Darwinism can't win even with loaded dice.

Researchers Ran a Massive Yearlong Experiment to Get Bacteria to Evolve. Guess What Happened?

Evolution News & Views

It's a struggle out there. You have to be fit to survive. When the pressure is on, nature favors the ones who can take the heat.

It's a theme that has been drummed into our heads since school. It's a cultural meme. Social Darwinists used it to justify atrocities -- see the new documentary The Biology of the Second Reich. Today's kinder, gentler Darwinists downplay the violence in the struggle for existence, yet the fact as they see it is inescapable: environmental circumstances select random genetic mutations that confer fitness, i.e., survival, by allowing organisms to adapt.

That in a nutshell explains the development of complex life forms. We're assured there are gobs of evidence for it, too.

Looking into a recent paper in PNAS about evolutionary fitness tradeoffs, you have to feel sorry for a team of five evolutionists from UC Irvine who did their level best to produce clear evidence for the favored story. They began with a startling revelation:

Despite the centrality of adaptation to evolution, surprisingly little is knownabout the diversity of mutations that contribute to adaptation or about their phenotypic and fitness effects (1). There are, in fact, only a few well-known examples linking genotype, phenotype, and adaptation in nature (2-4). (Emphasis added.)

Those references are worth a glance. Reference (1) is to H. Allen Orr (2005), "The genetic theory of adaptation: a brief history,"where he states, "Here I survey the history of adaptation theory, focusing on the rise and fall of various views over the past century and the reasons for the slow development of a mature theory of adaptation."

References (2-4) surely must represent what, in the authors' opinions, constitute the best "well-known examples linking genotype, phenotype, and adaptation in nature." What are they? #2 is about stickleback fish that gained or lost body armor, but the authors admit, like these ones do, that "the genetic and molecular basis of morphological evolution is poorly understood." #3 is about mice with varying coat colors due to a single mutation that allows light-colored mice to survive better on light backgrounds and dark-colored mice to survive better on dark backgrounds (a kind of "peppered mice" story). #4 is about a gene in butterflies that affects wing pattern mimicry. So these are their best examples linking genes to adaptation. What became of Darwin's finches and peppered moths?

Moving right along, the UC Irvine team next offers an excuse for this lack of evidence:

In nature, this connection is often complicated by factors such as varying selection pressures or underlying genetic heterogeneities. Although the task is difficult, the general inability to connect phenotype to genotype in the context of environmental adaptation has been a major failing in the field of evolution.

So they are here to fix that epic fail. After listing four complicating factors in their study, they say this in the last sentence of the paper:

Given the breadth of these complexities in a well-controlled experimental system, it is no wonder that the mapping of genotype, phenotype, and fitness continues to be a daunting task in natural populations.

In a moment we will see what they did and what went wrong, but first pause to be astonished.This is the theory that is so well-established by mountains of evidence, we are constantly told, that any criticism of it must be stifled as ignorant, and only this theory must be allowed to be considered scientific. They have just told us otherwise. "Surprisingly little is known" about it, and the best examples they could produce are all instances of trivial variations among existing species. If they had better examples, they surely would have brandished them proudly instead of giving excuses about how hard it is to find genetic evidence for adaptation.

The Experimental Test

Their experiment should have been ideal for testing the genetics of adaptation: 2,000 generations of E. coli bacteria subjected to heat. "In total, we performed >800 fitness competitions, making this one of the largest studies of its kind." The games are on! Evolve or perish! Long live the fittest!

Their "large-scale experiment" started with an "ancestral strain" of E. coli bacteria that they replicated 115 times and subjected to high temperatures (42.2 °C, or 108 °F) for 2,000 generations. "At the end of the experiment, fitness was measured at 42.2 °C for a single clone from each of 114 lineages; on average, fitness increased ∼40% during the yearlong experiment" (meaning, there were still some that hadn't died of heat exhaustion).

The hunt was on for genetic mutations that conferred ability to take the heat. "We sequenced the genome of these 114 clones, identifying 1,258 mutations relative to the ancestral genome," they say. To decide which mutations most likely had something to do with fitness, they identified two "adaptive pathways," both affecting RNA polymerase (RNAP). Clones could survive with one or the other mutation, but not the two together: "mutations in the two pathways were strongly negatively associated." (This is called negative epistasis; more on that later).

Their challenge of linking genetic mutations to fitness, though, was only beginning.

Our thermal stress experiment has identified many putatively beneficial mutationsthat lead to higher fitness under thermal stress. However, we still do not know the phenotypic consequences of these mutations or their relationship with fitness. Do the apparently distinct adaptive pathways converge on similar phenotypes? Or might the two pathways ... lead to alternative phenotypic solutions to a common selective pressure?

Here we begin to address these questions by measuring a complex phenotype: the magnitude of fitness tradeoffs across a thermal gradient. Evolutionary tradeoffs, which are defined as reduced fitness in a nonselected environment, are of great interest in their own right; they are widely observed and frequently assumed to govern and constrain trait evolution.

The operative word there is "assumed." For example, all these mutations may have been neutral, with no phenotypic consequences. Or, mutations for better survival in heat might have had negative consequences for surviving cold (an evolutionary trade-off), with no overall gain in fitness. "Whatever the cause, tradeoffs have rarely been linked to specific genetic variants" -- another embarrassing revelation.

Paltry Results

In this ideal setup (one of the largest of its kind, remember), they were not even looking for a glamorous innovation, like a wing or an eye. Just connecting a particular mutation to a functional phenotype would have been rated a great success, even if all it meant was shifting the germ's optimum temperature range by a few degrees. Trade-offs notwithstanding, so what if the fittest germ in the hot tub would shiver in the cold bath? They would at least be able to connect "genotype, phenotype and adaptation" together -- the kind of evidence neo-Darwinians need and want.

They found that half the clones shifted their thermal range upward by a few degrees (losing ability to survive cold -- the trade-off), and others survived the heat without losing ability to survive cold. Then they found two independent mutations in the RNAP gene that appear relevant to those shifts, as long as they don't occur together. Success? Not so fast.

For one thing, they don't know why those mutations had that effect. They suggested that they might slow RNAP down when its tendency under heat stress is to speed up, thus improving its likelihood to finish a protein synthesis, but this was not clear. Also, to their surprise, the ancestral strain could sometimes bounce back from doom through the "Lazarus effect" (resurrection from the dead) -- but they don't know how that effect works.

Surprisingly, however, w_a [absolute fitness] of the ancestor was negative (w_a = −0.290) but not significantly <0 .00="" 45.0="" able="" and="" at="" fig.="" nbsp="" s1="" s2="" strong="" style="border: 0px; margin: 0px; outline: 0px; padding: 0px;">This unexpected behavior

 was caused by the occasional sudden recovery of populations whose densities had initially declined markedly, a phenomenon known as the "Lazarus effect".

So how is Lazarus coming out of the grave? They don't know. Maybe there is some "preadaptation" to heat in these bacteria:

At the upper end of the thermal niche, most (>95%) of the clones persist at 45 °C, signaling an expansion of their niche at least 2 °C beyond that of the ancestor (Fig. 1B). This observation contrasts with a previous study in which only one of six 42 °C-adapted lines expanded their upper thermal limit but suggests a degree of "preadaptation" to temperatures beyond the clones' immediate experience. Above 45 °C the analyses become complicated by the Lazarus effect, in whichdeclining populations suddenly recover, presumably due to major effect mutations. Indeed, the ancestral clone, which is habituated to laboratory conditions of 37 °C, does not persist at 43 °C but often recovers at 45 °C (Fig. S2). We do not yet know the molecular processes underlying the Lazarus effect, but two seem possible: either the fitness effects of mutations change as a function of the intensity of stress or the mutation rate increases under high stress (33, 34). We do not yet know which of these two mechanisms predominates.

