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.

Despite this usage, most of us know that randomness has something to do with probability, and that it often implies a lack of conscious intentionality. But what do mathematicians and scientists mean when they say something is random? Can a random process lead to an ordered, even predictable outcome? Is there evidence that God makes use of random processes to fulfill his creative purposes?

These are big questions, and we won’t address them all today. But I think randomness is an important topic to cover for two reasons: 1) it is integral to many processes in biology (and math, physics, chemistry, etc.), and 2) it is commonly misunderstood to be incompatible with Christianity.

As I said above, most of us know that randomness has something to do with probability. If you pick a card “at random” from a shuffled deck, you have a small probability of drawing an ace (4 out of 52, or a 7.7% chance). If you flip a coin, you have an equal probability of getting heads or tails.

Randomness also seems to imply a lack of intentionality or purposefulness. After all, you might hope for an ace when you draw a card, but you can’t choose one on purpose. You might call heads when you flip a coin, but you can’t know beforehand what the outcome will be. Thus the outcome is indeterminate, but is it purposeless? Not necessarily. Indeterminacy simply means the result cannot be predicted from the outset.

It should be noted that indeterminacy does not imply that God does not have foreknowledge of future events. Christians ought not to be uncomfortable with the idea of God interacting with his creation through chance. We often describe a seemingly-random (i.e. unplanned by us) sequence of events as being “providential,” or planned by God.

In biology, it is very hard or impossible to calculate precise probabilities for most processes, so when we say a process is random, we typically mean it is extremely unpredictable. Eventually we will discuss randomness within biological evolution, but first we must consider some simpler processes, like the self-assembly of a virus.

Viruses are remarkably efficient entities. Coiled tightly within a protein-based shell is a small amount of DNA needed for self-replication. The shell, called a capsid, is made of many repeating protein subunits and is therefore highly symmetrical (see figure). Important biomedical insights have certainly been gleaned from structural studies of viruses, but viruses also teach us about the emergence of order from non-order.

The virus life cycle has four main steps: 1) enter a host cell, 2) hijack the cell’s replication and translation machinery to make many copies of itself, 3) assemble into many virus particles, and 4) exit the cell to invade another host.

When I first learned about this process, I found it very hard to believe it just “happens.” The idea that a bunch of molecules bumping into each other inside a crowded cell could spontaneously assembly into a fully-functional virus seemed a bit far-fetched. Many viral capsids have over 100 protein subunits that must interact with each other in just the right way, or it won’t work. Surely there must be something driving this process, right?

There is! Random motion. I had to see it to believe it. I distinctly remember sitting in class during my first year of graduate school when the professor demonstrated self-assembly of a virus using a 3D model as shown in the following video. In less than 30 seconds, you can watch a jumbled heap of proteins become a beautifully ordered structure.

As the narrator explains, sub-assemblies form and break apart en route to the most stable structure, the full capsid. As the sub-assemblies begin to form, further associations with free subunits become more favorable and as a result occur rapidly, while the final steps may take considerably longer. While the subunits in the model are rigid, in reality the proteins take on multiple conformations, allowing the capsid to “breathe.”

Amazing as it is, the system we just considered—one virus capsid in a jar—is pretty simple. One wonders how self-assembly can happen in a crowded cell, where there are countless other molecules diffusing around, potentially getting in the way. We can’t directly see how it happens in a cell, but we can reconstitute the process in a test tube using different combinations of constituent molecules.

Consider two viruses, where each protein subunit in one virus is the mirror image of the corresponding subunit in the other. Putting the two viruses together by hand would be pretty tricky, because the constituent parts look so similar. But random motion can do the job in short order:

From this model, we can see clearly, in real-time, how distinct complex structures can arise from their parts randomly interacting with one another. Many large viruses also use special scaffolding proteins to assist in the assembly process, and some even use their own genomes as a scaffold. In addition, two closely-related viruses that happen to infect the same cell can exchange parts to create a new virus. This is one way viruses can evolve quickly to evade the host’s immune system.

Here we have seen how viruses demonstrate a principle inherent in God’s world—that order can emerge out of chaos from random processes. In my next post, we will look at some other biological processes that make use of—rather, depend on—randomness. This will set the stage for us to see that such processes can not only assemble a structure within seconds or minutes, but also generate complex, information-bearing molecules over billions of years. Even though the freedom inherent in nature sometimes produces unintelligently-designed structures (like viruses, which can kill us), we see that God has made, and continues to oversee by his providence, a good creation that, at least in part, is capable of creating itself.

Next weekend, we’ll continue this series about randomness and God’s divine will. Up next: how God created the body to heal itself, and how can random mutations can be both harmful and benign.

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.

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.

Suppose a man falls among thieves, or wild beasts; is shipwrecked at sea by a sudden gale; is killed by a falling house or tree. Suppose another man wandering through the desert finds help in his straits; having been tossed by the waves, reaches harbor; miraculously escapes death by a finger’s breadth. Carnal reason ascribes all such happenings, whether prosperous or adverse, to fortune. But anyone who has been taught by Christ’s lips that all the hairs if his head are numbered [Matt. 10:30] will look further afield for a cause, and will consider that all events are governed by God’s secret plan.

