Moon Mysteries and the Lunarlogos Foundation
Suppose you are keenly interested in the topography of one of the moons, named Y6-9. Suppose also that the books you first select to read on the topic are popular works, written by “experts” who are “living legends.” As you read through the works, you find paragraphs here and there about how utterly decrepit Y6-9 is, and how this space body exemplifies eons of random events. The authors argue that we already knew all there was to know about that moon back in 1859, and that the evidence demonstrates either that God doesn’t exist or that the deity left the cosmos to itself after the Big Bang.

You find, however, that these books almost totally ignore the findings of the billion-dollar missions sent to the surface of Y6-9 since the 1960s. Indeed, there is next to nothing in them about Y6-9’s actual geology.

So you contact the Lunarlogos Foundation, a Christian group that promotes such books. You tell them that you have a few specific questions about the Y6-9 mission findings. The response you get is that because you are a layman, you would not be able to comprehend the details. Besides, the Lunarlogos folks say, the mainstream experts have spoken authoritatively about the subject and that should be enough for you. As a consolation, though, they send you a CD that has songs that are sung by one of their founding members.

Now, more than disgruntled, you decide to write about what you have learned, citing the relevant literature in case someone might want to read about this topic themselves. After posting what you write on the Internet, Lunarlogos posts their reply. Their response reads something like this:

Okay. Sure. There are obnoxious monoliths littering Y6-9…everybody knows this. In fact, there are about a million of them. But they got there because of degenerative cosmic processes. While many of the structures Mr. X mentioned are suggestive of some possibly unknown cause that we have never denied, it is almost certain that much, if not most, of the Y6-9 surface is without any remarkable features. Besides, why would God put them there? They are simply nonsensical.

We have one more thing to say. We don’t appreciate how disrespectful Mr. X has been to our team of experts. Although Mr. X is a Ph.D. planetary scientist, he is not as qualified to write on this subject as scientists approved by Lunarlogos. So we ask him, for the sake of having meaningful dialogue: Please stop writing about this subject.

A Lunarlogos sympathizer writes on another blog:

We think you’re a nice guy, but your arguments are insane.

Then someone unaffiliated with Lunarlogos brings something to your attention. He shows you a map of the sister moon of Y6-9, called Q7-10. You are aware that Y6-9 and Q7-10 went their separate ways after a cosmic collision twenty-two million years ago. But something strange catches your eye. Q7-10 has polished black monoliths, too, except that they are pyramids instead of rectangles. That’s not the weirdest thing, though. The weirdest thing is that the geographical distribution of the monoliths on Y6-9 very nearly matches the geographical distribution of the monoliths on Q7-10.

Now what would you think?

That Strange SINE Signal…Again
The almost one-to-one correspondence of mouse-specific and rat-specific SINE insertion events along homologous regions of the two genomes is almost as remarkable as the matching geographical distributions of the monoliths in the analogy of the two moons. Remember the graph (from Figure 9c of Ref. 1):

We have two genomes that went their separate ways 22 million years ago. We have two lineages that have been subjected to different historical events. Yet, when we compare the chromosome locations of mouse B1s/B2s/B4s with those of rat IDs, they look almost the same. Where the ID SINEs rise in density, so do the B1s/B2s/B4s SINEs; where the ID SINE levels decrease, so also do the B1s/B2s/B4s SINE levels. Independent mutational events have generated equivalent genomic patterns. How can we causally account for this striking pattern?

In the paper written by Francis Collins and his colleagues, under the heading Co-localization of SINEs in rat and mouse¹, we read:

“The cause of the unusual distribution patterns of SINEs…is apparently a conserved feature, independent of the primary sequence of the SINE...” (Italics mine.)

Let’s unpack this part of the sentence. We have:

1) A cause of some sort.

2) A cause that is conserved between the mouse and rat.

3) A cause that is independent of SINE primary DNA sequences.

Thinking Like a Darwinian
Experts such as John Avise, Francisco Ayala, Francis Collins, and Darrel Falk tell us that we must think like Darwinians before we can begin to make sense of the data, since nothing else is scientific, or indeed even reasonable. So let’s play along and think like Darwinians, limiting ourselves to what Collins and his colleagues have authoritatively provided. Recall that they are:

• Chance mutations continually degrade genomes that are largely junk
  
• SINEs are for the most part nonsensical junk
  
• Natural selection is the sole creative force in evolution
  
• Except when genetic drift (neutral evolution) is also a factor

We can call this conceptual scheme the “BioLogos box.”

We’ll start, then, with chance mutations. We know that the enzymes encoded by the L1 retrotransposon copy and paste SINEs into mammalian genomes. So perhaps this is the causative agent that acts independently of primary DNA sequence? And since L1 is present in all mammalian genomes, we may just be on the trail of the “conserved cause.”

But wait. L1 also mobilizes itself. This is a problem, for when we compare LINE and SINE distributions along chromosomes, it is clear that in the regions where the former is abundant the latter is not, and vice versa. Remember the graph (from Figure 9d of Ref. 1):

But we have no plausible mechanistic explanation for why the mouse L1 machinery would have pasted B1s/B2s/B4s—over twenty-two million years, no less—into the same general locations and at much the same densities, as the rat L1 machinery pasted ID elements over the same period of time.

Not to fear. We still have to consider that worker of miracles, natural selection. This mechanism eliminates harmful features while preserving those that enhance survival. So let’s construct a hypothesis: Mouse and rat SINE distributions reflect the differential removal of these DNA repeats from regions where their presence would be harmful. In other words, we predict that sequences where mouse B1s/B2s/B4s and rat IDs peak in density are segments of the genome that are largely junk; conversely, in the sections where these SINEs taper off, functional coding regions are to be found.

Does this hypothesis point in the right causal direction? I don’t think so. Here is why. Remember the statement made by Falk in defense of Ayala contra Meyer:

He [Ayala] does say that on average there are about 40 copies of Alu sequences between every two genes, but this is simply a fact.

The cause of the unusual distribution patterns of SINEs, accumulating in gene-rich regions where other interspersed repeats are scarce, is apparently a conserved feature, independent of the primary sequence of the SINE... (Italics mine.)

Whatever the mystery cause is, it plucked out the species-specific SINEs from the junkety-junk LINE regions, and piled them high around the “twenty-five thousand genes” of the mouse and rat. Or it directed the SINEs to rain down on the gene-rich regions and in much lesser amounts elsewhere. This contradicts our selection hypothesis, unless the SINEs are doing something important in and around those protein-coding regions. But since so much ink has been spilled arguing that nothing of the sort is the case—these are junk elements, even harmful—we must turn to some other factor.

Reaching into the BioLogos box, we now pull out “genetic drift.” Neutral evolution means that a mutation—regardless of whether it is beneficial, neutral, or negative—can become fixed or lost in a lineage solely by chance. With respect to a SINE insertion, its persistence in a lineage would have to be a genetic coin toss: If heads, the SINE stays in a site; if tails, it is lost. So for a pure neutralist model to account for the graphs we have seen, ~300,000 random mutation events in the mouse have to match, somehow, the ~300,000 random mutation events in the rat.

What are the odds of that?

Thinking Outside the Box
Like the imaginary scientist trying to make sense of the far-from-random lunar evidence that Lunarlogos glossed over, I think we have to look elsewhere for the mystery cause of equivalent SINE patterns in the mouse and rat genomes. But where? A technical term was used in the sentence that I quoted above that you may have missed. I will highlight it for you:

“The cause of the unusual distribution patterns of SINEs, accumulating in gene-rich regions where other interspersed repeats are scarce, is apparently a conserved feature, independent of the primary sequence of the SINE and effective over regions smaller than isochores.”

