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.

Antibody fine-tuning

At this moment, millions of B cells are patrolling my spleen and lymph nodes, each sporting a different antibody on its surface. If a foreign molecule from the cold virus happens to stick to an antibody on a particular B cell, the cell can get “activated.”

Pathogens are like cockroaches. If you see one roach, you can bet there are many more lurking under cupboards and between walls. Just as one shoe won’t kill them all, one B cell can’t make enough antibodies to deal with an infection. Activation causes the B cell to reproduce, creating more and more B cells that can produce the same kind of antibody.

As is typical during cell division, most of the DNA in dividing B cells is copied with extremely high accuracy. But in the gene segments coding for the variable region of the antibody, mutations accumulate about a million times more often than normal. Why would this be? Isn’t the point of B cell replication to make more identical antibodies?

Almost. It turns out that these frequent random mutations contribute to optimize the antibody. A shopping story helps to illustrate. I was recently at the mall and found a fabulous pair of shoes on sale. Sadly they were out of my size, but it was such a good sale that I decided to buy the half-size down, figuring the shoes might stretch out a little and grow more comfortable with time. Bad idea! That great bargain turned out to be pretty expensive when I got blisters and never wore the shoes again. Clearly this was not an optimized choice.

Just because you can get your foot into a shoe does not mean it fits. Likewise, just because an antibody binds to an antigen does not mean the two are perfectly complementary. Descendents of the activated B cell have a mechanism to induce mutations so each one can make a slightly different version of the antibody. If one of the resulting B cells makes a better-fitting antibody than its kin, it will have a selective advantage and proliferate. The other cells will not become activated as often and will end up dying by apoptosis, a kind of cellular suicide. This mechanism of mutation and selection, called affinity maturation, produces a highly specific, strong interaction between the antigen and the antibody.

Antibody production and evolution both involve mutation and selection

I believe God is sovereign over all of creation, but I don’t imagine he is presently curing my cold by directly controlling the specific gene rearrangements and optimizing mutations in each of the millions of B cells in my body. Could he do so? Of course! But if that were the case, why bother making billions of antibodies in the first place? The evidence suggests that God has chosen to work through a random process, one which involves the routine creation and destruction of millions of cells that never get used. This is the ordinary means by which God maintains our health. The miracles of healing recorded in the Bible are miraculous precisely because they don’t occur by this normal, natural process.

In my last post, I stated that the generation of antibody diversity is an example in which God uses a “blind” system to sustain and preserve life. I then suggested a link to evolution by asking, “If God uses natural mechanisms that work over short time scales (less than a week) to evolve life-giving solutions to disease, could he also use a similarly elegant approach to create life over long periods of time?”

Some may argue that a small-scale process like antibody production isn’t comparable to the processes of mutation and natural selection that are supposed to have caused macro-evolution. Intelligent Design proponent Michael Behe, for example, accepts that all creatures (including humans) have a common ancestor, but he believes random mutations are not powerful enough to have brought about the diversity of life we see today. He argues that there is an “edge” of evolution: mutation can bring about drug resistance and other small-scale adaptations, but beyond a certain point it can’t really produce anything new.

Clearly, antibody production creates something new: the random recombining of whole gene segments generates highly specific, never-before-seen protein functionality within just a few days. The body can respond to any foreign entity, simply by sorting through billions of ready-made possibilities. Furthermore, a pretty-good solution can be made even better by generating many variations on a theme and sorting through these for the optimal antibody.

Evolution works by the same kinds of mechanisms, except the mutations occur in germ cells (which give rise to egg and sperm) rather than in B cells, and the sorting (selection) process occurs at the population level rather than the cellular level.

Though often neutral or destructive, mutations sometimes create new functionality

Most people are familiar with point mutations, in which a single DNA “letter,” or base, gets changed. However, mutations come in several other varieties. Short sequences of DNA can be inserted or deleted at random. Chunks of DNA can get cut out and inserted in the opposite direction. Individual genes or even whole chromosomes can get lost or duplicated. In rare cases, the entire genome can get duplicated!

The effect of a mutation principally depends on where it occurs, not on the size of the DNA segment affected. A large deletion occurring within a long stretch between two genes may do nothing at all. On the other hand, a single point mutation within a critical gene may cause a devastating disease. There is also a third possibility though: new functionality may emerge as a result of a mutation.

Let’s consider the protein hemoglobin, for example, which binds oxygen and transports it throughout the body in the blood. Hemoglobin is made from two pairs each of two amino acid chains, called α and β (blue and red in the figure at right). The corresponding genes that code for α and β have similar sequences to each other, and are believed to have arisen when an ancestral globin gene (still present in marine worms, insects, and some fish) duplicated and slowly changed over time. While the ancestral form can bind oxygen just fine, the four chains of hemoglobin cooperate to do so even better.

Both the α and β genes have undergone further duplications followed by smaller mutations. As expected, many of the resulting genes have become irreparably damaged by mutations, but they continue to exist in the genome as inert DNA “fossils.” Others, however, remain active and now perform specialized functions. For instance, one set of β genes binds more tightly to oxygen than the others; it becomes active only during development to ensure that the fetus gets enough oxygen from the mother’s bloodstream. A few months after birth, fetal hemoglobin turns off and the adult form turns on.

To summarize, mutations come in many forms (e.g. rearrangements, insertions, deletions, duplications) and can lead to good, bad, or neutral effects within an individual. B cells depend on random mutations to produce novel antibodies. A few are productive, but the vast majority of B cells die unused. Yet the entire process works for our good! In the same way, mutations in germ cells can lead to no effect, disease, or new and better solutions, as we saw in the hemoglobin example. These are the ordinary (but masterful!) means by which God creates and sustains life.

Editor's Note: For more on the evolution of the immune system, read Randy's Isaac's post "Complex Specified Information Without an Intelligent Source" at the ASA website.

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.

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.

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.

My valiant helper, a small-sized tiger
Sleeps sweetly on my desk, by the computer,
Unaware that you insult his tribe.

Cats play with a mouse or
with a half-dead mole.
You are wrong, though: it’s not out of cruelty.
They simply like a thing that moves.

For, after all, we know that only consciousness
Can for a moment move into the Other,
Empathize with the pain and panic of a mouse.

And such as cats are, all of Nature is.
Indifferent, alas, to the good and the evil.
Quite a problem for us, I am afraid.

Natural history has its museums,
But why should our children learn about monsters,
An earth of snakes and reptiles for millions of years?

Nature devouring, nature devoured,
Butchery day and night smoking with blood.

And who created it? Was it the good Lord?

