According to popular understanding, gene duplication is a major driving force of evolutionary change and the key mechanism underlying the emergence of new genes and biological processes. Scientists came to this hypothesis by recognizing the similarities of sequences and structures of some proteins, like hemoglobin vs. myoglobin. Gene duplication is often taken as sufficient evidence of the Darwinian mechanism.
 
A new gene is called a paralogous gene. At first, it has the same function as its sister gene. However, it usually evolves by having its own mutations and in due time it may acquire functions that differ from those of its sister gene. The original gene, however, also evolves, and such direct descendants of the original gene are called orthologous genes. [1]
 
According to Susumu Ohno, GD is the only way to get new genes and, by duplication of whole genomes, great changes can occur e.g. from invertebrates to vertebrates. [2]
 
The important question is, like with any scientific theory, what is the hard evidence supporting this hypothesis? Until today, the only evidence for GD, as a driving force of evolution, is the inference from gene similarities. As M. Hurles says:
 
 
However, just because two genes are similar, that does not necessarily prove their relatedness through gene duplications. There are numerous objections that make such origination improbable. For example, all the experiments of artificial GD carried out on mice resulted in lethality, rather than evolutionary development.
 
The production of tetraploid (4n) embryos has become a common experimental manipulation in mice. Although the development of tetraploid mice has generally not been observed beyond mid-gestation [i.e. it is fatal], tetraploid:diploid (4n:2n) chimeras are widely used as a method for rescuing extra-embryonic defects [i.e. a genetic defect that is normally fatal can be artificially made to survive in the chimera].[4]
 
If the result is not lethal, then a diseased condition is very probable. “Gene duplication may lead to mutation and certain disorders. For instance, duplications of oncogenes cause many types of cancer, such as in the case of P70-S6 Kinase 1 amplification and breast cancer.” [5]
 
Further Problems of GD
 Before less than 40 years ago, for Susumno Ohno, the varying degrees of gene sequence similarities in numerous duplicated genes gave proof for evolution. The duplicated genes generated during cell division, first functionless copies but later acquiring some beneficial mutations, would be selected by natural selection. Contrary to this opinion, Zhenglong Gu et al, in their work published in 2001 Jan. 2 issue of Nature magazine, propose that gene duplicates, as backup copies, compensate a DNA failure and thus make the genome robust. Confirming this standpoint in 2003, Axel Meyer wrote, “Duplicated genes are common in genomes, perhaps because they provide redundancy: if one copy is inactivated, the other can still work.” Wondering about the raw materials for evolution he noticed:
 
 
According to Gu et al, GD contributes (23-59%) to genetic robustness, thus preserving unbroken completeness of the genome. This forcefully denies one of the main pillars of evolutionary mechanism.
 
 In 2006, further discoveries supported the preservation role of gene duplicates, i.e. that the harmful mutations are neutralized by genetic redundancy. Basically, a well functional backup, like a duplicate gene, replaces a damaged gene. All duplicate, backup genes are inactive when everything is intact and become active when a particular gene is damaged. "We suggest that compensation for gene loss is merely a side effect of sophisticated design principles using functional redundancy." [7] In this statement, not only the preserving function of the gene duplicates are emphasized but also how this genetic system indicates design. Thus, although many scientists accept GD as a proof of evolution, saying that undirected biochemical mechanisms can generate genetic redundancy, new discoveries point to other, alternative conclusions.
 
 It would be expected that according to the evolution theory, the human genome (30,000 genes) [8] is the biggest. However, this is not so. Rice has about 50,000 genes [9] and the bacterium Epulopiscium fishelsoni has approximately 25 times more DNA than a human cell. One of its genes has been duplicated 85,000 times, yet it is still a bacterium. [10]
 
 The number of chromosomes is also bigger in some species than in humans. Cambarus clarkii (a crayfish) has 200, dog 78, chicken 78, human 46, Xenopus laevis (South African clawed frog) 36, Drosophila melanogaster (fruit fly) 8, Myrmecia pilosula (an ant) 2. All these results do not fit the predictions of the GD, namely that there should be a positive correlation between organismal complexity and gene number, genome size and/or chromosome number. Obviously, evidence contradicts expectations.
 
 As a matter of fact, according to the genetic evolutionist professor Steve Jones, the more DNA there is in a particular organism, the slower it is able to evolve. For example, weeds have small genomes, while more established plants are packed with DNA and can take a month to make a single egg cell. [11]
 
 In the light of all these problems with the popular GD explanation for the origin of biochemical systems, Michale Behe writes: “Many biologists think that one of the most important evolutionary routes for biochemical innovation is through gene duplication. According to this model, a gene undergoes duplication to produce an extra copy that then experiences mutations that eventually yield a new protein with novel function. In most cases, this putative evolutionary pathway must alter several amino acids.” However, there are some strong evidences to doubt this, as Behe continues, “In this report, researchers perform mathematical simulations to model this evolutionary process and demonstrate that it is nonviable for all practical purposes. Based on their modelling, for a new functional protein with 5 amino acid changes to emerge in 100 million generations, it would take a population size of 10²⁵ (10 trillion trillion) individuals. As these researchers note, ‘These numbers seem prohibitive.’ In light of this work, gene duplication coupled to mutations can’t explain the origin of new biochemical systems.” [12]
 
 Pennisi, although a bit different in her opinion from Behe says, “scientists cannot prove that [genome duplication] didn’t happen,” but she doubtfully adds, “but [if it did], it didn’t have a major impact. For me, it’s a dead issue…The existing experimental evidence does not support genome duplication as a source of new genes for at least populations of fewer than one billion.” [17]
 
In his paper ‘Evolution at Two Levels: On Genes and Form,’ Sean B. Carroll, although a supporter of evolution, mentions some shaking facts calling GD a mere belief. He writes: “Ever since Ohno [2], and indeed well before [13], there has been widespread belief and expectation that gene duplication has been a major driving force in evolution. Empirical evidence suggests, however, that while gene duplication has contributed to the evolution of form, the frequency of duplication events is not at all sufficient to account for the continuous diversification of lineages. This conclusion is based primarily upon two sets of observations.
 
 
 Rejecting GD as a driving force of anatomical evolution, Carroll rather proposes that it happened through the evolution of regulatory mechanism[21], as he says “the story must lie more in the way regulatory mechanisms evolve.” [18] Newest researches, however, reveal that this hypothesis is not possible to testify. “Mechanistic complexity and a paucity of data from nonmodel organisms have prevented testing and quantifying universal hypotheses about the macroevolution of gene regulatory mechanisms.” [19]
 
 Another problem with GD is that natural selection acts on gene duplications, most often by deleting them from the gene pool or by degrading them into non-functional pseudogenes. This is because fully functional duplicated genes, in combination with the corresponding parent gene, produce abnormally abundant quantities of transcripts. This over-expression often alters the fragile molecular balance of gene products on a cellular level, ultimately resulting in deleterious phenotypic consequences. [20]
 
All together, looking at the different genes in the lab, one can come to suggestive similarities and propose how one gene came from another through GD and mutation, but the whole hypothesis simply remains a speculative proposition, because of the lack of proof in laboratory experiments. Thus the theory of evolution through GD remains only a well thought out hypothesis and not a hard proven fact.
 
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