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

What you can expect

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

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

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

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

How you can help

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

Getting started

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

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

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

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

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

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

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

Notes

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

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

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

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

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

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

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

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

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

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

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

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

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

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

ER: What qualifies as a “rare disease”?

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

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

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

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

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

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

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

ER: How did RGI get started?

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

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

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

Excerpts from Michael Hickerson Interview

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

JL: Medical and scientific doxologist.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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.

Morality, or more strictly our belief in morality, is merely an adaptation put in place to further our reproductive end.

Important scientific theories invite philosophical and theological reflection. Dawkins, Ruse, and Wilson, have described their conclusions. But scientific theories are often compatible with multiple philosophical and religious interpretations. For example, Newton's laws of motion and gravity allow several competing theistic and atheistic interpretations.

To avoid Ruse and Wilson's philosophical conclusion, we need not dispute their scientific hypothesis about how morality evolved. We need only dispute their philosophical extrapolation as to why morality exists. Even if we restrict ourselves to an atheistic worldview, this extrapolation is questionable. Donald MacKay (1965) would call this an example of "the fallacy of nothing but-tery". This is the assertion that a description of something at one level renders other levels of description meaningless. From our everyday experience, we know that a successful description on one level does not invalidate other levels of description. For example. one might assert that a Shakespeare sonnet is "nothing but" ink blots on a page (MacKay 1965). True, one way to describe a sonnet is to precisely specify the page coordinates of every ink blot. This description is valid and complete on its own level; however, one could also analyze the sonnet linguistically, emotionally, socially, historically, and on other levels. If one is programming an inkjet printer, the most important description is in terms of ink blot coordinates. For almost every other purpose in life, however, that is an unimportant level of description. In the same way, a complete evolutionary description of the existence of morality does not necessarily invalidate the truth, utility, or significance of other levels of description of morality.

If we do not restrict ourselves to atheism and instead allow for the existence of a creator, the extrapolation from how morality evolved to why morality exists fails further. Consider an analogy. Suppose an inventor builds a robot which could do a variety of useful things-- mow the lawn, clean the house, grade homework, write book chapters, and so on. One thing this robot can do, given a complete set of spare parts, is build a replica of itself. Whenever the inventor needs another robot, she gives one robot a set of spare parts and has it build a replica of itself. Amongst all the software subroutines within this robot, there is a set of subroutines that govern the robot's self-replication, including the replication of those self-replication subroutines. Would it be correct to say that the purpose of the robot's existence is merely to reproduce those particular self-replication subroutines? Do all of the other software and hardware of the robot--which allow it to mow the lawn, and so on-- merely further the reproductive ends of those self-replication subroutines? At one level, the robot's hardware and software do serve to reproduce those self-replication software routines. At another level of analysis, however, those self-replication software routines serve the robot to produce more copies of itself. At still another level, those self-replication software routines serve the robot's creator. The creator of the robot should get the last world as to which of those levels of description is most important.

In humans, does morality exist to further the reproduction of certain genes, or do those genes exist in order to allow for the production of new human beings who can behave morally? If human beings have a creator, the creator gets the final word on the question of purpose. The mechanism which the creator used to make those genes-- whether de novo or via evolution-- is secondary. The creator's purpose in creating those genes decides the issue.

References

• Dawkins, Richard. 1976. Pp. 1-11 in The Selfish Gene. Oxford: Oxford University Press.
• MacKay, Donald. 1965. Christianity in a Mechanistic Universe. Chicago: InterVarsity.
• Ruse, Michael, and Edward O. Wilson. 1993. The approach of sociobiology: The evolution of ethics. In Religion and the Natural Sciences, ed. James E. Huchingson. Fort Worth: Harcourt Brace Javonovich.

If a cadre of outspoken, strong atheists wrote a litmus test for scientists, that might very well be question #1.

"Scientists, if you're not an atheist, you're not doing science right," PZ Myers -- a well-known blogger, biology professor and atheist -- regularly preaches.

But if this is true, then as many as half of scientists are doing science wrong. A 2009 study from the Pew Research Center polled members of the American Association for the Advancement of Science (AAAS). Fifty-one percent of respondents reported a belief in a higher power. Does this mean that it's too late for science? Has religion already pillaged the minds of researchers worldwide? No, of course it hasn't.

"It seems to me that we as a society have lately been caught in this false dichotomy where it's either God as the guy with the beard on the cloud or nothing at all," neuroscientist David Eagleman told Discovery News.

Staunch atheists often falsely characterize followers of religion as being "all-in" with their beliefs, opining that they ascribe to the whole creationist, woo-y shebang. "Where's your evidence?" atheists mockingly question. "You can't prove that God exists!" they accuse (correctly). Yet, hypocritically, strict atheists are guilty of the exact same crime: belief without evidence.

"We know too little to commit to a position of strict atheism. [But] we know way too much to commit to any particular religious story," Eagleman said.

