Question: If your brand-new car breaks down and you take parts from an older car to fix it, is your new car closer to becoming a Model T?

Answer: No!

So why do some claim that if you take pieces from two very closely related genes and put them together, you’ve recovered the function of an “ancient” gene and essentially reversed evolution?

ScienceDaily1 and other news outlets report on an article recently published in Developmental Cell,2 claiming that scientists have been able to recreate an ancient Hox gene in mice by using this “reversal” method.

It’s all about presuppositions

Both the news articles and research articles are laden with the scientists’ evolutionary presuppositions. For example, “The process of one gene splitting into multiple genes, which then mutate, has occurred many times in evolution, but no one has put it back together again. … It illuminates the mechanisms and processes that evolution uses, and tells us more about how Mother Nature engineers life.”1

The purported ancient gene, Hox1, is a combination of the protein-coding region of the Hoxa1 gene and a portion of the regulatory region of the Hoxb1 gene.2 Hox genes in general are crucial for proper embryonic development. Hoxa1 and Hoxb1 are important for brain development in embryos. The 39 Hox genes present in humans and other mammals are theorized by some evolutionists to be the result of multiple gene duplications (plus mutations and loss of genes) from an original complement of 13 Hox genes.1 How do the scientists know this? The support for this idea is based solely on an increase in the number of Hox genes present in modern humans and mammals compared to putative ancient animals, as represented by the evolutionary tree. The amplification of Hox genes seen in current species is totally based on their assumption that the evolutionary tree is true. The problem is that the support for the evolutionary tree being correct is commonly based on genetic evidence, including the amplification of Hox genes! This type of circular reasoning proves nothing.

God designed organisms to have the Hox genes necessary to develop properly. These genes are critical in development, and even small mutations can have large effects on the organism—such as fruit flies growing legs where antennae should be. Since mammals share similar body plans, it shouldn’t be surprising that a common Designer used similar genes in many animals. These genes exist in a wide variety of animals because of functional constraints: certain designs are most effective and, for this reason, are used over and over.

Copying mistakes—the driving force of evolution?

The evidence cited for the Hox gene amplification is two-fold gene duplication and mutation over time. Gene duplication is often cited by evolutionists as a way for organisms to gain genetic information. This is simply not true (see Copying confusion). If you buy a book and a friend gives you a copy of the same book, do you have more information? No.

This is where evolutionists claim mutation plays a role. They argue that mutations could accumulate in the extra copies of the gene, possibly leading to new functions in the protein produced without harming the original function of the protein. There are several problems with this idea. First, mutations lead to a loss of information, not a gain.3 If you hand-copied a book, there would probably be errors in the copy that may lead to problems in understanding what is written. You would certainly not end up with more information.

Some argue that mutations, such as antibiotic resistance in bacteria, can be beneficial. However, the mutations are only beneficial to the bacteria when antibiotics are present. The mutated bacteria usually cannot effectively compete with their normal counterparts in an antibiotic-free environment.4 If you copied an English book and translated some of the sentences into Spanish, you have improved the book for Spanish-speaking individuals, because they now can understand a small portion of the book. But for English-speaking individuals you have made the book less understandable. The “error” is only beneficial under certain circumstances.

Another major problem with crediting mutations for changing a gene (and the function of the protein produced) is the number of mutations that would be required and the ability to accumulate them over time. Many mutations, called “silent mutations,” do not lead to a noticeable change in protein structure and function. Those proteins would not be selectable because they do not lead to improved fitness at the whole organism level, the only place where natural selection works.5,6 Considering that mutations are either harmful or neutral and cannot accumulate within one individual’s germ line, it would be unlikely for extra copies of a gene to lead to beneficial changes.

Conclusion

One thing that surprises scientists is the fact that the Hox gene family has mutated and gained new functions (neofunctionalization) over millions of years.2 In order to make their theory of evolution fit the evidence, the scientists claim that the Hox genes have undergone “functional partitioning, a process termed ‘subfunctionalization’.”2 Creationists conclude that God designed the Hox genes, including Hoxa1 and Hoxb1, with different functions as a part of the original creation. Hoxa1 and Hoxb1 have similar sequences, and their proteins may perform similar functions within varying organisms. Depending on your starting point this could either imply common ancestry or common design. But the evidence clearly denies common ancestry and points to a common Designer.

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Footnotes

  1. Scientists Reverse Evolution: Ancient Gene Reconstructed From Descendants, ScienceDaily, August 7, 2006. Back (1) Back (2) Back (3)
  2. Petr Tvrdik and Mario Capecchi, Reversal of Hox1 Gene Subfunctionalization in the Mouse, Developmental Cell, 11:239–250, 2006 Back (1) Back (2) Back (3) Back (4)
  3. See Mutations—part of evolution’s engine? Back
  4. See “Superbugs not super after all,” Creation 20(1). Back
  5. J.C. Sanford, Genetic Entropy and the Mystery of the Genome, Ivan Press, 2006. Back
  6. See Evolution or Adaptation? Back