In this passage, Calvin presents belief in “fortune” as evidence of carnal reasoning, and statements like this one have contributed to a widely-held notion that modern scientific understandings of the role that randomness plays in nature is inconsistent with belief in divine providence. In other words, if “randomness” equals blind and capricious “fortune,” then how can God be said to be working all things to his ends?

But Calvin could not have known of the very different understanding of randomness held by today’s scholars. Physical scientists, mathematicians, and statisticians have not yet agreed on a single unambiguous definition of the term “randomness,” but among these scientists, the term consistently refers to a family of related concepts focusing on unpredictability of the outcomes of single events and the absence of pattern in sequences of outcomes. I like this statement by John Polkinghorne, “Chance doesn't mean meaningless randomness, but historical contingency. This happens rather than that, and that's the way that novelty, new things, come about.” In Polkinghorne’s view, chance is an agent of creativity and can be perceived as being purposeful.

In fact, there are abundant examples of phenomena in nature in which randomness plays a role one could understand as being purposeful. For example, osmosis is a marvelous mechanism that enables all 10 trillion cells in our bodies to be nourished – it depends on the random motion of molecules. The human immune system is able to defend the body against attacks from millions of different microorganisms using a relatively small number of building blocks and random combinations of these to fashion defenses specific to each adversary. We never take a breath and find it to be all nitrogen or carbon dioxide – random motion of molecules keeps oxygen close to uniformly distributed throughout the atmosphere.

In 2007, a British statistician, David Bartholomew published God, Chance, and Purpose in which he argues that God “can have it both ways”—that he can use low level randomness to accomplish divine purposes while simultaneously maintaining order at a higher level. Of course, we cannot prove that God ordained these random processes to achieve divine purposes in the world. But to a person of faith, such an interpretation in both consistent with the observations we make in science and with the Scriptural notion of God’s providential care for the world.

Considerations like these led the John Templeton Foundation to provide a generous grant of $1.69 million to support a new research initiative on the theme of Randomness and Divine providence. Beginning this past summer, the program has the purpose of providing support for solid theoretical exploration of the kinds of ideas and possibilities expressed above—involving theology, philosophy, natural science, mathematics, and statistics. The grant will support individual scholars and teams of scholars who are willing to devote a significant amount of time between March of 2013 and June of 2015 to such work, and the project’s request for proposals suggests the following as questions researchers might pursue:

• How might God work providentially through indeterminate processes? Can recent advances in understanding the nature of randomness offered by algorithmic information theory, physics, biology, and other sciences provide insight into this question?
• Can we bring clarity to the concept of "randomness"? Philosophers and scientists have tried on occasion to give precise definitions of when a process is random, but more work needs to be done on the question. How do (or should) conceptions of randomness vary across academic disciplines?
• What are some possible implications of randomness for hiding or unfolding divine creativity and purpose in the world? Could God use randomness to (1) generate creativity, (2) hide divine actions, or (3) unfold information? Why might God do so?
• How might we identify and come to understand a significant collection of nondeterministic processes in which agents could intentionally employ randomness to bring about purposeful results?
• How might we mathematically and physically model random processes in ways that help us understand how divine providence could be exercised in a "chance-governed" world?
• How do "laws and orders" in nature interplay with "chance and randomness" in bringing about results that can be interpreted as aspects of divine providence?
• Might randomness be evidence of limitations in human knowledge but nothing more? Or might it be evidence of ontological indeterminism? Might this be tested?
• What implications does randomness have for aspects of God’s relationship with the physical world such as God’s relationship to time and God’s role in causation? How might randomness be reconciled with God’s foreknowledge?
• How might an understanding of providence based on an extended Molinism and/or open theology incorporate randomness? For example, could an extended Molinism provide a plausible account of the relationship between quantum mechanics and divine providence?
• What are some theodical implications of randomness, particularly for the issue of natural evil?
• How have the theological traditions of Augustine, Maimonides, Aquinas, Luther, and Calvin addressed chance and fortune? In what ways might they incorporate ontological randomness?
• How do or could religions other than the Judeo/Christian tradition understand and incorporate randomness?
• How is the concept of randomness understood by advocates of secularism, naturalism, and new atheism? What are the strengths and weaknesses of these usages?
• How might an understanding of randomness in the world alter our conceptions of divinity, especially our understanding of divine providence?

Despite the range of issues mentioned above, research is by no means restricted only to these topics. In fact, the structure of the program is designed to foster collaboration and build community between scholars, with the end of expanding the range and integration of their work: two conferences will be held to bring scholars together with each other and then with members of the public—one at Calvin College in 2013 and the other at Fuller Theological Seminary in 2015. To get more information and to learn how to submit a proposal, see the project website; then join us in exploring the truth that all creation glorifies God—even randomness!

In my previous essay, I discussed “Darwin’s finches” and how surprisingly little Charles Darwin himself had to say about them. In fact, it was actually the British ornithologist David Lack (1910-1973) who conducted the critical research that immortalized the finches in biology textbooks and popular lore. In 1973, the eminent German zoologist Ernst Mayr wrote:

Already well known among professional ornithologists, his work on the Galapagos finches gave David Lack world fame… There is no modern textbook of zoology, evolution or ecology which does not include an account of his work.¹

Ernst W. Mayr

Decades have passed since Mayr wrote these words, and David Lack’s name has largely faded from public discourse. On the other hand, the Galapagos finches have become one of the most recognized symbols of evolution in the world today. Does it really matter whether Lack or Darwin gets credit for describing the evolution of these remarkable birds?

