On I.D and expectations.

Horns of a Dilemma: Does Intelligent Design Do Too Little -- or Too Much?
Evolution News & Views 

An irony about intelligent design is that it is attacked from, so to speak, front and behind. Some, including theistic evolutionists, criticize ID's minimalism -- it declines to name a designer, to describe the act of design (so that you could picture it happening), to say when or how often the design is instantiated in life, among other things.

So goes the complaint. Let's see here.

When: Different scientific fields tell us different things. Astronomy doesn't tell us when the earth formed. But geology does. That doesn't mean astronomy is less a science because it can tell us things that geology cannot. ID tells us whether something was designed or whether it arose via material causes. ID doesn't tell you when the designer acted. But other fields can. Fields like geology (dating methods), paleontology (looking at fossils), or molecular biology (molecular clock methods) can potentially tell you when the designer acted to implement some design.

How often: As we learn more and more about where we should detect design, and as other fields tell us when that design happened, we can begin to get a handle on "how often" the designer acted. So this question is definitely not off limits to intelligent design and ID can help address it.

Identity of the designer: True, ID doesn't tell you who the designer is. That is because the scientific evidence doesn't tell us. This is a good example of ID . respecting the limits of science  Some see it as a weakness of ID. In fact, it's a strength. As William Dembski has said , "This is not a matter of being vague but rather of not pretending to knowledge that we don't have."

We're accustomed to Darwinists saying things they don't know (scientifically) to be true. That's doesn't mean we get to say things that we don't know (scientifically) to be true.

In a special irony, many theistic evolutionists tout methodological naturalism, criticizing ID for supposedly bringing God into science. These same individuals then pivot and complain that ID fails to identify the designer as God.

Meanwhile, design advocates are slammed for maximalism, or worse. Much worse. A friend shares with us these choice comments:

Evolutionary biologist Massimo Pigliucci (2002): ID is "bent on literally destroying science as we know it."

Physicist Marshall Berman (2005): "The current Intelligent Design movement poses a threat to all of science and perhaps to secular democracy itself."

Science journalist Robyn Williams (2006): "ID is, in a way, terrorism."

Whoa. So which is it, folks? Does ID do too little -- or too much? And why the hysteria?

ID may be limited, but if it can show that even one feature in living things is designed by an intelligence (no matter when,where, or how), the whole edifice of materialism collapses. That's why Darwinists are terrified. They cannot allow an intelligent foot in the door.


As for our theistic evolutionary friends, well, they've abandoned the principle of non-contradiction. Everything and nothing follows from that.

A simple lifeform ?II

Kamikaze cells wage biowarfare and fight viruses with viruses
By Michael Le Page

Giants, self-sacrifice, biological warfare: this story has them all. A voracious marine predator plagued by a giant virus has a defence system we’ve never seen before – it fights back by making its very own virus.

The individuals that make these bioweapons sacrifice themselves for the greater good, saving their fellow predators in the process.

The single-celled predator, Cafeteria roenbergensis, is common in coastal waters around the world, where it snacks on bacteria (the biologists who discovered it in 1988 near the Danish town of Roenbjerg sat discussing their find in the local… yes, you guessed it).

But Cafeteria has a deadly enemy of its own, the giant CroV virus.

Most viruses are little more than a protein shell encapsulating a handful of genes. They depend entirely on the machinery of the cells they infect to make more copies of themselves.

But giant viruses, discovered only in 2003, are more like living cells than normal viruses. They have the machinery to make proteins, which means they are vulnerable to viral attack themselves. For example, maviruses infect CroVs, forcing them to make more maviruses instead of CroVs, as Matthias Fischer, now at the Max Planck Institute in Germany, discovered in 2011.

That, of course, is good news for Cafeteria, because mavirus halts the spread of CroV.

And Cafeteria has evolved to exploit the concept that the enemy of my enemy is my friend. Rather than waiting for maviruses to arrive by chance when CroVs attack, it actually carries the genes that code for mavirus inside its own genome.

These genes are usually dormant, but they get turned on when Cafeteria is invaded by CroV. “It acts as an inducible antiviral defence system,” write Fischer and his colleague Thomas Hackl in a new preprint paper.

The infected Cafeteria cell still dies – but when it breaks apart it releases maviruses rather than CroVs, preventing the spread of the infection. This, then, is altruistic behaviour, which turns out to be surprisingly common among microbes. For instance, some bacteria kill themselves as soon as they are infected by viruses to prevent the infection spreading.

Other microbes form spore-bearing structures, with the cells making the stalk sacrificing themselves to give the spore-forming cells at the top a chance of surviving.

Bioweapons at the ready
Cafeteria may not be the only animal to use living bioweapons to defend itself. A wide range of animals, from sea anemones to crocodiles, harbour genetic elements called Maverick transposons that closely resemble the mavirus genes. It’s possible that some of these organisms can also unleash viruses that attack giant viruses.

It is common for viral genes to end up inside the genomes of animals. In fact, our genomes are littered with the mutant remains of viruses and genetic parasites.

Many viruses deliberately insert their genes into the genomes of the animals they attack, so they can lie dormant and emerge when conditions are favourable. In response, most animals have evolved ways of shutting down genes that code for viruses.

It is, however, extremely unusual for an animal to deliberately trigger virus production, as Cafeteria does – but then mavirus is unusual, too, because it targets another virus rather than Cafeteria itself.

What is common is for genes that originally came from viruses to be co-opted for new purposes. Genes of viral origin play a key role during pregnancy, for instance.

And some bacteria have “spearguns” that they use to attack other bacteria. These spearguns evolved from the apparatus that bacteria-attacking viruses use to inject their genes into their victims.


Journal reference: Biorxiv, DOI: 10.1101/068312

On physics' search for a theory of everything.

Should physics even try to converge on a grand unified theory?
Posted by News under Cosmology, Intelligent Design

From Manjit Kumar at Physics World , reviewing Peter Watson’s Convergence: the Deepest Idea in the Universe, , expresses some caution about that:

Wherever experimental evidence can be coaxed out of nature, it suffices to corroborate or refute a theory and serves as the sole arbiter of validity. But where evidence is sparse or absent, other criteria, including aesthetic ones, have been allowed to come into play – both in formulating a theory and evaluating it. Watson believes that because of this, in some ways “physics has become mathematics”, arguing that we are currently “living in an in-between time, and have no way of knowing whether many of the ideas current in physics will endure and be supported by experiment”.

