Michael J. Behe A (R)evolutionary Biologist

Articles

In addition to his books and academic writings, Michael Behe writes regularly at Evolution News. Of note, Behe and his colleagues have written at great length in response to objections to his arguments and expanded on many of his key concepts, such as irreducible complexity and the edge of evolution.  
Academic Writing

Academic Writing

Getting There First: An Evolutionary Rate Advantage for Adaptive Loss-of-Function Mutations

Michael J. Behe

Biological Information: New Perspectives, edited by R. J. Marks II, M. J. Behe, W. A. Dembski, and B. L. Gordon. World Scientific Publishing, Hong Kong, 450-473.

Abstract: Over the course of evolution organisms have adapted to their environments by mutating to gain new functions or to lose pre-existing ones. Because adaptation can occur by either of these modes, it is of basic interest to assess under what, if any, evolutionary circumstances one of them may predominate. Since mutation occurs at the molecular level, one must look there to discern if an adaptation involves gain- or loss-of-function. Here I present a simple, deterministic model for the occurrence and spread of adaptive gain-of-function versus loss-of-function mutations, and compare the results to laboratory evolution experiments and studies of evolution in nature. The results demonstrate that loss-of-function mutations generally have an intrinsic evolutionary rate advantage over gain-of-function mutations, but that the advantage depends radically on population size, ratio of selection coefficients of competing adaptive mutations, and ratio of the mutation rates to the adaptive states.

Experimental evolution, loss-of-function mutations, and “the first rule of adaptive evolution”

Michael J. Behe

The Quarterly Review of Biology 85(4) (December 2010), pp. 419-45.

Abstract: Adaptive evolution can cause a species to gain, lose, or modify a function; therefore, it is of basic interest to determine whether any of these modes dominates the evolutionary process under particular circumstances. Because mutation occurs at the molecular level, it is necessary to examine the molecular changes produced by the underlying mutation in order to assess whether a given adaptation is best considered as a gain, loss, or modification of function. Although that was once impossible, the advance of molecular biology in the past half century has made it feasible. In this paper, I review molecular changes underlying some adaptations, with a particular emphasis on evolutionary experiments with microbes conducted over the past four decades. I show that by far the most common adaptive changes seen in those examples are due to the loss or modification of a pre-existing molecular function, and I discuss the possible reasons for the prominence of such mutations.

Simulating evolution by gene duplication of protein features that require multiple amino acid residues

Michael J. Behe, David W. Snoke

Protein Science, Volume 13, Issue 10 (October 2004), pp. 2651-2664.

Abstract: Gene duplication is thought to be a major source of evolutionary innovation because it allows one copy of a gene to mutate and explore genetic space while the other copy continues to fulfill the original function. Models of the process often implicitly assume that a single mutation to the duplicated gene can confer a new selectable property. Yet some protein features, such as disulfide bonds or ligand binding sites, require the participation of two or more amino acid residues, which could require several mutations. Here we model the evolution of such protein features by what we consider to be the conceptually simplest route—point mutation in duplicated genes. We show that for very large population sizes N, where at steady state in the absence of selection the population would be expected to contain one or more duplicated alleles coding for the feature, the time to fixation in the population hovers near the inverse of the point mutation rate, and varies sluggishly with the λth root of 1/N, where λ is the number of nucleotide positions that must be mutated to produce the feature. At smaller population sizes, the time to fixation varies linearly with 1/N and exceeds the inverse of the point mutation rate. We conclude that, in general, to be fixed in 108 generations, the production of novel protein features that require the participation of two or more amino acid residues simply by multiple point mutations in duplicated genes would entail population sizes of no less than 109.

Irreducible Complexity: Obstacle to Darwinian Evolution

Michael J. Behe, David W. Snoke

In Debating Design: from Darwin to DNA, Ruse, M. and Dembski, W.A., eds. (Cambridge University Press: 2004), pp. 352-370.

Reply to My Critics: A Response to Reviews of Darwin’s Black Box: The Biochemical Challenge to Evolution

Michael J. Behe

Biology and Philosophy, Volume 16, (2001) pp. 683–707.

