Dr. Edward Max on Plagiarism & Shared Genetic Mistakes
I have found much misleading information at Talk Origins and I have been examining those articles in detail for over a year now. One of the most subtle is Edward Max’s comparison of the GLO gene in humans and apes.
He notes the fact that apes and humans cannot produce Vitamin C, (picture at left from Wikipedia) and assumes that this is because of a broken GULO gene. He compares this situation to a plagiarism case in the 1940’s, and leads readers to believe that this is strong evidence of common descent.
But this is misleading. Let’s take a look.
First, Dr. Max admits that both the Creationist and the Evolutionist explanations seem consistent with the data …
1.2 The creationist view of species similarities leads to a deadlock
However, creationists have an alternative interpretation of the amino acid sequence similarities reflected in the evolutionists’ trees. They say that such sequence similarities in “related” species simply reflect the creator’s choice to design similar species to function similarly, not only at the level of bones, muscles and organs, but also at the level of protein function–hence the amino acid sequence similarities.
Thus the similarities between species in anatomy and protein structure can be interpreted in two entirely different ways. The evolutionists say that the similarity between features of, for example, humans and apes reflects the fact that these features were inherited from a common ancestor; that is, the similar features of humans and apes are determined by modern copies of genes that once existed in species that was ancestral to both apes and humans. The creationists say that apes and humans were created independently but were designed with similar features so that they would function similarly. Both the gene copying and the independent creation views seem consistent with the similarity data, but which view is correct?
Dr. Max then proposes an analogy to resolve the deadlock which, at first glance, sounds plausible. But when you look at the details, it is not plausible at all and does nothing to “resolve the deadlock.”
1.3 A possible rationale to resolve the deadlock
One way to distinguish between copying and independent creation is suggested by analogy to the following two cases from the legal literature. In 1941 the author of a chemistry textbook brought suit charging that portions of his textbook had been plagiarized by the author of a competing textbook (Colonial Book Co, Inc. v. Amsco School Publications, Inc., 41 F. Supp.156 (S.D.N.Y. 1941), aff’d 142 F.2d 362 (2nd Cir. 1944)). In 1946 the publisher of a trade directory for the construction industry made similar charges against a competing directory publisher (Sub-Contractors Register, Inc. v McGovern’s Contractors & Builders Manual, Inc. 69 F.Supp. 507, 509 (S.D.N.Y. 1946)). In both cases, mere similarity between the contents of the alleged copies and the originals was not considered compelling evidence of copying. After all, both chemistry textbooks were describing the same body of chemical knowledge (the books were designed to “function similarly”) and both directories listed members of the same industry, so substantial resemblance would be expected even if no copying had occurred. However, in both cases errors present in the “originals” appeared in the alleged copies. The courts judged that it was inconceivable that the same errors could have been made independently by each plaintiff and defendant, and ruled in both cases that copying had occurred. The principle that duplicated errors imply copying is now well established in copyright law. (In recognition of this fact, directory publishers routinely include false entries in their directories to trap potential plagiarizers.)
Can “errors” in modern species be used as evidence of “copying” from ancient ancestors? In fact, the answer to this question appears to be “yes,” since recent molecular genetics investigations have uncovered some examples of the same “errors” present in the genetic material of humans and apes. To understand these findings it is necessary to know a little about DNA, the chemical molecule in which genetic information is stored.
Max continues with some good, basic information about genetics, but he makes a fundamental error in logic. What is his error?
1. THE “ERRORS” IN THE GULO GENE ARE NOT KNOWN TO BE ERRORS, WHEREAS THEY ARE KNOWN TO BE ERRORS WITH THE TEXTBOOK.
2. THE “ERROR TEXT” IN THE GULO GENE IS NOT IDENTICAL, WHEREAS IT IS IDENTICAL IN THE CASE OF THE TEXTBOOK.
Yes, it is true that duplicated errors in a book would make a very strong case for plagiarism, but this is because the errors are identical.
In the case of the ape and human GULO genes, they are not identical. Close, but not identical.
