If it's not natural selection, then it must be...

The folks at the Discovery Institute (DI) are engaged in an extensive attempt to rebut my friend Dennis Venema's critiques of Stephen Meyer's surprisingly lame ID manifesto, Signature in the Cell. There are several aspects of this conversation that I hope to address in the coming days and weeks, but one jumped out at me today: the consistent confusion about natural selection in depictions of evolutionary theory by design advocates.

Consider this excerpt from a recent blog post by a writer at the Discovery Institute:

...we need a brief primer in fundamental evolutionary theory. Natural selection preserves randomly arising variations only if those variations cause functional differences affecting reproductive output.

A few sentences later, the same claim is repeated:

Indeed, given that natural selection favors only functionally advantageous variations, ...

Those claims were first made in a piece written by unnamed DI "fellows" mocking the work and conclusions of Joe Thornton, an evolutionary biologist at the University of Oregon and the University of Chicago. And the claims are badly misleading.

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Common ancestry, bottlenecks, and human evolution

Human evolution has been in the news quite a lot recently.

• New genetic data suggest that ancient humans included both Neanderthals and Denisovans, which colonized different parts of the world but subsequently interbred with so-called modern humans and left telltale traces of this history in the genomes of living humans.
• New analysis of current genetic diversity suggests that human population size underwent interesting fluctuations throughout the history of our species, but concludes that the population never dipped below a few thousand reproducing individuals.

Unsurprisingly, these findings have been discussed in the context of Christian views of human origins. In the context of some of these discussions (among Catholics, for example), I have noticed some confusion regarding the implications of common ancestry. I will illustrate the error with a stylized example, then explain why it is an error.

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Harmful genes, and sneaky, too: Genetic hitchhiking in the human genome

Genetic hitchhiking is thought to be an inevitable result of strong positive selection in a population. The basic idea is that if a particular gene is strongly selected for (as opposed to selected against), then the chunk of the genome that carries that gene will become very common in the population. The result is a local loss of genetic diversity: all (or nearly all) of the individuals in the population will have that same chunk of genetic information, whereas before the selection process acted, there might have been a lot of variation in that chunk throughout the population. And this means that areas of the human genome that are less variable between people are suspected sites of recent positive selection. Within that chunk, there are potentially many genes and genetic elements that became more common in the population by virtue of their placement near the gene that was actually selected for. Those other genes are the hitchhikers. And it's likely that some hitchhikers are bad news – they're harmful mutations that would normally become rare or extinct in the population, but instead have become common by hitchhiking.

In the last few years, large amounts of genetic information have become available that have enabled biologists to look for evidence of such phenomena in the human genome. Specifically, two major projects have collected genetic data for the purpose of analyzing genetic variation among humans. One project, the International HapMap Project, mapped and quantified sites in the human genome that are known to vary among humans by a single genetic letter. These sites are called single nucleotide polymorphisms, or SNPs (pronounced "snips"). The project has mapped millions of these sites in a group of 270 humans representing various lineages. Another project that has made the news recently is the 1000 Genomes Project, which also seeks to provide a picture of human genetic variation using more people (more than 1000 at present) and slightly different technology. Efforts like these have taken analysis of the human genome to a new level. No longer do we merely wonder what "the" human genome is like – we can begin to learn about how genetic differences give rise to biological differences such as susceptibility to particular diseases.

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New limbs from old fins, part 3

The third installment of my series at BioLogos is now up.* It discusses the developmental mechanisms that underlie the construction of limbs, and the striking fact that these mechanisms are the same ones used to construct fish fins. Watch for an appearance by Sonic Hedgehog.

*Edit July 2020: The series was consolidated into a single article on the BioLogos site. The link now goes to that single article.

Genetic hitchhiking in English

The next post will discuss recent evidence for genetic hitchhiking in humans. So, what do we mean when we say that genes can hitchhike? To make sense of this phenomenon, we first need to review chromosomes and sexual reproduction.

Most people know that sexual reproduction creates offspring that are genetically distinct from both of the their parents. That's true, but the genetic scrambling that occurs is more significant than is sometimes reported. Let's start by looking at chromosomes.

