How Are New Genes Made?

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The evolutionary apologist Jerry Coyne describes Darwinian evolution as,

life on earth evolved gradually beginning with one primitive species—perhaps a self-replicating molecule—that lived more than 3.5 billion years ago; it then branched out over time, throwing off many new and diverse species.1

Ignoring the nonsensical suggestion that a single molecule “lived,” Coyne illustrates that evolution requires some very elaborate and dramatic forms of change. Indeed, evolution claims that during the course of earth history invertebrates transformed into vertebrates, non-flying creatures developed wings and started flying, and marine animals evolved legs and began walking.

The Evolution Motor?

The standard scenario is that chromosomal DNA undergoes changes (e.g., mutations) that can eventually form new genes. These new genes can alter the physical features and abilities of an organism. Eventually, enough new genes can change a dinosaur into a bird. Thus, evolutionists conclude that “the birth of new genes is an important motor of evolutionary innovation.”2

How Are New Genes Made?

Evolutionists offer two basic mechanisms:

  1. Gene Duplication. During chromosome replication occasionally an extra copy of a gene will be formed. If this extra copy is not needed by the organism, then subsequent mutations can transform it from the original gene to a new gene.3 Similar genes in other organisms are assumed to be related—providing an evolutionary lineage of the new gene.
  2. de novo Genes. Unused DNA in the chromosome can serve as a type of “gene nursery.” This DNA can be from the so-called “junk” DNA or sometimes from other sources, such as viral or horizontally transferred DNA. All DNA is potentially subject to mutations, so this “unused” DNA can begin to randomly mutate. Because the DNA supposedly has no function, presumably it is free to mutate until something useful is formed. From this unused DNA, genes can evolve from scratch (i.e., de novo).4 These de novo formed genes are sometimes called orphans because they "suddenly" appear in the evolutionary record with no apparent lineage of similar genes in other organisms.

Does This Work?

There are several problems with these scenarios. First, real-time analysis of mutations fails to support these claims. For example, overexpression of P450 genes contributes to insect resistance of DDT.5 This overexpression results from mutations that reduce a regulatory control. Bacteria can become resistant to some types of antibiotics following a mutation that eliminates specific transport proteins.6 Mice can gain a protective camouflaging of fur color when a mutation decreases the amount of fur pigment produced.7 Mutational loss of specific proteins on the surface of human blood cells can contribute to resistance of AIDS8 and malaria.9 The cotton bollworm gains resistance to some insecticides by mutations that prevent production of a transporter protein.10

Each of these mutations can be considered “beneficial” for the survival of the organism. Each of these mutations is commonly cited as an example of “evolution.” Each of these mutations is also at the expense of a pre-existing genetic system (i.e., activity of enzymes, transport proteins, regulatory factors, and so on, are diminished or eliminated). Each of these demonstrate how “beneficial” changes frequently result from degenerative mutations; the very opposite of forming new genes.

Therefore, simply because a mutation provides an adaptive benefit to the organism does not mean a new gene or regulatory system was formed (a very common misconception).

Simply because a mutation provides an adaptive benefit to the organism does not mean a new gene or regulatory system was formed.

What is more, experimental data show that seven or more mutations are typically necessary to transform a protein-coding gene into a different protein-coding gene.11 A variety of simulated estimates also illustrate that it likely would take millions of years for even a few of these “gene-transforming” mutations to occur and become fixed within a population.12 Coupled together, the two situations present a major obstacle for Darwinian evolution. There is simply not enough time, even by its lengthy historical timescale, to achieve the necessary gene transformation.

The proposition for de novo gene formation is even less plausible. At best, evidence that genes will form from scratch is derived by a historical reconstruction. Such reconstructions assume a Darwinian evolutionary history, and then make an interpretation based upon this assumption. For example, humans and chimpanzees supposedly share a common ancestor, yet humans may have over 600 genes that are not found in primates.13 These human genes are assumed to have formed de novo from unused (“junk”?) areas of our chromosomes during the past few million years as we traveled a different evolutionary path than gorillas and chimpanzees. So, any gene in humans that is not similar to a gene in primates is interpreted as a de novo origination. Because all organisms likely contain numerous such orphan genes (10–30% of their genome14), this reasoning is applied throughout the biological world. If similar genes are not found elsewhere, then there is no evolutionary lineage and the gene is assumed to have formed from scratch.15

However, historical reconstructions are only as good as the assumptions of the reconstruction.

What does de novo formation of a new gene involve? If it takes at least seven mutations to transform a functional gene into a different gene, then it would require far more mutations to truly evolve a de novo gene. One problem is that the more mutations required, the greater the potential that some will be harmful. An even greater problem, as Jacob admits, is “the probability that a functional [gene] would appear de novo . . . is practically zero.”16 In fact, this was the assessment (with experimental verification17) for many decades until it was realized that evolution could not account for orphan genes without drawing upon this “practically zero” event.

