So, I’ve decided to try a slightly different approach for the next while—one that has these sorts of folks in mind. From time to time, you can still expect those more in-depth, technical articles, or perhaps a discussion of some new research that makes the popular press, or even an analysis of some new argument from the IDM or RTB. These will be breaks from the new routine, however. For the most part, we’re going to stick to the basics, much like you would if you took an introductory evolution course at a university. Don’t worry, though: this course doesn’t have any prerequisites! All that’s needed is a willingness to learn.

What you can expect

The goal of this course is straightforward: to provide evangelical Christians with a step-by-step introduction to the science of evolutionary biology.  This will provide benefits beyond just the joy of learning more about God’s wonderful creation. An understanding of the basic science of evolution is of great benefit for reflecting on its theological implications, since this reflection can then be done from a scientifically-informed perspective. From time to time we might comment briefly on some issues of theological interest (and suggest resources for those looking to explore those issues further), but for the most part, we’re going to focus on the science. For folks interested in the interaction between science and Christianity, I heartily recommend Ted Davis’ recent series as a fabulous introduction to the topic.

You can also expect a slow, patient pace. Since this course is intended for folks with little or no background in biology, we’re going to take our time to make sure no one gets left behind. This might be frustrating to folks who already know a fair bit about evolution. Hopefully even more knowledgeable readers will learn some new and interesting details along the way—but the goal will primarily be to help folks who are less well versed in evolution increase their understanding.

You can also expect a survey of many different areas that have some bearing on evolution. We’ll examine geology, paleontology, biogeography, genetics, and a host of other topics in order to provide a “big picture” overview. This broad-brush approach means that any given individual post will not necessarily be “convincing” to folks who have doubts about evolution. Think about assembling a large jigsaw puzzle: placing any individual piece, on its own, doesn’t convincingly demonstrate what the overall picture will show. This course will be like that. Each topic we cover will put a few pieces in place here and there, slowly building towards the final overall picture.

Since evolution is an active science, this process will also highlight where there are “missing pieces” that are still being sought by scientists. All of this is well and good, since the purpose of this course is not so much to convince anyone of the validity of evolutionary theory, but rather to inform readers about the nature and scope of evolution as a scientific theory in the present day. My goal is to provide readers with a basic understanding of what evolution is and how it works. Given that as the primary goal, if one finds the scope of the evidence ultimately convincing (or not) is somewhat beside the point. The intent here is to provide readers with information they can use to make their own, informed decision.

How you can help

First and foremost, you can help by spreading the word about this series to folks you think would be interested in learning more about evolution in a non-threatening environment. Secondly, you can help me by asking questions in the comments. One of the challenges of being a specialist is having the ability to put oneself in the shoes of someone just starting out. What might seem obvious to me may not seem obvious to you, and I hope you’ll feel that no question is too basic or too simplistic. If you’re wondering about something, it’s almost guaranteed that other folks are, too! So, please don’t be shy. I’ll do my best to answer questions in the comments, though I hope that some of our more skilled commenters will (respectfully!) help out here, as well. Finally, you can help by letting me know what broader areas of evolution you find confusing. I have my own ideas about what areas of evolution are commonly misunderstood, but I’d love to hear from readers about what areas they find difficult to understand. I’ll use this input to shape the topics I will cover as we go forward.

Getting started

In the next post in this course, we’ll dive into the course content by introducing two key areas: how scientific theories work in general, and how evolution in particular works as the current organizing theory of modern biology. 

Such remnants are also found in our genomes.  Humans, unlike most mammals, cannot synthesize (make) our own vitamin C, but we carry the genes for synthesizing vitamin C.  One of these genes encodes the GLO (L-gulonolactone oxidase) enzyme, and this gene in humans contains inactivating mutations and is therefore a “pseudogene.”  This pseudogene and the genes that encode the enzymes of the vitamin C biosynthetic pathway are the remnants of our own evolutionary lineage from an ancestor that was able to synthesize its own vitamin C.⁴ Furthermore, the GLO pseudogene is just one of a graveyard of inactivated genes, transposons, retroviruses and other non-functional sequences that litter our genome.  While some of these sequences have been co-opted for particular functions, many of them have no known function.⁵ We share many of these non-functional sequences with chimpanzees.  The very presence of these genomic and anatomical flotsam and jetsam only makes sense if evolution has occurred.⁶

A third piece of evidence for evolution comes from biogeography.⁷ The flora and fauna of islands such as those of the Galápagos and Hawaii are radically unbalanced in that they lack many types of plants and animals but contain a profusion of clusters of similar species.  Hawaii, for example, has no native mammals, reptiles, or amphibians, but a profusion of fruit flies and silversword plants.⁸ One third of the 2,000 species of fruit flies are found on the Hawaiian Islands, which only covers 2 percent of the land on earth.  These islands were never connected to the continents and arose as a result of volcanic activity and were, at least initially, completely uncolonized.  The colonization of these islands occurred by means of occasional introduction of creatures from the mainland that then rapidly speciated on these islands to fill every available ecological niche.  Thus, the organisms most closely related to island species come from the closest mainland areas, and often include those creatures most likely to find their way to islands, such as birds and flying insects. 

The Galápagos Islands provide an excellent example of how biogeography provides evidence for evolution. The Galápagos have fourteen species of finch whose closest relative is probably the South American grassquit (Tiaris), yet only four of these finch species feed on seeds as finches normally do, while two others feed on cacti, seven eat insects, and another eats almost exclusively leaves.⁹ Darwin, while visiting the Galápagos, still thought that species only varied within a particular kind (though he would not have used that terminology) but could adapt to various local environments and become particular subspecies. Therefore, he originally listed the warbler finch (Certhidea olivacea) as a wren and listed the small cactus finch (Geospiza scandens) as a member of the Icteridae or the family of meadowlarks and orioles.  Only after Darwin had deposited his Galápagos specimens with the British ornithologist John Gould did Darwin discover (in a meeting with Gould that occurred during March, 1877), that his finch collection included thirteen or fourteen species of unusual finches that were all so closely related, Gould classified them in a single group all their own.  This meeting showed Darwin that the immutable barrier between kinds of species did not exist.  The Galápagos Islands were not a distinct “center of creation,” but a workshop for evolution in which an ancestral species made it to the yet uncolonized island and underwent a massive degree of speciation to adapt to the environment of the island.¹⁰ This is precisely what one would expect if the species of islands had arisen by evolution. 

A scientific theory also allows scientists to make predictions, and good theories provide accurate predictions.  Can the theory of evolution allow accurate predictions?  The answer, once again, is yes.  Darwin himself predicted that the earth must be very old for evolution to occur.  He did not know the age of the earth, but further research has shown that the earth is 4.55 billion years old, which is plenty of time for evolution to occur.  Darwin also predicted that since plants on islands were most closely related to certain mainland plant species, the seeds of these plants should be able to withstand immersion in sea water for long periods of time, and again, Darwin was shown to be right.¹¹ Many decades after Darwin, we now know that variation in organisms is due to mutations in DNA and that these mutations are inherited, just as Darwin predicted.¹² Also, Darwin’s principle of natural selection predicts that particular sequences of DNA should behave in a manner that benefits only themselves and not their carriers, which modern research has thoroughly confirmed with the discovery of transposons and other types of “selfish DNA.”¹³

Is evolutionary theory a good scientific theory?  It has been repeatedly tested for over 150 years since its inception, and it has passed those tests successfully.  The theory has been modified in response to new data, but the outlines of the theory have remained largely intact.  It has existed at risk from new data.  During the molecular biology revolution that began with the discovery of the structure of DNA by Franklin, Watson and Crick in 1953, the explosion of new data could have shown contemporary evolutionary theory to be wrong.  However, some of the most powerful evidence for the theory of evolution has come from a field of science that did not even exist during Darwin’s time.  The ability of a theory to withstand such intense scrutiny is a clear sign it is robust and enduring.  As shown, the theory of evolution has predictive power, and it also integrates and makes sense of data from several fields of science, including ecology, paleontology, genetics, historical geology, paleoclimatology, and comparative anatomy and biochemistry.  The highly integrative nature of evolutionary theory makes it a fine theory by any measure. 

In conclusion, when measured against the standards of a good scientific theory, modern evolutionary biology clearly qualifies as good science.  Ongoing debates within evolutionary biology exist about mechanism, rates, and causes, but not over whether evolution occurred.  Such a question has been largely settled by the last 150 years’ worth of research.  The future certainly looks bright for this field of science and I cannot imagine a more exciting topic to study. 

Notes

1. Davit-Béal, Tiphaine,Abigail S. Tucker, and Jean-Yves Sire. “Loss of Teeth and Enamel in Tetrapods: Fossil Record, Genetic Data and Morphological Adaptations.” Journal of Anatomy 214, no. 4 (2009): 477–501. 

2. Tian, Natasha M. M.-L., and David J. Price. “Why Cavefish are Blind.” BioEssays 27 (2005): 235–38; Yamamoto Y, Stock DW, and Jeffery WR (2004) Hedgehog Signalling Controls Eye Degeneration in Blind Cavefish. Nature 431:844–7; Jeffery, W. R. “Adaptive Evolution of Eye Degeneration in the Mexican Blind Cavefish.” Journal of Heredity 96, no. 3 (2005): 185–196. 

3. Bejder, L., and B. K. Hall. “Limbs in Whales and Limblessness in Other Vertebrates: Mechanisms of Evolutionary and Developmental Transformation and Loss.” Evolution and Development 4, no. 6 (2002): 445–58. 

4. Lachapelle, M. Y., and G. Drouin. “Inactivation Dates of the Human and Guinea Pig Vitamin C Genes.” Genetica 139, no. 2 (2011): 199–207.

5. Avise, John C. Inside the Human Genome: A Case for Non-Intelligent Design. New York: Oxford University Press, 2010.   Romano, C. M., F. L. Melo, M. A. Corsini, E. C. Homes, and P. M. Zanotto.  “Demographic Histories of ERV-K in Humans, Chimpanzees and Rhesus Monkeys.” PLoS One 2, no. 10 (2007): e1026. http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0001026. 

6. Max, “Plagiarized Errors and Molecular Genetics,” http://www.talkorigins.org/faqs/molgen.

7. Coyne, Jerry A. “Intelligent Design: The Faith that Dare Not Peak Its Name.” In Intelligent Thought: Science Versus the Intelligent Design Movement, edited by John Brockman, 3–23. New York: Vintage, 2006. 

8. Kricher, John. Galápagos: A Natural History. Princeton, NJ:  Princeton University Press, 2006. 

9. Grant, Peter R., and Rosemary B. Grant. How and Why Species Multiply: The Radiation of Darwin’s Finches. Princeton, NJ: Princeton University Press, 2011. 

10. Sulloway, Frank J. “Why Darwin Rejected Intelligent Design.” In Intelligent Thought: Science Versus the Intelligent Design Movement, edited by John Brockman, 107–25. New York: Vintage, 2006. 

11. Darwin, Charles. “On the action of sea-water on the germination of seeds.” Journal of Proceedings of the Linnean Society of London (Botany). 1 (1857): 130–140.

12. Futuyma, Douglas J. Evolution. 3rd ed. Sundbury, MA: Sinauer Associates, 2013. 

13. Dawkins, Richard. The Selfish Gene. New York: Oxford University Press, 2006.

JIMMY LIN: Currently I’m on faculty at Washington University at St. Louis, where I am a research instructor in the pathology department. Also, a year and a half ago, I founded the Rare Genomics Institute (RGI)—a nonprofit that helps find cures for people with rare diseases.

ER: What qualifies as a “rare disease”?

JL: These are diseases like cystic fibrosis and Huntingdon’s disease—diseases that affect less than 200,000 Americans each year. There are over 7000 different rare diseases, and less than 5% of them have any therapy. Altogether, they affect about 25-30 million people.

This creates what we call a “long tail problem”—it’s hard for a top-down research system to create research programs for all 7000 rare diseases. So instead, we are creating a bottom-up platform from which the patients themselves can create research projects and help fund them. We connect patients with physicians and researchers, customize a research program with top medical universities, design the experiment, and then use an online fundraising platform to fund the study through [mostly] friends and family of the patient.

Basically, we create a “foundation in a box.” By partnering with the Rare Genomics Institute, patients and their friends and families who want to study rare diseases don’t have to go through the hoops of creating their own nonprofit or lab—we do that for them. So, instead of creating 7000 different nonprofits, we create a generalized platform from which studies can be conducted.

ER: Who qualifies for care through the Rare Genomics Institute?

JL: Anyone with a rare disease can come to us. The main thing we’re doing right now is diagnosis. When families come to us, they either don’t know the disease that’s affecting them or their child, or they don’t know the gene that’s wrong.

For instance, if a child had a condition that doctors couldn’t identify, his or her parents might come to us for help. What we’d do then is sequence the genes of the mother, father, and child, and compare them to reference genome to determine what mutations each of the parents have. Depending on what the disease is and what the gene causing it is, we can filter out mutations that don’t mean anything using the parents’ genomes—then, after filtering, we can potentially pinpoint the genes that fit the genetic pattern of the disease. This is the first step.

After that, we are building infrastructure to determine the effect of these changes and a way to help. For example, after looking at the literature, we can perhaps design experiments using cells extracted from the patient; this part of the process is different for every disease. Then, if we can determine that there is, for instance, a pathway missing a specific enzyme, we can try using drugs, a bone marrow transplant, or gene therapy to try to put healthy cells into the child… But there’s a variety of diseases, of course, so there’s a variety of different approaches—and we’re just starting to explore these aspects.

ER: How did RGI get started?

JL: It really started when I was in medical school at Johns Hopkins—there was this boy that came to our clinic to be seen. My research was in cancer genome sequencing, and the family had come to our department looking for answers about what was wrong with their son. At that point, the family was almost hopeless—they had gone to so many doctors, run so many tests—I decided I wanted to try to help children like this. That’s when my friends and I decided to start the Rare Genomics Institute.