But being close really doesn’t tell us anything we did not already know. We already knew that ape and human genes are close, but as I have emphasized repeatedly in debating with evolutionists …
Close similarity is not diagnostic of Common Descent or Common Design. It would be expected within either theory.
I recently had a discussion of Dr. Max’s article at the Richard Dawkins Forum here http://richarddawkins.net/forum/viewtopic.php?t=13262
and here http://richarddawkins.net/forum/viewtopic.php?t=13847
During the discussion, I referred to an article by Dr. Daniel Criswell of the Institute for Creation Research (ICR) www.icr.org
Adam and Eve, Vitamin C, and Pseudogenes
by Daniel Criswell, Ph.D.*
In 1994, a group of Japanese scientists identified a DNA sequence in humans that had many similarities to the rat gene that codes for the enzyme (L-gulono-γ-lactone) that catalyzes the last step of vitamin C synthesis (Nishikimi et al. 1994). The human pseudogene sequence discovered has four of these 12 exons. (Exons are the modular coding regions of a gene.) These four human exon sequences have many characteristics of a pseudogene. There is a 70-80% sequence homology between the rat and human sequences depending on the exon, and two stop codons. Later analysis confirmed that these four exons are present in other primates as well (Inai, Ohta, and Nishikimi 2003). Humans are missing only the final enzyme for the last step in synthesizing vitamin C, but have all of the other enzymes necessary to convert glucose into vitamin C.
It would seem from the evidence of a potential human pseudogene for L-gulono-γ-lactone and the presence of the other enzymes necessary for synthesizing vitamin C that humans have lost the ability to make vitamin C. However, there is more to this story. There are only four exons for the gene encoding L-gulono-γ-lactone in humans. Two-thirds of the homologous rat gene is completely missing. Most pseudogenes represent 90% of the entire functional gene. This DNA sequence, labeled as a pseudogene, might have an entirely different function than the rat gene.
Stating that only the last enzyme is missing for the pathway to convert glucose to vitamin C might imply to the untrained individual that there is a biochemical pathway that leads to a dead end. Actually, the biochemical pathway that leads to the synthesis of vitamin C in rats also leads to the formation of five-carbon sugars in the pentose phosphate pathway present in virtually all animals (Linster and Van Schaftingen 2007). There are several metabolic intermediates in this pathway illustrating that these substances can be used as precursors for many compounds in the cell. In the pentose phosphate pathway, five-carbon sugars are made from glucose (a six-carbon sugar) to be used in the synthesis of DNA, RNA, and many energy producing substances such as ATP and NADPH (Garrett 1999). Animals that synthesize vitamin C can use both pathways illustrated in the simplified diagram below. Humans and the other animals “less fortunate” than rats only use the pentose phosphate pathway.
There is no dead end or wasted metabolic intermediates, and there is no need to have the enzyme to make vitamin C since humans are able to get all of the vitamin C they need from food substances.
Thousands of human pseudogenes have been catalogued, but in spite of the similarities to functional genes, the exact role of pseudogene sequences in the genome are not known by any scientist. It is not necessary to assume that pseudogenes are remnants of once functioning genes that have been lost and now clutter the genome like junk in a rubbish heap. It is possible that these regions of DNA do have a role in human and animal genomes and this role has not been discovered yet. Over 100 years ago, Robert Wiedersheim hypothesized that the human body had more than 80 organs that lacked any function simply because it was unknown at the time what these organs did (Wiedersheim 1895). They were assumed to be vestigial or “junk” leftovers from evolutionary history and several of these organs are still presented this way in biology textbooks today. The science of genomics is in the same position today. Just because scientists do not currently know the function of a portion of DNA does not mean that it does not have any function and therefore it is an evolutionary leftover. It has been reported that pseudogenes play a regulatory role in yeast for the functional genes that they share sequence homology with (Hirotsune et al. 2003). There needs to be more research in this area to verify these claims, but at least there are some indications of a functional role for pseudogenes in the human genome.
