Gene Duplication Is Not a Credible Source of Evolutionary Progress

Belief triumphs over facts in an evolutionist’s claim
that duplicate genes can evolve new functions

 

by Jerry Bergman, PhD

A long paper, titled The Failures of Mathematical Anti-Evolutionism by anti-creationist mathematics Professor Jason Rosenhouse, is a good illustration of the fact that evolution is a belief, and that facts, evidence and reason often have little effect on Darwin ‘true believers.’

Rosenhouse has research interests in Algebraic Graph Theory, Recreational Mathematics, Science Education, and Analytic Number Theory. His publications include the 2012 book, Among the Creationists: Dispatches From the Anti-Evolutionist Front Line, published by Oxford University Press. In the preface he openly admits “I am an atheist. That means that I do not believe in God.” The reason he is an atheist, he says, is that “Atheism just makes the fewest demands on my credulity.”

In his book, which covers many topics, Rosenhouse quoted me when I spoke at a conference where I mentioned my three thick volumes documenting in detail the cases of persons whose careers were ruined because of their criticism of evolution and their support of the creation worldview. Rosenhouse, calling me “a prominent creation speaker and writer,” responded curtly toward my comments regarding this Darwin-Doubters trilogy, stating that “Creation urban legends about ‘Darwin doubters’ having their careers summarily destroyed almost never include all of the relevant facts.”[1] He did not give any details about his claim, nor ask for information about my books which were carefully supported by documents stored in four full file cabinets. And, as far as I know, he never bothered to read any of them that he curtly dismissed.

 

Can Evolution Progress by Gene Duplication?

I will focus on one claim made in Rosenhouse’s paper The Failures of Mathematical Anti-Evolutionism,[2] namely that evolution can produce new information by the process of gene duplication. Rosenhouse stated that

Anti-evolutionists frequently refer to the technical minutiae of information theory in their discourse, but such references do nothing to help their argument. Known genetic mechanisms are fully adequate to explain the growth of genetic information through the evolutionary process. One especially important mechanism plays out when a gene duplicates itself, thereby leaving the organism with two copies of a gene that previously occurred only once. The second copy is then free to acquire mutations without harming the organism because the first gene is there to carry out the original function.

This process is analogous to increasing the information stored on a computer by inserting a thumb drive. Inserting the drive is comparable to the duplication event; it increases the information storage capacity of the computer just as the duplication increases the storage capacity of the genome. When new files are placed on the drive, the quantity of information stored on the computer has increased, just as mutations in the duplicate copy lead to new genetic information.[3]

Having taught genetics at the college level for several years, I am aware that this specific claim is not made by professional geneticists, and thus is not in any of the major genetics textbooks. Rather, it is made by evolutionists who have not considered the various problems with this idea. A major error with this concept is that when two genes are located in the genome that are very similar, the default assumption is that this condition is caused by genetic duplication.[4] Evolutionists further assume that “neo-functionalization” occurred with the duplicated gene, which was free to evolve a new function.

Creationists argue that the similarity must have existed in the original design because both genes are necessary for survival. Indeed, determining how the gene similarity occurred (i.e., discovering the specific mechanism responsible) is an entirely different challenge than just assuming it has occurred.

Several mechanisms can result in accidental gene duplication. For example it

can occur as the result of an error in recombination or through a retrotransposition event. Duplicate genes … can result in a large number of mutations accumulating in the duplicate gene code. This may render the gene non-functional or in some cases confer some benefit to the organism. There are multiple mechanisms by which gene duplication can occur. Duplications can arise from unequal crossing-over that occurs during meiosis between misaligned homologous chromosomes. The product of this recombination is a duplication at the site of the exchange and a reciprocal deletion. Ectopic recombination is typically mediated by sequence similarity at the duplicate breakpoints, which form direct repeats. Repetitive genetic elements, such as transposable elements, offer one source of repetitive DNA that can facilitate recombination.[5]

Hurdles Facing Gene Duplication

A gene duplication event can influence evolution only if the genes duplicated are in the germ cells (the sperm and eggs), not somatic cells which are not passed on to the offspring. And, of the trillions of germ cells, the cell with the duplicated genes must be the one that is fertilized to be passed on to its offspring. And it must normally occur very early in the cell division to ensure that all of the cells in the new organism have the aberration. At the least, the germ cells for the next generation must have the aberrant trait and produce the seeds of the next generation to allow the duplicated gene to become a new cell line and also a new strain of an organism.

