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Defending the Christian Worlview, Creationism, and Intelligent Design

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Defending the Christian Worlview, Creationism, and Intelligent Design » Intelligent Design » Information Theory, Coded Information in the cell » Overlapping codes - the second code of DNA

Overlapping codes - the second code of DNA

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Codes Within Codes: How Dual-Use Codons Challenge Statistical Methods for Inferring Natural Selection

The double function of the genetic code points to design
 1. An “overlapping language” has been found in the genetic code
2. One language describes how proteins are made, and the other helps direct genetic activity in cells. One language is written on top of the other, which is why this other language went undiscovered for so long.
3. The original paper by Stergachis et al. writes about “evolutionary constraints” of the overlapping codes. They wrote: “Our results indicate that simultaneous encoding of amino acid and regulatory information within exons is a major functional feature of complex genomes. The information architecture of the received genetic code is optimized for the superimposition of additional information.  TF [transcription factor] binding within exons may serve multiple functional roles.
4. According to the research, natural selection constrains or eliminates change (purifying selection)and is not helpful for creating new organs or functions. 
5. The words: information, architecture, optimized, and function are always and only referring to an intelligent agent with thinking feeling, and willing. Other proposed agents cannot on their own give information, design, optimize, or execute tasks. This has never been demonstrated to be possible.
7. Such an intelligently designed complex genetic code with double or even triple functions could have been created only by a brilliant superintelligent designer.

Besides there being overlapping coding that is, hierarchically, above the coding of DNA, we find that there also is overlapping coding within DNA as well:

Multiple Overlapping Genetic Codes Profoundly Reduce the Probability of Beneficial Mutation 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].

“There is abundant evidence that most DNA sequences are poly-functional, and therefore are poly-constrained. This fact has been extensively demonstrated by Trifonov (1989). For example, most human coding sequences encode for two different RNAs, read in opposite directions i.e. Both DNA strands are transcribed ( Yelin et al., 2003). Some sequences encode for different proteins depending on where the translation is initiated and where the reading frame begins (i.e. read-through proteins). Some sequences encode for different proteins based upon alternate mRNA splicing. Some sequences serve simultaneously for protein-encoding and also serve as internal transcriptional promoters. Some sequences encode for both a protein-coding and a protein-binding region. Alu elements and origins-of-replication can be found within functional promoters and within exons. Basically, all DNA sequences are constrained by isochore requirements (regional GC content), “word” content (species-specific profiles of di-, tri-, and tetra-nucleotide frequencies), and nucleosome binding sites (i.e. All DNA must condense). Selective condensation is clearly implicated in gene regulation, and selective nucleosome binding is controlled by specific DNA sequence patterns – which must permeate the entire genome. Lastly, probably all sequences do what they do, even as they also affect the general spacing and DNA-folding/architecture – which is clearly sequence-dependent. To explain the incredible amount of information that must somehow be packed into the genome (given the extreme complexity of life), we really have to assume that there are even higher levels of organization and information encrypted within the genome. For example, there is another whole level of organization at the epigenetic level (Gibbs 2003). There also appears to be an extensive sequence-dependent three-dimensional organization within chromosomes and the whole nucleus (Manuelides, 1990; Gardiner, 1995; Flam, 1994). Trifonov (1989), has shown that probably all DNA sequences in the genome encrypt multiple “codes” (up to 12 codes).
Dr. John Sanford; Genetic Entropy 2005

Moreover, there are very good mathematical reasons why overlapping coding within DNA will prevent one creature from ever being changed into another creature.

Multiple Overlapping Genetic Codes Profoundly Reduce the Probability of Beneficial Mutation  John C. Sanford 4 – May 2013
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 that 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?

A very simple way to understand the monumental brick wall any evolutionary scenario faces with the multiple overlapping coding found in DNA is with the following puzzle found on page 141 of the book ‘Genetic Entropy’ by Dr. Sanford.