Yes, undoubtedly, they are innocent,
Spiders, mantises, sharks, pythons.

We are the only ones who say: cruelty.

Our consciousness and our conscience
Alone in the pale anthill of galaxies
Put their hope in a humane God.

Who cannot but feel and think,

Who is kindred to us by his warmth and movement,

For we are, as he told us, similar to Him.

Yet if it is so, then He takes pity
On every mauled mouse, every wounded bird.
Then the universe for him is like a Crucifixion.

Such is the outcome of your attack on the cat:
A theological, Augustinian grimace,
Which makes difficult our walking on this earth.

–Czeslaw Milosz,¹
 translated by the author and Robert Hass

The Problem

The poem above communicates in a very poignant and profound way the essence of the theological problem of death, pain, and suffering in the natural world—what has been referred to as “natural evil.” As we will see, it may also point to at least one aspect of a Christian response.

I have become convinced that one of the fundamental issues underlying much of the resistance of many Christians to an ancient, evolving creation is that of the problem of “natural evil.” “Natural evil” is also very often a primary focus of those who reject a personal and compassionate God, as it was for Darwin himself. The issue of theodicy thus seems not only to drive many people of Christian faith away from an acceptance of the conclusions of modern science, but also to drive members of the scientific community away from a serious consideration of the claims of the Christian faith. The topic is important, then not because its solution is central to the validity of the Christian faith, but because it often serves as an unnecessary stumbling block to a productive engagement of both science and faith.

The tension generated by our understanding of God’s character, as revealed in the Bible, and by the reality of the natural world around us has been the focus of much theological and philosophical debate within the Christian church since the first century. This article sets out to examine critically several of the proposed solutions to this problem, viewing them from the perspective of a geologist, paleontologist, and orthodox evangelical Christian.

The theological problem of death and pain emerges from the following propositional statements:

1. Scripture consistently declares the absolute goodness of God and the very goodness of his creation. Furthermore, Scripture declares God’s love and care for creation, and the glory and praise it returns to him.
2. Scripture also confesses a transcendent God who is omnipotent in power, yet immanent in creation as well. God’s creative activity is not described as being confined to some past event at the beginning of time, but as a present and continuing reality. God upholds creation in its being from moment to moment, and is creatively active in its history. This understanding of God’s relationship to creation has been well articulated by Jürgen Moltmann.²
3. In seeming conflict with these confessions of God’s character, we observe death, pain, and suffering as ubiquitous, even integral, aspects of the creation around us.

The apparent conflict between God’s goodness and the presence of pain and suffering is made especially acute when we consider the nonhuman creation.³ How can we accommodate the death and suffering of animals within a theology that declares both God’s omnipotence and goodness? C. S. Lewis forcefully puts the issue before us in his book The Problem of Pain:

The problem of animal suffering is appalling; not because the animals are so numerous ... but because the Christian explanation of human pain cannot be extended to animal pain. So far as we know beasts are incapable either of sin or virtue: therefore they can neither deserve pain nor be improved by it.⁴

Because the issue of animal pain so directly impacts our understanding of the goodness of creation, I will focus particularly on solutions to the problem as posed by Lewis.

How do we then reconcile the goodness of God who is immanent and active in his creation with the death, pain, and suffering we see embedded within it? There seem to be two basic alternative approaches to this dilemma.⁵

1. Natural evil can be attributed to something independent of God and acting against his will. This position threatens to limit God’s power and freedom.
2. Natural evil can be considered a part of God’s good purpose for creation, and either directly willed or permitted by him. Such a view would seem to bring into question God’s goodness and love for his creatures.

The tension between these alternatives—and efforts to avoid their negative theological consequences—surface in many of the proposed solutions to this problem.

In part 2, we start to look at some of the proposed solutions, beginning with the idea that a perfect creation was corrupted by a fall.

Notes

1. This poem was included in a collection of poems that was one of two works by Czeslaw Milosz mentioned in a review article by Michael Ignatieff, “The Art of Witness,” New York Review of Books (March 23, 1995). I thank Carol Regehr for bringing my attention to this work.
2. Moltmann refers to this aspect of God’s creative activity in history as “continuous creation.” Jürgen Moltmann, God in Creation (Minneapolis, MN: Fortress Press, 1993), 206–14.
3. I will not address here arguments concerning the degree to which animals experience pain. This issue is considered by Robert Wennberg in “Animal Suffering and the Problem of Evil,” Christian Scholar’s Review 21 (1991): 120–40. It is obvious to me that, for many animals at least, pain and suffering are a very real conscious experience.
4. C. S. Lewis, The Problem of Pain (New York: Macmillan Publishing, 1962), 129.
5. As stated by John Hick, in Evil and the God of Love, rev. ed. (New York: HarperCollins Publishers, 1977): “For every position that maintains the perfect goodness of God is bound either to let go the absolute divine power and freedom, or else to hold that evil exists ultimately within God’s good purpose” (pp. 149–50).

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.

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.

In his essay for that series, Jeff Schloss addressed the question of whether animal death is a natural evil, but also noted that such theological considerations aside, death does not actually “drive evolution” in the way most people imagine—especially when they think of violence in the natural world. This more complicated sense of death’s role is partially the result of modern evolutionary science recognizing the importance of cooperation and inter-relation among species, rather than just direct competition. But just as important is the knowledge that evolution is significantly shaped not by the deaths of individual creatures, but by extinction, the loss of species over time. In this post, we explore some aspects of how extinction acts as both a destructive and creative force in evolutionary history, including the evolutionary history of mammals.

Sporadic extinction

Extinction is actually a common feature of life on earth when viewed over long (e.g. geological) timescales. By some estimates, over 99% of the species that have ever lived have gone extinct. One factor that promotes extinction is the fact that evolution does not produce species that are optimally adapted to their environment, but only better adapted than their local competitors. Invasive species testify to this fact: local (endemic) species are not always the best-adapted species for their own environment. Examples abound where species from other environments are actually better-suited to out-compete endemic species. Here in my own province, the invasive Himilayan blackberry (Rubis discolor) easily outcompetes many endemic species. If endemic species were optimally adapted to their environment, this would not be possible, as they would outcompete all exotic species. Instead, exotic species, by chance, might be better adapted to an ecosystem they did not evolve in. These exotics may be capable of eliminating endemic species altogether.

Such an extinction event (of a single species, or perhaps a handful of species) alters the environment of other remaining species in an ecosystem. This, in turn, may influence the ability of some of these remaining species to reproduce compared to other species. For example, the extinction of a competitor might allow a species to increase in population size. Conversely, the extinction of a species that provides a benefit (such as a pollinator) may reduce a species in number. As the ecosystem landscape shifts due to loss of species, new biological opportunities, or niches, might arise. These new niches are then available to support new species to fill them.

