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.

What does it mean for humanity to be created “from the dust of the ground?”

In many ancient Mesopotamian creation stories, human beings were depicted as deriving from some physical part of the gods. Often this was the result of conflict: humans arose from the blood, flesh or tears of gods slain by other gods. Humans created in this fashion were supposed to serve the gods by performing menial work that the gods had tired of doing themselves. The lot of humanity, then, was one of violence and servitude.

In the Israelite creation stories reflected in Genesis 1 and 2, however, humans are made from the ordinary material of creation: “dust.” Humans are made of earth-stuff, not god-stuff.

At first glance, it may seem that this lowers the status of the human creature. We might ask the question raised by Eliphaz in the book of Job:

Can a mortal be more righteous than God?
Can even a strong man be more pure than his Maker?
If God places no trust in his servants,
if he charges his angels with error,
how much more those who live in houses of clay,
whose foundations are in the dust, who are crushed more readily than a moth! (Job 4:17-19)

Indeed, our humble origins ought to remind us of the fragility of our lives. As the Psalmist says,

You turn people back to dust, saying, “Return to dust, you mortals.”
A thousand years in your sight
are like a day that has just gone by,
or like a watch in the night.
Yet you sweep people away in the sleep of death—
they are like the new grass of the morning:
In the morning it springs up new,
but by evening it is dry and withered.

The elements of which our bodies are made are ordinary and abundant. Science tells us that approximately ninety-three per cent of the mass in a living human body is comprised of elements first formed through nuclear fusion in the hearts of stars. Through almost unimaginably vast and ancient cycles of stellar formation and supernova explosions, this “stardust” of elements has been spread throughout the universe. It is as though God scattered the stars across space and time to seed the universe for life, including your life and mine. And we are thereby inseparably connected to each other, to the air we breathe, to the ground we tread, to all the creatures that fill the skies and crawl upon the earth and teem in the seas, to the depths of all the heavens. We are not transcendent of creation. We are creatures.

Yet we are creatures into which God breathed the “breath of life.” We are stardust and more than stardust. We are not reducible to our constituent chemicals. A “man” or a “woman” is not just a gooey sack of water, carbon and trace elements. Hydrogen, oxygen and carbon are not aware of their own existence. These elements cannot reason or pray or love or write poems. Conjunctions of these elements cannot carry any persistent identity across time. They do not exercise will or intentionality or agency. They are not “selves.”

Most of the cells in a human body are in constant flux: aging, dividing, dying, being replaced. The surface layer of human skin is renewed completely about every two weeks. An adult’s skeleton is entirely remade over approximately ten year periods. It may be that only the neurons of the cerebral cortex and a few other types of cells persist throughout the lifetime of a human body. And eventually, it all does return to “dust.”

Yet we think of ourselves as persisting over time, as comprising an “identity,” a “self.” Perhaps the cerebral cortex provides the stable biological platform for identity and selfhood, but something new emerges from the chemical-electrical soup, new patterns of organization, a different level of causation. We can even make choices that reshape ourselves, both physically and psychologically. The very wiring of our brains changes when we make conscious choices. Mind is both shaped by matter and supervenes on matter.

Materialists who wish to collapse all of human identity into brain chemistry overstep the bounds of “science.” A fundamental principle of scientific practice is testability: is it possible to demonstrate empirically whether a proposition is false ? As Saint Augustine observed many centuries ago, the fact that I acknowledge I could be “wrong” about something means that I am a “self” who is capable of making real choices about things that are in fact true or false. “Si fallor, sum” Augustine said – if I can doubt, if I can be wrong, then I must exist. One who is a true materialist “all the way down” cannot test his or her materialism. There is no possibility of “being” right or wrong, indeed no possibility of “being” – there is nothing but chemistry.

Spiritualists who wish to degrade matter in favor of the soul or spirit likewise are not expressing a Christian anthropology. Indeed, one of the first heresies that encountered the early Christian church was Gnosticism. A core belief of Gnosticism was that matter, including the human body, was essentially evil. Salvation for the Gnostics involved the soul’s escape from the prison of embodiment and materiality. The Gnostics treated the body either with disdain – engaging in extreme ascetic practices – or with antinomian abandon – engaging in extreme sexual license. Either way, their practices were rooted in the belief that matter and the body were unimportant. It’s easy to see how this view continually creeps into both our popular culture and our Church cultures.

Christian theology asserts that humans are spiritual creatures, a unity of body and spirit or “soul,” integrated, not reducible downwards to mere matter or upwards to mere spirit. Perhaps there is no better way to bring these themes together than with a Psalm — here is Eugene Peterson’s paraphrase of Psalm 139 in The Message:

God, investigate my life; get all the facts firsthand.
I’m an open book to you;
even from a distance, you know what I’m thinking.
You know when I leave and when I get back;
I’m never out of your sight.
You know everything I’m going to say
before I start the first sentence.
I look behind me and you’re there,
then up ahead and you’re there, too—
your reassuring presence, coming and going.
This is too much, too wonderful—
I can’t take it all in!

Is there any place I can go to avoid your Spirit?
to be out of your sight?
If I climb to the sky, you’re there!
If I go underground, you’re there!
If I flew on morning’s wings
to the far western horizon,
You’d find me in a minute—
you’re already there waiting!
Then I said to myself, “Oh, he even sees me in the dark!
At night I’m immersed in the light!”
It’s a fact: darkness isn’t dark to you;
night and day, darkness and light, they’re all the same to you.