Insofar as evolutionary theory contrasted with religious belief, it makes a big difference. In a culture that is eager to equate evolution with atheism, it should come as no surprise that these birds are only known as “Darwin’s finches”. Darwin’s personal struggles and ultimate rejection of Christianity are well documented, and people are eager to link his loss of faith to his evolutionary theory. David Lack, on the other hand, began his scientific career as an agnostic, but shortly after publishing his famous book on the evolution of Galápagos finches, he converted to Christianity! ²

A Christian at the forefront of evolutionary biology

Lack’s Christian conversion did not mark the end of his scientific achievements, either. In fact, he continued as a prolific researcher until just weeks before he died. Among his many achievements, he was Director of the Edward Grey Institute of Field Ornithology (1945-1973), Fellow of the Royal Society, and President of both the International Ornithological Congress (1962-66) and the British Ecological Society (1964-65). His fellow scientists held him in great esteem:

He was described as one of the most outstanding among world ornithologists; he was certainly this, but he was also one of the world’s leading evolutionists. All the time one saw developing his use of birds as material for the study of wider, deeper, biological problems.³

David Lack at the International Ornithological Congress, 1962.

Clearly David Lack was an outstanding scientist, and his commitment to Christianity did not tarnish, hinder, or undermine his research on evolution. But we might also ask, what was Lack like as a Christian? Did he keep his faith hidden from view, afraid that it might compromise his reputation as a scientist? Ernst Mayr, who interacted with David Lack professionally and personally for nearly 40 years, had this to say:

I have known only few people with such deep moral convictions as David Lack. He applied very high standards to his own work and was not inclined to condone shoddiness, superficiality and lack of sincerity in others. This did not always go well with those who preferred to compromise in favour of temporary expediency. David had been raised in an environment in which great stress was layed on moral principles and this attitude was later reinforced by his Christian faith. This explains his extraordinary unselfishness and modesty, and his great devotion to his family, to his students, to his friends, and to all the things that he lived for. The equanimity, indeed serenity, with which he faced death after his terminal cancer had been diagnosed is further evidence of the strength which his faith gave him.⁴

Like Asa Gray⁵ before him, and Francis Collins⁶ after, David Lack was an sincere, devout Christian, as well as a leading scientist who employed evolutionary theory to make brilliant discoveries about the natural world. Though Lack did not see any conflict between his scientific and Christian beliefs, he was sympathetic to the concerns of his fellow Christians. Therefore, ten years after publishing his masterpiece on Darwin’s Finches, Lack wrote another book entitled Evolutionary Theory and Christian Belief: The Unresolved Conflict.

Originally published in 1957, this book deals with the very same science and faith questions that Christians struggle with today— topics like randomness and chance, death in nature, miracles, and evolutionary ethics. While it would be unreasonable to expect anyone to completely resolve these matters, Lack offered numerous insights both as a devout Christian and one of the world’s leading biologists.

Let’s take a brief look at how Lack addressed some of these questions.

Blind Chance or Divine Plan?

Evolutionary theory does not invoke supernatural forces in explaining the history of life on Earth; instead, it relies on naturally-occurring processes to account for the vast diversity of life. Additionally, it explains animal behavior largely in terms of survival and reproduction, without appealing to any higher purpose of life. Taken together, does this imply that God is absent, and that our lives are ultimately meaningless?

David Lack responded,

Behind the criticism that Darwinism means that evolution is either random or rigidly determined lies the fear that evolution proceeds blindly, and not in accordance with a divine plan. This is another problem that really lies outside the terms of reference of biology. It is true that biologists have inferred that, because evolution occurs by natural selection, there is no divine plan; but they are being as illogical as those theologians whom they rightly criticize for inferring that, because there is a divine plan, evolution cannot be the result of natural selection.⁷

When rendering judgment on the ultimate meaning of life, biologists are speaking from their person beliefs, not from scientific authority. Moreover, Lack pointed out that many science enthusiasts have employed the concept of “randomness” in ambiguous and misleading ways:

Mutations are random in relation to the needs of the animal, but natural selection is not. Selection, as the word implies, is the reverse of chance.⁸

In support of his view, Lack pointed out that convergent evolution has produced uncanny resemblances between distantly-related species across the world, notably among marsupials in Australia. Different evolutionary trajectories can lead to very similar results.⁹

Death in Nature

After addressing concerns about the seeming “randomness” of evolution, Lack turned to another great concern, the role of death in natural selection:

Various writers–some Christian and others agnostic–have been troubled about natural selection not only because it seems too random, but also because it is so unpleasant.¹⁰

Image courtesy John Marsh Photography via Flikr

Genetic mutations are generally harmful, and for evolution by natural selection to produce new forms of life, an awful lot of organisms must die. For many Christians, it is inconceivable that a loving and merciful God would allow death on such a vast scale.

But Lack also pointed out that rejecting evolutionary theory doesn’t actually get rid of the problem of death. Regardless of what we think about evolution, the brute fact of mass extinction remains. Fossils of innumerable animals, plants, and microorganisms clearly demonstrate that the vast majority of species that have ever lived are now dead. It may be quite troubling for us to observe that our planet is a giant graveyard of natural history, but rejecting evolution will not change this fact.

