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.

Grantees will benefit from in-person interaction through a series of summer workshops in 2013, 2014, and 2015. These meetings will not only foster a broader knowledge base, but will build a sustained network of scholars and church leaders, both young and seasoned, who are serious about addressing the concerns of the church about evolution. Also in 2015, in connection with the third summer workshop, BioLogos will host a large conference open to scientists, scholars, and church leaders from around the world.

ECF History

In January 2012, BioLogos was awarded a multi-million dollar grant from the John Templeton Foundation to fund the work of scholars and church leaders on evolution and Christian faith. In spring 2012 we worked hard to get the word out. You may have seen announcements on the BioLogos website, in our newsletters, on the Books & Culture, Leadership Journal, or First Things websites, on your professional society’s listserv, or perhaps on your friend’s blog.

The response was overwhelming: we received 225 letters of intent for a total request of $21 million—about seven times the amount we had to offer. We needed to invite the most promising applicants to submit a full proposal, but recognizing the projects with highest potential would require broad expertise. From the beginning, we envisioned that a panel of scientists, pastors, and scholars would oversee the application and review process as well as play key advisory roles throughout the project. A team of eight highly qualified individuals came on board in the early months of the project. They reviewed each proposal and together recommended that BioLogos invite 86 applicants to submit full applications.

The deadline for submissions was October 1, 2012. As in the previous round, the ECF panel evaluated each proposal. In addition, we asked 55 other experts to participate, so that each proposal received 3-4 scores. Criteria for the decision included significance of topic, project design, creativity and innovation, long-term impact potential, feasibility, and budget.

The panel then met together November 29-30, 2012, to make the final funding decisions. In the end, they recommended that BioLogos give 37 awards, ranging from $23,000 to $300,000. BioLogos staff notified applicants of their awards on December 14, 2013.

The Grantees

As part of our objective to create a network of scholars and leaders, we awarded grants to organizations across the U.S. and the world. Thirty of the 37 grantees are domestic; seven are international, hailing from Canada, France, Great Britain, Netherlands, and Spain.

Two-thirds of the accepted projects will be led by teams—some with three or more Project Leaders. We expect that the teamwork and time spent together at our summer workshops will be the start of a long-lasting network of people dedicated to helping the church think carefully about origins.

Applicants chose to apply under one of three program tracks: interdisciplinary scholarship (Track 1), intra-disciplinary scholarship (Track 2), and translational projects (Track 3). Track 1 projects focus on both the collaboration between individuals in different disciplines and the development of projects at the interface of different content areas. Track 2 projects focus on work done within a specific discipline. Track 3 focuses on projects that encourage Christians, especially those within more conservative traditions, to engage in meaningful and productive dialogue to reduce tensions between mainstream science and the Christian faith. The numbers of grantees in Tracks 1, 2, and 3 are 6, 8, and 23, respectively.

Many of the scholarly projects tackle questions about Adam and Eve, the Fall, human identity, and Original Sin—some of the most critical interpretive issues for evangelical theology.  Some examples: 

• Theologian Oliver Crisp of Fuller Seminary will take an analytic theology approach to ask to what extent a theological account of the origin of human sin depends upon the evolution of modern humans from one and only one ancestral pair—especially if that pair does not appear to correspond to what we would think of as modern human beings. 

• Pastor Michael Gulker and philosopher James Smith, leading a large team from The Colossian Forum, ask a related question: if humanity emerged from non-human primates—as genetic, biological, and archaeological evidence seems to suggest—then what are the implications for Christian theology’s traditional account of origins, including both the origin of humanity and the origin of sin? 

• Biologist Dennis Venema of Trinity Western University and New Testament scholar Scot McKnight of Northern Seminary will write a book on the evidence for evolution and population genetics, with informed theological reflection on how these issues interact with orthodox Christianity.

• Biologist David Wilcox of Eastern University will develop an updated model of human identity which reflects the complex recent scientific advances in genetics and paleoanthropology and yet is sensitive to theological concerns.  

These are just a few of the scholarly awards; check out the Grantees page for full descriptions of all Track 1 and Track 2 projects.

All projects have translational potential, but Track 3 projects are designed to meet the needs of a particular constituency within the evangelical church. These projects run the gamut from ethics to education to media production to ministry resources.  Some examples include:

• Theologian Lee Camp of Lipscomb University will produce “The Questions in Monkey Town,” an episode of Tokens, a live variety show that features musical performances, comedic sketches, brief interpretive monologues, and dialog with authors and scholars. The episode will be performed and filmed on the site of the famous Scopes Trial in Dayton, Tennessee.

