The Non-Universality of the Genetic Code
(And Its Implications)
Introduction
Original
studies of the genetic code demonstrated that it was constant throughout the
plant, protists, and animal kingdoms. It was taught (even in my college days)
that the genetic code should be universal as predicted by the theory of
evolution, since alterations of the genetic code would be lethal in those
individuals that acquired genetic code mutations. Recently, many examples of
variations in the genetic code have been discovered in many species of unrelated
organisms. Although first shown in 1979 by Barrell et. al (1),
subsequent studies have demonstrated that the genetic codes differs in diverse
groups of unrelated animals, plants, and protists (2).
There is no pattern of change in the code of related groups of organisms and
none of the organisms that possess altered genetic code exhibit any form of
evolutionary descent or common ancestry, which might imply that the genetic code
had evolved.
Introduction to the genetic code and protein translation:
The molecule depicted on this page (Figure 1) is transfer RNA (tRNA). This molecule is responsible for translating messenger RNA (mRNA) to protein. Amino acids are esterified (bound) to the 3' end of the molecule. The anticodon portion of the molecule binds to the complimentary codon of mRNA, subsequently adding the amino acid to the growing peptide (protein) chain. The anticodon site of the tRNA molecule provides specificity to the genetic code, since each specific tRNA's bind to a specific mRNA codon sequence. All organisms that differ from the "universal" genetic code do so through a single nucleotide substitution in the anticodon site of the tRNA. In all the examples given in this paper, this single nucleotide substitution causes the tRNA to bind to a completely different mRNA codon (see Figure 2). Therefore, all codons that coded for this one amino acid would now be substituted by another amino acid. This kind of mutation would result in wholesale changes to all or nearly all of the proteins of an organism, which would be lethal to 100% of these mutants.


Figure 2. Translation of same mRNA by (A), wild type and (B), tRNA mutant
Since evolution requires a process by which the genetic code would be altered, evolutionists propose that organisms that express a non-standard genetic code must be genetic mutants. The problem is that this single point mutation would result in an organism that could not survive (in fact, the fertilized ovum of such a mutant would be unable to undergo even one round of cell division). This is not just my opinion. Even proponents of evolution agree that 100% of these tRNA mutants would be unable to survive. Dr. T. H. Jukes (University of California, Berkeley) has stated, "Any mutational change in the code would be lethal, because it would produce widespread alterations in the amino acid sequences of proteins. Such changes would destroy protein function, and hence would be intolerable." What these scientists have really found to be "intolerable" is what these "mutations" disclose about the theory of evolution.
tRNA "Mutants" of the "Universal" Genetic Code
What kinds of changes would tRNA mutations result in? Table 1 describes a number of these tRNA mutants, including the kinds of organisms and the changes in amino acids coded for. One can see that many of these mutations substitute amino acids that stabilize a-helical structures (the most common tertiary structure in proteins) for those that destabilize a-helical structures or, alternatively, those that destabilize a-helical structures for those that stabilize a-helical structures. A substitution that changes the configuration of a protein is virtually guaranteed to destroy its function. It actually gets worse in other instances. In some of the genetic code mutants, former stop codons (which cause protein translation to halt when the protein reaches the proper size) now code for amino acids, which would result in longer proteins. Although many proteins undergo post-translational modification, those that don't undergo post-translational modification will undergo conformational changes resulting in inactivation of function. The most lethal of all these mutants would be the ones that changed from coding for arginine to coding for the stop sequence. This mutant would produce proteins with very short polypeptide chains, since protein translation would stop at every instance where arginine (AGR) was coded. Some proteins would not be made at all and virtually all other proteins would be non-functional.