Just as it's a leap of faith for a religious person to assert that God incontrovertibly exists, it's an equally large leap for a strict atheist to declare, without question, that God does not exist. As Carl Sagan eloquently explained:

An atheist is someone who is certain that God does not exist, someone who has compelling evidence against the existence of God. I know of no such compelling evidence. Because God can be relegated to remote times and places and to ultimate causes, we would have to know a great deal more about the universe than we do now to be sure that no such God exists. To be certain of the existence of God and to be certain of the nonexistence of God seem to me to be the confident extremes in a subject so riddled with doubt and uncertainty as to inspire very little confidence indeed.

Absence of evidence is not evidence of absence. As this statement applies to science, so does it apply to religion. History is replete with signs that an all-powerful deity may not exist, but such substantiation is nowhere near tantamount to proof -- especially, as Albert Einstein said, in a universe as incomprehensibly vast as our own:

The human mind, no matter how highly trained, cannot grasp the universe. We are in the position of a little child, entering a huge library whose walls are covered to the ceiling with books in many different tongues. The child knows that someone must have written those books. It does not know who or how. It does not understand the languages in which they are written. The child notes a definite plan in the arrangement of the books, a mysterious order, which it does not comprehend, but only dimly suspects. That, it seems to me, is the attitude of the human mind, even the greatest and most cultured, toward God. We see a universe marvelously arranged, obeying certain laws, but we understand the laws only dimly.

Ultimately, the key is not to be swayed to one extreme or the other -- fundamentalist religion or strict atheism -- but to walk a reasoned middle path. Eagleman believes that path is "possibilianism," the concept of holding multiple beliefs or hypotheses whilst exploring new ideas.

"The goal is to avoid committing to any particular story," Eagleman told Discovery News, "whether that's religious fundamentalism or strict atheism. The goal of possibilianism is to retain the wonder that drives us all into science in the first place and to avoid acting as though we know the answers to things we can't possibly know at the moment."

Strict atheists do the world an incredible service by promoting the scientific method, skepticism, and critical thinking. But they do a disservice by campaigning against religion or touting -- as pure truth -- the non-existence of God, for those actions (especially the latter) are just as unscientific as a blind belief in all aspects of religion.

This summer, a worldwide poll showed that atheism is on the rise and religiosity is on the decline. It is my hope that these "New Atheists" and agnostics won't narrowly focus on denigrating religion, but will instead focus on encouraging open-mindedness and discouraging fundamentalism.

That would surely make the world a more enlightened place.

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.

There are more things in heaven and earth, Horatio, than are dreamt of in your philosophy.

—Hamlet Act 1, Scene 5

We live in a world driven by the gods of economics, technology and science. Particularly in a time of economic austerity, it is tempting to see the arts or humanities as an optional “extra”—a happy by-product of those true engines of society when they are running smoothly. But in this article we will look at how a biblically informed worldview might turn this perspective on its head, and what the humanities might have to tell us about the present contours of the science and faith conversation.

In his iconic 1959 Rede lecture, “The Two Cultures,” CP Snow noted the dysfunctional relationship between science and the humanities, arguing that the situation is principally the result of our educational system in the West. Ken Arnold, from the medicine and arts focused Wellcome Collection in London, believes that the split continues today, but with the further extension that

In emerging countries . . . amongst the middle classes there is a strong pressure to join the ranks of doctors and scientists and engineers because they see that as the place where future economies are growing. . . . In some ways you could almost begin to feel sorry for the arts and the humanities because they seem to be worth less than the sciences.¹

Is Protestant Christianity also peculiarly prone to such thinking? A skepticism of art in religious spaces as a result of iconoclasm and the reformation, combined with a proud history of the protestant work ethic, economic success, and a profound influence on the history of science, might lead Protestants to be more inclined towards the sciences and technology than to the arts. However, there are more corrosive reasons that science has usurped the humanities in our culture than merely educational or theological bias.

In the early 20th century, logical positivists regarded the humanities as expressions merely of our inner states and desires, but having nothing to do with objective reality. Such imperialistic claims to knowledge denied that other knowledge claims referred to any true reality, and were therefore not really forms of knowledge at all. Bertrand Russell writes,

But if there is a world which is not physical, or not in space-time, it may have a structure which we can never hope to express or to know … Perhaps that is why we know so much physics and so little of anything else.²

Christian scientists are of course very sensitive to this, and work hard to explain that science cannot answer questions of ultimate meaning or the existence of God, which are beyond the scope of science. Often, this line of thinking can be narrow in focus, delineating the limits of the science, and naming those assumptions made by science that cannot be justified empirically. Such arguments can be very fruitful within this narrow context, but we should not be led into thinking that our true perception of reality is limited to such analytic and evidential approaches. There are fields of inquiry that science isn’t able to explain (such as metaphysical judgments, ethics, and beauty), and even our confidence in mathematics— upon which so much of science itself is based—rests upon assumptions that cannot be experimentally demonstrated.

The human condition

Mathematics and the sciences do seem to provide tools by which we are able to perceive the external world and its regularities. However, the arts and humanities, too, are a way of understanding reality, and they tell us less about external reality than the internal human condition. The problem is that the ‘human condition’ seems to have been relegated by many to the realm of mere desire and subjective feeling and, therefore, not reality.

The modernist account of science is that, through our reason, we are somehow able to get outside of nature and describe it objectively. The biblical account, though, has human beings as part of the created order, and so embedded in nature—made from the dust of the earth. Given that, human thought life is also part of the natural world, even despite the fact that it is not best described by the sciences.