• Chaplain Joshua Hayashi and Educator Diane Sweeney of the Punahou School in Hawaii will lead a team to produce multimedia curricula aimed at helping high school students connect with their biology curricula and, at the same time, deepen their Christian faith.

• Physics teacher and pastor Benoît Hébert of Science et Foi Chrétienne in France will lead an international, multi-denominational team of French speaking Evangelical scientists, pastors and church leaders to produce a large number of resources on evolutionary creation.

• Pastor Seung-Hwan Kim of Grace Truth Community Church, a Southern Baptist church in Cambridge, Massachusetts, will produce teaching and preaching materials about evolution for church leaders.

• President Gregory Wolfe and Director of Resource Development for IMAGE will gather artists and writers of faith whose work explores the dialogue between evolutionary science and faith practice, convening a conversation between them and scientists, theologians, and church leaders in private and public conferences.

Again, this is just a taste of the diversity of Track 3 projects. Read more about each project on the Grantees page. You can look forward to an incredible variety of resources coming out of the ECF program, many of which will be featured right here on the BioLogos Forum.

A common argument leveled against the theory of evolution is that scientists have not been able to produce the expected transitional fossils that show the change of one species into another. If evolution were true, wouldn’t there be instances of clear intermediary species, like, for example, a species that was half whale and half hippo to show the transition between those two? In this BioLogos podcast, Kelsey Luoma addresses this misconception about what a transitional fossil actually is. Rather than a mix between two related species, transitional fossils point back to the common ancestors that modern species share. The fact is that the number of transitional species is massive and it grows with each passing year. Given the rarity with which organisms are actually fossilized, the amazing thing is actually the completeness of the fossil record, not its incompleteness. The transitional species story strongly supports, and certainly does not disprove, evolutionary theory. ¹

1. To hear the full audio clips which have been referenced go to:

• Rational Response Debate with Kirk Cameron (from Way of the Masters)
• Behind the Scenes with Dr. Neil Shubin (from Cincinnati Museum Center)
• Mark Norell Publishes New Archaeopteryx Findings (from American Museum of Natural Sciences)
• Texas A&M Professor Discusses Findings of Autralopithecus Sediba and its Relationship to Humans (from Texas A&M University)
• Intro/outro music composed by Martin Minor (Minor2Go).

An audio only version of the podcast can be downloaded here.

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

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

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

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

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

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

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

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

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

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

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

Behe and IC

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

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

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

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

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

(Darwin’s Black Box, p. 39)

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

Behe and exaptation

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

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

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

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

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

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

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

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

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

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

For further reading:

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

The origins of human chromosome 2: a brief review

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

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

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

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

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

Enter the Denisovans

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

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

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

Implications for understanding our “becoming human”

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

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

Darwin’s finches are some of the most visible and recognizable symbols of evolution in the world today. Biology textbooks feature them prominently, and the National Academy of Sciences has enshrined them in the entrance of their headquarters in Washington, DC. Surely the finches that Darwin collected on the Galápagos islands were a central feature of his evolutionary theory, right?

Lobby of The National Academies Building. Courtesy of CPNAS. Photo by Robert Lautman

Actually, the Galápagos finches are never even mentioned in Darwin’s famous work On the Origin of Species. Nor do they appear in Darwin’s famous notebooks on “Transmutation of Species”, in which he formulated the idea of evolution by natural selection.¹ Even Darwin’s private diary of his voyage on the HMS Beagle only mentions the Galápagos finches briefly in passing.²

It was only in 1845, in the second edition of The Voyage of the Beagle, that Darwin included a tantalizing sentence about the Galápagos finches:

Seeing this gradation and diversity of structure in one small, intimately related group of birds, one might really fancy that from an original paucity of birds in this archipelago, one species had been taken and modified for different ends.³

However insightful this statement may have been, Darwin never published anything else about the Galápagos finches for the rest of his life. Nor did he publically present these birds as direct evidence for this theory of evolution.⁴

If these finches were so important to Darwin’s evolutionary theory, why did he remain silent about them? One of his comments in The Voyage of the Beagle provides us with a clue:

Unfortunately most of the specimens of the finch tribe were mingled together; but I have strong reasons to suspect that some of the species of the subgroup Geospiza are confined to separate islands.⁵