Extinction, en masse

One way to appreciate how extinction opens up new niches is to examine mass extinction events – geologically brief periods where large numbers of species go extinct at the same time. Over the history of life on our planet there have been several mass extinction events. The largest such event, at the end of the Permian (~250 million years ago) appears to have been caused, at least in part, by intense volcanic activity over several hundred thousand years. This activity likely shifted CO2 levels and eventually led to a “runaway” greenhouse effect that dramatically raised global temperatures and led to anoxic (i.e. oxygen-depleted) oceans, though the exact contributions of these varied factors remains an area of scientific debate. What appears certain is that during this period environmental changes were too rapid for most species to keep evolutionary pace with, and as a result over 90% of the world’s species alive at that time went extinct. Obviously this represents destruction of biodiversity on an unimaginable scale, and the destructive effects of this event are with us to this day.

Speciation, en masse

This destruction, however, is not the whole story. Following on from the Permian mass extinction, we observe a steady increase in new species. These are species previously unknown in the fossil record. In fact, this pattern (a “radiation” of new species following an extinction event) is the rule, not an exception – we see the same effect after every mass extinction in the fossil record. Extinction is a driving force for novelty.

Perhaps the most famous mass extinction event is the Cretaceous – Paleogene (KPg) extinction, and it too follows this standard pattern. This mass extinction took place 65 million years ago when an asteroid ~10 kilometers in diameter struck the Yucatan peninsula. (Note: this event was formerly known as the Cretaceous – Tertiary (K-T) extinction, but that terminology is in decline within the scientific community). This extinction event is famous since it is the one that eliminated the dinosaurs (with the exception of the ancestors of modern birds). As with the Permian extinction, the elimination of so many species shifted the evolutionary landscape for the remaining species, and the result was a burst of speciation that appears rapid when viewed in geological time. Significantly for our own species, following the KPg extinction event is a burst in mammalian speciation, as small mammals that survived the event diverge and fill niches left empty by the dinosaurs. Without this event, the trajectory of mammalian evolution would certainly look very different.

Clearing the deck, and re-filling the niches

One interesting fact to note is that biological features that make a species resistant to usual, sporadic extinction are not necessarily the same features that will be useful during a mass extinction event. While species are continually under selection at the local level, there is no mechanism for (pre) selection to survive a mass extinction. As such, only species that happen to have the right combination of traits will survive, and often spread widely after a mass extinction. These so-called “disaster species” are usually generalists, and will later be displaced by more specialized species as they arise. As such, where sporadic extinction allows for more gradual turnover in species, mass extinction events are major “resets” of evolution that can radically shift what constitutes “well adapted” in a geological eyeblink. For mammals at the KPg boundary, small body size and an omnivorous diet (including the ability to scavenge detritus) were the “winning” combination of traits that allowed them to survive where larger, more specialized animals (think Tyrannosaurus rex) could not. From this rather humble station, mammals would come to dominate the world’s ecosystems over the coming eons – including a lineage that would someday lead to our own species. Far from only a destructive force, extinction is a powerful mechanism to allow evolutionary innovation, and one that was of significant importance to us.

For further reading:

Meredith, R.W. et al (2011). Impacts of the Cretaceous Terrestrial Revolution and KPg Extinction on Mammal Diversification. Science 334; 521-524.

Fastovsky, D.E. (2005). The Extinction of the Dinosaurs in North America. GSA Today (15); 1052-5173.

Benton, M.J. and Twitchett, R.J. (2003). How to kill (almost) all life: the end-Permian extinction event. TRENDS in Ecology and Evolution (18); 358-365.

The Evolutionary Role of Death & Natural Evil

In addition to providing a general theological critique of the endemic—as opposed to post-hoc or intrusive—origins of death in the natural world, John Laing’s imminently fair-minded essay also takes theological aim at the role death and natural evil play in the evolutionary diversification of life. It is one thing to say that death is primordial; it is another to view it not just as an ancient byproduct, but as the central means of creation. The understandable theological uneasiness expressed by John and many others about this issue ultimately rests not just on an understanding of God’s creative activity, but also on a particular representation of evolution. In this regard John makes two important claims:

• a) “…natural selection, with its emphasis on a natural state characterized by competition for limited resources and a general struggle for survival, is the primary means by which speciation takes place…”
• b) “death actually functions as a mechanism for life. Death plays a vital role in natural selection by rooting out weakness and driving evolutionary development.”

For reasons I discussed in the previous section, it is not entirely clear that death constitutes an evil that is incommensurate with divine activity. However, the fact is that the above depiction of evolution—which is not unique to John amongst public commentators and is largely commensurate with Darwin’s own views—does not adequately portray current discussions within evolutionary biology. There are three problems with this portrayal that I’d like to address in turn—three aspects of evolutionary theory that need to be better understood.

First, while there is no uncertainty about common descent or about natural selection as a cause of evolutionary change, there is considerable discussion over the extent to which natural selection is “the primary means” by which speciation takes place. For one thing, there are manifold other agents of evolutionary change: drift, gene flow, systems of mating, mutation itself unfiltered by selection. A tremendous amount of variation may be adaptively neutral, being invisible to natural selection. For another thing, some claim that evolution proceeds most rapidly and speciation occurs most precipitously in the relaxation of selection—when ecological times are good and the culling effects of the environment are minimized. We may see this in the contingency-driven formation or colonization of a new habitat or the exploitation of a new resource that does not displace previous variants. Or, speciation events or species-level innovations may be the results of chromosomal rearrangements or symbiogenesis that are not the cumulative results of selection. Finally, there exist manifold and admittedly controversial proposals that are critical of neo-Darwinism as a whole, claiming that natural selection may be a necessary, but is neither a sufficient nor a primary cause of large-scale evolutionary change.¹

Second, notwithstanding Darwin’s formulation of natural selection in terms of competitive struggle as (accurately) cited by John, the modern understanding of evolution and competition is considerably more differentiated and complicated. For one thing, competition is neither a necessary nor a sufficient condition for natural selection. Natural selection is formally defined as the differential reproduction of genotypes (or information.) Some sets of genes are replicated with greater efficiency than are others. Competition is formally defined as the negative impact of two organisms (or two species) on one another’s fitness. You can have all sorts of competition that does not result in natural selection. And importantly, you can have differential reproduction by natural selection without the negative fitness impacts of competition. Colonists to a new under-exploited habitat, or two species that are partitioned onto separate resources in a way that minimizes competition might well have some variants that leave more offspring than others without displacing them. This is natural selection.