Abstract: In Darwin’s Black Box: The Biochemical Challenge to Evolution I argued that purposeful intelligent design, rather thanDarwinian natural selection, better explains some aspects of the complexity that modern science has discovered at the molecular foundation of life. In the five years since itspublication the book has been widely discussedand has received considerable criticism. Here Irespond to what I deem to be the mostfundamental objections. In the first part of the article I address empirical criticisms based on experimental studies alleging either that biochemical systems I discussed are not irreducibly complex or that similar systems have been demonstrated to be able to evolve byDarwinian processes. In the remainder of the article I address methodological concerns, including whether a claim of intelligent design is falsifiable and whether intelligent design is a permissible scientific conclusion.

Self-Organization and Irreducibly Complex Systems: A Reply to Shanks and Joplin

Michael J. Behe

Philosophy of Science 67, (2000) 155-162.

Abstract:

Some biochemical systems require multiple, well-matched parts in order to function, and the removal of any of the parts eliminates the function. I have previously labeled such systems “irreducibly complex,” and argued that they are stumbling blocks for Darwinian theory. Instead I proposed that they are best explained as the result of deliberate intelligent design. In a recent article Shanks and Joplin analyze and find wanting the use of irreducible complexity as a marker for intelligent design. Their primary counterexample is the Belousov-Zhabotinsky reaction, a self-organizing system in which competing reaction pathways result in a chemical oscillator. In place of irreducible complexity they offer the idea of “redundant complexity,” meaning that biochemical pathways overlap so that a loss of one or even several components can be accommodated without complete loss of function. Here I note that complexity is a quantitative property, so that conclusions we draw will be affected by how well-matched the components of a system are. I also show that not all biochemical systems are redundant. The origin of non-redundant systems requires a different explanation than redundant ones.

An overabundance of long oligopurine tracts occurs in the genome of simple and complex eukaryotes

Michael J. Behe

Nucleic Acids Research, Volume 23, Issue 4 (February 25, 1995), pp. 689–695.

Abstract: A search of sequence information in the GenBank flies shows that tracts of 15–30 contiguous purines are greatly overrepresented in all eukaryotlc species examined, ranging from yeast to human. Such an overabundance does not occur in prokaryotlc sequences. The large Increase in the number of oligopurine tracts cannot be explained as a simple consequence of base composition, nearest-neighbor frequencies, or the occurrence of an overabundance of oligoadenosine tracts. Oligopurine sequences have previously been shown to be versatile structural elements in DNA, capable of occuring in several alternate conformations. Thus the bias toward long oligopurine tracts in eukaryotic DNA may reflect the usefulness of these structurally versatile sequences in cell function.

The protein-folding problem: the native fold determines packing, but does packing determine the native fold?

Michael J. Behe, E E Lattman, and G D Rose

Proceedings of the National Academy of Sciences (PNAS), (May 15, 1991)

Abstract: A globular protein adopts its native three-dimensional structure spontaneously under physiological conditions. This structure is specified by a stereochemical code embedded within the amino acid sequence of that protein. Elucidation of this code is a major, unsolved challenge, known as the protein-folding problem. A critical aspect of the code is thought to involve molecular packing. Globular proteins have high packing densities, a consequence of the fact that residue side chains within the molecular interior fit together with an exquisite complementarity, like pieces of a three-dimensional jigsaw puzzle [Richards, F. M. (1977) Annu. Rev. Biophys. Bioeng. 6, 151]. Such packing interactions are widely viewed as the principal determinant of the native structure. To test this view, we analyzed proteins of known structure for the presence of preferred interactions, reasoning that if side-chain complementarity is an important source of structural specificity, then sets of residues that interact favorably should be apparent. Our analysis leads to the surprising conclusion that high packing densities–so characteristic of globular proteins–are readily attainable among clusters of the naturally occurring hydrophobic amino acid residues. It is anticipated that this realization will simplify approaches to the protein-folding problem.

Binding of p-Nitrophenyl Phosphate and Other Aromatic Compounds by β-Lactoglobulin

Harold M.Farrell Jr., Michael J.Behe, Judith A. Enyeart

Journal of Dairy Science, Volume 70, Issue 2 (February 1987), pp 252-258

Abstract: Results obtained from gel filtration showed that β-lactoglobulin binds p-nitrophenyl phosphate with a stoichiometry of 1 mol of ligand per 18,360 monomer. Circular dichroic spectra confirmed the binding and implicated tryptophan and phenylalanine residues in the interaction. Fluorescence of the protein was quenched on binding also supporting complex formation; analysis of these data indicates that p-nitrophenyl phosphate binds to β-lactoglobulin A with a dissociation constant of 31 μM. The B and C genetic variants of β-lactoglobulin bind p-nitrophenyl phosphate with dissociation constants of 63 and 70 μM, respectively. In addition, a series of other nitrophenyl compounds and pyridoxal phosphate were also investigated by fluorescence analysis and found to bind to the protein. These results are discussed with respect to a recent hypothesis that β-lactoglobulin binds retinol and is structurally related to serum retinol binding protein.