Some Christians conclude that death could not have been part of the divine plan; instead, it must be the work of the devil, or the result of human sin. But this interpretation contains an implicit assumption that death is always evil. Is this really true? David Lack offered two intriguing insights:

Blue-cheeked Bee-eater (Merops persicus) pair in
courtship, seen in Basai, Gurgaon, India.
Image courtesy Koshy Koshy.

1. For a population to maintain a stable size, all births must be balanced by a corresponding number of deaths. A world in which no animals die is a world in which no animals are born. That means no reproduction, no courtship, and by implication, no singing birds—much to the dismay of ornithologists and people in love!

2. Some people, taking cues from Isaiah 11:6-7, suppose that in a perfect world, animals only eat plants. But in fact, plants themselves depend on the bacterial decay of dead organisms. If animals didn't die, then essential nutrients would disappear from the ground, and plants could not continue to grow. Eventually, there would be nothing left for animals to eat, and all life would cease.¹¹

Miracles

Many Christians are uncomfortable with evolutionary theory because it denies a miraculous, supernatural origin of life. They fear that if those miracles are denied, it might lead people to reject the possibility of miracles altogether, including the central feature of the Christian faith—the resurrection of Jesus from the dead.

As a devout Christian, David Lack certainly affirmed the fundamental tenets of the gospel. But at the same time, he explained to his readers that invoking miracles to account for unusual features of the natural world is not particularly helpful when trying to deepen our understanding of God’s great multitude of creatures:

[The biologist's] research depends on repeated observations. It need not, as popularly supposed, consist solely, or even mainly of measurements and experiments, but unless events are repeated, they cannot be assessed by science. Hence truly unique events come outside the domain of science, though biologists are not usually convinced when told they must, therefore, leave such problems as miracles to others. For one of the chief ways in which research has advanced is through the discovery of apparent exceptions to the known rules, and if further study shows the exceptions to be replicable, new regularities are revealed from which modified rules can be propounded. This method has been so successful that the biologist tends to doubt whether there are any types of irregularity, or seeming irregularity, that will not yield to it.¹²

But just because a scientist cannot repeat a particular event doesn’t mean it didn’t happen. Both natural history and human history contain unique events that only happened once. As we peer into the past, the difficulty of discerning fact from fiction inspires us to further investigate the mysteries that surround us.

Conclusion

David Lack’s book Evolutionary Theory and Christian Belief was quite insightful, but his enduring achievements took place in evolutionary biology, a place where many Christians are afraid to tread. While it is significant that he himself found no contradiction between his faith and his science, perhaps the greatest testament to the compatibility between Christian faith and evolution is the life he led as a believer in both. As we saw in Ernst Mayr’s candid praise, Lack reflected the light of Christ through both his personal and his professional relationships.

Today, many voices in our culture still insist that evolution is incompatible with a sincere faith in Jesus, but a careful look at history demonstrates otherwise. In the future, perhaps more people of faith will have confidence to study biology knowing that one of the most iconic symbols of evolution—the Galapagos finches—owe their fame in large part to a devout Christian named David Lack.

Notes

1. Mayr (1973) “David L. Lack.” Ibis: 433.
2. Larson, E. J. Evolution's Workshop: God and Science on the Galapagos Islands. New York, Basic Books, 2001: 218. See also Lack, David. (1973) “My life as an amateur ornithologist.” Ibis: 431.
3. Alister C. Hardy (1973). "David L. Lack." Ibis: 436.
4. Mayr (1973) “David L. Lack.” Ibis: 433.
5. For more about Asa Gray, see the BioLogos FAQ “How have Christians responded to Darwin’s Origin of Species?”
6. See Francis Collins’ autobiography The Language of God: A Scientist Presents Evidence for his Belief (New York: Free Press, 2007) (book info)
7. Lack, David. Evolutionary Theory and Christian Belief: The Unresolved Conflict. Methuen & Co., 1957: 67.
8. Lack, p65.
9. For more on convergent evolution and the possibility that evolution could be compatible with some form of divine purpose, see the work of Simon Conway Morris, especially The Deep Structure of Biology: Is Convergence Sufficiently Ubiquitous to Give a Directional Signal? Templeton Press, 2008.
10. Lack, p72.
11. Lack, pp75-76.
12. Lack, p82.

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.

For more, be sure to read Randall Pruim's recent series Randomness and God’s Governance, Kathryn Applegate's post That's Random: A Look at Viral Self-Assembly, and our FAQ How Do Randomness and Chance Align with Belief in God's Sovereignty and Purpose?.

Author's Note

I am so thankful that I grew up in a Christian environment, which both kindled and nurtured my relationship with Jesus Christ. The Biblical instruction I received from my parents, pastors, and teachers has been invaluable as I walk out my love for the Lord from day to day. However, there was one specific topic growing up which was not fully addressed, namely evolutionary theory.

Coming from a conservative Christian background, evolution was given little or no thought because of its seeming contradiction to the creation story in Genesis. To me, evolution meant a monkey became a human, and as far as I knew, I had never seen that happen! So, of course, it appeared too improbable to hold any truth. When it was discussed, an inadequate picture of its ideas was often painted, which caused immediate suspicion and rejection of the theory. I don’t think this was intentional, but most Christians have never learned an unbiased, in-depth theory of evolution that is completely detached from societal agendas and philosophical conclusions. Therefore, their explanations of the theory are often misinformed.

