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Tuesday, 1 November 2016

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."

Sunday, 30 October 2016

A clash of Titans. XXXV

File under "Well said" XL

"I was really too honest a man to be a politician and live." Socrates

Questioning JEHOVAH God:The Watchtower Society's commentary.

Three Questions People Would Like to Ask God:


SUSAN’S questions about God began at age seven, when her nine-year-old friend Al was hospitalized with polio and confined to an iron lung. She wrote about her experience in the January 6, 2013, issue of The New York Times.

After visiting Al in the hospital, Susan asked her mother: “Why would God do that to a little boy?”

“The priest would say God must have his reasons,” her mother replied, “but I don’t know what they could be.”

Two years later, in 1954, Jonas Salk’s polio vaccine became available, and Susan’s mother suggested that perhaps God had guided his research.

“Well, God should have guided the doctors a long time ago so that Al wouldn’t be in an iron lung,” Susan replied.

Susan summed up the account of her childhood experience by writing: “[Al] was to die only eight years later, by which time I was a committed atheist.”

Like Susan, many people who have suffered from tragedy or have witnessed it are unable to find satisfying answers to their questions about God. Some become atheists. Others may not entirely deny God’s existence, but they become skeptical.

It is not that atheists and skeptics are completely unfamiliar with religion. On the contrary, their experience with religion is often what pushes them toward disbelief. Organized religion, they may feel, has failed to answer life’s tough questions. What kind of questions? Ironically, they are often the same questions that people who claim to have faith in God struggle with. Consider three questions that many people would like to ask God, if given the chance, and the answers that the Bible provides.

1 “WHY DO YOU ALLOW SUFFERING?”

Why ask that question?

‘A loving God would prevent life’s tragedies,’ many conclude.

TO THINK ABOUT: We might find the habits and customs of people from another culture to be strange—perhaps even shocking. We could easily misinterpret their actions. For example, in one culture people feel that maintaining eye contact is a sign of sincerity; in another they see it as a sign of disrespect. Yet even in such cases, there would be no reason to say that they are wrong. Instead, we just need to get to know them better.

Could something similar happen when it comes to understanding God? Many believe that the presence of suffering proves that God does not exist. Others, though, who have come to understand why God has allowed suffering, are confident that he does exist.

WHAT THE BIBLE SAYS: God’s thoughts and ways are different from ours. (Isaiah 55:8, 9) Because of that, his actions, as well as his reasons for waiting before he acts, may at first seem strange to us.

Still, the Bible does not ask us to accept such hollow expressions as “God works in mysterious ways.” Instead, it encourages us to learn more about God, helping us to understand why and when he acts as he does.* We can even draw close to him.—James 4:8.

2 “WHY IS RELIGION FULL OF HYPOCRISY?”
Why ask that question?

‘If God appreciated sincerity,’ some might reason, ‘there wouldn’t be so much pretense among those who claim to worship him.’

TO THINK ABOUT: Imagine a son who rejects his father’s fine upbringing and leaves home to lead a corrupt life. Although the father does not approve, he allows his son to make that choice. Could those who later meet the son rightfully conclude that he had a bad father or even that he had no father at all? Of course not! Likewise, hypocrisy in religion only proves that God allows people to choose their own path in life.

WHAT THE BIBLE SAYS: God hates religious hypocrisy. (Jeremiah 7:29-31; 32:35) At the same time, he allows people to exercise free will. Many who claim to believe in God choose to follow man-made religious teachings and their own brand of morality.—Matthew 15:7-9.

In contrast, religion that God approves is not hypocritical.* Jesus said: “By this all will know that you are my disciples—if you have love among yourselves.” (John 13:35) This love must be “without hypocrisy.” (Romans 12:9) Most religions have failed to live up to that standard. During the 1994 genocide in Rwanda, for example, tens of thousands of religious people slaughtered members of their own faith, simply because those people were of a different tribe. In contrast, Jehovah’s Witnesses did not share in the massacre, and many of them protected fellow believers and others, even risking their life to do so. Such selfless acts prove that religion can be free of hypocrisy.
3 “WHY ARE WE HERE?”
Why ask that question?

Some may wonder: ‘Why do humans live for only 80 or 90 years and then die? What is the purpose of such a brief existence?’


TO THINK ABOUT: Many who do not believe in God still recognize the need to account for the complexity, intricacy, and order of the natural world. They perceive that our planet, other planets, and the moon are configured in just the right way to sustain life on earth. They describe the natural laws that govern the universe as being fine-tuned, perfectly set so that even the slightest alteration would make life on earth impossible.

WHAT THE BIBLE SAYS: While many people view our relatively brief life span as proof that there is no God, the natural world gives ample evidence that there is a Creator. (Romans 1:20) He had a purpose in making these things, and the reason for our existence is closely linked to his purpose. God created humans to live forever on the earth, and he has not abandoned his purpose.—Psalm 37:11, 29; Isaiah 55:11.

While we can discern God’s existence and even some of his qualities through the natural world, God did not intend for us to perceive his purpose that way. For us to know God’s purpose, and hence the meaning of our existence, we need communication from God. In the Bible he ­communicates with us, using simple, direct terms.* JEHOVAH'S Witnesses invite you to take a fresh look at the answers found there.

For the reason why God allows suffering, see chapter 11 of the book What Does the Bible Really Teach? published by Jehovah’s Witnesses. Also available at www.jw.org.

For more information, see chapter 15 of the book What Does the Bible Really Teach? published by Jehovah’s Witnesses. Also available at www.jw.org.

For more information, see chapter 3 of the book What Does the Bible Really Teach? published by Jehovah’s Witnesses. Also available at www.jw.org.

HE FOUND ANSWERS TO HIS QUESTIONS:
As a boy, Harry never understood why a loving God permitted suffering. As a young man, he witnessed firsthand the horrors of war and asked, “If there is an almighty Creator, why would he permit such conditions to afflict so many people, especially innocent children?”
Despite his university education and his examination of various religions, Harry’s questions persisted. After wrestling with the issue for years, he concluded that “perhaps there was no God after all.”


Harry kept an open mind when he heard what the Bible had to say on the matter. He learned that God is not the source of wickedness; rather, God hates it and feels pain when others suffer. (Proverbs 6:16-19; Isaiah 63:9; James 1:13) Harry found out that ultimately all pain and suffering can be traced to humans’ rejecting God’s authority and using their free will to decide for themselves what is right and what is wrong. (Deuteronomy 32:4, 5; James 1:14, 15) He also saw that God did not stand back and take an ‘I told you so’ posture. Instead, God immediately set in motion arrangements to eradicate wickedness and suffering. He will completely undo all the damage that has been done. Harry came to realize that in the meantime, God has provided comfort and support to help individuals endure.—Genesis 3:15; Romans 8:20, 21; Revelation 21:4.
These answers did more than satisfy Harry’s curiosity about a fundamental question. They helped him to weather the emotional turmoil he later experienced when tragedy touched him personally.

For some the circus is no laughing matter.