Additional gene duplications in the germ cells must occur many times. This is the only way a Darwinian process could ensure that the cell has sustained all of the mutations required to evolve a new function. The novel gene must produce a novel protein capable of conferring a survival advantage to the organism compared to the individual that does not have it. This is only the beginning of problems with the notion that gene duplication is a source of new genetic information.

Another problem is, if only one gamete possesses the duplicated gene—depending on how large the duplicated gene is—the gamete’s chromosomes may not pair correctly in zygote formation. For the duplication to be passed on to the progeny, it must become part of the allele pair that produces the next generation. And the same unlikely scenario must occur many times to create a future progeny so that the duplicated gene has become fixed to the point of improving the survivability of the descendants and the population.

Further Problems

When gene duplication occurs, cell repair processes will often attempt to correct the error by removing the duplicated genes. In cases where the aberrant genes are not removed, the evolutionary argument must consider additional hurdles required for the duplicate to successfully add new information. To function properly, genes require the correct regulatory factors related to gene expression. Regulatory elements can be adjacent to the genes they regulate, or they may be either upstream or downstream from it. Sometimes they are found at a significant distance away from the gene they regulates. So if the required regulatory genes were not also duplicated, evolution comes to a stop; the duplicated gene will normally not function properly, if at all.

Transposition is a system designed to produce genetic variety by the movement of genes from one location to another in the genome. This is another process requiring regulation. Many cases exist of transposition causing problems, including cancer, due to improper regulation. Assuming the regulatory system was also duplicated (an unlikely event) the gene copy will continue doing what the original gene did. This can cause up-regulation of the resulting protein, which may not be beneficial. More is not always better.

As is true of the location of words in a book, the location of the gene in the genome is also critical. Duplication of words in a book will most often interfere with the story, distorting the meaning of the affected text. Assuming that no problems are encountered up to this point, the duplicated gene will continue to produce the protein coded for by the original gene. Rosenhouse’s claim that the duplicated gene will, due to mutations, evolve to perform another function, is naïve.

Evolving the Novel Gene

Assuming that the organism has survived thus far, Rosenhouse argues the duplicated gene will begin to sustain mutations and the original gene will experience fewer or no mutations—a very implausible assumption. For the sake of argument, this unrealistic notion will be ignored in this discussion. The new gene will also be useless or worse until it has sustained the mutations required to produce a protein of use to the organism. This protein, moreover, must give it at least a slightly greater survival advantage than other organisms of the same type. This is a very unlikely scenario given the fact that 99.9 percent of the mutations that are not repaired will be deleterious, or at least near-neutral, 99 percent of the time. Furthermore, both the original gene and the duplicate gene will experience mutations primarily in locations called hot spots. If not repaired, as 99.99 percent of the time they will be, this will cause both genes to become useless and the cells with them will die and may be recycled.

Another problem is that the vast majority of mutations that are not repaired are in the above-mentioned hot spots. (Note: most of the genes that do not sustain many mutations are called cold spots.)[6] In cancer cases, we know that a majority of the mutations are in these hot spots. Hot spots are one reason why most mutations are near-neutral or deleterious. The mutations in the duplicated gene will almost always cause damage to the cell and will not become functional genes. For these reasons, life cannot be built from mutations.