Complicating matters even more are things like "negative epistasis" (mutations that counteract each other) and "antagonistic pleiotropy" (unintended consequences of a "beneficial" mutation on other parts of the genome).

In short, it was hard to find anything beyond a "suggestion" or a "scenario" that these bacteria improved their fitness in any way by genetic mutations, other than the gross observation that some of the clones managed to survive at 45 °C. But even the ancestor could do that sometimes through the "Lazarus effect." The authors also ignored the possibility that E. coli have ways to generate their own mutations under stress. That would be supportive of intelligent design, as would the notion that bacteria contain "a degree of preadaptation" to temperatures beyond their immediate experience.

Some experiment. What we learn from this paper is that under ideal conditions, with the best methods, scientists have a devil of a time trying to establish neo-Darwinian theory in a scientifically rigorous way. A look at their references shows a debt to Lenski's methods that similarly produced paltry results on one of the longest-running experiments in history trying to demonstrate evolution in a lab.

Is this a theory that deserves to rule the world?

Microevolution+Microevolution=? II

Nature's Microevolutionary Gems Part 2: Bird-Sized Evolutionary Change
Casey Luskin 

In Nature's evolution-evangelism packet, two of Nature's "evolutionary gems" looked at birds. The first such gem showed "Differential dispersal in wild birds" -- but before we get caught up in the jargon, let's just cut to the main question: What sort of evolutionary change was observed? From reading Nature's evolution-evangelism packet, one is told that the "findings illustrate the large effect of immigration on the evolution of local adaptations and on genetic population structure" or that "evolutionary differentiation can be rapid and occur over surprisingly small scales." So exactly what was this rapid, large evolutionary change?
In one study it turns out that female members of the bird species Parus major (common name: "great tit") bred on the western end of the Dutch island of Vlieland tend to lay 1.15 � 0.14 eggs per clutch more than females bred in populations on the east end of the islands. You read that right. The birds native to the island are still reproductively compatible with "immigrant" birds. The fact that evolutionary biologists consider a difference of 1.15 � 0.14 eggs per clutch to be a "large effect" on a population shows just how desperate they are to find evidence of biological change in nature. (See Erik Postma & Arie J. van Noordwijk, "Gene flow maintains a large genetic difference in clutch size at a small spatial scale," Nature 433:65-68 (January 6, 2005).)

Another study cited in this "gem" promised to show "marked evolutionary differentiation" at "small spatial and temporal scales." Readers learned that over a span of about 35 years, great tits from the eastern part of the Wytham woodland in southern England saw a decrease in adult body size that amounted to a net average change of about 1 gram (less than 10 percent of total body mass). Fledgling birds likewise saw a small change in body mass. (Birds in the northern part of the wood did not experience such a change.) (See Dany Garant, Loeske E.B. Kruuk, Teddy A. Wilkin, Robin H. McCleery & Ben C. Sheldon, "Evolution driven by differential dispersal within a wild bird population," Nature 433:60-65 (January 6, 2005).)

Recall that Nature's introduction to the packet boasts that "all life evolved by natural selection" and claims that this is "a fact, in the same way that the Earth orbits the Sun is a fact." Nature claimed the packet would show "just what is the evidence for evolution by natural selection." But if such featured "evolutionary gems" are among the best that evolutionary scientists have to offer, which is what the packet implies, then that leaves a large gap between the observed data and Nature's grand claims.

Meanwhile, what treatment of microevolutionary changes would be complete without a discussion of Darwin's Galapagos finches? The packet explains that "When Charles Darwin visited the Galapagos Islands, he recorded the presence of several species of finch that all looked very similar except for their beaks," further noting that "Darwin speculated that all the finches had a common ancestor that had migrated to the islands." We've all heard this story before -- but is there more too it?

According to the British Natural History Museum, "Mockingbirds from the Galapagos Islands, not finches, gave Charles Darwin his ideas about evolution. ... Darwin's finches are the better-known birds connected with helping Darwin come to his conclusions on evolution. However, it was the little-known mockingbirds that were the key." Likewise, historian of science Frank Sulloway debunks the finch myth, stating that, "far from being crucial to his evolutionary argument, as the legend would have us believe, the finches were not even mentioned by Darwin in the Origin of Species." (See: Frank J. Sulloway, "Darwin and His Finches: The Evolution of a Legend," Journal of the History of Biology, Vol. 15(1):1-53 (Spring, 1982).)

Island Biogeography observes that it is "unclear whether [the mockingbird] genus (Nesomimus) is sufficiently distinct morphologically to warrant separation from the mainland genus (Mimus)" (Robert J. Whittaker, Island Biogeography: Ecology, Evolution, and Conservation, p. 96 (Oxford University Press, 1998)), or as Explore Evolution explains, the mockingbirds "show only small-scale variations in existing traits."

Setting aside Nature's perpetuation of common myths about the Galapagos finches, modern-day field studies of these finch species are commonly cited as examples of evolution. So again we must ask, How much evolutionary change are we talking about? Here, the packet is somewhat forthright, acknowledging that we're in fact only talking about "small differences in the depth, width or length of the beak." The packet then refers readers to a study that investigated the genetic basis of these small changes in beak morphology. It's an interesting paper, but as the packet explains, these changes in beak morphology may be caused by mere "differing expression of the gene for calmodulin, a molecule involved in calcium signaling that is vital in many aspects of development and metabolism." (See Arhat Abzhanov, Winston P. Kuo, Christine Hartmann, B. Rosemary Grant, Peter R. Grant,, and Clifford J. Tabin, "The calmodulin pathway and evolution of elongated beak morphology in Darwin's finches," Nature, Vol. 442:563-567 (August 3, 2006).)

So what's at issue here is mere differential expression of a gene (rather than the evolution of an entirely new gene) causing "small differences" in beak morphology. For the Darwin-critic, this is interesting since such differences in beak shape are well-known throughout a variety of bird groups (such as Hawaiian honeycreepers), making it unsurprising that commonly observed forms of biodiversity have a small-scale genetic basis. None of this suggests how large-scale evolutionary change could occur. While the origin of the beaks (and the birds) themselves may remain unexplained, perhaps diverse beak morphologies are designed to evolve.

Microevolution+Microevolution=?

Nature's Microevolutionary Gems Part 1: Lizards, Fish, Snakes, and Clams
Casey Luskin

Early in 2006, the journal Science published a long article titled "Evolution in Action" purporting to give three examples showing the glory of Darwinian evolution. As I discussed at that time, what it really showed was "microevolution in action." Last year during the bicentennial anniversary of Darwin's birth, Nature tried to top Science by releasing a packet titled "15 Evolutionary Gems." The packet purported to show "just what is the evidence for evolution by natural selection." Yet much like the Science piece, many of the examples in the Nature packet entail trivial examples of small-scale evolution. This first installment of Nature's "microevolutionary gems" will look at the evidence cited there for evolution among lizards, snakes, clams, and birds.
Size Matters in Stickleback fish and Anolis lizards
One of Nature's "gems" was said to show "Natural selection in speciation." The study cited found that reproductive isolation between different populations of stickleback fish was established based upon the trait of body size: "Levels of reproductive isolation are well accounted for by differences in a single trait, body size." Since body size can be determined by genes or the environment, it wasn't entirely clear whether the selected traits were heritable. In fact, when individuals from different stickleback populations were manipulated in the lab to the "preferred" body size of a different "ecotype" (e.g. a member of the same species from a different habitat), mating occurred even though the sticklebacks had previously been from different reproductively isolated populations.

While this study is a nice demonstration of how assortative mating can lead to sympatric speciation (so long as we define "speciation" as mere "reproductive isolation" and don't expect significant morphological change), what this shows is that even after untold generations of reproductive isolation, these fish are still reproductively compatible so long as they like the "size" of their partner. And what sort of morphological divergence is observed between the different stickleback populations? A difference of 2-3 centimeters in length. It goes without saying that small changes in the size of stickleback fish are not going to explain the evolution of sticklebacks in the first place. Have we really witnessed differences that show large-scale evolutionary change is possible, or even "speciation"?

