This series of claims appears to offer irrefutable evidence in favor of evolution by common descent and has been often repeated on blogs and news Web sites. The premise of these claims is that if all life evolved from a common ancestor, there should be genetic remnants of our evolutionary past still present in the genomes of all organisms. Initially, these claims may sound insurmountable as evidence for our supposed evolutionary ancestry. However, several important points need to be made to clarify this “evidence.” Further, these alleged evidences are easily explained and do not support common descent.
Before addressing the claims, a few points need to be made regarding terminology. First, these claims use the term “genes” without clarifying exactly what is meant, which is very common in popular media. The term gene was coined by a Danish biologist named Wilhelm Johannsen over 100 years ago to describe the units of inheritance identified in Gregor Mendel’s research (“1909: The Word Gene Coined,” 2013). While this was a convenient way to describe these “units of inheritance,” our understanding of these factors has expanded dramatically in recent years. The idea that a single gene controls a specific trait or feature is generally an oversimplification. In other words, a visible trait (known as a “phenotype”) is the product of a series of genetic factors (known as the “genotype”). For example, eye color in humans results from the combination of specific versions (called alleles) of at least two different genes. More modern definitions have linked the idea of a gene to a sequence of DNA that is used to produce a protein. However, even this fails to capture the full idea of what a gene is since a number of DNA sequences are functional (and influence phenotype) without producing a protein product.
Applying this understanding to the claims being addressed above, it should be noted that the use of the word “gene” is misleading at best. The “genes” in some of the above questions are actually part of the sophisticated network of protein-coding and non-protein coding genes involved in body plan development (i.e., that control the development of structures and physical features while an organism is developing). These genes participate in an impressively well-orchestrated ballet that controls the location of body structures in embryos during development. So, there really aren’t specific “genes for legs” or “genes for tails.” Instead, alteration of the temporal and spatial presence of the protein products of development-regulating genes will alter the physical structures of a developing embryo.
A “gene” generally refers to a sequence of DNA that contains the information that is transcribed into RNA and translated into a protein product. This DNA ▶ RNA ▶ protein process is known as the “Central Dogma” of molecular biology. While this concept is true, it is an oversimplification and there is now known to be many more ways that DNA and RNA are used. So, protein production is not the only goal of DNA. For example, there are many non-protein coding genes that make functional RNA products. Further, many RNA molecules serve gene regulatory roles often by controlling how protein-coding genes are used and when they are expressed (i.e., used to make a protein).
Second, genes involved in body plan development are important to multicellular organisms, and there are several genes involved in development that have homologous (similar) genes that are present in very diverse sets of organisms. For example, the homeobox or HOX genes are a family of genes that are found in a wide array of organisms. These genes are involved in body plan development and slight changes to these genes can have extreme consequences on the structure and viability of an organism (McGinnis and Krumlauf, 1992, pp. 283-302; Mallo, et al., 2010, pp. 7-15). The tight regulation of HOX genes is evident from experimental results showing that mutations in HOX can alter body plan and neural development and even cause cancer (Philippidou and Dasen, 2013, pp. 12-34; Quinonez and Innis, 2014, pp. 4-15). This function underscores the fact that these genes are critical and must be precisely regulated in order for body plans to develop properly. While mutations in HOX genes can lead to extra limbs or other features, the additional features often are nonfunctional and are usually detrimental to the organism.
Third, HOX genes and other genes involved in development are often hailed as evidence of evolution by common descent. This is because HOX homologs are found in many different organisms, which is interpreted as evidence that these genes arose during evolution and passed from one life form to the next. However, it is proposed that some genes (including genes involved in growth and development) evolved independently multiple times (Irimia and Garcia-Fernandez, 2008, pp. 1521-1525). In other words, some homologous genes present in unrelated organisms arose independently, rather than from a common ancestor. According to this interpretation, evolution solved some of the same problems several times (i.e., in different lineages, independently). Rather than suggesting that these genetic discordances are evidence of common design, the concept of convergent evolution was invented to “explain away” these coincidences (Bergman, 2001, pp. 26-33). While convergent evolution is a convenient concept, it does not explain how these genes or sets of genes evolved once, let alone multiple times independently (Meyer, 2013).