Like every other animal (or plant or pretty much any other organism), your genetic endowment is carried in chunks of DNA called chromosomes. You have 23 of these chunks, which are rather like volumes in a set of encyclopedias. More completely, you have 23 pairs of these volumes; one set was contributed by your mother and the other by your father. Each of your parents had a complete set, also consisting of a set from Mom and a set from Dad. When your mother made the egg that became the zygote that became you, she provided you with one copy of each volume in the set, and she chose those copies randomly. For example, she may have chosen her dad's copy of chromosome 1, but her mom's copy of chromosome 2. Just by virtue of this random picking process, she made an egg with a shuffled version of her own genetic cards. Dad did the same when he made his sperm, and so your genetic complement is an amalgamation of your parents' genomes which were amalgamations of your grandparents' genomes, and so on.

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New limbs from old fins, part 2

Titktaalik roseae.
Image from
https://tiktaalik.uchicago.edu/index.html

The second post in my series on limb evolution is now up at the BioLogos site. This installment reviews the fossil evidence on fin-to-limb evolution, introducing the famous Tiktaalik. Next up: evidence from developmental biology.
The first post at BioLogos outlined limb structure and some historical background. The series at BioLogos was spawned by an idea here at QoD, which aimed to discuss some new findings in the fins-to-limbs story. Those new findings will be discussed in the final installment of the series at BioLogos.

*Edit July 2020: The series was consolidated into a single article on the BioLogos site. The link now goes to that single article.

"The stamp of one defect": an endless series on harmful mutations

Not surprisingly, Hamlet weighed in on the nature vs. nurture question, at least once.

So, oft it chances in particular men,
That for some vicious mole of nature in them,
As, in their birth,―wherein they are not guilty,
Since nature cannot choose his origin,―
By the o’ergrowth of some complexion,
Oft breaking down the pales and forts of reason,
Or by some habit that too much o’er-leavens
The form of plausive manners; that these men,
Carrying, I say, the stamp of one defect,
Being nature’s livery, or fortune’s star,
Their virtues else, be they as pure as grace,
As infinite as man may undergo,
Shall in the general censure take corruption
From that particular fault: the dram of eale
Doth all the noble substance of a doubt,
To his own scandal.

– Hamlet, Act I, Scene IV, The Oxford Shakespeare

It is certainly true that "the stamp of one defect" can wreak havoc on the scale that Hamlet describes, and whether the result is a debilitating physical limitation or damage to "the pales and forts of reason," the outcome is tragic by any measure.

Reflecting on the reality of inherited dysfunction, we might be tempted to assume that a "vicious mole of nature" is something seen only "in particular men," and that those who are not so characterized (let's call them "normal people") have been dealt a genetic hand that lacks such devilish cards. Normal people don't have bad genes.

Okay, so in the real world I suspect that most people are not so naïve; if you're reading this blog, then you probably know that bad genes can be carried by normal, healthy people. Nevertheless, when we think about bad genes – or more technically, deleterious mutations – we are likely to think that they are not very common.

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New limbs from old fins, part 1

Last month, I started a series on the topic of limb evolution, here at Quintessence of Dust. That series has been transformed (through a series of intermediates) into a series of posts* at the BioLogos site. The first installment is now up, and it provides an expanded introduction to the topic and a little historical context. Subsequent posts will tackle fossils, developmental biology, genetics, the explanatory role of design, and related themes.

So go check out the introduction, and feel free to contribute comments, questions and suggestions here. And enjoy the image below, from Wellcome Images, which is featured in the post at BioLogos. Cool, huh?

*Edit July 2020: The series was consolidated into a single article on the BioLogos site. The link now goes to that single article. 

Molecular evolution: improve a protein by weakening it

In the cartoon version of evolution that is often employed by critics of the theory, a new protein (B) can arise from an ancestral version (A) by stepwise evolution only if each of the intermediates between A and B are functional in some way (or at least not harmful). This sounds reasonable enough, and it's a good starting point for basic evolutionary reasoning.

But that simple version can lead one to believe that only those mutations that help a protein, or leave it mostly the same, can be proposed as intermediates in some postulated evolutionary trajectory. There are several reasons why that is a misleading simplification – there are in fact many ways in which a mutant gene or protein that seems to be partially disabled might nevertheless persist in a population or lineage. Here are two possibilities:

1. The partially disabled protein might be beneficial precisely because it's partially disabled. In other words, sometimes it can be valuable to turn down a protein's function.