When Darwin was exploring the Galápagos himself in 1835, he had not formulated his theory of evolution yet, and thus he did know what data would be necessary to make definitive conclusions about finch evolution. In particular, he did not keep careful track of which of his specimens came from which islands. Moreover, as was customary among naturalists at that time, Darwin only collected a small number specimens—he brought home only 31 finches and 64 total birds from the Galápagos.⁶

Though Darwin sensed that these birds were truly special, he lacked sufficient evidence to reach any specific conclusions about their evolutionary origins. It would be up to the rest of the scientific community to carry out the necessary empirical research. Subsequent expeditions in 1868, 1891, 1897, and 1905 brought back thousands of Galápagos finch specimens, but instead of unlocking the mysteries of evolutionary theory, the Galápagos finches became a great enigma.⁷

A century after Darwin's voyage, scientists still struggled to explain the staggering variety of finches on this tiny, remote archipelago. By the mid-1930’s, British Museum ornithologist Percy Lowe argued that the finches presented a "biological problem of first class importance", and he told the British Association for the Advancement of Science that the finches displayed a "bewildering diversity, intergradation, and distribution".⁸ Who would be up to the challenge of making sense of such tremendous biological complexity? It was David Lack.

David Lack

Ornithologist David Lack

David Lack had an exceptionally keen eye for bird-watching, and he possessed a passion to match it. By age 15, he had already observed 100 distinct species of birds, and before entering college, authored his first scientific paper. At Cambridge University in the early 1930’s, Lack was disappointed to find that his zoology professors taught “nothing about evolution, ecology, behavior or genetics, and of course nothing about birds.”⁹ In fact, at that time, there were only two professional ornithologists in all of Britain!

Thus David Lack took it upon himself to create his own learning opportunities. As an undergraduate, he became the president of the Cambridge Ornithological Club, traveled to Greenland for a bird-watching expedition, and cultivated a relationship with the prominent biologist Julian Huxley (grandson of Thomas Henry Huxley). Huxley was an inspiring mentor and encouraged Lack to expand his research further by studying tropical birds.¹⁰ Following this advice, Lack embarked on a research trip to Tanzania in the summer of 1934, but his greatest adventure was yet to come.

In 1937, Lack became fascinated by the scientific mysteries surrounding the Galápagos finches. But in order to study their behavior, Lack would need to travel to remote islands halfway around the world. How could he possibly get there? Once again, Julian Huxley was tremendously supportive and raised funds from two prominent scientific societies to pay for his expedition. After a long delay, David Lack and five companions finally set off on their journey.

Instead of residing in comfortable quarters aboard a royal naval ship, Lack’s group subsisted on a shoestring budget, traveled on commercial steamers, and stayed with local settlers. Their experience was definitely not a romantic tale of imperial expedition:

The Galápagos are interesting, but scarcely a residential paradise. The biological peculiarities are offset by an enervating climate, monotonous scenery, dense thorn scrub, cactus spines, loose sharp lava, food deficiencies, water shortage, black rats, fleas, jiggers, ants, mosquitoes, scorpions, Ecuadorian Indians of doubtful honesty, and dejected, disillusioned European settlers.¹¹

Whereas Charles Darwin spent only nineteen days on the shores of the Galápagos, Lack and his crew conducted more than five months of meticulous and exhausting study in the harsh climate. At that time, even the finches themselves provided little solace. Lack wrote,

Darwin’s finches are dull to look at, not only in their orderly ranks in museum trays, but also when they hop about the ground or perch in the trees of the Galápagos, making dull unmusical noises. Only the variety of their beaks and the number of their species excite attention.¹²

Large Cactus Finch on Española Island in the Galápagos Islands

The repetitive tedium requisite for important scientific discoveries is rarely discussed in public, and even today many bright-eyed science students become disillusioned by the painstaking work demanded by their Ph.D. programs. But one of the things that distinguishes great scientists is their unwavering commitment and tenacity in completing major projects. David Lack's efforts were not in vain:

"Despite his personal discomforts (or perhaps because of them), Lack did see something on the Galápagos that no one had ever seen before—natural selection at work among its finches through interspecies competition." ¹³

When the birds’ breeding season ended in 1939, Lack was ready to return to his home in England. But the captive finches that he had brought with him fared so badly on the voyage home that he detoured to San Francisco and put them in the care of the California Academy of Sciences. Turning this mishap into an opportunity, Lack stayed there for five additional months to study the Academy’s enormous collection of Galápagos finch specimens.¹⁴