The works of Shakespeare, for instance, are part of the created order, as are the poems of Wordsworth, the sculptures of Michaelangelo, and the music of Bach, not to mention children’s nursery rhymes, home decoration, and humming tunes whilst waiting for the bus. As C. S. Lewis wrote, "This is not panache, it is our nature." ³

A little reflection on life reveals something very strange going on here. Somehow, the mythic ‘war’ between science and religion has become the dominant battleground for defending the Christian faith, and competing explanations of the material world are used as apologetic weapons. But the reality is that science plays a peripheral role in our experience of life, not least our life as Christians. Of course that is not to deny the enormous impact of science on the material conditions of our lives, or the prevalence of the products of science. Instead, it is to observe that science plays a facilitatatory role, enabling us to carry out the real core business of our lives, which does not revolve around science. Cars, trains and airplanes are modes of transport to take us to work, or to see family, or go on holiday. Social media provide another way of being in relationship with people. Health services are not an end in themselves, but aim to make people well, so that they can get on with their lives. Why then, when life is not about science, does science dominate our way of thinking about life?

In focusing so much energy on opposing positivism are we not being inadvertently drawn into a positivist way of thinking, that science and material explanations of things are, indeed, our basic reality, what is ultimately true?

A biblical model

“We feel,” wrote the philosopher Ludwig Wittgenstein, “that even when all possible scientific questions have been answered, the problems of life remain completely untouched.” ⁴ Likewise, philosopher Susanne Langer questions any philosophy which claims to be able to explain everything:

Philosophers in every age have attempted to give an account of as much experience as they could. Some have indeed pretended that what they could not explain did not exist; but all the great philosophers have allowed for more than they could explain, and have, therefore, signed beforehand, if not dated, the death-warrant of their philosophies.⁵

Fortunately, the Bible preserves us from total positivist oblivion. There are a great many types of literature represented in the Bible, with the notable exception of scientific writing. If we long to be able to express our deepest emotions, we have the psalms; if we are looking for wise advice, we have the proverbs; if philosophical reflection, Ecclesiastes. There is poetry, song, history, biography, but there is no science. In addition, the Bible refers to the use of the visual arts in, for example, the designs of the tabernacle and temple. The Bible does seem to think the arts and humanities are fundamental for human life, but it doesn’t seem to think that what we think the physical world is constructed of matters much at all.

Do we sometimes read the Bible more like a science textbook than a novel or a poem? Most will agree that each type of literature needs to be read in its own way, but lip-service to that idea notwithstanding, recent arguments prove that it is still possible to read a poem with a scientific mentality—looking out for the ‘facts.’ Is that because we have too high a view of science, or because we have too low a view of the humanities? To say something is poetic is not to declare it ultimately untrue, futile and meaningless—it is to say it is more profound and meaningful and true than many other modes of expression.

According to Langer, part of the problem is the priority that has been accorded to discursive language as the only valid way we have of representing reality to each other. She observes that a study of symbolism shows us that this is actually only one way humans use to abstract from reality, and in fact, the situation even with discursive language isn’t as simple as has been made out. She notes that our sensory organs mediate our perceptions of the world and are already on the job— formulating, framing the world to us—before our cognitive apparatus gets to work. It must be so, or we would not be able to evaluate the importance of the vast array of sensory data we receive and reality would appear as a blur.

A linguistic symbol carries a concept we associate with it, which in turn denotes a reality. In language there is a commonly agreed definition for each word we use, thus enabling communication. But each person also has associations unique to him or her which color any particular concept. Though such personal associations with words are present all at once, they can only be expressed and communicated one at a time, because language is also sequential.

A picture also acts symbolically, though in a different way. Even something as ‘realistic’ as a photograph is likewise a representation of reality and not the reality itself. It also carries with it layers of meaning which reflect the subjective intentions of the person who took the photograph, and opens up for interpretations and associations of the person ‘reading’ the picture. A picture, though, is not sequential. All the information comes at once, and individual blotches of color carry no significance on their own, but only as part of the whole.

No amount of words could ever describe a picture in full. The number of blotches of color and their relations to each other are vast in their complexity, and one could never read words quickly enough to carry the meaning a picture brings in an instant, even if it warrants a far longer period of contemplation. Indeed, though we are only speaking here of visual perception, the same is true of our other sensory inputs, too: they all carry knowledge in quite distinct and profound ways, whilst we, in line with the Greeks, have tended to give sight a special place as the most ‘objective’ of our senses.

As we dig down into empirical science and explore the mechanisms by which sights and sounds and textures are transmitted and processed by the brain, we discover that the meaning of the sense-data which we perceive and which we attempt to describe is likewise profoundly limited by the use of words—much less mathematics—and that our science, as such, represents a tiny fraction of reality.

To suggest, then, that science is the only true way of representing reality—as positivism has done—or to exclude the humanities from our world, leaves us without a proper or even adequate means of expressing the significance we attach to even the most mundane day-to-day activities. Science is very good at describing the regularities of the physical world, but the experience of being human is no less part of the real natural world than are the structure of proteins or the movement of planets, and science does not have the appropriate tools to explore our inner worlds.