Which is translated ;


This ancient puzzle, which dates back to at least 79 AD, reads the same four different ways, Thus, If we change (mutate) any letter we may get a new meaning for a single reading read any one way, as in Dawkins weasel program, but we will consistently destroy the other 3 readings of the message with the new mutation (save for the center).
This is what is meant when it is said that a poly-functional genome is poly-constrained to any random mutations.
This poly-constrained principle is why we never see the unlimited plasticity in organisms that was, and is, imagined by Darwin and his followers, and is also why random mutations, that have effects that great enough that we are able to measure them, are almost always deleterious in the effects that are measured:

“Whatever we may try to do within a given species, we soon reach limits which we cannot breakthrough. A wall exists on every side of each species. That wall is the DNA coding, which permits wide variety within it (within the gene pool, or the genotype of a species)-but no exit through that wall. Darwin’s gradualism is bounded by internal constraints, beyond which selection is useless.”
R. Milner, Encyclopedia of Evolution (1990)

Moreover, at the morphological and behavioral level, we find that Chimps and Humans are far more different than is commonly believed.
In fact, King and Wilson, who were the first ones to suggest that we are 98% similar to chimps at the genetic level, said that since the morphological and behavioral disparity between chimps and humans is so great then the morphological and behavioral disparity between humans and apes must be due to variations in their genomic regulatory systems since such similarity in the protein-coding regions obviously could not explain that great morphological and behavioral disparity between chimps and humans.

In “Science,” 1975, M-C King and A.C. Wilson were the first to publish a paper estimating the degree of similarity between the human and the chimpanzee genome. This documented the degree of genetic similarity between the two! The study, using a limited data set, found that we were far more similar than was thought possible at the time. Hence, we must be one with apes, mustn’t we? But…in the second section of their paper King and Wilson honestly describe the deficiencies of such reasoning:
“The molecular similarity between chimpanzees and humans is extraordinary because they differ far more than sibling species in anatomy and way of life. Although humans and chimpanzees are rather similar in the structure of the thorax and arms, they differ substantially not only in brain size but also in the anatomy of the pelvis, foot, and jaws, as well as in relative lengths of limbs and digits (38).
Humans and chimpanzees also differ significantly in many other anatomical respects, to the extent that nearly every bone in the body of a chimpanzee is readily distinguishable in shape or size from its human counterpart (38).
Associated with these anatomical differences there are, of course, major differences in posture (see cover picture), mode of locomotion, methods of procuring food, and means of communication. Because of these major differences in anatomy and way of life, biologists place the two species not just in separate genera but in separate families (39). So it appears that molecular and organismal methods of evaluating the chimpanzee human difference yield quite different conclusions (40).”

King and Wilson went on to suggest that the morphological and behavioral between humans and apes,, must be due to variations in their genomic regulatory systems.
David Berlinski – The Devil’s Delusion – Page 162&163
Evolution at Two Levels in Humans and Chimpanzees Mary-Claire King; A. C. Wilson – 1975

In fact, so great are the anatomical differences between humans and chimps that a Darwinist, since pigs are anatomically closer to humans than chimps are, actually proposed that a chimp and pig mated with each other and that is what ultimately gave rise to humans. (I guess even hybridization knows no limits in the minds of some Darwinists).
Moreover, Physorg published a subsequent article showing that the pig-chimp hybrid theory for human origins is much harder to shoot down than some other Darwinists, who opposed McCarthy’s radical theory, had first supposed it would be:

Human hybrids: a closer look at the theory and evidence – July 25, 2013
Excerpt: There was considerable fallout, both positive and negative, from our first story covering the radical pig-chimp hybrid theory put forth by Dr. Eugene McCarthy,,,By and large, those coming out against the theory had surprisingly little science to offer in their sometimes personal attacks against McCarthy.
,,, Under the alternative hypothesis (humans are not pig-chimp hybrids), the assumption is that humans and chimpanzees are equally distant from pigs. You would therefore expect chimp traits not seen in humans to be present in pigs at about the same rate as are human traits not found in chimps. However, when he searched the literature for traits that distinguish humans and chimps and compiled a lengthy list of such traits, he found that it was always humans who were similar to pigs with respect to these traits. This finding is inconsistent with the possibility that humans are not pig-chimp hybrids, that is, it rejects that hypothesis.,,,

Of course, there is not one single scrap of empirical evidence that suggests that such radically different creatures, such as pigs and chimps, could ever successfully produce viable offspring.
But alas, when your theory is built on storytelling in the first place, (and not on any real empirical evidence), then of course you are not going to be able to shoot down another ‘just so story’ just because you don’t like how the narrative contradicts your preferred narrative of man ascending from monkeys:

“We have all seen the canonical parade of apes, each one becoming more human. We know that, as a depiction of evolution, this line-up is tosh (i.e. nonsense). Yet we cling to it. Ideas of what human evolution ought to have been like still colour our debates.”
Henry Gee, editor of Nature (478, 6 October 2011, page 34, doi:10.1038/478034a),