Ever heard of “isochores”? Well, they are to DNA sequence organization along a chromosome what mountains and valleys are to a continent. Imagine buying a book about the geographical features of Africa and not finding a single word about Mount Kilimanjaro or the Great Rift Valley.

Imagine finding instead a lot of musings about what God couldn’t or wouldn’t have done with Africa. What would you think about such a book?

Well, turn to the index of Francis Collins’s The Language of God, or John Avise’s Inside the Human Genome: A Case for Non-Intelligent Design, and look for “isochore.” You won’t find it.

Isochores might provide a clue to cause of the mystery signal, but the cause—whatever it may be—is outside the BioLogos box.

Reference
¹ Rat Genome Sequencing Project Consortium. 2004. Genome sequence of the Brown Norway rat yields insights into mammalian evolution. Nature 428: 493-521.

The blue line indicates the distribution of SINEs along a 110-million base pair interval of rat chromosome 10. (From Fig. 9d of Ref. 1.)

Taxon-Specific Elements: The SINEs Aren’t The Same
Intriguing as this non-random distribution of repetitive elements may be, it gets even more interesting when one realizes that SINEs are specific to taxonomic groups. Each primate genome has distinct subfamilies of the Alu sequence. The mouse genome, on the other hand, has no Alus but it does have three unique SINE families called B1, B2, and B4. While mouse B1 shares some sequence similarity with Alu, it has no relationship to the B2 or B4 elements; the latter two are also unrelated to each other. What then about the rat SINEs along chromosome 10, which were depicted as a blue line? Well, the genome of the rat has one main SINE family called ID, for the “Identifier” sequence. The ID elements have nothing in common at the DNA sequence level with the mouse B1s, B2s, or B4s, and they are wholly dissimilar to Alus.

Now, the mouse and rat are estimated to have diverged twenty-two million years ago. During that interval, individual SINEs have been coming and going and going and coming, in and out of chromosomes. This ongoing insertion/deletion of these retrotransposons is precisely the “degenerative process” that Francisco Ayala referred to when mentioning Alus.

For the twenty-two million years that have occurred since the mouse and rat lineages went their separate ways, both genomes have been subjected to hundreds of thousands—if not millions—of separate SINE insertion events. Putting on our “junk DNA” thinking caps, let’s try to predict what the outcomes of such long-term mutational bombardments would be vis-à-vis the linear distributions of SINEs along a chromosome. To do this, let’s connect these two statements:

1) “…almost certainly much, if not most, of the DNA plays no role…"

2) “Perhaps one could attribute the obnoxious presence of the Alu sequences to degenerative biological processes…”

Two Moons, Picking Up Impacts Independently – A Thought Experiment
Okay. What do we expect in general from degenerating processes that have no functional consequences? Let’s do a thought experiment. Consider the surfaces of two moons that were once part of the same planetary body 22 million years ago. Since their separation, both have been subjected to independent collisions with asteroids, meteorites, and other pieces of space debris. Question: Would you expect the scar patterns on both to be different or identical? (It may seem like a silly question, but bear with me.)

Replace now the word “moons” with the “mouse and rat genomes” and “asteroids and meteorites and other pieces of space debris” with SINEs, and you will see what I am asking. So I’ll rephrase my question. What should we expect regarding the linear distribution of independent SINE impacts along mouse and rat chromosomes?:

A. Completely independent patterns—like meteorite impact sites on moons;
B. A few overlapping patterns, due to chance; or
C. Nearly identical patterns.

This is a second figure from the article co-authored by Francis Collins. (From Fig. 9c of Ref. 1.) The scale on the x-axis is the same as that of the previous graph—it is the same 110,000,000 genetic letters of rat chromosome 10. The scale on the y-axis is different, with the red line in this figure corresponding to the distribution of rat-specific SINEs in the rat genome (i.e., ID sequences). The green line in this figure, however, corresponds to the pattern of B1s, B2s, and B4s in the mouse genome.

Was it what you expected from a degenerative process? Why?

At this point the theistic evolutionist might say—Silly Rick: Common descent explains this pattern!

Wrong, wrong, wrong.

Let me repeat—each graph denotes only lineage-specific mutational insertions.

The mutational signal from mouse B1s, B2s, and B4s is equivalent to the mutational signal of rat IDs. It almost looks as if, say, the rat graph was copied, slightly redrawn, labeled “mouse,” and then pasted above the previous line. (Of course, it wasn’t.) How strange that two independently-acting degenerative processes—affecting mostly “junk DNA”— would lead to the same higher-order pattern.

It’s a bizarre pattern. And this correlation occurs throughout both genomes.

Not A Secret, Folks: Collins et al. Discussed This “Unusual” Finding
The Rat Genome Consortium—and thus Francis Collins—apparently thought it worthy to devote a whole section to the phenomenon. Titled Co-localization of SINEs in rat and mouse,¹ the section states:

Despite the different fates of SINE families, the number of SINEs inserted after speciation in each lineage is remarkably similar: ~300,000 copies…Figure 9c displays the lineage-specific SINE densities on rat chromosome 10 and in the mouse orthologous blocks, showing a stronger correlation than any other feature. The cause of the unusual distribution patterns of SINEs, accumulating in gene-rich regions where other interspersed repeats are scarce, is apparently a conserved feature, independent of the primary sequence of the SINE and effective over regions smaller than isochores. (Italics mine.)

• The strongest correlation between mouse and rat genomes is SINE linear patterning.
• Though these SINE families have no sequence similarities, their placements are conserved.
• And they are concentrated in protein-coding genes.

Am I suggesting that extraterrestrials were fiddling with rodent DNA? No. Am I implying that we are seeing the “language of God” in rodent-script? I haven’t the foggiest notion. What I am saying is that we know a lot about the genome that is being glossed over in the popular works that the theistic evolutionists write. I am also saying that instead of finding nothing but disorder along our chromosomes, we are finding instead a high degree of order.

Is this an anomaly? No. As I’ll discuss later, we see a similar pattern when we compare the linear positioning of human Alus with mouse SINEs. Is there an explanation? Yes. But to discover it, you have to think outside the BioLogos box.

Reference
1. Rat Genome Sequencing Project Consortium. 2004. Genome sequence of the Brown Norway rat yields insights into mammalian evolution. Nature 428: 493-521.

Hirsch insisted again and again that God must be understood as acting with complete freedom in the world, both as it is now and as it was in the process of creation. Accordingly, Hirsch was critical of the then-new Darwinian evolutionary theory. The history of creation was one in which God’s thoughts emerged and freely influenced the shapes of nature: “They are not the result of some force working blindly, but the work of One thinking Being, creating them with intention and purpose”

You can read more here.

In a rejoinder to Meyer, Darrel Falk defended Ayala and claimed although “a number of functional regions have been discovered within Alu sequences,” there “is no question that many Alu sequences really have no function.”

In my last blog, I showed that the vast majority of the genome is transcribed, either into protein-coding genes or into regulatory RNAs. The technical literature—some of which I cited in that blog—reports that the genome is an RNA-coding machine. Clearly, most DNA really does have function.

In this and subsequent posts, I will provide other sorts of evidence that so-called “junk DNA” is not junk at all, but functional.

Now, the reason we are drawn in by such stories is obvious: The signals have serious implications for the characters. It could mean the survival of mankind after a thermonuclear war; it could mean that there are other sentient beings in the universe. That is why we would quickly lose interest in the plot if, say, in every scene where a scientist appeared before an important governmental group and said, “The outer space signal contains over sixty thousand, multidimensional pages of complex architectural plans,” she were countered with, “This is exactly the predicted outcome of billions of years of cosmic evolution—you see, random interstellar events lead to just this kind of complex specified information…we are not impressed.” We would want our money back.