Nowadays it seems that Christian cultural life has also too-often failed to fully acknowledge other ways of representing reality than materialist science—ironic because this state of affairs is so at odds with the Bible’s model of using the arts and humanities to profoundly explore the human condition. Perhaps it is time to recover that side of the biblical witness, and remind ourselves that there are more ways of representing the world to each other than positivism has ever dreamt.

Notes

1. BBC Radio 4, “The Life Scientific”, Tuesday 25th September 2012.
2. Bertrand Russell, “Philosophy”, New York. W.W.Norton &Co, 1927, page 265, quoted by Susanne K. Langer, Philosophy in a New Key, Harvard University Press, 1979, page 88.
3. C. S. Lewis, “Learning in War Time” in Fernseed and Elephants and other Essays on Christianity, Fontana, 1975, page 28.
4. Ludwig Wittgenstein, Tractatus Logico-Philosophicus. Routledge and Kegan Paul, 1951, page 187.
5. Susanne K. Langer, Philosophy in a New Key: A Study in the Symbolism of Reason, Rite and Art. Harvard University Press, 1979, p 5.

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.

There are several different kinds of arguments that people bring along these lines; I want to talk about just one. So first… the Heidelberg catechism, one of the forms of unity of the church I go to (the Christian Reformed Church), says

Providence is the almighty and ever-present power of God, by which he upholds as with his hand heaven and Earth and all creatures and so rules them, that leaf and blade, rain and drought, fruitful and lean years, food and drink, health and sickness, prosperity and poverty. All things, in fact, come to us not by chance, but from his fatherly hand.

And part of the way it comes to us—not by chance, but from his fatherly hand—part of the way God has designed our world, is that there is a great deal of regularity and dependability in our world. Of course, if it were not for this regularity and dependability, we couldn’t do the things that we actually do. I mean, for example, if I just wanted to walk off the stage—if, for example, all the sudden those stairs over there suddenly turned into a ladder going up—well, that would make it really difficult.

If you are trying to build a house, for example, you have this hammer, but all the sudden the hammer turns in to a goose or a pigeon. Again, that would make things really difficult…or if the nail turned into a worm…or if you get in the car and turn the key and the car turns into a camel, things would be really hard, much harder than they are. This regularity and dependability in our world is an essential condition of our being able to live in the world in which we actually do.

If the world were irregular enough, we would not even be able to live in it, but there are also, according to classical Christianity here (the Heidelberg catechism, for example) there are also special divine actions; sometimes God does things specially. There are miracles in Scripture: the parting of the Red Sea, for example, Jesus walking on water, Jesus changing water into wine. There are miraculous healings: Jesus rising from the dead, Jesus raising Lazarus from the dead, and so on. And according to classical Christians, many of them, perhaps most of them, are special divine actions. God, for example, responds to prayers. He works in the hearts and minds of his children to effect sanctification. There is, what Calvin called, the internal testimony or witness of the Holy Spirit, and there is what Thomas Aquinas called the internal instigation of the Holy Spirit. So, these things are all special actions on the part of God. God constantly causes events in the world. Ok, so far fair enough—what is the problem?

Many theologians seem to think there is a science-religion problem here. I don’t think any of the theologians of Biola think this, (I don’t know, but I doubt it) but many theologians do. For example, Rudolf Bultmann says, “The historical method,” which of course he thinks that is the method we should use, “includes the presupposition that history is a unity in the sense of a closed continuum of effects in which individual events are connected by the succession of cause and effect. This continuum, furthermore, cannot be rent by the interference of supernatural, transcendent powers.”

That’s what he says. Alright, there is this continuum that cannot be rent by the interference of supernatural (that would be God) or transcendent powers. So, it is a little bit like the laws of the Medes and Persians. You probably remember Daniel. Daniel was a favorite of King Darius, and well, the other courtiers became jealous of Daniel (they didn’t like it that the king liked him so well). So, they came to the king and said, “Oh king, live forever, we think it would be a great idea if you passed an edict to the effect that you alone can be worshipped. Everybody has to worship you and nothing else.” Well the king thought that over for a minute, and that sounded pretty good to him so he said, “I guess that it is a pretty good idea.” So he made this edict; he made this declaration: “Only King Darius is to be worshipped—no one else, nothing else.”

These courtiers knew that Daniel worshipped God, and they thought probably Daniel would keep right on worshipping God despite this edict. So they were watching Daniel, and he was, in fact, worshipping God. So they came to the king. Now the penalty for worshipping something else was to be thrown into the lion’s den and they said, “Well, king live forever, looks like Daniel has been violating this edict. You have got to throw him in the lion’s den.”

Well, the king didn’t want to do this because he really liked Daniel. He thought this was a miserable way to proceed, and he didn’t want to do it, but then they said to him, “O king live forever, and remember a law of the Medes and Persians cannot be abrogated, even by the king himself.” So once it’s put in place, not even the king himself can change it or abrogate it or go against it.

That is sort of the suggestion that you get here from Bultmann. Bultmann thinks, “Maybe God created the world and set it up in a certain way, but once he did that, not even he can interfere in it”—he uses that word interference—“not even he can do anything in it. He just has to keep hands off.” It is like the law of the Medes and the Persians.