In further note to King and Wilson’s observation that ‘nearly every bone in the body of a chimpanzee is readily distinguishable in shape or size from its human counterpart’, this observation by King and Wilson, by itself, places another severe constraint on the Darwinian evolution that, once again, calls the entire theory into question.
Simply put, since nearly every bone is readily distinguishable between chimps and humans, then multiple simultaneous coordinated changes are required instead of just individual changes, as is envisioned in Darwinism, so as to prevent catastrophic results:

Connecting The Dots: Modeling Functional Integration In Biological Systems – June 11, 2010
Excerpt: “If an engineer modifies the length of the piston rods in an internal combustion engine, but does not modify the crankshaft accordingly, the engine won’t start. Similarly, processes of development are so tightly integrated temporally and spatially that one change early in development will require a host of other coordinated changes in separate but functionally interrelated developmental processes downstream” (1)

“This is the issue I have with neo-Darwinists: They teach that what is generating novelty is the accumulation of random mutations in DNA, in a direction set by natural selection. If you want bigger eggs, you keep selecting the hens that are laying the biggest eggs, and you get bigger and bigger eggs. But you also get hens with defective feathers and wobbly legs. Natural selection eliminates and maybe maintains, but it doesn’t create….
(Quoted in “Discover Interview: Lynn Margulis Says She’s Not Controversial, She’s Right,” Discover Magazine, p. 68 (April, 2011).)

“The real number of variations is lesser than expected,,. There are no blue-eyed Drosophila, no viviparous birds or turtles, no hexapod mammals, etc. Such observations provoke non-Darwinian evolutionary concepts. Darwin tried rather unsuccessfully to solve the problem of the contradictions between his model of random variability and the existence of constraints. He tried to hide this complication citing abundant facts on other phenomena. The authors of the modern versions of Darwinism followed this strategy, allowing the question to persist. …However, he was forced to admit some cases where creating anything humans may wish for was impossible. For example, when the English farmers decided to get cows with thick hams, they soon abandoned this attempt since they perished too frequently during delivery. Evidently such cases provoked an idea on the limitations to variability… [If you have the time, read all of the following paper, which concludes] The problem of the constraints on variation was not solved neither within the framework of the proper Darwin’s theory, nor within the framework of modern Darwinism.” (IGOR POPOV, THE PROBLEM OF CONSTRAINTS ON VARIATION, FROM DARWIN TO THE PRESENT, 2009,

Perhaps that is why so many engineers support intelligent design since they can readily see the impossibility of the ‘engineering problem’ for Darwinian processes. Namely, Design must be implemented top down, with all the pieces coordinated with one another, so as to avoid catastrophic results for the system as a whole.
Moreover, in further note to King and Wilson’s contention that the morphological and behavioral disparity between humans and apes must be due to variations in their genomic regulatory systems, (since the genetic similarity obviously cannot explain that great morphological and behavioral disparity between chimps and humans), we find that it is indeed in the genetic regulatory regions that we find ‘orders of magnitude’ and ‘species specific’ differences between not only chimps and humans, but also in other species as well:
Just a reminder, genetic similarity is far more widespread, across very different species, than Darwinists expected the genetic similarity to be

Shark and human proteins “stunningly similar”; shark closer to human than to zebrafish – December 9, 2013
Excerpt: “We were very surprised to find, that for many categories of proteins, sharks share more similarities with humans than zebrafish,” Stanhope said. “Although sharks and bony fishes are not closely related, they are nonetheless both fish … while mammals have very different anatomies and physiologies.

Kangaroo genes close to humans
Excerpt: Australia’s kangaroos are genetically similar to humans,,, “There are a few differences, we have a few more of this, a few less of that, but they are the same genes and a lot of them are in the same order,” ,,,”We thought they’d be completely scrambled, but they’re not. There is great chunks of the human genome which is sitting right there in the kangaroo genome,”
[url= News/idUSTRE4AH1P020081118][/url]

First Decoded Marsupial Genome Reveals “Junk DNA” Surprise – 2007
Excerpt: In particular, the study highlights the genetic differences between marsupials such as opossums and kangaroos and placental mammals like humans, mice, and dogs. ,,,
The researchers were surprised to find that placental and marsupial mammals have largely the same set of genes for making proteins. Instead, much of the difference lies in the controls that turn genes on and off.