To complete his systematic research, Lack then travelled across the United States to study the Galápagos finch collection housed at the American Museum in New York.¹⁵ Altogether, Lack examined more than 8000 specimens and specifically measured the length, width, and depth of all their beaks.¹⁶

Lack’s final obstacle was in getting his research published. Though he completed his academic manuscript “The Galápagos Finches—A Study in Variation” in 1940, paper shortages during World War II delayed its publication by the California Academy of Sciences until 1945. Were he only interested in making an original contribution to science, Lack could have stopped here and congratulated himself on a job well-done. However, his motivation sprung from a deeper source:

David Lack's drawing of 14 species of Galápagos finches, p. 19 of Darwin’s Finches

"I did not watch birds primarily for scientific reasons but for sheer enjoyment, and from the age of 15 onward returned day after day in a glow of excitement after seeing a new bird or a new habit." ¹⁷

Lack’s joyful fascination with the Galápagos finches inspired him to continue developing his conclusions long after returning from his expedition. While waiting for his academic paper to be published, he began writing a book that would enable students and the general public to share his excitement about these remarkable birds and the evolutionary processes that shaped them.

First published in 1947, Lack’s book became tremendously influential. Before this time, biology textbooks had never even mentioned the Galápagos finches. But after David Lack’s study, the finches became a primary example of evolution by natural selection, specifically adaptive radiation. Not only did textbooks fully rely on Lack’s findings, they also followed his lead in calling them “Darwin’s finches”, the title of Lack’s famous book.¹⁸

Iconic Finches

What was it about these birds that made them such a prominent symbol of evolution? As Darwin himself pointed out, the numerous Galápagos finch populations each have distinctive beaks, and he speculated that they could have evolved from an ancestral species that came to the islands. But a complete picture of finch evolution would have to wait another hundred years, when David Lack arrived.

During his five months on the Galápagos, including both the rainy and dry seasons, Lack observed that these beak differences enable the finches to subsist on different kinds of food:

The beak differences between most of the genera and subgenera of Darwin's finches are clearly correlated with differences in feeding methods. This is well borne out by the heavy, finch-like beak of the seed-eating Geospiza, the long beak of the flower-probing Cactornis, the somewhat parrot-like beak of the leaf, bud, and fruit-eating Platyspiza, the woodpecker-like beak of the woodboring Catcospiza, and the warbler-like beaks of the insect-eating certhidea and Pinaroloxias.¹⁹

Lack's image of beak adaptations from Darwin’s Finches

Specializing in such different sources of food enables these finches to live in close proximity without directly competing with each other or driving populations to extinction. The fact that so many of these closely related finches are able to co-exist is a remarkable fact in itself. As Lack himself put it, “It is not only the origin, but also the persistence, of new species which require explanation.”²⁰

But it is also fascinating to consider how these birds got to be so different in the first place. How did a finch come to have a beak like a “parrot”, “woodpecker”, or “warbler”? The answer lies in the distinct characteristics of the Galápagos. Because the islands are so remote, no actual parrots, woodpeckers, or warblers ever settled on it. In the absence of these species, the Galápagos finches were able to adopt feeding habits and forms that they would never have taken on a large continent full of other birds competing for food. The isolation of these islands offered just the right conditions for us to see living examples of adaptive radiation.²¹

Conclusion

Considering the immense popularity of the Galápagos finches, it is quite surprising to learn that Charles Darwin himself had so little to say about them. In fact, it was actually David Lack, one century later, who conducted the critical research that immortalized the finches in biology textbooks and popular lore. By naming his landmark book Darwin’s Finches,²² Lack paid homage to the man whose voyage on the HMS Beagle helped transform the study of natural history. But at the same time, Lack also obscured the fact that evolutionary biology is an enterprise conducted by a large community of brilliant scholars, not just the product of one man’s efforts.

This tendency to immortalize “great men of science” has also led many people to refer to modern evolutionary theory as Darwinism, despite the fact that it has substantially changed and developed over the past 150 years. It is important to give credit where credit is due, and if that’s the case, we should seriously reconsider how we refer to the Galapagos finches. Evolutionary biologist Dolph Schluter, who studied the finches several decades after David Lack, had this to say:

I find Lack's intuition really stunning given how little information he had. He's my hero actually… They should be called Lack's finches.²³

In the second part of this series, we’ll explore the fact that David Lack, in addition to being a world-renowned evolutionary biologist, was also a devout Christian. His study of evolutionary theory did not cause him to lose his faith; in fact, he actually converted to Christianity after completing his Galápagos finch research.