Saving Darwin?

Does Karl Giberson represent the new face of American evangelicals, “accepting” Darwin?
November 23, 2015 Posted by News under Christian Darwinism, Intelligent Design

As some might hope? Where would that leave evangelicals now that Darwin is being re-evaluated in so many other places?

Dragging in here late, with the last of the religion coverage for the week:

Further to: “Karl Giberson? But at this point who cares what Darwin’s Christian huffs at Huffpo? (We all rate a better informed class of critic. Especially now.)

There we looked at Nazarene process theologian Karl Giberson’s fact-free claims about the Discovery Institute, sponsor of ID theorists …

Sounded odd, but he had been in the files for years. So I went back to see what else one might learn about a figure on the Christian lecture circuit who wants to “save Darwin.”

From my notes:

–  Giberson helped genome mapper Francis Collins found Templeton-funded Darwin apologist group (2008), BioLogos. He has served as vice-president (2008–2010) Collins resigned from BioLogos when appointed NHS director in 2008. However, in 2011, Giberson also left both BioLogos and Eastern Nazarene College in Boston, where he had taught physics.

– He considers Darwin’s theory of evolution to be “confirmed beyond a reasonable doubt by science,” though as Bill Dembski notes, “No theory is that good.”

– In 2008, Karl Giberson wrote a book called Saving Darwin (Harper One, 2008). That positions him clearly, considering that, as far-left The Nation (2012) noted, Christian Alvin Plantinga, non-materialist atheist Thomas Nagel, and materialist atheist Jerry Fodor (well-known philosophers all) agree on doubting Darwin. And it is becoming a trend.

– In the book  co-authored with Collins, The Language of Science and Faith (IVP Books, 2011), readers are told, “We avoid using the ‘E-word.’” [evolution]

Theistic evolution is the belief that God created life using natural processes, working within the natural order, in harmony with its laws. So, why don’t we simply use the term evolution to describe our view? We don’t use the term, at least not at this point in our discussion, because it is associated with negative ideas, including atheism, and many readers would have a constant uncomfortable feeling while thinking about it. The word evolution carries emotional baggage that we are tossing overboard. (pp. 19–20)

Of course, the history of the word “evolution” is not emotional baggage. It is the best evidence for what the word usually means: 78% of evolutionary biologists are pure naturalist atheists.

– Giberson, along with Collins, seems to display a deep attachment to Darwinism that comes out in his theology. For example, in response to the question of whether God planned us in any sense, Giberson and Collins are quite clear in The Language of Science and Faith, that God is not in the details like us:

… we hope readers will agree with us that the relevant part of our origins is not the story of how we acquired the specific details of our body plan—ten fingers, two ears, one nose—or how we lack a marsupial pouch to carry our newborns, or why potty-training takes so long. Nothing about these details is critical to what makes us human. Our humanness is embedded more holistically in our less tangible aspects and could certainly be embodied in creatures that looked nothing like us …

Many may find this thought unsettling and strangely at odds with their understanding of creation, which celebrates that God created us “in his image.”We suggest that this is due to the influence that actual artistic images have had on our view of God and ourselves Because God became incarnate in Jesus, who looks like us, we all too quickly slip into the assumption that God also looks like us. (p. 201, p. 204-5. )

This feels disingenuous. The question isn’t whether God looks like us (a notion with which the Scriptures are clearly comfortable) but whether God intends us to look the way we do. On a Darwinist reckoning, no. On a Christian reckoning, yes.

– In Saving Darwin, Giberson offers a doctrine of the fall of man that most orthodox Christians would not recognize:

Selfishness, in fact, drives the evolutionary process. Unselfish creatures died, and their unselfish genes perished with them. Selfish creatures, who attended to their own needs for food, power, and sex, flourished and passed on these genes to their offspring. After many generations selfishness was so fully programmed in our genomes that it was a significant part of what we now call human nature. ( p. 12.)

In other words, the fall was not a human choice after all. And salvation now means getting the better of that selfish gene.

– More significantly, Giberson also tells us, “Jesus would believe in evolution and so should you.” Jesus thus stands revealed as a mere man among men—a good, honest man who wants to believe the correct things. As it happens, orthodox Christians regard him as the Word who created the entire cosmos. In that case, for Jesus, belief is superfluous. He knows how he made life.

– There has been conflict among Nazarenes in recent years over “emergent” (open, process) theology, as denominational news stories attest, with some asking, about Giberson, “What is this guy doing teaching in an allegedly evangelical school?”

– Process/open theology affirms that

1) love is uniquely exemplified by God, 2) love is the human ethical imperative, 3) God and creatures enjoy free and mutually-influencing relations, 4) and the future is open and not settled.

Open theology affirms that God knows everything that may happen in the future. God knows all possibilities. But God does not know with absolute certainty what every free creature will someday actually do.

Note: This summary is from the page of Thomas Jay Oord, a Nazarene theologian supported by Giberson.

Process theology would be most helpful to anyone promoting Darwinian evolution as an account of the history of the human race among Christians. But most evangelicals have rejected it in the past, due to its sharply diminished view of the sovereignty of God.

However, in 2011 Christianity Today went to considerable trouble to highlight—favourably, it seemed—Giberson’s approach to origins, grounded in process theology. As I used to write for that mag, I took an interest, and will unpack that episode next Sunday if possible.

Meanwhile, is Christianity Today onto something, that a Darwinized human origins story is gaining ground among American evangelicals? Or what?

Note: Giberson currently has a Web site, “Exploring America’s creation-evolution controversy* * probably not going to hell,” which doubtless updates any of the forgoing. – O’Leary for News

On Spaceship earth.

Molecular biology v. Darwinism

Look at All that Goes into Translating a Gene
Evolution News & Views 

In Nature, Marlene Oeffinger gives readers a tour of the ribosome, in particular how it is built. This wonder of the cell translates messenger RNA into proteins. Prepare to be astonished. Here’s the overture:

Production of the cell's translational apparatus, the ribosome, requires the orchestrated function of hundreds of proteins. A structure of its earliest precursor yields unprecedented insight into ribosome formation. [Emphasis added.]
For the first movement, she calls forward an ensemble of scientists led by Markus Kornprobst. They published in the journal Cell a composition about the “pre-ribosome” in eukaryotes. The 3-D structure of this protein, revealed through cryo-electron microscopy, shows that it engulfs the “pre-rRNA” (one of the large, complex RNA molecules that will comprise the ribosome) during construction. The pre-ribosome itself has about 70 assembly factors. Are we sounding irreducibly complex yet? The work has only begun. Oeffinger comments,

The structure reveals, for the first time and in stunning detail, the arrangement of and interactions between many proteins that have been implicated in ribosome assembly, shedding light on a crucial step in early ribosome formation.
Keep in mind we are only looking so far at one crucial step in early ribosome formation.