Where could we have learned but from – Sept. 28, 2014
Excerpt: “We have basically the same 20,000 (30,000?) protein-coding genes as a frog, yet our genome is much more complicated, with more layers of gene regulation.”

Yet it is exactly in these genetic regulatory networks that ‘orders of magnitude’ differences are found between species:

Evolution by Splicing – Comparing gene transcripts from different species reveals surprising splicing diversity. – Ruth Williams – December 20, 2012
Excerpt: A major question in vertebrate evolutionary biology is “how do physical and behavioral differences arise if we have a very similar set of genes to that of the mouse, chicken, or frog?”,,,
A commonly discussed mechanism was variable levels of gene expression, but both Blencowe and Chris Burge,,, found that gene expression is relatively conserved among species.
On the other hand, the papers show that most alternative splicing events differ widely between even closely related species. “The alternative splicing patterns are very different even between humans and chimpanzees,” said Blencowe.,,,

Gene Regulation Differences Between Humans, Chimpanzees Very Complex – Oct. 17, 2013
Excerpt: Although humans and chimpanzees share,, similar genomes, previous studies have shown that the species evolved major differences in mRNA (messenger RNA) expression levels.,,,

“Where (chimps and humans) really differ, and they differ by orders of magnitude, is in the genomic architecture outside the protein-coding regions. They are vastly, vastly, different.,, The structural, the organization, the regulatory sequences, the hierarchy for how things are organized and used are vastly different between a chimpanzee and a human being in their genomes.”
Raymond Bohlin (per Richard Sternberg) – 9:29 minute mark of video

On Human Origins: Is Our Genome Full of Junk DNA? Pt 2. – Richard Sternberg PhD. Evolutionary Biology
Excerpt: “Here’s the interesting thing, when you look at the protein-coding sequences that you have in your cell what you find is that they are nearly identical to the protein-coding sequences of a dog, of a carp, of a fruit fly, of a nematode. They are virtually the same and they are interchangeable. You can knock out a gene that encodes a protein for an inner ear bone in say a mouse. This has been done. And then you can take a protein that is similar to it but from a fruit fly. And fruit flies aren’t vertebrates and they certainly are not mammals., so they don’t have inner ear bones. And you can plug that gene in and guess what happens? The offspring of the mouse will have a perfectly normal inner ear bone. So you can swap out all these files. I mentioning this to you because when you hear about we are 99% similar (to chimps) it is almost all referring to those protein-coding regions. When you start looking, and you start comparing different mammals. Dolphins, aardvarks, elephants, manatees, humans, chimpanzees,, it doesn’t really matter. What you find is that the protein-coding sequences are very well conserved, and there is also a lot of the DNA that is not protein-coding that is also highly conserved. But when you look at the chromosomes and those banding patterns, those bar codes, (mentioned at the beginning of the talk), it's akin to going into the grocery store. You see a bunch of black and white lines right? You’ve seen one bar code you’ve seen them all. But those bar codes are not the same.,, Here’s an example, aardvark and human chromosomes. They look very similar at the DNA level when you take small snippets of them. (Yet) When you look at how they are arranged in a linear pattern along the chromosome they turn out to be very distinct (from one another). So when you get to the folder and the super-folder and the higher-order level, that’s when you find these striking differences. And here is another example. They are now sequencing the nuclear DNA of the Atlantic bottle-nose dolphin. And when they started initially sequencing the DNA, the first thing they realized is that basically, the Dolphin genome is almost wholly identical to the human genome. That is, there are a few chromosome rearrangements here and there, you line the sequences up and they fit very well. Yet no one would argue, based on a statement like that, that bottle-nose dolphins are closely related to us. Our sister species if you will. No one would presume to do that. So you would have to layer in some other presumption. But here is the point. You will see these statements throughout the literature of how common things are.,,, (Parts lists are very similar, but how the parts are used is where you will find tremendous differences)

Moreover, unlike protein-coding regions where there is some ‘non-catastrophic’ tolerance to random mutations, randomly mutating gene regulatory networks is found to be ‘always catastrophically bad':