My senior year of high school, I took AP Biology, and finally learned the scientific reasoning supporting this theory. I was surprised by how logical and obvious the mechanisms of change (such as mutations, natural selection, genetic drift, and so on) were that gave rise to new species. My subsequent response was, “No wonder people believe evolution occurred.” At that point, I was convinced that microevolution (evolution within a species) existed, but I was still questioning macroevolution.

Now, being at Point Loma Nazarene University as an undergrad in the Biology-Chemistry major and a year-round, student intern at BioLogos, my understanding of evolution has expanded enormously. I have enjoyed critically thinking through the evidence for evolution and reading articles that tackle difficult issues at the interface of science and Christian faith. Ultimately, I know that God has created all things, but the processes he used surpass my small understanding.

My personal wrestling with evolution and quest for truth has led to times of prayer and studying God’s Word, which has deepened my love for him in ways I cannot express. The first chapters of Genesis, in particular, have come alive. My whole life, the creation story was a straightforward list of facts about the creation of the world; I never searched further. I didn’t even perceive the truths Genesis declared over my very identity and God’s character. The more I study his Word and handiwork, I glimpse the awesomeness and majesty of the Creator, who loves me much more than I know. There is still so much to learn, but I am confident that he will lead me into all truth as I seek him out.

I desire to give others the opportunity to see evolution accurately and to distinguish it from the traditional, philosophical, and personal conclusions that too often cloud the scientific theory. I believe these conclusions alienate Christians from evolution more than the scientific theory itself. Ultimately, I do not mean to convince someone about evolution, but simply to give them the freedom to understand it.

Therefore, my goal for this podcast is two-fold:

• First, to offer a new perspective on randomness within natural processes that removes its negative connotations (especially as it relates to evolution).
• Second, to expose why evolution is powerless to support conclusions beyond the physical realm.

This will hopefully encourage others to study evolutionary theory and draw their own conclusions about its meaning in the framework of their faith.

Many of the games I enjoyed playing involve a combination of strategy and randomness: card games of various sorts, backgammon, and board games like Monopoly and Parcheesi. Some games that rely exclusively on chance (like War and Candy Land) or too heavily on chance (like Sorry) quickly became uninteresting to me. In fact, for Sorry, War, and several other games, I introduced additional rules to change the balance of strategy and luck—for example, by allowing each player to hold a hand of cards rather than merely flip a card and follow its bidding.

When my children were young, I played many games with them, especially those involving some amount of chance. I always play to win, so games of pure strategy like chess gave me too great an advantage—at least when they were still young. I still remember the first time I played the German game Mitternachtspartie with my children and some of their cousins. The game uses a die on which the number 5 has been replaced with the image of Hugo the ghost. Each player rolls the die and moves one of his figures the specified number of squares, unless Hugo is rolled, in which case Hugo moves instead.

I quickly worked out the expected distance Hugo would move for each of my turns and the expected number of squares I would get to move my own figures each turn. Using that information, I could strategically place my figures in the opening portion of the game. I fully expected to win this first game, since my young children were going to have to learn from experience what I already knew by the mathematics of probability. I lost—badly. As it turned out, the die had two Hugos on it. So compared to my expectations, Hugo moved twice as often, and my figures moved slightly less far. That combination turned the carefully calculated positioning of my figures into a disaster.

From Fun and Games to Science

I still enjoy playing games, including games that involve chance. But these days I encounter randomness even more often in my profession. I was trained as a mathematician and now work at the intersection of mathematics, statistics, and computer science. Like many scientists, I use randomness on a daily basis as part of our toolkit for modeling and investigating all sorts of phenomena. Models known as stochastic models, which explicitly incorporate random components, often via simulation in computer software, are used to model everything from diffusion to genetics to quantum mechanics. Insurance companies and financial institutions use stochastic models to manage risk. If we include all the applications of statistics, then almost no area of science is untouched by the use of randomness.

Most of the time, scientists and game players alike don’t devote much thought to just what makes randomness tick. But they both know that the better they understand the probabilities, the more successful they are. Nevertheless, if you ask many of them what it means for something to be random, they may struggle to put it into words. I won’t try to give a precise definition either, but it is important that we have some idea what we are talking about, so let’s consider one of the prototypical examples of randomness: the tossing of a fair coin.

If I flip a coin, the result could be heads or tails. Until I flip the coin, I don’t know which it will be. In this sense, the coin toss is unpredictable. If the coin is fair, each result is equally likely, so while I cannot say in advance whether a particular result will be heads or tails, I can say something about a large number of flips: approximately half should be heads and the other half tails.

A little mathematics even allows me to determine a range around 50% in which the percentage will almost surely lie. For example, if I flip a fair coin 1,000 times, the percentage of heads will most likely be between 45% and 55% (where “most likely” means a 99% chance). If the percentage of heads lies outside this range—especially if it is quite far outside this range—I am going to be suspicious that the coin flipping process is not fair. That’s one of the key ideas in statistics: not only can we calculate the frequency with which an event occurs, but we can compare data to a stochastic model to see if they are compatible or incompatible.

There are several interesting things we can learn by considering a coin toss. First, probability calculations rely on assumptions. If the assumptions are incorrect, then the probability calculations will also be incorrect. For example, if the coin is biased (such as one that is heads 60% of the time), but we assume it is fair, then the probability calculations given above will be wrong. Of course, if the assumptions are not too far from correct, the results may still be sufficiently accurate for scientific conclusions. If we have an appropriate way to collect data, then we can test our assumptions by comparing data to projections made based on the assumptions.