(See Jeffrey S. McKinnon, Seiichi Mori, Benjamin K. Blackman, Lior David, David M. Kingsley, Leia Jamieson, Jennifer Chou & Dolph Schluter, "Evidence for ecology's role in speciation," Nature, 429:294-298 (May 20, 2004).)

Another "gem" claimed to find "Natural selection in lizards." Well, it wasn't exactly "natural" selection. Somewhat like the way researchers once glued peppered moth on trees to see if they'd be eaten by birds, evolutionary researchers artificially introduced a predatory lizard to small islands in the Caribbean to see if there was any impact upon populations of smaller Anolis lizards native to the islands. And they didn't just introduce the lizards to the island. They also artificially released "curly-tailed" predatory lizards right in front of their would-be prey, the lizard species Anolis sagrei, to see how Anolis lizards would respond. Here's what your taxpayer-funded NSF grant dollars supported:

On four of the experimental islands, we conducted focal animal observations on individual A. sagrei to investigate their immediate reaction to the introduction of curly-tailed lizards. Lizards were approached and an experimental object -- either a live curly-tailed lizard (n � 24) or, as a control, an inanimate object of approximately the same size (n � 23) -- was placed 0.5-1.0m from the lizard on the ground and clearly in its visual field.
(Jonathan B. Losos, Thomas W. Schoener & David A. Spiller, "Predator-induced behaviour shifts and natural selection in field experimental lizard populations," Nature 432:505-508 (November 25, 2004).)

That the experiment was not entirely "natural" is no great reason to criticize it and in fact it does serve as a nice illustration of what natural selection might be able to do. Confirming prior studies, the Anolis lizards were found to undergo selection for both larger body sizes (in females) and longer limb (in males) because this allowed them to better escape the predatory "curly-tailed" lizards. And Anolis lizards may be small but they aren't stupid: they also started spending less time on the ground and perched higher up in trees to escape their newfound predators. I'm sure that the slower, smaller Anolis lizards didn't appreciate falling prey (literally) to this experiment -- in Darwin's words, such experiments show "Nature red in tooth and claw" at its finest. But we've still seen nothing beyond extremely small-scale changes in lizard sizes. Much like the peppered moth story said nothing about the origin of moths, what does this study tell us about the origin of lizards? Not much.

Toxic Examples of Evolution
It's long been discussed by critics of neo-Darwinian that the evolution of antibiotic resistance entails the evolution of essentially no new functional biological information in the genome. Nature calls "Toxin resistance in snakes and clams" an "evolutionary gem," but what's really going on in the studies cited?

In the case of snakes, a species of garter snakes predate upon certain newts which produce the toxin tetrodotoxin (TTX). The toxin "causes paralysis and death by binding to the outer pore of voltage-gated sodium channels and blocking nerve and muscle fiber activity." It turns out that by substituting valine for isoleucine in a gene for a particular protein involved in the sodium ion channel, a small amount of resistance to TTX is gained. A couple other amino acid substitutions in certain snake species also seem to confer additional resistance. Meanwhile, the sodium ion channels continue to perform their functions. So we see that toxin-resistance requires small-scale genetic changes that entail the origin of no new genes.

(See Shana L. Geffeney, Esther Fujimoto, Edmund D. Brodie III, Edmund D. Brodie Jr, & Peter C. Ruben, "Evolutionary diversification of TTX-resistant sodium channels in a predator-prey interaction," Nature 434:759-763 (April 7, 2005).)

As for the clams, the packet reports that "Resistance to the toxin in the exposed populations is correlated with a single mutation in the gene that encodes a sodium channel, at a site already implicated in the binding of saxitoxin." (See V. Monica Bricelj, Laurie Connell, Keiichi Konoki, Scott P. MacQuarrie, Todd Scheuer, William A. Catterall & Vera L. Trainer, "Sodium channel mutation leading to saxitoxin resistance in clams increases risk of PSP," Nature 434:736-767 (April 7, 2005).)


In both cases, we're talking about strong selection pressure causing a couple changes (or even just one change) in the amino acid sequence of structural proteins. No new functions or structures are evolving and all we've seen is the loss of the ability of a toxin to bind to its target -- a protein involved in sodium channels. This is similar to the breaking down of a function -- losing the ability to bind through a mutation. Interesting and important research for sure, but if we're trying to showcase "just what is the evidence" for the grander claims of Darwinian evolution, this will not suffice.

Evaluating Darwinism's evangel

Evaluating Nature's 2009 "15 Evolutionary Gems" Darwin-Evangelism Kit
Casey Luskin 

Last year, during the bicentennial anniversary of Darwin's birth, Nature released a free online packet titled "15 Evolutionary Gems." Its subtitle was "A resource from Nature for those wishing to spread awareness of evidence for evolution by natural selection." It might have been better subtitled 'A evangelism packet for those wishing to spread the good news about Darwinism.' After all, when Nature announced the packet, they said they were heeding a prior call which "urged scientists and their institutions to 'spread the word'" about evolution and "highlight reasons why scientists can treat evolution by natural selection as, in effect, an established fact." The packet is to be used not just in schools, but also in home evangelism or relationship evangelism. At least, that's basically what Nature said:
This week we are following our own prescription. Readers will find at www.nature.com/evolutiongems a freely accessible resource for biologists and others who wish to explain to students, friends or loved ones just what is the evidence for evolution by natural selection. ... In a year in which Darwin is being celebrated amid uncertainty and hostility about his ideas among citizens, being aware of the cumulatively incontrovertible evidence for those ideas is all the more important. We trust that this document will help.
("Announcement: Evolutionary gems," Nature, Vol. 457 (January 1, 2009).)


If all that weren't enough, the back page of the packet shows a picture of a smiling young Darwin with animals flocking about him (lizards, birds, monkeys, flowers, sponges, turtles, etc.), much like the pictures of Jesus posing with lions and lambs on some cheesy religious tract. You have to see the packet to believe it:Should we be surprised that Nature -- one of the world's top scientific journals -- is promoting evolution in this fashion? The respected historian of evolution Peter J. Bowler explains that Nature itself was originally founded in the late 19th century by T. H. Huxley and others for the express purpose of promoting a "campaign" to support Darwinism:

By exploiting their position in this network, Huxley and his friends ensured that Darwinism had come to stay. (Ruse, 1979a). They controlled the scientific journals -- the journal Nature was founded in part to promote the campaign -- and manipulated academic appointments. Hull (1978) has stressed how important these rhetorical and political skills were in creating a scientific revolution. The Darwinists adopted a flexible approach which deflected opposition, minimized infighting among themselves, and made it easy for others to join their campaign. Many, like Huxley himself, were not rigidly committed to the theory of natural selection; they were simply anxious to promote the case for evolution.
(Peter J. Bowler, Evolution: The History of an Idea, p. 185 (University of California Press, 3rd ed., 2003).)

The packet is simply an extension of Nature's "campaign" for Darwin. But it is quite useful in one important respect: the packet is from the world's top scientific journal and purports to show us "just what is the evidence for evolution by natural selection." So if the evidence isn't very strong, then that should tell you something.

As we'll see, far from being "incontrovertible," most of the "evolutionary gems" in the packet do not show any significant amount of evolution and might be best views as "microevolutionary" gems. A couple of the "gems" have little to do with evolution, but an evolutionary interpretation is added in after-the-fact.

Finally, the few "gems" that do deal with large-scale change face serious problems and might be termed "lumps of coal." For the "lumps of coal," their strategy is the same: ignore dissent and overhype the evidence.

At the end of this series, all the posts will be combined into a single PDF file which can be downloaded and distributed or printed off freely.