So, despite the improbability, Abrusán insists that “de novo origination of genes is not questioned anymore.” This conclusion is not based on observational data, but rather on evolutionary necessity. The presumption of evolution is so prevalent in biology that it trumps everything else, even if it means depending upon events with a “practically zero” chance of occurring. To borrow an observation, some ideas become so thoroughly entrenched in scientific thought that they become “vampirical more than empirical—unable to be killed by mere evidence.”18

I am not aware of any experiments that show splicing even similar genes together yields a functional product, let alone random sequences of DNA naturally mutating to become a functional gene. Several frequently cited examples, the Sdic, Adh-finnegan, and Adh-twain genes of Drosophila, may only be rearrangements of pre-existing genes with no clearly identified function—suggesting they might actually be more degenerative than innovative. In addition, relocating a gene to an alternate regulatory system, activating a silent gene, or horizontally transferring a pre-existing gene does not constitute formation of a new gene. Yet many popular examples of new gene “evolution” simply involve these processes. Certainly contemporary genetics has shown that portions of chromosomes can be very dynamic, yet this does mean that de novo gene formation can result.

Terms such as tinkering and cobbling together are frequently found in the evolutionary literature of de novo gene evolution. These hardly present a viable mechanism for gene formation. Typical animal genes contain exons, introns, open reading frames, start and stop sequences, flanking regions, and adjacent (and even distant) regulatory regions controlling expression of the gene—all providing coordinated genetic function. Thus, it takes far more than “cobbling” together pieces of pre-existing genes to claim a gene was formed from scratch. No wonder Singer admits that “creating a gene from a random DNA sequence appears as likely as dumping a jar of Scrabble tiles onto the floor and expecting the letters to spell out a coherent sentence.”19 Yet she simply concludes that somehow it must happen.

As noted, the time needed to transform a functional gene into a different gene bursts the evolutionary timescale. The de novo formation of new genes takes this problem to even greater magnitudes. Humans, for example, are supposed to have evolved from a primate ancestor in just 4–6 million years. Even by the most generous calculations, this is insufficient time for the de novo construction of the hundreds of human orphan genes. Clearly, this presents a significant problem for any evolutionary scenario—there simply is not enough time.

What is more, this time constraint is based upon calculations that are assuming de novo formation can actually occur. In contrast, real-time natural mutation studies, as discussed above, give us little grace for this assumption. Rather, example after example shows that “beneficial” mutations are still degenerative. Other than evolutionary presupposition, we have no basis to assume that random “junk” sequences of DNA can mutate into anything other than different random “junk” sequences of DNA. Even when starting with pre-existing genes, experiments demonstrate that random mutations typically reduce or eliminate the activity or regulation of that gene. This is the antithesis of new gene formation.

Experiments demonstrate that random mutations typically reduce or eliminate the activity or regulation of that gene.

In fact, geneticists generally admit that “most amino-acid changing mutations are deleterious.”20 Thus, at best, evolutionary assumptions are relying on those exceptionally rare events—a protein-changing mutation that is neither deleterious nor degenerative (even if beneficial). Perhaps such mutations occur, but their distinct rarity makes them an extremely weak mechanism to account for Coyne’s grand claims about Darwinian evolution.

Less-Is-More. In light of this rarity, genetic loss has been proposed as a major driving force of evolution instead. This “less-is-more” model recognizes that degeneration (and not formation) of genes is actually behind most “beneficial” mutations.21 However, evolutionary transformation (e.g., human evolution) requires a genetic mechanism that accounts for the origin of specialized features, such as vision, cognition, dexterity, and so on. A “less-is-more” mechanism cannot account for the origin of the genetic systems it is ultimately eliminating. Thus, it assumes that previous mutations have built the genetic machinery, and other mutations will continue to build (or rebuild) the machinery. So this model requires what has not been observed—the formation of new genes from scratch, in order to achieve what has been observed—loss of those genes.

Fits Biblical Model. Instead, the evidence fits within a biblical creation model, where humans, animals, plants were created with a fully functional genome. Since this initial creation, subsequent changes in the genome have introduced many mutations and other alterations to the DNA. Some of these have even provided a specific (and likely limited) adaptive benefit. Yet these benefits result from degenerative mutations, not the formation of new genes.

Answers in Depth

2016 Volume 11

Kevin Anderson (PhD, Microbiology) serves as director of the Van Andel Creation Research Center in Chino Valley, Arizona.