For Discussion

Further Reading

• Grant, Peter R.; Grant, B. Rosemary. How and Why Species Multiply: The Radiation of Darwin's Finches, Princeton University Press, 2008.
• Sulloway, Frank J. (Spring 1982), "Darwin and His Finches: The Evolution of a Legend" (PDF), Journal of the History of Biology 15 (1): 1–53.
• Weiner, Jonathon. The Beak of the Finch: A Story of Evolution in Our Time. Vintage Books, 1995.

Notes

1. Sulloway, F. (1983). "Darwin and his finches: The evolution of a legend." Journal of the history of biology 15(1): 32. Darwin’s notebooks on transmutation mentioned Galapagos tortoises and mockingbirds, not finches.
2. Lack, David. Darwin’s Finches. Cambridge University Press, 1947: 9. Confirmed by Sulloway (1983), p5.
3. Darwin, Charles. Journal of researches into the natural history and geology of the countries visited during the voyage of H.M.S. Beagle round the world. London: John Murray. 2d ed. 1845: 379-80. This edition of the book also contained the drawings of four different finches that have become enshrined in biology textbooks and on the walls of the National Academy of Sciences in Washington, DC.
4. Sulloway, p35. Sulloway points out that the first published evolutionary account of the Galapagos finches was not until 1876, by Osbert Salvin: "On the Avifauna of the Galapagos Archipelago." Trans. Zool. Soc. London, 9:447-51.
5. Darwin (1845), p395.
6. Sulloway, p40.
7. Sulloway, p40.
8. Larson, E. J. Evolution's Workshop: God and Science on the Galapagos Islands. New York, Basic Books, 2001: 166-67.
9. Lack, David. (1973) “My life as an amateur ornithologist.” Ibis: 424.
10. Lack (1973), 425-27.
11. Lack (1947), p1.
12. Lack (1947), p11.
13. Larson, 167-68.
14. The California Academy of Sciences sponsored an expedition to the Galapagos in 1905-06 and collected nearly 9000 Galapagos finch specimens (Sulloway, p40).
15. In New York, Lack roomed with the curator of the finch collection—German émigré zoologist Ernst Mayr. By developing this relationship, Lack had close ties with two of the biggest figures in the neo-Darwinian synthesis, Julian Huxley and Ernst Mayr (Larson, 168).
16. Larson, p168.
17. Lack (1973), p424.
18. Larson, p198.
19. Lack (1947), p60.
20. Lack (1947), p158.
21. See Lack’s concluding chapter on “Adaptive Radiation”, pp146-159 of Darwin’s Finches (1947).
22. British ornithologist Percy Lowe originally proposed the name “Darwin’s finches” in 1935, but the name did not catch on until Lack used it in his book. See P.R. Lowe, (1936) "The Finches of the Galapagos in Relation to Darwin's Conception of Species." Ibis, 13th ser., 6:310-321. (Cited in Larson, p287)
23. Schluter, in an interview with Edward Larson, 16 March 2000.

Eugene Dubois

13 years before, in 1877, Dubois had arrived in Amsterdam to study medicine, but always harboring a desire to study the ancestry of modern humans. So, after four years at the University there, he accepted an invitation to go to the University of Utrecht to study comparative anatomy and devote himself to the latest thinking about the origins of the human species. It was during his time at Utrecht (from 1881 to 1887) that Dubois became enamored of Haeckel’s views on human origins, which differed from those of Darwin. While Darwin argued that humans had evolved in Africa, the region in which our closest living relatives—the chimpanzees and gorillas—still live, Haeckel believed that the origins of humanity lay in East Asia. This was so, he believed, because of his own observations of gibbons that walk bipedally when on the ground.

Haeckel also believed that there had once been a large landmass called Lemuria between the continents of Africa and Asia. In his view, Lemuria had since become submerged, leaving the modern islands of Madagascar and the East Indies as its only remains. The idea of submerged continents was not unusual for the late 19th-century, as people struggled to understand the character of biological diversity present in the world and why there were such striking similarities between animals that were geographically dispersed. The geographical distribution of marsupial fossils in South America and Australia is an example of this sort of problem, and one that was not solved until the second half of the 20th century when continental drift reconstructions suggested that ancient marsupials had used Antarctica as a conduit between the other two continents. Not only did such theories make sense of modern distributions, they were confirmed with later discoveries of marsupial fossils in Antarctica.