2. The effects of the disabling mutations might be masked, partially or completely, by other mutations in the protein or its functional partners. In other words, some mutations can be crippling in one setting but not in another.

In work just published by Joe Thornton's lab at the University of Oregon*, reconstruction of the likely evolutionary trajectory of a protein family (i.e., the steps that were probably followed during an evolutionary change) points to both of those explanations, and illustrates the increasing power of experimental analyses in molecular evolution.

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Let's see a show of autopods. Part 1.

The discovery of deep homology was a milestone in the history of evolutionary thought. Anatomical structures in distantly related organisms, structures with only the barest of functional similarities, were found to be constructed under the influence of remarkably similar genetic pathways. The original and classic example from 1989 involves genes controlling pattern in both insects and mammals – the famous Hox genes. Another great example emerged from the study of limb development and evolution in vertebrates, work beautifully described by Neil Shubin in Your Inner Fish.

The idea that the limbs of various animals are homologous – meaning that they are variations on a theme inherited from common ancestors – is certainly not new, with roots in the exploration of 'archetypes' by the great Sir Richard Owen. But deep homology goes, well, deeper, suggesting that even basic themes like 'limb' or 'eye' or even just 'thing-sticking-out-of-the-body-wall' can be identified and seen to be conserved throughout the biological world. And, importantly, deep homology points to genetic mechanisms that underlie basic themes, structural concepts so distinct that they would not be judged to be related by structural criteria alone. Consider, for example, limb development in vertebrates.

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What a selfish little piece of...

"The Selfish Gene." "Selfish DNA." Oh, how such phrases can get people bent out of shape.  Stephen Jay Gould hated such talk (see a little book called The Panda's Thumb), and Richard Dawkins devoted more time to answering critics of his use of the term 'selfish' than should have been necessary. Dawkins' thesis was pretty straightforward, and he provided real examples of "selfish" behavior of genes in both The Selfish Gene and its superior sequel, The Extended Phenotype. But there have always been critics who can't abide the notion of a gene behaving badly.

Leaving aside silly bickering about the attribution of selfishness or moral competence to little pieces of DNA, let's consider what we might mean if we tried to imagine a really selfish piece of DNA. I mean a completely self-centered, utterly narcissistic little piece of DNA, one that not only seeks its own interest but does so with rampant disregard for other pieces of DNA and even for the organism in which it travels. Can we imagine, for example, a piece of DNA that deliberately harms its host in order to propagate itself?

Sure, we might picture genes acting in naked self-interest, perhaps colluding to create an organism that can fly and mate but can't eat. We can picture genes driving organisms to take outrageous risks in order to reproduce. And we can picture millions and millions of "jumping genes" that don't seem to care at all about the host's welfare while they hop about in bloated mammalian genomes. (If you are one who prefers to think of these transposable elements as beautifully-designed marvels of information transfer and storage, you can have a pass on that last one for now, because you won't like where we're going with this.) But can we picture a gene that actively harms its host in order to get ahead?

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Evolution cheats, or how to get an old enzyme to do new tricks

It is of course a cliche to state that eukaryotic cells (i.e., cells that are not bacteria) are complex. In the case of an animal, tens of thousands of proteins engage in fantastically elaborate interactions that somehow coax a single cell into generating a unique and magnificent organism. These interactions are often portrayed as exquisitely precise, using metaphorical images such as 'lock-and-key' and employing diagrams that resemble subway maps.

Many of these interacting proteins are enzymes that modify other proteins, and many of those enzymes are of a particular type called kinases. Kinases do just one thing: they attach phosphate groups to other molecules. This kind of modification is centrally important in cell biology, and one way to tell is to look at how many kinases there are: the human genome contains about 500 kinase genes.

Now, kinases tend to be pretty picky about who they stick phosphate onto, and this specificity is known to involve the business end of the kinase, called the active site. The active site is (generally) the part of the kinase that physically interacts with the target and transfers the phosphate. You might think that this interaction, between kinase and target, through the active site, would be by far the most important factor in determining the specificity of kinase function. But that's probably not the case.

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Design and falsifiability

Last month I had an interesting conversation with Casey Luskin of the Discovery Institute (DI), at Evolution News and Views (ENV), a DI blog/site that recently opened some articles to comments. The topic of the original post was common ancestry in humans and other primates, but Casey and I discussed various aspects of design thought.