Indeed, imagine an infinite habitat with non-limiting resources and no competition at all: as long as there were adaptively salient mutations, there would be natural selection—some of those new genotypes would reproduce more effectively than others. Competition, to whatever extent it exists in nature, is a consequence of finitude and not a necessary precondition of natural selection. And finally, the role of cooperation in evolution has itself been massively reconsidered in recent years. It would not be entirely unfair to say that on the basis of mathematical models and empirical data, the proposal that cooperation “is now seen as a primary creative force”² and a “fundamental principle of evolution”³ has moved from being a cult-alternative to a widely accepted paradigm. Indeed, cooperation and increasing scales of cooperative interdependence are seen not only as a formative process but also as a recurring product of evolutionary change, which may even be viewed as “progress.”⁴ A biologically significant and theologically salient thematic trend across major evolutionary transitions, is that cooperative interdependence itself – and the wondrous properties of life mentioned in the first installment of this essay – seem to be amplified through selection.⁴ Through evolution, God may be seen to confer life and confer it in greater abundance.

Third, the claim that “death drives evolutionary development” turns out to be problematic. Recent discussions of death and senescence (organismic decay) between various branches of the biosciences are spirited and fascinating. One of the vexing characteristics of living creatures is the internalization of death and senescence: even if an individual is not killed by external forces, it will die from the inside out—virtually no species is immortal.⁶ One account of this—the rate of living theory of senescence—understands it not in terms of selection for reduced mortality but in terms of biophysical or allometric constraints relating rate of metabolism to rate of wearing out. Though it views senescence differently, the prevailing evolutionary theory of senescence, with several variants, does not affirm death or decay—at least the kind of death and decay that is intrinsic to organismic development—as a prerequisite to evolution by natural selection either.⁷

Indeed, internalized death is viewed not as driving but as deriving from, not as a necessary requirement for but as a byproduct of, natural selection. Specifically, mutations or traits with detrimental impacts later in life may not be eliminated by or may even be favored by selection if their contribution to reproduction early in life is sufficient. Now, neither theory completely dismisses the shaping role of death. Under certain but not all conditions, differential mortality may have adaptive import (and it is not even the longer-lived organisms that always have adaptive advantage). Extrinsic sources of death may also shape the internalization of death.⁸ But the view that death drives evolution does not adequately represent emerging scientific understanding of the relationship between natural selection and senescence.

Scientifically death does not “drive” evolution. And theologically, although neither evolutionary change nor ecological interaction “solve” the ultimate puzzle of human death, they may nevertheless mitigate the proximal existence of creaturely death by amplifying the complexity and vibrant abundance of living forms.

Darwin famously closed The Origin by observing “There is a grandeur in this view of life, with its several powers, having been originally breathed by the Creator into a few forms or into one…from so simple a beginning endless forms most beautiful and most wonderful have been, and are being evolved.”⁹ Unlike John, I do not see anything in evolutionary theory to reduce, and I see much to augment the sense of grandeur and (for that matter) the appreciation of sheer goodness—both earthly and divine—evoked by the wonders of the living world.

Yet grandeur and goodness are not perfection. My Dad is still dying. I still wince at the suffering of clearly sentient animals. And, truth be told, I tremble at the biblical images of universal herbivory: even metaphors are metaphors of something, and in the case of biblical revelation, that something can be taken to be real and important. So like John, I confess to profound gratitude tempered with a lingering unease at the state of nature. Though I believe in a Fall, this unease is not rationally relieved by attributing to an Adam the present state of all nature. Nor is it resolved by the various alternative considerations I’ve described and which, taken together, seem to have considerable merit but not sufficiency. Notwithstanding, I thankfully affirm that “I have known the goodness of the Lord in the land of the living.” And I look to the day when we may say together, “My ears had heard of You, but now my eyes have seen You.” (Job 42:5)

Notes

1. E.g., Salthe, S. 2008. “An Anti-Neo-Darwinian View of Evolution.” Artificial Life. 14:231-233; David Depew and Bruce Weber (eds). Darwinism Evolving: Systems Dynamics and the Genealogy of Natural Selection. 2004. MIT Press
2. Michod, Richard and Denis Roze. 2001. “Cooperation and Conflict in the Evolution of Multicellularity.” Heredity. 86:1-7. Page 2
3. Nowak, Martin. Evolution, Games, and God: The Principle of Cooperation. Martin Nowak & Sarah Coakley, eds. Forthcoming from Harvard University Press.
4. Sigmund, Karl and Eörs Szathmáry. 1998. “Merging Lines and Emerging Levels.” Nature. 392: 439-441.
5. John Maynard Smith and Eörs Szathmáry. 1998. The Major Transitions in Evolution. Oxford University Press. Brett Calcott & Kim Sterelny (eds). 2011. The Major Transitions in Evolution Revisited. MIT Press.
6. “Virtually” is an important qualifier: while senescence has been documented in nearly all organisms examined, there are some cell lines and species in which this may not be the case.
7. Williams, George. 1957. “Pleiotropy, Natural Selection, and the Evolution of Senescence.” Evolution. 11:398-411.
8. This relationship is complex and not invariant. E.g., Williams, Paul and Day, Troy. 2003. “Antagonistic Pleiotropy, Mortality Source Interactions, and the Evolutionary Theory of Senescence.” Evolution. 57(7): 1478-1488.
9. Darwin, Charles. 1876. The Origin of Species By Means of Natural Selection, or the Preservation of Favored Races in the Struggle for Life. 6th Edition. John Murray. p. 429.

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.

With the first part of my essay as background, I now respond directly to Dembski’s analysis of “Darwinism” and how BioLogos differs from the view he critiques. He begins by posing a question, “Is Darwinism theologically neutral?” He goes on to describe two contrasting views:

1. Those of the agnostic philosopher, Michael Ruse, who claims Christianity and Darwinian evolution are compatible and,
2. Those of individuals who hold a young earth view and claim Christianity and Darwinian evolution are incompatible.

Dembski suggests that Ruse, in order to claim compatibility (neutrality), redefines Christianity. I agree he does this. Without belief in the bodily resurrection of Jesus, Christianity is dead and, as Paul says, Christians are of all people most to pitied. (1 Corinthians 15:19).

Dembski also states that a belief in common descent can be consistent with Christian faith (i.e. neutral), and here I agree with Dembski again. As he points out, Christianity is not defined by the mechanism that God chose to use in accomplishing his purposes in creation.