Footnotes

  1. Jerry Coyne, Why Evolution is True (New York: Penguin Books, 2009), 3.
  2. Jorge Ruiz-Orera et al., “Origins of de novo Genes in Human and Chimpanzee,” PLoS Genetics 11, no. 12 (2015): e1005721, doi:10.1371/journal.pgen.1005721.
  3. Ibid.
  4. Ibid.
  5. Richard H. ffrench-Constant, “The Molecular Genetics of Insecticide Resistance,” Genetics 194, no. 4 (2013): 807–815.
  6. Kevin Anderson, “Is Bacterial Resistance to Antibiotics an Appropriate Example of Evolutionary Change?,” Creation Research Society Quarterly 41, no. 4 (2005): 318–326.
  7. Hopi Hoekstra et al., “A Single Amino Acid Mutation Contributes to Adaptive Beach Mouse Color Pattern,” Science 313, no. 5783 (2006): 101–104.
  8. Kristina Allers et al., “Evidence for the Cure of HIV Infection by CCR5Δ32/Δ32 Stem Cell Transplantation,” Blood 117, no. 10 (2011): 2791–2799, doi:10.1182/blood-2010-09-309591.
  9. Terence Hadley and Stephen Peiper, “From Malaria to Chemokine Receptor: The Emerging Physiologic Role of the Duffy Blood Group Antigen,” Blood 89, no. 9 (1997): 3077–3091; Martha Hamblin et al. “Complex Signatures of Natural Selection at the Duffy Blood Group Locus,” American Journal of Human Genetics 70, no. 2 (2002): 369–383, doi:10.1086/338628.
  10. Wee Tek Tay et al., “Insect Resistance to Bacillus thuringiensis Toxin Cry2Ab is Conferred by Mutations in an ABC Transporter Subfamily A Protein,” PLoS Genetics 11, no. 11 (2015): e1005534, doi:10.1371/journal.pgen.1005534.
  11. Ann Gauger and Douglas Axe, “The Evolutionary Accessibility of New Enzyme Functions: A Case Study from the Biotin Pathway,” BIO-Complexity 1 (2011): 1–17.
  12. John Sanford et al., “The Waiting Time Problem in a Model Hominin Population,” Theoretical Biology and Medical Modelling 12, no. 1 (2015): 18, doi:10.1186/s12976-015-0016-z.

    Rick Durrett and Deena Schmidt, “Waiting for Two Mutations: With Application to Regulatory Sequence Evolution and the Limits of Darwinian Evolution,” Genetics 180, no. 3 (2008): 1501–1509, doi:10.1534/genetics.107.082610.

  13. Ruiz-Orera et al., “Origins of de novo Genes . . . ”
  14. Lothar Wissler et al., “Mechanisms and Dynamics of Orphan Gene Emergence in Insect Genomes,” Genome Biology and Evolution 5, no. 2 (2013): 439–455, doi:10.1093/gbe/evt009.
  15. Aoife McLysaght and Daniele Guerzoni, “New Genes from Non-coding Sequence: The Role of de novo Protein-coding Genes in Eukaryotic Evolutionary Innovation,” 370, no. 1678 (2015): 20140332, doi:10.1098/rstb.2014.0332.
  16. Francois Jacob. “Evolution and Tinkering,” Science 196, no. 4295 (1977): 1164.
  17. Douglas Axe, “Estimating the Prevalence of Protein Sequences Adapting Functional Enzyme Folds,” Journal of Molecular Biology 341, no. 5 (2004): 1295–1315, doi:10.1016/j.jmb.2004.06.058.
  18. Akshat Rathi, “Scientists Falter as Much as Bankers in Pursuit of Answers,” The Conversation, December 4, 2013, http://theconversation.com/scientists-falter-as-much-as-bankers-in-pursuit-of-answers-21136.
  19. Emily Singer, “A Surprise Source of Life’s Code,” Quanta Magazine, August 18, 2015, https://www.quantamagazine.org/20150818-a-surprise-source-of-lifes-code.
  20. Kirk Lohmueller, “The Distribution of Deleterious Genetic Variation in Human Populations,” Current Opinion in Genetics & Development 29 (2014): 139–146, doi:10.1101/005330.
  21. MV Olson, “When Less is More: Gene Loss as an Engine of Evolutionary Change,” American Journal of Human Genetics 64, no. 1 (1999): 18–23, doi:10.1086/302219; Jinchun Zhu et al., “Comparative Genomics Search for Losses of Long-Established Genes on the Human Lineage,” PLoS Computational Biology 3, no. 12 (2007): e247, doi:10.1371/journal.pcbi.0030247; Xiaoxia Wang et al., “Gene Losses during Human Origins,” PLoS Biology 4, no. 3 (2006): e52, doi:10.1371/journal.pbio.0040052; Hey Ji Oh et al., “Loss of gene function and evolution of human phenotypes,” BMB Reports 48, no. 7 (2015): 373–379.

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