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. 

Antibody fine-tuning

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

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

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

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

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

Antibody production and evolution both involve mutation and selection

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

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

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

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

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

Though often neutral or destructive, mutations sometimes create new functionality

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

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

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

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

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

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

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.

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

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

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

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

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

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

And who created it? Was it the good Lord?

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

We are the only ones who say: cruelty.

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

Who cannot but feel and think,

Who is kindred to us by his warmth and movement,

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

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

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

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

The Problem

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

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

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

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

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

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

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

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

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

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

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

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

Notes

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

As we discussed yesterday, the most dramatic innovation yet observed in the E. coli Long Term Evolution Experiment (LTEE) was the ability, acquired by one of the twelve cultures, to use citrate as a carbon source under aerobic conditions. When we last discussed the LTEE in 2011, we noted what was known then about the mutations that eventually combined to produce the Cit+ trait:

Tracking down the nature of this dramatic change led to some interesting findings. The ability to use citrate as a food source did not arise in a single step, but rather as a series of steps, some of which are separated by thousands of generations:

1. The first step is a mutation that arose at around generation 20,000. This mutation on its own does not allow the bacteria to use citrate, but without this mutation in place, later generations cannot evolve the ability to use citrate. Lenski and colleagues were careful to determine that this mutation is not simply a mutation that increases the background mutation rate. In other words, a portion of what later becomes “specified information for using citrate” arises thousands of generations before citrate is ever used.
2. The earliest mutants that can use citrate as a food source do so very, very poorly – once they use up the available glucose, they take a long time to switch over to using citrate. These “early adopters” are a tiny fraction of the overall population. The “specified information for using citrate” at this stage is pretty poor.
3. Once the (poor) ability to use citrate shows up, other mutations arise that greatly improve this new ability. Soon, bacteria that use citrate dominate the population. The “specified information for using citrate” has now been honed by further mutation and natural selection.
4. Despite the “takeover”, a fraction of the population unable to use citrate persists as a minority. These cells eke out a living by being “glucose specialists” – they are better at using up glucose rapidly and then going into stasis before the slightly slower citrate-eaters catch up. So, new “specified information to get the glucose quickly before those pesky citrate-eaters do” allows these bacteria to survive. As such, the two lineages in this population have partitioned the available resources and now occupy two different ecological niches in the same environment. As such, they are well on their way to becoming different bacterial species.

As such, we noted three distinct steps observed by the Lenski group: steps they call potentiation, actualization, and refinement. Potentiation mutations do not themselves result in the ability to use citrate under aerobic conditions, but they are necessary for it to appear later. Actualization is the mutation that first brings about the Cit+ trait, though, as we noted, this step produced only a very weak Cit+ effect. This nascent ability, however, then undergoes refinement through additional mutations and selection to give the final, robust Cit+ trait observed in the culture.

While some things were known about these steps when the Lenski group last published on this topic (in 2008), the precise details remained unclear. What was needed was a complete characterization of the Cit+ bacteria through whole-genome sequencing to help indentify the changes. These long-awaited results are now available in a new paper published last month by the Lenski group, and they shed light on all three stages of the process.

Lights, camera, actualization

The key step - and the one of greatest interest - is of course actualization: the mutation that converted a Cit- cell to a Cit+ one. This is also one of the easiest steps to study, since the mutation provides the cell with a new feature that can be detected experimentally. Though E. coli cannot use citrate as a carbon source in the presence of oxygen, they are capable of using citrate in anoxic conditions (i.e. when oxygen is absent). To do so, they employ a protein that imports citrate in to the cell while at the same time exporting a compound called succinate. Since this protein is already present in the E. coli genome, it was long suspected that a genetic regulatory change that turned on its production in the presence of oxygen could be the key innovation that produced the first Cit+ bacterium in the culture. As we discussed yesterday, Behe notes that this change could result from a loss-of-FCT or a gain-of-FCT mutation:

“If the phenotype of the Lenski Cit+ strain is caused by the loss of the activity of a normal genetic regulatory element, such as a repressor binding site or other FCT, it will, of course, be a loss-of-FCT mutation, despite its highly adaptive effects in the presence of citrate. If the phenotype is due to one or more mutations that result in, for example, the addition of a novel genetic regulatory element, gene duplication with sequence divergence, or the gain of a new binding site, then it will be a noteworthy gain-of-FCT mutation.”