In the nucleolus, three of four ribosomal RNAs undergo assembly before leaving to work in the cytoplasm. Many other proteins, called ribosome biogenesis factors, will be involved in construction of the pre-ribosome. (Remember, this is just for the pre-ribosome.) As the complexity grows, tension increases in the orchestration:

During its transcription, the long pre-rRNA is assembled with r-proteins, ribosome biogenesis factors and small nucleolar RNAs to form a large 90S pre-ribosome. Following the first stage of pre-rRNA processing, the complex splits into two pre-ribosomes, dubbed pre-40S and pre-60S, which are eventually exported to the cytoplasm where they undergo further maturation steps and then join as 40S and 60S subunits to form the mature ribosome.
Along with the identities of the biogenesis factors came the realization that they numbered a vast 200 to 300 in eukaryotes. In the yeast Saccharomyces cerevisiae, the 90S pre-ribosome alone contains about 70 ribosome biogenesis factors -- almost as many as the number of proteins in a mature ribosome. Hence, a recurring question in the field is: why does ribosome production require so many accessory proteins?

Kornprobst’s team provided a partial answer. All these dozens of proteins are involved in multi-part complexes that work together to build the pre-ribosome.

The requirement for so many extra proteins is explained by the authors' observation that many accessory proteins are arranged around the folded pre-rRNA molecule in previously defined multi-protein complexes called UTP-A, UTP-B and UTP-C. Of these, UTP-A and UTP-B form a scaffold, within which the newly transcribed pre-rRNA is encased and so can be securely processed, modified and assembled with r-proteins.
Explained, perhaps, but not simplified! Oeffinger’s cartoon illustration of these complexes shows the pre-rRNA being threaded into a mold formed by UTP-A, UTP-B, and another factor named U3. “Encased within this mould, the pre-rRNA is safely folded and processed,” she explains. But then, we still only have the Pre-40S and Pre-60S parts of the ribosome constructed.

The role of this scaffold is reminiscent of the way in which chaperone proteins aid folding of other proteins -- a common process that prevents aggregation of proteins into non-functional structures. But although chaperone-mediated protein folding has been long established, the idea of chaperone moulds is new to RNA biology.
Keep that in mind as we talk later about the implications for the origin of life. That little U3 factor, by the way, has two functions. Half of it forms part of the scaffold. The other half is buried deep within the pre-ribosome, “presumably interacting with the pre-rRNA.” It clings to a spacer molecule that gets cleaved from the pre-rRNA. This step “is crucial for the separation of the processed 90S pre-rRNAs into pre-40S and pre-60S complexes, and the progression of ribosome production.”

We’re getting into gory details on purpose. We need to hear the complex counterpoint going on, so that the standing ovation at the end of the composition will be deserved. Remember, we are still just trying to get the “pre-ribosome” finished. Bear with us:

Kornprobst and colleagues also identified the position of the pre-18S rRNA (which will become the rRNA component of the 40S subunit) in their structure. When comparing the pre-18S structure with that of the mature 18S rRNA, the authors observed that the molecule underwent progressive folding, beginning in the domains closest to the site where transcription began. In the 90S, these regions were folded to resemble the mature 18S, whereas domains farther from the transcriptional start site were seemingly still in transitory states. This observation fits well with a previous model of hierarchical rRNA assembly.
All this and we still don’t have a working ribosome yet -- just a pre-ribosome. At this point, though, we can give hearty applause for the first movement of the symphony. Oeffinger is sure thrilled with it.

Kornprobst and colleagues have visualized in detail what, until now, has been seen through electron microscopy only as small black balls on strings of pre-rRNA. Holding a magnifying glass to the early steps of ribosome biogenesis, the authors have finally revealed a role for the multitude of ribosome biogenesis factors as a chaperone mould that provides a secure environment for the processing and folding of pre-rRNA.
The rest of the story is bound to be good. For now, we can ponder these members of a large orchestra playing together, interacting in complex sequential ways, and ask some important questions. Chiefly, could any of this have arisen by chance?

Origin-of-life researchers sometimes leap from random building blocks to a cell, or a replicator, without considering all the factors involved. They think RNA is the magic molecule that can fulfill the dual roles of metabolism and coding. Simplistic accounts, like this one on Phys.org, make it seem an “RNA World” could have preceded the DNA-protein world of life as we know it.

Actual RNA, though, is extremely delicate and nearly impossible to form in water. With copious amounts of guidance and protection by intelligent investigators in a lab, RNA can do simple things like cut itself in half or make crude copies of parts of itself. What it cannot do is code for proteins that can help it assemble. That’s putting the cart before the horse. If it needs proteins to guide and protect it into a hierarchical sequence of stages leading up to a mature ribosome, you can’t invoke raw RNA as a stepping stone for what it has to have to exist.

And no fair attributing sentience to the RNA molecules. In a sense, they’re dumb. They have no goal, and no desire to organize on a cell-making project. Some origin-of-life researchers have a bad habit of envisioning the molecules wanting to get together to form a cell. RNA starts out holding some code and metabolic function, they will say, then it “hands off” the coding to DNA and the metabolism to proteins. For a materialist, that’s cheating.

Italian biochemist Pier Luigi Luisi calls the RNA World scenario a “baseless fantasy.” See his reasons in an interview with Susan Mazur in her book The Origin of Life Circus (pp. 360-363 in particular), where he dismisses it as so unrealistic on several levels that he states that a new start is needed, a “beginner’s mind revolution” away from the RNA-DNA-centric models.

The real problem is to make ordered sequences of amino acids, and of course ordered sequences of nucleic acids – and on that the prebiotic RNA world is absolutely silent. But this view of the prebiotic RNA world is still the most popular. I think it is a case of social science psychology more than science itself (p. 363).
We do know of a cause, however, that is capable of sequencing building blocks into ordered structures. It can organize dozens of complex parts that can interact in detailed ways, in a hierarchical structure, working in sequence toward a goal. That cause (need it be said again?) is intelligence.


Intelligence is not magic. It is a cause we know and use every day. It is a cause that is necessary and sufficient for these kinds of highly ordered operations. Because of this, and because blind chance is utterly incapable of such things, intelligence is the cause that we should use in our scientific explanations.

Is there still cause for doubt?

Do New Ediacaran Fossils Muffle the Cambrian Explosion?
Evolution News & Views 

Whenever the mainstream journals discuss the Cambrian explosion, you can expect three things:

They will try to explain the Cambrian radiation using only unguided material causes like oxygen, temperature or chemistry. Mind and intelligence is forbidden.

They will use anthropomorphic words or appeal to magic, saying that the Cambrian animals appeared, developed, innovated, arose, emerged, filled new ecological niches, or engaged in an evolutionary arms race.

They will completely ignore the argument in Stephen Meyer's book Darwin's Doubt: that the sudden appearance of the Cambrian animals required vast amounts of information expressed hierarchically in new cell types, tissues, organs, and body plans. Since this is beyond the capabilities of neo-Darwinism, and the only cause we know that can produce this kind of information is intelligence, the Cambrian explosion provides powerful evidence for intelligent design.

