A visitor to Stephen Meyer’s Facebook page asked about an article by biologist and theistic evolutionist Dennis Venema, “Genesis and the Genome: Genomic Evidence for Human-Ape Common Ancestry and Ancestral Hominid Population Sizes,” and what our response would be. It should be pointed out first that ID does not have an “official” position on common descent. Guided common descent would be compatible with intelligent design. However, many ID theorists do question the evidence offered for universal shared ancestry. On human evolution in particular, our book Science and Human Origins is a must read, especially Chapter 5.
That said, many of Dr. Venema’s arguments are suspect. They have been dealt with in other articles, as well in Science and Human Origins and Jonathan Wells’s book The Myth of Junk DNA. Here is a very quick and dirty rundown of what’s wrong with his main arguments:
(1) Dr. Venema argues that high human-chimp genetic similarity is at least 95%, and that this shows common our ancestry.
Response: Dr. Venema overstates the degree of human-chimp similarity and seems to disregard the obvious the possibility of common design for human-chimp functional genetic similarities. See:
- Human/Ape Common Ancestry: Following the Evidence
- Critically Analyzing the Argument from Human/Chimpanzee Genetic Similarity
- The Mismeasure of Man: Why Popular Ideas about Human-Chimp Comparisons Are Misleading or Wrong
For some technical references supporting these arguments, see Jon Cohen, “Relative Differences: The Myth of 1%,” Science, 316 (June 29, 2007): 1836.
(2) Dr. Venema argues that redundancy in codon-use (e.g., reuse of synonymous codons) is far in excess of what is required for functionality, suggesting common ancestry.
Response: Dr. Venema’s argument depends on the standard evolutionary presumption that synonymous mutations are phenotypically equivalent. This is a good example of how evolutionary biologists use molecular biology that is outdated; while synonymous codons do encode the same amino acids, they can have different, and important phenotypic or functional effects relating to gene expression. See:
- Codes Within Codes: How Dual-Use Codons Challenge Statistical Methods for Inferring Natural Selection
- Does Natural Selection Leave “Detectable Statistical Evidence in the Genome”?
This means there could be functional reasons for using specific synonymous codons, so his argument holds no water. As a 2010 paper in Science stated, “The discovery [reported in a research paper] that synonymous codon changes can so profoundly change the role of a protein adds a new level of complexity to how we interpret the genetic code.” (“New Roles for Codon Usage,” Science, 329:1473-74, Sept. 17, 2010; “Differential Arginylation of Actin Isoforms Is Regulated by Coding Sequence-Dependent Degradation,” Science, 329:1534-37, Sept. 17, 2010.)
There are additional technical references supporting the claim that different synonymous codons can have important phenotypic effects upon gene expression, meaning Dr. Venema’s argument is simply wrong. See: Li et al., “The anti-Shine-Dalgarno sequence drives translational pausing and codon choice in bacteria,” Nature (2012) doi:10.1038/nature10965 (published online March 28, 2012); Cannarozzi et al., “A Role for Codon Order in Translation Dynamics,” Cell, 141: 344-354 (April 16, 2010); Tuller et al., “An Evolutionarily Conserved Mechanism for Controlling the Efficiency of Protein Translation,” Cell, 141: 344-354 (April 16, 2010); Moleirinho et al., “Evolutionary Constraints in the ?-Globin Cluster: The Signature of Purifying Selection at the ?-Globin (HBD) Locus and Its Role in Developmental Gene Regulation,” Genome Biology and Evolution, Vol. 5(3): 559-571 (2013).
(3) He argues that the highly similar spatial organization of the genes (synteny) across different species suggests common ancestry.
Response: Again, Dr. Venema’s molecular biology is outdated. He assumes the ordering of genes (or chromosomal structure) is functionally unimportant, but molecular biology has discovered that nothing could be further from the truth. As the revolution in epigenetics has taken hold, molecular biologists now know that the structure of chromosomes, and their 3-dimensional arrangement(s) within a cell, are important parts of genomic regulation. For one example of this, see: Paper: “Irreducible Organization” of DNA Necessary for Genetic Regulation.