So far we are on exactly the same page. Ruse claims Darwinism is neutral, but only by departing from Christian theology. Some young earth creationists claim Darwinism is not neutral, but they focus on common descent and this, by itself, does not depart from Christian theology. However, as Dembski quickly notes at that point in his essay, he has not yet carefully defined Darwinism and Christianity. He goes on to describe what he considers to be some non-negotiables of each.

Dembski suggests that among the core non-negotiable principle beliefs of Christianity are: (a) divine creation, (b) reflected glory, (c) human exceptionalism, and (d) bodily resurrection of Jesus. I agree that these are non-negotiables; take away any of these beliefs and you no longer have Christianity. We’re still on the same page.

What about non-negotiables of “Darwinism?” They are, he says, (a) common descent, (b) natural selection, (c) human continuity, (d) methodological naturalism. With that, he proceeds to analyze each.

Common Descent

Common descent, which today is at the core of the biological sciences, was a fundamental tenet for Darwin. Dembski sees no significant theological problem with common descent. “By themselves [the Christian non-negotiables described above] allow that God might have specially created living forms or brought them about via an evolutionary process,” he writes. He sees no theological conflict with this Darwinian tenet, even though he does not subscribe to it.

Natural Selection

Dembski indicates that natural selection, as defined by Darwin, is in tension with two of the four Christian non-negotiables—divine creation and reflected glory. His primary concern is that Darwin’s view of natural selection is non-teleological. Insomuch as this is true (and Darwin’s views on teleology are complex and contested), I agree. If Darwin’s non-teleological views were correct, this would be incompatible with some of the non-negotiables in Christianity. As Dembski says, “to say that something is undetectable is not to say that it doesn’t exist....” I concur that Darwin had no scientific basis for concluding that the evolutionary process did not end up exactly the way that God intended in the beginning. If Darwin reached non-teleological conclusions on the basis of his data then he allowed his philosophical and theological commitments to influence his conclusions. Like Dembski, I believe God did call our existence into being; there is a teleological basis for our presence on earth. We are by no means an accident and to the extent that Darwin thought we are, he was wrong.

So far, I see no significant difference between BioLogos and the non-negotiables presented by Dembski. Intriguingly, however, Dembski goes on to state, “it seems odd, given C1—[divine creation], that God would create by Darwinian processes, which suggest that unguided forces can do all the work necessary for biological evolution.” Here we part company. As indicated in my introductory comments above, I believe that the natural activity of God is not less divine than the supernatural activity of God, something borne out by the Scriptures themselves. This does not mean that I think that no supernatural activity occurred in life’s history; I just don’t see why it would be “odd” if God chose to create life’s diversity through his natural activity. How would we know what is odd as it relates to the activity of God? The only reliable source of what is odd and what is not is God’s revelation through his Word. But I see no scripturally-based rationale for determining the expected ratio of natural vs. supernatural divine activity in creation. Scripture is silent on the issue and so far at least, science is as well—other than demonstrating that many biological features and mechanisms previously thought by some to be evidence of supernatural action can now be explained via God’s regular activity—that associated with his natural laws. For the present, I think it is best to withhold judgment about the extent to which God suspends his ongoing regular activity in favor of miraculous supernatural activity in the history of the creating life’s diversity.

I now come to the most fundamental point of disagreement between the Intelligent Design movement and BioLogos. Dembski states:

Given that science is widely regarded as our most reliable universal form of knowledge, the failure of science to provide evidence of God, and in particular Darwin’s exclusion of design from biological origins, undercuts C2 [reflected glory].

Furthermore, he also writes:

If God does occlude his purposeful activity in nature, that raises a tension with (C2), which states that the world clearly reflects God’s glory (Psalm 19) and that this fact should be evident to all humanity (Romans 1).

I don’t think that God occludes or masks his activity. Thanks in no small part to science, we now recognize that there are “signposts” (C.S. Lewis’s term) all over the place directing our attention to the existence of our Creator. The question is whether those “signposts” can be developed into scientific hypotheses that can be scientifically tested in a manner that parallels how one goes about testing the hypothesis that smoking causes cancer or that DNA is the genetic material. The heavens do declare the glory of God (Psalm 19), and, “ever since the creation of the world, his eternal power and divine nature, invisible though they are, have been understood and seen through the things he has made” (Romans 1:20). God has not occluded his activity. It is all around us. From the birth of a baby to the birth of a star; from a universe which is mathematically coherent to one which is exquisitely fine-tuned; from our sense of shame to our ability to recognize the good and the right—from all of these and so much more, we see signposts all pointing to our Creator. Individually each hints at something beyond ourselves. Together they shout out with the message of God’s glory. Still, can they be tested scientifically—in a manner that parallels whether penicillin kills bacteria or the mitochondrion is the cell’s energy factory—to determine whether God is at work in them? Can intelligent people who choose not to believe come up with feasible alternative explanations that do not include God? Sure, they do it all the time and, as Romans 1 tells us, they have been doing it from the beginning of human existence.

Given the way that God has worked through his regular natural activity, why should we expect to be able to develop a test for the activity of God? God is always active, but scientific testing of God’s activity would require a “control” where God is not active. How can we conduct an experiment which studies the “presence vs. absence of God” when God is always present as sustainer as well as creator?

Human Continuity

Dembski quotes from Darwin’s Descent of Man:

The difference in mind between man and the higher animals, great as it is, certainly is one of degree and not of kind. We have seen that the senses and intuitions, the various emotions and faculties, such as love, memory, attention, curiosity, imitation, reason, etc., of which man boasts, may be found in an incipient, or even sometimes in a well-developed condition, in the lower animals.

Even if all that Darwin says here were more or less true, it would still say nothing about that which makes humans truly exceptional, because—our linguistic and cognitive abilities aside—what makes us truly exceptional has less to do with biology than with the fact that God chose to enter into a unique relationship with humankind. Dembski paraphrases an ideologically strict Darwinian view of man as "not worthy of special divine attention, and with no prerogatives above the rest of the animal world." But Christians recognize that our material ordinariness is radically transformed by the presence and promises of God. Exactly as with the people of Israel among the nations, so humans among the animals: our special identity rests in the free choice of the Creator to give us his himself and his name. If we recognize that human specialness rests on God’s fellowship with and call upon us, and that we—alone of all creatures—are enabled by God to bear his image in the world, then anything Darwin said about the physical continuity between humans and animals is irrelevant. In the way that matters most, we are not continuous with animals. For philosophical and theological reasons, Darwin did not recognize this. Darwin, I believe, was wrong. I, like Dembski and like Southern Baptists in general, am not a Darwinist.

Methodological Naturalism

Dembski defines methodological naturalism in the following way:

The physical world, for purposes of scientific inquiry, may be assumed to operate by unbroken natural law.