| "Mutant" Code ("Normal" amino acid) | Stabilize a-helix? | "Mutant" amino acid ("Universal" Code) | Stabilize a-helix? | Where "mutant" found |
|---|---|---|---|---|
| AUA (isoleucine) | no | methionine (AUG) | yes | human mitochondria |
| UGA (stop) | N/A | tryptophan (UGG) | yes | human mitochondria |
| UGA (stop) | N/A | tryptophan (UGG) | yes | Mycoplasma spp. |
| UAA and UAG (stop) | N/A | glutamine (GAA, GAG) | no | ciliated protozoa, Acetabularia |
| UGA (stop) | N/A | cysteine (UGC, UGU) | yes | E. octacarinatus |
| CUG (leucine) | yes | serine (UCN) | no | Candida spp. |
| CUN (leucine) | yes | threonine (ACN) | no | yeasts |
| AAA (lysine) | no | asparagine (AAU, AAC) | yes | platyhelminths and echinoderms |
| UAA (stop) | N/A | tyrosine (UAU, UAC) | yes | planaria |
| AGR (arginine) | no | serine (AGU, AGC) | no | several animal orders |
| AGR (arginine) | no | stop (UGA, UAA, UAG) | N/A | some vertebrates |
| A = Adenine C = Cytosine G = Guanine U = Uracil N = Adenine and Guanine R = Cytosine or Uracil |
The evidence is overwhelming and the problem an extremely profound one. The scientific community and even the community of creationary scientists, despite its obvious implications, have largely ignored this problem. Those who have proposed evolutionary explanations have done so using mechanisms that are so improbable as to be statistically impossible. Here is their explanation:
We propose that the changes are typically preceded by loss of a codon from all coding sequences in an organism or organelle, often as a result of directional mutation pressure, accompanied by loss of the tRNA that translates the codon. The codon reappears later by conversion of another codon and emergence of a tRNA that translates the reappeared codon with a different assignment (2).
The Problem of Mechanism
Here is the essence of what evolutionists are proposing. They propose that every instance of a specific codon in the DNA is mutated and replaced by another codon. This requires replacement of 1-5% of the entire genetic sequence of an organism. Although this doesn't seem like a large amount of the genome, it is the specificity of replacement that makes this mechanism statistically impossible. In the case of vertebrates, this replacement would involve the specific replacement of millions of nucleotide pairs. There is no "directional mutation pressure" that would cause only one codon sequence to be replaced in an organism, even according to evolutionary theories. Evolution states that selection acts on the protein structure to improve its function. Since we are talking about all the proteins in an organism, there is no one selective pressure that would work to improve the function of all proteins simultaneously (especially by substituting only one specific amino acid for another). It would make much more sense from an evolutionary viewpoint that gene duplication of tRNA would occur, followed by mutation of the duplicated tRNA and gradual conversion of genetic sequences from those that bound to the universal tRNA to those that bound the mutant tRNA. However, such a scenario would be expected to produce intermediate forms of organisms (possessing both forms of tRNA), since the process would obviously be a long one. Even though there are dozens of examples of tRNA mutants, none of them exist as these hypothetical intermediates, indicating that this is not a reasonable mechanism.
The Problem of Descent
The existence of genetic code mutants in diverse groups of unrelated organisms presents a significant problem in evolutionary theory. Since all life must be related to their relatives, the genetics must reflect this fact. These mutants present a glaring problem in terms of descent. One would expect that related organisms would exhibit some form of evolutionary tree in regard to the genetic code mutants. Instead, what we find are randomly isolated individual species of organisms which possess these genetic code mutations. If the mechanism for producing these mutations was evolution, we would expect to find whole families and orders of organisms with these kinds of mutations. Alternatively, we must accept that all of these mutations occurred relatively recently, such that there would be no record of descent.
Conclusion 
In conclusion, there is no reasonable evolutionary mechanism by which tRNA point mutations can occur in such a diversity of organisms. Evolutionists must believe in a magical directional mutation pressure that replaces all of one specific codon sequence in a variety of unrelated species. In addition, they must believe that none of these species have evolved once this mutation occurred, since there is no evidence of descent. The alternative, that a Creator designed tRNA "mutants" to show us that He and not blind chance is responsible for life, is intolerable to those whose "faith" is evolution.
Related Resources 
Fazale Rana (Ph.D.
in chemistry), vice president of research and apologetics at
Reasons To Believe, has written a
new book,
The Cell's Design: How Chemistry Reveals the Creator's Artistry, that
attempts to show that cellular biochemistry points to the existence of the
Creator who designed it. Whereas most intelligent design books attempt to show
the existence of design by demonstrating the existence of irreducible
complexity, Dr. Rana examines the cell's biochemistry with broad strokes of how
everything works together with such marvelous fidelity. So, even if a single
piece or line of evidence might be dismissed as a statistical outlier, the
weight of evidence makes a powerful case for design by a Creator.
References 
- G. Barrell, A. T. Bankier, and J. Drouin. 1979. Nature [London] 282: 189-194.
- Osawa S. Jukes TH. Watanabe K. Muto A. 1992. Microbiological Reviews 56 (1): 229-64.
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