My purpose for bringing up this subject is that I have a mysterious genomic signal for you to see—which I will show you tomorrow. We detected it some time ago and it has aroused the interest of some genomicists, but you will find no mention of it books such as Francis Collins’s The Language of God—which is peculiar. But I have another aim in mind, too, for broaching this possible chromosomal code: A key first indicator of functionality is a distinctly non-random pattern. The persistence of a distinct signal in different contexts often suggests functional constraints are operative—that is why genomicists look for them. And since I want to focus on the global functions of such Short Interspersed Nuclear Elements (SINEs) as human Alus and their mouse and rat counterparts, their far-from-random placement cannot be elided. In fact, I will argue that it is a critical part of the genome story that the folks at Biologos aren’t telling you.

To prepare for the mysterious genomic signal, though, I want to draw your attention to this figure:

What you are seeing are the relative densities of Long Interspersed Nuclear Element (LINE) L1s and SINEs along 110,000,000 DNA letters of rat chromosome 10.¹ (From Fig. 9d of reference 1.) The x-axis represents the sequence of letters in DNA and the blue line indicates where SINEs occur—what Ayala calls “obnoxious sequences” that are supposedly due to “degenerative biological processes that are not the result of ID.” The red line indicates where LINE sequences occur.

By the way, Francis Collins is a principal author of the Nature paper where these results are published.

Both LINEs and SINEs are types of mobile DNA, namely, retrotransposons, and together they can comprise around half of the mammalian genome. As should be clear from the figure, LINEs tend to peak in abundance where SINEs taper off and vice versa (see the blue boxes). We have known about this pattern since the late 1980s, so it is no surprise to someone who has been following the subject. What should be surprising to anyone, however, is that the same machinery is responsible for the movement of both types of retrotransposon. A complete L1 element encodes the proteins necessary to “reverse transcribe” an RNA copy of itself back into DNA, and to insert the generated duplicate into some chromosomal site. SINEs, by way of contrast, rely on the L1-specified proteins for all their copying and pasting routines.

This compartmentalization of LINEs and SINEs along the mammalian chromosome can also be detected by using molecular probes for L1 or Alu(-like) sequences²:

For junkety-junk elements that can make up fifty percent of a mammal’s mostly junkety-junk genome, the rule seems to be: Location, location, location.

Interestingly, this higher-order pattern cannot be detected when small sections of DNA are examined. It only becomes evident when stretches that are millions of nucleotides long are studied.

This banding pattern has been known for decades—but for some reason it is rarely (if ever) discussed by “junk DNA” advocates. The bands on the chromosome arms fall into two general categories:

• R bands: DNA compartments that are enriched with the genetic letters G and C, have a high concentration of protein-coding genes, a preponderance of Alu or Alu-like repetitive elements (e.g., mouse B1s), and replicate early in the DNA synthesis phase of the cell cycle.
  
• G bands: DNA compartments that are enriched with the genetic letters A and T, have a low concentration of protein-coding genes, a high density of the L1 retrotransposon, and replicate late in the DNA synthesis phase of the cell cycle.

There are other strong functional correlations, also, such as the distribution of types of chromatin and how the genome is packaged in the nucleus. But I’m getting way ahead of myself.

Now, some questions. Which DNA regions of the mammalian genome are enriched in the codes for the most essential functions? Precisely where you find Alus and Alu-like sequences (the dark blue bands on the chromosome). Which sections of the mammalian genome have the highest rates of transcription? Precisely where you find Alus and Alu-like sequences. Where do you find the strongest organizational correlations between any two mammalian genomes? Precisely where you find Alus and Alu-like sequences.

Aren’t these correlations a bit strange for genomes that supposedly consist mostly of junk and are constantly being corrupted by “degenerative processes”? Why do such “obnoxious sequences” have any kind of conserved higher-order “bar code” pattern? These facts of mammalian chromosome biology have been known for years, if not decades. But, alas, no mention of them is to be found in the literature that wants to emphasize the unintelligent design of our genome. To make up for this lack, then, I am going to discuss such facts in more detail after I show you the mystery signal tomorrow.

References
¹ Rat Genome Sequencing Project Consortium. 2004. Genome sequence of the Brown Norway rat yields insights into mammalian evolution. Nature 428: 493-521.

² Chen TL, Manuelidis L. 1989. SINEs and LINEs cluster in distinct DNA fragments of Giemsa band size. Chromosoma 98: 309-316;
Korenberg JR, Rykowski MC. 1988. Human genome organization: Alu, lines, and the molecular structure of metaphase chromosome bands. Cell 53(3): 391-400;
Costantini M, Clay O, Federico C, Saccone S, Auletta F, Bernardi G. 2007. Human chromosomal bands: nested structure, high-definition map and molecular basis. Chromosoma 116: 29-40.

Anyone who similarly doesn’t quite “get it” should read our friend and colleague Wesley J. Smith’s new and important book on the animal-rights movement, A Rat Is a Pig Is a Dog Is a Boy. If you follow conservative journalism, you’ve likely heard about the book from the contentious deliberation it has received in National Review and on NR’s website. This started with a review by speechwriter Matthew Scully, similarly a friend and a gifted polemicist. Scully is the vegetarian and champion of animals who, for the 2008 Republican convention, wrote the best speech ever given by that great white hunter, Governor Palin.

As a reviewer for Wesley Smith’s book, Matthew Scully was a surprising choice. Scully's own book, Dominion: The Power of Man, the Suffering of Animals, and the Call to Mercy, received a wounding review in The Weekly Standard some years back from none other than Wesley Smith and it comes in for criticism again in Smith’s book. I can’t understand NR’s decision to match these two valued friends of the magazine against each other. Matthew wrote, I am sorry to say, a distorting and unfair review of Wesley’s book, to which NR then let Wesley reply, generating additional discussion on the website but less illumination than the subject deserves.

So let’s highlight Smith’s contribution to public understanding of why the Darwin debate matters. His recounting of terrorist and other heinous acts by animal-rights extremists (even grave-robbing!), his exploration of the wicked views of “personhood” theorist Peter Singer, author of A Darwinian Left and the manifesto Animal Liberation -- these tell us about the leading edge of what you might call the animalist view, equating humans with animals.

A chimpanzee, dog, or pig…will have a higher degree of self-awareness and a greater capacity for meaningful relations with others than a severely retarded infant or someone in a state of senility. So, if we base the right to life on these characteristics, we must grant these animals a right to life as good as, or better than, such retarded or senile human beings.

Obviously, these are monstrous views, sustainable by an otherwise decent person only in the kind of privileged academic setting where scholars live and think in isolation from reality. Unfortunately, it’s precisely the philosophical foundations of decency that are undermined by the Darwinian perspective. If taken deeply to heart, Darwinism erases the distinction, the right of protection, that a human being earns simply by being human. After all, there’s nothing special about belonging to our species over any other. All the species are part of a continuum of life bubbling up from history without guidance, purpose or meaning.

The respect in which such ideas are held in prestige society can’t help but have a morally corrosive effect that trickles down and outward to the rest of the culture. When they are honest with themselves, Darwinists admit this. In his book, Smith quotes Richard Dawkins, who entertains a fond daydream in which scientists find a living human/chimp hybrid, able to breed with both species and thus finally proving that human beings are just another kind of animal:

We need only discover a single survivor, say a relict Australopithecus in the Budongo Forest, and our precious system of norms and ethics could come crashing about our ears. The boundaries with which we segregate our world would be shot to pieces.