The journal Geology just published new research dealing with the Ediacaran period -- that lazy world of sessile marine animals that preceded the Cambrian. Let's see if they live up to our expectations or have something new to say. Unless they find a gradual neo-Darwinian path from Precambrian microbes to trilobites, appealing to only material causes, without using magic words, we will have to call Strike Three.

Pour Sand, Add Cement, Mix

Derek E. G. Briggs, a Darwin proponent we called out last October, lends his name to a paper by lead author Lidya Tarhan and three others writing in Geology, "Exceptional preservation of soft-bodied Ediacara Biota promoted by silica-rich oceans." Tarhan's team took a closer look at the type sequence in Australia where the Ediacarans were first identified. Their goal was to understand how such soft creatures could be perfectly preserved as fossils in sandstone. In short, they propose that if you add the right silica cement to the sandy seafloor fast enough, you can get beautiful molds and casts of creatures before they decay.

Here we present evidence from the Ediacara Member of South Australia that Ediacara-style preservation was due to rapid, early-stage precipitation of silica cements, facilitated by the high silica saturation state of the oceans prior to the appearance of prolific silica biomineralizers. An early silicification model provides a coherent, mechanistic and empirically supported explanation for the widespread preservation of soft-bodied organisms of Ediacaran-early Paleozoic age as sandstone casts and molds. The prevalence of early silicification confirms that Ediacara-style fossil assemblages can provide an accurate window into life on the Ediacaran seafloor that can be used to reconstruct critical steps in the development and diversification of early animal ecosystems. [Emphasis added.]
You see right off the bat their focus is on the fossilization process, not on evolution. If you can explain the creatures' preservation, they say, you can "reconstruct critical steps in the development and diversification of early animal ecosystems." But that doesn't follow. It's only a half-truth. You might open a window on the conditions that existed when they were fossilized, but you can't leap from there to a theory of how animals "developed" (euphemism for evolved) and "diversified" (another evolutionary euphemism).

In a nutshell, their premise is that a "taphonomic window" (opportunity for fossilization) opened in Precambrian days that permitted a unique kind of "Ediacaran-style preservation," as can be seen in their beautifully detailed photos of Ediacarans, those mysterious frond-like and pillow-like multicellular colonies illustrated in Illustra's film Darwin's Dilemma. This taphonomic window persisted for "hundreds of millions of years" well into the Ordovician.

So why don't we find Ediacarans after the Cambrian explosion? As the story goes, the new critters used up the cement. Modern oceans are undersaturated in silica, thanks to drawdown by diatoms, sponges, and radiolarians. That wouldn't have been the case back in the Ediacaran. With more dissolved silica in the water, the Precambrian creatures could have been cemented in the sand, forming casts and molds before their tissues decayed away. But later, the silica-hungry newcomers broke the molds; that's why the Ediacarans stopped being preserved. Most likely this reflected a global change in the chemistry of the oceans. What are the implications of their model?

Evidence for early silicification across a wide range of tissue types demonstrates the importance of a global and persistent environmental control on fossilization, i.e., high marine silica concentration. Resolving this long-standing taphonomic paradox allows genuine evolutionary signals (e.g., extinction events) to be distinguished from preservational artifacts. An early silicification taphonomic model indicates that the geologically abrupt appearance and subsequent disappearance of the Ediacara Biota is a valid evolutionary signal. It also provides the first empirical support for the contention that Ediacara-style fossil assemblages truly reflect the diversity, trophic complexity, and community-level ecology of Earth's oldest fossil animal ecosystems.
That's not helpful. For Darwinians, that is. They just said that the abrupt appearance and disappearance of the Ediacarans "is a valid evolutionary signal." Meyer agrees that the Ediacarans appeared explosively (DD, pp. 86-88), and disappeared before the Cambrian explosion. He would only disagree that this is a valid evolutionary signal. Next.

Signals in the Desert

In a desolate area east of Death Valley, a team of scientists found "Two new exceptionally preserved body fossil assemblages from Mount Dunfee, Nevada, USA" (Geology). They were hopeful this site would shed light on the Cambrian explosion, because

Evaluation of hypotheses that relate environmental to evolutionary change across the Ediacaran-Cambrian transition has been hampered by a dearth of sections that preserve both the last appearance of Ediacaran body fossils and the first appearance of Treptichnus pedum [an index fossil for the start of the Cambrian] within carbonate-rich strata suitable for chemostratigraphic studies. Here, we report two new exceptionally preserved latest Ediacaran fossil assemblages from the Deep Spring Formation at Mount Dunfee, Nevada (USA). Further, we report these occurrences in a high-resolution carbon isotope chemostratigraphic framework, permitting correlation on a regional and global scale.
It's a significant find. They've got the latest Ediacaran all the way to the first Cambrian. In between, they identified a "worm world" of ichnofossils (trails and burrows), some small shelly fossil traces, and -- get this -- the "carbon isotope excursion" that evolutionists believe indicates a global change in ocean chemistry and the carbon cycle. Their detailed geological cross-sections show this transition across 100 meters of strata. They can correlate some fossils with similar ones from China. It's a perfect setup to refute Darwin's Doubt.

The data presented here represent the tightest relationship documented to date between the negative δ13C excursion and biological turnover at the Ediacaran-Cambrian boundary, consistent with an environmental disturbance eliminating the last of the Ediacaran biota and paving the way for the Cambrian radiation.
Alas, things are not so simple. Once again, they agree that the Ediacarans went extinct before the Cambrian event. That means those weird sessile creatures didn't have anything to do with the new Cambrian body plans. The Nevada site lacks the frond-like and mattress-like creatures for which the Ediacaran period is best known. As for Cloudina, (once considered a "small shelly fossil" but later reclassified), its classification as a metazoan living in the Ediacaran period seems questionable. It looks like a pile of cups, and has no organs or specialized tissues. It went extinct at the base of the Cambrian, so it cannot have been an ancestor to the new Cambrian phyla. T. pedum is hardly a better contender; it's known by its burrows, and probably lacked hard parts.

The team's geological chart shows lots of strata between the first and second fossil assemblages where transitional forms could be hiding, but they're not there. You have Ediacarans, then blank space, then some tubular things, then the Cambrian index fossil T. pedum higher up. No evolution is obvious. No pre-trilobites. No pre-Anomalocaris. A Darwinian would be batting the air to consider this outcrop helpful for explaining the Cambrian Explosion.

As for that carbon isotope excursion, we've observed that its significance is questionable, since it doesn't correlate tightly around the world. At best it is an effect of the explosion, not the cause of it. Similarly, T. pedum shows up in different places around the world, so it's not exactly a precise marker either. Moreover, their correlations of the few worm-like body fossils with similar ones in China appear dubious. And embarrassingly, one fossil they call Conotobus used to be considered an ancestor to Cloudina, but here in Nevada it appears in strata above its descendent! So as noteworthy as the Nevada site is, it leaves the Cambrian explosion completely unexplained. Another strikeout.