In any case, in 1888 Dubois joined the army and set out for the Dutch East Indies to pursue his ideas. For the next two years, he would comb Sumatra attempting to locate the hominin remains that Haeckel promised would be there. In hindsight, what Dubois was attempting was something that had never been done before: discovery of hominin material through the tools of archaeological excavation. Up to this point, all of the human fossils had been found on the surface, eroding out of the side of a bank, or as a result of farming. It had not occurred to anyone to go looking for human ancestors.

Now, with his supply of prison workers dwindling due to desertion and fever, he had almost run out of options and was on the verge of failure. Using almost all of his remaining resources, he decided to abandon his excavations on Sumatra and turn to the nearby island of Java. Emboldened by the fact that early modern human fossils had been discovered there (at Wadjak), he arrived and settled in at Trinil, on the banks of the Solo River, in 1890.

Figure 1: Dubois' Pithecanthropus erectus

The very next year, Dubois’ long-standing efforts were finally rewarded, first with the discovery of a skullcap (calvaria) of a hominin cranium, and then with an intact femur (Figure 1). Judging by what he knew of cranial anatomy, Dubois estimated that the skull would have been approximately 900 cubic centimeters (cc) in volume, placing it below even the lowest threshold of modern humans. Further, he noticed that it was not like modern humans in shape, being too long and low. He concluded that it showed “evidence of a form intermediate between man and the anthropoid apes” (Dubois, 1896). Dubois envisioned a sequence of forms in which the gibbon gave rise to a form of chimpanzee called Anthropopithecus sivalensis, which then gave rise to the form represented by the Trinil remains, after which Homo sapiens arose (Turner, 1895).

Dubois spent the next twenty years on the road with his find, trying to drum up support for its place in human prehistory. As with Raymond Dart’s discovery of the first australopithecine thirty-three years later, Dubois did not receive a warm reception. Most critics simply said that he had gotten it wrong and that the femur did not belong to the same individual as the obviously-primitive skull cap. Some of the criticism Dubois suffered could have been mitigated had he been more open to sharing the Trinil materials; but, instead, he allowed very little access to the bones, so that very few people knew exactly what they looked like. Adding to Dubois’s credibility problems was the 1911 “discovery” of Piltdown. This intentional hoax turned the paleoanthropology world on its head for forty years, sending researchers down innumerable rabbit holes. As I noted in a previous post, the Piltdown remains made all of the other hominin finds appear too “ape-like” to be on the road to humanity and informed many opinions about finds such as those from Trinil.

On the other hand, some critics of Dubois’ new hominin claim were vicious, and questioned both his academic abilities and his judgment (Shipman & Storm, 2002)—in addition to the interpretation of the find itself. It was in reference to Dubois’ work that the term “Missing Link” was first used with reference to a particular human fossil, originating with Charles Lyell (1863) and describing palaeontological gaps. And ironically, it was in one of the most stinging criticisms of Dubois’ work that the name that would eventually stick was first used: “Homo erectus.” Eventually, many other finds in the same general area and across Southeast Asia demonstrated that what Dubois had found was a real, previously-unknown hominin form, and the first to colonize the Asian continent and the islands leading off towards Oceania.

Homo erectus across South East Asia:

Figure 2: Sangiran 17

Sangiran

The earliest point at which Homo erectus appears to have begun to colonize the greater East Asian region is around 1.8 million years ago, represented first by the partial child’s skull found at the site of Modjokerto, and then, at around 1.66 million years ago, at the site of Sangiran, in Trinil, where Dubois had made his landmark discovery. This site was rich, yielding the remains of many crania, perhaps best represented by Sangiran 17 (Figure 2), an almost complete skull.

The material from the Sangiran site is very diverse morphologically, with some crania having capacities of as little as 700 to 800 cc, and other, larger heads with volumes in the range of 1000 cc. As with the late Homo ergaster finds from Africa, the remains from Sangiran yielded crania that were still widest at their bases, possessing large brow ridges. Some have thick cranial bones and are very robust (Sangiran 4), while others are very gracile (Sangiran 31). What this variation means is not clear, but most workers believe it represents a very diverse diachronic population (that is, one group living and moving around over a long period) rather than separate species inhabiting the area. The Sangiran site yielded fossil material in an almost continuous succession from approximately 1.66 million years ago to less than 800,000 years ago.

Because the area of the excavations—the Sangiran Dome—is a volcanic deposit, the layers have been securely dated by the ⁴⁰Ar/³⁹Ar method, although questions remain about the historical sequence and distribution of other animals that lived there through the ages (its faunal succession). The problem is that many of the fossils were not found in context, and relating them directly to the stratigraphy is tenuous. Despite this, most workers are comfortable with the earliest hominins in the region being at least 1.5 million years old.