This, Watson explains, deeply worries the likes of cosmologists Joseph Silk and George Ellis. At the end of 2014, Silk and Ellis argued in a Nature comment piece that some scientists appear to have “explicitly set aside” the need for experimental confirmation of our most ambitious theories, “so long as those theories are sufficiently elegant and explanatory”. They further complain that we are at the end of an era, “breaking with centuries of philosophical tradition” of defining scientific knowledge as empirical.

As Silk and Ellis point out, this situation has come about because particle physicists have struggled to go beyond the Standard Model. Their most prominent attempt has been the theory of supersymmetry, but the problem is that no supersymmetric particles have been found, and Silk and Ellis fear that its advocates will simply “retune” their models “to predict particles at masses beyond the reach of the LHC’s power of detection”.More.


Put simply, the war on falsifiability advances.

On darwin's defenders.

Robert Richards and Evolutionary Apologetics
Evolution News & Views 

Evolutionary apologetics is the defense of Darwinian theory against all challenges -- scientific and otherwise. That Darwinism has not coincidentally been put to evil ends, while not in itself evidence of invalid science, would seem indisputable.

Its role in shaping Nazi ideology would also seem clear enough to anyone who has read a little about the subject. Because Hitler's Germany can't be topped for evil, the defense of Darwinism must have a refutation of the Darwin-Hitler connection.

Over at the website This View of Life, promising "Anything and everything from an evolutionary perspective," SUNY Binghamton biologist David Sloan Wilson wraps up a series of essays by various scholars seeking "A New Social Darwinism." Wilson writes:

Truth and reconciliation for Social Darwinism involves acknowledging the misuse of evolutionary theory, but it also involves acknowledging false accusations and the omission of benign uses of evolutionary theory.

From an apologetic perspective, those "false accusations" to be dealt with must include the stain of Hitler, an "invented history." Invented? To show as much the series features an essay -- "Was Hitler a Darwinian? No! No! No!" -- by University of Chicago historian of science Robert Richards that takes shots at our colleagues Richard Weikart and David Berlinski, the film Expelled, and the "gossamer logic" of the "Intelligent Design crowd."

Plenty of other scholars have recognized Hitler's Darwinism, however crude and derivative. Richards mentions Hannah Arendt, John Gray, and the otherwise "astute historian" Peter Bowler, notably absent from the ranks of the "Intelligent Design crowd."

In any event, Professor Weikart has already dealt with Dr. Richards in a series of posts here:

"'Was Hitler a Darwinian?' Reviewing Robert Richards"

"Ignoring Evidence, Caricaturing Critics: Robert J. Richards's Was Hitler a Darwinian?"

"Is Robert Richards Right to Deny that Hitler Was a Darwinian?"

"Why My Critics Care So Much About the Darwin-Hitler Connection"

Why all the clamor to erase the Darwin-Hitler link? Weikart is characteristically astute:

[W]hy do they care about this at all? If they believe, as many do, that morality is simply "an illusion fobbed off on us by our genes," as evolutionary biologist E.O. Wilson and philosopher Michael Ruse famously put it, then what makes the illusions of some people superior to Hitler's illusions? Why do everything possible -- even denying obvious historical facts -- to obscure the historical linkages between Darwin and Hitler? I have a hunch that at some level they recognize that their evolutionary account of morality is inconsistent with reality.

As to the facts, Richards "misquotes and/or ignores the context of quotations," "ignores mountains of evidence," "caricatures the positions of those he disagrees with," "conflates certain key concepts," " totally ignores many of the most salient points I set forth in my books," "even creates a new historical 'fact.'"


Quite simply, evolutionary apologetics must have its own historical alternative reality. The defense of Darwin demands it, and so the dish is served.

Michael Behe v. the critics

Irreducible Complexity and the Evolutionary Literature: A Response to Critics

Michael Behe 

Editor's note: In celebration of the 20th anniversary of biochemist Michael Behe's pathbreaking book Darwin's Black Box and the release of the new documentary Revolutionary: Michael Behe and the Mystery of Molecular Machines, we are highlighting some of Behe's "greatest hits." The following was published by Discovery Institute on July 31, 2000. Remember to get your copy of Revolutionary now! See the trailer here.

I. Summary

Although several persons have cited numerous references from the scientific literature purporting to show that the problem of irreducible complexity I pointed out in Darwin's Black Box is being seriously addressed, the references show no such thing. Invariably the cited papers or books either deal with non-irreducibly complex biochemical systems, or do not deal with them in enough detail for critical evaluation. I strongly emphasize, however, that I do not prefer it that way. I would sincerely welcome much more serious, sustained research in the area of irreducible complexity. I fully expect such research would heighten awareness of the difficulties of Darwinian evolution.

II. Web Spinners

The necessary starting point of Darwin's Black Box was the contention that, despite the common assumption that natural selection accounts for adaptive complexity, the origins of many intricate cellular systems have not yet been explained in Darwinian terms. After all, if the systems have already been explained, then there's no need to write. While most scientist-reviewers disagreed (often emphatically) with my proposal of intelligent design, most also admitted to a lack of Darwinian explanations. For example, microbiologist James Shapiro of the University of Chicago declared in National Review that "There are no detailed Darwinian accounts for the evolution of any fundamental biochemical or cellular system, only a variety of wishful speculations." (Shapiro 1996) In Nature University of Chicago evolutionary biologist Jerry Coyne stated, "There is no doubt that the pathways described by Behe are dauntingly complex, and their evolution will be hard to unravel. . . . [W]e may forever be unable to envisage the first proto-pathways." (Coyne 1996)

In a particularly scathing review in Trends in Ecology and Evolution Tom Cavalier-Smith, an evolutionary biologist at the University of British Columbia, nonetheless wrote, "For none of the cases mentioned by Behe is there yet a comprehensive and detailed explanation of the probable steps in the evolution of the observed complexity. The problems have indeed been sorely neglected -- though Behe repeatedly exaggerates this neglect with such hyperboles as 'an eerie and complete silence.'" (Cavalier-Smith 1997) Evolutionary biologist Andrew Pomiankowski agreed in New Scientist, "Pick up any biochemistry textbook, and you will find perhaps two or three references to evolution. Turn to one of these and you will be lucky to find anything better than 'evolution selects the fittest molecules for their biological function.'" (Pomiankowski 1996) In American Scientist Yale molecular biologist Robert Dorit averred, "In a narrow sense, Behe is correct when he argues that we do not yet fully understand the evolution of the flagellar motor or the blood clotting cascade." (Dorit 1997)