An Evangelistic Opening
Nature's evolution-evangelism packet opens with one of the most dogmatic statements imaginable in support of evolution. According to the packet, "Most biologists take for granted the idea that all life evolved by natural selection over billions of years ... natural selection is a fact, in the same way that the Earth orbits the Sun is a fact." Surely, if their claim is true (and not a bluff) then we will find no notable scientific dissent from the view that "all life evolved by natural selection."

Just a couple years ago science journalist Susan Mazur (who is no friend of intelligent design) wrote that "hundreds of other evolutionary scientists (non-Creationists) who contend that natural selection is politics, not science, and that we are in a quagmire because of staggering commercial investment in a Darwinian industry built on an inadequate theory." Two of those scientists might be National Academy of Sciences members Philip Skell and Lynn Margulis, staunch critics of the claim that "all life evolved by natural selection":

"Darwinian evolution -- whatever its other virtues -- does not provide a fruitful heuristic in experimental biology. This becomes especially clear when we compare it with a heuristic framework such as the atomic model, which opens up structural chemistry and leads to advances in the synthesis of a multitude of new molecules of practical benefit. None of this demonstrates that Darwinism is false. It does, however, mean that the claim that it is the cornerstone of modern experimental biology will be met with quiet skepticism from a growing number of scientists in fields where theories actually do serve as cornerstones for tangible breakthroughs." -- Philip Skell
"[The] Darwinian claim to explain all of evolution is a popular half-truth whose lack of explicative power is compensated for only by the religious ferocity of its rhetoric. 
-- Lynn Margulis

And of course there's the 800+ scientists  scientists who have courageously signed a statement agreeing that they are skeptical of the creative power of natural selection: "We are skeptical of claims for the ability of random mutation and natural selection to account for the complexity of life. Careful examination of the evidence for Darwinian theory should be encouraged."

But there's a deeper point here. If the claim that "all life evolved by natural selection" is "a fact, in the same way that the Earth orbits the Sun," then shouldn't it be as self-evident as the fact that the Earth orbits the Sun? But no one is making packets to evangelize for heliocentrism -- because in that case the evidence is so overwhelming that no one of any consequence disagrees.

Nature's evolution-evangelism packet seems like a politically motivated attempt to spread the good news about Darwin. And given the power that the journal Nature wields within the scientific community, its dogmatic treatment of natural selection serves to stifle academic freedom and dissent from Nature's viewpoint. This leads me to suspect that the journal might overstate the evidential case for natural selection. Over the course of eight subsequent posts, we'll see just how far these "gems" actually go to support the view that "all life evolved by natural selection" is "a fact, in the same way that the Earth orbits the Sun" is a fact.

File under "Well said" XXXVIII

"Great is the guilt of an unnecessary war". John Adams

On Ruse V. Nagel and strawman?

Roasting a Straw Man: Evolutionist Michael Ruse on Thomas Nagel
Jonathan Witt 

If you're driving along and notice that a bright philosopher has just mangled beyond recognition the argument of another bright philosopher, a tap on the brakes and a bit of careful rubbernecking is in order.

If you then notice that the one who has done the mangling is Darwinist Michael Ruse, and what he mangled is an argument by eminent philosopher Thomas Nagel against Darwinism, then it's worth pulling over and taking an even closer look.

And if upon doing this you find that Ruse has not only badly mischaracterized Nagel's argument but is pouring lime powder on it beside an open grave, then it's time to get out of your car and call out something like, Hey buddy, cut that out. You don't have to do this. There's a better way.

The illustration does not exaggerate. Let's lay Ruse's characterization and dismissal of Nagel's argument beside Nagel's actual argument, then you decide.

The Ruse

The mangling occurred earlier this week at an Oxford University Press blog ("Darwinism as religion: what literature tells us about evolution"). And by the way, Ruse and Nagel are both atheists. Here's the key passage from Ruse:

Just as we have the proselytizing Darwinian New Atheists, so we have today a vocal anti-Darwinian party, consisting somewhat surprising not only of the evangelical Christians of the American South but of some of today's most eminent atheist philosophers, notably Thomas Nagel, OUP author of Mind and Cosmos: Why the Materialist Neo-Darwinian Conception of Nature is Almost Certainly False (2012). As his subtitle reveals, Nagel's worry is less about the science and more about its supposed religious-cum-metaphysical implications, namely that Darwin plunges us into a hateful world without value and meaning.
Ruse makes Nagel sound a bit like someone who has just learned that, Gosh, scientists are telling us the earth actually revolves around the sun instead of the other way around, and goodness, mightn't that make us feel rather marginal and inconsequential? Do we really want to go there?

Now, maybe Nagel, following Matthew Arnold, does worry that, thanks to Darwinism, our world

Hath really neither joy, nor love, nor light,
Nor certitude, nor peace, nor help for pain;
And we are here as on a darkling plain
Swept with confused alarms of struggle and flight.
Where ignorant armies clash by night.
But whether or not Nagel carries this worry, it isn't his argument against Darwinism, never mind Ruse's suggestion.

Nagel's Actual Argument Against Darwinism

Nagel's case against Darwinism is complex and nuanced. But it has at least two key parts. I'll only mention the first one, and do a bit more unpacking of the second one, since the second one comes closer to Ruse's straw-man characterization.

First, Nagel argues that modern evolutionary biology, a physical theory, cannot account for consciousness. Since evolutionary theory purports to explain the origin of humans, the theory's inability to explain human consciousness is a major strike against it. One finds this laid out plainly in the introduction to Mind and Cosmos.

Ruse is free to agree or disagree with that argument, but he shouldn't mischaracterize it as only the worry that "Darwin plunges us into a hateful world without value and meaning."

And here is a second pillar of Nagel's argument, in his own words, from Mind and Cosmos: "Evolutionary naturalism provides an account of our capacities that undermines their reliability, and in doing so undermines itself."

Nagel makes the same point at a bit more length on the same page ofthe book:

The evolutionary story leaves the authority of reason in a much weaker position. ... Evolutionary naturalism implies that we shouldn't take any of our convictions seriously, including the scientific world picture on which evolutionary naturalism itself depends. (28)
Darwinian evolution might have selected for true and reliable reasoning about the natural world around us, but it might also have selected for all sorts of other ways of arriving at conclusions -- maybe a mix of several -- and who's to say which has predominated? So, for instance, perhaps natural selection opted for a line of primates with an ability to form convictions more readily than the evidence allowed, since in "nature red and tooth and claw," sometimes the worst decision is the delayed decision.

If Darwinism undermines the ground of reason, Nagel asks, what ground do we have to stand on to insist that reason reliably guides us to the supposed truth of Darwinism?

Darwin Anticipates Nagel

We have oceans of evidence for the human tendency to irrationality. And Darwin made extra room for irrational animal behavior through his complementary theory of sexual selection. So the concern that Darwinian evolution saddled humanity with profoundly unreliable faculties for reasoning about biological origins is hardly an idle worry.

Darwin himself didn't consider it an idle concern. John West points this out in a review of Mind and Cosmos:

This objection is not new. Indeed, it reaches back to Charles Darwin himself. Darwin published a lengthy tome, The Descent of Man, purporting to prove that his theory of unguided evolution could explain basically everything, including man's mind and morals. Yet in his private writings, he expressed a lingering reservation over the impact of his theory on the trustworthiness of reason. In a letter written in 1881, he disclosed that "with me the horrid doubt always arises whether the convictions of man's mind, which has been developed from the mind of the lower animals, are of any value or at all trustworthy. Would any one trust in the convictions of a monkey's mind, if there are any convictions in such a mind?"
Remember, though: Nagel isn't arguing that we shouldn't trust our natural faculties. He's arguing that since we are properly confident of our natural faculties (even if they aren't foolproof and we are free to indulge in irrational behavior), then the fact that Darwinism logically entails that we can't trust our natural faculties is itself a strike against Darwinism.