Novel Proteins Must Be Team Players

To achieve the close-to-impossible feat of producing a functional protein by duplication, the cell must also evolve the many required regulation-controlling systems for it to work. These include accessory parts, such as chaperones (also complex molecular machines) that work to help the new protein fold properly. Any newly evolving protein, furthermore, must be compatible with the downstream cellualr factories that perform post-translational processing. Much of this occurs in the endoplasmic reticulum, where molecular machines perform multiple vital roles in the synthesis, folding, modification, and transport of proteins. Also, the protein requires compatibility with the Golgi apparatus. This complex organelle serves in further post-processing of proteins that have been transported from the endoplasmic reticulum, to package and sort them for transport to their eventual destinations.

Summary

In short, the gene duplication process has close to a zero probability of adding information to the cell. Expecting that duplication of existing information might generate a novel protein that could evolve to give the organism an advantage by natural selection is a false hope. Gene duplication, therefore, cannot be a major, or even a minor, source of genetic variety in evolution. Many other reasons exist to support this conclusion aside from the concerns listed here.[7]

Genes are designed to resist mutational aberrations in order to maintain homeostasis. This is obvious from the history of life when considering the large number of living fossils—organisms that have not changed[8] for millions of supposed Darwin Years. Little evidence exists to support the conclusion that gene duplication is a significant source of new genetic information. One University of South Carolina molecular evolutionist’s conclusion was clear: scientists cannot “prove that [genome duplication] didn’t happen, but [if it did], it didn’t have a major impact. … For me, it’s a dead issue.”[9]

References

[1] Rosenhouse, Jason. 2012.  Among the Creationists: Dispatches From the Anti-Evolutionist Front Line. New York, NY: Oxford University Press, p. 200.

[2] Rosenhouse, Jason. 2022. The Failures of Mathematical Anti-Evolutionism. Skeptical Inquirer

46(3), May/June. https://skepticalinquirer.org/2022/05/the-failures-of-mathematical-anti-evolutionism/

[3] Rosenhouse, 2022. Italics added.

[4]  Bansal, Mukul S., and Oliver Eulenstein. 2008. The multiple gene duplication problem revisited. Bioinformatics 24(13): i132–i138, July 1. doi: 10.1093/bioinformatics/btn150.

[5] Libretext. 2020. Gene Duplications and Divergence. https://bio.libretexts.org/Bookshelves/Introductory_and_General_Biology/Book%3A_General_Biology_(Boundless)/18%3A_Evolution_and_the_Origin_of_Species/18.4%3A_Evolution_of_Genomes/18.4D%3A_Gene_Duplications_and_Divergence.

[6] Si, W. 2015. Widely distributed hot and cold spots in meiotic recombination as shown by the sequencing of rice F₂ plants. New Phytologist 206(4):1491-1502.

[7] Bergman, Jerry. 2006. Does Gene Duplication Provide the Engine for Evolution? Journal of Creation 20(1):99-104. https://creation.com/does-gene-duplication-provide-the-engine-for-evolution.

[8] Silverberg, Robert. 1966. Forgotten by Time: A Book of Living Fossils.  New York, NY: Thomas Crowell Co.

[9] Pennisi, E., 2001. Genome Duplications: The Stuff of Evolution? Science 294(5551):2458–2460, December 21.

---

Dr. Jerry Bergman has taught biology, genetics, chemistry, biochemistry, anthropology, geology, and microbiology for over 40 years at several colleges and universities including Bowling Green State University, Medical College of Ohio where he was a research associate in experimental pathology, and The University of Toledo. He is a graduate of the Medical College of Ohio, Wayne State University in Detroit, the University of Toledo, and Bowling Green State University. He has over 1,300 publications in 12 languages and 40 books and monographs. His books and textbooks that include chapters that he authored are in over 1,500 college libraries in 27 countries. So far over 80,000 copies of the 40 books and monographs that he has authored or co-authored are in print. For more articles by Dr Bergman, see his Author Profile.