A prominent claim I made in Darwin's Black Box is that, not only are irreducibly complex biochemical systems unexplained, there have been very few published attempts even to try to explain them. This contention has been vigorously disputed not so much by scientists in the relevant fields as by Darwinian enthusiasts on the Internet. Several web-savvy fans of natural selection have set up extensive, sophisticated sites that appear to receive a significant amount of notice. They influence college students, reporters, and, sometimes, academic reviewers of my book such as Cal State-Fullerton biochemist Bruce Weber, who lists the addresses of the websites in his review in Biology and Philosophy as "summaries of the current research that Behe either missed or misrepresented" (Weber 1999), and Oxford physical chemist Peter Atkins, who writes:

Dr. Behe claims that science is largely silent on the details of molecular evolution, the emergence of complex biochemical pathways and processes that underlie the more traditional manifestations of evolution at the level of organisms. Tosh! There are hundreds, possibly thousands, of scientific papers that deal with this very subject. For an entry into this important and flourishing field, and an idea of the intense scientific effort that it represents (see the first link above) [sic]. (Atkins 1998)

The link Atkins refers to is a website called "Behe's Empty Box" that has been set up by a man named John Catalano, an admirer of Oxford biologist Richard Dawkins (his larger site is devoted to Dawkins' work, schedule, etc.). The Empty Box site is, I think, actually a valuable resource, containing links to many reviews, comments and other material, both critical and favorable, related to my book. One subsection of the site is entitled "Alive and Published," and contains citations to a large number of papers and books which Catalano believes belie my claim that "There has never been a meeting, or a book, or a paper on details of the evolution of complex biochemical systems." (Behe 1996) (p. 179) The citations were solicited on the web from anyone who had a suggestion, and then compiled by Catalano.

Something, however, seems to be amiss. The assertion here that very many papers have been published clashes with statements of the reviews I quoted earlier which say, for example, that "The problems have indeed been sorely neglected." (Cavalier-Smith 1997) Would reviewers such as Jerry Coyne and Tom Cavalier-Smith -- both antagonistic to my proposal of intelligent design -- be unaware of the "hundreds, possibly thousands, of scientific papers that deal with this very subject"? Both claims -- that the problems have been neglected and that the problems are being actively investigated -- cannot be correct. Either one set of reviewers is wrong, or there is some confusion about which publications to count. Which is it?

In the context of my book it is easy to realize that I meant there has been little work on the details of the evolution of irreducibly complex biochemical systems by Darwinian means. I had clearly noted that of course a large amount of work in many books and journals was done under the general topic of "molecular evolution," but that, overwhelmingly, it was either limited to comparing sequences (which, again, does not concern the mechanism of evolution) or did not propose sufficiently detailed routes to justify a Darwinian conclusion. Yet the Catalano site lists virtually any work on evolution, whether it pertains to irreducible complexity or not. For example it lists semi-popular books such as Patterns in Evolution: The New Molecular View by Roger Lewin, and general textbooks on molecular evolution such as Molecular Evolution by Wen-Hsiung Li.

Such books simply don't address the problems I raise. Molecular Evolution by Wen-Hsiung Li (Li 1997) is a fine textbook which does an admirable job of explicating current knowledge of how genes change with time. That knowledge, however, does not include how specific, irreducibly-complex biochemical systems were built. The text contains chapters on the molecular clock, molecular phylogenetics, and other topics which essentially are studies in comparing gene sequences. As I explained in Darwin's Black Box, comparing sequences is interesting but cannot explain how molecular machines arose. Li's book also contains chapters on the mechanisms (such as gene duplication, domain shuffling, and concerted evolution of multigene families) that are thought to be involved in evolution at the molecular level. Again, however, no specific system is justified in Darwinian terms.

Here is an illustration of the problem. Li spends several pages discussing domain shuffling in the proteins of the blood-clotting cascade (Li 1997). However, Li himself has not done work on understanding how the obstacles to the evolution of the clotting cascade may have been circumvented. Since those investigators who do work in that area have not yet published a detailed Darwinian pathway in the primary literature1, we can conclude that the answer will not be found in a more general text. We can further assume that the processes that text describes (gene duplication, etc.), although very significant, are not by themselves sufficient to understand how clotting, or by extension any complex biochemical system, may have arisen by Darwinian means.

Catalano's site lists other books that I specifically discussed in Darwin's Black Box, where I noted that, while they present mathematical models or brief general descriptions, they do not present detailed biochemical studies of specific irreducibly complex systems. (Gillespie 1991; Selander et al. 1991) There is no explanation on Catalano's website of why he thinks they address the questions I raised. The site also points to papers with intriguing titles, but which are studies in sequence analysis, such as "Molecular evolution of the vertebrate immune system" (Hughes and Yeager 1997) and "Evolution of chordate actin genes: evidence from genomic organization and amino acid sequences." (Kusakabe et al. 1997) As I explained in Darwin's Black Box, sequence studies by themselves can't answer the question of what the mechanism of evolution is. Catalano's compendium also contains citations to papers concerning the evolution of non-irreducibly complex systems, such as hemoglobin and metabolic pathways, which I specifically said may have evolved by natural selection. (Behe 1996) (pp. 150-151; 206-207)

III. Equivocal Terms

Another website that has drawn attention (as evidenced from the inquiries I receive soliciting my reaction to it) is authored by David Ussery (Ussery 1999), associate research professor of biotechnology at The Technical University of Denmark. One of his main goals is to refute my claim concerning the dearth of literature investigating the evolution of irreducibly complex systems. For example, in a section on intracellular vesicular transport he notes that I stated in Darwin's Black Box that a search of a computer database "to see what titles have both evolution and vesicle in them comes up completely empty." (Behe 1996) (p. 114) My search criterion, of having both words in the title, was meant to be a rough way to show that nothing much has been published on the subject. Ussery, however, writes that, on the contrary, a search of the PubMed database using the words evolution and vesicle identifies well over a hundred papers. Confident of his position, he urges his audience, "But, please, don't just take my word for it -- have a look for yourself!" (Ussery 1999)