Here's Nagel on page 29 of Mind and Cosmos:

The failure of evolutionary naturalism to provide a form of transcendent self-understanding that does not undermine our confidence in our natural faculties should not lead us to abandon the search for transcendent self-understanding. There is no reason to allow our confidence in the objective truth of our moral beliefs, or for that matter our confidence in the objective truth of our mathematical or scientific reasoning, to depend on whether this is consistent with the assumption that those capacities are the product of natural selection. Given how speculative evolutionary explanations of human mental faculties are, they seem too weak a ground for putting into question the most basic forms of thought. Our confidence in truth of propositions that seem evident on reflection should not be shaken so easily (and, I would add, cannot be shaken on these sorts of grounds without a kind of false consciousness).
He turns the line of his argument squarely against Darwinism:

It seems reasonable to run the test equally in the opposite direction: namely, to evaluate hypotheses about the universe and how we have come into existence by reference to ordinary judgments in which we have very high confidence. It is reasonable to believe that the truth about what kind of beings we are and how the universe produced us is compatible with that confidence. After all, everything we believe, even the most-far-reaching cosmological theories, has to be based ultimately on common sense, and on what is plainly undeniable.
So Why Did the Intelligent Ruse Mangle a Skeptical Nagel?

That's Nagel's argument in a nutshell. And he gives us what I've conveyed above all in the book's introduction and the chapter immediately following the introduction. In other words, Ruse didn't need to read far into the book to get this.

But if Ruse did get it, he didn't give it to us in his OUP post. Instead he gave us an unrecognizable mischaracterization of Nagel's critique.

Three possibilities. (1) Ruse isn't smart enough to understand Nagel's argument. We can reject that. Ruse is an intelligent man. (2) Ruse didn't read far enough into the book and relied on someone else for a summary of Nagel's position. Perhaps, but the argument is so central to Nagel's book that this explanation seems unlikely. Or (3) Ruse willfully misrepresented Nagel's core argument because it was so much easier to dispense with an attack on Darwinism from a distinguished philosopher and fellow atheist simply by mischaracterizing the attack.


I don't mean that Ruse necessarily did this consciously. It might have been wishful thinking working hand-in-glove with this or that pressing publication deadline. Who knows? The good news is that Ruse's philosophical position on that human enterprise called scientific reasoning allows plenty of room for the possibility of irrational behavior on the stage of science, so Ruse should be well positioned dispositionally to consider why he behaved as he did.

Eels vs. Darwin

Eel Migration Comes to Light
Evolution News & Views

In his new book Evolution:Evolution: Still a Theory in Crisis  Institute biologist Michael Denton gives example after example of living things -- microbes, animals, and plants -- whose traits could not have arisen by a Darwinian process. He describes one of the most bizarre of all, a fish whose life cycle and migration has challenged biologists for over a century: the European freshwater eel. Inhabiting most of the rivers of Europe and the British Isles, the eel undergoes radical metamorphoses, transforming from transparent, flat larvae to cylindrical "glass eels" and then again to yellow eels and, finally, silver eels that migrate to the Sargasso Sea to mate.

During these transitions, digestive and sex organs move about the anatomy. Early scientists were not even sure they were the same species. Individuals can apparently switch sexes depending on the environment, spending some time as hermaphrodites. Denton tells how young Sigmund Freud became baffled trying to find the gonads on an eel. They must develop later in the life cycle, Freud concluded before he abandoned biology for his more famous work in psychology.

"Their life cycle is no less baroque than their sexual development," Denton continues. These vulnerable prey fish manage somehow to swim thousands of kilometers from their freshwater habitats out into the salty ocean to the Sargasso Sea, where they breed. Yet to this day, "no one has observed their mating and spawning of freshwater eels in the wild."

Denton's readers may be gratified to hear that scientists have, for the first time, tracked the migration routes of some of the eels using geolocators. That's bound to be interesting. You may remember the geolocators attached to the feet of Arctic terns in Illustra's film Flight: The Genius of Birds, but how does one fasten a tracking device to an eel, the veritable icon of slipperiness? The authors of an open-access paper in Science Advances used some clever intelligent design for this challenge.

Before tagging, eels were anesthetized using metomidate [d1-1-(1-phenylethyl)-5-(metoxycarbonyl) imidazole hydrochloride] at the concentration of 40 mg/liter. Eels tagged in the Mediterranean were anesthetized with Aqui-S (Aqua-S) at a concentration of 600 mg/liter. Fish were measured and weighed, and, where possible, their fat content was measured using a Distell Fatmeter .... Surgical implantation of i-DSTs was achieved by pushing the tags through a small (~1 cm) incision into the body cavity from the ventral surface. After tag insertion, the incision was closed with two independent single sutures and dusted with Cicatrin antibiotic. [Emphasis added.]
One cannot be sure that any animal will behave normally after radical surgery like this, but the multi-national European team is pretty confident it didn't affect the eels too much. The tags consisted of external PSATs (pop-up satellite archival tags) and DSTs (data storage tags). Though not capable of continuous data recording, they monitored position, temperature and pressure every 2 minutes, and transmitted the data to low-earth orbit Argos satellites at set intervals or if the tag became detached. Considering that many of the 707 eels tagged succumbed to predators, it's remarkable that over 80 of them collected enough data to reconstruct their migratory paths. Here were some of the key findings:

The eels did not make a beeline for the Sargasso Sea. Instead, they tended to congregate near the Azores islands, and then head west. Even so, there was variability depending on the release location.

Not all the eels swam at the same speed. Even though tests in artificial tanks show they can swim at 0.7 body lengths per second for 173 days, individual speeds varied from 3 to 47 kilometers per day, probably because of factors like currents or predator abundances.

Remarkably, the eels dive deep (as deep as 1000 m) during the day, and rise to near the surface at night. This probably helps them avoid predators, but it also exposes them to radically different lighting conditions, pressures and temperatures -- sometimes as low as the freezing point of water. It also adds considerable distance to their overall travel.

The authors avoided any mention of evolution. We can infer, however, that these creatures are even better designed than previously known. They don't just drift with prevailing currents. Like sea turtles and salmon, they know where they need to go and will battle currents to get there, even if it requires taking a roundabout path.

Historically, migration routes to the spawning area have been assumed to be "as the crow flies" from escapement to the Sargasso Sea...; however, as we have shown, migration routes were not simply error-free great-circle routes (that is, the shortest possible route to the Sargasso Sea from the departure points). Instead, many of the routes were in the reverse direction of the northern part of the subtropical gyre in the North Atlantic Ocean, which is consistent with the hypothesis that eels follow olfactory cues originating in the spawning area or that eels navigate using oceanic cues imprinted or learned during the leptocephalus [juvenile] phase. However, our reconstructions showed that the routes taken by eels contain meanders or deviations from a simple point-to-point migration along the shortest possible route. These meanderings are possibly related to entrapment within eddies or navigational responses to other hydrographic or bathymetric features [exemplified by leatherback turtle behavior in contrast to the "perfect" migration assumed in modeling studies].
Surely "olfactory cues" would be diluted to nothingness so far from the destination. How do they do it? Are eels equipped with magnetosensing, like salmon, sea turtles and Monarch butterflies? The authors don't elaborate, but eels must engage multiple sensory modalities to navigate, especially when swimming in the dark at night. And like sea turtles, their "map" is inherited at birth, so that tiny juveniles 5mm long born in the Sargasso Sea know where their native stream is in Europe, and the adults that develop from them will be able to find the Sargasso Sea years later.

These new findings pile on problems for functionalist explanations. Neo-Darwinism would predict bare-minimum adaptation sufficient for survival. Travelling 5,000 to 10,000 km in open sea, rife with predators, makes no sense in evolutionary theory. Undergoing major morphological changes makes no sense, either. Evolution is indeed still a theory in crisis.