Currently, there are about 50 researchers associated with the organization, and we are all volunteers. It’s growing much, much faster and been more amazing than we’ve ever imagined—we’re already making an impact. In May of last year, we were able to discover a new disease using the world’s first crowd-sourced, crowd-funded genome. Working with researchers at Yale, we delineated a disease of which our patient was the first identified.

Right now, we’re in the middle of raising funding and hiring staff to make this organization one that is self-sustaining, and to increase its impact even more.

Excerpts from Michael Hickerson Interview

MH: …you call yourself a doxologist. What’s the full term you used in your Jubilee bio?

JL: Medical and scientific doxologist.

MH: How did you decide on that term and what does it mean to you?

JL: I listen to a bunch of teaching by J.I. Packer , who teaches theology at Regent College and is one of the leading thinkers on these things. Interestingly, before any one of his classes, he says “Theology is for doxology,” and then the whole class sings the Doxology together out loud in class. I thought, “Wow, that is so great,” because everybody sometimes learns theology just for intellectual things [instead of for worship].

That’s not just true for theology, it’s for everything: biology is for doxology; chemistry is for doxology. That’s when I started to think, I should consider myself, first and foremost, as a person who praises God in what I do. And then no longer make “Christian” the adjective, right? “Doxologist” is the noun. But then what kind of doxologist am I? So I call myself a medical and scientist doxologist. I would call someone, for example, in the marketplace, a business doxologist. Or, someone who does art, an artistic doxologist. To really have the noun as our identity, and then our vocation as just a descriptor of how we do that.

MH: That’s a great point. A noun is always stronger than the adjective. So, you want that to be the focus, rather than the add-on.

JL: In our current culture, we’re defined by our jobs. It’s having a vocation. I wanted to shift away from that. I didn’t want to be a doctor first and foremost, or a scientist, but one who praises God. And evidently, within science you don’t want to call yourself a Christian Scientist. That’s another religion, so . . .

MH: [laughs] That’s right. I run into that, as well, when I’m teaching or talking about science to Christians. You always run into that stumbling block.

JL: With “scientific doxologist,” people don’t confuse them. You do have to explain what it means. And that gets in a little story actually, on what it means about vocation. It’s a small lesson — a teaching point when you do talk to people about vocation and calling. That’s why I use it.

MH: I guess my final question would be what spiritual practices help sustain you? What helps you stay in contact with God and keep a good foundation?

JL: First, I am interested in many, many different things. I sort of mix it up in terms of spiritual practices. Besides the fundamentals, of course, of quiet time, devotional reading, and scriptural reading, I do theological study because I have to do that academically. I find a lot of time with God through the spiritual disciplines, such as times of solitude — which is very interesting for someone who is in academics to no longer think about ideas but just to be quiet before God — how silence, time to think by yourself, or sitting in silence is also something you should foster.

In terms of spiritual formation, what you really need is definitely a good community of people. I have a very supportive community at my church. I’m the deacon of devotions, so that of course keeps me on track. It encourages me as I, in my own spiritual walk, encourage other people. Fundamentally, I think for all Christians, whether you are academic or no matter your vocation or calling, being in the Word and prayer are the most important things. Doing that and being spiritually fed is what is important.

DOUG LAUFFENBURGER: It could look like a lot of things. One way to envision what I mean is to put yourself back a hundred years. For instance, in 1913, an electronic computer was unimaginable. But using physics, quantum physics, leading to semiconductors and devices like that, people figured out over the next 20 to 30 years how you could build a machine to do calculations and so forth. And then, of course, all sorts of thing happened…

We’re roughly at that stage with biology, even though it seems like things are more imaginable because—and we don’t have to go strictly century by century here—because we can already guess the way some things might change, whereas in 1913 there was no inkling, really, as to what would happen in the computer revolution.

So, to enumerate some of the things that are conceivable—let’s just start with computers, because we were just there.

There’s a notion that computers get faster and cheaper by making their logic gates smaller, and how you improve a design with physics keeps bumping up against how you make these little units smaller. Well, using biology, the solution seems self-evident—you just line up the pieces of DNA, and if you put the right pieces of DNA in the right places, the resulting parts are so much smaller than the things we can do with physics. You can imagine, even though it’s just a theory now, computers continuing to become many times smaller and cheaper—and be made via environmentally benign manufacturing processes—through biomolecular construction.

Now that’s exciting from one point of view, but from another, it’s not that revolutionary, because you’re just using DNA as a piece of physics. It’s not really biology—it’s merely a biological molecule being used to make better physics.

For a different example, if you think about the way we make things, the way we manufacture plastics, gasoline, energy—we have to do all that using chemistry, and to make that chemistry happen, we have to input a lot of energy—in fact, one of the most costly industries in terms of energy usage is the energy industry. You have to put in so much energy to refine petroleum and things like that. And to make plastics, ceramics—things of that nature—is also very energy intensive, and it’s also where a lot of pollution comes from, because you’re mixing together all these chemicals that really didn’t want to be mixed together. You get what you want, but you get a lot of byproducts, toxins, etc.

Well, people have started to realize that a lot of this work can be redone through the use of biology. You can turn corn into fuel or plastic, and you can make magnetic or electrical storage devices out of biological units (viruses can pattern the crystals, so instead of using mixtures of toxic chemicals, you just pull the viruses with the right properties together). Right on this tabletop, you could make materials that by current manufacturing processes would otherwise cause a great amount of environmental hazard.

As for another exciting development—well, to preface, one of the problematic things about modern agriculture is the necessity of using fertilizers (there are insecticides to be concerned about, too), but fertilizer manufacturing is terrible for the environment. You have to make fertilizer out of ammonia and that’s a horribly polluting and energy-intensive manufacturing process. What you could potentially do, instead, is program into bacteria the genes that take nitrogen out of air, turning it into organic nitrogen then just scatter the bacteria onto the field—and you wouldn’t need to make ammonium using the current very caustic processes.

These are the sorts of things I mean—and we haven’t even touched on medicine, yet. People tend to think about medicinal advances, first, but before you even get to medicine, you can think about energy, manufacturing, materials, and agriculture. In 50 years, we should be able to do things in ways we don’t do them now, that will be cheaper, less toxic, less polluting, more efficient, and so forth.

ER: A lot of people are nervous about the idea of “programming” life. Can you respond to this fear as a Christian?

DL: As a Christian, I would say that God gave humankind dominion over the earth, to do good things—he gave us minds, a passion for understanding how things work, and then he put in this world all these fascinating processes, which, if we figured them out, we could do good things, could feed more people—could feed more people without causing extensive damage to the environment. And cure disease and injury. And the list goes on. I think all that is good, and that God would be pleased that we would be using His creation to live better—I’m not saying more luxuriously, but more happily, contentedly, with each other.

ER: But back to the topic—advances using biology in the next century. You had just mentioned medicine…

DL: So, yes, there’s also medicine. Now, obviously, in thinking about this, the use of stem cells comes to immediately the fore. There are a lot of diseases out there that you really do need to correct using cellular processes. Right now, we try to make these corrections through chemistry. For instance, we give you a pill, and that pill should interfere with something that’s going wrong in your body—and yet it’s really never adequate to just interfere with something that goes wrong in the body, because you don’t really set it right just by getting in the way of it.

The opportunity with stem cells is that you can say, “I’ll replace the cells in the body that are doing something wrong with cells that are actually doing it right again.” If you program cells to be neurons, heart cells, or bone cells, you can regenerate properly functioning physiology. Rather than, say, replacing a hip with a metal part, you could regenerate the bone, itself, or you could regenerate neurons in Alzheimer’s patients. Never in the past has medicine been able to regenerate a proper physiology; it’s only tried to replace it with an inadequate surrogate, or minimize how much damage a disease is doing. With the use of stem cells, you can actually imagine returning the body to its proper physiology.

A different use of stem cells is to generate human tissue in the laboratory for better studies of human physiology and pathology and improved testing of drug effectiveness and toxicity.  This will be a major advance over animal models, because of the significant disparities between animal physiology and human physiology.

A key point to emphasize is that there are different kinds of stem cells, which involve big differences in potential concerns. For Christians, clearly, stem cells derived from embryos present a tremendous ethical issue. Fortunately, a good proportion of stem cell technologies can be pursued using stem cells from adult tissue. These cells can be stimulated to develop into certain tissue-specific physiological behavior, or can now even be “re-programmed” to become quite similar to the more broadly flexible stem cells derived from embryos but now not requiring the embryonic source. Happily, the days of reliance on embryo-derived stem cells appear to be over for purposes of beneficial technologies.

We also should consider genomic medicine, and what’s attractive about that field is that with the way we do medicine now, which is chemistry-based—say you have a disease, and we might give you a pill to correct it—well, the biggest problem with that is that while I think this pill will help ameliorate your condition, maybe it won’t. Maybe that drug only works in ten percent of the patients and not ninety percent.

For example, consider cancer. You’ve got a particular kind of cancer, and we prescribe a certain treatment… well, hopefully you’re among the lucky ten percent, and you’ll be in much better shape in two or three years. If you’re not, then we’ve wasted your time. In fact, we’ve probably hurt you rather than helped you, because we’re using chemistry to interfere with things, and even though we might be reducing the damage of some things, we’re probably causing toxicity elsewhere in the system, because that same chemistry is also interfering over there.

So the value of genomic medicine is to get enough information about you through sequencing your genome that we can say, “Ah, for you this particular pill is not a good idea; it will actually do more damage than good. But for your brother, it’s likely to work, and the ratio of benefit to harm is much better.” This is the reason genomic medicine is more imminent—it’s what’s closest on the horizon to being realized—because we can use the same drugs we have now, we’ll just be using them more effectively. At the moment, we can sequence genomes, and we do have these treatments that help, and it’s just a matter of matching up these two technologies.

Now, on the other hand, when you think about genome sequencing, you can find out all sorts of things, and you have to decide, “What if I learn something negative?”

EDITOR’S NOTE: Join us next week as we continue the conversation about genomic medicine, bioengineering, and being a Christian in science.

Genesis 8:1: But God remembered Noah and all the wild animals and all the domestic animals that were with him in the ark. And God made a wind blow over the earth, and the waters subsided; 2 the fountains of the deep and the windows of the heavens were closed, the rain from the heavens was restrained, 3 and the waters gradually receded from the earth.

The Flood narrative of Genesis 7-9 has played a prominent role in science and religion debates for over three hundred years and gave rise in earlier centuries to geological theories such as old earth catastrophism. While literary studies have uncovered the chiastic structure of the Flood story (see Gordon Wenham, “The Coherence of the Flood Narrative” Vetus Testamentum 28 (1978):336-48) and with it the theological pivot point of the entire narrative (Gen. 8:1 – “And God remembered Noah…), much of the popular attention remains on the questions regarding details (Is there THAT much water in the world to cover ALL the mountains to a depth of 15 cubits? Could you really fit two or seven of every animal species in an ark that size?)

Looking at a smaller matter, we find at the beginning and the middle of the narrative indications of an ancient Near Eastern worldview. As the story is told, the flood was not merely the result of excessive rain, but actually the convergence of the waters above the earth with the waters below the earth. It is, as one translation puts it, as if the sluice gates at the deep and of the heavens were thrown open and water poured in from above and below. This is a consistent picture from the Old Testament of a three-tiered universe—a dome above the earth holding back the heavenly waters, a flat earth with water on its surface, and water under an earth which is held up by pillars.

That the story is told using the cosmology of its time should not be unduly unsettling, nor that the story is reinterpreted as new understandings of the universe come into favor. By way of example, consider John Calvin and his understanding of the structure of the universe. Although committed to the principle of sola Scriptura, Calvin recognized that the Bible would have been written in terms its original recipients would have understood.

Calvin inherited the medieval cosmology of his time, a way of viewing the world heavily influenced by Greek thought and one which was about to receive shocks from astronomers such as Copernicus and Galileo. But not just yet. Calvin still subscribed to the common conception of his day in which the four elements—earth, air, fire, and water—comprised the earthly sphere and possessed unique characteristics. The nature of air and fire was to rise, while the nature of earth and water is to sink. Earth, being heavier than water, should sink to the center of the cosmos and water should compose the next layer. Both earth and water are spherical, i.e., naturally form spherically around the cosmic center. Thus the heavier spherical element of earth should be encased entirely within the lighter spherical element of water.

Notice what this does to the flood story. For Calvin, the amazing thing is that the world isn’t constantly under water and subject to flooding. In the cosmology of Calvin’s day, it does not take an act of God to cause a universal flood, but rather an actively present and restraining hand of God to keep the waters back in everyday circumstances and make inundation by water something other than universal.

Obviously, Calvin was wrong. Or perhaps we should say that medieval cosmology was flawed and justifiably gave way to new conceptions of the universe. The answer is not to return to an ancient Near Eastern cosmology, but to reinterpret cautiously within new and better cosmologies and to pay closest attention to the text and the theology of scripture.

The geological and planetary sciences bring their own unique contributions and are of more interest than the latest expedition to discover the ark on Mt. Ararat. Is the flood story a universalization of a catastrophic regional event that burned itself into the psyche of ancient cultures in the Mediterranean basin? Various theories regarding a Black Sea venue for a catastrophic flood event are still in process of being sorted out. It’s intriguing. Or the question where the water on Planet Earth comes from? Was it always here as an emanation of vapors from the earth’s crust in its early formation, or has it accumulated over eons through the steady bombardment of earth by small, icy comets? It’s an intriguing scientific question that is in the midst of determination through testing.

Preaching Suggestions

When preaching on the story of the Flood, it is easy to get lost in the debates over particulars. As mentioned elsewhere, to tackle all the peripheral issues threatens to turn a sermon into a geology lecture. Other settings are better suited to addressing those questions, and those are best addressed open-endedly.

A brief explanation of ancient Near Eastern cosmology can be helpful to contextualize the story. If there are those who are tempted to think that a cosmology embedded in the Bible must be inspired and definitive, one can note that cosmology has changed by the New Testament. The Bible itself isn’t wed to a particular structure of the universe.