One of the things hampering workers in this region is the comparative paucity of recovered stone tools. Those that have been found suggest a technological stage similar to the late Oldowan design, equivalent to that being created by the Homo ergaster populations inhabiting the area of Dmanisi and East Africa. Unfortunately, none of the tools have been associated with the hominins directly so it is not exactly clear who made them.

Figure 3: Sambungmacan 3

Sambungmacan

Another major find from the area where Dubois brought Homo erectus to light is the cranium from the site of Sambungmachan. This skull was reportedly found in 1977 but was then illegally sold to the antiquities market, where is spent considerable time in different collections before being “rediscovered” in 1998—in a New York nature curio shop called Maxilla and Mandible, Inc. (Delson et al., 2001). This was an almost-complete calvaria (Figure 3), with only part of the base missing. It is equivalent in size to the fossils from Sangiran, with a cranial capacity of around 1000 cc. It has a large brow ridge extending all of the way across the top of the eyes, a long, low cranium with a sloping forehead and a maximum width near the cranial base—all features that are also characteristic of the late African H. ergaster and Sangiran crania. Although we will never know exactly how old this cranium is, its morphology is consistent with that of the material from Sangiran.

Figure 4: Ngandong 6

Ngandong

Later in time, but also located on the Solo River, is the site of Ngandong, excavated by Oppenoorth in the early 1930s. At this site, fourteen calvaria have been discovered, all of which show advanced Homo erectus characteristics: long and low in shape, with thick-bones and a distinctive brow-ridge. (Figure 4). As with the other Indonesian finds, dating the Ngandong material has been problematic. The deposits at the site were originally thought to be around 100,000 years old, but this interpretation was turned on its head in 1996, when Swisher and colleagues claimed that the deposits were no older than between 27,000 and 53,000 years old (Swisher et al., 1996). These age estimations were made on the associated fauna, however, and as Rainer Grün and the late Alan Thorne pointed out, the faunal material does not match the skulls either in color or in texture and is likely not from the same time. Recently, Swisher and colleagues revisited the dating of the site and derived internally-consistent dates of at least 143,000 years before the present (Indriati et al., 2011). As with the Trinil remains, however, there are no associated stone tools.

Homo erectus in China

The Chinese Homo erectus material is very widely scattered and working in the region has presented many difficulties for researchers in terms of transport, language barriers and funding. Consequently, we know less about this region and its previous inhabitants than we do about most other areas of the Old World. Although there are between ten and fifteen sites that have yielded Homo erectus material, I will only touch on the most important ones.

Lantian:

Figure 5: Lantian

In the early 1960s, a cranium and mandible were found in the cave of Lantian, Shaanxi province, whose characteristics matched other remains from China designated as Homo erectus. Paleomagnetic dating has yielded a date no earlier than 1.15 million years ago for the skull, with the consensus being that it is around 800,000 years old. A date of approximately 650,000 years before the present was derived for the mandible. The cranium is heavily encrusted and suffered from postmortem deformation (Figure 5). When reconstituted, it was found to have a capacity of around 780 cc (low for Homo erectus) and the bones on the sides of the head are the thickest yet recorded. At this site some flake tools, mammal remains, and an ash deposit were all recovered, suggesting hunting and control of fire.

Figure 5: Hexian

Hexian

Another almost-complete calvaria was found at Longtandong cave in the province of Hé Xiàn, dated to between 400,000 and 500,000 years ago. This find exemplifies typical Homo erectus in many ways in that it is long and low, with heavy muscle markings toward the base and the rear of the skull (Figure 6). The cranial capacity is around 1000 cc, a third-again greater than that of the Lantian calvaria. Its cranial shape is very similar to those found in Southeast Asia, suggesting that it straddles the Southeast Asian and Chinese boundary.

While both Lantian and Hexian were significant finds, another site in China boasted the single largest collection of Homo erectus fossils ever found at one site, as well as presenting one of the greatest mysteries in paleoanthropology. Tomorrow, in the conclusion of our look at Homo erectus in Asia, we’ll peer into the Zhoukoudian caves and consider how this species fits into the lineage of man.

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

There are two opposite errors which need to be countered about the fossil record: 1) that it is so incomplete as to be of no value in interpreting patterns and trends in the history of life, and 2) that it is so good that we should expect a relatively complete record of the details of evolutionary transitions within all or most lineages.

