This is the next post of evidence for Rize. This is where I will talk about the genetic evidence for the common descent of humans and modern apes from an ape-like ancestor.
To recap where we are so far: We have seen that unless we throw out the standard geological dating techniques, we must conclude that humans are a very recent arrival on Earth, slightly more recent than the broader group of "apes". We have seen that a separate creation for humans violates an observed law of nature (biogenesis), and that evolution is the only known means of making the recent appearance of humans on earth consistent with this law. We have seen an almost linear progression of skull size over time in fossil organisms that are morphologically similar to both apes and humans and that appear in the fossil record between the oldest apes and the first Homo sapiens. We would not have expected to find this fossil data if special creation were true, but we must expect to find them if evolution is true. We have seen that creationists have difficulties in finding alternative explanation for this fossil data. And now, we move on to the genetic.
Most everyone who has debated creationism is aware of fact one:
Humans and chimpanzees share 98% of their DNA sequences. Of course if humans and apes must each carry much of the DNA of their ancestors (all that has not been lost or changed). Finding such similar DNA patterns can easily be interpreted as evidence for evolution. Creationists have an alternate explanation. They explain this as a result of "similar structures for similar functions," then go another step to explain that similar DNA is used to build similar structures. On the surface, this explanation works. It does leave some questions open about why, exactly, God would want His "prized creation" to have so much in common (function-wise) with His "lesser" creations, but that can be chalked up to God working in mysterious ways. On a deeper examination, this explanation doesn't work on a large subset of DNA homologies (similarities).
Creationists are also apt to point out that 2% of DNA sequence dissimilarity represents a very large number of nucleotides, and potentially a large number of genes. In other words, they point out that 2% is quite a lot of DNA. The fact is, that 2% is still a very small minority. It takes a very long strand of DNA to make a gene, and it usually takes several genes to make a significant difference in the gross morphology of an organism.
It should also be noted that the majority of differences in chimp and human DNA lie in the non-coding regions. When we look only at the coding regions of DNA, humans and chimps are much more similar.
This leads us to the types of DNA homology that will not answer to "similar design for similar function". Generally, I am talking about non-coding DNA. Estimates of the percentage of our genome that codes for proteins have fallen recently from about 10 % to about 2%. But, whether 10% or 2% code for proteins, the majority of our DNA does not. The majority of our DNA is involved in regulatory or structural function, or has no function at all. There are segments of DNA that are involved in regulating the expression of genes, and these may (to the best of my knowledge) require certain sequences for their function. Non-coding regulatory DNA is only one of many types of DNA sequence that do not code for proteins, and it is the only one where the DNA sequence could possibly relate to its function. I should qualify this: some non-coding DNA may have a function
only in an evolutionary context - in being available for "back-mutations" (that restore a previous functionality) or to provide the basis for future mutations that may yield new genes with new functions. Nevertheless, for expression of phenotype (that is, the anatomical and physiological characteristics of an organism), the majority of DNA has no purpose, or works independently of the nucleotide sequence. Bear in mind that when we are talking about DNA homology (or similarity), we are talking about nucleotide sequence. For genes that are expressed, it is the nucleotide sequence that governs what proteins are made, and how they are assembled in the cell.
When there is DNA homology in the non-coding DNA, we are talking about similarities that cannot simply be explained by "similar DNA for similar structures for similar functions," because the sequence (the part that is similar) has no bearing on the development of structures or physiological function.
Non-coding DNA comes in many forms. There are repeating line segments (bits of DNA that have been copied and inserted repeatedly into the genome). There are retroviral insertions (bits of DNA that were insterted by a virus that incorporated part of its own DNA into the germ-line DNA of one of our ancestors). There are transposons (bits of DNA that were lifted from one gene, and set down unceremoniously in the middle of another). And then there are pseudogenes: bits of DNA very similar to a gene that codes for a protein, but that have mutations that interfere with the protein synthesis either because they have "stop" codons that prematurely terminate transcription, or because they have accumulated mutations that make the protein itself unviable.
"Similar structure for similar function" does not account for shared pseudogenes. I will be pointing out two specific pseudogenes that are shared between humans and other primates, one of which is shared nearly identically, and the other of which accounts for an obvious maladaption that we share with primates. After that, I will be pointing out a piece of genetic evidence that does not have to do specifically with sequence similarity.
The first pseudogene that I will point out is the urate oxidase pseudogene (thanks, chickenman!).
chickenman started a thread about this and discussed it in depth. His thread is
here. He points out that the transcription of this gene is terminated prematurely by a stop codon. (It actually has more than one premature stop codon). Now, looking at the sequence, I might have missed one or two, but I was only able to find three nucleotide differences between our copy of the pseudogene and the chimpanzee's. The premature stop codon that terminates transcription is in exactly the same place in humans, chimpanzees, and orangatans. Without these premature stops, this DNA would code for the urate oxydase enzyme. You will notice that there is significant homology (though not nearly as complete) between the primate pseudogenes and the working gene found in the owlmonkey. As evolution predicts, the pseudogene is more similar to the apes' (our near cousins) than the monkeys (our more distant cousins).
Creationists cannot account for this with "similar genes for similar organisms," because this gene
doesn't work. The alternative interpretation is usually that the gene was broken after the fall. This leaves unexplained why the gene the stop codon that makes the gene non-functional occurs in
exactly the same place and in
exactly the same way in both chimpanzees and humans. The odds of this occuring by chance are extremely low.
The next psuedogene is the human LGGLO gene. It codes for a L-gulono-gamma-lactone oxidase, a key enzyme used in the synthesis of vitamin C. That's right, with a working copy of LGGLO, humans would never get scurvy, because they could manufacture their own vitamin C like most other organisms can. Other primates share this disadvantage, and a broken gene with close homology to that of humans. The only non-primate that shares it is the guineau pig, whose broken gene is not broken by the same mutations as the primate version.
Now, if God had designed humans and other primates to require vitamin C from their food, he could just as well have left out this gene (and others involved in the synthesis of vit C). Clearly, similar genes for similar functions fails the creationist on this count. But! We could rescue the idea by postulating that God created humans and apes and all the other critters with a functioning LGGLO gene and, due to the curse, humans became vulnerable to mutations that damaged that gene. And so did apes. But monkeys didn't. And neither did mice. And neither did goldfish. Or orange trees. Etc., etc., etc. Coincidentally it was
only apes and humans that lost function by the same mutations in this gene, and only apes, humans and one other species that lost this function by mutations to this gene at all. The weakness of the explanation that this genetic trait was a similar design that was later broken explanation should be obvious.
I have one or two other genetic examples to add to this before I finish. I will wait until my next post to once again add up the points of the cumulative case.