Summing Up

The editors of Geology put the best spin on things that they can. James D. Schiffbauer, a geologist from the University of Missouri, reviews the papers in a piece titled, "The age of tubes: A window into biological transition at the Precambrian-Cambrian boundary." He recalls his delight at reading Wonderful Life, Stephen Jay Gould's marvelous description of the Burgess Shale. He remembers his astonishment at the newly discovered Ediacaran fauna in 1992, wondering what it meant for evolution. He says that the Ediacaran-Cambrian interval "has become one of the most intensively studied time slices in the geological and paleontological records." Then he laments:

The past twenty years have brought significant new data to the table regarding the Ediacaran-Cambrian Earth system and biosphere, but a great many questions remain unanswered. Foremost of which, the pattern(s) of and mechanism(s) for biotic change during the Ediacaran-Cambrian transition are still largely unresolved.
Did these two papers offer new hope? Well, they helped rule out some unworkable ideas, like the "Cheshire Cat" theory that posited the Ediacarans disappeared gradually. No, Schiffbauer admits, "we observe that the fossil record of Ediacara organisms was truncated at this transition -- whether by disappearance of their preservational regime, or by disappearance of the organisms themselves."

As excited as Schiffbauer is about the new Nevada site with its tubular whatzits, he ends with more stories, more magical anthropomorphic talk, and more promissory notes. His last paragraph even discounts some of his own previous publications.

These tubular and other vermiform (worm-like) organisms have recently been implicated in marginalizing and competitively wedging out the classic Ediacaran forms, owing to such ecological novelties as ecosystem engineering and macropredation (Schiffbauer et al., 2016). However, as shown here in direct context with an isotopic record of environmental perturbation, perhaps the combined ecological and environmental stressors provided an insurmountable double whammy, forcing a coda for the classic Ediacarans. While the terminal Ediacaran of the Deep Spring Formation had been previously examined (e.g., Gevirtzman and Mount, 1986; Signor et al., 1987), Smith et al.'s new work has served to prop the window open for further refinement of the taxonomy of these tubular forms, as well as detailed investigation of their taphonomy and paleoecology. These "wormworld" organisms (Schiffbauer et al., 2016) inhabit an important transition, and their continued investigation may yield clarity into the patterns and mechanisms of biotic turnover at the Ediacaran-Cambrian boundary.

OK, when he finds said clarity, we'll be glad to give him another chance at bat. Till then, we must call it as we see it. Strike three.

On suboptimal design re:the human body.

Is the Human Form Riddled with Bad Design?

Jonathan Witt


"You have no idea how awful the human body is," Matan Shelomi begins in a recent Medical Daily article. He goes on to argue that the human body is badly designed in many ways, and that this shows we're the product of blind Darwinian trial-and-error evolution.

"To say that humans were 'intelligently designed' by a 'creator' is to insult God," Shelomi writes, "because our bodies show no intelligent design at all."

Wow, our bodies show no intelligent design at all? Even most atheist biologists grant that living things, including human beings, appear intelligently designed. Professional atheist Richard Dawkins, for instance, went so far as to define biology as the study of things in nature that have the appearance of having been designed for a purpose.

And it's now common knowledge in biology that the human genome is such a sophisticated information-processing system that it makes our most powerful computers look like a Roman abacus by comparison.

But Shelomi sets aside the engineering marvels of the human genome along with countless other marvels of the human body that far outstrip our most advanced human technologies, and instead focuses on a handful of features he insists are badly designed. The glass for him, in other words, isn't 99 percent full; it's one percent empty.

The Sweat Fret

"Like most mammals, we sweat to maintain our temperature, but most animals don't have as many sweat glands as we do," he writes. "We are the least efficient thermoregulators in the mammal world: only apes and (oddly) horses have as many sweat glands, mostly in the armpits, as we do."

Shelomi isn't finished complaining. "The way the eye is shaped, there is a spot that we literally cannot see, and the brain fills in the blanks," he writes. "All vertebrates have this, but not all animals. Octopuses have better-designed eyes that lack a blind spot. If we're so great, why do octopuses have better eyes?"

This is an old favorite of Darwinists. They talk about the "backward wiring" of our eyes. What they neglect to note is that this "backward wiring" improves oxygen flow. And as even professional Darwin defender Richard Dawkins concedes, its negative impact on vision is "actually probably not much."

The eyes of vertebrates (left) and invertebrates such as the octopus (right). 1: Retina 2: Nerve fibers 3: Optic nerve 4: Blind spot

This is yet another example of what engineers refer to as constrained optimization: in this case, a tiny blind spot in exchange for improved oxygen flow. Complaining about it is a bit like complaining that a heavy duty Silverado pickup doesn't have the handling and sporty feel of a Corvette.

The Problem of Pain

But our eyes go bad, and sometimes all too soon. "Then you have all of the eye problems like myopia, glaucoma, cataracts -- why do our eyes fail so often?" Shelomi asks.
"Who designed these faulty things? The answer can't be a God, because a God so incompetent in designing vision sensors isn't worth worshipping."

Notice he is now doing theology: A God worth worshipping would have designed our eyes and the rest of our bodies so that they are free of defects and disease. This element of his argument, in other words, is a version of the problem-of-pain argument: A good and all-powerful creator wouldn't allow pain and suffering in the world.

It's a fair question -- an important question. But if Shelomi is going to invoke a theological argument, he should engage the theological explanations, and for that matter, the sociological and historical record showing pretty clearly that, as Lord Acton famously put it, "Power tends to corrupt."

The Super Predator

That insight is particularly apropos because threaded throughout Shelomi's essay is the assumption that any intelligent designer worth his salt would surely have given humans all sorts of additional powers or capacities found elsewhere in the animal kingdom (for example, the ultraviolet vision he notes that bees possess). But let's pause and ask the question the mad scientists in all those science fiction movies never stop to ask: Is it really a good idea to loose a super-powered subspecies of human onto planet earth?

It's easy to think of reasons why it would actually be pretty stupid to do so. Man already is arguably too effective a predator. Just ask the megafaunal species of the Quaternary extinction event -- the wooly mammoths and giant sloths and such.

Michael Behe v. The philosophers.