What is important is to keep the theology of the text front and center, and in that theology there are at least three non-negotiables from the flood narrative. First, human sin and violence threatens to undo a good creation (the flood is a de-creation event, a return of the waters mentioned in Genesis 1:2). Second, God remembers Noah, and never forgets his promises. Third, the end of the flood is a covenant with the whole earth regarding the stability and endurance of the natural order.

About a year ago I posted the first article in this series, asking whether recent advances in genomics made any difference to the Judeo-Christian notion of humanity being made in the 'image of God'. That article focused on DNA sequencing data from our closest relatives. This article will focus on the issue of genetic determinism.

Theologians have spent many centuries mining the rich vein of the 'image of God' metaphor. Central to the idea is humanity with spiritual capabilities and responsibilities, equipped for moral decision-making and a relationally rich life in community. Historically, the idea has contributed to the conviction that each human individual has an absolute value, independent of their ethnicity, educational level, health status or income.

Do recent advances in genomics threaten or support such a view of humankind, or are they just neutral? Irrespective of one's belief in God, or not, this is of more than passing interest. Imagine the poor person wrestling for years with the great questions of life and finally deciding to become an atheist, only to then be informed that a cognitive bias derived from his particular set of genetic variants made that decision pretty much inevitable anyway. Such news might be equally unsettling for the person who had just struggled to faith following years of agnosticism. Our deepest human feelings are closely connected with the idea that we choose our own path through life.

The flourishing of genomics in the early part of the 21st century has certainly conveyed the message to many that one's destiny is written into one's genome. Whereas scientists are generally scrupulously careful not to give the impression that there is any such entity as a "gene for" some human trait, by the time the latest discovery appears in the media, such caution is often thrown to the winds. The past year has seen the trumpeting of a "gene for happiness," a "kindness gene" and a "believer gene." It is not even a question of education, but "genes are to decide" if you are a "caring person." Genetic testing websites assure us that "your genes are a road-map to better health," and we all know that road-maps are fixed. Small wonder that there is a creeping genetic fatalism around that subverts the idea of personal responsibility.

Fatalism in itself impacts on human behavior. Studies have shown that subjects exposed to the writings of authority figures doubting free-will are then more likely to cheat. Conversely, workers convinced of the reality of free-will are rated higher in the work-place than those whose beliefs tend more towards determinism.

The reality is that recent genetics research has continued to move steadily away from any notion of genetic fatalism, highlighting the sheer complexity of the genome, and providing some fascinating examples of the ways in which our choices impact upon our own genomes. There is no gene "for" any complex human trait because in fact genes encode proteins or other types of information-containing molecules, and thousands of genes collaborate together during human development in interaction with the environment to generate the unique human individual that each person represents. Those requiring an introduction for the non-specialist are referred to "The Language of Genetics."

Epigenetics adds further layers of variation and complexity. This refers to the chemical modifications of the DNA that cause genes to be switched on or off. It is such epigenetic modifications that generate the 220 specialized tissues of our bodies. Such acquired changes can even be inherited across several generations, certainly in plants and animals, and maybe in humans as well. In choosing to smoke, drink in excess, or take drugs, we also choose to modify our genomes.

So it turns out that even identical twins are not really genetically identical, developing different profiles of epigenetic modification as they go through life. This no doubt contributes to the otherwise surprising result that the age of death of identical twins, who share identical genomes, is comparable with that observed in non-identical twins, whose genomes are as different from each other as any two sibs. In one study of 184 pairs of twins in Spain, the difference in the age of death between the identical twin pairs was seven years on average, but such averages hide the fact that the age differences ranged from a couple of weeks to eighteen years. In the case of the non-identical twins, the difference in age at time of death was nine years, and the range was three to nineteen years. So there was really not that much in it.

What would happen if there was a genetic marker that identified nearly everyone in prison, marking them out as genetically distinct from half the world's population? What would that do to our ideas about genetic fatalism and convictions about moral responsibility? As it happens that marker already exists. Out of 131 countries worldwide, an average of 96 percent of the prisoners are male and, in this case, no complicated genetic studies are needed to know that the genetic marker that identifies this population is the Y chromosome. So universal is the correlation between the Y chromosome and criminality that we can safely say that no other genetic correlation will ever be found between a variant genome and criminality that surpasses this one. And yet we still hold nearly all males responsible for their criminal actions and put them in jail as soon as they're convicted. Furthermore, we note that most people who possess a Y chromosome go through life without committing a crime. So having a Y chromosome, with its unique set of genes, does not "determine" human criminality, although clearly we cannot go to the opposite extreme and say that it is completely irrelevant for patterns of human behavior.

The point in citing such examples is not to suggest that our genomes have nothing to do with our lives. They certainly do, not least in their significant contributions to our personality differences. The point rather is that the latest results in genetics provide no grounds for fatalism, instead highlighting the richness and diversity of the human population, and our own moral responsibilities, including the challenge to be good stewards of our genomes.

An argument for the existence of God this is not. But for those of us whose world-view is shaped by the conviction that we humanity are made in God's image, it is good to know that the latest genetics is consistent with such a perspective.

The story in Genesis is a story (full of the deepest suggestion) about a magic apple of knowledge; but in the developed doctrine [of the Fall] the inherent magic apple has quite dropped out of sight, and the story is simply one of disobedience. I have the deepest respect even for Pagan myths, still more for myths in Holy Scripture. I therefore do not doubt that the version which emphasises the magic apple, and brings together the trees of life and knowledge, contains a deeper and subtler truth than the version which makes the apple simply and solely a pledge of obedience. But I assume that the Holy Spirit would not have allowed the latter to grow up in the Church and win the assent of great doctors unless it also was true and useful so far as it went. It is this version which I am going to discuss, because, though I suspect the primitive version to be far more profound, I know that I, at any rate, cannot penetrate its profundities.¹

Whatever its theological profundities, though, Lewis is clear that Genesis 2-3 is probably not a straightforward narrative of historical events. “What exactly happened when Man fell, we do not know,” he later writes. “We have no idea in what particular act, or series of acts, the self-contradictory, impossible wish [to be our own masters] found expression. For all I can see, it might have concerned the literal eating of a fruit, but the question is of no consequence.”²

What, then, is of consequence for Lewis, we might ask? The real story of the Fall, says Lewis, is not the surface narrative about “the magic apple,” but rather what he refers to as “the developed doctrine” of the Fall, namely the doctrine of humankind’s depraved condition:

According to [the doctrine of the Fall], man is now a horror to God and to himself and a creature ill-adapted to the universe not because God made him so but because he has made himself so by the abuse of his free will. To my mind this is the sole function of the doctrine.³

The “sole function of the doctrine” for Lewis is to name the human condition for what it is, namely, shot through with corruption. Or, as Lewis put it in A Preface to “Paradise Lost,” “The Fall is simply and solely Disobedience—doing what you have been told not to do: and it results from Pride—from being too big for your boots, forgetting your place, thinking that you are God.” You might call this the “Mere Depravity” view of the Fall.

Throughout The Problem of Pain Lewis displays a remarkable degree of comfort with evolutionary theory, not least evolutionary accounts of human origins. A corollary of Lewis’s acceptance of evolutionary theory, of course, is that death pre-existed humanity. Lewis grasps this nettle in chapter IX of the book when he writes,

The origin of animal suffering could be traced, by earlier generations, to the Fall of man—the whole world was infected by the uncreated rebellion of Adam. This is now impossible, for we have good reason to believe that animals existed long before men. Carnivorousness, with all that it entails, is older than humanity.⁵

Here is not the place to go into Lewis’s postulation that Satan was responsible for animal predation. We need only note that he makes this suggestion precisely in order to show how a broadly Darwinian picture of natural history may be compatible with a broadly Christian view of the world. For some, severing the link between the Fall of man and death’s entry into the world, is anathema. But given Lewis’ mere depravity view of the Fall, this evolutionary understanding of natural history creates no real problem for Christian faith.

Moreover, for Lewis the evolutionary picture of the ascent of humankind presents no real objection to the Christian doctrine of the Fall, either:

Many people think that this proposition [that we are fallen creatures] has been proved false by modern science. “We now know,” it is said, “that so far from having fallen out of a primeval state of virtue and happiness, men have slowly risen from brutality and savagery.” There seems to me to be a complete confusion here…. If by saying that man rose from brutality you mean simply that man is physically descended from animals, I have no objection. But it does not follow that the further back you go the more brutal–in the sense of wicked or wretched–you will find man to be.⁶

Lewis goes on to note that the categories of virtue and vice simply do not apply to the animal kingdom–and therefore not to our pre-human ancestors either–because animals as such are not moral agents. Moreover, Prehistoric man is not to be presumed to be altogether reprobate simply on account of using only rudimentary tools, hunting and gathering, and the like. Primitivity ought not to be confused with sinfulness he argues. Thus, for Lewis, the discoveries of modern paleontology and archaeology can tell us nothing about when or whether our ancestors fell from a state of innocence, and so we are free to accept, as Lewis seems to have, man’s physical descent from animals without giving up the Christian doctrine of the Fall.

While Lewis may not have publically argued for the historicity of Adam and Eve, his private opinions might have been another matter. In his recent essay “Darwin in the Dock,” John G. West has argued that, regardless of what he said in print, Lewis privately “embraced the literal existence of Adam and Eve.”⁷ West chiefly bases his argument for Lewis’s private belief in a literal Adam and Eve on an anecdote involving one of Lewis’ Oxford colleagues, Helen Gardner, recounted in A.N. Wilson’s C.S. Lewis: A Biography.⁸ Upon being asked at a dinner party whom he would most like to meet after death, Lewis replied, “Oh, I have no difficulty in deciding…. I want to meet Adam.” Gardner, it is reported, replied by saying that “if there really were, historically, someone whom we could name as ‘the first man’, he would be a Neanderthal ape-like figure, whose conversation she could not conceive of finding interesting.”⁹ Lewis, we are told, gruffly responded, “I see we have a Darwinian in our midst” and never invited Gardner to dinner again.¹⁰

West takes this tense little interaction between Lewis and Gardner to indicate that Lewis’ belief in a literal historical Adam and Eve. However, it should be noted that such a conclusion seems somewhat overhasty in light of what Lewis says in The Problem of Pain, where he articulates a view rather similar to what Gardner said that evening:

I do not doubt that if the Paradisal man could now appear among us, we should regard him as an utter savage, a creature to be exploited or, at best, patronised. Only one or two, and those the holiest among us, would glance a second time at the naked, shaggy-bearded, slow spoken creature: but they, after a few minutes, would fall at his feet.¹¹

Given that Lewis actually believed what he wrote here, the difference between Lewis and Gardner seems not to have been either the question of “whether man is physically descended from animals” (which, as we have seen, Lewis was willing to grant) or the question of whether Paradisal man would be a “naked, shaggy-bearded, slow spoken creature,” a “Neanderthal ape-like figure.” Rather they differed over whether “Paradisal man,” as Lewis puts it, would have been someone, however primitive, to be revered, or whether, as Gardner seemed to believe, a mere brute. Taking Lewis’ written statements at face-value, it would appear that his irritation with Gardner owed less to her acceptance of evolution than it did to her dismissive presumption that our forebears were but dull savages.

Finally, it should be noted that Lewis was not even committed to the most basic element of a belief in a literal Adam and Eve, namely, that it was precisely two humans who fell and from whence our species came. He writes, “We do not know how many of these creatures God made, nor how long they continued in the Paradisal state. But sooner or later they fell.”¹² Lewis’s mere depravity view of the Fall and his belief in the mythical character of the Eden story gave him some latitude on the question of whether the Fall consisted of a historic first human pair going wrong at an easily identifiable moment. For Lewis, it was apparently quite possible that whole tribes of “Paradisal” Prehistoric humans could have gone about their business for generations—hunting, gathering, singing around the campfire, rearing children, painting in caves—before the spiritual and scientifically undetectable catastrophe of “the Fall” occurred. In other words, if Lewis were presented with the recent genomic evidence which suggests that our species arose from an initial population of several thousand rather than only two, it is doubtful that it would have flustered him. It simply makes no difference to Lewis’s argument how or how many humans initially “fell.” All that matters for Lewis is that God made humans (perhaps via evolution, perhaps not) and that we humans have gone quite wrong–so wrong, in fact, that it is beyond our powers to repair ourselves. Mere Christianity, for Lewis, does not logically depend on the historicity of the Adam and Eve story, but on the doctrine of our mere depravity.

In tomorrow's concluding post, we turn to C.S. Lewis' views on the compatibility of evolution and Christian faith.

Notes

1. Lewis, The Problem of Pain, (New York: Simon & Schuster, 1996), 63-64, my italics
2. Ibid.
3. Ibid, my italics
4. Lewis, A Preface to Paradise Lost, (New York: Oxford University Press, 1961), 70-71
5. Lewis, The Problem of Pain, 119
6. Ibid, 64
7. West, “Darwin in the Dock,” in The Magician’s Twin: C.S. Lewis on Science, Scientism, and Society, (Seattle: Discovery Institute Press, 2012), 121. West’s volume takes a markedly different view of Lewis and Lewis’s legacy regarding debates about Christianity and evolution. I intend to write a thorough critical review of West’s book in the near future.
8. Ibid
9. A.N. Wilson, C.S. Lewis: A Biography, (New York: W.W. Norton, 1990), 210
10. Ibid
11. Ibid
12. Ibid.

Behe and IC

Since we have previously explored Behe’s idea of irreducible complexity in an entire series, we will not revisit it here in great detail. It is important, however, to reemphasize how Behe defines irreducible complexity (IC). As we noted in the first part of that series, Behe frames his ideas on IC as a counter to Darwin’s ideas of gradualism.