One subject that came up was the falsifiability of design. I maintain that design arguments, whenever they also postulate the existence of an omnipotent deity (or any super-powerful being, for that matter), are inherently unfalsifiable. And I want some feedback on my argument.

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Conversing with Casey Luskin

Last month I wandered over to Evolution News and Views (ENV), a Discovery Institute (DI) blog, and read a piece by Casey Luskin on the topic of human/chimp common ancestry. I saw some stuff I didn't like, and left a comment, and an interesting exchange ensued. You can read it yourself, but here are some of my comments.

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Genetics, evolution, and sexual orientation: the gay extinction hypothesis

Three weeks ago, I went to the Cornerstone Music Festival with my two oldest kids. For the second year, I was an invited speaker in the festival's excellent seminar program. This year, my two series were entitled "Alien Worlds" and "Zombies on Jeopardy" – exploring extreme biology and human nature, respectively. It was fun, if a little too hot for a day or so.

At one point, I was discussing human intelligence and its genetic underpinnings. And I got a loaded question, paraphrased thus: "What happens when you substitute 'sexual orientation' for intelligence? Is homosexuality 'genetic' and if so, what does that mean for Christian views of sexuality?" (The Cornerstone Festival is a Christian music festival, known for embracing music at the 'fringes' while remaining consistent with most mainstream evangelical sensibilities, including a typically evangelical view of homosexuality.) I answered that sexual orientation also has a fairly significant heritable component, meaning that some of the variation in sexual orientation is accounted for by genetics. Then I got a followup question/comment, delivered with intriguing smugness, and paraphrased as follows: "Homosexuality can't be genetic, because homosexuals don't have kids and so the trait will be eliminated from the population." Without going into the complexity of sexual orientation as a biological phenomenon, I will critique this person's claim, since I hear it from Christians with disheartening frequency.

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Mapping fitness: ribozymes, landscapes, and Seattle

A few months ago, we were looking at the concept of a fitness landscape and how new technologies are creating opportunities for biologists to look in detail at relationships between genetics and fitness. The first post discussed the concepts of a fitness landscapes and adaptive walks, with some focus on the limitations of the metaphor. The second post summarized some recent work on bacterial fitness and mutation rates, with the concept of a fitness landscape as a theme, and the third post reviewed another recent paper, one that described techniques for studying fitness landscapes in detail by linking protein function (which can be screened and/or selected) and genetic information. Here we'll look at yet another approach to the problem, in which the subject of the analysis is not an organism (as in the first paper) or a protein (as in the second paper) but an RNA molecule.

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New reading on "junk DNA"

John Farrell runs an interesting blog at Forbes.com, and he regularly discusses genetics, design, and other topics of interest around here. His latest points to work by Larry Moran and Ryan Gregory, both of whom have debunked some of the "junk DNA" misinformation concocted by design theorists, then looks at some interesting new blogging from one Stanley Rice. It's interesting stuff.

Casey Luskin shows up in the comments. Nothing new there. Run over and check it out.

Alu need to know about parasitic DNA: telling the whole story about Alu elements and "design"

So, Alu elements are mobile DNA modules that can exert diverse influences on genomes and the organisms harboring them. They can affect genome function in constructive ways, by altering gene expression or supporting chromosome structure. And they can be damaging, even deadly. There are more than a million of them in the human genome, and we don't know what each one does. But, as I explained in the first post in this series, we do know that they can play both helpful and harmful roles, in the same way that other kinds of parasites can be good, bad, or indifferent.

Alu elements and other genome-wide repeats are a big problem for intelligent design (ID) theorists of some stripes. Any ID proponent who claims that genomes are carefully-designed, well-optimized systems must deal with the reality of the enormous numbers of mobile elements in (for example) the human genome. Now, I can think of various ways such an ID theorist might discuss Alu elements. She could propose that all of their characteristics (including their mobility) are part of their design, such that they can bring new design features quickly into being; she could propose that their mobility is a "bug" rather than a "feature," and perhaps speculate on how things went wrong; she could postulate that the damage caused by their expression and their mobility is being misattributed to the genome when it is instead caused by some other external process. (Or she could say, "We're still working on that one.")