Oh yes, you shaped me first inside, then out;
you formed me in my mother’s womb.
I thank you, High God—you’re breathtaking!
Body and soul, I am marvelously made!
I worship in adoration—what a creation!
You know me inside and out,
you know every bone in my body;
You know exactly how I was made, bit by bit,
how I was sculpted from nothing into something.
Like an open book, you watched me grow from conception to birth;
all the stages of my life were spread out before you,
The days of my life all prepared
before I’d even lived one day.

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.

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.

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.

(Click Image for Full Resolution)

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

For more, be sure to read our FAQs How are the ages of the Earth and universe calculated? and What scientific evidence do we have about the first humans?, as well as our recent infographic How Do We Know the Earth is Old?.

Author's Note from Joy Walters

As I mentioned in my first post, I grew up skeptical of the whole idea of evolution. One contributor to my disbelief was the lengthy timescale for the “tree of life” that was presented with the theory. I would hear, for example, that dinosaurs lived hundreds of millions of years ago, but there was no explanation of why this was true; it was just given as a fact. No one explained the methods of dating, and so I thought biologists simply estimated the ages of species to fit their preconceived notions of how long it would take for one species to emerge from another. It also seemed like the ages were periodically revised and extended farther back in time, and I figured scientists needed to manipulate numbers to make evolution plausible. This, in my mind, made the theory both unbelievable and dismissible.

Once I learned about the techniques used to date fossils, I realized that my first impressions were wrong; the ancient ages of species are scientific determinations rather than scholarly conjectures. However, I have found in recent conversations that Christians remain skeptical of old ages and the evolutionary time scale. For this reason, I wanted the videocast to address the process of fossil dating (what the methods are and why they are accurate) while focusing on cases where hominid fossils were discovered and dated using these very methods. My hope is that Believers would be informed about the evidence for human evolution and its scientific grounding.

Many posts on this Forum have suggested that the cosmological narrative in Genesis 1 is best read as being primarily about God’s identity and agency, rather than about the physical make-up or material history of the natural world. Similarly, we demonstrate our highest regard for Genesis 2’s account of the creation of Eve—the second fully human being—by looking to its meaning in terms of spiritual and interpersonal relationships, rather than genetic ones. While the specific “how” of our being made into the image of God will probably always remain a mystery, the Bible and creeds are clear on the “why” of our creation: we were made to worship the Lord, and be in relation with Him and each other. That intimate, conscious and deeply symbolic knowledge of our maker and fellow human beings is a profound difference that sets us apart from the other creatures.

I have frequently argued that poets are often the most clear on some of the important issues of our faith, including this one. Today we feature a work by Robert Siegel, who identifies the imagination as the faculty by which we recognize and name those spiritual relationships. As he says, “It's the imagination, hence language and art, that establishes the connections”; it is the imagination that allows us to conceive of and name the links between ourselves and creation, ourselves and each other, ourselves and the Creator God.

Though we often focus on Adam’s naming of the animals, and then even of Eve, Siegel helps us remember that it was in hearing his own name that Adam’s whole humanity came into being: he experienced the richness of being called by God to bear His likeness, but also of being called to by one that was profoundly “like him.” Put another way, we are speakers, but also equally hearers. May we, too, be awakened to ourselves and our image-bearing identity by a still, soft voice saying our name. May we, too, in gratitude and delight, call upon the name of the one, Jesus, who is both our God and our fellow man.

“Adam’s Dream”

by Robert Siegel

The Imagination may be compared to Adam's dream:
he awoke and found it truth. --Keats

He saw the garden spreading past the trees
he'd been warned to avoid (yet keep a special eye on).
He'd learned by scents, transported by the breeze,
myriads of roses and how, by hand, the scion

of one to graft on another--and what was edible:
whole families of legumes, grasses, roots,
melons, peaches, apples, pears. Incredible,
the variety of tastes just from the fruits!

But it wasn't enough. Even the breathing animals
with friendly grunt or sigh, silken warm side,
and large affectionate eye were not able
to speak. When he named them, none replied:

His words fell dead on the air--though he said
them everywhere, walking or running to each place:
to the mountain, which echoed back the sounds he made,
or the still pool, returning his own gaze.

But no one answered him until one night in a dream
he woke and heard a soft voice speak his name.

“Adam’s Dream” first appeared in issue 3 of Stonework, the literary journal of Houghton College. © 2001 Robert Siegel

Robert Siegel is the author of nine books of poetry and fiction, most recently A Pentecost of Finches: New and Selected Poems. He has received prizes and awards from Poetry, Prairie Schooner, The Transatlantic Review, the Ingram Merrill Foundation, and the National Endowment for the Arts, and his poems have appeared in numerous journals and anthologies. His fiction includes Alpha Centauri and the Whalesong trilogy, which received the Golden Archer and Matson awards. With degrees from Wheaton, Johns Hopkins, and Harvard, Siegel has taught at Dartmouth, Princeton, and Goethe University in Frankfurt, and for twenty-three years at the University of Wisconsin-Milwaukee, where he directed the graduate creative writing program and is currently professor emeritus of English. He is married to Ann Hill Siegel, a photographer, and lives on the coast of Maine.