Second, “random” does not imply “equally likely.” A fair coin should have equal probabilities of heads or tails, but a biased coin is no less random. It’s just different. It is not as simple to handle arithmetically as a situation in which all outcomes are equally likely, but it is not otherwise special. It is a common mistake to assume random events are equally likely when they are not (or when that assumption is not justified).

Third, randomness is about the process. It is a fun experiment to flip a penny 100 times, then spin a penny 100 times and record the side that is showing when it finally tips over, then to stand the penny on end (this takes a steady hand and a little practice) and record which side is showing after pounding the table. These are three different processes, and they do not yield the same results.

Fourth, random processes produce patterns. I sometimes ask my students to mentally flip a coin and record the results as a sequence of letters (e.g., “HTTHHTHT”). Then I have them actually flip a coin and record the results. If the sequences are long enough, I can almost always tell them which is which. The sequences imagined by the students tend to have too few runs of consecutive heads or tails. The sequences based on real coin flips usually include several heads in a row. People not familiar with randomness are often surprised at the patterns that result and assume that the process must not have been random when they perceive a pattern. Our eyes and minds are drawn to similarities and patterns—even those that are produced purely randomly. This can lead us to draw false conclusions from coincidences of all sorts.

Consider the image in Figure 1. It was constructed using a computer to randomly throw 300 darts at a square board. Every position on the board was equally likely to be hit by a dart. This does not, however, mean that the dots are evenly spaced. There are 100 smaller squares. The average is three dots per square. But your eye is likely drawn to some clusters and voids. My eye also catches a graceful downward swoop in the lower part of the upper left quarter. All of this is exactly what we should expect from this random process. If we repeated this experiment, we should expect similar results. Several of the smaller squares would be empty and some others would have two or three times the average number of dots, but these clusters and voids would appear in different places.

Finally, randomness can be used to produce patterns intentionally. Consider the two pictures in Figure 2. You may think the two pictures are identical, but they are not. However, they were each constructed using the same random process:

1. Start at the lower left corner of the big triangle.
2. Randomly choose one of the three corners of the big triangle.
3. Move half way to that corner, placing a dot at the new location.
4. Repeat steps 2 and 3, 50,000 times.

The first few steps of this process for each image are illustrated in Figure 3. Although the final images look very similar, the route taken to get there is very different. In fact, the only point the two images have in common is the starting point. As the creator of the program that generated these images, I knew full well that the result would resemble a fractal image known to mathematicians as Sierpinski’s Triangle, even though I did not know or exercise any control over how the individual points would be selected.

Despite our familiarity with children’s games and the importance of stochastic models throughout the sciences, many Christians have a reaction to randomness that falls somewhere between uneasy and antagonistic. And yet, those same Christians may well watch the evening news to learn about public opinion polls forecasting upcoming elections, take prescription drugs approved by the FDA based on statistics found in clinical trials, obtain electrical power from a nuclear power plant that uses random fission reactions, and insure their cars with companies that rely on stochastic models to set the rates. The foundation of each of these activities is a thorough understanding of randomness that begins with the simple description above.

So where does the uneasiness come from? Likely it comes from the feeling that taking randomness seriously means not taking God seriously. Or put more strongly, it comes from a fear that believing in randomness means not believing in God. Next week we’ll address that problem by asking the question, “Could God use randomness to achieve his purposes?”

In the 1950s, Cage began using various methods of “casting lots” to determine how elements of his music would be chosen and arranged—principally the Chinese system of I Ching. His controversial program was to distance himself from his own creative process, and he explored many additional strategies to transform the role of “creator” into one of “observer.” Most famous of these was his musical composition, “4.33,” which consisted of a pianist sitting at the instrument doing nothing at all for four minutes and thirty-three seconds, while musician and audience listened to the ambient sounds of the concert hall. Yet contrary to that main thrust of Cage’s work, a description of the activities during the week-long residency at the Mountain Lake Workshop where the New River Watercolor Series were made suggests that choice, constraint, and intention were integral and inescapable tools in putting randomness to work for creative ends.

Here’s art historian and theorist Howard Risatti’s description of Cage’s plan of action for the New River Watercolors, from the website of artist Ray Kass, who runs the Mountain Lake program and was Cage’s collaborator for his work there:

Following upon [a previous (1983) Mountain Lake workshop] “painting experiment,” stones collected from the New River were sorted into three groups according to size, which were separately numbered; numerous and varied brushes were divided into two separately numbered groups; likewise, feathers to paint with, colors and washes, and papers were also divided and numbered. In this way, chance procedures using pages of random numbers that were now generated by a computer program could be used to determine the specific materials utilized for each painting (e.g., which painting instruments, what type of paper and which colors, how many washes, which stones to paint around, where to locate the stones on the paper).

While this list enumerates all the specific variables that Cage and his team submitted to chance, there was an incredible level of personal engagement with the materials: Cage didn’t just show us drawings of where the I Ching said the rocks ought to be, he (or his assistants) placed them on the paper and used them as guides to paint around. Large custom brushes were constructed to lay on washes of color, and even the paints were hand mixed, combined, and diluted according to his desires.