Daniel Criswell has a Ph.D. in molecular biology and is a biology professor at the ICR Graduate School.
There was some discussion which ensued, most of which was not substantive at all, but there was one poster who made a very detailed post and sounded somewhat convincing. Here are links to her two posts …
http://richarddawkins.net/forum/viewtopic.php?t=13847&start=68, and http://www.richarddawkins.net/forum/viewtopic.php?t=9216&start=1973
Dr. Criswell responded to this via an e-mail to me and I have posted the relevant parts (with his permission) of his response below …
You will notice that no where in the paper did I say that humans definitely did or did not possess the enzyme necessary for vitamin C synthesis at one time. I presented both possibilities from a Creationist perspective. I am not interested in what evolutionists think. Evolution is a failed theory. It might be that we did have a vitamin C gene and lost it. That would certainly fit into any Creationist paradigm. All systems, especially biological ones, are in a state of decay. I do believe that the current evidence is stronger for never having this enzyme.
One of your adversaries mentioned that the enzyme necessary for vitamin C synthesis was an oxidase, which is correct and a trivial point in a paper written to an audience of non-scientists. If this would have been in a biochemistry journal (such as JMB) I would have used all of the technical aspects of the process (then no one in my readership would have understood the paper, including your opponents at Dawkins.org.) This is a typical method of trying to “discredit the witness” used by these people.
I was also accused of not providing any experimental data to support the assertion that pseudogenes may have other functions. This of course is a misrepresentation of what I wrote, as I clearly gave an example from the secular literature, cited the reference, and even suggested myself that this was insufficient and more research needed to be done in this area. Don’t let your opponents get away with this type of lie.
Finally, one of your opponents cut and pasted two biochemical pathways- one leading to vitamin C synthesis and the other into the pentose phosphate pathway. I’ll give him credit for knowing how to cut and paste. I suppose he and I could go-round-round on the semantics of these pathways. But look very carefully at the diagram. There is a pathway that leads to Ribose 5 phosphate – a pentose phosphate! Notice that this pathway can start from glucose and is directed along the same path that leads to vitamin C production. This is the same crude diagram that I gave in the paper. Remember, I am writing to a non-biochemical audience. Your adversary needs to understand that there are many substrates that can be shunted into the production of the pentose phosphate pathway. It can start from any metabolic intermediate that is in his diagram. My point was there is no dead end pathway without vitamin C. And you can see that from his diagram. There is no dead end. In fact nearly all biochemical pathways are designed (notice the word designed!) to utilize a variety of metabolic intermediates provided by the cell depending on the nutrients available to the cell and the cell’s current metabolic state. This is why we can use fats, proteins or carbohydrates for energy. They can all be plugged into Kreb’s cycle through a variety of metabolic intermediates. However with all that said. I will stand by my assertions that glucose can be directed to ribose 5-phosphate, vitamin C, and a host of other metabolic intermediates depending on cellular needs. There simply is no evolutionary dead end involved with the lack of a vitamin C enzyme. If there was, evolution might have a case. (I would also suggest that your opponents read the literature that I cited.)
You are free to do what you want with this information. You can contact me if you still are not clear about any point of this subject. I will not, however, respond to the on-line chat rooms.
Daniel Criswell, Ph.D.
Institute for Creation Research
Dr. Criswell addresses the frameshift issue in another email to me …
[RE:] … question raised over a frame shift in the human vitamin C pseudogene. … let me give you a quick run down of the characteristics of this proposed gene.
1) The four exons proposed to be the vitamin c oxidase share nearly a 70% homology with the rat vitamin c gene in question. This is the lower limit to identify pseudogenes, which in itself is an arbitrary standard. (We will give this to them since it is an interspecies comparison.)
2) Seven of the exons are completely missing. A fifth exon has been putatively identified. Where are the other exons?
3) A frame shift causing the loss of this gene function can only be assumed. If the only difference between the human and rat sequences was one or two indels then this would definitely infer loss of function due to a frame shift. There are at least four indels in the four exons, but more importantly, they have enough substitutions to lower the homology to 70%. Again, this is beginning to stretch the standards for pseudogenes. What came first, the indels or the substitutions? This is something that can’t be observed and is always inferred in light of evolutionary theory. (Maybe it was designed that way!)