The problem is that, as I stated in the book, I had restricted my search to the titles of papers, where occurrence of both words would probably mean they concerned the same subject. Ussery's search used the default PubMed setting, which also looks in abstracts.2 By doing so he picked up papers such as "Outbreak of nosocomial diarrhea by Clostridium difficile in a department of internal medicine." (Ramos et al. 1998) This paper discusses the "clinical evolution" (i.e., course of development) of diarrhea in hospitalized patients, who also had "vesicle catherization." Not only do the words evolution and vesicle in this paper not refer to each other, the paper does not even use the words evolution and vesicle in the same sense as I did. Since the word evolution has many meanings, and since the word vesicle can mean just a container (like the word "box"), Ussery picked up equivocal meanings.

The paper cited above shows Ussery's misstep in an obvious way. However, there are other papers resulting from an Ussery-style search where, although they do not address the question I raised, the unrelatedness is not so obvious to someone outside the field. An example of a paper that is harder for someone outside the field to evaluate is "Evolution of the trappin multigene family in the Suidae." (Furutani et al. 1998) The authors examine the protein and gene sequences for a group of secretory proteins (the trappin family) which "have undergone rapid evolution" and are similar to "seminal vesicle clotting proteins." The results may be interesting, but the seminal vesicle is a pouch in the male reproductive tract for storing semen -- not at all the same thing as the vesicle in which intracellular transport occurs. And trappins are not involved in intracellular transport.

A second example is "Syntaxin-16, a putative Golgi t-SNARE." (Simonsen et al. 1998) This paper actually does concern a protein involved in intracellular vesicular transport. However, as the abstract states, "Database searches identified putative yeast, plant and nematode homologues of syntaxin-16, indicating that this protein is conserved through evolution." The database searches are sequence comparisons. Once again I reiterate, sequence comparisons by themselves cannot tell us how a complex system might have arisen by Darwinian means.

Instead of listing further examples let me just say that I have not seen a paper using Ussery's search criteria that addresses the Darwinian evolution of intracellular vesicular transport in a detailed manner, as I had originally asserted in my book.

It is impossible for me to individually address the "hundreds, possibly thousands" of papers listed in these websites. But perhaps I don't have to. If competent scientists who are not friendly to the idea of intelligent design nonetheless say that "There are no detailed Darwinian accounts for the evolution of any fundamental biochemical or cellular system, only a variety of wishful speculations," (Shapiro 1996) and that "We may forever be unable to envisage the first proto-pathways" (Coyne 1996), then it is unlikely that much literature exists on these problems. So after considering the contents of the websites, we can reconcile the review of Peter Atkins with those of other reviewers. Yes, there are a lot of papers published on "molecular evolution," as I had clearly acknowledged in Darwin's Black Box. But very few of them concern Darwinian details of irreducibly complex systems, which is exactly the point I was making.

IV. Kenneth Miller

In Finding Darwin's God (Miller 1999) Kenneth Miller is also anxious to show my claims about the literature are not true (or at least are not true now, since the handful of papers he cites in his section "The Sound of Silence" were published after my book appeared). Yet none of the papers he cites deals with irreducibly complex systems.

The first paper Miller discusses concerns two structurally-similar enzymes, both called isocitrate dehydrogenase. The main difference between the two is simply that one uses the organic cofactor NAD while the other uses NADP. The two cofactors are very similar, differing only in the presence or absence of a phosphate group. The authors of the study show that by mutating several residues in either enzyme, they can change the specificity for NAD or NADP. (Dean and Golding 1997) Although the study is very interesting, at the very best it is microevolution of a single protein, not an irreducibly complex system.

The next paper Miller cites concerns "antifreeze" proteins. (Logsdon and Doolittle 1997) Again, these are single proteins that do not interact with other components; they are not irreducibly complex. In fact, they are great examples of what I agree evolution can indeed do -- start with a protein that accidentally binds something (ice nuclei in this case, maybe antibiotics in another case) and select for mutations that improve that property. But they don't shed light on irreducibly complex systems.

Another paper Miller cites concerns the cytochrome c oxidase proton pump (Musser and Chan 1998), which is involved in electron transfer. In humans six proteins take part in the function; in some bacteria fewer proteins are involved. While quite interesting, the mechanism of the system is not known in enough detail to understand what's going on; it remains in large part a black box. Further, the function of electron transfer does not necessarily require multiple protein components, so it is not necessarily irreducibly complex. Finally, the study is not detailed enough to criticize, saying things such as "It makes evolutionary sense that the cytochrome bc1and cytochrome c oxidase complexes arose from a primitive quinol terminal oxidase complex via a series of beneficial mutations." In order to judge whether natural selection could do the job, we have to know what the "series of beneficial mutations" is. Otherwise it's like saying that a five-part mousetrap arose from a one-part mousetrap by a series of beneficial mutations.3

Finally Miller discusses a paper which works out a scheme for how the organic-chemical components of the tricarboxylic acid (TCA) cycle, a central metabolic pathway, may have arisen gradually. (Melendez-Hevia et al. 1996) There are several points to make about it. First, the paper deals with the chemical interconversion of organic molecules, not the enzymes of the pathway or their regulation. As an analogy, suppose someone described how petroleum is refined step by step, beginning with crude oil, passing through intermediate grades, and ending with, say, gasoline. He shows that the chemistry of the processes is smooth and continuous, yet says nothing about the actual machinery of the refinery or its regulation, nothing about valves or switches. Clearly that is inadequate to show refining of petroleum developed step by step. Analogously, someone who is seriously interested in showing that a metabolic pathway could evolve by Darwinian means has to deal with the enzymic machinery and its regulation.