Say we discard the Biblical idea that the human countenance bears a divine stamp, the image of God. Then the standards advanced by Peter Singer seem entirely plausible. Moral value, writes Smith, would accordingly be based on the “capacities of each individual.” Such a “standard would obliterate universal human rights.” Smith cites Mortimer J. Adler, who explained what could all too easily follow from a society’s decision to cast off human exceptionalism:

Why, then, should not groups of superior men be able to justify their enslavement, exploitation, or even genocide of inferior human groups, on factual and moral grounds akin to those that we now rely on to justify our treatment of the animals we harness as beasts of burden, that we butcher for food and clothing, or that we destroy as disease-bearing pests or as dangerous predators?

Dear [Snip],

Greetings and thanks for your e-mail. ID is most definitely testable and falsifiable. It uses the scientific method and explains many patterns we observe in nature.

Let's start with how ID uses the scientific method. The scientific method is commonly described as a four-step process involving observations, hypothesis, experiments, and conclusion. ID begins with the observation that intelligent agents produce complex and specified information (CSI). Design theorists hypothesize that if a natural object was designed, it will contain high levels of CSI. Scientists then perform experimental tests upon natural objects to determine if they contain complex and specified information. One easily testable form of CSI is irreducible complexity, which can be discovered by experimentally reverse-engineering biological structures to see if they require all of their parts to function. When ID researchers find irreducible complexity in biology, they conclude that such structures were designed.

(1) Natural structures will be found that contain many parts arranged in intricate patterns that perform a specific function (e.g. complex and specified information).
(2) Forms containing large amounts of novel information will appear in the fossil record suddenly and without similar precursors.
(3) Convergence will occur routinely. That is, genes and other functional parts will be re-used in different and unrelated organisms.
(4) Much so-called “junk DNA” will turn out to perform valuable functions.

In this regard, ID is falsifiable. When we test these predictions, ID passes those tests. For example:

Regarding prediction 1, natural structures have been found that contain many parts arranged in intricate patterns that perform a specific function (e.g. complex and specified information), such as irreducibly complex machines in the cell. The bacterial flagellum is a prime example. The specified complexity of protein bonds and the simplest self-reproducing cell are other examples. For details, please see Intelligent design (ID) has scientific merit because it uses the scientific method to make its claims and infers design by testing its positive predictions or Asking the Right Questions about the Evolutionary Origin of New Biological Information or you might also enjoy reading the book Signature in the Cell by Cambridge University Ph.D. philosopher of science Stephen C. Meyer.

Regarding prediction 2, biological novelty appears in the fossil record suddenly and without similar precursors. The Cambrian explosion is the prime example. For details, please see Intelligent Design Has Scientific Merit in Paleontology.

Regarding prediction 3, similar parts have been found in organisms that even Darwinists see as separated by more closely related forms that do not contain the similar parts in question. Clear examples include genes controlling eye or limb growth in different organisms whose alleged common ancestors are not thought to have had such forms of eyes or limbs. For details, please see: A Primer on the Tree of Life.

Regarding prediction 4, genetic research continues to uncover functions for “junk-DNA,” include functionality for pseudogenes, introns, LINE, ALU elements, and many other types of "junk DNA." Examples of unknown DNA functions persist, but design encourages researchers to investigate functions, whereas Darwinism has caused some scientists to wrongly assume that non-coding DNA is junk. In fact, ID proponents have been predicting the collapse of the "junk DNA" paradigm for many years. For details, please see: Intelligent Design and the Death of the "Junk-DNA" Neo-Darwinian Paradigm.

These predictions are elaborated in "The Positive Case for Design." In this regard, below is a brief listing of some of the fields where ID provides a framework for predicting, understanding, and explaining the patterns we observe in nature from a wide variety of scientific fields:

Biochemistry, where ID explains and predicts the presence of high levels of complex and specified information in proteins and DNA;

Genetics, where ID predicts and explains function for so-called “junk” DNA while neo-Darwinism stifles such research;

Systematics, where ID explains why there are similarities between living species, including examples of extreme genetic “convergence” that severely conflict with conventional evolutionary phylogenies;

Cell biology, where ID explains why the cell resembles “designed structures rather than accidental by-products of neo-Darwinian evolution,” allowing scientists to better understand the workings of molecular machines;

Systems biology, where ID encourages biologists to look at various biological systems as integrated components of larger systems that are designed to work together in a top-down, coordinated fashion, which is what biologists are finding is the case;

Animal biology, where ID predicts function for allegedly “vestigial” organs, structures, or systems whereas evolution has made many faulty predictions here;

Bioinformatics, where ID explains the presence of new layers of information and functional language embedded in the genetic codes, as well as other codes within biology;

Information theory, where ID encourages scientists to understand where intelligent causes are superior to natural causes in producing certain types of information;

Paleontology, where ID's prediction of irreducibly complexity in biological systems explains paleontological patterns such as the abrupt appearance of biological life forms, punctuated change, and stasis throughout the history of life;

Physics and Cosmology, where ID encourages scientists to investigate and discover more instances of fine-tuning of the laws of physics and properties of our universe that uniquely allow for the existence of advanced forms of life;

Finally, you might benefit from an Educator's Briefing Packet on Intelligent Design. We don't recommend pushing ID into the curriculum in public schools, so if you're interested in more information on Discovery Institute's recommended science education policy, please visit Discovery Institute's Science Education Policy or feel free to write back seeking more information.We help many educators to better understand the debate over evolution. Contact us for more information!

Here is an example. While reading the ”critique” of Steve Meyer’s book, Signature in the Cell, by Francisco Ayala, a number struck me that I know to be incorrect. The integer that I am referring to is “25,000” and it is claimed to be the known tally of genes in our chromosomes:

The human genome includes about twenty-five thousand genes and lots of other (mostly short) switch sequences…

So the true number of genes in our DNA is probably >450,000 + 25,000 = >475,000. What is more, these >450,000 genes cover more than 88.5% of our 3 billion genetic letters. That’s right—most, if not close to all, of our chromosomal DNA consists of different types of genes that have only recently been discovered.

How do these facts square with this comment made by Falk?

but this still doesn’t negate the fact that almost certainly much, if not most, of the DNA plays no role, and in many cases can be harmful.

References
¹ Rederstorff M, Bernhart SH, Tanzer A, Zywicki M, Perfler K, Lukasser M, Hofacker IL, Hüttenhofer A. 2010 (In Press). RNPomics: Defining the ncRNA transcriptome by cDNA library generation from ribonucleo-protein particles. Nucleic Acids Research.

² Amaral PP, Dinger ME, Mercer TR, Mattick JS. 2008. The eukaryotic genome as an RNA machine. Science 319(5871): 1787-1789;

³ Dinger ME, Amaral PP, Mercer TR, Mattick JS. 2009. Pervasive transcription of the eukaryotic genome: functional indices and conceptual implications. Briefings in Functional Genomics and Proteomics 8(6): 407-423;

⁴ Mercer TR, Qureshi IA, Gokhan S, Dinger ME, Li G, Mattick JS, Mehler MF. 2010. Long noncoding RNAs in neuronal-glial fate specification and oligodendrocyte lineage maturation. BMC Neuroscience 11(1): 14.

Other criticisms, however, are fluffy confections, failing to achieve even the slightness of what Hume called “mere cavils and sophisms.” Let’s look at one such bonbon of sophistry, Shallit’s claim that weather forecasting represents a devastating counterexample to SITC's argument that complex specified information is, universally in human experience, produced by a mind or intelligence.

Even if we accept Meyer's informal definition of information with all its flaws, his claims about information are simply wrong. For example, he repeats the following bogus claim over and over:

p. 16: "What humans recognize as information certainly originates from thought - from conscious or intelligent human activity... Our experience of the world shows that what we recognize as information invariably reflects the prior activity of conscious and intelligent persons." [...]

