Another Confirmation of the Creationist View of the Genome

In my previous post, I discussed the new journal BIO-Complexity. I briefly discussed the first two articles in the journal, but I want to go into one of them in more detail, because the results are fascinating.

To understand the importance of the paper’s result, remember one of the ways evolutionists think information can be added to a genome. They think that gene duplication occurs, resulting in two identical genes. The copy of the gene can mutate freely, since it doesn’t really have to produce anything. After all, the original gene is still producing the protein that the organism needs, so if the duplicate gene doesn’t produce anything useful, there is really no problem. Since the copy is free to mutate, it can presumably become a completely different gene, adding information to the genome. This is supposed to play a major role in evolution.

So imagine you have this gene copy that is free to mutate. Since it can mutate a lot, it presumably can “explore” all sorts of possibilities as far as the new proteins it might make. When it hits on a protein that is beneficial to the organism’s survival, it will be naturally selected, and presto, there is new information in the genome of that species.

This idea sounds reasonable (ignoring annoying things like information theory), but it hinges on the assumption that a duplicated gene is free to mutate and that the cell continues to “sample” that mutating gene so as to “try out” the new proteins for which the duplicate is coding. Well, that didn’t happen in the experiment presented in the BIO-Complexity paper.

As I mentioned previously, the experiment begins with a strain of bacteria that has two mutations in the trpA gene, which is essential for the synthesis of tryptophan, an important amino acid. One of the mutations was fully-inactivating, which means the gene simply cannot work with that mutation. The other mutation was partially-inactivating, which means the gene will work with that mutation, but not very well.

The ability to produce tryptophan is a huge advantage for any organism. People can’t produce it, for example, so they have to eat it. As a result, it is called an essential amino acid for people. Many herbicides kill plants by inhibiting the ability of the plants to make tryptophan. Long term, that simply kills the plant, because without tryptophan, it cannot make the proteins it needs to survive. Obviously, then, bacteria like the ones used in the experiment are at a disadvantage, and if mutations could somehow repair the gene, it would make the resulting bacterium much more likely to survive and pass on the fixed gene to its progeny.

In order for this to happen for the bacteria in the experiment, only one mutation had to occur. If a mutation event corrected the fully-inactivating mutation, the gene would allow the bacteria to produce tryptophan, but not very efficiently. However, once the bacteria started producing tryptophan, presumably the gene would be naturally selected, and only the partially-inactivating mutation would be left. Later on, a mutation event could correct that mutation, making the bacteria capable of efficient tryptophan production.

The researchers did this experiment for a total of 9,300 generations involving more than 1012 cells. However, no bacteria became capable of even inefficient tryptophan production, much less efficient tryptophan production. In other words, after all those generations, not even the first mutation event occurred and was expressed.

This is surprising, because the experimenters showed that if they put just one of either mutation in a strain of bacteria, the bacteria would become efficient tryptophan producers in just a few generations. Thus, when the gene is one mutation away from efficient tryptophan production, mutational events can “fix” that mutation. However, when the gene is two mutations away from efficient tryptophan production, neither mutation gets fixed to the point where the bacterium can start producing tryptophan.

Why is this? Well, the experimenters say that the bacteria have two possible evolutionary paths. First, mutation events could fix the mutations in the tryptophan-producing gene so that the bacteria can produce tryptophan. They call this the “constructive” path. Second, the bacteria could become more efficient in their metabolism so that they could effectively use what little tryptophan the researchers gave them to eat in the experiments. How do they become more efficient in their metabolism? They acquire mutations that reduce the expression of nonfunctional genes, including the mutated trpA gene! The experimenters call this the “reductive” path.

When the bacteria are just one mutation away from efficient tryptophan production, the first path (the constructive one) seems to be the most likely to occur. Presumably, this is because efficient tryptophan production is achieved in just a few generations. However, when the bacteria are two mutations away from efficient tryptophan production, the second path (the reductive one) seems to be more likely to occur. Presumably, this is because fixing two mutations takes too many generations, so the gene’s expression is turned down so that cell stops producing the “junk” protein for which the nonfunctional trpA gene codes.

How does this relate to gene duplication and evolution? Think about it. In the evolutionary scenario in which gene duplication eventually produces something useful, the duplicate gene is supposed to be mutating away, and the cell is supposed to be producing the “junk” protein for which the gene codes. When just the right mutations occur, the cell produces a protein from the gene that is no longer junk, and the cell is now more likely to survive and pass on this new gene to its progeny.

This experiment, however, says that when resources are limited (the bacteria were given only a little tryptophan to ingest in the experiment), genes that are several generations away from producing useful proteins get “turned down” so that they don’t get expressed much. As a result, the cell doesn’t “sample” the gene very much. Thus, the idea of a freely-mutating gene being constantly expressed until something useful turns up doesn’t seem to be a very reasonable scenario. Indeed, the authors say that in their experiment, there may have been some bacteria whose trpA gene was fixed by a mutation event. However, because the gene’s expression had been so strongly reduced, a fixed gene incurred little or no advantage. After all, if the cell isn’t using the gene, it doesn’t matter whether or not the gene works.

So the results of the experiment do not provide much hope for people who want gene duplication to produce new genes in evolution. Obviously a lot more experiments like this would have to be done to see if this is a general trend, but in this particular case, it seems that when a gene doesn’t produce something useful for several generations, its expression gets turned down to the point where it isn’t sampled much. As a result, even if lucky mutations occur and produce something beneficial after lots and lots of generations, the organism won’t be any more likely to survive, since it is essentially ignoring the gene.

This, of course, is exactly what you would expect in a creationist view of the genome. The genome was designed to be efficient, and when inefficiencies arise, the genome reacts by reducing the effect of those inefficiencies. This result, of course, is not the only confirmation that bacteria have provided for the creationist view of the genome.