just-so story for multifunctional proteins and for alternatively spliced genes that are now found pervasively throughout biology.
Human Genes: Alternative Splicing (For Proteins) Far More Common Than Thought: Excerpt: two different forms of the same protein, known as isoforms, can have different, even completely opposite functions. For example, one protein may activate cell death pathways while its close relative promotes cell survival. http://www.sciencedaily.com/releases/2008/11/081102134623.htm Genes Code For Many Layers of Information - They May Have Just Discovered Another - Cornelius Hunter - January 21, 2013 Excerpt: “protein multifunctionality is more the rule than the exception.” In fact, “Perhaps all proteins perform many different functions by employing as many different mechanisms." http://darwins-god.blogspot.com/2013/01/genes-code-for-many-layers-of.html Time to Redefine the Concept of a Gene? - Sept. 10, 2012 Excerpt: As detailed in my second post on alternative splicing, there is one human gene that codes for 576 different proteins, and there is one fruit fly gene that codes for 38,016 different proteins! While the fact that a single gene can code for so many proteins is truly astounding, we didn’t really know how prevalent alternative splicing is. Are there only a few genes that participate in it, or do most genes engage in it? The ENCODE data presented in reference 2 indicates that at least 75% of all genes participate in alternative splicing. They also indicate that the number of different proteins each gene makes varies significantly, with most genes producing somewhere between 2 and 25. Based on these results, it seems clear that the RNA transcripts are the real carriers of genetic information. This is why some members of the ENCODE team are arguing that an RNA transcript, not a gene, should be considered the fundamental unit of inheritance. http://networkedblogs.com/BYdo8    Multiple Overlapping Genetic Codes Profoundly Reduce the Probability of Beneficial Mutation George Montañez 1, Robert J. Marks II 2, Jorge Fernandez 3 and John C. Sanford 4 - published online May 2013 Excerpt: In the last decade, we have discovered still another aspect of the multi- dimensional genome. We now know that DNA sequences are typically “ poly-functional” [38]. Trifanov previously had described at least 12 genetic codes that any given nucleotide can contribute to [39,40], and showed that a given base-pair can contribute to multiple overlapping codes simultaneously. The first evidence of overlapping protein-coding sequences in viruses caused quite a stir, but since then it has become recognized as typical. According to Kapronov et al., “it is not unusual that a single base-pair can be part of an intricate network of multiple isoforms of overlapping sense and antisense transcripts, the majority of which are unannotated” [41]. The ENCODE project [42] has confirmed that this phenomenon is ubiquitous in higher genomes, wherein a given DNA sequence routinely encodes multiple overlapping messages, meaning that a single nucleotide can contribute to two or more genetic codes. Most recently, Itzkovitz et al. analyzed protein coding regions of 700 species, and showed that virtually all forms of life have extensive overlapping information in their genomes [43].,,, Conclusions: Our analysis confirms mathematically what would seem intuitively obvious - multiple overlapping codes within the genome must radically change our expectations regarding the rate of beneficial mutations. As the number of overlapping codes increases, the rate of potential beneficial mutation decreases exponentially, quickly approaching zero. Therefore the new evidence for ubiquitous overlapping codes in higher genomes strongly indicates that beneficial mutations should be extremely rare. This evidence combined with increasing evidence that biological systems are highly optimized, and evidence that only relatively high-impact beneficial mutations can be effectively amplified by natural selection, lead us to conclude that mutations which are both selectable and unambiguously beneficial must be vanishingly rare. This conclusion raises serious questions. How might such vanishingly rare beneficial mutations ever be sufficient for genome building? How might genetic degeneration ever be averted, given the continuous accumulation of low impact deleterious mutations? http://www.worldscientific.com/doi/pdf/10.1142/9789814508728_0006 'It's becoming extremely problematic to explain how the genome could arise and how these multiple levels of overlapping information could arise, since our best computer programmers can't even conceive of overlapping codes. The genome dwarfs all of the computer information technology that man has developed. So I think that it is very problematic to imagine how you can achieve that through random changes in the code.,,, and there is no Junk DNA in these codes. More and more the genome looks likes a super-super set of programs.,, More and more it looks like top down design and not just bottom up chance discovery of making complex systems.' - Dr. John Sanford - Inventor of the ‘Gene Gun’ - 31 second mark - video http://www.youtube.com/watch?feature=player_detailpage&v=YemLbrCdM_s#t=31s
I imagine that to even attempt to try to concoct an evidence-free imaginary just-so story for this staggering level of complexity, would turn even the Darwinists' dream world of evidence free science into a nightmare.
Psalm 139:13-14 For you formed my inward parts; you knitted me together in my mother's womb. I praise you, for I am fearfully and wonderfully made.[a] Wonderful are your works; my soul knows it very well.
Junk science? Darn the luck! jstanley01

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