The second and more important point is that, while the paper is very interesting, it doesn't address irreducible complexity. Either Miller hasn't read what I said in my book about metabolic pathways, or he is deliberately ignoring it. I clearly stated in Darwin's Black Box metabolic pathways are not irreducibly complex (Behe 1996) (pp. 141-142; 150-151), because components can be gradually added to a previous pathway. Thus metabolic pathways simply aren't in the same category as the blood clotting cascade or the bacterial flagellum. Although Miller somehow misses the distinction, other scientists do not. In a recent paper Thornhill and Ussery write that something they call serial-direct-Darwinian-evolution "cannot generate irreducibly complex structures." But they think it may be able to generate a reducible structure, "such as the TCA cycle (Behe, 1996 a, b)." (Thornhill and Ussery 2000) In other words Thornhill and Ussery acknowledge the TCA cycle is not irreducibly complex, as I wrote in my book. Miller seems unable or unwilling to grasp that point.

V. A Plea for More Research

In pointing out that not much research has been done on the Darwinian evolution of irreducibly complex biochemical systems I should emphasize that I do not prefer it that way. I would sincerely welcome more research (especially experimental research, such as done by Barry Hall -- see my discussion of Hall's work in the essay on the "acid test" at this website) into the supposed Darwinian origins of the complex systems I described in my book. I fully expect that, as in the field of origin-of-life studies, the more we know, the more difficult the problem will be recognized to be.

References:

Atkins, P. W. (1998). Review of Michael Behe, Darwin's Black Box. http://www.infidels.org/library/modern/peter_atkins/behe.html

 .

Behe, M. J. (1996). Darwin's black box: the biochemical challenge to evolution. (The Free Press: New York.)

Cavalier-Smith, T. (1997). The blind biochemist. Trends in Ecology and Evolution 12, 162-163.

Coyne, J. A. (1996). God in the details. Nature 383, 227-228.

Dean, A. M. and Golding, G. B. (1997). Protein engineering reveals ancient adaptive replacements in isocitrate dehydrogenase. Proc.Natl.Acad.Sci.U.S.A 94, 3104-3109.

Dorit, R. (1997). Molecular evolution and scientific inquiry, misperceived. American Scientist 85, 474-475.

Furutani, Y., Kato, A., Yasue, H., Alexander, L. J., Beattie, C. W., and Hirose, S. (1998). Evolution of the trappin multigene family in the Suidae. J.Biochem. (Tokyo) 124, 491-502.

Gillespie, J. H. (1991). The causes of molecular evolution. (Oxford University Press: New York.)

Hughes, A. L. and Yeager, M. (1997). Molecular evolution of the vertebrate immune system. Bioessays 19, 777-786.

Kusakabe, T., Araki, I., Satoh, N., and Jeffery, W. R. (1997). Evolution of chordate actin genes: evidence from genomic organization and amino acid sequences. Journal of Molecular Evolution 44, 289-298.

Li, W. H. (1997). Molecular evolution. (Sinauer Associates: Sunderland, Mass.)

Logsdon, J. M., Jr. and Doolittle, W. F. (1997). Origin of antifreeze protein genes: a cool tale in molecular evolution. Proc.Natl.Acad.Sci.U.S.A 94, 3485-3487.

Melendez-Hevia, E., Waddell, T. G., and Cascante, M. (1996). The puzzle of the Krebs citric acid cycle: assembling the pieces of chemically feasible reactions, and opportunism in the design of metabolic pathways during evolution. Journal of Molecular Evolution 43 , 293-303.

Miller, K. R. (1999). Finding Darwin's God: a scientist's search for common ground between God and evolution. (Cliff Street Books: New York.)

Musser, S. M. and Chan, S. I. (1998). Evolution of the cytochrome c oxidase proton pump. Journal of Molecular Evolution 46, 508-520.

Pomiankowski, A. The God of the tiny gaps. New Scientist. 9-14-1996.

Ramos, A., Gazapo, T., Murillas, J., Portero, J. L., Valle, A., and Martin, F. (1998). Outbreak of nosocomial diarrhea by Clostridium difficile in a department of internal medicine. Enfermedades Infecciosas Y Microbiologia Clinica 16, 66-69.

Selander, R. K., Clark, A. G., and Whittam, T. S. (1991). Evolution at the molecular level. (Sinauer Associates: Sunderland, Mass.)

Shapiro, J. In the details . . . what? National Review, 62-65. 9-16-1996.

Simonsen, A., Bremnes, B., Ronning, E., Aasland, R., and Stenmark, H. (1998). Syntaxin-16, a putative Golgi t-SNARE. European Journal of Cell Biology 75, 223-231.

Thornhill, R. H. and Ussery, D. W. (2000). A classification of possible routes of Darwinian evolution. Journal of Theoretical Biology 203, 111-116.

Ussery, David (1999). A biochemist's response to "The Biochemical Challenge to Evolution".  http://www.indiana.edu/~ensiweb/behe.rev.html

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Weber, Bruce (1999). Irreducible complexity and the problem of biochemical emergence. Biology & Philosophy 14, 593-605.

Notes:

(1) See my essay on blood clotting  this website

.

(2) In a later version of his review (the website has been updated several times, making it a moving target that is hard to pin down precisely), Ussery did note explicitly that one needed to search abstracts as well as titles to come up with the total of 130 papers. He then noted that a total of just four papers have both words in the title. These papers were not picked up in my search because they either were published after my search was completed in 1995, or because the papers were published before the mid 1980s (which is outside the scope of a CARL search). None of the papers affects the questions discussed in this manuscript.

(3) See my discussion of "mousetrap evolution" on  this website.

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On the royal society's peek under the hood re:Darwinism.

The Road to the Royal Society: The Problems That Matter, the Problems That Don't
Paul Nelson

Starting next Monday, November 7, the Royal Society (RS) will convene a three-day meeting   at its London headquarters that has the potential to rival -- for historical significance --   the (in)famous 1980 Field Museum gathering  on macroevolution, or the  1966 Wistar symposium on mathematical challenges to the neo-Darwinian interpretation of evolution. Structured to include open-ended roundtable discussions, the RS meeting is premised on the view that current textbook evolutionary theory falls far short of what it needs to explain, and that mechanisms and processes outside its customary purview require careful attention.

Like Sherlock Holmes's dog that did not bark in the night, however, the RS meeting is noteworthy for those speakers who were not invited. We do not mean the obvious heretics or ID bad guys, such as Mike Behe, Doug Axe, or Steve Meyer. Their absence from the program is entirely predictable, if one understands that the paradigm actually controlling the boundaries of admissible scientific dissent is not neo-Darwinian evolution, or a scientific theory at all, but the underlying philosophy of materialism or naturalism.