A Listener’s Guide to the Meyer-Marshall Debate: Focus on the Origin of Information Question -Casey Luskin – December 4, 2013
Excerpt: “There is always an observable consequence if a dGRN (developmental gene regulatory network) subcircuit is interrupted. Since these consequences are always catastrophically bad, flexibility is minimal, and since the subcircuits are all interconnected, the whole network partakes of the quality that there is only one way for things to work. And indeed the embryos of each species develop in only one way.” –
Eric Davidson – developmental biologist

Thus, where Darwinists most need plasticity in the genome to be viable as a theory, (i.e. developmental Gene Regulatory Networks), is the place where mutations are found to be ‘always catastrophically bad’. Yet, it is exactly in this area of the genome (i.e. regulatory networks) where substantial, ‘orders of magnitude’, differences are found between even supposedly closely related species.
Needless to say, this is the exact opposite finding for what Darwinism would have predicted for what should have been found in the genome.
If Darwinism were a normal science, instead of being basically the unfalsifiable ‘blind faith’ religion of atheists, this finding, by itself, should have been more than enough to falsify neo-Darwinian claims.

Of supplemental note to Richard Sternberg’s ‘bar codes are not the same’ between species quote. It turns out that the bar code pattern that Dr. Sternberg alluded to is irreducibly complex in its organizational relation to the individual genes:

Refereed scientific article on DNA argues for irreducible complexity – October 2, 2013
Excerpt: This paper published online this summer is a true mind-blower showing the irreducible organizational complexity (author’s description) of DNA analog and digital information, that genes are not arbitrarily positioned on the chromosome etc.,,
,,, First, the digital information of individual genes (semantics) is dependent on the intergenic regions (as we know) which is like analog information (syntax). Both types of information are co-dependent and self-referential but you can’t get syntax from semantics. As the authors state, “thus the holistic approach assumes self-referentiality (completeness of the contained information and full consistency of the different codes) as an irreducible organizational complexity of the genetic regulation system of any cell”. In short, the linear DNA sequence contains both types of information. Second, the paper links local DNA structure, to domains, to the overall chromosome configuration as a dynamic system keying off the metabolic signals of the cell. This implies that the position and organization of genes on the chromosome is not arbitrary,,,

This has been a fairly long post, (even for me ), but hopefully, for the open-minded person who is honestly trying to see if either ID or Darwinism is true, this post has made it abundantly clear that neo-Darwinian explanations are grossly deficient on several different levels as to explaining the amazing integrated complexity we see in life, and that ID explanations are, by far, the most satisfactory explanations for that amazing integrated complexity that we see.

complementary notes:

Contrary to popular belief, the fossil record certainly, when looked at in its entirety, does not support the hypothesis of common descent,

(Disparity consistently precedes diversity in the fossil record)
[dih-spar-i-tee] noun, plural disparities.
1. lack of similarity or equality; inequality; difference:

In fact, the ‘argument from form’ also gives us very good evidence that we each must have a soul so as to explain how the billion-trillion protein molecules of a human body can possibly cohere as a single unified whole for ‘precisely a lifetime, and not a moment longer’ (Talbott).

Body plans, contrary to neo-Darwinian presuppositions, simply are not reducible to DNA, period! That finding pretty much renders any Darwinian argument for common ancestry based on DNA alone moot and void:

A Big Problem for Common Descent: Hundreds of "Active 'Foreign' Genes" Don't Fit the Standard Evolutionary Phylogeny

Some Problems in Proving the Existence of the Universal Common Ancestor of Life on Earth

A Primer on the Tree of Life

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 – May 2013
Excerpt: It is almost universally acknowledged that beneficial mutations are rare compared to deleterious mutations [1–10].,, It appears that beneficial mutations may be too rare to actually allow the accurate measurement of how rare they are [11].
1. Kibota T, Lynch M (1996) Estimate of the genomic mutation rate deleterious to overall fitness in E. coli . Nature 381:694–696.
2. Charlesworth B, Charlesworth D (1998) Some evolutionary consequences of deleterious mutations. Genetica 103: 3–19.
3. Elena S, et al (1998) Distribution of fitness effects caused by random insertion mutations in Escherichia coli. Genetica 102/103: 349–358.
4. Gerrish P, Lenski R N (1998) The fate of competing beneficial mutations in an asexual population. Genetica 102/103:127–144.
5. Crow J (2000) The origins, patterns, and implications of human spontaneous mutation. Nature Reviews 1:40–47.
6. Bataillon T (2000) Estimation of spontaneous genome-wide mutation rate parameters: whither beneficial mutations? Heredity 84:497–501.
7. Imhof M, Schlotterer C (2001) Fitness effects of advantageous mutations in evolving Escherichia coli populations. Proc Natl Acad Sci USA 98:1113–1117.
8. Orr H (2003) The distribution of fitness effects among beneficial mutations. Genetics 163: 1519–1526.
9. Keightley P, Lynch M (2003) Toward a realistic model of mutations affecting fitness. Evolution 57:683–685.
10. Barrett R, et al (2006) The distribution of beneficial mutation effects under strong selection. Genetics 174:2071–2079.
11. Bataillon T (2000) Estimation of spontaneous genome-wide mutation rate parameters: whither beneficial mutations? Heredity 84:497–501.