For Behe, the argument for IC is a critique of gradual evolutionary processes, of the kind that Darwin saw as necessary for his theory to hold. When Behe introduces and defines IC in his book Darwin’s Black Box, he has a key quote from Darwin on gradualism explicitly in view:

Darwin knew that his theory of gradual evolution by natural selection carried a heavy burden: "If it could be demonstrated that any complex organ existed which could not possibly have been formed by numerous, successive, slight modifications, my theory would absolutely break down."

It is safe to say the most of the scientific skepticism about Darwinism in the past century has centered on this requirement… critics of Darwin have suspected that his criterion of failure had been met. But how can we be confident? What type of biological system could not be formed by “numerous, successive, slight modifications”?

Well, for starters, a system that is irreducibly complex. By irreducibly complex I mean a single system composed of several well-matched, interacting parts that contribute to the basic function, wherein the removal of any one of the parts causes the system to effectively cease functioning. An irreducibly complex system cannot be produced directly (that is, by continuously improving the initial function, which continues to work by the same mechanism) by slight, successive modifications of a precursor system, because any precursor to an irreducibly complex system that is missing a part is by definition nonfunctional. An irreducibly complex biological system, if there is such a thing, would be a powerful challenge to Darwinian evolution.

(Darwin’s Black Box, p. 39)

The definition of an IC system is thus straightforward: it is a matched group of components, where all the components are necessary for the function of the system. The necessity of each component can be demonstrated by attempting to remove it – if the system no longer works if even one component is removed, it is by definition IC.

Behe and exaptation

The standard response to Behe’s argument from IC is to discuss the evolutionary concept of exaptation: that new systems and functions are cobbled together from components that have functional roles in other systems already present in the cell. Behe discusses, and ultimately dismisses this idea in Darwin’s Black Box as follows:

In Chapter 2 I noted that one couldn’t take specialized parts of other complex systems (such as the spring from a grandfather clock) and use them directly as specialized parts of a second irreducible system (like a mousetrap) unless the parts were first extensively modified. Analogous parts playing roles in other systems cannot relieve the irreducible complexity of a new system; the focus simply shifts from “making” the components to “modifying” them. In either case, there is no new function unless an intelligent agent guides the setup.

So for Behe, two points are clear: parts selected for function in one system cannot be exapted for use in other systems since they would require too many modifications; and the emergence of a new function is the indication that an intelligent agent is guiding the process.

Behe has responded to my previous posts to claim that the tandem duplication event that brought about the Cit+ actualization event should not be considered a gain-of-FCT mutation under his criteria:

The gene duplication which brought an oxygen-tolerant promoter near to the citT gene did not make any new functional element. Rather, it simply duplicated existing features. The two FCTs comprising the oxygen tolerant citrate transporter locus -- the promoter and the gene -- were functional before the duplication and functional after. I had written in my review that one type of mutation that could be categorized as a gain-of-FCT was gene duplication with subsequent sequence modification, to allow the gene to specialize in some task. Venema thinks the mutation observed by Lenski is such an event. He has overlooked the fact that there was no subsequent sequence modification; a segment of DNA simply tandemly duplicated, bringing together two pre-existing FCTs.

As an aside, quibbling over whether this mutation constitutes a “genuine gain-of-FCT” mutation is not my purpose here, since the definition is Behe’s to define, and I am not aware of anyone else in the scientific literature who uses Behe’s definitions. That said, I consider it passing strange to claim that a series of events that produced a gene that has a new sequence and functional properties distinct from either of its component parts does not constitute the production of a new “functional coded element.” If nothing else, it is a functional coded element that has not previously existed, cobbled together from parts of other functional coded elements, displaying new, adaptive properties. If according to Behe’s definition that’s not “new” or a “gain” then I guess it’s not, but that seems to me to torture the words “new” and “gain” beyond recognition. But I digress.

The important point for our purposes, however, lies elsewhere. Note carefully how Behe describes the Cit+ actualization event. By dividing the new aerobic citrate transporter gene into two previously existing FCTs, Behe is describing an exaptation event. The one FCT (the aerobic promoter) starts off as a necessary component of a gene transcribed when oxygen is present. As such it is under selection for that function, which has nothing to do with expressing a citrate transporter. The second FCT (the citrate transporter amino acid coding sequence) is under selection to be a citrate transporter, which has nothing to do with the function of the gene the promoter comes from. The Cit+ actualization event, then, exapts these two FCTs by placing them together to create a new function (which Behe does not mention).

And here’s the kicker: the new system (expression of the citrate transporter when oxygen is present) requires both FCTs in order to work. It has become a system of “well matched, interacting parts that contribute to the basic function” (i.e. transporting citrate in the presence of oxygen) “wherein the removal of any one of the parts causes the system to effectively cease functioning.”

In other words, it is a new IC system – a small and relatively simple system, yes, but nonetheless IC. Now, I’m fairly sure that Behe would not define this system as IC, since the documentation of an IC system evolving would seriously undermine his thesis. I am interested, however, in how he will handle this development, on two fronts. First, he would need to explain specifically why two exapted FCTs that are required together for a basic function does not constitute an IC system (if indeed he wishes to preserve his definition). Secondly, given that he allows for exaptation in this case, he needs to explain how exaptation is not a threat to IC in general. In Darwin’s Black Box he disallows exaptation altogether, but that option is no longer on the table.

In the next post in this series, we’ll continue to explore the evidence for exaptation as a means to build new FCTs, and go on to examine the implications of this evidence for Douglas Axe’s proposed limit to evolutionary mechanisms.

For further reading:

Blount, Z.D., Barrick, J.E., Davidson, C.J. and Lenski, R.E. (2012). Genomic analysis of a key innovation in an experimental Escherichia coli population. Nature 489; 513- 518.

Michael J. Behe, Darwin’s Black Box: The Search for the Limits of Darwinism (New York: Free Press, 2006).

Michael J. Behe, The Edge of Evolution: The Search for the Limits of Darwinism (New York: Free Press, 2007).

Michael J. Behe (2010). Experimental evolution, loss-of-function mutations, and “The first rule of adaptive evolution”. The Quarterly Review of Biology 85(4); 419-445.

This week we feature the third clip from the upcoming documentary “From the Dust”, directed by filmmaker Ryan Pettey. It is our sincere hope that, above all else, the film can become a focal point for some of the big questions that inevitably arise at the intersection of science and faith. We believe Ryan's work will inform faith and enrich discussion, and we feel that this week’s topic, the Fall, is of particular importance for Christians as we think through the ramifications of creation by evolutionary mechanisms.

To help foster such dialogue, we are once again including several discussion questions with this week’s clip. In the transcript below, you’ll find several prompts that are meant to help viewers dig deeper into the material being presented. Mouse over each highlighted region and a question will appear on the side. We encourage you to watch this video with your friends, your churches, your small groups and Sunday School classes, your pastors -- or anyone else for that matter – and take some time to discuss what is being said (and maybe even what isn’t). You may not all agree, but you will find yourselves engaged in fruitful and spirited conversation. And it is this kind of conversation that will help move the science and faith discussion forward.

The provided questions are just a few of the discussion questions that go with this transcript, and we'd be happy to send them to you to foster further conversation within your church or small group setting. If you’d like to see the questions, or if you have stories from your own small group discussions about the clip, we would love to hear from you at info@biologos.org.

Editor's Note: The full documentary is now available on DVD and Blu-ray. You can order the film here, and learn more about the project here.

“The Fall” Transcript

Dr. Jeff Schloss: “My friends and colleagues, who have concerns about evolutionary theory for theological reasons, are onto something, and one of them involves the Fall, the nature of the Fall, what it is. Even if it is a metaphor, it is a metaphor for something, and what is that something? And how would we make sense of that something in light of evolutionary theory? The other issue on this has been probably the most serious issue that not only Christians, but all theists who believe in a good and providential God have wrestled with, it is the problem of natural evil.”

Reverend Dr. Michael Lloyd: “The problem of evil is a real problem to religious faith. It was certainly the thing for Darwin himself. That is what made him question his faith, and I think rightly so. It does not look like the sort of system that a good and loving and benevolent God would have set up. Now, obviously that raises huge questions because we don’t see any evidence of a world that was harmonious. We only see evidence of a world that was at war with itself, and that obviously is the problem that Christian theologians face. For a long time I used to believe that the Genesis narratives paint a picture of a world completely at peace, completely harmonious until the human fall, and then something goes wrong. When I began to look at it more closely, I began to think that there is more to it than that. There is evidence from the text that things are already dislocated, already out of joint. For one thing, there is the serpent, and however you interpret the serpent, here is a bit of the created order that is actively talking against God, working against God—so there is already something that has gone wrong. Secondly, there is the command to fill the earth and subdue it. There is the suggestion that something needs to be subdued, something is not quite right that needs to be put right and humans beings are called to do that—to put it right. And thirdly, it is a garden. It is almost as if God has said, ‘Here is a little bit I have done for you, here is a little bit of order and harmony that I have done for you. Now you go and spread that order and that harmony throughout the rest of creation.’ The tragedy is, of course, that human beings don’t do that. Rather than put that right, they make it worse.”

Dr. Alister McGrath: “Clearly Scripture distinguishes humanity from the rest of creation by this idea of the image of God. And that is understood in a number of ways—one of which is relational. Human beings have this God-given capacity to be able to relate to God, which is simply not there for the rest of creation. How do we understand that phrase: the image of God? If we accept the narrative of biological evolution, we have to say that at some point humanity became sufficiently distinguished from the rest of the natural world to be able to have this relationship with God.”

Reverend Dr. Michael Lloyd: “If you have a very finely graded gas tap and you begin to turn it on, initially, there is not enough gas in the air for the gas to ignite. So, you turn it up some more, still nothing, a bit more, still nothing, and a bit more, still nothing. At a particular point, there will be enough gas to air ratio for the thing to ignite. So, you can have a completely smooth, upward development, and yet, you can have something decisive happening at a particular moment. You get an increase in that moral capacity and moral awareness; you get an increase in their relational ability, in their social ability. You get an increase in their tool-making ability. You get an increase in their language. At a particular point there is enough of all that. There is enough relational capacity; there is enough social capacity and moral awareness and spiritual awareness for God to deal with us in a new way: ‘They have enough creativity to reflect the fact that I am the creator. They have enough relational capacity to reflect the fact that I am love. This in some way reflects who I am, and I will stamp my image upon them.’”

Reverend Dr. John Polkinghorne: “As hominids evolved and became more complex, then self-consciousness, in the sense of projecting our minds into the remote future or past began to dawn in them. And that didn’t bring biological death into the world, because obviously it had been there for millions of years beforehand, but it brought into the world what you might call mortality. Because our ancestors were self-conscious, they knew they were going to die. Because they had turned away from God, they had alienated themselves to the only one who was the ground for the hope of a destiny beyond death. And so, mortality, meaning the sadness, the human sadness at transiency and decay dawned in human life. Another very subtle feature of the Genesis 3 story is that it is a fall upwards as people would sometimes say. It is the gaining of some knowledge, the knowledge of good and evil, the story says. And so, the dawning of self-consciousness is also the gaining of something that wasn’t there before. What the serpent whispers in Eve’s ear is, ‘eat this fruit, and you will be like God. You won’t need God anymore. You can do it yourself.’ That is the fundamental sin, the fundamental mistake in human life is believing that we can do it on our own, doing it my way, and spiritual death is to deliberately and persistently cut yourself off from that. It doesn’t occur as an angry God giving you a punishment for not falling into line. It is simply that you have punished yourself. You know, preachers sometimes say that the gates of hell are locked from the inside not to keep the creatures in, but to keep God out. And that, I think in the end, is what spiritual death is if you persist in it. But God is always, I am sure, at work, seeking to draw people back into the divine love. I think that is the work that is necessary to understand what Paul is getting at in Romans 5 when he says that death came into the world through one man. The cost of development is a degree of precariousness. The people need the grace of God if we truly are to live fulfilling lives.”

Dr. Thompson responded that while the essence of Sin is ultimately mysterious, he suggests that there are some ways to think about Sin in the language of interpersonal neurobiology.

On the other hand, Dr. Smith found the wisdom of St. Augustine in The Confessions quite helpful—The essence of Sin is loving the wrong things in the wrong ways. It’s a disordered love.

We need to have an account of Sin in terms of habit. A lot of Christians today think of “sins” and discreet choices, but historically Christians have thought of Sin as a habitual tendency and disordering. It is formed over time—that’s what a vice is. Virtue and sanctification require ongoing re-habituation, a counter-formation of our inclinations.

Dr. Thompson followed up with a reference to Malcolm Gladwell’s Outliers and noted that people who are really good at what they do generally acquire it through lots of practice. Thompson then asked the audience, “How are we, in an embodied way, going to practice Christianity for 10,000 hours?”

We hope you have enjoyed this video series. If you'd like to learn more, we encourage you to read Curt Thompson's The Anatomy of the Soul and James K.A. Smith's Desiring the Kingdom: Worship, Worldview, and Cultural Formation. Dr. Smith also has a new book coming out this winter entitled Imagining the Kingdom: How Worship Works. ]]> Fri, 05 Oct 12 04:00:00 -0700 Curt Thompson, Smith, James K.A. http://biologos.org/blog/series/decoding-encode-series?utm_source=RSS_Feed&utm_medium=RSS&utm_campaign=RSS_Syndication http://biologos.org/blog/series/decoding-encode-series?utm_source=RSS_Feed&utm_medium=RSS&utm_campaign=RSS_Syndication The BioLogos Foundation explains to the findings of the Encyclopedia of DNA Elements (ENCODE) project and responds to the claims that its discoveries challenge the theory of evolution, especially regarding so-called "junk DNA". In 2003, under the leadership of BioLogos founder Francis Collins, the Human Genome Project sequenced the full human genome, showing us for the first time the order of the 3.2 billion chemical “bases” that make up the rungs of DNA’s double helix structure. The project identified and mapped 23,000 genes that code for proteins, but those genes make up less than 2% of the total sequence—far fewer than originally predicted, given the complexity of humans. While many non-coding sequences were identified as having function as well, there were still vast swaths of the genome that had no obvious function. In fact, what was known about certain classes of sequences suggested that they had no functional role for humans—such as the sequences identified as either transposons or transposon fragments that make up nearly half of our genome. These sorts of sequences seemed to fit into what was popularly known as the “junk DNA” category.