Interestingly, the actualization mutation was indeed a change of regulation of the anoxic citrate / succinate transporter, and it arose through a gain-of-FCT mutation. The mutation turned out to be a side-by-side duplication of the citrate / succinate transporter gene, as well as portions of two genes on either side of it. This imprecise duplication placed a partial fusion of these flanking genes next door to one of the copies of the citrate / succinate transporter gene. This brought the copy under the control of promoter sequences derived from of one of its neighbors, a gene that is active when oxygen is present. The resulting product was a copy of the citrate / succinate transporter gene that was now very weakly expressed in aerobic conditions. Since this is an example of a mutation that duplicates a gene and simultaneously creates a new regulatory element for it (causing significant sequence divergence), this is a clear-cut example of a gain-of-FCT mutation.

Responding to the data

While Behe has not yet, to my knowledge commented on this particular development within the LTEE, one of his colleagues in the Intelligent Design Movement (IDM), microbiologist Ann Gauger, has offered her thoughts. Two themes emerge in her commentary: that the Cit+ trait is “not new”, and that the number of mutations it required were within the bounds set out by Behe and another member of the IDM, structural biologist Douglas Axe:

When is an innovation not an innovation? If by innovation you mean the evolution of something new, a feature not present before, then it would be stretching it to call the trait described by Blount et al. in "Genomic analysis of a key innovation in an experimental Escherichia coli population" an innovation [...]

The total number of mutations postulated for this adaptation is two or three, within the limits proposed for complex adaptations by Axe (2010) and Behe in Edge of Evolution. Because the enabling pre-adaptive mutations could not be identified, though, we don't know whether this was one mutation, a simple step-wise series of adaptive mutations, or a complex adaptation requiring one or two pre-adaptations before the big event.

But does this adaptation constitute a genuine innovation? That depends on the definition of innovation you use. It certainly is an example of reusing existing information in a new context, thus producing a new niche for E. coli in lab cultures. But if the definition of innovation is something genuinely new, such as a new transport molecule or a new enzyme, then no, this adaptation falls short as an innovation. And no one should be surprised.

While Gauger does not speak to the tension between her description of the Cit+ mutation as “not genuinely new” and Behe’s criteria that this should be classified as a gain-of-FCT mutation, it is clear that she views this event as within Behe’s “edge” – i.e. within the bounds of “what Darwinism can do.” Additionally, she sees it as falling within the scope of what is evolutionarily possible as proposed by Axe’s work. In the next installment of this series, we’ll revisit how Behe defines his (claimed) limit of what evolutionary processes can accomplish, with this new evidence in hand. In doing so, a careful examination of the potentiation and refinement phases of the Cit+ transition will be informative.

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, 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.

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

Sporadic extinction

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

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

Extinction, en masse

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

Speciation, en masse

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

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

Clearing the deck, and re-filling the niches

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

For further reading:

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

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

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

The Evolutionary Role of Death & Natural Evil

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

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

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

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

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

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

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

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

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

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

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

Notes

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

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.

Transitional Fossils

Some time ago, the Discovery Institute’s Casey Luskin commented on the human origins exhibit at the Smithsonian Institution, suggesting that palaeoanthropologists use evolutionary theory to describe the progression of the human lineage even when they don’t have transitional fossils with which to work. He writes:

What's ironic, however, is that if you ask the question How Do We Know Humans Evolved? the answer you’re given is, “Fossils like the ones shown in our Human Fossils Gallery provide evidence that modern humans evolved from earlier humans.” So whether you find fossils or you don’t, that’s evidence for evolution.

Indeed, it has become an article of faith for those espousing both the young earth creation (hereafter YEC) model and many who hold to the intelligent design model that transitional fossils do not exist and therefore evolution has not taken place. Support for this position usually entails attacking the weak areas of the fossil record, where burial processes have left us little with which to work, or the creation of straw men arguments in which transitional fossils are defined in such a way that none could ever be found. Often this centers on the concept of “missing link,” a term that is habitually used in the popular press and young earth creation and intelligent design literature when referring to fossil remains but which has little to no meaning for biologists or palaeontologists. As Ahlberg and Clack (Ahlberg and Clack 2006) write:

But the concept has become freighted with unfounded notions of evolutionary ‘progress’ and with a mistaken emphasis on the single intermediate fossil as the key to understanding evolutionary transitions. Much of the importance of transitional fossils actually lies in how they resemble and differ from their nearest neighbours in the phylogenetic tree, and in the picture of change that emerges from this pattern.

Contrary to common misconceptions, the fossil record does not record one single lineage for any family of organisms but rather a series of branches, with many related species coexisting synchronously. Darwin hypothesized that the evolutionary record reflected this bushiness and drew such a diagram in his journal. At the time, though, he had little in the way of fossil evidence to back up this position. Much has changed since his day.