I have a simple counterexample to all these claims: weather prediction. Meteorologists collect huge amounts of data from the natural world: temperature, pressure, wind speed, wind direction, etc., and process this data to produce accurate weather forecasts. So the information they collect is "specified" (in that it tells us whether to bring an umbrella in the morning), and clearly hundreds, if not thousands, of these bits of information are needed to make an accurate prediction. But these bits of information do not come from a mind - unless Meyer wants to claim that some intelligent being (let's say Zeus) is controlling the weather. Perhaps intelligent design creationism is just Greek polytheism in disguise!

Poor Zeus: stand-in deity for yet another counterexample. And he only gets union scale.

1. Collecting Meteorological Data

To see what’s wrong with this putative counterexample, begin by asking yourself if you know -- without peeking online at a weather page, or looking at a barometer -- what the atmospheric (barometric) pressure happens to be in your immediate neighborhood, right now.

Any guesses? Well, how about the temperature, or the wind speed and direction? Again, no peeking allowed. Give yourself a moment or two to write down the correct values. Okay, stop.

The fact is, unless you cheated, you don’t know the relevant measurements for your immediate surroundings (and nor do I, as I write this, for my neighborhood). So what would we need to obtain those data?

Measuring instruments, such as (a) a barometer, (b) a thermometer, (c) a wind speed indicator (an anemometer), (d) a wind direction indicator, and so on. So let’s suppose we have these instruments, and we retrieve data from all of them.

Can we now predict tomorrow’s weather? Do we have, as Shallit argues, complex specified information?

2. Turning Data into Predictions

No. We have a few data points. To create an accurate weather prediction, we’re going to need data retrieved from hundreds or thousands of instruments, distributed or coordinated across a wide geographic area, and taken over a range of time intervals.

We’re going to need something more, however, without which all those measurements will tell us nothing. We need an analytical model -- an algorithm -- and a computer to run that model.

Shallit glides over this essential step in how data become predictions with his innocent, almost blushingly naïve verb, “process”:

Meteorologists collect huge amounts of data from the natural world: temperature, pressure, wind speed, wind direction, etc., and process this data to produce accurate weather forecasts. (emphasis added)

Now, “process” can mean many things. What “process” manifestly does not mean in the case of weather forecasting, however, is the mechanical transmission of thousands of bits of data directly from measuring instruments to end-users. That would look like this:

Or this:

And we’d be none the wiser. There is a reason we don’t receive our weather predictions this way: raw data aren’t predictions at all. Collecting measurements from instruments, and mechanically transmitting those data, without any interpretation or analysis, does not (indeed, cannot) make any specified predictions.

To be sure, there is complexity aplenty in the data, but, as SITC explains, that complexity is unspecified. Unspecified complexity is what natural causes produce. And thus, because that “information” lacks specification, it is useless (by itself) for yielding genuine predictions. No specificity; no forecast.

By contrast, in real weather forecasting, data only become complex specified information -- that is, genuine predictions -- by passing through an intelligently-designed algorithm: a computer model, in most instances. But the measurements themselves don’t give us the model. They can’t.

3. The Intelligence in the Story

Meteorologists construct models, using their minds (their analytical intelligence). The useful, complex specified information that emerges from a computer model comes to us via the action of intelligent agents, and not otherwise. The true “process” therefore looks like this:

Shallit would succeed if he could show how raw meteorological data yield testable weather forecasts, without those data ever passing through the analytical filter of an intelligently designed model or algorithm.

Good luck with that.

One final point. In other writings, Shallit has indicated his hostility to the notion of human agency. In light of this, it’s perhaps not surprising that Shallit reduces the creative intellectual activity of meteorologists, who can improve their predictions by designing better and more powerful algorithms, to the bland and seemingly agency-free verb, “process.”

But unpacking that verb shows clearly that intelligent causation is actually indispensable, whether Shallit sees it or not.

Support your local meteorologist.

Darrell Falk at the Biologos Foundation was apparently responsible for inviting Ayala to comment on Meyer’s book, and has been drawn into the debate.

He published the first part of Meyer’s response to Ayala, but not without first offering his “background comments” about the debate. (I think David Klinghoffer has said what needs to be said about that.) The Biologos Foundation is committed to the “science-and-religion dialogue.” In my opinion, however, they have a peculiar way of fostering dialogue.

No one who even skimmed the book would say something this inaccurate. The inaccuracy is so blatant that I would think that Falk would be hoping that the embarrassing incident would soon be forgotten. But instead, he keeps re-opening the wound with another scratch. Now he’s offered another longish commentary on Ayala’s “essay” on Meyer’s book, “A Rejoinder to Stephen C. Meyer’s Response to Francisco Ayala.” And he promises that there are more to come.

Although he wisely doesn’t claim that Ayala actually read Meyer’s book, Falk starts by defending Ayala’s claim about “hundreds of pages”:

Meyer says he only spent 55 pages on the question. By Meyer’s definition of chance on page 176, and by the fact that Meyer himself refers to the competing hypotheses as “chance theories” (see pages 195,196, and 227, for example), I happen to think that Ayala is right--it is much more than 55 pages. However, this is a side issue to what I think we should really discuss.

Hmm. So the existence of three references to chance theories in a 508-page book confirms Ayala point? Hardly. In his statement, Ayala completely misrepresents Meyer’s thesis. The bit about hundreds of pages merely adds the patina of precise quantification to his misrepresentation.

Falk then raises two “concerns. The first, apparently, is that Meyer treats chance at all:

I began my post-graduate career in genetics over four decades ago. I have taught courses such as genetics, cell biology and molecular biology for almost 35 years. I cannot recall any textbook in any course that ever seriously considered what Dr. Meyer called the “chance hypothesis.” No one ever needed to do calculations of the sort that Meyer does in his book. To my recollection it was never seriously considered. Everyone knew it couldn’t have worked that way.

Meyer seems to imply (pages 204-213) that scientists were really engaged by this hypothesis for some period of time beyond a meeting in 1966 when it was first raised. He cites work in the late 1980s and up to 2007. He seems to imply that the chance hypothesis (pure chance, from building blocks) had actually engaged origin-of-life researchers throughout this time period.

A few responses to these charges:

(1) Prominent figures like Francis Crick and George Wald did entertain chance theories in the 1950s and 1960s. Here’s Wald (quoted in one of those pesky pages in Signature in the Cell where Meyer talks about chance): “Time is in fact the hero of the plot. . . . Given so much time, the impossible becomes possible, the possible probable, and the probable virtually certain.” And that’s exactly what Meyer points out in the book.

(2) Pure chance ceased to be a serious contender in the 1960s as Meyer points out for the reasons that he explains in the book. He is a clear-thinking philosopher of science, interested in explaining things for the general reader who lacks detailed background knowledge, and so he lays out the arguments, the reasons, the probabilities, and the evidence painstakingly.

(3) Meyer simply does not claim that pure chance hypotheses have been leading contenders in recent decades. In fact, he quite clearly says just the opposite. On p. 204, which Falk references, Meyer is talking about a conference in the 1960s. Later he talks about experimental evidence demonstrating the extreme rarity of functional sequences of amino acids—evidence that didn’t exist in the 1960s—but which, as he explains, has confirmed the earlier intuitions and judgments scientists about the insufficiency of chance by scientists in the 1960s who lacked this information.

(4) Chance nevertheless remains an important category of explanation because it continues to be a component in current theories such as the RNA world scenario. In fact, many current origin-of-life scenarios combine both chance and a selective mechanism as recommended by Jacques Monod’s famous book Chance and Necessity. Thus, Meyer’s analysis of the limits of chance as a plausible explanation (or aspect of an explanation) is highly relevant to assessing many current theories of the origin of life.