Philosophical Objections to Intelligent Design: A Response to Critics
Michael Behe 

I. Is Intelligent Design Falsifiable?

Some reviewers of Darwin's Black Box (Behe 1996) have raised philosophical objections to intelligent design. I will discuss several of these here, beginning with the question of falsifiability. To decide whether, or by what evidence, it is falsifiable, one first has to be sure what is meant by "intelligent design." By that phrase someone might mean that the laws of nature themselves are designed to produce life and the complex systems that undergird it. In fact, something like that position has been taken by the physicist Paul Davies and the geneticist Michael Denton in their recent books, respectively, The Fifth Miracle: The Search for the Origin and Meaning of Life (Davies 1999) and Nature's Destiny: How the Laws of Biology Reveal Purpose in the Universe. (Denton 1998) That stance also seems to pass muster with the National Academy of Sciences:


Many religious persons, including many scientists, hold that God created the universe and the various processes driving physical and biological evolution and that these processes then resulted in the creation of galaxies, our solar system, and life on Earth. This belief, which sometimes is termed "theistic evolution," is not in disagreement with scientific explanations of evolution. Indeed, it reflects the remarkable and inspiring character of the physical universe revealed by [science]. (National Academy In such a view even if we observe new complex systems being produced by selection pressure in the wild or in the laboratory, design would not be falsified because it is considered to be built into natural laws. Without commenting on the merits of the position, let me just say that that is not the meaning I assign to the phrase. By "intelligent design" I mean to imply design beyond the laws of nature. That is, taking the laws of nature as given, are their other reasons for concluding that life and its component systems have been intentionally arranged? In my book, and in this essay, whenever I refer to intelligent design (ID) I mean this stronger sense of design-beyond-laws. Virtually all academic critics of my book have taken the phrase in the strong sense I meant it.

In the strong sense ID is no longer approved by the National Academy, for a specific reason: "[I]ntelligent design . . . [is] not science because [it is] not testable by the methods of science." (National Academy of Sciences 1999, 25) In his review of Darwin's Black Box for Nature, Jerry Coyne, professor of evolutionary biology at the University of Chicago, explains why he also thinks intelligent design is unfalsifiable.

If one accepts Behe's idea that both evolution and creation can operate together, and that the Designer's goals are unfathomable, then one confronts an airtight theory that can't be proved wrong. I can imagine evidence that would falsify evolution (a hominid fossil in the Precambrian would do nicely), but none that could falsify Behe's composite theory. Even if, after immense effort, we are able to understand the evolution of a complex biochemical pathway, Behe could simply claim that evidence for design resides in the other unexplained pathways. Because we will never explain everything, there will always be evidence for design. This regressive ad hoc creationism may seem clever, but it is certainly not science. (Coyne 1996)
Coyne's conclusion that design is unfalsifiable, however, seems to be at odds with the arguments of other reviewers of my book. Clearly, Russell Doolittle (Doolittle 1997), Kenneth Miller (Miller 1999), and others have advanced scientific arguments aimed at falsifying ID. (See my articles on blood clotting and the "acid test" on this web site.) If the results with knock-out mice (Bugge et al. 1996) had been as Doolittle first thought, or if Barry Hall's work (Hall 1999) had indeed shown what Miller implied, then they correctly believed my claims about irreducible complexity would have suffered quite a blow. And since my claim for intelligent design requires that no unintelligent process be sufficient to produce such irreducibly complex systems, then the plausibility of ID would suffer enormously. Other scientists, including those on the National Academy of Science's Steering Committee on Science and Creationism, in commenting on my book have also pointed to physical evidence (such as the similar structures of hemoglobin and myoglobin) which they think shows that irreducibly complex biochemical systems can be produced by natural selection: "However, structures and processes that are claimed to be 'irreducibly' complex typically are not on closer inspection." (National Academy of Sciences 1999, p. 22)

Now, one can't have it both ways. One can't say both that ID is unfalsifiable (or untestable) and that there is evidence against it. Either it is unfalsifiable and floats serenely beyond experimental reproach, or it can be criticized on the basis of our observations and is therefore testable. The fact that critical reviewers advance scientific arguments against ID (whether successfully or not) shows that intelligent design is indeed falsifiable.

In fact, my argument for intelligent design is open to direct experimental rebuttal. Here is a thought experiment that makes the point clear. In Darwin's Black Box (Behe 1996) I claimed that the bacterial flagellum was irreducibly complex and so required deliberate intelligent design. The flip side of this claim is that the flagellum can't be produced by natural selection acting on random mutation, or any other unintelligent process. To falsify such a claim, a scientist could go into the laboratory, place a bacterial species lacking a flagellum under some selective pressure (for mobility, say), grow it for ten thousand generations, and see if a flagellum -- or any equally complex system -- was produced. If that happened, my claims would be neatly disproven.1

How about Professor Coyne's concern that, if one system were shown to be the result of natural selection, proponents of ID could just claim that some other system was designed? I think the objection has little force. If natural selection were shown to be capable of producing a system of a certain degree of complexity, then the assumption would be that it could produce any other system of an equal or lesser degree of complexity. If Coyne demonstrated that the flagellum (which requires approximately forty gene products) could be produced by selection, I would be rather foolish to then assert that the blood clotting system (which consists of about twenty proteins) required intelligent design.

Let's turn the tables and ask, how could one falsify the claim that, say, the bacterial flagellum was produced by Darwinian processes? (Professor Coyne's remarks about a Precambrian fossil hominid are irrelevant since I dispute the mechanism of natural selection, not common descent. I would no more expect to find a fossil hominid out of sequence than he would.) If a scientist went into the laboratory and grew a flagellum-less bacterial species under selective pressure for many generations and nothing much happened, would Darwinists be convinced that natural selection is incapable of producing a flagellum? I doubt it. It could always be claimed that the selective pressure wasn't the right one, or that we started with the wrong bacterial species, and so on. Even if the experiment were repeated many times under different conditions and always gave a negative result, I suspect many Darwinists would not conclude that the claim of its Darwinian evolution was falsified. Of complex biochemical systems Coyne himself writes "we may forever be unable to envisage the first proto-pathways. It is not valid, however, to assume that, because one man cannot imagine such pathways, they could not have existed." (Coyne 1996) If a person accepts Darwinian paths which are not only unseen, but which we may be forever unable to envisage, then it is effectively impossible to make him think he is wrong.

Kenneth Miller announced an "acid test" for the ability of natural selection to produce irreducible complexity. He then decided that the test was passed, and unhesitatingly proclaimed intelligent design falsified ("Behe is wrong"; Miller 1999, 147). But if, as it certainly seems to me, E. coli actually fails the lactose-system "acid test," would Miller consider Darwinism to be falsified? Almost certainly not. He would surely say that the experiment started with the wrong bacterial species, used the wrong selective pressure, and so on. So it turns out that his "acid test" was not a test of Darwinism; it tested only intelligent design. The same one-way testing was employed by Russell Doolittle. He pointed to the results of Bugge et al. (1996) to argue against intelligent design. But when the results turned out to be the opposite of what he had originally thought, Professor Doolittle did not abandon Darwinism.

It seems then, perhaps counterintuitively to some, that intelligent design is quite susceptible to falsification, at least on the points under discussion. Darwinism, on the other hand, seems quite impervious to falsification. The reason for that can be seen when we examine the basic claims of the two ideas with regard to a particular biochemical system like, say, the bacterial flagellum. The claim of intelligent design is that "No unintelligent process could produce this system." The claim of Darwinism is that "Some unintelligent process (involving natural selection and random mutation) could produce this system." To falsify the first claim, one need only show that at least one unintelligent process could produce the system. To falsify the second claim, one would have to show the system could not have been formed by any of a potentially infinite number of possible unintelligent processes, which is effectively impossible to do.