More Crises in Darwinian Fish Stories

Elizabeth Pennisi has more bad news for evolutionists. Writing for Science, she says, "Fossil fishes challenge 'urban legend' of evolution." What urban legend does she speak of? It's a favorite myth in Darwinian theory: the idea that gene duplication frees up a spare copy to evolve new innovations. Her fish story involves the most diverse group of vertebrates in the world.

Imagine a half-ton tuna laid out on a dock next to a seahorse, a minnow, and a moray eel. That's just a snapshot of the astonishing diversity found in the group of fishes called teleosts, or ray-finned fish, which today have 30,000 species -- more than all living mammals, birds, reptiles, and amphibians combined. For more than a decade, many researchers have assumed that teleosts' dizzying array of body types evolved because their immediate ancestor somehow duplicated its entire genome, leaving whole sets of genes free to take on other functions.
Now, an examination of the fish fossil record challenges that view. Despite duplicating their genome about 160 million years ago, teleost fish hewed to a few conventional body types for their first 150 million years. Meanwhile, the holostean fishes, a related group with genomes that never underwent a doubling, evolved a stunning diversity of body plans. The work "demonstrates beautifully how necessary it is to look at the fossil record when testing hypotheses about ... largescale evolutionary changes," says Robert Sansom, a paleontologist at the University of Manchester in the United Kingdom.

Pennisi's lesson is clear. How many times have lazily accepted assumptions blinded scientists from the truth? You have to look at the data. You have to test theories with observations.


One can get an idea of the trajectory of a scientific paradigm by watching how rapidly anomalies accumulate. Evolution is more a theory in crisis than Denton's first book was published in 1985. These entries show it has gained more crises since his second book was published earlier this year. Things do not look good for Darwinism. There's an alternative position that doesn't have these problems. Its evidence is growing year by year. It's called intelligent design.

The deprivileging of mankind's status continues apace.

From the "Nothing Special" Files -- Apes and Their Theory of Mind

David Klinghoffer

This is just in from the laboratories of Nothing Special that I wrote about here the other day. Reports Karen Kaplan in the Los Angeles Times, "[H]umans' thinking abilities aren't quite as special as we'd like to think" (emphasis added). She knows that because of a new study in Science, "Great apes anticipate that other individuals will act according to false beliefs."

Of all the creatures in the animal kingdom, only humans were given credit for being able to ascertain the unstated thoughts, beliefs and desires of others. (Of course, said credit was doled out by humans.) ...
Ask yourself: Why the sarcastic tone? She goes on:

A notable version of this skill is the ability to recognize when someone else believes something that's false....
A team led by evolutionary anthropologist Christopher Krupenye at Duke University and comparative psychologist Fumihiro Kano of Kyoto University chose 41 chimpanzees, bonobos and orangutans. The researchers showed the apes a series of videos starring a regular person and a man dressed up as King Kong. In a variety of scenarios, King Kong would try to hide a rock-like object from the person. If the person saw what was going on, he'd find the rock in the expected place. If not, he didn't.

To test whether the apes understood what was going on, the scientists showed them additional videos in which King Kong tried to hide in one of two haystacks. Sometimes the person saw where King Kong went, and sometimes he didn't. Using an infrared eye-tracker, the researchers could see where the apes were looking -- and thus, where they expected the human to go.

In a second experiment, the apes watched more videos of King Kong trying to hide a rock from the person. Again, the researchers used eye-trackers to see if the apes could anticipate what the person would do.

In both cases, the chimpanzees, bonobos and orangutans correctly anticipated the person's actions -- even when the person looked for King Kong or the rock in the wrong place.

The moral, of course, is that humans are Nothing Special:

Thanks to these results, the claim that only humans can ascertain the mental states of others "is starting to wobble," primatologist Frans de Waal of the Yerkes National Primate Research Center at Emory University wrote in a commentary that accompanies the study....
De Waal seconded that notion, saying the results highlight "the mental continuity between great apes and humans."

It's a useful reminder that humans shouldn't be so quick to put themselves on a pedestal, he added.

The paper in Science is only a little more restrained in drawing the same lesson:

We humans tend to believe that our cognitive skills are unique, not only in degree, but also in kind. The more closely we look at other species, however, the clearer it becomes that the difference is one of degree. Krupenye et al. show that three different species of apes are able to anticipate that others may have mistaken beliefs about a situation.... The apes appear to understand that individuals have different perceptions about the world, thus overturning the human-only paradigm of the theory of mind.
Yet the business about knocking us down from a pedestal is based on a false premise: that we are at all surprised by these results. I'm not. Given that canines with their high emotional intelligence clearly intuit "unstated thoughts, beliefs and desires of others," as anybody with experience with dogs knows, why would the same not be true of apes?

That we share a limited capacity like this with chimps and orangutans comes as no shock. Therefore nothing is "starting to wobble." The results of the research do little to span the chasm between chimp and man. Instead the Nothing Special crowd uses the "pedestal" as a setup, a momentary fiction useful only for being immediately knocked over.

As Wesley Smith reminds us, dumping dirt on human exceptionalism is a preoccupation of popular science journalism -- not to mention professional science. It goes to show how powerful the will is among many smart and otherwise thoughtful people to believe humans are nothing special, and to convince others of the same thing. Where does that power come from?

An email correspondent notes the irony:

I have never been able to understand why so many people want so badly to believe there is Nothing Special about us, but they do. Only thing I can figure is that some of them just feel saying this makes them look special in the eyes of others.
Yes, right. Status is the key, but the psychology is very strange. Obviously I understand polishing your sense of self by advertising your accomplishments, associations, and possessions. But what drives this weird dynamic where feeling special depends on obsessively disclaiming specialness? We all know people who take pride in their humility. This is different. It seems to be more about sticking it -- "Nothing Special" -- in the face of others. That is the whole point of the L.A. Times article.


I am stumped. If you have any insights, please drop me an email and let me know. (Hit the orange button at the top of the page.)

Darwinism and mathematics are natural enemies.

Biologic Institute's Groundbreaking Peer-Reviewed Science Has Now Demonstrated the Implausibility of Evolving New Proteins

Casey Luskin January 22, 2015 10:51 AM

 

Ann Gauger already provided an excellent series of articles discussing her recent paper co-authored in BIO-Complexity. She explains why it is important for demonstrating intelligent design (see here, here, here, here, and here). However, I wanted to give a slightly different framing of the new data. My purpose here and in a follow-up post will be to explain how this latest ID research (as well as prior work in the field) addresses fundamental questions in the debate over Darwinian evolution and ID -- and comes up with very positive results.When Michael Behe published Darwin's Black Box in 1996, he outlined the concept of irreducible complexity as a biochemical challenge to Darwinian evolution. According to his argument, some structures require all of their parts (or a certain core minimum number) in order to function. In this game of all or nothing, such "irreducibly complex" structures cannot be built in the step-by-step manner of Darwinian evolution because they provide no advantage, of the kind evolution requires, until all their parts are present.
At the time and since, evolutionists responded by arguing that irreducibly complex features can be built through co-option. Under this view, biological parts might exist elsewhere in an organism where they are used for a different function. Sometimes, when a gene is duplicated, the extra copy could then be borrowed, retooled, and "co-opted" to perform a new function in a new system. Sounds easy, right?
Not so fast. Darwin observed that his theory "breaks down" when large leaps of complexity are needed in order to provide some advantage. What if retooling proteins to perform new functions requires such leaps? What if multiple mutations are needed to convert a protein to perform some new function? Should we follow many evolutionists and simply wave our hands and assume the co-option model of protein evolution is sufficient, or should we behave like scientists and test the viability of that model? Researchers at Biologic Institute have decided to take the latter approach, and to test the co-option model of protein evolution.
In 2011, Ann Gauger and Douglas Axe published a paper in BIO-Complexity, "The Evolutionary Accessibility of New Enzymes Functions: A Case Study from the Biotin Pathway." They reported results of their laboratory experiments trying to convert one enzyme (Kbl₂) to perform the function of a very similar enzyme (BioF₂), thought to be very closely related to Kbl₂. Because these proteins are both members of the GABA-aminotransferase-like (GAT) family, and are believed to be very closely related, this is the sort of evolutionary conversion that evolutionists say ought to be easily accomplished under the standard co-option model. However, after trying multiple combinations of different mutations, they found otherwise:

We infer from the mutants examined that successful functional conversion would in this case require seven or more nucleotide substitutions.