(5) To make a clear and complete argument, chance needs to be treated as one of the logical possibilities. That’s what Meyer does in his book. Why doesn’t Falk get this simple point? Falk seems to think that because the community he’s been swimming in hasn’t bothered to reflect carefully on the full range of logically possible options, that’s it’s problematic that Meyer would do so.

(6) I’m guessing that Meyer’s ideal reader is the open-minded, logical person who can follow a good, clear argument, based on public evidence, and isn’t intimated into mental fogginess because of the social pressures not to discuss the topic of his book. Moreover, since his is a trade-press book, Meyer doesn’t have the luxury of assuming that every reader will know—as apparently does Falk—why chance is so extraordinarily implausible as a complete explanation for the origin of life. So he assumes his reader will need to have that information provided in the text.

(7) That said, I’m still glad that Falk (and apparently Ayala) agree with Meyer that pure chance is not, these days, a live alternative. Unfortunately, Falk doesn’t seem to realize that he is agreeing with Meyer on this point.

Falk’s second concern is with Meyer’s central positive claim. He argues that Meyer never justifies his central claim that “the activity of conscious and rational agents is the only known cause by which large amounts of new functional information arises, at least when starting from purely physical and chemical antecedents.”

He attempts to refute Meyer’s claim by asserting that the fact of biological evolution disproves Meyer’s contention. As he explains:

Virtually all biologists today consider it a fact that all multi-cellular organisms are derived from a single cell. Does not the information required to make the vast array of living organisms constitute Meyer’s definition of “huge?” Doesn’t the process of natural selection, group selection, genetic drift, and sexual selection fit his criteria of purely chemical and physical causes? There is nothing more foundational to biology than that huge amounts of information has arisen through physical and chemical antecedents.

Falk cites belief in biological evolution as a counterexample of Meyer’s claim. But Meyer, in the quote and in his book, is quite obviously talking about chemical evolution and the origin of life, not the evolution of life after the first reproducing cell. That’s why he says: “at least when starting from purely physical and chemical antecedents.” In other words, Meyer, without conceding the point about biological evolution, is arguing here only about the origin of biological information from physics and chemistry—about chemical evolution—and not about what happens once you have life. And contrary to what Falk says, Meyer extensively substantiates his claim about the power of, and the need for, intelligence in producing functional information (at least, if you are starting from physical and chemical, rather than living, antecedents). The only way to fully appreciate that, however, is to read the book (especially Chapters 15 and 16 where he develops his positive case in detail).

That said, even if Meyer’s book were about biological evolution, Falk’s argument would fall short. Falk is confusing sociology with biology. That most biologists assume that universal common ancestry is a fact isn’t evidence for said fact. It’s a fact about prominent beliefs within a community. And even if universal common ancestry is a fact, it’s not evidence that all the organisms that evolved from said ancestor did so purely by a process of chance and (merely physical) necessity without the contributions of intelligence. (Oddly, Falk wants to have it both ways, since he says: “I want to be quick to add that, as a Christian, I believe that it happened at God’s command and as the result of God’s presence. . . .”)

In any case, that many biologists believe that selection and random mutation can generate large amounts of new biological information is a sociological, not a biological, fact. And frankly, it’s not even a sociological fact. There are many biologists who doubt it, and get on quite well nonetheless.

Those who've been following the debate between Meyer and his critics know that there has been a bit of back and forth since Ayala was invited to critique SITC on the Biologos website. Meyer has responded this week, with the first of two parts on the Biologos site.

Discovery Institute would like to initiate a full-fledged, official debate between the two, and so we have already sent the following invitation to Dr. Ayala.

Dear Professor Ayala:

I am writing to you in my capacity as the Director of Research for the Center for Science and Culture at the Discovery Institute.

As you know, there is widespread interest but also widespread disagreement on the relationship between faith and science. Unfortunately, much of the dialogue on science and religion proceeds without careful examination of the scientific evidence in dispute in chemical and biological evolution. Surely one should consider, for instance, the evidence for a chemical evolutionary scenario before reflecting on its implications for religious belief.

In the same way, contemporary intelligent design arguments are often criticized on theological grounds, without first engaging ID arguments on scientific grounds. As a result, the scientific issues are rarely fully aired. For instance, you recently were asked by Biologos to comment on Stephen Meyer’s new book, Signature in the Cell. Unfortunately, the forum did not provide the opportunity for a full critique of the book, as well as a full response by Dr. Meyer.

I am writing to offer you just such an opportunity. I would like to invite you to participate in a public debate with Dr. Meyer on the thesis of Signature in the Cell at a time and place that is mutually convenient. To limit your own travel and expenditure of time, we would be happy to have the debate take place at the University of California, Irvine.

There would be many details to work out, of course; but I wanted first to extend a formal invitation for you to participate in such a forum. Please let me know at your earliest convenience.

Sincerely yours,

Jay Richards
Director of Research
Center for Science & Culture

As a former book review editor (at National Review), I take a professional interest in book reviews and all the things that can go right or wrong with them. I confess, though, I’ve never seen anything quite like the treatment of Stephen Meyer’s book, Signature in the Cell: DNA and the Evidence for Intelligent Design, on BioLogos, the curious website funded by the Templeton Foundation and specializing in Christian apologetics for Darwin. The site published what was clearly, unambiguously written to look like a review by biologist Francisco Ayala that, as Steve Meyer pointed out already, actually gave every evidence that Ayala had not read the book. (My colleague Dr. Meyer thinks Ayala did read the Table of Contents, but on this I must disagree.)

On what did Ayala base his views about Signature? This is a bit of a mystery. BioLogos president Dr. Darrel Falk is unstinting with fulsome praise for Ayala (“one of Biology’s living legends”). Falk claims he actually asked Ayala to respond to Falk’s review of Signature. Falk purports that in publishing Ayala’s review, he mistakenly failed to introduce it with the disclaimer that Ayala was reviewing Falk’s review, not Meyer’s book per se. Yeah, sure. Falk’s review did not provide Ayala with his absurd misrepresentation of Meyer’s argument. Instead Ayala gives every impression of having derived that from his own assessment of the book itself. As Ayala claims,

The keystone argument of Signature of the Cell [sic] is that chance, by itself, cannot account for the genetic information found in the genomes of organisms. I agree. And so does every evolutionary scientist, I presume. Why, then, spend chapter after chapter and hundreds of pages of elegant prose to argue the point?

What’s notable is that Falk in his own review, whatever its other faults or merits, never claimed that Signature is all about proving that “chance by itself, cannot, account for the genetic information found in genomes.” Falk doesn’t mention the word “chance.” So where did Ayala get his mistaken notion? All one can say is, not from the book, which he patently didn’t read, and not from Falk. Indeed, Ayala in his essay does not mention Falk or Falk’s review. Clearly, Ayala wanted readers to think he was reviewing Signature in the Cell—or Signature of the Cell as he repeatedly calls it. Thus, for example, he commends Meyer for his “elegant prose.” The idea that Ayala was merely acting in good faith on Falk’s assignment of responding to Falk’s review is hardly believable.

On top of this, there is Falk’s introduction to Meyer’s response to Ayala. Here he essentially ambushes Meyer by agreeing to publish his reply to Ayala and then introduces the reply, in italics above it and at some length, in a blatant and again disingenuous attempt to undercut its credibility. Thus Falk claims that Meyer originally agreed to limit himself in his response to “Ayala’s philosophical and theological arguments.” In Falk’s presentation, Meyer then stabbed him in the back by going ahead and writing about the science after all. In reality, in his full response, Meyer writes about philosophy (multiple competing hypotheses), theology (Ayala’s claims about junk DNA), and science. The three are inextricably linked.