I think Professor Coyne and the National Academy of Sciences have it exactly backwards. A strong point of intelligent design is its vulnerability to falsification. (Indeed, some of my religious critics dislike intelligent design theory precisely because they worry that it will be falsified, and thus theology will appear to suffer another blow from science. See, for example, (Flietstra 1998).) A weak point of Darwinian theory is its resistance to falsification. What experimental evidence could possibly be found that would falsify the contention that complex molecular machines evolved by a Darwinian mechanism?

II. What Is "Irreducible Complexity" and What Does It Signify?

Some reviewers have criticized the concept of irreducible complexity. In Boston Review University of Rochester evolutionary biologist H. Allen Orr agrees that many biological systems are "irreducibly complex," but argues that Darwinian evolution can, at least in theory, directly account for them. However, as I will show, his argument depends on changing the definition of irreducible complexity, which obscures the difficulty.

In his review Orr initially seems to clearly understand what I meant by "irreducible complexity" (quoted earlier). Of the example I used in Darwin's Black Box he writes: "A mousetrap has a clear function (crushing mice) and is made of several parts (a platform, a spring, a bar that does the crushing). If any of these parts is removed, the trap doesn't work. Hence it's irreducibly complex." (Orr 1996) So far, so good. Nonetheless, later in the review he seems to lose hold of the concept:

An irreducibly complex system can be built gradually by adding parts that, while initially just advantageous, become -- because of later changes -- essential. The logic is very simple. Some part (A) initially does some job (and not very well, perhaps). Another part (B) later gets added because it helps A. This new part isn't essential, it merely improves things. But later on, A (or something else) may change in such a way that B now becomes indispensable. This process continues as further parts get folded into the system. And at the end of the day, many parts may all be required. (Orr 1996)
Now, how can we square this paragraph with his initial agreement that if any part of a mousetrap is removed, it doesn't work? Thinking of the mousetrap example, what would correspond to "Some part (A)" that "initially does some job"? In fact, the whole point of the mousetrap example was to show that there is no "part (A)" that will initially do the job. There is no "part (B)" that helps gradually improve "part (A)." A gradual addition of parts is not possible for the mousetrap example (or at least it is very far from obvious that it is possible). Orr later gives a biological example of what he has in mind.

The transformation of air bladders into lungs that allowed animals to breathe atmospheric oxygen was initially just advantageous: such beasts could explore open niches -- like dry land -- that were unavailable to their lung-less peers. But as evolution built on this adaptation (modifying limbs for walking, for instance), we grew thoroughly terrestrial and lungs, consequently, are no longer luxuries -- they are essential. The punch-line is, I think, obvious: although this process is thoroughly Darwinian, we are often left with a system that is irreducibly complex. (Orr 1996)
In Orr's example, however, what is the irreducibly complex system? Is it the swim bladder? The lung? The whole organism? What is the function of the system? Is it "swimming," "breathing," "living," or something else? If we assume he meant that the irreducibly system is, say, the lung, can the lung be considered "a single system," as my definition requires (Behe 1996, p. 39)? What are the parts of the lung without which it will stop working, like a mousetrap without a spring? What is "part (A)" and what is "part (B)"? None of these things is clear at all -- certainly not as clear as the parts and function of a mousetrap.

Let me preface my remaining remarks on this subject by acknowledging that it is often notoriously difficult to rigorously define a concept, as exemplified by the problems encountered in trying to define "science," "life," or "species." Furthermore, I am no philosopher; my end purpose is not to come up with a string of words that completely defines the phrase "irreducible complexity." Rather, my purpose is to focus attention on a class of biochemical systems that pose a particular challenge to Darwinian evolution. The examples I gave in my book -- a mousetrap, cilium, clotting cascade, and so on -- clearly show the necessity for some systems of having a number of discrete parts working together on a single function. The examples, I think, better get across the concept of irreducible complexity than does the definition I offered (Behe 1996, 39), although I think the definition I gave does an adequate job.

With those comments in mind, it can be seen that Orr simply switched concepts in mid-review, as shown by his conflicting remarks quoted above. He jumped from my idea of irreducible complexity to a hazy concept that can perhaps be paraphrased as, "if you remove this part, the organism will eventually die." I'm happy to agree for purposes of discussion that a class of biological phenomena exists which are required for life and which can be changed gradually by natural selection, perhaps even including the swim bladder/lungs Orr mentions (although it is not nearly so obvious as he assumes it to be). It's just that they are not the same types of things as, nor do they somehow obviate the problem of, irreducibly complex systems like mousetraps and cilia. If they were, then Orr could have explained them away as easily as he does swim bladders and lungs. (After all, lung tissue contains cilia plus many, many other components; Orr should thus find it easier to explain cilia alone, rather than cilia-plus-other-components.) Implicitly changing the definition of irreducible complexity, as Orr did, does not tell us how the blood clotting cascade or the bacterial flagellum could have been produced. On the contrary, it distracts our attention from those features of the systems that make them recalcitrant to Darwinian explanation.

Other scientific reviewers have made arguments similar to Orr's which depend on implied definitions of irreducible complexity different from what I used. Writing in the Wall Street Journal Paul Gross compares biochemical systems to cities, where features can be added over time. (Gross 1996) But the analogy is poorly chosen because no city completely stops working when a part is removed, as does a mousetrap or cilium. In Boston Review Douglas Futuyma writes:

In mammals, successive duplications of the beta gene gave rise to the gamma and epsilon chains, which characterize the hemoglobin of the fetus and early embryo respectively, and enhance uptake of oxygen from the mother. Thus a succession of gene duplications, widely spaced through evolutionary time, has led to the "irreducibly complex" system of respiratory proteins in mammals. (Futuyma 1997)
But the several hemoglobins that Futuyma calls the "'irreducibly complex' system of respiratory proteins" in fact do not constitute an irreducibly complex system in my sense of the term. They do not interact with each other, as do the parts of a mousetrap or clotting cascade. They go their separate ways, and for the most part aren't even present at the same time in the organism. Like Allen Orr, Futuyma implicitly switches the meaning of "irreducibly complex." Unfortunately, that does not solve the problem I pointed out, but only obscures it. (As an aside, it is difficult to understand what Futuyma intends by the quotation marks around the phrase irreducibly complex. He can't be quoting me; I never used the term in connection with hemoglobin -- quite the opposite. He may intend them to be taken as "scare quotes," to warn the reader to take the phrase with a grain of salt. But since he is the one who decided to use the term in conjunction with hemoglobins and then to argue against it, the effect is that of setting up a straw man.)