With the complete genome sequence in hand, we knew the sequence and location of our genes, but what we didn’t know was how all those genes are regulated: how do the trillions of cells in our bodies know when to turn on or off all those genes? How do the hundreds of distinct cell types develop and function together, when they are all running on the same DNA “operating system?”

That’s where the ENCODE (short for Encyclopedia of DNA Elements) project comes in. Launched in September 2003, shortly after the announced completion of the Human Genome Project, the goal of the ENCODE project is “to build a comprehensive parts list of functional elements in the human genome, including elements that act at the protein and RNA levels, and regulatory elements that control cells and circumstances in which a gene is active.” In other words, the project seeks to understand how the genome “works.”

Early this month, researchers from ENCODE released more than thirty papers presenting their findings. During a Science magazine online chat, the project’s data coordinator, Ewan Birney, explained the outcome:

The ENCODE project aimed to start our understanding of how the human genome works. We know that (nearly) all the information that determines a human is in the genome, as we all start off as single cell with this DNA. However, we had a patchy understanding of how it works, in particular away from protein coding genes.

To work out how the genome works, we used the fact there are many tiny machines (proteins and RNA - RNA is very like DNA) in each of our cells which know how to "read" parts of the genome. By monitoring where these little molecular machines are on the genome, or how parts of the DNA are copied into RNA (there are quite a few different types of RNA as well), we start to gain some insight into the genome.

We did many such experiments, across different cell types (eg, one cell type was very similar to a liver cell type; another was very similar to a white blood cell). This way not only can we see what is similar, we can also see differences between these cell types.

There is a lot more to get to know and understand here - this is definitely closer to the start than the end. But it is a substantial amount of data, and analysis, to start on this journey.

According to the abstract of one of the lead papers from Nature, this extraordinary glut of data “enabled us to assign biochemical functions for 80% of the genome, in particular outside of the well-studied protein-coding regions.” Only 2% of the genome codes for proteins, but 80% or more has some biochemical function. As a Science news article put it, these 30 papers “sound the death knell for the idea that our DNA is mostly littered with useless bases.”

The pro-Intelligent Design organization The Discovery Institute has heralded the discovery as the “demise of junk DNA.” Casey Luskin writes for their blog Evolution News:

Let's simply observe that it provides a stunning vindication of the prediction of intelligent design that the genome will turn out to have mass functionality for so-called "junk" DNA. ENCODE researchers use words like "surprising" or "unprecedented." They talk about of how "human DNA is a lot more active than we expected." But under an intelligent design paradigm, none of this is surprising. In fact, it is exactly what ID predicted.

The extent to which the ENCODE project been able to identify function has been surprising—even exhilarating—though scientists have for some time been getting glimpses of the many ways in which segments of DNA can be “active.” Even in 1970 biologists knew that some non-coding DNA had function, and by 2003 there was a large body of work demonstrating that many non-coding elements acted as promoters, enhancers, insulators, and so on. Indeed, in recent years many have come to appreciate the fact that “junk” was never really an appropriate metaphor in the first place. Still, because sequencing of multiple genomes has shed such extraordinary light on key evolutionary mechanisms, many geneticists have focused on function primarily in terms of which regions do or do not contribute to the evolutionary fitness of their host, rather than whether they were merely "doing something" biochemically. What the impressive ENCODE project has done is open a treasure trove of new information that can only accelerate the pace at which researchers are able to explore the incredible subtlety and complexity of DNA, and refine the very concept of “functionality.”

So with all this in mind, is ENCODE a stunning victory for ID, as Luskin believes? Bryan College biologist Todd Wood thinks not. He writes, “I don't think that function equates to design, nor do I think that design requires or predicts function. They're not the same thing… my understanding of function does not require me to hypothesize God (or an anonymous designer, if you must) as the proximal cause.”

We agree. Indeed we would go on to say that evolution and design are not mutually exclusive. So while finding function is not sufficient to prove design, recognizing that function has arisen by way of evolution does not indicate that God was not at work. We at BioLogos believe God providentially works out his purposes—his designs—through the elegant processes of evolution, not in opposition to them.

Amazing as the new data are, it only strengthens and enhances our evidence for evolution. While much of the genome is “doing something” biochemically, it is still likely that the majority of the sequence is evolutionarily neutral (Senior Fellow Dennis Venema discusses the evidence for this “neutrality” in a post on our site, including a striking comparison between 29 different mammal genomes and the human genome). In fact, another ENCODE researcher participating in the Science magazine chat, John A. Stamatoyannopoulos of the University of Washington School of Medicine, thinks the findings align beautifully with evolutionary theory:

ENCODE's data provide a unique and powerful window through which to view evolutionary change. We can see those changes directly by lining up the genome sequences of many different organisms -- these line-ups have revealed millions of regions where all the genomes agree, indicating sequences that have been specially preserved by evolution while others have decayed away (ie freely changed their letter codes). We now see that a large proportion of these 'conserved' regions are lighted up by ENCODE annotations, indicating that they are marking spots in the genome that contain important instructions for cell function.

We’ve discussed “junk” DNA previously, including a multi-part series by Dennis Venema, and we’ve received many emails over the past few days asking for our comments on the ENCODE findings. On Monday and Tuesday, Dr. Venema will begin to offer his own thoughts on ENCODE.

A special thanks goes to Darrel Falk, Mark Sprinkle, Kathryn Applegate, Dennis Venema, and Tom Burnett for their contributions to this post.

Last time I introduced the idea that a Christocentric theology of creation is one of the hallmarks of Theistic Evolution, and I focused on the idea of the “Crucified God.” But the scientist-theologians who write about TE also think about creation and theodicy in terms of divine “kenosis” and eschatology. So today we’ll conclude our “implications” section by returning to creational theology, and then turn to the ways TEs re-think Adam and Eve in light of human evolution.

Kenosis, theodicy and eschatology

John Polkinghorne and others, citing Philippians 2:7, like to speak about divine “kenosis”, God’s choice to “empty himself” in taking on human form; they apply this also to the act of creating the world in a great work of self-sacrificial love. Although Wikipedia gives much information about the roots of this doctrine in Orthodox and Catholic circles, my knowledge is minimal and I cannot confirm what I find there (though it might all be correct). According to a theologian I once consulted, kenosis in soteriology was discussed by Lutherans in the 17th century (if not perhaps even earlier, by others), but was only extended to theology of creation in recent decades. The most I can say with confidence is this: one of the most striking features of Protestant thought about nature, during and since the Scientific Revolution, is the degree to which it is not Christocentric in the sense we are now discussing. In much Protestant and Evangelical literature devoted to the topic of creation, one often looks in vain even for references to Jesus, let alone to Jesus as the suffering servant through whom the world was made,. Only in the latter part of the 20th century do I find a clear emphasis on the idea that nature is the creation of the God who put aside power and was crucified. If this understanding is correct, then I would say that it’s high time, and let’s get on with it!

TEs (especially Polkinghorne) are also in the forefront of those Christian writers who are linking theodicy inextricably with eschatology. Yet another scientist-theologian, Robert Russell, offers this powerful eschatological vision in Cosmology From Alpha to Omega, drawing on all of the main ideas I’ve presented in this section:

[I]n order to move us beyond mere kenosis to genuine eschatology, I believe that both kenotic theology and eschatology must be structured on a trinitarian doctrine of God. The reason here is simple: it is the trinitarian God who will act to bring about the redemption of all of nature since it is this God who is revealed as God in and through the cross and resurrection of Jesus. A kenotic theodicy (that God suffers voluntarily with the world) in and of itself is not redemptive. Eschatology is required, in which the Father who suffers the death of the Son acts anew at Easter to raise Jesus from the dead. In turn, the involuntary suffering of all of nature--each species and each individual creature--must be taken up into the voluntary suffering of Christ on the cross (theopassionism) and through it the voluntary suffering of the Father (patripassionism).(p. 266)

George MacDonald (source)

Because this series is primarily focused on the history of approaches to understanding Science and the Bible, I will not delve more deeply into these important theological issues, but only direct readers to resources such as these. Still, I close this section with a quotation from George MacDonald’s Unspoken Sermons, the same passage that C. S. Lewis used in abbreviated form as an epigram for The Problem of Pain:

“the Son of God, who, instead of accepting the sacrifice of one of his creatures to satisfy his justice or support his dignity, gave himself utterly unto them, and therein to the Father by doing his lovely will; who suffered unto the death, not that men might not suffer, but that their suffering might be like his, and lead them up to his perfection...”

Adam, the fall, and sin

(5) TEs have to confront questions about human origins that are much easier for OECs or YECs to answer: Did Adam and Eve really exist as historical persons? Was the “fall” an actual historical event? If not, what is the origin of sin?

Michelangelo Buonarroti, “The Fall and Expulsion from the Garden of Eden,” Cappella Sistina, Vatican (1509-10)

My comments here are much briefer, but I don’t mean to imply that the questions are any less important than the one I’ve just dealt with. Polkinghorne does not hold a traditional view of the fall, but he likes Reinhold Niebuhr’s view “that original sin is the only empirically verifiable Christian doctrine!” (Belief in God in an Age of Science, p. 88) This reminds me of G. K. Chesterton, who famously remarked, “Certain new theologians dispute original sin, which is the only part of Christian theology which can really be proved” (Orthodoxy, chap. 2). In other words, anyone who doubts the idea that we are “fallen” creatures simply needs to look around—that is all the evidence of our strong bent to wickedness that you’ll ever need.

There are ways to finesse the fall and evolution in a quasi-concordistic manner, such as the “headship” model advocated by Denis Alexander. Others reject any appeal to Concordism, stressing the principle of divine accommodation. For example, Denis Lamoureux argues that in the revelatory process the Holy Spirit came down to the level of understanding of the ancient Hebrews and used their ancient conception of de novo creation, in which humans were created quickly and completely. Thus, in Genesis chapters 2 and 3, Adam and Eve are ancient vessels that deliver the inerrant spiritual truths that God created us and that we are sinners.

The views that have received the most attention among evangelicals, however, are probably those of biblical scholar Peter Enns, particularly his new book, The Evolution of Adam. Instead of trying to summarize them myself, I’ll link his discussion of “Mistakes in the Adam/Evolution Discussion”, since it parallels some of the content in the book. Also see his replies to some evangelical scholars who have been critical of the book.

One of the most original and thoughtful proposals I have seen comes from philosopher Robin Collins (for bibliographical information on this and the other works cited in the rest of this column, see below). Collins calls his model the “Historical/Ideal” view, because “the original state described in the Garden story represents an ideal state that was never realized,” showing “what an ideal relation with God would be like.” Adam and Eve represent every person who has ever lived, but they also represent “the first hominids, or group of hominids, who had the capacity for free choice and self-consciousness.” Just as the first hominids made sinful choices, so do we now, and original sin involves “the resulting bondage to sin and spiritual darkness that is inherited from our ancestors and generated by our own choices.” I can’t convey the subtlety and thoroughness of this account in a short space, so those who want to know more will have to read for themselves. Conveniently, Collins provides a link to a “near final version” of his paper on his web site. If someone wants to summarize his arguments in a few paragraphs below, it would be a real service to our “course.”

Problems with historicity

(6) Questions about the historicity of Adam & Eve are underscored by evolution, but they would still come up even if Darwin had never existed and no one had ever proposed that humans and other animals have common ancestors. The Bible places Adam & Eve in a Neolithic world, with cities and agriculture, whereas non-biological scientific evidence shows that humans existed for a very long time before cities or agriculture came into existence.

Read that again. It’s a crucial point. Far too many people believe—erroneously—that evolution is responsible for undermining the historicity of Adam, Eve, and the Garden of Eden. In fact, the relevant science here is almost entirely from anthropology, not biology, and it involves human antiquity, not common ancestry. Since the mid-nineteenth century, evidence has been building that creatures anatomically and behaviorally identical to us have been on this planet for a very long time, far longer than the biblical 6,000 years. We could leave Darwin and evolution entirely out of the picture, and we would still be having a conversation about the historicity of Genesis 2 and 3. The same issues pertain to any OEC scenario. Most proponents of ID can’t duck this, either, even though they get to say “officially” that ID isn’t about the Bible. Because most ID proponents are not YECs, they accept the general validity of the methods used to date rocks and fossils, and so (by implication) this is their problem, too, whether or not it’s acknowledged.

To illustrate my point historically, let me introduce readers to George Frederick Wright (read more here and here). Ronald Numbers, the leading historian of American religion and science, wrote a clear, detailed article about this (see the reference below) that I strongly recommend to anyone who’s interest has been piqued. An influential Congregationalist clergyman and theologian, Wright was mentored by Harvard botanist Asa Gray, served briefly under Thomas C. Chamberlin on the U. S. Geological Survey, and even contributed articles on early humans and the ice age—his specialty—to scientific journals. During the 1870s, he worked closely with Gray to promote what is usually seen as a type of Theistic Evolution. By the early twentieth century, however, he appeared in some of his writings to have almost completely reversed his views on evolution. He even contributed an essay on “The Passing of Evolution” to the famous pamphlets, The Fundamentals, that later gave its name to that movement.

In other writings, however, Wright seemed to remain convinced of evolution, at one point saying that, “it is difficult to resist the conclusion that, so far as his physical organism is concerned, man is genetically connected with the highest order of the Mammalia.” Whatever he really thought about common ancestry—whether he was really a TE, an OEC, or an ID (one could make a good case for each)—the question of human antiquity dogged Wright for decades, as he sought ways to reconcile the genealogies in Genesis with accumulating evidence that humans have existed much longer than 6,000 years. Fortunately for Wright’s Christian faith, which probably hung in the balance, the famous Princeton theologian Benjamin Breckenridge Warfield, together with the conservative biblical scholar William Henry Green, managed to persuade Wright that the Genesis genealogies had plenty of wiggle room. Anyone wanting to see the crucial details should read Green’s paper on “Primeval Chronology” at this point. Note Warfield’s own conclusion (same URL): “There is no reason inherent in the nature of the Scriptural genealogies why a genealogy of ten recorded links, as each of those in Genesis v. and xi. is, may not represent an actual descent of a hundred or a thousand or ten thousand links.”