Last edited by Otangelo on Sat Jan 02, 2021 2:10 am; edited 9 times in total


Duons: Parallel Gene Code Defies Evolution 1

Researchers have just characterized a new, previously hidden genetic code embedded within the same sections of genes that code for proteins—utterly defying all naturalistic explanations for its existence.1
In addition to supplying many different types of genetic code that regulate function, the genome also provides highly complex coded templates for making a wide diversity of functional RNA molecules and proteins.

Protein-coding genes—those containing the key information to make proteins—hold the most-studied type of genetic code. Some of the most important chunks of code in genes are the exons, which specify the actual template for protein sequences.

In exons, three consecutive DNA letters form what is called a codon, and each codon corresponds to a specific amino acid in a protein. Long sets of codons in genes contain the protein-making information that ends up being translated into entire proteins that may be hundreds of amino acids in length.
Before this study, scientists were aware that the protein-coding regions of genes had mysterious signals other than codons that told the cell machinery how to regulate and process the RNA transcripts (copies of genes) prior to making the protein. Researchers originally thought that these regulatory codes and the protein template codes containing the codons operated independently of each other.
In reality, the new results showed that these codes actually work both separately and together. While one set of codons specifies the order of amino acids for a protein, the very same sequence of DNA letters also specifies where necessary cellular machinery (transcription factors) are to bind to the gene to make the RNA transcript that codes for a protein. As a result of this new discovery, these dual-function code sites in exons have been labeled “duons.” Scientists just last year reported that transcription factors clamped onto some exons inside genes but did not understand this dual code system until now.2
The human mind struggles to comprehend the overall complexity of the genetic code—especially the emerging evidence showing that some genes have sections that can be read both forward and backward.3Some genes overlap parts of other genes in the genome, and now it has been revealed that many genes have areas that contain dual codes within the very same sequence.1,4
Even the most advanced computer programmers can’t come close to matching the genetic code’s incredible information density and bewildering complexity. An all-powerful Creator appears to be the only explanation for this astounding amount of seemingly infinite bioengineering in the genome.


[1]Stergachis, A. B. et al. 2013. Exonic Transcription Factor Binding Directs Codon Choice and Affects Protein Evolution. Science. 342 (6164): 1367-1372.

[2]Neph, S. et al. 2012. An expansive human regulatory lexicon encoded in transcription factor footprints. Nature. 489 (7414): 83-90.

[3]Tomkins, J. Bewildering Pseudogene Functions Both Forwards and Backwards. Creation Science Update. Posted on June 14, 2013, accessed December 19, 2013.

[4]Sanna, C. R., W. H. Li, and L. Zhang. 2008. Overlapping genes in the human and mouse genomes. BMC Genomics. 9: 169.

*Dr. Tomkins is Research Associate at the Institute for Creation Research and received his Ph.D. in genetics from Clemson University.


David Klinghoffer recently noted the discovery of dual-use codons, dubbed "duons," where a triplet of nucleotides can have multiple functions. Of course one of those is the standard function of encoding an amino acid. But now it turns out a codon can have another function as well: it can bind transcription factors which regulate the transcription of the gene. As many are now observing, this means that a single nucleotide sequence can have multiple levels of meaning. That is to say, there are multiple codes within the genetic code. In fact, one commentator observed that on the same analysis, codons may have more than two uses:

By this logic one could coin the term "trion" by pointing out that histone binding is also independently affected by A-C-T-G letter frequencies within protein-coding stretches of DNA.
But this isn't the first time that scientists have discovered multiple codes in biology. Earlier this year I discussed research that found an analog code in the DNA that helps regulate gene expression, in addition to the digital code that encodes primary protein sequence. In other cases, multiple proteins are encoded by the same gene! And then of course there's the splicing code, which helps control how RNAs transcribed from genes are spliced together in different ways to construct different proteins (see here and here).
It boggles the mind to think about how such "codes within codes" could evolve by random mutation and natural selection. But now it turns out that evidence of different functions for synonymous codons could threaten many standard methods used to infer selection in the first place

