One of evidences for evolution that has been strongly touted in recent years is the fact that the genomes of the human and chimpanzee are so similar. About 98.4% of the instructions in our genome match the chimp's. We must share a common ancestor, so goes the argument which doesn't worry about how humans and chimps could be so different. With a 98.4% match, evolution must be true. That, of course, is not a scientific argument. But leaving that aside, when we look under the hood we actually find that comparisons of the human and chimp genomes contradict evolution.It turns out that the differences between the human and chimp DNA instructions are not sprinkled, more or less at random, throughout our genome. Rather, these differences are found in clusters. Even more interesting, at these locations the chimp's genome is quite similar to other primates--it is the human that differs from the rest, not the chimp.
Evolutionists refer to these clusters as human accelerated regions (HARs) because they believe the human genome evolved from a human-chimp common ancestor. Often these HARs are found in DNA segments that do not code for genes (the majority of the genome does not code for genes). As we have seen, these HARs cause several problems for evolution. For instance, we must believe that evolution magically caused rapid changes to occur right where needed to improve function and eventually create a human. As one evolutionist wrote:
The way to evolve a human from a chimp-human ancestor is not to speed the ticking of the molecular clock as a whole. Rather the secret is to have rapid change occur in sites where those changes make an important difference in an organism’s functioning. HAR1 is certainly such a place. So, too, is the FOXP2 gene, which contains another of the fast-changing sequences I identified and is known to be involved in speech.
This is truly a whopper of a just-so story. But it doesn't stop here. Some HARs are found in DNA segments that do code for genes, and here we find another story of contradictions. For the ump-teenth time the evolutionary expectations are found to be false.
Of course the evolutionary expectation was that humans evolved from the chimp-human ancestor via natural selection acting on mutations, to improve the genes. That is, mutations happen to occur in the genes and occasionally a mutation was helpful or at least not harmful (neutral). In those cases it may well persist and eventually become established in the population.
But findings published earlier this year reveal nothing of the kind. Assuming evolution is true, the HARs that were found in protein coding genes showed evidence not of mutations that had been selected because they were genetically helpful, but rather the exact opposite. The genetic changes showed evidence that they were, in fact, at least slightly deleterious. They had become established in the population not because they were helpful (or not harmful), but in spite of being deleterious. As the evolutionists concluded, the results led to:
the provocative hypothesis that many of the genetic changes leading to human-specific characters may have been prompted by fixation of deleterious mutations.
Once again the results make little sense under evolution. This evolutionary conundrum is inferred from a series of observations. First, it was found that the differences found in the HARs had a suspicious trend: they strengthened the structure of the DNA molecule. Here is a brief explanation.
Instead of 26 letters, the DNA language consists of four letters. And instead of ink on paper, the DNA letters are represented by four different nucleotide molecules. The four nucleotides used in DNA are adenine, thymine, guanine and cytosine (abbreviated a, t, g and c, respectively). In the famous double helix structure, nucleotides from one DNA strand are paired with the corresponding nucleotide in the other strand.
Adenine and guanine are the larger nucleotides whereas thymine and cytosine are the smaller nucleotides. Not surprisingly, paired nucleotides consist of a big and a small nucleotide. Adenine is not found paired with guanine (two large nucleotides) nor is thymine found paired with cytosine (two small nucleotides).
This way the DNA double helix has a constant width. Furthermore, adenine is only found paired with thymine (barring error), and guanine is only found paired with cytosine. Each pair (a-t and g-c) has hydrogen bonds that precisely align, as can be seen below. Notice that the g-c pair has three hydrogen bonds whereas the a-t pair has only two hydrogen bonds. Therefore g-c pairs are stronger than a-t pairs.
Now back to our story. The HARs show a suspicious trend in that the differences observed in the human DNA (compared to the other species which are quite similar) typically increase the g-c content of that particular region of the DNA helix. That would not occur if the differences were produced by evolution as it enhanced the functionality of the protein that is encoded by the gene. That is, if natural selection were picking out DNA mutations that improved the protein, then the g-c content of the underlying gene should remain roughly constant. We would not expect a consistent trend toward increasing g-c content.
Furthermore, these HARs often are not limited just to the protein coding part of the gene, but instead extend beyond the border a bit into the flanking sequences. This further indicates that these differences observed in the human DNA are not a consequence of natural selection enhancing the protein that the gene encodes.
On the other hand, these HARs tend to cluster in a single part of a gene (in and around a single exon) rather than across the entire gene, and they tend to correlate with male recombination but not female recombination. These observations also make no sense on the theory of evolution.
There is more to the story, but it does not get any better for evolution, and evolutionists are left to speculate about why these strange patterns would be favored. For instance, evidence suggests that increased g-c content helps to increase gene expression. But as the evolutionists admit:
it is difficult to hypothesize why selection on g-c content would affect single exons and their flanking sequences rather than chromosomal domains or spliced transcripts.
Once again the evolutionary expectation is contradicted and under evolution the evidence is a mess. We're left with an increasingly contorted theory that is twisted and patched in its attempt to explain the data. It lent no helpful intuition in exploring the evidence, and leaves us even more confused after the investigation is over.