What then is the quality of the fossil record? It can be confidently stated that only a very small fraction of the species that once lived on Earth have been preserved in the rock record and subsequently discovered and described by science.

There is an entire field of scientific research referred to as "taphonomy" -- literally, "the study of death." Taphonomic research includes investigating those processes active from the time of death of an organism until its final burial by sediment. These processes include decomposition, scavenging, mechanical destruction, transportation, and chemical dissolution and alteration. The ways in which the remains of organisms are subsequently mechanically and chemically altered after burial are also examined -- including the various processes of fossilization. Burial and "fossilization" of an organism's remains in no way guarantees its ultimate preservation as a fossil. Processes such as dissolution and recrystallization can remove all record of fossils from the rock. What we collect as fossils are thus the "lucky" organisms that have avoided the wide spectrum of destructive pre- and post-depositional processes arrayed against them.

Soft-bodied organisms, and organisms with non-mineralized skeletons have very little chance of preservation under most environmental conditions. Until the Cambrian nearly all organisms were soft-bodied, and even today the majority of species in marine communities are soft-bodied. The discovery of new soft-bodied fossil localities is always met with great enthusiasm. These localities typically turn up new species with unusual morphologies, and new higher taxa can be erected on the basis of a few specimens! Such localities are also erratically and widely spaced geographically and in geologic time.

Even those organisms with preservable hard parts are unlikely to be preserved under "normal" conditions. Studies of the fate of clam shells in shallow coastal waters reveal that shells are rapidly destroyed by scavenging, boring, chemical dissolution and breakage. Occasional burial during major storm events is one process that favors the incorporation of shells into the sedimentary record, and their ultimate preservation as fossils. Getting terrestrial vertebrate material into the fossil record is even more difficult. The terrestrial environment is a very destructive one: with decomposition and scavenging together with physical and chemical destruction by weathering.

The potential for fossil preservation varies dramatically from environment to environment. Preservation is enhanced under conditions that limit destructive physical and biological processes. Thus marine and fresh water environments with low oxygen levels, high salinities, or relatively high rates of sediment deposition favor preservation. Similarly, in some environments biochemical conditions can favor the early mineralization of skeletons and even soft tissues by a variety of compounds (eg. carbonate, silica, pyrite, and phosphate). The likelihood of preservation is thus highly variable. As a result, the fossil record is biased toward sampling the biota of certain types of environments, and against sampling the biota of others.

In addition to these preservational biases, the erosion, deformation and metamorphism of originally fossiliferous sedimentary rock have eliminated significant portions of the fossil record over geologic time. Furthermore, much of the fossil-bearing sedimentary record is hidden in the subsurface, or located in poorly accessible or little studied geographic areas. For these reasons, of those once-living species actually preserved in the fossil record, only a small portion have been discovered and described by science. However, there is also the promise of continued new and important discovery.

The forces arrayed against fossil preservation also guarantee that the earliest fossils known for a given animal group will always date to some time after that group first evolved. The fossil record always provides only minimum ages for the first appearance of organisms.

Because of the biases of the fossil record, the most abundant and geographically widespread species of hardpart-bearing organisms would tend to be best represented. Also, short-lived species that belonged to rapidly evolving lines of descent are less likely to be preserved than long-lived stable species. Because evolutionary change is probably most rapid within small isolated populations, a detailed species-by-species record of such evolutionary transitions is unlikely to be preserved. Furthermore, capturing such evolutionary events in the fossil record requires the fortuitous sampling of the particular geographic locality where the changes occurred.

Using the model of a branching tree of life, the expectation is for the preservation of isolated branches on an originally very bushy evolutionary tree. A few of these branches (lines of descent) would be fairly complete, while most are reconstructed with only very fragmentary evidence. As a result, the large-scale patterns of evolutionary history can generally be better discerned than the population-by-population or species-by-species transitions. Evolutionary trends over longer periods of time and across greater anatomical transitions can be followed by reconstructing the sequences in which anatomical features were acquired within an evolving branch of the tree of life.

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

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

(Click Image to Enlarge)

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

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

(Click Image to Enlarge)

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

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

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

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

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

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

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

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

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

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

Testing IC with new research

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

For further reading:

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

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

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

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

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

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

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

Evolution: A Theory with Bite

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

Independent Lines of Evidence, but Contradictory Stories?

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

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

Signature in the SINE

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

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

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

For further reading:

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

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

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

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

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