The Origin of Biological Information, Part 6
If your heart is right, then every creature is a mirror of life to you and a book of holy learning, for there is no creature - no matter how tiny or how lowly - that does not reveal God’s goodness.
Thomas a Kempis - Of the Imitation of Christ (c.1420)
A brief recap of the series to date
This series of posts has been exploring the question of how new structures and functions arise through evolutionary mechanisms. This topic is one that is of considerable interest for Christians, since the Intelligent Design Movement claims that the generation of such features (what it terms Complex Specified Information, or “CSI”) is not possible for natural processes to produce in any significant measure. As such, it holds up examples of CSI in nature as evidence for a supernatural designer. Unfortunately, this approach has the effect that new scientific evidence that explains how CSI arises naturally diminishes the perceived evidence for God.
As we were careful to point out in the very first post in this series, understanding how natural processes create information is in no way a threat to God’s ordaining and sustaining of creation. If it were so, the obvious conclusion would be that “natural mechanisms” and “God’s actions” are effectively a zero-sum game where every scientific discovery diminishes God’s activity. Indeed, the ID argument strongly tends in this direction. This is certainly not a historic Christian view of science, and one we would do well to steer the church away from.
With these theological considerations in mind, we have explored several examples of new CSI arising through evolutionary processes (the posts in this series are linked in the sidebar for those who have not yet read them). In summary, we have seen that:
CSI does not need to arise all at once, but can arise piecemeal through independent mutation events.
Separate mutations that later combine to form CSI do not need to confer a specific advantage on their own. In other words, mutations that are “neutral” with respect to the survival of the organism can later be co-opted into CSI that does have a distinct survival advantage.
Neutral mutations may open up new future paths. For example, the brand-new ability of one bacterial population to use citrate as a food source required that a neutral mutation appear several thousand generations before it combined with other mutations to provide the CSI for using citrate (see Part 2). A second example we observed is how neutral mutations opened up new future possibilities during the evolution of hormone/hormone receptor complexes in vertebrates (see Part 3).
When CSI arises, it can be pretty poor at the beginning. Nascent CSI, though poor, provides a survival advantage because it is the “best game in town” at that time. Further mutation in, and natural selection on, the offspring of the original CSI-holder quickly refine the nascent information into ever-more “specified” CSI.
The detailed examples of new CSI arising through changes to existing proteins appear to apply generally to many, many protein families across multiple organisms (see Part 4). There is nothing about protein structure that prevents proteins from acquiring new functions through evolutionary means.
Comparative genomics evidence, especially evidence from synteny, strongly supports the hypothesis that large swaths of modern vertebrate genomes are the result of ancient whole-genome duplications, where some of the duplicated genes go on to acquire new functions through mutation and selection (see Part 5).
Comparative genomics and new CSI: details, details
One last way to assess the ability of natural processes to generate CSI that we will explore is based on comparing the genomes of two closely-related species that nonetheless have significant biological differences. The most detailed approach, of course, is to examine and compare the entire genomes of the species in question. Such a comparison shows us the total genetic differences that have arisen between the species since they parted ways:
It needs to be emphasized that only a subset of the observed differences will be meaningful. Put another way, many of the mutations that have occurred in the two lineages are neutral, having no discernable effect on the organisms in question. Indeed, the subset of truly meaningful differences is likely to be relatively small. Still, the subset of meaningful differences cannot exceed that of the total genetic differences. So, even if we do not, as of yet, understand all the details of how the species in question came to be biologically different, we can be sure that we know what the upper maximum is for the necessary mutations needed to bring about the differences we observe. So, while the total genetic differences between two species is an overestimation of the genetic changes needed to cause the differences, it is still a useful measure because we know that all of the meaningful changes must be accounted for within it.
Applying this test to humans and our closest (living) evolutionary relative, the chimpanzee, reveals that at a whole-genome level, we are over 95% identical. This value is even an underestimate, since it “counts” mutations that duplicate or delete sections of DNA as if they were separate mutations affecting individual DNA “letters” even though it was created by only one genetic change. Indeed if we use the same criteria to compare the diversity which exists within our own species, we humans are only 98% identical to each other. By whatever measure used, we are but a hand-breadth away from our evolutionary cousins at the DNA level (for those interested in a full treatment of how the human and chimpanzee genomes compare, please see this recent article).
Of interest for our purposes here is the simple realization that a relatively small number of subtle genetic changes undergird the large biological differences we observe between humans and chimpanzees. The increase in CSI associated with building the complex human brain and other distinctively human features in contrast to the body of our cousin, the chimpanzee does not appear to require huge changes at the genetic level. The differences we see, when examining these two genomes, are consistent with small changes,of the sort easily accessible to evolutionary mechanisms. While this observation does not rule out the possibility of God directing this stage of human evolution in a more supernatural way, the genomics evidence suggests that this stage was accomplished in gradual, incremental steps. This observation also matches what we see in the fossil record, with gradual increases in brain capacity, tool making, and other features that mark us out as distinctly human.
Evolution and new CSI: cause for fear or celebration?
So, for evangelical Christians, what is perhaps the most challenging evidence for new CSI arising through evolutionary means comes from within our own genomes. Here we see that, at the genetic level, we are but a stone’s throw from other primates such as chimpanzees. This realization leads to what may be for some an uncomfortable choice: either evolution is capable of generating significant novelty through mutation, genetic drift, and natural selection, or the differences between humans and other forms of life must be seen as insignificant. The only other option is to reject these lines of evidence altogether.
Of course, this response, for many, is one driven by fear: fear of having to re-consider the range of methods by which God creates, or perhaps how one interprets the opening chapters of Genesis. My hope is that this series, while challenging for some, would not ultimately be cause for fear. Indeed, this response plays into the false “natural versus God” dichotomy discussed above. Rather, my hope is that understanding some of the natural means God uses to bring about biodiversity on earth, including for our own species, will provide an occasion to offer thanks and praise to our Creator.
Dennis Venema is Fellow of Biology for The BioLogos Foundation and associate professor of biology at Trinity Western University in Langley, British Columbia. His research is focused on the genetics of pattern formation and signalling.