No, the noteworthy uninvited scientists look on casual inspection to be completely respectable, even highly distinguished. Cambridge University paleontologist Simon Conway Morris, for instance, or University of Zurich evolutionary biologist Andreas Wagner, both of whom have written extensively about how neo-Darwinian theory requires revision, are conspicuously absent from the program. Here is a speculation as to why.

Even One Part Per Billion of Teleology is One Part Too Much

Let's start with Wagner. Over the past decade, Wagner has challenged the sufficiency of neo-Darwinian theory, mainly on the grounds that random or undirected changes to any complex functional system are far likelier to end up lost in enormous non-functional regions than they are to land on the very much smaller neighborhoods where novel function or structure occur. In 2011, Wagner wrote:

...we know few of the principles that explain the ability of living things to innovate through a combination of natural selection and random genetic change. Random change by itself is not sufficient, because it does not necessarily bring forth beneficial phenotypes. For example, random change might not be suitable to improve most man-made, technological systems. Similarly, natural selection alone is not sufficient: As the geneticist Hugo de Vries already noted in 1905, 'natural selection may explain the survival of the fittest, but it cannot explain the arrival of the fittest.'"

This criticism of the neo-Darwinian premise of random change should be familiar: one finds the objection featured prominently, for example, in the arguments of the 1966 Wistar participants, not to mention the writings of ID theorists since the early 1980s. Functional complexity and randomness stand fundamentally at odds with each other. If you doubt this, ask yourself if you would like to fly on a passenger jet that had undergone, let's say, one dozen unknown random changes to its flight control system. ("But hey, we're going to take off anyway!" said the demented pilot over the intercom cheerfully, as everyone made for the exits.)

What is probably less familiar is Wagner's solution to the problem of randomness. Probabilistically favored paths, he argues, must exist through sequence and function space, to enable evolutionary processes to move from one novel island to another within the time available -- and those paths must have been built into the universe from the start. As Wagner writes at the conclusion of his 2014 book, The Arrival of the Fittest, "life's creativity draws from a source that is older than life, and perhaps older than time."

Bzzzzzzz! No Royal Society invitation for you, Andreas. Sounds like Platonism, right? And indeed it is, of a sort, anyway, as Wagner readily acknowledges. But if a universal library of Platonic forms enabled biological evolution to succeed, the materialist premise underlying neo-Darwinism must be wrong. ID skeptic and philosophical materialist Massimo Pigliucci can see where ideas of this coloring might be headed: danger, danger, Will Robinson. (He explains this week in "The Neo-Platonic Argument for Evolution Couldn't Be More Wrong.") Teleology is lurking behind those forms.

Teleology detectors also start buzzing loudly when the ideas of Simon Conway Morris come into view. Over the past 15 years, Conway Morris has contended that the "radical historical contingency" premise of neo-Darwinism -- namely, that the existence of Homo sapiens is the unexpected, unpredictable, or strictly one-off outcome of inherently random events -- is false. Rather, evolution was channeled from the start, and a species very much like Homo sapiens, if not H. sapiens itself, was destined to appear in the universe. You are not an accident of the cosmos.

Bzzzzzzz! Teleology jess don't sit right with us folks. No RS invite for Simon.

Philosophical Materialism and Its Invitation List

All joking aside, no one -- least of all, the troublemakers themselves -- really expects ID troublemakers to be invited to speak at major evolution meetings. If that happened with any regularity, or even occasionally, no one would be reading this site, because the intelligent design debate would be (1) pretty much over, (2) never started in the first place, or (3) entirely different in its nature.

But neither Andreas Wagner nor Simon Conway Morris advocates ID; in fact, both are opposed to the idea. Yet even the subtle teleology of their theories is too strong a flavor for the Royal Society. (Let me say I would love to be wrong about this speculation: it would be delightful to learn that Wagner and Conway Morris were invited by the Royal Society to speak, and couldn't make it, or declined the invitation.) Wagner's and Conway Morris's teleology would have been too strong a flavor for Darwin himself, in fact. "If I were convinced that I required such [teleological] additions to the theory of natural selection," Darwin wrote to Lyell in 1859, "I would reject it as rubbish."


But what if it's true -- namely, that teleology, or genuine purpose, is required to explain living things? Then materialism must give way to evidence. That is a problem that matters. Ultimately, the Royal Society, or anyone who wishes truly to understand the universe, must focus on the problems that matter. The ones that don't will take care of themselves.

Decanonising Darwin

So, You Thought Charles Darwin Discovered Natural Selection? Wrong
Jonathan Witt 

After marshaling evidence against the theory of evolution, skeptics sometimes throw Darwin a bone so as not to seem churlish. Hey, we say in essence, natural selection does accomplish things like spreading antibiotic resistance, and Charles Darwin deserves credit for discovering the principle of natural selection even if it isn't the bauplan-building wunderkind he made it out to be.

Yet this gives Darwin too much credit.

Natural Selection Comes to Edinburgh -- Before Darwin

Long before Darwin (or Alfred Russel Wallace), James Hutton, the father of modern geology, propounded the idea of evolution by natural selection. And at least two other men followed on his heels, doing the same well before Darwin articulated the idea.

A retrospect by Paul N. Pearson in the journal Nature reports:

Following the publication of On the Origin of Species in 1859, Charles Darwin learned (and duly acknowledged) that two previous authors had anticipated the theory of evolution by natural selection. The first account to come to light was by Patrick Matthew, who had briefly outlined the mechanism in an appendix to his 1831 book On Naval Timber and Arboriculture. The second was by the physician William Wells, who had speculated on selection and human evolution in 1818.

But some 50 years ago, E. B. Bailey described a still older version of the selection theory from a 1797 manuscript by the geologist James Hutton -- now chiefly famous for his early appreciation of geological time. Unfortunately, this work, entitled the Elements of Agriculture, never appeared in print. Now a more complete, published account has come to light from 1794.

