Genetic Redundancy
The following article reproduces the article "Über den Entwurf des Lebens: Genetische Redundanz" by Dr. Peter Borger, published in the "Studium Integrale Journal" (Vol. 29, Issue 2; October 2022). Quotes without further attribution originate directly from the aforementioned original article.
To a layperson, genetic redundancy can be translated as "fault tolerance" or a "backup." It means that genes are not "selfish" (each solely responsible for its own specific task of producing certain proteins), but rather that they work together in networks. As a result, a single task can be carried out by multiple genes, while only one of these genes is actually required for execution. If one of these genes fails, another gene takes over its function, so that there is no change in the phenotype (the sum of all traits).
This was discovered in laboratory mice using so-called "knockouts." A "knockout" means that a gene is completely switched off, so that the corresponding protein is no longer produced. Scientists initiated such knockouts expecting that they would lead to defective or deficient trait expressions in the phenotype. From this, conclusions about the gene's function could then be drawn. Today, there is a mouse knockout for almost all human genes that also occur in mice.
I will spare the layperson the exact explanation of how these knockouts are induced and identified in offspring. Those interested can read about it in the original article. In any case, a complete knockout only appears starting from the second filial generation once homozygosity has been established, since, as is well known, every organism has two genes of the same kind—one from each parent (see Mendelian inheritance rules).
Surprisingly, however, these knockouts did not lead to any noticeable phenotypic change. Within the framework of evolutionary origin, every single gene should have a measurable fitness and a selectable benefit. Accordingly, every knockout should also lead to a measurably altered phenotype. However, many knockouts result in no phenotypic change at all, or only do so after the inactivation of additional genes.
This means there are genes that are dispensable. They can be switched off without any—or with only very minor—effects on the phenotype. Many genes even appear to have no measurable function whatsoever (though they may still have an unknown function).
This graphic illustrates the principle of genetic redundancy:
What can be seen is a section of 4 nodes in a complex biological network. A can reach C via B or D. If, for example, B is switched off, C can still be reached via D, resulting in no phenotypic change.
Through various knockout experiments and investigations of naturally occurring knockouts, it has been shown that genetic redundancy is the rule rather than the exception.
This brings us to the problem for evolutionary theory:
In the book Evolution by Gene Duplication by Susumu Ohno, the idea is discussed that genetic redundancy arose through the doubling of genes (gene duplication). Sometimes a gene or a longer segment of biological information is duplicated during cell division. If this occurs in germline cells and thus becomes heritable, the same gene can appear twice in the offspring. Ohno suggests that duplications create genetic redundancies, which can subsequently accumulate mutations and take on new biological functions.
The argument is that duplicated DNA elements are not subject to natural selection and can therefore be freely converted into new genes. It is assumed "that over time, a duplicated gene can differ from the original gene in its phenotypic expressions or function due to mutations in the regulatory and coding segments of the duplicate." Advantageous duplicates are said to be favored by selection while simultaneously protecting the redundancy of old functions as new functions emerge.
According to Ohno's estimate, for every new duplicated gene, approximately 10 redundant copies must be added to the non-functional DNA base sequences.
This idea of evolution through duplications would also explain knockouts without phenotypic changes. In fact, a certain degree of redundancy would be expected if genes duplicate relatively often, "since duplicates provide an organism with backup genes." Ohno's theory thus predicts a connection between genetic redundancy and gene duplication.
This question was investigated by biologists using extensive data from common baker's yeast. A full 60% of the baker's yeast genes could be inactivated without changing the phenotype. However, in 1999, Winzeler and his colleagues reported in the scientific journal Science that only 9% of the dispensable genes in baker's yeast share sequence similarities with other genes in the yeast genome, meaning that only this 9% could be the result of gene duplication.
Thus, 91% of the dispensable genes (not all genes!) in common baker's yeast are not related to other genes in the yeast genome (if similarity is interpreted as a measure of relatedness), which suggests that they did not arise through gene duplication.
This was later confirmed by other scientists (Wagner 2000; Kitami & Nadeau 2002). Genetic redundancy is not the result of gene duplication, but of interactions between unrelated genes. Thus, the prediction derived from Ohno's theory was not fulfilled, proving his theory to be incorrect.
Another argument states: "If the evolution of protein-coding genes were primarily due to (nearly) neutral mutations, then mutations in genes less exposed to purifying selection should be retained more frequently because they are not selectively eliminated. Such non-essential genes should be able to change more easily and rapidly."
However, despite intensive scientific research, this prediction could not be confirmed:
A systematic analysis of mouse genes showed that essential genes do not change more slowly than dispensable genes (Hurst & Smith 1999).
E. coli proteins operating in large redundant networks can tolerate just as many mutations as unique single-copy proteins (Hahn, Conant & Wagner 2004).
Genome comparisons between humans and chimpanzees revealed that non-functional pseudogenes, which can be viewed as redundancies, have a similar percentage of nucleotide substitutions as essential protein-coding genes (Nachman & Crowell 2000).
Thus, Ohno's duplication argument was rendered void.
Genes work together in networks, overlap in functions, can replace and bypass one another. Individual failures can be coped with because genes are not arranged linearly (like a chain), but as a network. And this is a problem for evolutionary theory while simultaneously being an indication of an engineer:
The presence of provisions for potential future failures or errors demonstrates forward planning, which is typical of an intelligent engineer and cannot be explained by purely natural processes. Since redundant genes are not constantly needed, they are not subject to selection. This means that damaging mutations could destroy these genes without selection being able to slow down this process. Within the framework of macroevolution over millions of years, redundant genes could therefore never have survived this long. Redundant genes can be a few thousand years old, but never millions of years.
Genetic redundancy contradicts evolutionary theory and represents a clear indication of creation.
Literature:
Hahn M. W., Conant G. C. & Wagner A. (2004) Molecular evolution in large genetic networks: does conectivity equal constraint? J. Mol. Biol. 58, 203-211. ↩︎
Hurst L. D. & Smith N. G. C. (1999) Do essential genes evolve slowly? Curr. Biol. 9, 747-750. ↩︎
Kitami T. & Nadeau J. H. (2002) Biochemical networking contributes more of genetic buffering in human and mouse metabolic pathways than does gene duplication. Nat. Genet. 32, 191-194. ↩︎
Nachman M. W. & Crowell S. L. (2000) Estimate of the mutation rate per nucleotide in humans. Genetics 156, 297-304. ↩︎
Winzeler E. A. et al. (1999) Functional characterization of the S. cerevisiae genome by gene deletion and parallel analysis. Science 285, 901–906. ↩︎
Wagner A. (2000) Robustness against mutations in genetic networks of yeast, Nat. Genet. 24, 355-361. ↩︎
Comments