To be more specific, Meyer’s response does address—as he promised—Ayala’s main theological argument, namely, the argument that junk DNA shows that the human genome could not have been intelligently designed by God because it is chalk full of nonsense DNA. To refute Ayala’s theological argument Meyer shows it is based upon false scientific claims. But Falk declined to publish that part of his response until later in the week. Fair enough, but then why criticize Meyer for acting in bad faith in a preamble to the first part of his response on Monday knowing full well his response to Ayala’s theological argument is coming later?

You can only appreciate theistic evolutionists for finally agreeing to engage in dialogue, but arbitrarily limiting what can be said by the other side—tying one, or both, hands behind their back—is hardly an equitable way to hold a meaningful exchange of views. Anyone who has read the reviews in question knows that only a fool would agree to the condition of totally conceding the scientific facts to Ayala, especially since his theological argument is based upon false scientific claims. Implicitly accepting Ayala’s say-so on the science, “living legend” or not, would pull the legs out from under any philosophical or theological argument that Meyer chose to make. Steve Meyer, no fool, assures me that he never agreed to such a condition.

Falk is not a fool either, I assume. Neither is Ayala. So what, then, is wrong with these people?

The legal incentive to pair global warming with evolution in curriculum battles stems in part from a 2005 ruling by a United States District Court judge in Atlanta that the Cobb County Board of Education, which had placed stickers on certain textbooks encouraging students to view evolution as only a theory, had violated First Amendment strictures on the separation of church and state.

Although the sticker was not overtly religious, the judge said, its use was unconstitutional because evolution alone was the target, which indicated that it was a religious issue.

We do know one of the NY Times sources—and he’s not a lawyer. Kaufman’s original article cites Josh Rosenau of the NCSE to wrongly claim that Selman struck down policies that single out evolution, which means that, unfortunately, the NCSE gave inaccurate information to the NY Times which has now been promulgated around the country. (This is not the first time the NCSE gave bad facts which the NY Times reprinted uncritically.)

In fact, the only court ruling to buy the “no singling out” evolution argument was Judge Jones in the Kitzmiller v. Dover ruling; however, the authority that Judge Jones relied on to validate the “no singling out” evolution argument was the (now vacated) Selman decision which, as we have seen, rejected the “no singling out” evolution argument and instead held “[t]he School Board's singling out of evolution is understandable” because “evolution was the only topic in the curriculum, scientific or otherwise, that was creating controversy.” So Judge Jones chose the wrong authority to validate the “no singling out evolution” argument.

What the NY Times doesn’t tell you is that the highest court to deal with the “singling out” of evolution question in fact determined that it IS legally permissible to single out evolution in a curricular policy. In Freiler v. Tangipahoa Parish Board of Education, the Fifth Circuit Court of Appeals dealt with a lawsuit over an evolution-disclaimer, and validated a secular purpose underlying the disclaimer “to disclaim any orthodoxy of belief that could be inferred from the exclusive placement of evolution in the curriculum, and . . . to reduce offense to the sensibilities and sensitivities of any student or parent caused by the teaching of evolution.” The Fifth Circuit noted that “a purpose is no less secular simply because it is infused with a religious element,” and thus “the fact that evolution, the subject about which the School Board sought to disclaim any orthodoxy of belief, is religiously charged . . . and the fact that sensitivities and sensibilities to which the School Board sought to reduce offense are religious in nature, does not per se establish that those avowed purposes are religious purposes.” The court explicitly validated these legislative purposes because “local school boards need not turn a blind eye to the concerns of students and parents troubled by the teaching of evolution in public classrooms.” (Freiler v. Tangipahoa Parish Bd. of Educ. 185 F.3rd 337, 344-346 (5th Cir. 1999), cert. denied, 530 U.S. 1251 (2000) (striking down the policy on other grounds).)

In sum, there are 3 cases that have dealt with the “singling out evolution” argument: (1) Selman v. Cobb County (a vacated lower court ruling which said it’s OK to single out evolution), (2) Freiler v. Tangipahoa (a 5th Circuit Appellate court ruling which said it’s OK to single out evolution), and (3) Kitzmiller v. Dover (a lower court which said it is NOT OK to single out evolution, but mis-cited Selman as its authority to justify that point). That means that courts are 2-1 in favor of the constitutionality of singling out evolution, and the highest court to rule on the issue upheld the constitutionality of singling out evolution. (And the one case that disagreed mis-cited Selman, its authority.)

Since Selman was vacated (on other grounds), the ruling doesn’t hold much water anymore for anyone—whether for Judge Jones or for the NY Times or for me. Nonetheless, the Times said that Cobb County’s disclaimer “was unconstitutional because evolution alone was the target,” but the singling out of evolution was NOT the basis that the Selman court struck down the sticker. Whatever current law may say, that is not an accurate description of the Selman holding.

(For further details on these cases, see Does Challenging Darwin Create Constitutional Jeopardy? A Comprehensive Survey of Case Law Regarding the Teaching of Biological Origins.)

At the end of the day, all of the NY Times’ misinformation is part of a campaign to attack academic freedom for teachers to openly discuss all the scientific evidence regarding evolution in the classroom. To support academic freedom, visit AcademicFreedomPetition.com.

Fitness costs are real, and biological realities like fitness cost and other limits to evolution play a vital role in shaping strategies used to combat antibiotic resistance, antiviral resistance, and pesticide resistance. In fact, were it not for the existence of fitness cost, in many cases antibiotic resistant bacteria would proliferate and resistant strains would soon replace non-resistant strains. Because of fitness costs, resistant strains are outcompeted by non-resistant bacteria once selection pressure is relaxed, allowing doctors to combat antibiotic resistance through various drug usage strategies.

Not only is the NCSE’s mindset challenged by the evidence [4], but if it were true, the implications for medicine would be drastic: If biological realities like fitness cost and other limits to evolution did not exist, it would be pointless for medical doctors to try to combat antibiotic resistance or antiviral drug resistance, because evolution could always produce an adaptation such that bacteria would become resistant without incurring a fitness cost. Thankfully, Explore Evolution informs students about the realities of limits to bacterial evolution that give doctors and scientists empirically-based hope in the fight against antibiotic resistance.

The NCSE wrongly implies that fitness costs are a minor issue for those trying to fight antibiotic resistance and other forms of resistance, stating, “Mutations do not necessarily impair a protein's normal functioning nor impose a fitness cost.” After complaining that “Explore Evolution … says mutations do confer resistance but with a ‘fitness cost,’” the NCSE then claims that “Explore Evolution significantly misrepresents how antibiotic resistance arises in this description.” Unfortunately, it appears that the NCSE misunderstands both EE and the importance of fitness costs to evolutionary biologists.

Many scientific papers discuss the stark reality of fitness costs, supporting the emphasis that EE places on this topic. In fact, one paper cited by the NCSE acknowledges that the reality of fitness costs is vital to help scientists predict whether resistance will spread: “biological cost of resistance might be a more relevant predictor of the risk for resistance development.” [5] Another paper published in Environmental Toxicology and Chemistry found that “[t]he topic of fitness costs is a central theme in evolutionary biology” because “fitness costs constrain the evolution of resistance to environmental stress.” [6] Yet another paper observed that “[i]t is generally established that drug resistance mutations reduce viral fitness.” [7] Regarding the specific case of antibiotic resistance, one study in the Journal of Antimicrobial Chemotherapy observed that “[t]he biological fitness cost of antibiotic resistance is a key parameter in determining the rate of appearance and spread of antibiotic-resistant bacteria.” [8] Indeed, science journals are replete with documented examples of fitness costs, as the following selections amply demonstrate:

An article published in the journal Genetics in 2007 by Marciano et al. titled “A Fitness Cost Associated With the Antibiotic Resistance Enzyme SME-1 β -Lactamase” found that blaSME-1 β-lactamase gene, which confers antibiotic resistance to the use of carbapenems, has a fitness cost associated with mutations in its signal sequence. Only by artificially swapping the gene’s signal sequence with the signal sequence from a different gene could this fitness cost be alleviated; there was no natural evolutionary elimination of this fitness cost. The article found that identifying this fitness cost barrier to evolution helped them prevent the spread of antibiotic resistant bacteria: “The identification of a SME-1-mediated fitness cost allows the direct application of genetic techniques that have been utilized to understand structural features of β-lactamase function and evolution.” See David C. Marciano, Omid Y. Karkouti and Timothy Palzkill, “A Fitness Cost Associated With the Antibiotic Resistance Enzyme SME-1 β-Lactamase,” Genetics, Vol. 176: 2381–2392 (August, 2007).