I asked a colleague to send me some papers discussing how chromosomal structure and gene ordering can be functionally important, and he overloaded me with papers. Here are some of the references:
Jachowicz et al., “Heterochromatin establishment at pericentromeres depends on nuclear position,” Genes & Development, 27: 2427-2432 (2013); Verdaasdonk et al., “Centromere Tethering Confines Chromosome Domains,” Molecular Cell, 52: 1-13 (December 26, 2013); Filion et al., “Systematic Protein Location Mapping Reveals Five Principal Chromatin Types in Drosophila Cells,” Cell, 143: 212-224 (October 15, 2010); Giacomo Cavalli, “From Linear Genes to Epigenetic Inheritance of Three-dimensional Epigenomes,” Journal of Molecular Biology (2011); Justin M. O’Sullivan, “Chromosome Organizaton in Simple and Complex Unicellular Organisms,” Current Issues in Molecular Biology, 13: 37-42 (2011); Dirar Homouz and Andrzej S. Kudlicki, “The 3D Organization of the Yeast Genome Correlates with Co-Expression and Reflects Functional Relations between Genes,” PLoS One, 8: e54699 (January, 2013); Stephen A. Hoang and Stefan Bekiranov, “The Network Architecture of the Saccharomyces cerevisiae Genome,” PLoS One, 8: e81972 (December, 2013).
Consider the following quote from another paper my colleague sent me:
The association of chromosomes with each other and other nuclear components plays a critical role in nuclear organization and genome function. … Genomes are highly ordered yet dynamic entities in which chromosomal positions, structures and interactions are controlled in order to regulate nuclear processes. Recent research (Mitchell and Fraser, 2008; Spilianakis et al., 2005) using microscopy (e.g. Berger et al., 2008; Bolzer et al., 2005) and Chromosome Conformation Capture strategies (i.e. 3C (Dekker et al., 2002), 4C (Simonis et al., 2006) and 5C (Dostie et al., 2006)) has begun to unravel the structural (Guelen et al., 2008) and functional (Spilianakis et al., 2005) significance of chromosomal interactions at specific loci including the b-Globin locus (Dostie et al., 2006; Simonis et al., 2006), the Igf2/H19 imprinting control region (Ling et al., 2006; Zhao et al., 2006), and the TH2 locus (Spilianakis et al., 2005).
(Rodley et al., “Global identification of yeast chromosome interactions using Genome conformation capture,” Fungal Genetics and Biology, 46: 879-886 (2009).)
In other words chromosomal structure and organization matters — a lot. OK, one more quote:
The spatial organization of the chromosomes is crucial for gene expression and development.
(O’Sullivan et al., “Repeated elements coordinate the spatial organization of the yeast genome,” Yeast, 26: 125-138 (2009).)
Part of Dr. Venema’s “synteny” argument pertains to chromosomal fusion, which also is not an argument for human-ape common ancestry. See:
- And the Miller Told His Tale: Ken Miller’s Cold (Chromosomal) Fusion (Updated)
- What the Literature Says about Chromosomal Fusion and Why It Says It
- Guy Walks Into a Bar and Thinks He’s a Chimpanzee: The Unbearable Lightness of Chimp-Human Genome Similarity
- A Reply to Francis Collins’s Darwinian Arguments for Common Ancestry of Apes and Humans
(4) Dr. Venema argues that shared pseudogenes suggest common ancestry.