Temperature‐dependent conformational transitions in poly(dG‐dC) and poly(dG‐m5dC)

Michael J. Behe, Gary Felsenfeld, Shousun Chen Szu, Elliot Charney

Biopolymers, Volume 24, Issue2 (February 1985), pp. 289-300

Abstract: The double‐stranded helical complexes of poly(dG‐dC) and of poly(dG‐m5dC) are shown to convert from B‐ to Z‐DNA‐type conformations at moderate or low ionic strengths, lower for the 5‐methyl than for the non‐methyl species, in a highly cooperative temperature‐dependent equilibrium. In the presence of low concentrations of divalent ion, e.g., Mg2+, the temperature at which the B → Z transition occurs is virtually independent of the salt concentration and the B‐conformation is favored at lower temperature, while the Z‐conformation is favored at higher temperature. Since the Debye‐Hückel screening parameter changes rapidly with ionic strength in this region, electrostatic interaction with the free ions appears to be only a small factor in the forces that promote the transition; the temperature dependence must derive principally from effects on the solvent. The temperature dependence at high salt concentrations is also reported.

Evolution News

Evolution News

Important Medical Effects but Modest Mutations

I was asked to address a comment left by a viewer of one of Discovery’s YouTube videos. The comment is:1 Some monkeys have a mutation in a protein called TRIM5 that results in a piece of another, defunct protein being tacked onto TRIM5. The result is a hybrid protein called TRIM5-CypA, which can protect cells from infection with retroviruses such as HIV. Here, a single mutation has resulted in a new protein with a new and potentially vital function. New protein, new function, new information. A bit of Googling shows that the text was taken word-for-word from an old article (2008) on the New Scientist website2 (perhaps by way of intermediate copying). That was during a period when the 150th anniversary of the publication of the Origin of Species was fast approaching, and many

Darwin on Trial — As Fresh and Relevant as Ever

Editor’s note: Phillip E. Johnson, Berkeley law professor and author of Darwin on Trial and other books, died on November 2. Evolution News is sharing remembrances from Fellows of Discovery Institute. Dr. Behe’s most recent book is Darwin Devolves. The following essay appeared originally as the Foreword to the 20th Anniversary edition of Darwin on Trial. Twenty years can be a virtual eternity in modern science, so rapidly do new discoveries accumulate. Twenty years ago the idea of determining the entire DNA sequence of even a tiny living organism such as a bacterium, let alone the genetic endowment of a large animal such as a mammal, seemed a dream. Yet shortly before I wrote this foreword, the 1000th kind of bacterial genome was sequenced. The DNA code of humans was

Darwin Devolves — Evidence Keeps Rolling In

Several new papers have appeared that reinforce key points of my recent book, Darwin Devolves. (Hat tip to Paul Nelson.) The first one — “Quantifying the pathways to life using assembly spaces” — is from a group of theoreticians at Arizona State and the University of Glasgow. (The work was discussed by one of the authors, Sara Imari Walker, at a meeting this July in Italy, “Mind Matters: Intelligence and Agency in the Physical World.” Walker is a frequent collaborator of Paul Davies.)  Reeking of ID The paper investigates phenomena that reek of intelligent design, but the authors ascribe design either to an extrinsic agent or to (presumably undirected) evolution. Herein, we present the foundations of a new theoretical approach to agnostically quantify the amount of

Puppy Dog Eyes for Darwin

A new study published in the Proceedings of the National Academy of Sciences reports on the canine musculature that underlies “puppy dog eyes.” The study has gotten tons of affectionate press, probably because puppies are so darned cute. The story is also cast in an evolutionary framework. The researchers found that a particular muscle abbreviated LAOM is almost always present and well-developed in dogs but is often missing or much less well-developed in wolves. The muscle allows dogs to raise their inner eyebrows in a way that humans find attractive. Since dogs are descended from wolves, the change is ipso facto “evolution.” The authors go on to speculate that the trait was selected over time by humans adopting the dogs that seemed cutest. Well, okay, why not. However,