A paper in BiomedCentral’s journal Evolutionary Biology titled “Acetylcholinesterase alterations reveal the fitness cost of mutations conferring insecticide resistance” found that some insects exposed to insecticides which target acetylcholinesterase, an important enzyme involved in the nervous system of insects, evolve resistance that comes only at a fitness cost. According to the article, “Our findings suggest that the alteration of activity and stability of acetylcholinesterase are at the origin of the fitness cost associated with mutations providing resistance.” As the paper put it, “higher the number of [resistance-conferring] mutations, the lower the stability of the mutant” enzyme. When seeking mutations that compensated for loss of stability in the mutant enzymes, the study found that “no mutation increased the stability of the enzyme, all combinations resulted in proteins still less stable.” In other words, there was a clear fitness cost faced by insecticide-resistant mutant insects. See David C. Marciano, Omid Y. Karkouti and Timothy Palzkill, “A Fitness Cost Associated With the Antibiotic Resistance Enzyme SME-1 β-Lactamase,” Genetics, Vol. 176: 2381–2392 (August, 2007).

A paper in the Journal of Antimicrobial Chemotherapy, titled “Nitrofurantoin resistance mechanism and fitness cost in Escherichia coli,” observes the reality of fitness cost, stating: “The biological fitness cost of antibiotic resistance is a key parameter in determining the rate of appearance and spread of antibiotic-resistant bacteria.” The paper found that because of the fitness cost associated with E. coli that are resistant to Nitrofurantoin, “even though resistant mutants will appear in the bacterial population in the bladder, they will be unable to become enriched and establish an infection because of their impaired growth at these therapeutic antibiotic concentrations.” The article further observes, “Resistance to antibiotics is most often accompanied by a biological cost, observed as a decrease in fitness, i.e. a reduced growth rate or virulence.” Ironically, the paper cited by this study to bolster this claim—a claim that corroborates EE’s statements about fitness cost—is Andersson (2006) [see below], the same paper that the NCSE cites to back its claim that “not all mutations produce fitness costs!” It seems that research scientists have interpreted Andersson (2006) differently than the NCSE. See Linus Sandegren, Anton Lindqvist, Gunnar Kahlmeter, and Dan I. Andersson, “Nitrofurantoin resistance mechanism and fitness cost in Escherichia coli,” Journal of Antimicrobial Chemotherapy, Vol. 62, 495–503 (2008).

Andersson (2006) explicitly observes that fitness cost is important to understanding whether resistant populations will persist after selection is relaxed:

A key parameter influencing the rate and trajectory of the evolution of antibiotic resistance is the fitness cost of resistance. Recent studies have demonstrated that antibiotic resistance, whether caused by target alteration or by other mechanisms, generally confers a reduction in fitness expressed as reduced growth, virulence or transmission. These findings imply that resistance might be reversible, provided antibiotic use is reduced. However, several processes act to stabilize resistance, including compensatory evolution where the fitness cost is ameliorated by additional mutation without loss of resistance, the rare occurrence of cost-free resistance mechanisms and genetic linkage or co-selection between the resistance markers and other selected markers. Conceivably we can use this knowledge to rationally choose and design targets and drugs where the costs of resistance are the highest, and where the likelihood of compensation is the lowest.

Thus, Andersson (2006) observes that “cost-free resistance mechanisms” are “rare” and that fitness cost is a very common phenomenon, stating that antibiotic resistance “generally confers a reduction in fitness.” EE thus properly discusses this common phenomenon, and Andersson (2006) actually bolsters the points of EE. We find it unfortunate that the NCSE has misused this paper in its attempt to downplay the importance and reality of fitness costs. Additionally, Andersson (2006) states, “A rational antibiotic design strategy is therefore to identify targets for which the resistance mechanism has the most negative effect on fitness.” This is a good strategy, but it would be pointless if bacteria didn’t face evolutionary limits and could essentially always evolve to avoid fitness costs, as the NCSE implies. Again, we see that fitness cost is a real phenomenon and is vitally important to understand as microbiologists seek to slow the spread of antibiotic resistant bacteria. EE is justified in discussing it. See Dan I Andersson, “The biological cost of mutational antibiotic resistance: any practical conclusions?,” Current Opinion in Microbiology, Vol. 9:461–465 (2006).

Many similar examples could be cited. Given the scientific literature, how can the NCSE seriously maintain that fitness cost is not an important issue in microbiology or that EE is mistaken by highlighting its importance to evolutionary processes? The NCSE asserts that EE “significantly misrepresents how antibiotic resistance arises” when EE states that “[e]xperiments show that once antibiotics are removed from the environment, the original (non-resistant) strain ‘out-competes’ the resistant strain, which dies off within a few generations.” But studies like those discussed here directly corroborate this claim of EE. And the existence of fitness costs are vital to helping biologists to fight antibiotic resistance, antiviral resistance, and pesticide resistance. For the sake of medical progress, thank goodness the NCSE is wrong.

[Note: This post was adapted from Antibiotic Resistance Revisited, a response to the NCSE, which was originally co-authored with Explore Evolution co-author Ralph Seelke, Professor of Biology at University of Wisconsin-Superior.]

References Cited
[1] National Center for Science Education. 2008. Section on “Bacteria” in the NCSE critique of Explore Evolution. Available at http://ncseweb.org/creationism/analysis/bacteria as of January 16, 2009.

[4] See R. Seelke and S. Ebnet. “An unexpectedly low evolutionary potential for a trpA 49V,D60N double mutant In Escherichia coli.,” Presented at the 107th Annual Meeting, Abstract R-055, American Society for Microbiology, Toronto, Canada, May 21-25, 2007; R. P. Mortlock (ed.), Microorganisms as Model Systems for Studying Evolution (Plenum Press, New York, 1984). Note: This book contains seven examples of situations in which evolution fails to produce a new function.

[5] Dan I Andersson, “The biological cost of mutational antibiotic resistance: any practical conclusions?,” Current Opinion in Microbiology, Vol. 9:461–465 (2006).

[6] Lingtian Xie and Paul L. Klerks, “Fitness costs constrain the evolution of resistance to environmental stress in populations,” Environmental Toxicology and Chemistry, Vol. 23(6):1499–1503 (2004).

[7] M. Cong, D.E. Bennett, W, Heneine and J.G. García-Lerma, “Fitness Cost of Drug Resistance Mutations is Relative and is Modulated by Other Resistance Mutations: Implications for Persistance of Transmitted Resistance,” Antiviral Therapy, Vol. 10, Suppl 1:S169 (June 7-11, 2005).

[8] Linus Sandegren, Anton Lindqvist, Gunnar Kahlmeter, and Dan I. Andersson, “Nitrofurantoin resistance mechanism and fitness cost in Escherichia coli,” Journal of Antimicrobial Chemotherapy, Vol. 62, 495–503 (2008).