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Exploring the protein universe: a response to Doug Axe

One of the goals of the intelligent design (ID) movement is to show that evolution cannot be random and/or unguided, and one way to demonstrate this is to show that an evolutionary transition is impossibly unlikely without guidance or intervention. Michael Behe has attempted to do this, without success. And Doug Axe, the director of Biologic Institute, is working on a similar problem. Axe's work (most recently with a colleague, Ann Gauger) aims (in part, at least) to show that evolutionary transitions at the level of protein structure and function are so fantastically improbable that they could not have occurred "randomly."

Recently, Axe has been writing on this issue. First, he and Gauger just published some experimental results in the ID journal BIO-Complexity. Second, Axe wrote a blog post at the Biologic site in which he defends his approach against critics like Art Hunt and me. Here are some comments on both.

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How do fish adapt to life in hydrogen sulfide?

To find out, and to read some of the best recent blogging on evolution, visit the new Carnival of Evolution, 35th Edition, at Lab Rat. And go to the official carnival page to learn more about the Carnival of Evolution and perhaps to sign up as a future host.

Alu need to know about parasitic DNA: Alu elements and blindness

Age-related macular degeneration (AMD) is a leading cause of blindness in humans, and the leading cause of visual impairment during advanced age. The condition comes in two basic forms, the most severe of which is untreatable. Called geographic atrophy (GA), this condition involves the steady destruction of the retinal pigment epithelium, a layer of tissue in the eye that is essential for the health and maintenance of the photoreceptors in the retina. Loss of the pigment epithelium means certain death for the photoreceptors, and that means visual impairment and then blindness for the affected person.

A major publication in Nature last month (Kaneko et al., "DICER1 deficit induces Alu RNA toxicity in age-related macular degeneration," Nature 17 March 2011) now points to one likely cause of AMD, and in the process provides a chilling example of what can happen when the parasitic Alu elements in our genomes (see the previous post for an introduction) are left unrestrained.

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Alu need to know about parasitic DNA: Introduction to Alu elements

Defenders of intelligent design theory often dwell on the topic of "junk DNA," which has been molded into a masterpiece of folk science. The ID approach to "junk DNA" involves a fictional story about "Darwinism" discouraging its study, and a contorted and simplistic picture of a "debate" about whether "junk DNA" has "function." The fictional story is ubiquitous despite being repeatedly debunked. But the picture of an ongoing "debate" about "function" is harder to sort out. Like most propaganda, that picture contains enough truth to sound plausible. (Browse my "Junk DNA" posts, and work by Ryan Gregory and Larry Moran, for more information on errors and folk science associated with these topics.)

There is, in fact, some scientific disagreement about functions of various elements in genomes, but it's not the crude standoff that ID apologists depict, and it has very little to do with "Darwinism." The debate, if we must call it that, is about at least two matters: 1) the extent to which certain genomic elements contribute to normal function or development of organisms; and 2) the means by which we might determine this. The debate is not about whether non-coding DNA can have function, or even about whether some segments of non-coding DNA do have function. That debate was invented by anti-evolution propagandists.

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34th Carnival of Evolution

Welcome to the 34th Edition (1 April 2011) of the Carnival of Evolution, and welcome to Quintessence of Dust. It's nice to be hosting this fine carnival, and to see that it's still going strong.

I've organized the carnival under some chapter and section headings that I got from some old Victorian's magnum opus, but I think you'll find the topics require no further creative embellishment.

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Mapping fitness: protein display, fitness, and Seattle

A couple of months ago we started looking at the concept of fitness landscapes and at some new papers that have significantly expanded our knowledge of the maps of these hypothetical spaces. Recall that a fitness landscape, basically speaking, is a representation of the relative fitness of a biological entity, mapped with respect to some measure of genetic change or diversity. The entity in question could be a protein or an organism or a population, mapped onto specific genetic sequences (a DNA or protein sequence) or onto genetic makeup of whole organisms. The purpose of the map is to depict the effects of genetic variation on fitness.

Suppose we want to examine the fitness landscape represented by the structure of a single protein. Our map would show the fitness of the protein (its function, measured somehow) and how fitness is affected by variations in the structure of the protein (its sequence, varied somehow). It's hard enough to explain or read such a map. Even more daunting is the task of creating a detailed map of such a widely-varying space. Two particular sets of challenges come to mind.

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