Response: Here Dr. Venema is assuming that what we don’t understand is functionless. in this case, we have lots of evidence that many pseudogenes — including pseudogenes that are prominent examples used by ID-critics — are likely functional. For some examples, see:
- Dover Revisited: With Beta-Globin Pseudogene Now Found to Be Functional, an Icon of the “Junk DNA” Argument Bites the Dust
- Paper Rebuffs Assumption that Pseudogenes Are Genetic “Junk,” Claims Function Is “Widespread”
- Et tu, Pseudogenes? Another Type of “Junk” DNA Betrays Darwinian Predictions
- Unitary Pseudogenes and RNA Editing
Darwin-skeptics charge that evolutionary assumptions about pseudogenes being “junk” have hindered our discovery of their functions. Because a pseudogene may only function in specific tissues during particular stages of development, function may be difficult to discover. While it’s true that there’s a lot about pseudogenes we still don’t know, an RNA Biology paper concludes: “the study of functional pseudogenes is just at the beginning,” and it predicts that “more and more functional pseudogenes will be discovered as novel biological technologies are developed in the future.” That paper concludes functional pseudogenes are “widespread.” Indeed, when we do carefully study pseudogenes, however, we often find function. One paper in Annual Review of Genetics tellingly observed: “pseudogenes that have been suitably investigated often exhibit functional roles.”
For some references documenting functions for pseudogenes, see: Moleirinhoet al., “Evolutionary Constraints in the ?-Globin Cluster: The Signature of Purifying Selection at the ?-Globin (HBD) Locus and Its Role in Developmental Gene Regulation,” Genome Biology and Evolution, 5 (2013): 559-571; Tam, et al., “Pseudogene-derived small interfering RNAs regulate gene expression in mouse oocytes,” Nature, 453 (2008): 534-538; Poliseno et al., “A coding-independent function of gene and pseudogene mRNAs regulates tumour biology,” Nature, 465 (2010): 1033-1038; Poliseno, “Pseudogenes: Newly Discovered Players in Human Cancer,” Science Signaling, 5 (242) (September 18, 2012); Pink et al., “Pseudogenes: Pseudo-functional or key regulators in health and disease?” RNA, 17 (2011): 792-798; Wen et al., “Pseudogenes are not pseudo any more,” RNA Biology, 9 (January, 2012): 27-32; Zheng and Gerstein, “The ambiguous boundary between genes and pseudogenes: the dead rise up, or do they?,” Trends in Genetics, 23 (May, 2007): 219-224; Hirotsune et al., “An expressed pseudogene regulates the messenger-RNA stability of its homologous coding gene,” Nature, 423 (May 1, 2003): 91-96; O. Tam et al., “Pseudogene-derived small interfering RNAs regulate gene expression in mouse oocytes,” Nature, 453 (May 22, 2008): 534-538; Pain et al., “Multiple Retropseudogenes from Pluripotent Cell-specific Gene Expression Indicates a Potential Signature for Novel Gene Identification,” The Journal of Biological Chemistry, 280 (February 25, 2005):6265-6268; Zhang et al., “NANOGP8 is a retrogene expressed in cancers,” FEBS Journal, 273 (2006): 1723-1730; Balakirev and Ayala, “Pseudogenes, Are They ‘Junk’ or Functional DNA?” Annual Review of Genetics, 37 (2003): 123-51.
In closing, what’s going on here? While ID is compatible with common ancestry, Dr. Venema’s arguments represent a basic difference in philosophy between Darwinian evolutionists and proponents of intelligent design. Darwinian evolutionists tend to assume that many poorly understood aspects of our genomes (e.g., the prevalence of synonymous codons, the widespread existence of synteny, or non-coding DNA) do not have important functions and exist simply due to unguided mutations. In contrast, ID proponents predict that if our genomes were designed, then many of these mysterious features will turn out to have important functional purposes. And indeed, in each of these four areas, Dr. Venema’s argument depends on the presumption that the similarity between humans and chimps (whether  protein sequence or overall genome similarity;  similar use of synonymous codons;  synteny; and  shared “pseudogenes”) is functionally unimportant–i.e., it’s a “junk” property of the genome. And in each of these four areas, the latest findings of molecular biology show that the property is not “junk” or unimportant, but in fact represents newly discovered important functional elements of molecular biology.
Yes, there’s still a lot we don’t know about the genome. But as time goes on, ID’s predictions are being confirmed. Meanwhile, Darwinian presumptions — that many aspects of genomes exist for no reason other than “they were put there by unguided evolutionary mechanisms” — are turning out to be wrong.