Déjà Vu at National Review

Some guy once wrote that there’s nothing new under the sun. He must have had political conservatives’ pro-Darwin arguments in mind. Yesterday National Review posted an essay by Razib Khan. (See here and here for more on that.) Khan is a Wikipedia-described atheist, writer, and doctoral student in genetics. He is also a self-described conservative. The essay seeks to assure conservatives that Darwin’s theory is “a crowning achievement of Western civilization and a rejoinder to the modern myths of the Left.” Conservatives should happily embrace whatever is claimed in Darwin’s name because “The science built upon the rock of Charles Darwin’s ideas is a reflection of Western modernity’s commitment to truth as a fundamental value.” What’s more, coos Khan,

Can’t Anybody Here Make Distinctions?

This is the fourth in a series of posts responding to the extended critique of Darwin Devolves by Richard Lenski at his blog, Telliamed Revisited. Professor Lenski is perhaps the most qualified scientist in the world to analyze the arguments of my book. He is the Hannah Distinguished Professor of Microbial Ecology at Michigan State University, a MacArthur (“Genius Award”) Fellow, and a member of the National Academy of Sciences with hundreds of publications. He also has a strong interest in the history and philosophy of science. His own laboratory evolution work is a central focus of the book. I am very grateful to Professor Lenski for taking time to assess Darwin Devolves. His comments will allow interested readers to quickly gauge the relative strength of arguments against the

Thanks, Professor Lenski, the LTEE Is Doing Great!

This is the third in a series of posts responding to the extended critique of Darwin Devolves by Richard Lenski at his blog, Telliamed Revisited. Professor Lenski is perhaps the most qualified scientist in the world to analyze the arguments of my book. He is the Hannah Distinguished Professor of Microbial Ecology at Michigan State University, a MacArthur (“Genius Award”) Fellow, and a member of the National Academy of Sciences with hundreds of publications. He also has a strong interest in the history and philosophy of science. His own laboratory evolution work is a central focus of the book. I am very grateful to Professor Lenski for taking time to assess Darwin Devolves. His comments will allow interested readers to quickly gauge the relative strength of arguments against the

A Response to My Lehigh Colleagues, Part 3

Recently two of my Lehigh University Department of Biological Sciences colleagues published a seven-page critical review of Darwin Devolves in the journal Evolution. As I’ll show below, it pretty much completely misses the mark. Nonetheless, it is a good illustration of how sincere-yet-perplexed professional evolutionary biologists view the data, as well as how they see opposition to their views, and so it is a possible opening to mutual understanding. This is the third of a three-part reply. It continues directly from Part 2. See here for Part 1. Of Course Proteins Are Machines A basic difference between the views of Greg Lang and Amber Rice and my own concerns the nature of the molecular foundation of life. They object that I consider many biochemical systems to be actual

A Response to My Lehigh Colleagues, Part 2

Recently two of my Lehigh University Department of Biological Sciences colleagues published a seven-page critical review of Darwin Devolves in the journal Evolution. As I’ll show below, it pretty much completely misses the mark. Nonetheless, it is a good illustration of how sincere-yet-perplexed professional evolutionary biologists view the data, as well as how they see opposition to their views, and so it is a possible opening to mutual understanding. This is the second of a three-part reply. It continues directly from Part 1. A Limited Accounting of Degradation Greg Lang and Amber Rice cite a number of articles to show that loss-of-function mutations are just a small minority of those found in studies of organisms. However, the truth is that loss of function mutations account

A Response to My Lehigh Colleagues, Part 1

Recently in the journal Evolution, two of my colleagues in the Lehigh University Department of Biological Sciences published a seven-page critical review of Darwin Devolves. As I’ll show below, it pretty much completely misses the mark. Nonetheless, it is a good illustration of how sincere-yet-perplexed professional evolutionary biologists view the data, as well as how they see opposition to their views, and so it is a possible opening to mutual understanding. This is the first of a three-part reply. I’d like to begin by enthusiastically affirming that the co-authors of the review, Greg Lang and Amber Rice, are terrific young scientists. Greg’s research is on the experimental laboratory evolution of yeast, and he’s an associate editor at the Journal of Molecular Evolution.