Another theologian who agrees is John Macquarrie, who says,

The way of understanding miracle (and that would be one kind of special divine action) that appeals to breaks in the natural order and to supernatural intervention belongs to the mythological outlook, and cannot commend itself in a post-mythological climate of thought. The traditional conception of miracle is irreconcilable with our modern understanding of both science and history. Science proceeds on the assumption that whatever events occur in the world, can be accounted for in terms of other events that also belong within the world, and if on some occasion, we are unable to give a complete account of some happening, the scientific conviction is that further research will bring to light further factors in the situation that will turn out to be just as imminent and this worldly as the factors already known.

Ok again, no room there for special action. And the third thinker here, Langdon Gilkey (still another theologian), says something similar, but I will pass. I will not read that one in the interest of saving a little bit of time, but these three theologians, plus many others want to assert that there is something wrong with the idea of God acting in the world, acting in the world in a way that goes beyond creation and sustaining, or creation and holding things in existence. So they think, “Ok, God created the world; God sustains it in existence”…that is ok with them, but anything beyond that, God performing any miracles, raising Jesus from the dead, or for that matter working in somebody’s heart and mind in a special way, that, they say, is a real problem. The question is, what is the problem?

Well, the next little bit here…according to the Christian and theistic idea, God is a person; he has knowledge, loves, and hates. He has aims and ends. He acts on the basis of his knowledge to achieve his ends. He is all-powerful, all-knowing, and wholly good. Thirdly (noted above by the Heidelberg catechism), God has created the world. Fourth is God conserves and sustains and maintains in being this world he created, but fifth, at least sometimes, God acts in a way going beyond creation and conservation in miracles, but also in his providential guiding of history, his working in the hearts of people, his internal instigation of the Holy Spirit, and so on, and it is with that fifth category that these people have a problem. It is God’s special action in the world—action beyond conservation and creation—and miracles would be an example.

So we might think of these theologians as endorsing what we could call hands off theology. God has got to keep his hands off. God could create the world. God conserves the world, sustains it in being, but he can’t do anything else—that is as far as he could go. It is hands off theology, and Bultmann, even in this context, even talks about interfering. I mean if God did something in the world that would be interfering, which, when you think about it, is a sort of strange thing to say—I mean if God created the world, he is the omnipotent, omniscient, holy, good creator of the world—when you accuse someone of interfering, you are saying they are doing something they should not be doing, right?

So Bultmann thinks if God did something in the world that would be interfering, and he should be ashamed of himself. Ok, now why is this a problem? Their suggestion is that somehow it is contrary to science. It is contrary to science the suggestion that God acts specially in the world. I didn’t read that bit, but Gilkey says, "The causal nexus in space and time which the enlightenment science and philosophy introduced into the western mind is also assumed by modern theologians and scholars. Since they participate in the modern world of science, both intellectually and existentially, they can scarcely do anything else.”

From a presentation sponsored by Biola University’s Center for Christian Thought, and delivered February 12, 2012 at EV Free Church, Fullerton, CA. Used by permission.

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

Judging from the flurry of headlines over the past week, one might be tempted to think that proof positive of God’s existence (or lack thereof) had just appeared out of a 27-km-tunnel buried beneath the Swiss-French border. This frenzy of news headlines and blog titles hailed the recent news that CERN’s Large Hadron Collider has discovered a brand new particle of a mass of 125-126 GeV, which is assumed to be the Higgs boson, or the so-called “God particle.” The discovery of the Higgs boson would certainly be a breakthrough for particle physics and cosmology, but would such a finding also radically redefine theology’s understanding of God or challenge the existence of such a deity? Is there actually any theological or religious significance in Higgs physics at all?

The short answer is “no,” which becomes apparent when one considers the widely-reported story of how it got named. In 1993, Nobel Laureate physicist Leon Lederman, along with science writer Dick Teresi, wrote a book detailing the history of particle physics starting with Pre-Socratic Greek philosophy Democritus and culminating with the hunt for the Higgs boson. Until this latest discovery, the Higgs boson was the elusive final missing piece of the puzzle known as the Standard Model—a collection of the fundamental particles that constitute our universe and the complex and mathematically-sophisticated relationships between them. Considering how incredibly difficult finding the Higgs boson was proving to be, Lederman wanted to name the book after that “goddamn particle,” according to some of his collaborators. His editor, however, would not allow it and so the name was shortened to “The God Particle: If the Universe Is the Answer, What is the Question?” And thus ‘the God particle’ was born, carrying with it more than enough social baggage for such a miniscule particle.

Particle physicist Dr. Zosia Krusberg (at right) is visiting assistant professor of physics and astronomy at Vassar College and thinks “the term ‘god particle’ is unfortunate. The Higgs boson is no more (or less) divine or spiritually significant than any other elementary particle within the standard model of particle physics.” It may be fundamental to explaining one of the most basic characteristics of the universe—namely the existence of matter and mass in addition to energy—but “it is no more (or less) important than any other physics principle underlying the Standard Model.”