Can this really be true, without straining the whole idea of historicity? Davis Young’s skepticism seems appropriate here. How far back can we place Adam and Eve and still have contact with the biblical period? In my opinion, a clear and convincing picture of an historical Adam and Eve, reconciling the biblical picture with human antiquity, has not yet been produced, and I am doubtful that we will ever have one. Those who want more information about the possibilities and the difficulties are invited to consult the articles (cited below) by anthropologist James Hurd, evolutionary biologist David Wilcox, and anthropologist Dean Arnold. To the best of my knowledge, Hurd and Wilcox are TEs, while Arnold is an OEC. It’s up to you, my “students,” to consult these sources and place summaries and comments below. I’ve done enough already.

Looking Ahead

In about two weeks, I’ll conclude with a short history of Theistic Evolution. There’s plenty to think about in the interval. Please follow some of these links, borrow some of these books, and add your views to mine.

Citations

Dean Arnold, “How Do Scientific Views on Human Origins Relate to the Bible?” in Not Just Science, edited by Dorothy F. Chappell & E. David Cook (Zondervan, 2005), 129-40.

Robin Collins, “Evolution and Original Sin,” in Perspectives on an Evolving Creation, edited by Keith B. Miller (Eerdmans, 2003), 469-501.

James P. Hurd, “Hominids in the Garden?” in Perspectives on an Evolving Creation, 208-33.

Ronald L. Numbers, “George Frederick Wright: From Christian Darwinist to Fundamentalist,” Isis 79 (1988): 624–45.

David Wilcox, “Finding Adam: The Genetics of Human Origins,” in Perspectives on an Evolving Creation, 234-53.

The Denisovans, an extinct hominid group that interbred with modern humans, made the news again lately with the publication of a more detailed study of their genome. One of the many interesting findings was that the Denisovans share the same chromosome 2 fusion that modern humans have. In this post, I review what we know about the origins of human chromosome 2, and then discuss the new Denisovan findings and their implications.

The origins of human chromosome 2: a brief review

Though I have discussed the evidence for a fusion event leading to human chromosome 2 before, perhaps a brief review of the evidence is in order. The human genome is made up of 23 pairs of chromosomes (for a total of 46 chromosomes). This makes us something of an oddity among living great apes, all the rest of whom have 24 pairs of chromosomes (for a total of 48). Given that there are many independent lines of evidence that support the conclusion that we share a common ancestor with other great apes, this poses something of a conundrum: how is it that our species arrived at this specific chromosome number? If we were to represent this “problem” on a phylogeny, or tree of relatedness, it would look something like this (not to scale):

Our closest living relatives, chimpanzees and bonobos, both have 48 chromosomes, as do all other great apes such as gorillas and orangutans. This pattern has one of two explanations, one of which is much more likely than the other. Either the common ancestor to these species had 48 chromosomes, and there was an event that reduced that number to 46 specifically on the lineage leading to humans (option A), or the common ancestor species had 46 chromosomes, and there were independent, repeated events that increased chromosome number in all other great ape species (option B). We can compare these options by placing the required event(s) on the phylogeny (again, not to scale):

It should be obvious that the option that requires the fewest events is the more likely one – in this case option A with an event that reduces chromosome number in the lineage leading to humans. The other option, that of repeated, independent events to increase chromosome number, remains a formal, but unlikely, possibility. Events that reduce chromosome number are not frequent occurrences, so Option A is more likely than Option B.

We can also find further support for Option A, because it predicts a specific type of event, namely one that reduces chromosome number. Since loss of a large amount of chromosomal material is almost always detrimental, we need an event that reduces chromosome number without losing information. One way for this to happen is for two chromosomes to fuse together and become one. Initially, this event would produce an individual with 47 chromosomes, where two different chromosomes get stuck together. Contrary to what is often assumed, this individual would be fertile and able to interbreed with the others in his or her population (who continue to have 48 chromosomes). In a small population, over time, two relatives who both have one copy of the fusion chromosome may mate and produce some progeny with two copies of the fused chromosome, or the first individuals with 46 chromosomes. Since either a 48-pair set or a 46-pair set is preferable for ease of cell division, this population will either eventually get rid of the fusion variant (the most likely outcome), or by chance will switch over completely to the “new” form, with everyone bearing 46 chromosome pairs. While not overly likely, this type of event is not especially rare in mammals, and we have observed this sort of thing happening within recorded human history in other species. Some mammalian species even maintain distinct populations in the wild with differing chromosome numbers due to fusions, and these populations retain the ability to interbreed.

Further evidence for a fusion event in the lineage leading to modern humans comes from comparing synteny, or gene locations and orders on chromosomes within modern great apes – an issue we have discussed here before. In brief, what we see in human chromosome 2 is exactly what we would predict for a fusion event. When compared to other great apes, we see the genes on human chromosome 2 match up, in order, with two smaller ape chromosomes. We also see that sequences used at the tips of chromosomes are present at the proposed fusion site, and that human chromosome 2 has not one but two sites for the cell cytoskeleton to attach to for cell division – but that one of the sites is mutated and not functional, though it lines up precisely with the location of this site on the appropriate ape chromosome. Together, this evidence consistently supports both common ancestry for humans and great apes, and specifically that the difference we see in our chromosome numbers arose due to a single fusion event. I briefly discussed this evidence in my last post where I describe how I teach some of this material and the compelling impact it has on students exploring the evolution question for the first time.

Enter the Denisovans

With that as background, we are now prepared to appreciate a new finding that comes from genomics work done on the Denisovan hominids, an archaic species that is more closely related to Neanderthals than to us, but that nonetheless interbred with some anatomically modern humans as they migrated out of Africa and populated the globe. (For those not familiar with the Denisovans, or the evidence for our interbreeding with them, both Darrel Falk and I have written on this previously, here and here). Recently, a more detailed understanding of the Denisovan genome was published, and nested in the new information is the discovery that the Denisovans share the 46 chromosome set with the same fusion that we have. This strongly supports the hypothesis that the fusion event predates the separation of our species. If we were to represent this on a phylogeny, we can now place this event with more accuracy than before (as before, the phylogeny is not to scale):

Despite this new information, one obvious question remains. Did the Neanderthals also have the 46-pair set? From looking at the phylogeny above, we can see that the most likely answer is that they did, since the fact that the Denisovans had it strongly implies that the last common ancestor of humans and Neanderthals / Denisovans had it as well, and the Neanderthal-Denisovan split comes later. While the Denisovan DNA samples are of high enough quality to make this assessment, we do not yet have Neanderthal DNA of high enough quality to do the same analysis with current methods (though one additional feature of the new work on the Denisovan genome is developing more sensitive DNA sequencing techniques that may resolve this question in the future).

In other words, this fusion seems to be an ancient one, predating our species by several hundred thousand years. Present estimates of the last common ancestor between humans and Neanderthals / Denisovans range at about 800,000 years ago.

Implications for understanding our “becoming human”

The main implication from this work is that it places the fusion event well before the advent of our species. I’ve often chatted informally with Christians about evolution, and at times some have thought that this fusion event was what “started” our species, or made our species unable to interbreed with other groups. Some have even suggested that perhaps the fusion event was what produced the first human (i.e. Adam).

Note that thinking this way suggests a misunderstanding of how chromosome fusions occur and what effect they have on their hosts. A fusion does not precipitate a speciation event, but rather the individual with the fusion remains a part of his or her population, and able to interbreed, even if with reduced fertility. Also, there is no necessary biological effect or change that the fusion produces on the appearance of the organism. These misunderstandings aside, however,what this new evidence shows is that this fusion event took place long before modern humans arose at around 200,000 years ago. Indeed, the 800,000 years ago date for the last human - Denisovan common ancestor means that this is the most recent date possible for the fusion. While it is an interesting piece of our evolutionary history, it doesn’t seem to have much to do with how we came to acquire the traits that set us apart from, and ultimately outcompete, other similar species.

Recently, an elegant and powerful experiment was done to further investigate a question of interest to many evangelicals: how is it that we are so different from our closest biological relative (the chimpanzee) when our DNA is so very similar? Even when using estimates that maximize the differences, our genomes are 95% identical. The conclusion, that I have discussed here in the past is that a dispersed set of numerous small changes can have large effects on the form and function of an organism. Of course, small changes are what evolution specializes in: tinkering here and there, one mutation at a time, as we have directly observed in laboratory experiments. Before we discuss how this pivotal new study was done, however, a brief review of how genes work is in order.

Review: gene structure and function

If you’ve been following the ongoing Understanding Evolution series here at BioLogos, you will recall that we discussed gene structure and function not long ago, in the context of discussing non-functional DNA sequences (so-called “junk DNA”):

Genes have a typical structure (obviously simplified here somewhat). First off, there is the actual DNA sequence that specifies the protein product sequence (the so-called “coding sequence”, shown in blue). This sequence is usually broken up into segments in mammalian genes, and these sequences are spliced together when the DNA sequence of the gene is transcribed into a “working copy” called mRNA – a short duplicate of the code that can be used by the cell’s machinery to actually build the specified protein.

In addition to the actual coding sequences, other sequences are needed to tell the cell when and where certain genes should be transcribed into mRNA. Every cell in an organism has the same genes in their chromosomes, but not all are transcribed. Using different genes in different combinations is what makes cells take on distinct roles – for example, cells in your small intestine need different genes (for absorption of nutrients) than do cells of the immune system (for fighting off pathogens). Regulatory sequences make sure any given cell type has the right genes transcribed and made into protein products. Some of these sequences are part of the mRNA transcript (shown in red), and others are not transcribed but only part of the chromosomal DNA sequence (such as the “promoter” region that directs the enzymes responsible for making the mRNA transcript (shown in blue).

With this background in mind, we can now extend our understanding slightly further. DNA in cells is “packaged up” when not in use by winding it around a class of proteins called histones. This packaging keeps the DNA in a compact form, and it is useful in helping cells prevent genes they don’t need from being transcribed. For any given chromosome - which is one long strand of DNA – some regions will be packed away (and the genes there not transcribed), while other regions are unpacked (less tightly associated with histones) with the genes there actively undergoing transcription. The open regions allow for transcription because enzymes and other proteins needed for the process can gain access to the DNA there.

Comparing gene transcription across species at the genomic level

Because of the overwhelming similarity between the human and chimpanzee genomes (and the even greater similarity when examining only their protein-coding regions) it has long been hypothesized that changes in “where and when” genes are transcribed will be a major player in what makes our two species different (in contrast to the idea that we are different because of the relatively tiny changes in the coding regions of our genes). From an evolutionary point of view, there are a few ways to explore how differences in gene transcription arise once species go their separate ways, such as when our ancestors parted ways with our last common ancestor with chimps around 4-6 million years ago. The main idea is to compare the same cell type in both species: human skin cells versus chimp skin cells, for example. Determining what specific genes are transcribed (or not) in human cells and comparing the results to chimpanzee cells gives us an idea of how gene transcription differences arose in the two lineages since they last shared a common ancestor. The challenge, up until now, is that there was no easy way to indentify the changes in regulatory DNA that led to those differences in transcription. The problem arises because of the overwhelming similarities between our genomes: changes in transcription due to changes in DNA sequence are hard to find simply by looking for sequence differences, since in most cases the differences will be very small. There are also many small differences between our genomes that have no effect on gene transcription, so we cannot simply look for any difference at all. What we need is a way to identify which small changes led to differences in gene transcription.

Old hypotheses, new technology

Back in 2008, a method for addressing this issue was devised. As we have seen, DNA undergoing transcription is “unpacked” and accessible to enzymes. Researchers have long known about a certain enzyme, called DNAse I, that can cut exposed DNA but leave histone-packaged DNA alone. This means that DNA from any given cell type can be cut using this enzyme specifically at “DNAse I hypersensitive sites” (DHS’s) where regulatory DNA is unpackaged and a nearby gene is being transcribed. While this technique is decades old, what is new is a way to then go on to sequence the DNA next to each of these sites. This requires what is known as “next-generation” or “deep” DNA sequencing methods that can use a linker sequence to attach to the DNAse I cut sites and then amplify and sequence individual DNA fragments attached to the linker. Since we have the entire genome sequence of humans and chimps it is then trivial to take the sequencing results and map them to either genome. The results are a detailed map of what chromosome regions are unpacked and regulating transcription in each cell type. These maps can then be compared with related species across entire genomes.

It was only a matter of time before these powerful methods were applied to the human-chimp question, and the first results became available last month. The research group was of course interested in differences between the two species, and the results are fascinating. The researchers looked at several different cell types, and found similar results in all cases. The results for any given gene fall into one of several categories when compared to the human-chimp (H-C) last common ancestor:

• No differences in regulatory DNA relative to the H-C last common ancestor (1259 genes)
• Gain of regulatory DNA in humans relative to the H-C last common ancestor (836 genes)
• Loss of regulatory DNA in humans relative to the H-C last common ancestor (286 genes)
• Gain of regulatory DNA in chimpanzees relative to the H-C last common ancestor (676 genes)
• Loss of regulatory DNA in chimpanzees relative to the last common ancestor (211 genes)

While it was not surprising to find a significant percentage of unchanged genes, it was interesting to note the large percentage of differences in regulatory DNA, despite the overwhelming genomic similarity between the two species. Small changes had a large impact on gene regulation. The researchers went on to examine the new regulatory regions they had identified, and found that they showed evidence of being under natural selection. These mutations had not only brought change, but provided an advantage to their hosts.

