Posted by: adventlife | May 21, 2013

Gary Gilbert, Spectrum, and Pseudogenes, by Arthur V. Chadwick, Ph.D.

Art_ChadwickIn October of 1992, Spectrum Magazine ran an article written by a young physician, Gary Gilbert, in which he attempted to justify his loss of faith on the basis of the existence of pseudogenes.

Pseudogenes are regions of DNA that have codes very similar to known genes, but often have stop codes in every reading frame, so that no protein could ever be produced from the code they contain. They were presumed by evolutionists to be copies of protein-coding genes that, through the process of evolution, have been mutated so extensively that they are no longer functional.

Gilbert learned that there was a pseudogene within the five functional genes of the beta globin gene family on chromosome 11 that was present in both humans and chimpanzees. Since the likelihood of a functional gene being similarly disabled in both humans and chimpanzees is very low, Gilbert concluded, in his Spectrum article, that both humans and chimpanzees were descended from a common ancestor that had that pseudogene.

Gilbert decided, on that basis, that the Biblical account of origins could not be correct and therefore concluded that we humans arose as a result result of evolutionary processes. Of course, this was a huge stretch, but it was enough for Gilbert; and his article was the basis for a number of Adventists losing their sense of direction in scripture, especially with regard to origins.

Are pseudogenes functionless?

For decades, I have explained to students in molecular biology that pseudogenes are not functionless and never were. In the case of the beta globin gene, I pointed out to them that the two pseudogenes in the beta globin gene family (there are five globin genes which occur on the chromosome in the same order as they are utilized in the developmental process) are so placed that one of them is located just before the genes that are activated in ontogeny (at the beginning of fetal development), and the other one is located just before the two beta globin genes that are utilized in the adult. That was, for me anyway, clear evidence for regulatory functionality. So, I instructed my students to this concept.

In philosophy class, I handed out or at times gave, as part of the final exam, Gilbert’s article as required reading for my students. I required them to analyze his logic and conclusions. Almost always the students concluded that Gilbert was not coming to the data to find answers, but he was seeking to use science to support his own pre-determined philosophical position.

It has taken some years for our understanding of pseudogenes to come out of the dark. First came indications that many pseudogenes were functional. Then certain experiments that knocked them out indicated that quite a number were in fact essential (1, 2). More recently, in 2012, the startling revelations of the ENCODE project (3) demonstrated that almost all DNA was functional. This discovery was soon followed by articles boldly proclaiming that “Pseudogenes are not pseudo any more” – such as an article by Wen et. al. (4) In this particular article the authors note:

“The study of functional pseudogenes is just at the beginning. There remain many questions to be addressed, such as the regulatory elements controlling the cell or tissue specific expression of pseudogenes. But, definitely, the so-called pseudogenes are really functional, not to be considered any more as just “junk” or “fossil” DNA. Surely, many functional pseudogenes and novel regulatory mechanisms remain to be discovered and explored in diverse organisms.” [emphasis added]

Finally, within the last year, the hemoglobin pseudogenes have themselves been the object of some study, specifically the HPPB1 gene that sits amidst the “functional” genes of the beta globin locus. As we had suspected on the basis of a considered study of placement, it is not only highly conserved (something Gilbert could have seen early on), but is essential for function. Even a single base change in the pseudogene region is responsible for pathology in humans (6).

What is the take home lesson from this? When we think we find evidence that a clear reading of the Bible story of origins is wrong, it would be well to consider the mantra of the skeptic: “An extraordinary claim requires extraordinary evidence.”

Before you decide God was wrong when He wrote with his finger in stone (7) that he made the earth in six days, perhaps we would be well served to consider all the evidence, and then, with humility, acknowledge our own ignorance and bow before the Creator in reverence and awe.

Who knows, had the author of this article reserved judgment, or better yet, had he pursued the functionality of the pseudogene, perhaps we could be talking about the Adventist Nobel Laureate who discovered the functionality of pseudogenes? – instead of lamenting for a soul who chose to abandon the Biblical account of origins to follow the philosophies of Darwinism.

1. Shinji Hirotsune, Noriyuki Yoshida, Amy Chen, Lisa Garrett, Fumihiro Sugiyama, Satoru Takahashi, Ken-Ichi Yagami, Anthony Wynshaw-Boris & Atsushi Yoshiki. 2003. An expressed pseudogene regulates the messenger-RNA stability of its homologous coding gene. Nature 423, 91 – 96;
2. Evgeniy S. Balakirev and Francisco J. Ayala. 2003. Pseudogenes: Are They “Junk” or Functional DNA? Annual Review of Genetics, Vol. 37, pp. 123-151
3. The ENCODE Project Consortium. 2012. An Integrated Encyclopedia of DNA Elements in the Human Genome. Nature. 489: 57-74
4. Yan-Zi Wen, Ling-Ling Zheng, Liang-Hu Qu, Francisco J. Ayala and Zhao-Rong Lun. 2012. RNA Biology 9:1, 27–32.
5. Moleirinho A, Seixas S, Lopes AM, Bento C, Prata MJ, Amorim A. 2013. Evolutionary Constraints in the β-Globin Cluster: The Signature of Purifying Selection at the δ-Globin (HBD) Locus and its Role in Developmental Gene Regulation. Genome Biology and Evolution. 5: 559–571.
6. Giannopoulou E, Bartsakoulia M, Tafrali C, Kourakli A, Poulas K, Stavrou EF, Papachatzopoulou A, Georgitsi M, Patrinos GP. 2012. A Single Nucleotide Polymorphism in the HBBP1 Gene in the Human β-Globin Locus is Associated with a Mild β-Thalassemia Disease Phenotype. Hemoglobin. 36 (5): 433-445.
7. Genesis 31:16-18


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