So, what should we make of these claims? Let us examine each one briefly to understand what the claims are and what the evidence is. First, do whales have “genes for legs”? While whales have developmental genes just like other mammals, they do not have specific “genes for legs.” In fact, the only reason that “legs” are even mentioned is because of the presumed evolutionary ancestry of whales. In other words, why not call these “genes for extra fins/flippers”? Further, it should be noted that there are a few extreme cases that have been documented in whales where bones around the pelvic region have been expanded and/or additional bones are present (Andrews, 1921, pp. 1-6). Contrary to some claims, the pelvic region in whales is not a vestigial structure. Rather, the bones in this region anchor the reproductive organs (Wieland, 1998, pp. 10-13; Dines, et al., 2014, pp. 3296-3306). Cases of “growths” or extra bones, while interesting, do not mean that whales once had legs. Is it possible that these occurrences are within the natural genetic variation of organisms? Take for example, the more recent story of a dolphin with a second set of fins (Wieland, 2006). Perhaps this is an example of our lack of understanding of the natural genetic variation found within these creatures? Again, the only reason that these structures are claimed to be “legs” is because of the evolutionary interpretation placed on top of the data. The fact that these anomalies exist does not negate Creation in any way. Rather than supporting common descent, these examples of variations and mutations really suggest a common design, including common developmental circuits built into the genomes of organisms (Ham, 2006; Sarfati, 2014).
Second, humans do not have genes for tails. This claim arises from the presumption that we evolved from ape-like ancestors and is based on two observations. First, there are newborns that have fatty tissue appendages on the rear of the child, which may appear tail-like. However, these appendages do not display characteristics of a tail in structure or function (Lamb, 2007). Further, these incidences are clearly the result of mutation—breaking gene function rather than developing something new. The second source of this claim comes from the appearance of a developing human embryo. During embryonic development, it may appear like humans have a tail, but this actually develops into the spinal column and coccyx. The coccyx is no longer considered a vestigial organ (Bergman and Howe, 1990, p. xii). So, there never is a “tail” even as an embryo. But what of the cases of extra bones beyond the coccyx? There are some documented cases of this, but this only supports the idea that there is variation among humans and not that humans have leftover “tail genes.” [For a more detailed discussion of “human tails,” see a series of articles by Casey Luskin (2014).] Further, there are numerous examples of anatomical variation among humans including cervical ribs, extra fingers or toes, absent muscles, and even differences in the branching pattern of the aorta (Moore, et al., 2014). Each of these examples suggest that anatomical variation is normal and highlights the differences in development that result from an individual’s unique genetic make-up.
Third, regarding humans having the genes for egg yolk, this claim is weak at best. The claim originates from a single published report suggesting that humans have remnants of a gene used to make a protein found in egg yolk (Brawand, et al., 2008, p. e63). When the data is examined, the “remnants” are a few very short sequence segments—most of which contain multiple mutations when compared to the sequences found in chickens [see supporting information in (Brawand, et al.)]. Unlike the claim that “humans have genes for egg yolks,” we in fact have a few short sequences (sequences represent portions of two to three exons out of 35 exons in the VIT1 gene) which poorly correspond to fragments of the rather large genes for these proteins. In fact, I would suggest that these sequence correspondences really are not remnants at all. Some of the sequences in question are actually part of other human genes. So, instead of being remnant sequences, these are more likely coincidental sequence similarities.
Homologous proteins are those that have similar structure (resulting from similar DNA/protein sequence) and function. The evolutionary assumption is that homologous features—including structures, proteins, etc.—are the result of evolution by common descent. However, homology does not necessarily imply common ancestry. Instead, we would argue from a biblical model these are excellent examples of common design features that were created to accomplish common functions.
Fourth, the claim that birds have genes for teeth likely centers around a 2006 study of a mutation in chickens called talpid2, which is a lethal recessive mutation that causes several developmental defects in chick embryos (Harris, et al., 2006, pp. 371-377). This mutation has been studied for over 60 years, and the 2006 study suggested that embryos with this mutation appeared to be developing a tooth-like structure before death (Harris, et al.). Evolutionary interpretations of these findings suggest that this mutation must indicate that there is some vestigial genetic programming for tooth development leftover in the genomes of chickens (“Mutant Chickens Grow Teeth,” 2006). But important points need to be made regarding those interpretations. First, the talpid2 mutation is known to impact the developmental gene called sonic hedgehog (shh), which plays critical roles in body plan patterning and development. Thus, it is no surprise that this mutation may cause drastic changes in body structure. Second, this mutation is lethal; so, clearly, it does not offer any benefit for the organism. Third, at the time of the 2006 study, the actual gene involved in this mutation was unknown. However, that gene has now been identified as C2CD3 (Chang, et al., 2014, pp. 3003-3012). This study noted that the actual function of the protein produced from this gene is not known, but they provided evidence that a deletion within this gene caused the talpid2 phenotype (Chang, et al.). Interestingly, this gene is somehow involved in production of cilia and the protein product is detectable in cells. Thus, far from being a “gene for teeth,” this gene appears to be important in embryonic development and somehow plays a role in cilia formation. Certainly, more details will be forthcoming as research continues, but this example does not support the idea that “birds have genes for teeth.” That said, it should be noted that there are examples of birds with teeth (e.g., Archaeopteryx; also, there is an egg tooth that is used to break out of eggs). So, we would not be surprised to find other birds with the genetic information to produce such structures, but the existence of those abilities in no way implies that birds evolved from animals with teeth. Further, it is also possible that there may be birds that have lost the ability to produce teeth through genetic mutation, but again, the talpid2 mutation does not appear to be such a case.