The account appears in a 1794 tome, An Investigation of the Principles of Knowledge. There Hutton wrote the following:

If an organised body is not in the situation and circumstances best adapted to its sustenance and propagation, then, in conceiving an indefinite variety among the individuals of that species, we must be assured, that, on the one hand, those which depart most from the best adapted constitution, will be most liable to perish, while, on the other hand, those organised bodies, which most approach to the best constitution for the present circumstances, will be best adapted to continue, in preserving themselves and multiplying the individuals of their race.

After quoting the passage, Pearson continues:

For example, Hutton describes that in dogs that relied on "nothing but swiftness of foot and quickness of sight" for survival, "the most defective in respect of those necessary qualities, would be the most subject to perish, and that those who employed them in greatest perfection would be best preserved, consequently, would be those who would remain, to preserve themselves, and to continue the race." But if an acute sense of smell was "more necessary to the sustenance of the animal," then "the natural tendency of the race, acting upon the same principle of seminal variation, would be to change the qualities of the animal, and to produce a race of well scented hounds, instead of those who catch their prey by swiftness." The same "principle of variation" must also influence "every species of plant, whether growing in a forest or a meadow."

One might object that this was buried deep in a long book and mostly forgotten. Perhaps, but Hutton was a major scientific figure, and he disseminated his ideas not just by book but also by lecture and conversation.

And as Pearson also notes, Wells and Matthew -- the other two men known to have articulated the idea of evolution of natural selection before Darwin had -- just so happen to have been "educated in Hutton's home town of Edinburgh, a place famous for its scientific clubs and societies."

So here's the lay of the land: Hutton was born, and died, in Edinburgh, attended the University of Edinburgh, and returned to live in the city as an adult, where he was a member of the Royal Society of Edinburgh and a leading figure in the Scottish Enlightenment. This man, the father of modern geology and a fixture of Edinburgh scientific society, propounds a theory of natural selection, and a generation later two other scientists educated in that same scientific community articulate the same idea in their works. (See a post at Genomicron by T. Ryan Gregory for more on Wells's and Matthew's early musing about natural selection.)

Darwin, keep in mind, was also educated at the University of Edinburgh. So four of the earliest articulations of the idea of natural selection are by Edinburgh men, and Darwin is the last of the four.

Darwin Rediscovers

Pearson generously reconstructs this eyebrow-raising coincidence:

It may be more than coincidence that Wells, Matthew and Darwin were all educated in Hutton's home town of Edinburgh.... Studies of Darwin's private notebooks have shown that he came to the selection principle independently of earlier authors, as he always maintained. But it seems possible that a half-forgotten concept from his student days resurfaced afresh in his mind as he struggled to explain the observations of species and varieties compiled on the voyage of the Beagle.

I suspect that's about right. I have a hard time believing that Darwin knowingly and fiendishly stole Hutton's idea and then, even in his notebooks, carefully pretended he'd never heard it before. And I find it hard to believe that the idea of natural selection was not in the air of Edinburgh when Darwin was there as a student, at least in the scientific community. Hutton was too towering a scientific figure, and the idea of natural selection popping up three times in the written works of three separate Edinburgh-trained scientists following in his wake is surely more than coincidence.

In any case, Darwin didn't discover the idea of natural selection. He either resurfaced the idea on his Beagle voyage and didn't realize he was remembering rather than discovering it; or he came upon the idea independently after three other Edinburgh men had articulated it.

And No, Darwin Doesn't Get Points for Theatrical Overstatement

But wasn't it Darwin who first realized the full power of natural selection? In his Nature article, Paul Pearson is careful to note that Hutton did not extend the idea in the way Darwin had. Hutton thought natural selection's effects were limited to generating different races or breeds within a species.

Also, neither William Wells in 1818, nor Patrick Matthew in 1831, applied the idea of natural selection beyond the species level. So the common defense of Darwin at this stage is to remind readers that it's the Victorian gentleman of Down House who gets the credit for discovering the full power and import of natural selection.

But if natural selection actually cannot produce all the biological variety we see around us, if it can only produce variety within species and just a bit beyond the species level (see Michael Behe's The Edge of Evolution), then Darwin was most original precisely where he was wrong.


Darwin did galvanize attention on the process of natural selection, but he did so in much the way those who started the legend of the Seven Cities of Gold encouraged exploration of the American Southwest. In both cases, a tall tale spurred attention and exploration. And in both cases, some worthwhile things were discovered. But the gold? Not so much.

Pre Darwinian design v. Darwinism.

Twenty Years of "Revolutionary" Machines: The Case of ATP Synthase
Evolution News & Views 




It was a Eureka! moment. When Michael Behe saw that diagram of a bacterial flagellum in his biochemistry textbook,  he says, "That's an outboard motor! That's designed. That's no chance assemblage of parts." Thousands of other students must have ignored the obvious, or else meekly accepted what their professors told them, that natural selection was capable of creating such things. But Dr. Behe self-admittedly has a stubborn streak that wouldn't tolerate simplistic answers. From such qualities a   Revolutionary was born. This year we've been celebrating the 20th year since he published  Darwin's Black Box, the book that first put intelligent design on the map.

Twenty years ago another rotary engine was to earn its discoverers the 1997 Nobel Prize in Chemistry. ATP synthase was known previously by its chemical function, but its mode of action was a black box. When Paul Boyer and John E. Walker opened the box and saw a rotary engine one tenth the size of the bacterial flagellum, they were astonished. In the years since, more details have come to light. It's hard to find any paper describing this machine that doesn't call it "amazing" or "remarkable." (Readers may wish to view our animation of ATP synthase, above.) And as Behe discovered in researching the flagellum, hardly anyone tries to explain how it could have come about by neo-Darwinian processes.

John Walker has continued research on this molecular motor since earning the Nobel. Now at age 75, he must be gratified that all the parts have been described, although details about the extraction of torque from a flow of protons remain to be understood. His latest paper, just published by the Proceedings of the National Academy of Sciences  (PNAS) with three colleagues from Cambridge, shows that the surprises keep coming.