He goes on from there to write that if one assumes that miracles were performed in salvation history, then it would seem to be arbitrary to assume that God would not also perform miracles in natural history as well. Although I do not rule out the occurrence of miracles in natural history, the purpose of miracles in the biblical narrative seems to stem from God’s desire to reveal himself to humankind, reminding us of and guiding us in our relationship with him and each other. Given that, I do not see why it is arbitrary to think that God may not have used miracles to accomplish his purposes in nature before humans were around to observe them.

However, I strongly disagree with Dembski that if one believes God has worked primarily through natural processes in creation as a whole, this makes belief in the resurrection less tenable. The two ought not to be tied together in this way, especially since I have already stated that I reject the notion that the ordinary and regular processes of creation are any less God’s—than what I have called supernatural processes. One’s conclusion about the mechanism of creation has no logical extension to one’s views about the historicity of the bodily resurrection of Jesus.

In conclusion, I think Dembski takes some steps that are both theologically unnecessary and scientifically unjustified in rejecting what careful study tells us about God’s marvelously ordinary processes of creation: ordinary because they follow his natural laws so faithfully, marvelous because they have resulted in a world of complex and beautiful life. On the other hand, I agree with Dembksi that Darwin’s views were not theologically neutral. Darwin’s views on teleology, human exceptionalism, and miracles were not compatible with Christianity. Quite simply, this is why I do not consider my views to be Darwinian and why I am not a Darwinist.

For further reading:

The BioLogos website offers many resources to acquaint readers with the incredibly strong scientific evidence for common descent and other facets of evolutionary biology.

Evolution: just a theory

One game that my (young) children like to play is a guessing game where both players select a character from among many choices, and by process of elimination, tries to guess the character the other has selected. Questions like “does your character have red hair? glasses?” etc., are used to narrow down the possibilities. Once you have guessed correctly which character your opponent has selected, you can perfectly predict the answer to every question thereafter (and a good many parents likely prolong the questioning to keep the hopes of victory alive for their children). When considered separately, the individual features of each character—glasses, brown hair, purple hat, and so on—mean almost nothing, since they could be features shared with other characters in the game. Only the convergence of multiple features is indicative of a good guess, and the accuracy of that guess is put to the test every time a new question is asked.

A good theory is something like this: an educated guess, based on and consistent with all past work on the topic to date. It allows you to predict how future tests should pan out. In the guessing game, there are limited options to choose from (so the analogy, like all analogies, eventually breaks down). In science, we don’t really know the true way things actually work. What we have are theories—broad explanatory frameworks supported by experimentation, that make sense of our current collection of facts—that we can use to make testable predictions about the natural world. All theories in science are provisional in that they are not complete descriptions of how the world actually works and are subject to future revision; but at the same time they are robust frameworks that can be used to predict how experiments should behave with almost boring regularity. So, far from the colloquial usage of “theory” as speculation, “just a theory” is high praise in science.

The current understanding of evolutionary theory in all its scope and diversity is far more complex than Darwin himself could have ever envisaged. (As a geneticist, I’ve often wished I could have a cup of tea with him to show him how far his theory has grown, especially given his confusion about how heredity worked.) Our understanding of how evolution works has grown by leaps and bounds since the 1850s. What is remarkable is just how much Darwin got “right” given his time and place. His main hypotheses—that species descend from ancestral forms through descent with modification, that and natural selection acting on heritable variation is a significant force in that process—remains the core of modern evolutionary theory. We’ve added a lot of detail since then (population genetics, kin selection, neutral evolution/genetic drift, symbiosis, horizontal gene transfer, molecular exaptation, and so on), but Darwin’s core ideas have produced a wealth of successful predictions. They were a very good “guess” that continues to pay rich scientific dividends.

Whale evolution: an example of converging lines of evidence

One of the things I personally find quite enjoyable about evolutionary theory is the counter-intuitiveness of some of the predictions it makes. One example that is a personal favorite, and one I often use to illustrate how evolution makes sense of converging lines of evidence, is cetacean (whale) evolution. Let’s set up the “problem” that evolutionary biology forces upon us:

• Modern cetaceans are mammals – they nourish their young in utero through a placenta, give birth to live young, and feed newborns with milk – all features of standard mammalian biology.
• Mammals are tetrapods – organisms with four limbs. Mammalian life shows up in the fossil record as an innovation within tetrapods, so mammals are “nested within the set” of tetrapod forms. Not all tetrapods are mammals (amphibians, for example) but all mammals are tetrapods.
• Tetrapods are by and large terrestrial creatures. Having four limbs for locomotion is a distinctly land-based adaptation.

The “problem”, of course, is that modern whales are emphatically not terrestrial, nor do they have four limbs – they have two front flippers and a tail, with no hind limbs in sight. Yet they are mammals, which forces evolution’s hand as it were. Evolution thus is dragged, under protest, to the prediction that modern whales, as mammals, are descended, with modification, from ancestral terrestrial, tetrapod ancestors. 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”.

Going out on a limb

Anyone who has seen a modern whale skeleton in a museum and noted it carefully may have noticed that though whales lack hind limbs, they do have a bit of bone back there where the hind limbs ought to be. While this is suggestive of a vestigial characteristic (a feature in a modern organism that has a reduced role relative to the role the structure played in an ancestral species), it’s hardly a smoking gun for evolution. Still, it’s consistent with the idea.

When we look at the cetacean fossil record, we also see forms suggestive of a progressive loss of hind limb function and structure over time, as David Kerk and Darrel Falk have elegantly explained before. Again, if one were resistant to evolutionary explanations, it would be possible (if a bit strained) to interpret these creatures as having been created directly as we find them in the fossil record. The facts that we do not see these forms in the present day, and that they seem to blur the distinctions between terrestrial tetrapods and whales might make one a bit uncomfortable, however.

Recent work on cetacean embryogenesis (how whales and their relatives develop from fertilized eggs into fully-formed baby whales) has shed even more light on the issue for modern species, however. Dolphin embryos actually have four limbs early in their development, as well as a few facial hairs, just as any good mammal should have. The hind limbs and hairs are lost later in development, and work on the molecular signaling events that halt hind limb growth and cause the limb bud to regress into the body wall have now been worked out in some detail. Moreover, early in dolphin development the nostrils are distinct and on the front of the face, and only fuse into a blowhole and migrate to the top of the head later in development. Early dolphin embryogenesis is distinctly mammalian and uncannily tetrapod-like.