Last week’s discovery was monumental in that it may have finally provided experimental evidence for the Higgs Mechanism and defined the specific energy of the resulting Higgs boson, but even this “breakthrough” for particle physics leaves many scientific questions unresolved. Finding the Higgs boson completes the Standard Model, but it does not do away with many other questions and shortcomings of the current state of particle physics, such as the constituent particles of dark matter, a quantum theory of gravity, and other “mathematically subtle problems.” Not to mention that there is still significant work to be done to determine the exact nature of this newly-found particle. According to Dr. Krusberg, this particle might behave just as the Standard Model predicts or it could instead be “a Higgs-like particle that will serve as a gateway into explorations of physics beyond the Standard Model." Krusberg continued, “And I guarantee that it is this latter scenario that most of us are hoping for: physicists love nothing more than discovering the shortcomings of their theories, since this is the first step toward more fundamental theories with even more predictive power!”

No, finding the Higgs boson does not answer all the questions of particle physics, much less lend insight into the existence (or not) of God. For that reason, Dr. Krusberg (like most physicists) bemoans the term ‘God particle’ and insists, “There really is nothing either literally or metaphorically god-like about the Higgs boson.” Indeed, one writer for the British journal The Guardian reached such a point of frustration about the name that he ran a competition for alternatives. The winner was “the champagne flute boson,” ostensibly because the bottom of a champagne bottle is an excellent and oft-used demonstration of the energy potential of the Higgs Mechanism. Or then again, perhaps it is simply because physicists thought that finally finding this shy particle would call for some of the bubbly.

On the other hand, some science writers and scientists can appreciate the ‘educational benefits’ of such a mysterious and controversial name because it attracts the attention of the general public and puts a relatable face on an extremely esoteric physics concept. Krusberg herself admits that “People are naturally drawn to the mysterious and the controversial, providing educators with great teaching opportunities.” But she worries about the larger social implications involved in “mixing the vernacular of physics and spirituality,” not least because such uncritical mixing can lead the non-scientific community to draw conclusions about the authority and reach of science that are not justified.

Understanding that the Higgs boson is not the literal stuff of God and that it does not prove or disprove God’s existence (as the name seems to suggest) extinguishes the fire under any sort of religious outcry. But this does not mean that its discovery is irrelevant to the discussion of science and faith, nor to the Christian community as a whole. As Dr. Krusberg remarks, “The recent discovery of [this] new boson at the LHC perfectly embodies the scientific process at its best (and thereby illustrates to the public why and how science works).” Scientific exploration of nature is not a fool-proof endeavor; healthy skepticism and accountability to a wide community of other researchers are absolutely critical to its success. But such evidence of the power and finesse of well-executed science as we saw last week is a testament to our ability to explore and understand the ‘how’ of the universe. God has equipped humanity with the desire, the intellectual abilities, and the collective will to recognize and explore the cosmic order and beauty of his creation. God has made our home knowable, and has given us the tools and capacities by which to know it.

At left, Cern researchers present their findings to a few hundred of their colleagues in Melbourne, Australia. Image © 2012 CERN

It is valuable, then, for the Christian community to understand and appreciate how science works, in part to recognize that there are many instances in which science and the church work in tandem in order to better understand and better serve the world. But I think there is something else we can draw from the story of the Higgs boson, too. The nickname ‘the God particle’ has touched nerves in religious communities because it implies that science has the ability to prove or disprove divine existence by physical means. Even though the physics community is by no means claiming insight into the divine, it is sometimes assumed by the religious community that scientists view their work as chipping away at God’s existence when they begin to understand something that was previously unknown, or known only “by faith” in esoteric theories and models.

And yet, regardless of motives or metaphysical interpretations, perhaps physicists' search for the Higgs boson is in fact an apt picture of our own search for God. How many times have we stared up at the starry ceiling in times of crisis and prayed fervently for some kind of sign from God to assure us of his presence? And how many times has that much-desired evidence appeared only in retrospect, when we look back to see God’s hand faithfully and elegantly working in ways inscrutable at the time? It took a community of physicists to discern the presence of the Higgs boson. But even so, they could only do so after the fact from the cascade of particle decays it sparked; they could not observe the particle itself directly. In a similar way, though we often do not see the working of God directly, “in the moment,” we still trust in his presence and providence, often depending on friends, family and the community of the church to help us see his hand in hindsight.

So while the discovery of the Higgs boson does not itself explain God, we rejoice at the subtle yet striking new insight we have into God’s creative genius via the Higgs boson and at the way God gives evidence of his faithfulness in the ordered creation itself. Perhaps, however, the greatest insight we can glean from this breakthrough is an analogy for the way God calls us to seek him and find him together, in the community of those who follow his son.

Tomorrow, Baylor University physicist Gerald Cleaver answers the question, "What is the Higgs boson?"

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.

A scientist, my dear friends, is a man who foresees; it is because science provides the means to predict that it is useful, and the scientists are superior to all other men. --Henri de Saint-Simon¹

Scientism is a rather strange word, but for reasons that we shall see, a useful one. Though this term has been coined rather recently, it is associated with many other “isms” with long and turbulent histories: materialism, naturalism, reductionism, empiricism, and positivism. Rather than tangle with each of these concepts separately, we’ll begin with a working definition of scientism and proceed from there.