Living cells need fuel in the form of adenosine triphosphate, or ATP, to stay alive. This fuel is generated by a molecular machine made of two motors joined by a rotor. One generates rotation by using energy provided by oxidative metabolism or photosynthesis; the other uses energy transmitted by the rotor to make ATP molecules from its building blocks, adenosine diphosphate, or ADP, and inorganic phosphate. The structure has been determined of a fungal machine, isolated from its cellular power stations, the mitochondria, where the machine operates. It provides unsuspected details of the blueprint of the machine and how it works. The working principles of the fungal machine apply to similar machines in all species.
Before now, only about 85 percent of the structure had been determined. That last 15 percent was hidden inside the membrane that anchors the machine. By extracting working motors from a fungus and combining it with counterparts from a cow's mitochondrial version, the team of Vinothkumar, Montgomery, Liu, and Walker was able to glimpse the machinery with unprecedented clarity:

As described here by cryo-EM, we have determined the structure of the entire monomeric F-ATPase complex from the mitochondria of the moderately thermophilic fungus, Pichia angusta, bound to the inhibitory region of the natural bovine inhibitor protein, IF1 (inhibitor of F1-ATPase). This structure fills significant gaps in our knowledge of the mechanism of the F-ATPase. First, it contributes to our understanding of the coupling mechanism by providing unsuspected details of the peripheral stalk and how it is attached to both the catalytic F1-domain and the membrane sector of the enzyme. Second, it provides an independent description of the transmembrane proton pathway for protons, helping both to define common features in the proton translocation mechanism in bacterial and mitochondrial F-ATPases and to explain human pathological mutations in the subunit.
That last clause reinforces Behe's concept of irreducible complexity. Mutations break things. If one of the parts is broken or missing, people get sick or die. Although there are variations in ATP synthase between bacteria and eukaryotes, particularly in the number of c-subunits in the rotor, most parts are "highly conserved" between kingdoms and species. The authors speak of parts that are "strictly conserved" or "absolutely conserved." There are so many essential parts in this machine, it cannot function unless everything is in place and matched for functional interaction.

The authors note that these motors spin at up to 350 Hz. That's a whopping 21,000 rpm! Think about that. Every rotation yields 3 ATP molecules, which are used for most energy-consuming processes in the cell.  a kinesin machine walking down a microtubule, every motion of actin in muscle, every advance of a polymerase translating DNA consumes ATP. If one ATP synthase motor generates 63,000 ATP molecules a minute, imagine how many ATP molecules are being created by thousands of the motors in a single cell. No wonder you can create up to your body weight in ATP in a single busy day.

Walk up to one of these machines in your mind's eye. It's rotating so fast it's a blur. The bottom half spins like a turbine in a hydroelectric power plant, turned not by water but by protons. The upper half assembles the ATP in three pairs of lobes that continuously run "a cycle of substrate binding, ATP formation, and product release. Thus, each 360° rotation produces three molecules of ATP." How could the scientists study something moving so fast? They couldn't. They had to slow it down with an "inhibitor protein" so they could get a good look at it.

They realized that the catalytic upper part rumbles. At top speed, the constant insertion and ejection of substrates generates lateral forces. Without a really steady brace, the machine would vibrate itself out of commission. And a steady brace is just what they found:

Although the relevant interactions are still not fully resolved, the current structure demonstrates that the attachment to the catalytic domain is much more extensive and robust than had been thought, probably involving both the N- and C-terminal domains of the OSCP [oligomycin sensitivity conferral protein] and the N-terminal regions of all three α-subunits. The structure has also provided evidence that, at the lower end of the peripheral stalk (distal from the F1-domain), the hydrophobic N-terminal region of the b-subunit is, as predicted, folded into two transmembrane α-helices, bH1 and part of bH2. It interacts with aH1 and aH2, and bH2 with aH5 and aH6, and most likely, in addition, with the loop between aH3 and aH4. It has also confirmed that the middle part of the peripheral stalk, consisting of the central α-helical pillar that is about 160 Å long and provided by bH2, is augmented by roughly parallel α-helices from subunit d and most likely from subunit h (as in the related bovine F6). Thus, it has the characteristics of a seemingly rigid and inflexible structure.
We include those details to emphasize the complexity of this machine. Without the robust stator and all its interactions, the machine could not handle the lateral forces of its high-speed operation.

But wait; there's more! The central stalk that confers stability also flexes! Why?

The second role of the peripheral stalk is to help keep the a-subunit in contact with the rotating c-ring, possibly by exerting lateral pressure toward the central axis, thereby ensuring the integrity of the transmembrane proton pathway. Subunit ATP8 may contribute here via its C-terminal region. It is known that the longer C-terminal region of bovine ATP8 extends from the membrane into the peripheral stalk, where it interacts with subunits b and d, thereby providing another brace in addition to subunit b to hold subunit a against the rotating c-ring.
In other words, as protons enter the spinning rotor on the bottom half, the stator provides lateral pressure to keep the protons from leaking out. How well-designed must that be?

Another finding concerns "supernumerary subunits" unrelated to the catalytic activity of the machine. Some of these appear to have a role in arranging multiple motors into efficient rows in the mitochondria:

The supernumerary subunits have no known direct role in ATP synthesis, but some of them mediate interactions between monomeric F-ATPase complexes in dimers [pairs of motors] of the complex that are associated in rows along the edges of the mitochondrial cristae.
The authors found another aspect that challenges Darwinian theory. Different versions of the machine work similarly despite different amino-acid sequences (and thus DNA codes) for particular parts. This was unexpected, they say:

A comparison of the current structures of the bacterial and mitochondrial enzymes (Fig. 4) illustrates their known similarities in overall architecture and in the detailed structures of the catalytic and proton translocating regions. Somewhat unexpectedly, the peripheral stalk regions of mitochondrial and bacterial enzymes are also similar, despite significant differences in subunit composition and lack of similarity in sequence of their constituent subunits.... Thus, peripheral stalks from bacteria, chloroplasts, and eukaryotes have similar designs, and presumably similar physical properties, to allow them to perform their roles in ensuring the maintenance of an intact proton pathway in the interface between rotor and stator and in keeping the stator together.
This means that function is conserved even when the sequence is not. If natural selection could not build one irreducibly complex version of a machine, how much less could it build multiple versions?


If there is any aspect of nature that should arouse our awe, it should be to find rotary engines operating with multiple well-matched parts at high speeds at fantastically tiny scales. The details of what Walker's team found can be explored in this open-access paper in PNAS. It doesn't mention "evolution" anywhere, but it does mention design (see above). We hope you will look at the pictures, read the descriptions, and notice their emotional response as they say, "The structure provides more insights into the workings of this amazing machine."