How does a gene list the amino acids? As shown in the illustration above, it does so by using the four nucleotide bases known as cytosine (C), guanine (G), thymine (T), and adenine (A). A group of three nucleotide bases codes for a specific amino acid. For example, when a gene has three thymines in a row (TTT), this means “use the amino acid called lysine.” When it has three guanines in a row (GGG), it means “use the amino acid called proline.” So by grouping its four nucleotide bases three at a time, a gene specifies which amino acid should be used in building a protein.
Here’s the catch: There are only 20 amino acids in the standard proteins of life. As a result, there need to be only 20 codes to specify them. However, there are 64 possible ways you can group four nucleotide bases three at a time. Thus, there are 64 different possibilities for how a gene can specify an amino acid, but there are only 20 amino acids the gene needs to specify. As a result, most amino acids are specified by more than one set of three nucleotide bases. As I said above, a sequence of three thymines (TTT) means “use the amino acid called lysine.” However, two thymines followed by a cytosine (TTC) means the same thing. This is why we say the genetic code is degenerate. It has multiple ways it can specify most amino acids.
Why is the genetic code degenerate? There is one obvious reason. If the genetic code used only 20 of its 64 possibilities*, the remaining ones would be meaningless. As a result, if a mutation caused a change in one three-nucleotide-base sequence, the result would most likely be something meaningless, which would terminate the production of the protein. To avoid this, all combinations are used. That way mutations don’t stop the protein from being produced. It might change the amino acid that is used, which might change the protein a bit, but at least the protein would still be produced. As a result, there would be a chance for it to continue to do its job. As one biochemistry textbook succinctly puts it:1
Thus, degeneracy minimizes the deleterious effects of mutations.
For many years, scientists have thought that was the only reason for DNA’s degeneracy. However, new research has uncovered a completely different reason!
A team made up of two Harvard biologists and one biologist from the University of Chicago decided to specifically look at the differences in how quickly proteins are made when different sequences are used for the same amino acid. The results were surprising, to say the least. When there was an ample supply of a given amino acid, the rate at which a protein was produced was not strongly affected by which specific sequence was used to code for that amino acid. However, when the amino acid was in short supply, the rate of protein production changed dramatically. Genes that used one sequence to specify the amino acid ended up producing almost no protein at all, while genes that used a different sequence for the same amino acid ended up producing proteins up to 100 times faster!
This seems to indicate that there is a hierarchy of importance among the different sequences that code for the same amino acid. Some sequences seem to be used in “low-priority” proteins that are simply not made if the amino acid is in short supply. Other sequences seem to be used in “high-priority” proteins that are made regardless of how much amino acid is available. The authors say that this lifts the degeneracy of the genetic code, showing that different sequences for the same amino acid are not necessarily the same.
Why would the code be built this way? Here’s what the authors suggest:2
Therefore lifting the degeneracy of the genetic code might emerge as a general strategy for biological systems to expand their repertoire of responses to environmental perturbations.
In other words, this might be a way for the cell to know what proteins must be made and what proteins can be ignored when the supplies for making that protein run low. If this is true, it represents yet another level of information that is stored in the genetic code. As I wrote previously, the information storage capacity of DNA is already mind-blowing. This research suggests it might be even more mind-blowing than previously thought.
The more I study science, the more amazed I am at the handiwork of the Creator!
REFERENCES
1. John L. Tymoczko, Jeremy M. Berg, and Lubert Stryer, Biochemistry: A Short Course, Second Edition, W. H. Freeman, 2013, p. 676
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2. Arvind R. Subramaniam, Tao Pan, and Philippe Cluzela, “Environmental perturbations lift the degeneracy of the genetic code to regulate protein levels in bacteria,” Proceedings of the National Academy of Sciences of the United States of America doi:10.1073/pnas.1211077110, 2012
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* Please note that there are really only 61 possibilities for amino acid codes, because three of the possibilities (ATC, ATT, and ACT) are used to tell the cell that the sequence is finished.
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Interesting article. I’d be curious to know how an evoultionist would explain that your DNA has safety mechanisms that resist changes by mutation, considering that mutation is one the main arguments for how one species becomes another.
Evolutionists have no idea how the genetic code came about, Evan. Indeed, there are so many proposed scenarios trying to explain the origin of life that it is clear evolutionists are flailing about. As Dembski and Wells put it in their book, The Design of Life, “An embarrassment of riches [so many origin-of-life scenarios] points not to the solution of a problem but to vain gestures at a solution. Indeed, the very claim that ‘there are many plausible solutions’ suggests that none is plausible.” (p. 241).
However, a typical evolutionist would say that early on, there was a lot of mutation without hardly any checks against it. This led to a lot of death, but it also led to a lot of innovation. Once life was established, however, the ability to survive became fairly important, so any organism that was built on a code which limited mutations to some extent had a better chance of passing its code on. At the same time, however, a code that was 100% impervious to mutations would not produce any innovation. Thus, as time went on, a balance was struck. The current genetic code we have today represents such a balance. Mutations can happen, and some will lead to innovation (in an evolutionist’s mind). However, mutations are not frequent, which produces long-term stability as well.
Slightly off subject…
What do you know about fossilized giant humans? Have such things actually been found, or is that Christian myth?
Grace, I have never seen any human fossil that is larger than Robert Pershing Wadlow, who died in 1940 and was 8 feet 11.1 inches tall. Of course, I am not a paleontologist, so I might have missed something in the literature. I know there are people who claim to have fossils from giants, but none of them (to my knowledge) have produced actual fossils. They have models to be sure, but I have not seen any actual fossils.
How does this affect Dr. John Sanford’s arguments about genetic entropy in his book Genetic Entropy & the Mystery of the Genome?
I am not sure it relates to the argument, David. This isn’t really about the degradation of the genome. It is about how the cell deals with a lack of resources.
Just out of curiosity, have there been any observed cases where an organism actually recieved a net benefit from a mutation?
There certainly have been cases in which a mutation causes a net benefit to an organism, Evan. Streptomycin, for example, is an antibiotic. It kills bacteria by attaching to the ribosome, making it nonfunctional. Because of this, the bacteria can’t make proteins, and they die. A mutation that degrades the ribosome makes the bacterium resistant to streptomycin, because the ribosome becomes so misshapen that Streptomycin can’t attach to it anymore. At the same time, however, the mutation also causes the ribosome to be very inefficient at making proteins. [Gartner, T. and Orias, E., “Effects of mutations to streptomycin resistance on the rate of translation of mutant genetic information,” Journal of Bacteriology 91:1021–1028, 1966.]
In the end, the bacteria benefit from the mutation, because they don’t die in the presence of Streptomycin. However, the key is that this mutation didn’t add something novel to the genome. Instead, it degraded something that was already there. Not long ago, I wrote of another example of mutation causing a benefit but not producing anything new in the genome. If flagellate-to-philosopher evolution were true, we should see mutations adding novel things to the genome. However, no such observation has been made.
Wow! Thanks!