Cage’s use of chance, then, was not a “hands off” process, but neither was it a matter of total control: Cage selected processes to create a space of play between himself and the materials he used: the feather between himself and the paper, for instance, introduced variability of resistance and spring, its ability to hold paint, the width of the line. All of these things were elements of material ‘freedom,’ areas in which Cage asked the stuff he used to make the paintings to take part in the process—to contribute its own identity to the intentional, purposeful, and determined work of creating “based on chance.” This should not be surprising, as all art, all creation that we can observe, happens as a dialectic between materials and the creator, and such engagement and interaction in no way lessons the purpose of making, the end in sight.

Kass’ book The Sight of Silence: John Cage’s Complete Watercolors, gives a much more complete account of the tools, processes, and interpersonal reactions between Cage, Kass, and the team of student assistants who helped at almost every stage of the creation of the works. The book goes to great length to honor Cage’s ideal of being present in but not controlling the outcomes (not least by nearly always putting words like “choice” in quotation marks), but the description of his process makes the centrality of Cage’s personal aesthetic and artistic motives inescapable, even more than his physical engagement. What comes through perhaps even more than the way Cage intended to allow chance to ‘guide the creative process’ is that way Cage, himself, not only set the parameters of the chance he allowed into the system, not only engaged directly with the materials during the process, but also exercised judgment over the results, both in process and at the end:

“Cage decided he didn’t want the images of the stones to overlap or go off the sides of the paper. To guarantee this restriction, he created conditions and rules to limit their possible placements.” (p. 51)

“For this single painting [Series IV, #1, pictured above] Cage chose to confine the images of the rocks to a lower area of the paper that represented the proportion of the “golden rectangle. . .” (p. 57)

“While “choice” established much of the work’s nature, “chance” highlighted the intrinsic nature of the materials to reveal a refreshing presence.” (p. 59)

“[H]e initially decided to remove [the first painting of Series III] from the group, and then, liking it more, changed his mind and returned it to the group that would be signed.” (p. 56)

This last note is particularly interesting in that it highlights the fact that Cage was claiming these paintings, naming himself as their author, and was attentive to which ones he approved of enough to call his own. There is no way around the fact that Cage was subjectively as well as objectively the maker of these works: the author of the procedures by which they came to be, but well as the judge (and sometimes redeemer) of the results. For Cage, randomness was a tool, no different than the brushes or rocks or paints is that its specific parameters were chosen at the outset, and always used within the context of his over-arching vision. Perhaps we may likewise think of God’s use of chance—constrained by and tuned to the material conditions he established at the birth of the cosmos—as a way to both engage with and allow freedom for the creation itself.

With any work of art it is reasonable to ask, “Is it beautiful?” or more tellingly, “Would I hang this on my wall?” Seeing Cage’s watercolors for first time without any knowledge of the process or the relative fame of Cage himself, some might be intrigued by the structure of the work (the proportions of the golden rectangle, the overlapping stone shapes, the colors of the paint) while others would be completely uninterested, perhaps even after hearing about how they were made and seeing them in the context of the rest of the New River Watercolor series. But if you had been there in the shop as an assistant, or even observer, if you had been party to the relationships that developed even over the few days Cage spent at the Mountain Lake Workshop, your sense of the beauty of these paintings (and perhaps even scraps of paper Cage used to try out brushes or washes), would take on a different meaning, in much the way we treasure the crayon drawings of our children not because they are spectacular art, but because they are tokens of our relationship.

I make that observation to emphasize one other aspect of Cage’s creative process: that Cage was the instigator first and foremost of relationships of creation. His process created not only paintings but the fellowship that developed as the work was being done. That social, interpersonal dimension is what gives the objects a depth of meaning beyond their material composition, and suggests the particular roles humanity has been given by God. One role is to join into the creative process as lesser, but not unimportant co-creators with him; the other is to observe, recognize and celebrate his activity in the world. Where some will see randomness as evidence of an absent God, our knowledge of this most personal and participatory aspect of creation points us to the God who is with us.

With God’s creation as with human art, we may (or may not) marvel at any one particular “work,” or even think the specifics of how it was made are interesting or attractive; but knowledge of and fellowship with the artist transforms our appreciation of the process as well as its results. When we know the maker, we come to recognize and treasure even the most “random” bits of his handiwork, and name them as his, nonetheless.

For Further Reading:

Ray Kass. The Sight of Silence: John Cage’s Complete Watercolors, 2011.

Website for John Cage Centennial Festival, Washington, DC. September 2012.



]]> Sun, 13 May 12 12:53:04 -0700 Mark Sprinkle http://biologos.org/blog/understanding-evolution-theory-prediction-and-evidence-2?utm_source=RSS_Feed&utm_medium=RSS&utm_campaign=RSS_Syndication http://biologos.org/blog/understanding-evolution-theory-prediction-and-evidence-2?utm_source=RSS_Feed&utm_medium=RSS&utm_campaign=RSS_Syndication We have already discussed hind limb and hair loss in whales, and now we turn to one of the remaining questions: tooth loss in the lineage leading to modern toothless whales. One of the challenges for discussing evolution within evangelical Christian circles is that there is widespread confusion about how evolution actually works. In this (intermittent) series, I discuss aspects of evolution that are commonly misunderstood in the Christian community. In this post, we continue to explore how whale evolution is supported by converging lines of evidence from developmental biology and genetics.