These results underscore a few important points:

• Species become different because differences accumulate in both lineages once a common ancestral population splits into two. The differences we see in modern species are due to changes both species have accumulated over time.
• Tweaking the regulation of numerous genes appears to be a widespread mechanism for generating evolutionary novelty. Both gaining and losing regulatory sequences is common.
• These gains or losses in regulatory DNA require only very small changes at the DNA sequence level, but they can have profound impacts on how genes are transcribed.
• These changes appear to be widespread in genomes, and able to accrue in short evolutionary timescales.
• Small changes are exactly the sort of thing that evolution is known to be able to accomplish easily, one mutation at a time.
• These small changes bear the marks of natural selection, indicating that they were selected for as they arose.
• Anyone who wishes to call these differences “insignificant” will have to contend with the observation that the biological differences we observe between humans and chimpanzees are significant.
• Small, incremental changes at the genomic level fit nicely with the fossil evidence for human evolution, which, though fragmentary, indicates gradual changes in skeletal morphology over the same timescale.

Of course, this study is just the beginning, and future studies are sure to examine and compare additional cell types found in humans and our evolutionary cousins. These results have already added to the troubles of antievolutionary groups that wish to portray the differences between us as too great for evolutionary mechanisms to bridge. I suspect these troubles will only worsen in the coming years as these new techniques come into their own.

For further reading:

Shibata Y, Sheffield NC, Fedrigo O, Babbitt CC, Wortham M, et al. (2012). Extensive Evolutionary Changes in Regulatory Element Activity during Human Origins Are Associated with Altered Gene Expression and Positive Selection. PLoS Genetics 8(6): e1002789. doi:10.1371/journal.pgen.1002789

http://www.plosgenetics.org/article/info%3Adoi%2F10.1371%2Fjournal.pgen.1002789

In the last post in this series, we introduced a paper by Chen and colleagues that sought to identify new genes in various Drosophila (fruit fly) species. The youngest (i.e. the most recently evolved) gene they found is one specific to Drosophila melanogaster, the species of fruit fly beloved by geneticists as a model organism. The gene is named “p24-2” (not the most imaginative name, but it serves its purpose) and the gene it is duplicated from is called “Éclair”. The Éclair gene is found in a number of Drosophila species. A simplified “family tree” of three Drosophila species (D. melanogaster, D. simulans and D. erecta) is shown below. The duplication event that generated the p24-2 gene happened within the lineage leading to D. melanogaster, but after D. melanogaster and D. simulans separated as distinct species:

Since the entire genomes of these species are now sequenced and available online, it is possible to look at the chromosome region where the Éclair gene is found in all three. By looking at this region in D. melanogaster, we see that the brand-new p24-2 gene is almost right next door to its “parent” gene, Éclair. Below is a screen shot taken when looking at this region using a Drosophila “genome browser” that is freely available online. The red arrow indicates the Éclair gene, and we can see p24-2 is just one gene over, and seems to be nested within another gene called “Unc-115b”. The green arrows are pointing to two different “versions” of how p24-2 is made into an mRNA working copy. The Unc-115b gene (blue arrow) has five different mRNA versions. (One of the p24-2 mRNA versions has a lot of Unc-115b sequence that is not used when the p24-2 protein is made).

(Click Image to Enlarge)

Finding a duplicated gene next door to the sequence it is copied from is pretty common in genomes – when chromosomes are copied or recombined during cell division, side-by-side copies of parts of chromosomes show up every now and then. It’s also not surprising to see a new gene cobbled together with another gene. In this case, Unc-115b and p24-2 are overlapping but separate functional entities: they each have their own protein sequences, but each includes the code of the other as a sequence that does not actually translate into protein. The details of how this “cobbling” happens aren’t important for this discussion, other than to note that the mechanisms are known and not rare. In the chart above, then, the orange sections indicate the active parts of the transcribed sequence, while the gray are sections that are included in the RNA molecule, but do not get used directly to code for the new protein.

When we look at this same chromosome region in D. simulans and D. erecta, however, p24-2 is missing. Éclair and Unc-115b are there, but p24-2 is not, since it arose after D. melanogaster separated from its common ancestors with the other species. (Note: this entire region is a mirror image in D. simulans and D. erecta when compared to D. melanogaster due to a large scale chromosome inversion that covers this whole area. So, while it looks “backwards” compared to the image above, that is not surprising, it’s expected):

(Click Image to Enlarge)

So, with the p24-2 gene in D. melanogaster, we have a bona-fide, recent gene duplication event. This gene is brand new, evolutionarily speaking (less than 3 million years old, given the calculated speciation times of D. melanogaster and D. simulans). Not only is it brand new, it is also essential for survival in D. melanogaster: if you remove it, the fly dies. Obviously, since every other Drosophila species lacks p24-2, this gene is not essential for survival for any other species. It’s new, and now it’s necessary.

Do new, essential genes refute the Intelligent Design (ID) argument from Irreducible Complexity (IC)?

So far, nothing we have discussed explicitly threatens the ID argument from IC, though it does threaten the ID argument that new information cannot arise through evolution, a topic we have discussed in detail before. Michael Behe, the main ID proponent of the argument from IC, has commented on this research by Chen and colleagues (thanks to commenter “Bilbo” for pointing this out). Behe’s rejoinder was to a blog post by biologist and atheist blogger Jerry Coyne, who used the paper by Chen and colleagues to attack Behe’s ideas. Since Behe’s reply deals with his understanding of how gene duplication relates to his argument from IC, I will quote it here at length:

I have never stated, nor do I think, that gene duplication and diversification cannot happen by Darwinian mechanisms, or that “they play almost no role at all” in the unfolding of life. (As a matter of fact, I discussed several examples of that in my 2007 book The Edge of Evolution. That would be silly — why would anyone with knowledge of basic biochemical mechanisms deny that, say, the two gamma-globin coding regions on human chromosome 11 resulted from the duplication of a single gamma-globin gene and then the alteration of a single codon? What I don’t think can happen is that duplication/ divergence by Darwinian mechanisms can build new, complex interactive molecular machines or pathways. Assuming (since he is in fact critiquing them) Professor Coyne has been attentive to my arguments, one background assumption that he may have left unexpressed is that he thinks the newer duplicated genes discovered by Professor Long’s excellent work represent such complex entities, or parts of them.

There is no reason to think so. A gene can duplicate and diversify without building a new machine or network, or even changing function much. The above example of the two gamma-globin genes shows that duplication does not necessarily result in change in function. The examples of delta- and epsilon-globin, which, like gamma-globin, presumably also resulted from the duplication of an ancestral beta-like globin gene, show that sequence can diversify further, but function remain very similar. Even myoglobin, which shares rather little sequence homology with the other globins, has not diverged much in biochemical function.

In his recent work Professor Long discovered that many of the new genes were essential for the viability of the organism — without the gene product, the fruitflies would die before maturity. Perhaps Professor Coyne thinks that that means the genes necessarily are parts of complex systems, or at least do something fundamentally new. Again, however, there is no reason to think so. The notion of “essential” genes is at best ambiguous. We know of examples of proteins that surely appear necessary, but whose genes are dispensable. The classic example is myoglobin. It is also easy to conceive of a simple route to an “essential” duplicate gene that does little new. Suppose, for example, that some gene was duplicated. Although the duplication caused the organism to express more of the protein than was optimum, subsequent mutations in the promoter or protein sequence of one or both of the copies decreased the total activity of the protein to pre-duplication levels. Now, however, if one of the copies is deleted, there is not enough residual protein activity for the organism to survive. The new copy is now “essential”, although it does nothing that the original did not do.

The main points of Behe’s reply can be summarized as follows:

1. Gene duplications and subsequent changes to the copies (diversification) can and do happen, but the results are nothing really “new”— no new molecular machines or pathways (nor parts of such pathways), nor much in the way of new functions.
2. Duplicated genes can become essential simply by “sharing” the original function, and then reducing their share to a minimum, perhaps through the amount of protein that each copy makes. Again, this is not anything really new, since the copy doesn’t do anything that the original didn’t do already. So, the finding that some gene copies are essential genes is not a threat to the IC argument.

Note that Behe’s reply makes predictions that can be tested with further research. These predictions might be summarized in this way:

1. If IC is correct, duplicated genes will not be part of new, complex molecular pathways or machines.
2. If IC is correct, duplicated genes that are both essential should “share” the original function.

Testing IC with new research

Behe’s reply to the Chen paper is of course hypothetical and speculative – as demonstrated by his own comment that “there is no reason to think” that the duplicated genes are components of new complex pathways or systems. Accordingly, the validity of Behe’s reply depends on its ability to hold up over time as more work is done. Of note, the functions of p24-2 and its parent gene Éclair have been studied intensively since 2010. These studies, as we shall see in the next post in this series, shed quite a bit of light on these questions.

For further reading:

Behe, M.J. Darwin’s Black Box: the Biochemical Challenge to Evolution. Free Press, New York, 1996.

Behe, M.J. The Edge of Evolution: the Search for the Limits of Darwinism. Free Press, New York, 2007.

Chen, S., Zhang, Y, and Long, M (2010). New genes in Drosophila quickly become essential. Science 330; 1682-1685.

In the previous post in this series, we explored how evolution can force science into making predictions that seem counter-intuitive. For cetacean (whale) evolution, we saw that the preliminary lines of evidence (the fact that whales are vertebrates, and mammals, for instance) pointed to the prediction that modern whales are descended from four-limbed, land-dwelling ancestors. As we then noted:

Instantly this prediction raises a host of uncomfortable questions: where did their hind limbs go? How did they acquire a blowhole on the top of their heads when other mammals have two nostrils on the front of their faces? How did they transition to giving birth in the water? What happened to the teeth of the baleen whales? What happened to the hair characteristic of mammals? and so on. In some ways, evolutionary thinking about whales creates more difficulties than it appears to solve.

And yet, these difficulties are the stuff of science. If indeed our “educated guess” of terrestrial, tetrapod ancestry for whales is correct, the evidence will show that these transitions, challenging though they may seem, did indeed occur on the road to becoming “truly cetacean”.

We have already discussed hind limb and hair loss in whales, citing evidence from embryonic development in modern whales that shows how hair and hind limbs develop early in their embryogenesis, but then are lost at later stages. We now turn to one of the remaining questions: tooth loss in the lineage leading to modern toothless whales (order Mysticeti). To obtain their food these whales pass seawater through a baleen, a large sieve-like structure that filters out plankton, small fish and other food items. Some recent genetics sleuthing has investigated a portion of this riddle, and adds further details to the story of how the baleen whales came to be.

Evolution: A Theory with Bite

If indeed modern whales are descended from ancestral, four-limbed, terrestrial ancestors, then those ancestors, like mammals in general, had teeth. Modern toothed whales (order Odontoceti) have retained those teeth to the present day, but baleen whales have adopted a new way of life as filter-feeders. Researchers were curious to see if traces of a “toothed past” could be found in the genomes of modern baleen whales, so they went hunting for remnants of genes devoted to making teeth. Such defective gene remnants would be examples of pseudogenes, and we have discussed pseudogenes previously in this series. While pseudogenes in and of themselves are powerful evidence for evolution, pseudogenes that are “out of place” are especially so. One such example we have seen before is the human vitellogenin pseudogene, the remains of a gene used for yolk production in egg-laying organisms found in the exact location in the genome that evolution would predict for it. As mammals that receive embryonic nourishment through a placenta, we have no need of egg-yolk genes. Similarly, baleen whales have no need for genes responsible for making teeth, and finding the remnants of such genes would make a strong case for an evolutionary origin of baleen whales as the modified descendents of toothed whale ancestors.

Independent Lines of Evidence, but Contradictory Stories?

Some of the genes known to be used in all mammals for tooth formation were the obvious candidate genes to start with: the products of the ameloblastin, amelogenin, and enamelin genes are all used in the formation of tooth enamel, the hardest structure in the vertebrate skeleton. Researchers went looking for these genes in several Mysticete (i.e. toothless whale) species. The results showed that all the species studied did indeed have these three genes present as pseudogenes (and more specifically, as unitary pseudogenes, a special class of pseudogene we have discussed in detail previously). Finding these genes as pseudogenes in toothless whales was exactly what evolution predicted, but there was a catch: none of the mutations that removed the functions of these three genes were shared between different species, suggesting that these genes lost their function independently in the species studied. This finding was at odds with data from the fossil record, which suggested that teeth were lost only once, and early in the lineage leading to all modern toothless whales. So, the researchers seemed to have two lines of evidence that at face value contradicted each other. The fossil record suggested that tooth loss occurred once in the common ancestor of all toothless whales, but these three genes seemed to have been inactivated independently, several times over, suggesting that loss of teeth should be happening later in Mysticete evolution, and more than once.

One proposed explanation for the apparent discrepancy (among several put forward) was to predict that a fourth gene required for enamel formation was lost early in Mysticete evolution. The loss of any one gene necessary for forming enamel would be enough to prevent the process altogether. In this case, the loss of this fourth gene would prevent tooth enamel from forming, even though the genetic sequences of the other three enamel genes would still be intact. Once enamel function was lost, random mutations in the remaining enamel genes could then accumulate later in Mysticete evolution after speciation in this group was already underway. To test this hypothesis, the research group went hunting for other enamel genes in toothless whales.

Signature in the SINE

The smoking gun for tooth loss in Mysticetes turned out to be exactly what was predicted: a fourth gene, necessary for enamel production, and mutated with the same inactivating mutation in all modern toothless whales. The gene in question, named enamelysin, was destroyed when a mobile genetic element called a SINE transposon inserted into it, breaking it into two halves and removing its function:

The fact that the same SINE insertion mutation at an identical location is found in all modern Mysticete species indicates that this mutation happened once in a common ancestor and then was inherited by the entire group. Since this must have occurred early in the evolution of toothless whales in order to happen in the common ancestor of the entire group, the picture from the genetics and the fossil record match. Once again, findings in one discipline (in this case, paleontology) can be used to make very detailed predictions about what another, unrelated discipline (comparative genomics) should reveal. These results are also entirely consistent with the observation, made in the 1920s, that toothless whales form tooth buds during embryogenesis that are later reabsorbed prior to the point when the deposition of enamel would begin. As with the hind limb story in whale evolution, lines of evidence from genetics, paleontology and embryology converge to support the hypothesis that modern toothless whales descend, through modification, from toothed ancestors.