Historian Richard G. Olson defines scientism as “efforts to extend scientific ideas, methods, practices, and attitudes to matters of human social and political concern.” ² But this formulation is so broad as to render it virtually useless. Philosopher Tom Sorell offers a more precise definition: “Scientism is a matter of putting too high a value on natural science in comparison with other branches of learning or culture.” ³ MIT physicist Ian Hutchinson offers a closely related version, but more extreme: “Science, modeled on the natural sciences, is the only source of real knowledge.” ⁴ The latter two definitions are far more precise and will better help us evaluate scientism’s merit.

A History of Scientism

The roots of scientism extend as far back as early 17th century Europe, an era that came to be known as the Scientific Revolution. Up to that point, most scholars had been highly deferential to intellectual tradition, largely a combination of Judeo-Christian scripture and ancient Greek philosophy. But a torrent of new learning during the late Renaissance began to challenge the authority of the ancients, and long-established intellectual foundations began to crack. The Englishman Francis Bacon, the Frenchman Rene Descartes, and the Italian Galileo Galilei spearheaded an international movement proclaiming a new foundation for learning, one that involved careful scrutiny of nature instead of analysis of ancient texts.

Descartes and Bacon used particularly strong rhetoric to carve out space for their new methods. They claimed that by learning how the physical world worked, we could become “masters and possessors of nature.” ⁵ In doing so, humans could overcome hunger through innovations in agriculture, eliminate disease through medical research, and dramatically improve overall quality of life through technology and industry. Ultimately, science would save humans from unnecessary suffering and their self-destructive tendencies. And it promised to achieve these goals in this world, not the afterlife. It was a bold, prophetic vision.

As this new method found great success, the specter of scientism began to emerge. Both Bacon and Descartes elevated the use of reason and logic by denigrating other human faculties such as creativity, memory, and imagination. Bacon’s classification of learning demoted poetry and history to second-class status.⁶ Descartes’ rendering of the entire universe as a giant machine left little room for the arts or other forms of human expression. In one sense, the rhetoric of these visionaries opened great new vistas for intellectual inquiry. But on the other hand, it proposed a vastly narrower range of which human activities were considered worthwhile.

The Enlightenment

A century later, many of the Enlightenment intellectuals continued their love-affair with the power of natural science. They claimed that not only could science enhance the quality of human life, it could even promote moral improvement. The Encyclopedist Denis Diderot aimed to collect, organize, and preserve all human knowledge so that “our children, becoming better instructed, may become at the same time more virtuous and happy.” ⁷ Many of the French philosophes even claimed that science could be a substitute for religion. In fact, during the French Revolution, numerous Catholic churches were converted into “Temples of Reason” and held quasi-religious services for the worship of science.⁸

Positivism

The 19th century witnessed the most powerful and enduring formulation of scientism, a system called positivism. Its founder was August Comte, who built his positive philosophy from a deep commitment to David Hume’s empiricism and skepticism. Comte claimed that the only valid data is acquired through the senses. Nothing was transcendent, and nothing metaphysical could have any claim to validity.⁹ The task of scientists was twofold—first, to demonstrate how all phenomena, including human behavior, are subject to invariable natural laws.¹⁰ Second, they would reduce these natural laws to the smallest possible number, and ultimately unify them under the laws of physics.¹¹

Comte also subsumed all of human intellectual history into a single process which he called the Law of Three Stages. In his view, each branch of knowledge passes through three stages: the theological or fictitious, the metaphysical or abstract, and lastly the scientific or positive state. He believed that through the continual advancement of human understanding, religion would fade away, philosophy and the humanities would be transformed into a naturalistic basis, and all human knowledge would eventually become a product of science. Any ideas outside that realm would be pure fantasy or superstition.

Logical Positivism

Positivism did not lose its appeal in the 20th century. To the contrary, a group known collectively as The Vienna Circle reinvigorated the fundamental tenets of positivism with enhanced symbolic logic and semantic theory. They called their approach, fittingly, logical positivism. In this system, there are only two kinds of meaningful statements: analytic statements (including logic and mathematics), and empirical statements, subject to experimental verification. Anything outside of this framework is an empty concept.¹²

Given its sweeping claims, logical positivism came under heavy scrutiny. Karl Popper pointed out that few statements in science can actually be completely verified. However, a single observation has the potential to invalidate a hypothesis, and even an entire theory. Therefore, he proposed that instead of experimental verification, the principle of falsifiability should demarcate what qualified as science, and by extension, what can qualify as knowledge.¹³

Another weakness of the positivist position is its reliance on a complete distinction between theory and observation. Observations, essential to the empirical approach of science, were claimed by positivists to be brute facts which one could use to establish, evaluate, and compare the theories. However, W.O. Quine pointed out in his “Two Dogmas of Empiricism” that observations themselves are partly shaped by theory (“theory-laden”).¹⁴ What counts as an observation, how to construct an experiment, and what data you think your instruments are collecting—all require an interpretive theoretical framework. This realization does not deal a death-blow to the practice of science (as some post-modernists like to claim), but it does undermine the positivist claim that science rests entirely on facts, and is thus an indisputable foundation for knowledge.