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

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

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

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

Evolution: A Theory with Bite

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

Independent Lines of Evidence, but Contradictory Stories?

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

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

Signature in the SINE

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

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

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

For further reading:

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

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

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Perusing the writings of atheistic scientists and philosophers like Daniel Dennett, one could easily get the impression that arriving at a simpler explanation for something equates to a revelation that things are “lower, cruder, and more trivial.” But at the heart of Barr’s critique is the observation that in fundamental physics and advanced mathematics, “simpler” does not mean more chaotic and inchoate, but rather more elegant and beautiful. Those who hold to a philosophical reductionism “overlook the hidden forces and principles” that govern the processes of cosmic evolution.

Barr’s article lays out the way that the work of scientists and mathematicians exploring the fundamental principles of physics (from Kepler to Einstein to those currently running the Large Hadron Collider in Switzerland) actually suggests “that order does not really emerge from chaos, as we might naively assume; it always emerges from greater and more impressive order already present at a deeper level.” This excerpt gives his first example, the starting point from which he guides us into strangely beautiful world of particle physics, and towards the discovery that “matter, although mindless itself, is the product of a Mind of infinite profundity and infinite simplicity.”

Fearful Symmetries

“Let’s start with a simple but instructive example of how order can appear to emerge spontaneously from mere chaos through the operation of natural forces. Imagine a large number of identical marbles rolling around randomly in a shoe box. If the box is tilted, all the marbles will roll down into a corner and arrange themselves into what is called the “hexagonal closest packing” pattern. (This is the same pattern one sees in oranges stacked on a fruit stand or in cells in a beehive.) This orderly structure emerges as the result of blind physical forces and mathematical laws. There is no hand arranging it. Physics requires the marbles to lower their gravitational potential energy as much as possible by squeezing down into the corner, which leads to the geometry of hexagonal packing.

At this point it seems as though order has indeed sprung from mere chaos. To see why this is wrong, however, consider a genuinely chaotic situation: a typical teenager’s bedroom. Imagine a huge jack tilting the bedroom so that everything in it slides into a corner. The result would not be an orderly pattern but instead a jumbled heap of lamps, furniture, books, clothing, and what have you.

Why the difference? Part of the answer is that, unlike the objects in the bedroom, the marbles in the box all have the same size and shape. But there’s more to it. Put a number of spoons of the same size and shape into a box and tilt it, and the result will be a jumbled heap. Marbles differ from spoons because their shape is spherical. When spoons tumble into a corner, they end up pointing every which way, but marbles don’t point every which way, because no matter which way a sphere is turned it looks exactly the same.

These two crucial features of the marbles—having the same shape and having a spherical shape—should be understood as principles of order that are already present in the supposedly chaotic situation before the box was tilted. In fact, the more we reduce to deeper explanations, the higher we go. This is because, in a sense that can be made mathematically precise, the preexisting order inherent in the marbles is greater than the order that emerges after the marbles arrange themselves. This requires some explanation.

Both the preexisting order and the order that emerges involve symmetry, a concept of central importance in modern physics, as we’ll see. Mathematicians and physicists have a peculiar way of thinking about symmetry: A symmetry is something that is done. For example, if one rotates a square by 90 degrees, it looks the same, so rotating by 90 degrees is said to be a symmetry of the square. So is rotating by 180 degrees, 270 degrees, or a full 360 degrees. A square thus has exactly four symmetries.

Not surprisingly, the hexagonal pattern the marbles form has six symmetries (rotating by any multiple of 60 degrees: 60, 120, 180, 240, 300, and 360 degrees). A sphere, on the other hand, has an infinite number of symmetries—doubly infinite, in fact, since rotating a sphere by any angle about any axis leaves it looking the same. And, what’s more, the symmetries of a sphere include all the symmetries of a hexagon.

If we think this way about symmetry, careful analysis shows that, when marbles arrange themselves into the hexagonal pattern, just six of the infinite number of symmetries in the shape of the marbles are ex-pressed or manifested in their final arrangement. The rest of the symmetries are said, in the jargon of physics, to be spontaneously broken. So, in the simple example of marbles in a tilted box, we can see that symmetry isn’t popping out of nowhere. It is being distilled out of a greater symmetry already present within the spherical shape of the marbles.”

In the full essay, Barr gives a richer description of how this most basic kind of symmetry is just one sort of order, and how even this form points to other much more complex kinds of symmetry whose properties may be described only through the tools of complex mathematics. As he says, “the symmetries that characterize the deepest laws of physics are mathematically richer and stranger than the ones we encounter in everyday life.” But even more important than the fact that such mathematical concepts exist and are beautiful, more important even than the way such esoteric mathematical symmetries have suggested imminently practical experimental projects, is the way they point to a universe that is anything but brutish and trivial, though its elegance may be hard to see:

“It is true that the cosmos was at one point a swirling mass of gas and dust out of which has come the extraordinary complexity of life as we experience it. Yet, at every moment in this process of development, a greater and more impressive order operates within—an order that did not develop but was there from the beginning. In the upper world, mind, thought, and ideas make their appearance as fruit on the topmost branches of an evolutionary tree. Below the surface, we see the taproots of reality, the fundamental laws of physics that shimmer with ideas of profound simplicity.”

This essay appears with the permission of First Things. To read Barr’s complete essay, please click here.

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.”