Because of redundancy in the genetic code, there are anywhere between two and six codons that will encode any given amino acid that life uses. These are called "synonymous codons" because they all have the same standard function in the genetic code: encoding the same amino acid. But this new study shows that codons can have other functions as well -- like binding transcription factors. The paper concludes:

Our results indicate that simultaneous encoding of amino acid and regulatory information within exons is a major functional feature of complex genomes. The information architecture of the received genetic code is optimized for superimposition of additional information and this intrinsic flexibility has been extensively exploited by natural selection. Although TF [transcription factor] binding within exons may serve multiple functional roles, our analyses above is agnostic to these roles, which may be complex.
(Stergachis et al., "Exonic Transcription Factor Binding Directs Codon Choice and Affects Protein Evolution," Science, Vol. 342: 1367-1372 (December 13, 2013).)
Of course "exploited by natural selection" is another way of saying "these codons are rife with different types of potentially useful functions." A news article in Science elaborates on the findings:
Despite redundancy in the genetic code, the choice of codons used is highly biased in some proteins, suggesting that additional constraints operate in certain protein-coding regions of the genome. ... The authors determined that ~14% of the codons within 86.9% of human genes are occupied by transcription factors. Such regions, called "duons," therefore encode two types of information: one that is interpreted by the genetic code to make proteins and the other, by the transcription factor-binding regulatory code to influence gene expression. This requirement for transcription factors to bind within protein-coding regions of the genome has led to a considerable bias in codon usage and choice of amino acids, in a manner that is constrained by the binding motif of each transcription factor.
The paper argues that because there's often a bias towards certain synonymous codons over other synonymous codons, this shows a "code" where transcription factors can "prefer" to bind to certain codons during processes that regulate gene expression. Because they haven't elucidated the exact workings of this "code," it's hard to say for sure whether codon biases result from an actual "code," or just preferences of the binding motifs of transcription factors. To understand how exactly these mechanisms work, more work will need to be done.
Nonetheless, one thing is clear: there ARE biases towards certain synonymous codons, meaning synonymous codons have some function, meaning synonymous codons are NOT functionally neutral. Given that we know that synonymous codons can preferentially bind transcription factors (or other molecules, like histones), we have a good idea of what kinds of functional mechanisms are causing certain synonymous codons to be preferred.

All of this poses a major conundrum for statistical methods that evolutionists use to infer natural selection in studies purporting to explain the evolution of genes. Last summer here on ENV, I discussed and critiqued such statistical methods. According to this way of thinking, an excess of nonsynonymous mutations implies "positive selection" is preserving mutations that change amino acid sequence. An excess of synonymous mutations implies selection is at work to "weed out" mutations that change amino acid sequence -- i.e., there is no "positive selection." If synonymous and nonsynonymous mutations are fixed at a proportional rate, this indicates no selection pressure, and the gene is undergoing "neutral" evolution.

To use these statistical techniques, evolutionary biologists rely on the crucial assumptions that (1) synonymous mutations are selectively neutral because they don't modify amino acid sequence in a protein or perform any other selectable functions, and (2) nonsynonymous mutations which change the amino acid sequence are preserved because they cause some selectable change in protein function. In my article last summer I cited multiple studies that challenge both assumptions. For example, the first assumption is challenged by a paper in Science which said the "discovery that synonymous codon changes can so profoundly change the role of a protein adds a new level of complexity to how we interpret the genetic code."[***] In other words, synonymous codons can have functions in addition to encoding an amino acid. This recent study in Science, however, provides additional strong evidence refuting the first assumption that synonymous mutations are selectively neutral.

(Indeed, the news article in Science also challenged the second assumption, stating, "Intriguingly, a large fraction of the variants that result in a nonsynonymous change are predicted not to alter protein function.")

But the main point of this new study is as follows: particular synonymous codons can be preferred for functional reasons. This means synonymous codons can have important functions in addition to encoding an amino acid, suggesting that the numerous studies which have purported to detect natural selection in genes, operating under the assumption that synonymous codons are selectively neutral, should be viewed with extreme skepticism.

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