In the next post in this series, we’ll examine a few more lines of evidence for whale evolution, and extend our discussion to converging lines of evidence for the evolution of our own species.

For further reading:

Meredith, R.W., Gatesy, J., Cjeng, J., and Springer, M.S. (2011). Pseudogenization of the tooth gene enamelysin (MMP20) in the common ancestor of extant baleen whales. Proceedings of the Royal Society B: 278 (1708); 993 – 1002. Available online: http://rspb.royalsocietypublishing.org/content/early/2010/09/16/rspb.2010.1280.full.pdf

Ridewood, W.G. (1923). Observations on the skull in foetal specimens of whales of the genera Megaptera and Balaenoptera. Philosophical Transactions of the Royal Society of London B: 211; 209 - 272. Available online: http://rstb.royalsocietypublishing.org/content/211/382-390/209.full.pdf

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Today's video is courtesy of filmmaker Ryan Pettey, director/editor of Satellite Pictures, and features Dr. Rick Colling, biologist and author of Random Designer.

In today’s video, Dr. Rick Colling states that one of the biggest difficulties in communicating compatibility between evolution and faith is a misunderstanding of what evolution is. Evolution is not, he says, about the imposition of death and destruction and survival of the fittest. Rather, it is about second chances. Our bodies contain thousands of genes, which duplicate like a computer back-up copy and can serve as raw material. When an organism encounters adverse environmental condition, this raw material can be used to help adapt and survive.

“God is so creative," says Colling, "that he’s actually put into place a mechanism to start doing these gene changes in advance before they’re even needed. And God has given us a second change through the evolutionary process of creating duplicate genes that give rise to new raw material that give rise to new possibilities, and that really more accurately describes the process of evolution. It’s redemption, it’s possibility, and it’s hope.”

Do genomes have non-functional sequences?

There are various ways to test the hypothesis that certain regions of DNA are non-functional, and in this series we will explore some of them. One way to estimate the fraction of non-functional DNA in a particular genome is to determine which portions of the genome can be freely altered by mutation without consequence to the organism. DNA sequences that cannot be mutated freely without a loss in function are said to be under purifying selection: as mutated forms of this sequence arise in a population, the loss of function associated with the mutated sequence reduces the likelihood that the organism will pass this mutation on to future generations. This type of mutation, in a functional sequence, has deleterious consequences. Another way to put it is that functional sequences are subject to natural selection, which acts as a filter to “purify” the genome at a particular location, but that non-functional sequences are free from the constraints of selection, and “anything goes” with respect to mutation.

Tell us again, Grandpa!

One way to think about this is to consider a humorous story that is told within an extended family (I think every family has these types of stories – I know my kids love to hear certain ones told and retold again). Certain incidental details of the story can be altered from telling to telling, and perhaps Uncle Joe tells it a certain way but Uncle Jeff tells it another with respect to those types of details. There are, however, certain features of the story that are absolutely non-negotiable, or the story doesn’t “work” (and telling these parts incorrectly will generate protests and corrections from the kids who know how the story goes and insist that you are not telling it correctly). These types of stories, like genomes, have some bits that can freely change and others that can’t. The bits that can’t change are under constraint and, in biological terms, subject to selection. The same factors apply in more concise form to jokes: some bits can change (and do, as the joke is told and retold) – but some bits cannot (for example, the punch line).

The best way to test for purifying selection is to compare the genomes of related organisms that have been separate species for some time. (To continue our analogy, you could determine what parts of the story are really important by comparing how each of the uncles tells it and listing out the parts that are the same in all the various versions). The genomes in the two species are modified versions of the same genome present in the common ancestor species: they started as virtually identical but have since experienced mutations in different locations over time. Mutations in functional sequences will have been subject to purifying selection to remove loss-of-function mutations, whereas mutations will have freely accumulated in non-functional sequences. The two genomes are thus a collection of similarities and differences, as we have discussed before:

In some ways, comparing the DNA sequence between related organisms is like reading alternative history novels. The hypothesis of common ancestry between similar organisms makes a very straightforward prediction about their genomes: it simply predicts that they were once the same genome, in the same ancestral species. This hypothesis also predicts that these two genomes, having gone their separate ways in the diverged species, will have accumulated changes once they separated. Like an alternative history, each genome has the same backstory, and then a history independent from the other after the point of separation.

These similarities and differences, however, will not be randomly distributed. Sequences subject to purifying selection will have fewer differences than sequences that can freely mutate. Accordingly, when compared side-by-side, the two genomes should have regions where differences are common, and where differences are rare. For example, consider a genome segment in two related species where there is one gene present. This gene has some regions that cannot be changed without significant consequences (the DNA letters that code for the amino acid sequence of the gene product, for example) and some regions that can be mutated without consequence (such as some sequences inside introns, the non-coding segments that separate gene coding segments and are spliced out of the final gene product):

What biologists observe when comparing sequences like this between two related organisms is that coding sequences, which obviously are required for the gene’s function, have far fewer differences between them than do sequences found in introns or in between genes. The idea is not that mutations are preferentially happening in those areas, but that mutations can occur everywhere in the genome, but are more likely to be selected out of populations if they alter functional sequences.

The expanding data set

This type of analysis gets easier to do the longer two species have been separated, and the more species one has to compare to each other. Very recently separated species will have a very high degree of genetic similarity simply because neither species has had appreciable mutations to a common ancestral genome. As such it is difficult to pick out the sequences that have been subject to selection, since functional and non-functional sequences are both still highly similar (virtually identical). It is only as species have been separated for a long time that a pattern begins to emerge: sequences that are functional remain “constrained” by purifying selection to remain more similar, and non-functional sequences accumulate mutations in the separate lineages that make them less and less alike.

Now that biologists have access to a wide range of mammalian genomes, this type of analysis has been done on the human genome with ever-increasing precision. Early studies comparing the human genome to other genomes, such as the mouse genome (compared in 2002) and dog genome (2005), suggested that only a small fraction of the human genome was subject to purifying selection (about 5%). Recent work published a few months ago has taken this approach to a whole new level: a genome-wide comparison of 29 mammalian species (!). These results are exciting from a biological perspective because this work helps scientists tease out what bits of the human genome are under selection, and what bits aren’t (which isn’t always obvious, because we don’t always know what sequences are functional or non-functional). This type of approach is non-biased: it requires no prior hypotheses of what types of sequences to look for, but rather simply looks for what has been selected to remain more similar over time. The results, based on the (very nearly) whole-genome sequences of 29 placental mammals, are in keeping with previous estimates: about 5-6% of the human genome is under purifying selection, and the rest appears to be rather free to accumulate changes. As a species, our genome seems to be about 95% incidental details and 5% punch line.

So, what sorts of things lurk out there in the “other” 95%? In the next post in this series, we’ll head out into the wilds of the human genome and have a look.

Editors Note: So now that you've read the essay, see if you can surmise the meaning of the figure at the top. This is a tiny stretch of DNA, 21 bases (units of code) long. Why do you think position #4 shows only an A and position #5 shows only a G, whereas other positions are not restricted in this manner? Pretend that you could represent the genome as a whole in this manner. Of the 3 billion bases in our genome, how many of them would be configured like position #4 or #5? What about the rest? Is the specific base (unit of code) functionally important for that set? Upon what, do you base your conclusions.? Finally do the presuppositions of the Intelligent Design Movement and Reasons to Believe pivot on how to interpret this data? How would such proponents interpret the data differently than mainstream biologists? Feel free to address these questions in the comment section or, if you prefer, just reflect on them.

For further reading:

Lindblad-Toh, K., et al. (2011). A high-resolution map of human evolutionary constraint using 29 mammals. Nature 478 (27), 476-482.
http://www.nature.com/nature/journal/v478/n7370/full/nature10530.html

I’d like to suggest that this argument is in significant ways misplaced. The participants in this debate all seem to agree that what makes us “human” can be defined by genes and population studies. There is a pressing need for them to conform theology to population genetics, or to conform population genetics to theology, because the story of our genes is implicitly equated with the story of what it means to be “human.” The hypothesis that there was a “first human” – a capital-A “Adam” – can be tested in our genes.

But “genes” do not make us “human.” What makes us “human” is the irreducible phenomena of all of our material and immaterial being as persons.

Nothing we observe in the universe is flat. By “flat” I mean having only one aspect or “layer.” Consider, for example, an apple. What is it? Is it the fruit of an apple tree? The seed-carrier – the potentiality – of new apple trees? Beautiful and delicious? Skin, flesh, and core? Water and organic molecules? Caloric energy and roughage? Hydrogen, oxygen, and carbon? Physical laws? All of these things comprise some of what we mean by “apple,” but none of them are what an “apple” is. The reality that is “apple” cannot be reduced to any one of its aspects or layers.

It is possible to think of these aspects or layers hierarchically, with “higher” layers that emerge from “lower” ones. Physical laws emerge from quantum probabilities; molecules emerge from physical laws; seeds, skin, flesh and core emerge from complex arrangements of molecules; beauty and delight emerge from the connection of skin, flesh and core to human sense perception;¹ “apple” emerges from all of this (and more) combined with the human cultural experience of this thing we call “apple.”

Notice that some “layers” can impinge or “supervene” on lower ones – for example, human sense perception and cultural experience do something to this thing confronting the subject in order for it to become “apple.” But notice also that “apple” is not merely a cultural construction. The word or signifier “apple,” of course, could be arbitrary, but there is an objective reality to the thing signified. The layer of human sense perception and cultural experience supervenes upon, but does not create, the lower-order reality from which it emerges.

Sociologist Christian Smith draws these strands together in a critical realist framework in his excellent book What Is a Person?: Rethinking Humanity, Social Life, and the Moral Good from the Person Up. In a critically realist approach to culture and human personhood, Smith suggests, “[h]uman beings do have an identifiable nature that is rooted in the natural world, although the character of human nature is such that it gives rise to capacities to construct variable meanings and identities….” Culture is a social construction, but it is not merely a social construction. Human beings are social, but they are not subsumed by the social. The reality we inhabit is “stratified”: it includes both the reality of individual conscious human agents and the reality of the social structures that emerge from the cultures created by those agents. These “personal” and “cultural” layers of the world interact with each other dynamically, each continually informing and changing the other.

Smith’s approach is helpful, but perhaps it does not go far enough. For Smith, as for critical realists in general, the phenomena of human culture remain subject to some degree of granular disaggregation, at least analytically. A phenomenological approach suggests that no “thing” can be broken into components and still comprise that “thing” – the genes that encode for apple trees are not apple seeds, apple seeds are not apple trees, and apple trees are not apples. The critical realist framework of stratification, emergence, and supervenience functions as a very useful heuristic device, but to describe what an apple is, we must approach the phenomenon of “apple” in its fullness. To know whether something falls into the kind “apple,” we must hold an ideal of everything an apple is, and compare the subject to the ideal.

And because of the transcendence of the ideal concept of “apple,” we can begin to speak of the relative excellence of particular instantiations of apples. What is an “excellent” apple? What distinguishes the excellent apple from a poor one? We can only ask such questions if “apple” means something more than the particular physical specimen in hand, whether firm, sweet and tart, or bruised and sour.

The same is true of human “persons.” We can say almost nothing about a “person” merely by observing genes, because genes are not “persons.” Populations genetics studies can provide models of the dispersion of genes through groups of biological entities, but they can tell us nothing whatsoever about when the first “human person” emerged. Indeed, for population genetics qua population genetics, there simply are no “persons” – for this is a science of the movement of genes, not a philosophical, sociological, or theological description of “persons.”

So what of “Adam?” It is often suggested that in Romans 5:12 Adam is a type of Christ. But, in fact, in Paul’s thought, as well as for the early Church Fathers, Christ is the type, the typos, a notion derived from the “stamp” or “seal” on an official document. There is a hint in Romans 5 of a truth that would only become clarified later in Christian theology – that the pre-incarnate Christ, the second person of the Trinity, always was. Whereas Arius declared that “there was a time when he [Christ] was not,” Nicea established the orthodox Christology of Christ’s eternal sonship. Thus Christ is and was the Redeemer, the one for whom creation was made and in whose death and resurrection creation always finds its fulfillment. Adam’s failure was that he went against type – he did not conform to Christ but rather tried to become something else, and thereby the true nature of humanity was broken.

Is the typos of Christ reducible to a set of genes? Surely not. It resides not in genes or in any other created thing but rather in the Triune life of God Himself. We might speak, in a roughly analogical way, of ideas we hold in our minds – say, the idea of a perfect Bordeaux, ruby-red, silky, smoky, plummy, luxurious. We could labor to instantiate that idea, combining genes and terroir and water and light and care, and perhaps we might achieve it, to the point where upon taking a sip we exclaim, “this – this – is Bordeaux. Nothing else is worthy of that name.”

This is what God said of Adam, when he gave him breath and a name. It is not something that God said of any other creature, even apparently some creatures that a modern population geneticist or paleoanthropologist might designate as ancestrally human based on genes or bones. Yet that Adam, and each of us in that Adam, fail to participate fully and unreservedly in the true nature of the true human, the nature of Christ. And so Pontius Pilot, an unwitting prophet, said of Christ: “behold, the man” (John 19:5, KJV). And so also Paul invites us to see: the sinful man, the broken seal, the first created Adam; and the true type, the seal of humanity’s future, the perfect Adam, the Christ. None of this is about the definitions and categories of modern science, as helpful and important as they may be for the progress of scientific thought. It is, rather, about the fullness of what it means to be human.

Notes

1. Human sense perception, of course, is an emergent property of an even more complex set of relations that give rise to the human “person.”