Scientism of Today

Scientism today is alive and well, as evidenced by the statements of our celebrity scientists:

The Cosmos is all that is or ever was or ever will be. –Carl Sagan, Cosmos

The more the universe seems comprehensible, the more it also seems pointless. –Stephen Weinburg, The First Three Minutes

We can be proud as a species because, having discovered that we are alone, we owe the gods very little. –E.O. Wilson, Consilience

While these men are certainly entitled to their personal opinions and the freedom to express them, the fact that they make such bold claims in their popular science literature blurs the line between solid, evidence-based science, and rampant philosophical speculation. Whether one agrees with the sentiments of these scientists or not, the result of these public pronouncements has served to alienate a large segment of American society. And that is a serious problem, since scientific research relies heavily upon public support for its funding, and environmental policy is shaped by lawmakers who listen to their constituents. From a purely pragmatic standpoint, it would be wise to try a different approach.

Physicist Ian Hutchinson offers an insightful metaphor for the current controversies over science:

The health of science is in fact jeopardized by scientism, not promoted by it. At the very least, scientism provokes a defensive, immunological, aggressive response from other intellectual communities, in return for its own arrogance and intellectual bullyism. It taints science itself by association.¹⁵

Noting that most Americans enthusiastically welcome scientific advancements, particularly those in health care, transportation, and communications, Hutchinson suggests that perhaps what the public is rejecting is not actually science itself, but a worldview that closely aligns itself with science—scientism.¹⁶ By disentangling these two concepts, we have a much better chance for enlisting public support for scientific research than we would by trying to convince millions of people to embrace a materialistic, godless universe in which science is our only remaining hope.

Distinguishing science from scientism

So if science is distinct from scientism, what is it? Science is an activity that seeks to explore the natural world using well-established, clearly-delineated methods. Given the complexity of the universe, from the very big to very small, from inorganic to organic, there is a vast array of scientific disciplines, each with its own specific techniques. The number of different specializations is constantly increasing, leading to more questions and areas of exploration than ever before. Science expands our understanding, rather than limiting it.

Scientism, on the other hand, is a speculative worldview about the ultimate reality of the universe and its meaning. Despite the fact that there are millions of species on our planet, scientism focuses an inordinate amount of its attention on human behavior and beliefs. Rather than working within carefully constructed boundaries and methodologies established by researchers, it broadly generalizes entire fields of academic expertise and dismisses many of them as inferior. With scientism, you will regularly hear explanations that rely on words like “merely”, “only”, “simply”, or “nothing more than”. Scientism restricts human inquiry.

It is one thing to celebrate science for its achievements and remarkable ability to explain a wide variety of phenomena in the natural world. But to claim there is nothing knowable outside the scope of science would be similar to a successful fisherman saying that whatever he can't catch in his nets does not exist.¹⁷ Once you accept that science is the only source of human knowledge, you have adopted a philosophical position (scientism) that cannot be verified, or falsified, by science itself. It is, in a word, unscientific.

Notes

1. "Un savant, mes amis, est un homme qui prévoit; c’est par la raison que la science donne le moyen de prédire qu’elle est utile, et que les savants sont supérieurs à tous les autres hommes." Translated into English by Valence Ionescu in The Political Thought of Saint-Simon. Oxford University Press, 1976. Page 76
2. Olson, Richard G. Science and Scientism in Nineteenth-Century Europe. Urbana, University of Illinois Press, 2008.
3. Sorell, Tom. Scientism: Philosophy and the Infatuation with Science. New York: Routledge, 1991.
4. Hutchinson, Ian. Monopolizing Knowledge: A Scientist Refutes Religion-Denying, Reason-Destroying Scientism. Belmont, MA: Fias Publishing, 2011.
5. Descartes, Rene. Discourse on Method
6. Sorell, p176
7. Sorell, p35
8. Ozouf, Mona. Festivals and the French Revolution. Harvard University Press, 1988.
9. Zammito, John H. A Nice Derangement of Epistemes : Post-Positivism in the Study of Science from Quine to Latour. Chicago: University of Chicago Press, 2004.
10. This view is a form of strict determinism, and current popularizers of continue to enthusiastically endorse it. Perhaps they are “determined” to do so?
11. This view is a form of extreme reductionism, also widely endorsed by current popularizers of science.
12. Zammito, p8
13. Popper, Karl. Logic of Scientific Discovery. 1959
14. For an extended discussion, read Zammito’s chapter “The Perils of Semantic Ascent: Quine and Post-positivism in the Philosophy of Science” in A Nice Derangement of Epistemes. University of Chicago Press, 2004.
15. Hutchinson, p143
16. Hutchinson, p109
17. Giberson, Karl, and Mariano Artigas. Oracles of Science: Celebrity Scientists Versus God and Religion. Oxford: Oxford University Press, 2009.

Ultimately, however, Finch remarks that "science can neither prove nor disprove the existence of God." To him, those who proselytize atheism under the banner of "science" do a disservice to science. The goal of scientists is to understand the physical world around us, and most scientists go into their labs to discover something wonderful about the world, rather than to comment on the existence of God.

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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