… and passing the test

Taken in isolation, these facts about whales are interesting trivia. Taken together, however, they begin to form a picture entirely consistent with the prediction that modern whales are derived from terrestrial ancestors. The true strength of evolution as a scientific theory for the origin of whales is this: not that we can prove it, (for no theory is ever proven in science due to its permanently provisional nature), nor that we have full access to every bit of data we would like (consider how fragmentary the fossil record is, for example), but rather that we haven’t been able to disprove it yet, despite our best efforts. Descent with modification remains a productive educated guess that grows stronger with each investigation.

In the next post in this series, we’ll explore some additional lines of evidence for cetacean evolution that further illustrate the predictive power of evolutionary theory.

For further reading

Evidences for Evolution, Part 2a: The Whale's Tale

Evidences for Evolution, Part 2b: The Whale's Tale
J. G. M. Thewissen, M. J. Cohn, L. S. Stevens, S. Bajpai, J. Heyning, and W. E. Horton, Jr. (2006). Developmental basis for hind-limb loss in dolphins and origin of the cetacean bodyplan. Proceedings of the National Academy of Sciences 103 (22), 8414–8418. available freely online.

In our last two BioLogos podcasts, we looked at the question of transitional fossils and the genetic evidence for evolution. In our final installment of this three part series, we move on to the question of speciation and macroevolution. A common challenge to evolutionary theory is that while life does indeed change over time (what is known as microevolution), no one has ever seen one species evolve into another species (macroevolution). For example, no one has seen a dog evolve into something other than a dog. Because speciation has never been observed, and because science is based on observation, evolution cannot be considered scientific.

In fact, examples of speciation have been observed by scientists. We must also remember that we are able to observe just a tiny window of the long history of life on Earth, and the fact that any speciation has been noted at all is impressive indeed.

Transcript

It’s pretty clear to most of us that life can change over time. For those who aren’t convinced, just take a quick trip to your local animal shelter. Each of the dog breeds there, from the Great Dane to the Chihuahua, descended from a single ancestral population. As you probably already know, that ancestral group was a wolf-like species. -How did these drastic changes take place? Well, basically, genetic variation within that original population was acted upon by selective forces. Now, just to be clear, the selection at work here wasn’t natural. It was the result of breeding done over hundreds of years. But the basic principle is the same. Genetic variation plus some sort of selection results in genetic change. This is evolution.

For the most part we are ok with accepting this. Yet many people still have a problem with the Theory of Evolution. Those suspicious of evolutionary Theory generally split evolution into two categories. Instead of arguing that evolution is completely impossible, they will say something like, “I know microevolution is real, but I just can’t accept macroevolution.”

Kent Hovind, an especially outspoken opponent of evolutionary theory, often makes this argument in his presentations:

“Maybe you’re talking about macroevolution. That’s where an animal changes into a different kind of animal. Nobody’s ever seen that. Nobody’s seen a dog produce a non-dog. I mean you may get a big dog or a little dog, I understand, but you’re going to get a dog, okay?” (source)

But what does this mean? What is the difference between micro and macroevolution anyway, and why is one of them ok while the other is condemned?

Well, like many terms used in the evolution debate, the definitions tend to differ depending on who you talk to. This can make rational discussion difficult. Most opponents of evolution, like Kent Hovind, say that macroevolution refers to one “type” or “kind” of organism evolving into another “kind”. Microevolution, they might say, is evolution within a “kind”. Evolution of one dog breed into another, they would say, is microevolution. Evolution of a “dog into a non-dog”, as Hovind puts it, would be “macroevolution.”’

One big problem with this argument is that “kind” is not clearly defined. It is a subjective term referring to organisms that seem similar to each other. Now, this is a definition that can easily be manipulated. And it doesn’t work very well when asking scientific questions. Because there is disagreement about what they actually mean, the terms micro and macroevolution aren’t often used in scientific literature. But when biologists do refer to “macroevolution”, most define it as “evolution above the species level”.

(Sources: http://ib.berkeley.edu/courses/ib200a/lect/ib200a_lect26_Lindberg_macroevolution.pdf, http://www.nescent.org/media/NABT/, http://evolution.berkeley.edu/evosite/evo101/VIADefinition.shtml, http://www.nhm.ac.uk/hosted_sites/paleonet/paleo21/mevolution.html)

In other words, at the smallest scale, macroevolution is the development of a new species. This definition is more useful because you can objectively determine whether two organisms are members the same species, but “kind” has no specific definition.

So what does “species” mean anyway? How is it different from “kind?” Well, the term species can be hard to define. Life is complex, and categorizing it into clear groups can be tricky. The currently accepted definition of species comes from what we call the “biological species concept.” Basically, the biological species concept says that a species is made of populations that actually or potentially interbreed in nature.

So, two populations that cannot mate to produce successful offspring are by definition separate species. Now, this definition doesn’t always work. For example, when you have a species that reproduces asexually, finding the boundaries between species can be a little tricky. But in most cases it does a pretty good job. It’s a good way to objectively determine where one species stops and another one begins.

The Biological Species Concept is especially useful when you have two species that look and act very similar. Eastern and Western Meadowlarks are a good example of this. They look almost exactly the same. But they cannot interbreed successfully. Therefore, they are separate species. This definition also helps when we study evolution. Where can we draw the line between microevolution and macroevolution? Well, it’s never easy, but having a working definition of this thing called a species helps out a lot. When enough genetic changes accumulate in a population, eventually it loses the ability to mate with others of its species. Then, by definition, it becomes a new species. In other words, macroevolution has occurred.

As we just discussed, many critics claim that macroevolution can never happen—one species can never cross over to become another one. This statement might sound valid, but a little bit of investigation shows that it is not well supported by evidence. For one thing, the only difference between micro and macroevolution is scope. When enough micro changes accumulate, a population will eventually lose its ability to interbreed with other members of its species. At this point, we say that macroevolution has occurred.

The same processes—random mutation and natural selection—cause both micro and macro evolution. There are no invisible boundaries that prevent organisms from evolving into new species. It just takes time. Usually, the amount time required for macroevolution to occur is significant—on the order of thousands or millions of years. That’s why you don’t normally see brand new forms of life appear every time you step out your front door. And that’s also why some people think that speciation never happens at all.

But sometimes macroevolution doesn’t take that much time. In fact, the evolution of new species sometimes happens so quickly that we can actually see it take place! Let’s look at a few recent examples.