For Dreams of Darwinian Evolution, First Rule of Adaptive Evolution Is an Insuperable Problem

This is the second in a series of posts responding to the extended critique of Darwin Devolves by Richard Lenski at his blog, Telliamed Revisited. Professor Lenski is perhaps the most qualified scientist in the world to analyze the arguments of my book. He is the Hannah Distinguished Professor of Microbial Ecology at Michigan State University, a MacArthur (“Genius Award”) Fellow, and a member of the National Academy of Sciences. With hundreds of publications, he also has a strong interest in the history and philosophy of science. His own laboratory evolution work is a central focus of the book. I am very grateful to Professor Lenski for taking time to assess Darwin Devolves. His comments will allow interested readers to quickly gauge the relative strength of arguments against the

Bullet Points for Jerry Coyne

As noted here earlier, University of Chicago evolutionary biologist Jerry Coyne reviewed Darwin Devolves for this past Sunday’s Washington Post. As you might expect, it’s written in the venerable style of Richard Dawkins’s review of The Edge of Evolution for the New York Times back in 2007: long on sneering, smearing, and assertion; short to nonexistent on telling readers what the book’s actual arguments are. Alas, Coyne’s piece has too little intellectual content to sustain any real engagement. So I’ll simply proceed from its beginning to its end, with lines from his review in bullet points and italics. My comments follow directly after each.  “intelligent design” arose after opponents of evolution repeatedly failed on First Amendment grounds to get Bible-based

Lessons from Polar Bear Studies

This is the first in a series of posts responding to the extended critique of Darwin Devolves by Richard Lenski at his blog, Telliamed Revisited. Professor Lenski is perhaps the most qualified scientist in the world to analyze the arguments of the book. He is the Hannah Distinguished Professor of Microbial Ecology at Michigan State University, a MacArthur (“Genius Award”) Fellow, and a member of the National Academy of Sciences with hundreds of publications, who also has a strong interest in the history and philosophy of science. His own laboratory evolution work is a central focus of the book. I am very grateful to Professor Lenski for taking time to assess Darwin Devolves. His comments will allow interested readers to quickly gauge the relative strength of arguments against the

Train Wreck of a Review: A Response to Lenski et al. in Science

Last week Science unexpectedly published a scathing pre-publication review,1 by Richard Lenski and two co-authors, of my book Darwin Devolves. I have already posted a short gleeful reply,2 noting their almost complete lack of a response to the book’s main argument, but I had planned to say more. This lengthier post will address such points as they do make, grouped into four themes: supposed counter-examples they cite; stale arguments they bring up; Lenski’s own evolution work; and a clear conclusion to draw. For readers who don’t have time to plow all the way through, here are the take-home lessons: gene-level counter-examples cited by the reviewers are shamelessly question-begging; the reviewers simply gesture at genes and assume they were produced and/or integrated

Coyne and Polar Bears: Why You Should Never Rely on Incompetent Reviewers

Over at his blog, Why Evolution Is True, the eminent evolutionary biologist Jerry Coyne seems unwisely to be relying for his information about Darwin Devolves on one of the fellows who authored the mind-bogglingly shoddy review in Science. Coyne paraphrases some of his and another guy’s claims about my discussion of the polar bear thus: Behe claims that this is true for the polar bear: that the genes that turned the ancestral coat white and changed the fat metabolism were broken genes. But when you examine the paper supposedly supporting Behe’s claim, you find, argue Lents and Hunt, that about half of them don’t seem to have any damaging mutations, and that perhaps “none of the 17 most positively selected genes in polar bears are ‘damaged’.” In fact, we can even

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Featured Articles

A Response to My Lehigh Colleagues

Recently in the journal Evolution, two of my colleagues in the Lehigh University Department of Biological Sciences published a seven-page critical review of Darwin Devolves. As I’ll show below, it pretty much completely misses the mark. Nonetheless, it is a good illustration of how sincere-yet-perplexed professional evolutionary biologists view the data, as well as how they see opposition to their views, and so it is a possible opening to mutual understanding. This is the first of a three-part reply. I’d like to begin by enthusiastically affirming that the co-authors of the review, Greg Lang and Amber Rice, are terrific young scientists. Greg’s research is on the experimental laboratory evolution of yeast, and he’s an associate editor at the Journal of Molecular Evolution.