This presents a serious problem for Darwinian evolution since a 2010 paper by Axe found that a feature that would require more than two maladaptive mutations, or more than six neutral mutations, before providing an advantage could not arise in the entire history of the earth. Gauger and Axe (2011) concluded:

[E]volutionary innovations requiring that many changes would be extraordinarily rare, becoming probable only on timescales much longer than the age of life on earth. Considering that Kbl₂ and BioF₂ are judged to be close homologs by the usual similarity measures, this result and others like it challenge the conventional practice of inferring from similarity alone that transitions to new functions occurred by Darwinian evolution.

Their 2011 study thus provided a "disproof of concept" of the co-option model. However, it only looked at two proteins. What if other proteins are more easily convertible? Last December, in a landmark peer-reviewed paper published in BIO-Complexity, Axe, Gauger, and biologist Mariclair Reeves presented new research on additional proteins in the same family. They showed that these proteins too are not amenable to an evolutionary conversion to perform the function of BioF₂.
Now in their new study, "Enzyme Families-Shared Evolutionary History or Shared Design? A Study of the GABA-Aminotransferase [GAT] Family," Reeves, Gauger, and Axe examine nine other enzymes from the same GAT family. Once again, the idea was to see if it is possible to convert them to perform the function of BioF₂. They tested proteins that are closer to BioF₂, or more distant from BioF₂, than the enzyme they tested in their prior study (Kbl₂). But all of the proteins studied are in the same family, and are thought to be closely related.
First, they sought to determine if the enzymes could be converted to perform the function of BioF₂ through a single mutation. They created mutation libraries with every single possible mutation in those nine enzymes. No BioF₂ function was ever detected. As they explain:

The present study has added to our previous examination of these problems in several respects. We have shown, based on sequence alignment of α-oxoamine synthases (a subset of the GAT family), that our previous use of rational design did indeed target regions of Kbl₂ that are likely to be functionally significant. Furthermore we have now shown that the lack of a simple evolutionary transition to BioF₂ function is not at all unique to our initial choice of Kbl₂ as the starting point. Single mutations cannot convert any of eight other members of the GAT family to that function, despite the fact that all of these enzymes are regarded as close evolutionary relatives.

Then they tried double-mutation libraries. They were able to try 70 percent of the double-mutations in two enzymes that are thought to be the most likely candidates for conversion to function like BioF₂: Kbl₂ and another enzyme, BIKB, which is said to have both BioF₂ and Kbl₂ functions. They write:

[W]e have demonstrated that converting either Kbl₂ or BIKB to perform the function BioF₂ with two DNA base substitutions is at least mildly unlikely, in that neither conversion was found after examining over two thirds of the possibilities. Of course, many possibilities remain unexamined. Although it is certainly possible for a working combination to be among those unchecked possibilities, we think it is more informative at this point to ask the fundamental question of whether the available evidence as a whole really supports the idea that evolutionary recruitment is the cause of functional diversity in enzyme families.

This suggests that at least two mutations would be necessary to convert a protein in this family to perform the function of BioF₂. But it's likely that additional mutations would be necessary for these evolutionary conversions. To be specific, the co-option model requires that a gene become duplicated, and then overexpressed before it can evolve some new function. Thus, at least two more mutations are needed -- one to duplicate the gene and another to overexpress it.
However, one of their citations makes a compelling case that the gene duplication step poses a major obstacle to gene recruitment via gene duplication and mutation. They cite a paper from PLOS Genetics, "The Extinction Dynamics of Bacterial Pseudogenes," which notes:

In bacteria, however, pseudogenes are deleted rapidly from genomes, suggesting that their presence is somehow deleterious. The distribution of pseudogenes among sequenced strains of Salmonella indicates that removal of many of these apparently functionless regions is attributable to their deleterious effects in cell fitness, suggesting that a sizeable fraction of pseudogenes are under selection.

It concludes, "Although pseudogenes have long been considered the paradigm of neutral evolution, the distribution of pseudogenes among Salmonella strains indicates that removal of many of these apparently functionless regions is attributable to positive selection."
Don't miss the profound importance of this. What it means is that there is very likely a fitness cost associated with carrying an extra, useless copy of a gene, and therefore it can be advantageous to delete duplicate version. This has major implications for the co-option model of protein evolution, because it shows that producing a new protein does not involve "neutral evolution," but rather requires steps that very likely will impose a deleterious effect upon the organism.
Similar results were obtained in a 2010 BIO-Complexity paper reporting ID research, "Reductive Evolution Can Prevent Populations from Taking Simple Adaptive Paths to High Fitness," by Gauger and biologist Ralph Seelke. This paper found that when merely two mutations along a stepwise pathway were required to restore function to a bacterial gene, even then the Darwinian mechanism failed. But the reason why Darwinism failed is important.
Although one mutation restored partial function, the function was very slight. In the experiments, the gene was deleted before the second mutation could occur and restore full function. It was more advantageous to delete a weakly functional gene than to continue to express it in the hope that it would "find" the mutations that fixed the gene. This means that carrying a weakly functional gene is disadvantageous, and that it's more advantageous to just get rid of a gene duplicate that isn't contributing very much to the success of the organism.
So a fundamental component of the co-option model -- duplicating a gene -- very likely involves a deleterious step. What does that say about the potential for evolving complex traits? ID research has already addressed that question.
In a 2010 research paper that Douglas Axe published in BIO-Complexity, "The Limits of Complex Adaptation: An Analysis Based on a Simple Model of Structured Bacterial Populations," he determined that when deleterious mutations are involved, a trait that requires more than two disadvantageous mutations could never form over the history of the earth. In other words, if you are trying to evolve a trait that requires more than two deleterious mutations, it's not going to evolve.
Let's return now to the 2014 paper by Reeves, Gauger, and Axe. They experimentally found that at least two mutations would be necessary to convert the most likely co-option candidates in this enzyme family to function like BioF₂. But other mutations would be necessary as well -- at least one to duplicate the enzyme and another to overexpress it. This suggests at least four mutations would be required for this conversion. Given that, as we just saw, some of these mutations (such as duplication) would initially impose a disadvantage, the math says it would take some 10¹⁵ years for the necessary mutations to arise to co-opt a protein to function like BioF₂ -- over 100,000 times longer than the age of the earth! They thus conclude:

Based on these results, we conclude that conversion to BioF₂ function would require at least two changes in the starting gene and probably more, since most double mutations do not work for two promising starting genes. The most favorable recruitment scenario would therefore require three genetic changes after the duplication event: two to achieve low-level BioF₂ activity and one to boost that activity by overexpression. But even this best case would require about 10¹⁵ years in a natural population, making it unrealistic. Considering this along with the whole body of evidence on enzyme conversions, we think structural similarities among enzymes with distinct functions are better interpreted as supporting shared design principles than shared evolutionary histories.

This new paper thus provides a robust disproof of the co-option model, overturning a cornerstone argument that evolutionists have long used when trying to answer ID arguments like irreducible complexity. By testing the co-option model, Biologic Institute is not just asking the right questions and doing innovative research that addresses key issues in the debate over Darwinian evolution and intelligent design. They're also finding data that confirms that ID's earliest arguments were right all along.