It is very important that we carefully examine the scientific evidence behind common claims that purport to show irrefutable evidence for evolution. An examination of the actual data shows that the evidence is not what it claims to be. It is important, however, that creationists also not oversimplify complex data. The details of science often make a big difference in interpretation of the data, as is seen with the talpid2 mutation example.
From a biblical worldview perspective, none of the above “evidences” are at odds with a Creation model. In fact, the presence of mutations and variation is consistent with the genetic degeneration anticipated in the modern concept of the Creation model (Sanford, 2008). Living on Earth after the Fall, with many generations of mutations already present in the genomes of organisms around the world, we must recognize that genetic degeneration continues to remind us of both the consequences of the Fall and the hope we have in Christ our Redeemer Who will clothe us with a new body (Philippians 3:21).
“1909: The Word Gene Coined” (2013), http://www.genome.gov/25520244.
Andrews, R.C. (1921), “A Remarkable Case of External Hind Limbs in a Humpback Whale,” American Museum Novitates, :1-6.
Bergman, Jerry (2001), “Does Homology Provide Evidence of Evolutionary Naturalism?,” Journal of Creation, 15:26-33.
Bergman, Jerry and George F. Howe (1990), “Vestigial Organs”Are Fully Functional: A History and Evaluation of the Vestigial Organ Origins Concept (Terre Haute, IN: Creation Research Society Books).
Brawand, D., W. Wahli, and H. Kaessmann (2008), “Loss of Egg Yolk Genes in Mammals and the Origin of Lactation and Placentation,” PLoS Biology, 6:e63.
Chang, C.F., E.N. Schock, E.A. O’Hare, et al. (2014), “The Cellular and Molecular Etiology of the Craniofacial Defects in the Avian Ciliopathic Mutant Talpid2,” Development, 141:3003-3012.
Dines, J.P., E. Otarola-Castillo, P. Ralph, et al. (2014), “Sexual Selection Targets Cetacean Pelvic Bones,” Evolution, 68:3296-3306.
Ham, K. (2006), “Dolphin Found with ‘Remains of Legs,’” https://answersingenesis.org/theory-of-evolution/evidence/dolphin-found-with-remains-of-legs/.
Harris, M.P., S.M. Hasso, M.W. Ferguson, and J.F. Fallon (2006), “The Development of Archosaurian First-Generation Teeth in a Chicken Mutant,” Current Biology, 16:371-377.
Irimia, M., I. Maeso, and J. Garcia-Fernandez (2008), “Convergent Evolution of Clustering of Iroquois Homeobox Genes across Metazoans,” Molecular Biology and Evolution, 25:1521-1525.
Lamb, A. (2007), “Human Tails and Fairy Tales,” http://creation.com/human-tails-and-fairy-tales.
Luskin, C. (2014), “Human Tails: Another Evolutionary Icon that Coyne, Giberson, and Other Darwin Defenders Would be Wise to Abandon,” http://www.evolutionnews.org/2014/05/human_tails_ ano085671.html.
Mallo, M., D.M. Wellik, and J. Deschamps (2010), “Hox Genes and Regional Patterning of the Vertebrate Body Plan,” Developmental Biology, 344:7-15.
McGinnis, W. and R. Krumlauf (1992), “Homeobox Genes and Axial Patterning,” Cell, 68:283-302.
Meyer, Stephen C. (2013), Darwin’s Doubt : The Explosive Origin of Animal Life and the Case for Intelligent Design (New York: HarperOne).
Moore, K.L., A.M.R. Agur, and A.F. Dalley (2014), Clinically Oriented Anatomy (Baltimore, MD: Lippincott, Williams, & Wilkins).
“Mutant Chickens Grow Teeth” (2006), http://news.sciencemag.org/2006/02/mutant-chickens-grow-teeth.
Philippidou, P. and J.S. Dasen (2013), “Hox Genes: Choreographers in Neural Development, Architects of Circuit Organization,” Neuron, 80:12-34.
Quinonez, S.C. and J.W. Innis (2014), “Human Hox Gene Disorders,” Molecular Genetics and Metabolism, 111:4-15.
Sanford, J.C. (2008), Genetic Entropy & the Mystery of the Genome (Waterloo, NY: FMS Publications).
Sarfati, J. (2014), The Greatest Hoax on Earth? Refuting Dawkins on Evolution (Atlanta, GA: Creation Book Publishers).
Wieland, C. (1998), “The Strange Tale of the Leg on the Whale,” Creation, 20:10-13.
Wieland, C. (2006), “A Dolphin with Legs—Not,” http://creation.com/a-dolphin-with-legs-not.