Here's How to Tell if Scientists are Exaggerating

How much can the public trust confident claims by scientists? Especially about morally or politically or philosophically charged topics? Alas, not so much, as the New York Times Magazine reminds us once again in a recent article, “How Beauty Is Making Scientists Rethink Evolution.” The subtitle asks, “The extravagant splendor of the animal kingdom can’t be explained by natural selection alone — so how did it come to be?” Butterfly Wings Great question. But wait a second — haven’t we all been told that Darwin’s natural selection has already been shown to explain pretty much everything? Forget about pretty flowers or cute puppies. Whole scholarly books have been written claiming that Darwin’s theory explains mind, law, literature, music, and

Waiting Longer for Two Mutations

A roll-up of "Waiting Longer for Two Mutations", Parts 1-5
An interesting paper appeared recently in an issue of the journal Genetics, “Waiting for Two Mutations: With Applications to Regulatory Sequence Evolution and the Limits of Darwinian Evolution” (Durrett, R & Schmidt, D. 2008. Genetics 180: 1501-1509). As the title implies, it concerns the time one would have to wait for Darwinian processes to produce some helpful biological feature (here, regulatory sequences in DNA) if two mutations are required instead of just one. It is a theoretical paper, which uses models, math, and computer simulations to reach conclusions, rather than empirical data from field or lab experiments, as The Edge of Evolution does. The authors declare in the abstract of their manuscript that they aim “to expose flaws in some of Michael Behe’s arguments

Science, E. coli, and the Edge of Evolution

Dear Readers, As I wrote in The Edge of Evolution, Darwinism is a multifaceted theory, and to properly evaluate the theory one has to be very careful not to confuse its different aspects. Unfortunately, stories in the news and on the internet regularly confuse the facets of Darwinism, ignore distinctions made in The Edge of Evolution, or misstate the arguments of intelligent design. The disregard for critical distinctions blurs the issues badly. Over the next few days I will briefly respond to four separate stories 1) A few months ago an interesting paper in Science, “Adaptive mutations in bacteria: high rate and small effects”, by the group of Isabel Gordo demonstrated that beneficial mutations in E. coli were more frequent than had been thought. In fact, the authors

Whether Intelligent Design is Science

A Response to the Opinion of the Court in Kitzmiller vs Dover Area School District
Senior Fellow, Dr. Michael Behe, testified as an expert witness in the Kitzmiller v. Dover Area School Board intelligent design trial in 2005. Judge Jones issued a ruling against the school board and in so doing asserted that intelligent design was not based on science. Dr. Behe disagrees, and here we publish his direct responses to many claims of the Court. Dr. Behe writes:  The Court’s reasoning in section E-4 is premised on: a cramped view of science; the conflation of intelligent design with creationism; the incapacity to distinguish the implications of a theory from the theory itself; a failure to differentiate evolution from Darwinism; and strawman arguments against ID. The Court has accepted the most tendentious and shopworn excuses for Darwinism with great charity

Michael Behe on Molecular Exploitation and the Theory of Irreducible Complexity

NOTE: Comments from biochemist Dr. Michael Behe, Senior Fellow, Discovery Institute’s Center for Science & Culture in response to Science magazine’s forthcoming article “Evolution of Hormone-Receptor Complexity by Molecular Exploitation,” and regarding irreducible complexity, evolution and intelligent design. The study by Bridgham et al (2006) published in the April 7 issue of Science is the lamest attempt yet — and perhaps the lamest attempt that’s even possible — to deflect the problem that irreducible complexity poses for Darwinism.  The bottom line of the study is this: the authors started with a protein which already had the ability to strongly interact with three kinds of steroid hormones (aldosterone, cortisol, and “DOC” ). After introducing

Design for Living

The Basis for a Design Theory of Origins
Bethlehem, Pa. |— IN the wake of the recent lawsuits over the teaching of Darwinian evolution, there has been a rush to debate the merits of the rival theory of intelligent design. As one of the scientists who have proposed design as an explanation for biological systems, I have found widespread confusion about what intelligent design is and what it is not. First, what it isn’t: the theory of intelligent design is not a religiously based idea, even though devout people opposed to the teaching of evolution cite it in their arguments. For example, a critic recently caricatured intelligent design as the belief that if evolution occurred at all it could never be explained by Darwinian natural selection and could only have been directed at every stage by an omniscient creator.