Reasons to doubt the trinity III

Yet More on life's anti Darwinian bias IV

Armed Forces in the Cell Keep DNA Healthy
Evolution News & Views September 8, 2015 3:01 AM

Science reporters struggle for metaphors to describe the complex operations they see going on in the cell. For example:

The Orchestra

News from the University of Geneva likens the human genome to a "complex orchestra." Their research led to "unexpected" and "surprising" findings showing "harmonized and synergistic behavior" in the regulation of genes. The metaphor of a conductor keeping all the various players in harmony came to mind:

A team of Swiss geneticists from the University of Geneva (UNIGE), the École Polytechnique Fédérale de Lausanne (EPFL), and the University of Lausanne (UNIL) discovered that genetic variation has the potential to affect the state of the genome at many, seemingly separated, positions and thus modulate gene activity, much like a conductor directing the performers of a musical ensemble to play in harmony. These unexpected results, published in Cell, reveal the versatility of genome regulation and offer insights into the way it is orchestrated. [Emphasis added.]
The Armed Forces

Another metaphor popular among reporters is "armed forces." This metaphor will prove instructive as we read about DNA protection and damage repair. Let's look at some of the stages in this process where we will find soldiers, emergency medical technicians, ambulances and military hospitals in action, each well trained and equipped for defense.

Surveillance and Inspection

Any disciplined military operation requires high standards. Soldiers at boot camp know that drill sergeants can be ruthless when inspecting rifles, shoe shines, and barrack beds. Similarly, machines in the genome inspect DNA for errors and won't tolerate less than perfection. A news item from North Carolina State University describes MutS, a machine that inspects unzipped DNA strands looking for errors. Any mismatch makes this drill sergeant stop and stare the recruit in the face, even if he is one in a million.

Fortunately, our bodies have a system for detecting and repairing these mismatches -- a pair of proteins known as MutS and MutL. MutS slides along the newly created side of the DNA strand after it's replicated, proofreading it. When it finds a mismatch, it locks into place at the site of the error and recruits MutL to come and join it. MutL puts a nick in the newly synthesized DNA strand to mark it as defective and signals a different protein to gobble up the portion of the DNA containing the error. Then the nucleotide matching starts over, filling the gap again. The entire process reduces replication errors around a thousand fold, serving as our body's best defense against genetic mutations and the problems that can arise from them, like cancer.
First Response

If casualties occur, they have to be detected. A protein named ATF3 is captain of a squad that acts as "first responder" to DNA damage, as this from Georgia Regents University explains. Let's say a DNA strand breaks because of sunlight, chemotherapy or a cosmic ray. If not corrected quickly, the cell could become cancerous or die. What happens first?

In the rapid, complex scenario that enables a cell to repair DNA damage or die, ATF3, or activating transcription factor 3, appears to be a true first responder, increasing its levels then finding and binding to another protein, Tip60, which will ultimately help attract a swarm of other proteins to the damage site.
Combat Operations

Viruses have invaded! The armed forces go into high alert. The Salk Institute for Biological Studies describes the flurry of activities that result, because every organism "must protect its DNA at all costs."

Before panicking, the cell's commanding officers need intelligence. If a DNA break puts the cell in stress, was it a natural break, let's say from a cosmic ray, or from a virus, like an insurgent tossing a grenade? A false move could lead to friendly-fire casualties.

The researchers explain how the cell figures out if the DNA damage was internal or external. First, the MRN complex gives the "all hands on deck" signal. It stops replication and other cell operations until the break is mended.

What's interesting is that even a single break transmits a global signal through the cell, halting cell division and growth," says O'Shea. "This response prevents replication so the cell doesn't pass on a break."
The viral response begins the same way, the article continues, but doesn't give the global alarm. Instead, the alarm is localized, and sentries in the area dispatch the invaders. There's a reason for this. "If every incoming virus spurred a similarly strong response, points out O'Shea, our cells would be frequently paused, hampering our growth." But when the cell becomes preoccupied with DNA damage repair, the viruses can infiltrate.

A video clip in the article applies the armed forces metaphor:

Govind Shah: "DNA repair proteins serve as security guards inside the nucleus. They catch virus DNA and escort them out of the cell. If a cell experiences a huge amount of DNA damage, then these security guards will be pulled away from the viral DNA and allow the viral DNA to replicate to high levels."
Clodagh O'Shea: "We discovered that if you have DNA damage in your own genome, and the alarm goes off, actually that recruits in all of the forces: all of the police, national guard--everyone's there. All the forces are dealing with your own DNA damage, and there's nothing left to actually even see or actually turn off the virus."

This gave them an idea. Shah says, "So why not use this to kill cancer cells" with viruses engineered to enter tumor cells? The programmed response they discovered will cause the cell to let the viruses in while it's preoccupied with fixing DNA breaks. "If the cell can't fix the DNA break, it will induce cell death-a self-destruct mechanism that helps to prevent mutated cells from replicating (and thus prevents tumor growth)."

Medics

We're all familiar with the images of battlefield helicopters delivering medics to give first aid to the wounded, or airlifting them to the nearest triage station or hospital. The cell nucleus has hospitals, an article at Biotechniques says, and "A molecular ambulance for DNA" knows how to get the casualties to the emergency room.

Double-strand breaks in DNA are a source of stress and sometimes death for cells. But the breaks can be fixed if they find their way to repair sites within the cell. In yeast, one of the main repair sites resides on the nuclear envelope where a set of proteins, including nuclear pore subcomplex Nup84, serves as a molecular hospital of sorts. The kinesin-14 motor protein complex, a "DNA ambulance," moves the breaks to repair sites, according to a new study in Nature Communications.
Researchers at the University of Toronto found it "very surprising" was that the ambulance driver is the well-known motor protein kinesin-14 (see our animation of kinesin at work).

Hospital Staff

News from the University of Texas MD Anderson Cancer Center introduces some of the specialists in the DNA repair hospital: fumarase. a metabolic enzyme; DNA-PK, a protein kinase; and histone methylation enzymes that regulate the repair process. These skilled doctors perform restorative surgery for "DNA double-strand breaks (DSBs)," which "are the worst possible form of genetic malfunction that can cause cancer and resistance to therapy."

Clean-up Crew

Cells invest a lot of energy in their ribosomes, the organelles that translate DNA. Ribosomes are assembled from protein and RNA domains. What happens with the leftovers? An item from the University of Heidelberg describes molecular machines that barcode the fragments for delivery to a barrel-shaped shredder called the exosome. Though not described in military terms, the agents are under strict orders and required to pass through checkpoints.

According to Prof. Hurt, the production of ribosomes is an extremely complex process that follows a strict blueprint with numerous quality-control checkpoints. The protein factories are made of numerous ribosomal proteins (r-proteins) and ribosomal ribonucleic acid (rRNA). More than 200 helper proteins, known as ribosome biogenesis factors, are needed in the eukaryotic cells to correctly assemble the r-proteins and the different rRNAs. Three of the total of four different rRNAs are manufactured from a large precursor RNA. They need to be "trimmed" at specific points during the manufacturing process, and the superfluous pieces are discarded. "Because these processes are irreversible, a special check is needed," explains Ed Hurt.
The number of "armed forces" personnel involved in DNA defense and cell quality control is astonishing. It's beyond a well-conducted orchestra. It's like a military operation, with strict protocols, hierarchical command structure and trained specialists. These systems are goal-oriented: they exist to protect the genome. They are on duty inspecting components even when nothing is wrong. And when things do go wrong, they know just what to do, as if well-trained in following orders.

We aren't surprised to notice that these articles say nothing about evolution. Why? Because we all know from our experience that phenomena characterized by hierarchical command and control systems with documented procedures and skilled agents are always intelligently designed.

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