Biologists Peter and Rosemary Grant had been studying finches since 1973. They lived on an island called Daphne Major in the Galapagos. It was here that they conducted their studies. When they first began their studies, only two species of Finch lived on Daphne Major: the medium ground finch and the cactus finch. But, in 1981, Peter and Rosemary noticed that an odd new finch had immigrated to the island. It was a hybrid, a mix between a cactus finch and a medium ground finch. It didn’t quite fit in with the other birds. The odd misfit had an extra large beak, an unusual hybrid genome, and a new kind of song. But somehow he was still able to find a mate. The female was also a bit of a misfit and had some hybrid chromosomes of her own. So their offspring were very different from the other birds on the island.

Rosemary and Peter continued to carefully watch the odd hybrid line. They wondered if the birds would become isolated from the other finch species on the island or if they would eventually re-assimilate. After four finch generations, a drought killed off many of the birds on Daphne Major. In fact, almost the entire hybrid line was exterminated. Only a brother and sister pair remained. The two family members mated with each other, producing offspring that were even more unique than their parent line. From that point on, as far as biologists Peter and Rosemary could tell, the odd population of finches mated only with each other. They were never seen to breed with the cactus finches or the medium ground finches on the island. The finches with the strange song had become a brand new species.

(Source: http://www.pnas.org/content/106/48/20141.full)

Another example of speciation, or macroevolution, also took place on an island—this time, on the beautiful Portuguese island of Madeira. According to history books, the Island of Madeira was colonized by the Portuguese about 600 years ago. The colonizers brought with them a few unassuming European House Mice, which they accidentally left on the island. It’s also possible that a group of Portuguese House Mice was dropped off later on.

Recently, Britton-Davidian, an evolutionary biologist at University Montpellier 2 in France, decided to collect samples of the Madeira mice and see how those original populations had changed over time. What she found was surprising. Rather than just one or two species of mouse, she found several. In only a few hundred years, the original populations of Mice had separated into six genetically unique species. The first mouse populations had 40 chromosomes altogether. But the new ones were quite different. Each new variety had its own unique combination of chromosomes, which ranged in number from 22 to 30.

What seems to have happened is that, over time, the mice spread out across the island and split into separate groups. Madeira is a rugged volcanic island with crags and cliffs. So it makes sense that this would have been easy to do. There were many isolated corners for the mice to occupy. Over time, random mutations occurred—some chromosomes became fused together.

Now, In order to reproduce successfully, both parents must have the same number of chromosomes. So when a population develops a chromosome fusion, suddenly that group cannot mate with the other members of its species. It becomes a brand new species. That’s exactly what happened on Madeira. And because of this phenomenon, 6 new species evolved from just 1 or 2 in an extremely short amount of time.

(Sources: http://onlinelibrary.wiley.com/doi/10.1111/j.1365-294X.2009.04345.x/full, http://www.genomenewsnetwork.org/articles/04_00/island_mice.shtml, http://www.nature.com/hdy/journal/v99/n4/full/6801021a.html)

Another fascinating example of macroevolution was recently observed by researchers at Pennsylvania State University. This time, two species combined to make a single new one. In 1997, researchers at Penn State noticed a fruit maggot infestation on some recently introduced Asian Honeysuckle bushes. They decided to investigate the Honeysuckle fly population and determine how it was related to the other flies nearby. When they examined the honeysuckle fly’s genes, the researchers discovered something interesting. The fly appeared to be a hybrid of two native species—the blueberry fly and the snowberry fly.

But the honeysuckle fly’s genetic material was not an exact balance between that of the two parent species. The ratios of DNA varied from fly to fly. This showed the researchers that the honeysuckle flies had been breeding amongst themselves for many generations—probably at least 100. Also, they found that the Honeysuckle Flies were very unlikely to breed with any other species. They bred only on their host Honeysuckle plants. So they weren’t likely to mix with flies that lived on a different host.

According to Dr. Dietmar Schwarz, post-doctoral researcher in entomology, as far as the researchers can tell, “The new species is already reproductively isolated. They seem to be in a niche on the brushy honeysuckle where the parent species cannot compete."

(Source: http://www.psiee.psu.edu/news/2005_news/july_2005/hybrid_insects.asp)

While this kind of speciation—two species hybridizing to create a new one—seems odd, it is a significant mechanism of macroevolution. And it’s especially common in plants. In fact, a new species of weed recently arose this way in Great Britain. In 1991, Richard Abbot, a plant evolutionary biologist from St. Andrews University, noticed an unusual weed growing next to a car park in York. He discovered that the species, an unassuming scruffy weed, was a natural hybrid between the common groundsel and the Oxford ragwort, a plant that was introduced to Britain only 300 years ago. The York Groundsel lives in a different niche, or microenvironment, than either of its parent species. It is able to breed and reproduce, but only with other York Groundsel plants. It cannot successfully reproduce with any other species, including either of its parent plants. Thus, by definition, the York Groundsel is its own new species.

(Sources: http://www.nerc.ac.uk/publications/planetearth/2003/summer/sum03-evolution.pdf, http://www.nature.com/hdy/journal/v69/n5/abs/hdy1992147a.html)

So, as we have seen, macroevolution is an established process. Usually it takes thousands of years to occur, but sometimes we get lucky and catch it in the act. When Kent Hovind said that, “no one has ever seen a dog produce a non-dog” he was technically quite correct. But this statement infers that macroevolution means a drastic and obvious change from one type of organism into another. Those who think this way believe that macroevolution is something like two dogs breeding to suddenly produce a cat, or two guinea pigs mating to produce a mouse.

But this is not how evolution works at all. Over millions of years, a dog-like animal may indeed evolve into a something that looks completely unlike a dog. However, this is not something that we would expect to be able to observe. It just takes too much time. To put the scale of evolution into perspective, consider this. If the average lifespan of a United Stated citizen, 78 years, were a single minute, then single-celled life has been around for nearly 100 years. On this scale, all we get to see is one minute. And even in that time frame we sometimes see new species forming. God’s time is not our time and we tend to forget this. What we do expect to observe is a very slow step-by-step accumulation of tiny genetic changes that eventually result in speciation. And indeed, as we discussed today, this is exactly the sort of evidence revealed in nature.

So, macroevolution is not a “myth” by any means. It is supported by a vast amount of evidence. That evidence includes the fossil record and genetics, as discussed in previous BioLogos podcasts, and, when we get lucky, direct observation of speciation. God, being who God is, could conceivably have created species out of thin air in a single instant. But what if instead if God created and sustained the process by which new species are created? Does that make him less powerful or less "god-like"? Is it somehow more God’s process if it happened in an instant, than it is if it happened over a long period of time? Presumably even if it happened in an instant, it would still happen by some sort of process—only faster.

God’s time is not our time, and perhaps it’s a good idea for all of us to simply stand back in amazement while God does God’s work in God’s time through God’s process.

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