In Defense of the Irreducibility of the Blood Clotting Cascade

Response to Russell Doolittle, Ken Miller and Keith Robison
A system of this kind cannot just be allowed to free-wheel. The success of the coagulation process is due to the finely tuned modulation and regulation of all of the partial proteolytic digestions that occur. Too little or too much activity would be equally damaging for the organism. Regulation is a central issue in blood coagulation.Torben Halkier (1992, 104) I. Summary In Darwin’s Black Box: The Biochemical Challenge to Evolution I devoted a chapter to the mechanism of blood clotting, arguing that it is irreducibly complex and therefore a big problem for Darwinian evolution. Since my book came out, as far as I am aware there have been no papers published in the scientific literature giving a detailed scenario or experiments to show how natural selection could have built the

Teach Evolution

And Ask Hard Questions
BETHLEHEM, Pa. — The debate leading the Kansas Board of Education to abolish the requirement for teaching evolution has about the same connection to reality as the play ‘Inherit the Wind’ had to the actual Scopes trial. In both cases complex historical, scientific and philosophical issues gave way to the simplifying demands of the morality play. If the schoolchildren of Kansas and other states are to receive a good science education, however, then we’ll have to forgo the fun of demonizing each other, take a deep breath and start making a few distinctions. Regrettably, the action of the Kansas board makes that much more difficult. Not only are teachers there now discouraged from discussing evidence in support of Darwin’s theory, results questioning it

A Mousetrap Defended

Response to Critics
Introduction In Darwin’s Black Box: The Biochemical Challenge to Evolution I coined the term “irreducible complexity” in order to point out an apparent problem for the Darwinian evolution of some biochemical and cellular systems. In brief, an irreducibly complex system is one that needs several well-matched parts, all working together, to perform its function. The reason that such systems are headaches for Darwinism is that it is a gradualistic theory, wherein improvements can only be made step by tiny step,(1) with no thought for their future utility. I argued that a number of biochemical systems, such as the blood clotting cascade, intracellular transport system, and bacterial flagellum are irreducibly complex and therefore recalcitrant to gradual construction, and

"A True Acid Test"

Response to Ken Miller
I. Summary In this essay I reply to what I consider to be the most important claim made by any critic of intelligent design: that direct experimental evidence has shown that evolution can indeed generate irreducibly complex biochemical systems. As I will show below, the claim is false. Briefly, in his book Finding Darwin’s God (Harper Collins, 1999) Kenneth Miller quite rightly says that a “true acid test” of Darwinism is to see if it could regenerate an irreducibly complex system that was knocked out using the tools of molecular biology. He then discusses work from the laboratory of Barry Hall of the University of Rochester on the lac operon of the bacterium E. coli. Miller strongly implies that natural selection pieced together the whole pathway in Hall’s

The Sterility of Darwinism

As it struggles to comprehend nature, science sometimes has to completely re-think how the world works. For example, Newton’s laws apply to everyday objects but can’t handle nature’s tiny building blocks. Propelled by this discovery, quantum mechanics overthrew Newton’s theory. Revolutions in biology have included the cell theory of life in the 19th century, as well as the slow realization in this century that cells are composites of enormously complex molecular systems. Newton’s theory remains very useful, and we can still learn many things by studying whole animals or cells. When explaining the nuts and bolts of the world, however, those views must yield to more basic descriptions. A mechanical engineer can’t contradict a physicist on fundamental

Darwin Under the Microscope

Pope John Paul II’s statement last week that evolution is “more than just a theory” is old news to a Roman Catholic scientist like myself. I grew up in a Catholic family and have always believed in God. But beginning in parochial school I was taught that He could use natural processes to produce life. Contrary to conventional wisdom, religion has made room for science for a long time. But as biology uncovers startling complexity in life, the question becomes, can science make room for religion? In his statement, the Pope was careful to point out that it is better to talk about “theories of evolution” rather than a single theory. The distinction is crucial. Indeed, until I completed my doctoral studies in biochemistry, I believed that Darwin’s

Molecular Machines

Experimental Support for the Design Inference
Editor’s Note: This article presents an overview of the key ideas in biochemist Michael Behe’s book Darwin’s Black Box: The Biochemical Challenge to Evolution. A more detailed discussion of these ideas can be found in the book itself. Those interested in the debate over intelligent design in biology should also check out Michael Behe’s extensive responses to various critics. Darwinism’s Prosperity Within a short time after Charles Darwin published The Origin of Species the explanatory power of the theory of evolution was recognized by the great majority of biologists. The hypothesis readily resolved the problems of homologous resemblance, rudimentary organs, species abundance, extinction, and biogeography. The rival theory of the time, which posited

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