4) Stop codons are not automatically the result of frame shifts. The genetic code is arranged in such a way as to minimize the effects of base changes including preventing the introduction of a stop codon. (Notice I said this is not automatic, it can happen. It has been my experience that your opponents will take this and say, “Criswell says there is never a stop codon introduced when a frame shift happens, ha ha”.) The reason why stop codons are used as a measurement of pseudogenes is because they are so common in pseudogenes. I might do a comparison of the rate of stop codons in pseudogenes compared to possible stop codons due to frame shifts in functioning genes to see how significant the difference is. There is a difference. It needs to be quantified.
5) Your opponents are assuming the only explanation is that we lost the vitamin C gene through evolution. Maybe we did lose it, but as a result of the “Fall”. I discussed that possibility. Losing genetic information will not make evolution happen though. I am always amused when evolutionists discuss their theory this way. In fact there are many observable examples of lost information (genetic diseases), but no observation for the production of a new gene (although mutation can create a variation in an existing gene). Loss of information is not going to evolve a primate, rat, or amoeba into a human.
Daniel Criswell, Ph.D.
Institute for Creation Research
I have had several posters at forums tell me that they used to believe the Bible, but they don’t anymore because of this issue. Too bad for them. They jumped to a conclusion without understanding the evidence!
More discussion HERE followed by my conclusion as follows …
LOTS OF EFFORT BY GLADIATRIX … BUT WHAT DOES IT ALL MEAN?
Gladiatrix … I have to hand it to you. You are a very conscientious and detailed researcher and you seem to have a very good grasp on how things work. I wish that all posters followed the example set by you and CK1 and a handful of others who seek to support the things that you post, rather than just typing and typing and typing endlessly with no support, wasting bandwidth with nothing but insults, twisting and distorting the things I say, etc.
So you make some good points about how things work. However, as Crick makes clear …
Francis Crick, What Mad Pursuit: A Personal View of Scientific Discovery, Basic Books, 1988pp. 138-139
Biologists must constantly keep in mind that what they see was not designed, but rather evolved. [I’ll forgive Crick for the moment for this injection of quasi-religious opinion] It might be thought, therefore, that evolutionary arguments would play a large part in guiding biological research, but this is far from the case. It is difficult enough to study what is happening now. To try to figure out exactly what happened in evolution is even more difficult. Thus evolutionary arguments can usefully be used as hints to suggest possible lines of research, but it is highly dangerous to trust them too much. It is all too easy to make mistaken inferences unless the process involved is already very well understood.
knowing how things work and how things supposedly evolved are quite different.
What you have done is made a case for the position that humans and apes once had a functioning GULO gene, but it was inactivated by mutation.
Creationists acknowledge this as a possibility, so there is no point arguing about this.
Our difference lies in the answer to this central question …
Are shared mistakes “proof” of common ancestrty?
Creationists would say “NO.”
Evolutionists say “YES.”
And therein lies our fundamental difference.
However, the truth of the matter is that the bare facts can be accommodated by BOTH theories. The bare facts are that …
1) GULOP shares 70% homology to RAT GULO (the “P” denotes “pseudogene”)
2) Apes and humans both have GULOP which is more than 70% similar, but not identical (as I was led to believe back at AtBC)
3) Guinea pigs also have GULOP and share many similarities with human GULOP
So there are similarities, but that is all we can say.
We cannot say, “There are similarities … therefore, apes and humans share a common ancestor.”
We also cannot say, “There are similarities … therefore, they have a Common Designer.”
GULOP does not help us decide between Common Descent and Common Design as Dr. Max proclaims that it does.
So, while we could argue until we are blue in the face about this topic, the only point that is important to me is …
Dr. Max’s article is misleading. Shared Mistakes do NOT help us decide between Common Ancestry and Common Design.