An analogy for understanding this “bushiness” was best described by Prothero and Buell (Prothero and Buell 2007). They suggest that the reader consider his or her own genealogy. You and your siblings are the direct descendents of your parents and, while you are similar to them, each of you has different characteristics not shared with them as well as characteristics that you do share. Your parents have siblings as well (your aunts and uncles), and your grandparents are their last common ancestors. These siblings have their own children (your cousins), who have different and similar traits relative to their parents. They are broadly recognizable as being related to you (“oh, I see you have Aunt Edna’s nose”) but three or four generations out, they will become less and less so. These are the “nearest neighbours” that Ahlberg and Clack describe. In this analogy, each of these cousins represents a transitional form from what was (your grandparents) to what will be down the road.

For example, no one would confuse a frog with a salamander but if you trace the fossil record of each back in time, eventually you encounter a fossil, Gerobatrachus hottoni which was recently discovered (Anderson et al. 2008) that is best described as a “frogamander,” having the basal characteristics of both frogs and salamanders. Had we seen such an animal at the time, it is likely we would not have found it remarkable because it would have resembled the species around it. One lineage eventually diverged into frogs, salamanders and other amphibians. Most (just like Darwin proposed in his tree diagram with the little hatch marks at the tip of many branches) went extinct.

Taxonomy and the Beginnings of Human Origins

All life is classified based on a system devised by Carolus Linneaus in 1735 in his remarkable work Systema Naturae. This system gives all recognized species an individual place based on a system of hierarchy. The study of classification is known as taxonomy. A taxonomic ranking for humans would be this:

When a fossil is excavated, the first thing that the palaeontologist does is make a taxonomic assessment of where it fits in a sequence of known fossils. Traits that are shared with other like species or genera are referred to as primitive traits. Examples of this in humans are five fingers and the presence of three arm bones. We share this with all mammals. Traits that are new or are not shared with other like species are referred to as derived traits. Examples of this in humans are the skeletal changes in the pelvis and the foot to allow for walking upright. We do not share these with any other primates.

Transitional fossils in the human fossil record are distinguished at both the genus and species level. This group includes the extinct genera Ardipithecus and Australopithecus and the current genus Homo. All species except Homo sapiens are extinct. Much of the recent study of early humans focuses on the transition from Ardipithecus (‘Ardi’) to Australopithecus (‘Lucy’ and similar fossils) and from Australopithecus to Homo, the genus that led eventually to us. While each of the australopithecine species identified in the fossil record has derived characteristics that separate them from their ancestors and from each other, only one led to the genus Homo.

In future posts, I will describe the evidence for human evolution and why this evidence is compelling. It suggests that we have had a long, varied history filled with great leaps of change, crushing defeat, and eventual expansion into all areas of the globe.

Notes

Ahlberg, P. & J. Clack (2006) A firm step from water to land. Nature, 440.

Anderson, J. S., R. R. Reisz, D. Scott, N. B. Frobisch & S. S. Sumida (2008) A stem batrachian from the Early Permian of Texas and the origin of frogs and salamanders. Nature, 453, 515-518.

Prothero, D. & C. Buell. 2007. Evolution: What the fossils say and why it matters. Columbia Univ Pr.

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.

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

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

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

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

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

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

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

Common Descent

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

Natural Selection

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

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

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

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

Furthermore, he also writes:

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

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

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

Human Continuity

Dembski quotes from Darwin’s Descent of Man:

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

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

Methodological Naturalism

Dembski defines methodological naturalism in the following way:

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

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

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

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

For further reading:

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

Evolution: just a theory

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

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

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

Whale evolution: an example of converging lines of evidence

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

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

The “problem”, of course, is that modern whales are emphatically not terrestrial, nor do they have four limbs – they have two front flippers and a tail, with no hind limbs in sight. Yet they are mammals, which forces evolution’s hand as it were. Evolution thus is dragged, under protest, to the prediction that modern whales, as mammals, are descended, with modification, from ancestral terrestrial, tetrapod ancestors. Instantly this prediction raises a host of uncomfortable questions: where did their hind limbs go? How did they acquire a blowhole on the top of their heads when other mammals have two nostrils on the front of their faces? How did they transition to giving birth in the water? What happened to the teeth of the baleen whales? What happened to the hair characteristic of mammals? and so on. In some ways, evolutionary thinking about whales creates more difficulties than it appears to solve.

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

Going out on a limb

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

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

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

… and passing the test

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

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

For further reading

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

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

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

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

Transcript

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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