If you scramble about 90% of a protein sequence—randomly replacing amino acids with different ones—would the protein still work? That is what evolutionists are implying in order to make sense of their theory. The problem is that evolution’s explanations for de novo genes are unlikely and very unlikely. In the case of the T-urf13 de novo gene, the two choices seem to be (i) a one in ten million shot that protein coding sequences just happened to be lying around waiting for use or (ii) only about 10% of the T-urf13 sequence really matters and you can scramble the rest with no effect.
BackgroundAn obvious problem with evolution is that it calls for vast banks of biological programs to arise on their own. One example of this is the protein coding genes within DNA. Evolutionists usually say that these resulted from the reuse of existing protein coding genes. For instance, we are able to see in color because the photocells in our retina contain different proteins that are sensitive to different colors of light.
And how did the genes for these different proteins arise? Easy, take one such gene, duplicate it and throw in a few mutations to modify the color sensitivity. Of course there are
massive problems with this narrative which evolutionists fail to recognize, but that’s another story.
Also, there is the question of from where did the first such gene come? If new genes come from pre existing genes, then from where did the first gene come? Ever since David Hume, evolutionists have argued against an infinite regress of causation so they have to have a starting point. But they have no explanation for such massive complexity beyond vague speculation which amounts to “See, poof, it happened.”
In an effort to bridge this enormous gap, evolutionists have constructed a new narrative based on de novo genes. These are genes that were not predicted but now, amazingly, evolutionists are using them as proof that evolution can indeed create new protein coding genes.
That is the argument evolutionists use for the de novo gene T-urf13 which was found in the mitochondrial genome of certain varieties of corn. The problem is that T-urf13 provides no such evidence. Indeed, if anything, it is yet another de novo gene that contradicts evolutionary theory. Let’s have a look.
Two choices: Unlikely and very unlikelyThe T-urf13 gene sequence appears to come from two separate sequences already residing in the mitochondrial genome. The two sequences are in, and flanking, an RNA gene. In other words, it appears that two sequences came together, along with a short unidentified segment, to form this new gene.
But the story is more complicated than the mere reuse of pre existing coding sequences. Under the theory of evolution, the RNA and flanking sequences are not designed to have a role in coding for
proteins. Evolution does not have the foresight, for instance, to imbed secondary functions for future use in the DNA information.
Evolutionists therefore cannot say the T-urf13 gene arose from the duplication of an existing
protein gene. They could say that T-urf13 is a lucky strike—that the RNA and flanking sequences just happened to have protein coding properties even though they were not designed or used as such. As
explained elsewhere this is unlikely (probably far worse than a one in ten million shot).
Or evolutionists can agree that, yes, the RNA and flanking sequences were not originally protein-coding like segments, but mutations evolved them into a protein coding sequence. The problem here is that we don’t find very many mutations at work. This is a difficult argument for evolutionists to make because there is so little sequence information added to the sequence. What we find is a couple dozen point mutations out of about 340 nucleotides (about 93% of the nucleotides are conserved), along with several insertions and deletions.
This second option is probably worse than the first option. For evolutionists would have to say that a sequence that has no protein-coding properties—that was not designed or selected for such information and therefore is no better than a random sequence insofar as protein-coding is concerned—can be converted into a protein-coding gene by swapping only a relatively few nucleotides. The resulting protein would have only a few percent of the amino acids modified, along with some insertions and deletions.
One way to test this evolutionary hypothesis would be to introduce mutations at those T-urf13 nucleotide sites that share identity with the original RNA and flanking sequences. In other words, scramble the majority of the T-urf13 gene. While we cannot know for sure, certainly our current knowledge suggests the resulting gene would be junk. You cannot scramble ninety percent of a gene and reasonably expect a folding, functioning, fitness-adding protein.
And if the mutated gene is junk, then we would conclude that T-urf13 owes its protein-coding abilities, probably in large part, to those original RNA and flanking sequences and that the evolutionary hypothesis makes little sense.
SummaryEvolution is not well supported by the scientific evidence. Yet evolutionists continue to reinterpret the evidence in creative ways to prop up the theory. In the case of the T-urf13 gene evolutionists have claimed that, in spite of the science, the gene is a result of a routine evolutionary capability to produce new genes.