A different question about irreducible complexity is asked by David Ussery on his web site. He notes that, whereas a bacterial flagellum in E. coli requires about 40 different proteins, in H. pylori only 33 are required. Since fewer proteins are required, how can the flagellum be irreducibly complex? Two responses can be made. First, some systems may have parts that are necessary for a function, plus other parts that, while useful, are not absolutely required. Although one can remove the radio from a car and the car will still work, one can't remove the battery or some other parts and have a working car. Ussery himself seems to recognize this when he writes "I would readily admit that there is STILL the problem of the evolution of the 'minimal flagellum,'" (Ussery 1999) but he hopes gene duplication will explain that. Second, one must be careful not to identify one protein with one "part" of a biochemical machine. For example, genes coding for two proteins in one organism may be joined into a single gene in another. A single protein in one organism may be doing the jobs of several polypeptides in another. Or two proteins may combine to do one job (an example is the α- and β-subunits of tubulin, which together make microtubules, a "part" of the eukaryotic cilium).

In his review Ussery mistakenly attributes to me the belief that 240 separate proteins are required for the bacterial flagellum. The confusion apparently arose because at the end of a chapter on the eukaryotic cilium and bacterial flagellum, I stated that a typical cilium contains over two hundred different kinds of proteins. In the next paragraph I wrote, "The bacterial flagellum, in addition to the proteins already discussed, requires about forty other proteins for function." (Behe 1996, p. 72) Although I meant in addition to the flagellar proteins I had discussed a few pages earlier in the chapter, Ussery interpreted the statement to include the several hundred ciliary proteins as well. Ordinarily I would simply overlook such a mistaken attribution, since it should be obvious to informed readers that I wouldn't be lumping the proteins of cilia and flagella together -- after all, they are completely different structures that occur in separate kinds of organisms. In his review in Biology and Philosophy, however, Bruce Weber writes "Behe cannot imagine how anything short of the full 240 components of the flagellum could propel a bacterium. But only 33 proteins are needed to produce a functional flagellum for Helicobacter pylori." (Weber 1999) And Weber then cites Ussery's web site as his source. Since Ussery's misreading of my book seems to be spreading, and since naive readers might be more impressed by a drop from 240 to 33 than by a change from 40 to 33, I have to state for the record that I did not mean the bacterial flagellum requires the proteins of the eukaryotic cilium!

Several reviewers have questioned whether irreducible complexity is necessarily a hallmark of intelligent design. James Shapiro, who has worked on adaptive mutations, writes in the Boston Review (Shapiro 1997) of "some developments in contemporary life science that suggest shortcomings in orthodox evolutionary theory" while arguing for "a growing convergence between biology and information science which offers the potential for scientific investigation of possible intelligent cellular action in evolution." Thus Shapiro appears to think that irreducibly complex biochemical structures might be explained in a non-Darwinian fashion without invoking intelligence beyond the cells themselves. In Biology and Philosophy Bruce Weber (1999) writes that the work of Stuart Kauffman and others on self-organizing phenomena "disrupts the dichotomy Behe has set up of selection or design." Most explicitly, Shanks and Joplin argue in Philosophy of Science that self-organizing phenomena such as the Belousov-Zhabotinsky reaction demonstrate that irreducible complexity is not necessarily a pointer to intelligent design. (Shanks and Joplin 1999) I have responded to Shanks and Joplin's argument in a separate paper. (Behe 2000) Briefly, complexity is a quantitative feature; systems can be more or less complex. Although it produces some complexity, the self-organizing behavior so far observed in the physical world has not produced complexity and specificity comparable to irreducibly complex biochemical systems. There is currently little reason to think that self-organizing behavior can explain biochemical systems such as the bacterial flagellum or blood clotting cascade.

The underlying point of all these criticisms that needs to be addressed, I think, is that it is possible future work might show irreducible complexity to be explainable by some unintelligent process (although not necessarily a Darwinian one). And on that point I agree the critics are entirely correct. I acknowledge that I cannot rule out the possibility future work might explain irreducibly complex biochemical systems without the need to invoke intelligent design, as I stated in Darwin's Black Box. (Behe 1996, 203-204) I agree I cannot prove that studies of self-organization will not eventually show it to be capable of much more than we know now. Nor can I definitively say that Professor Shapiro's ideas about self-designing cells might not eventually prove true, or that currently unknown theories might prevail. But the inability to guarantee the future course of science is common to everyone, not just those who are supportive of intelligent design. For example, no one can warrant that the shortcomings of self-organization will not be exacerbated by future research, rather than overcome, or that even more difficulties for natural selection will not become apparent.

I agree with the commonsense point that no one can predict the future of science. I strongly disagree with the contention that, because we can't guarantee the success of intelligent design theory, it can be dismissed, or should not be pursued. If science operated in such a manner, no theory would ever be investigated, because no theory is guaranteed success forever. Indeed, if one ignores a hypothesis because it may one day be demonstrated to be incorrect, then one paradoxically takes unfalsifiability to be a necessary trait of a scientific theory. Although philosophers of science have debated whether falsifiability is a requirement of a scientific theory, no one to my knowledge has argued that unfalsifiability is a necessary mark.

Because no one can see the future, science has to navigate by the data it has in hand. Currently there is only one phenomenon that has demonstrated the ability to produce irreducible complexity, and that is the action of an intelligent agent. It seems to me that that alone justifies pursuing a hypothesis of intelligent design in biochemistry. In his recent book Tower of Babel: The Evidence against the New Creationism, however, philosopher of science Robert Pennock argues that science should avoid a theory of intelligent design because it must of necessity embrace "methodological naturalism." (Pennock 1999) I have responded to Pennock elsewhere. (Behe 1999) Briefly, science should follow the data wherever it appears to lead, without preconditions. Further, the question of the identity of the designer remains open (see below) -- just as the cause of the Big Bang has been open for decades. Thus, science can pursue theories with extra-scientific implications (such as the Big Bang2 or intelligent design) as far as it can, using its own proper methods.

III. Can We -- May We -- Detect Design in the Cell?

Several reviewers have argued against the legitimacy of reasoning to a conclusion of intelligent design based on biochemical evidence. In the same review discussed above Allen Orr raises an intriguing question of how we apprehend design. He writes:

We know that there are people who make things like mousetraps. (I'm not being facetious here -- I'm utterly serious.) When choosing between the design and Darwinian hypotheses, we find design plausible for mousetraps only because we have independent knowledge that there are creatures called humans who construct all variety of mechanical contraptions; if we didn't, the existence of mousetraps would pose a legitimate scientific problem. (Orr 1997)

So, Orr says, we know mousetraps are designed because we have seen them being designed by humans, but we have not seen irreducibly complex biochemical systems being designed, so we can't conclude they were.

Although he makes an interesting point, I think his reasoning is incorrect. Consider the SETI project (Search for Extraterrestrial Intelligence), in which scientists scan space for radio waves that might have been sent by aliens. Those scientists believe that they can distinguish a designed radio wave (one carrying a message) from the background radio noise of space. However, we have never observed space aliens sending radio messages; we have never observed aliens at all. Nonetheless, SETI workers, funded for years by the federal government, are confident that they can detect intelligently designed phenomena, even if they don't know who produced them.

The relevance to intelligent design in biochemistry is plain. Design is evident in the designed system itself, rather than in pre-knowledge of who the designer is. Even if the designer is an entity quite unlike ourselves, we can still reach a conclusion of design if the designed system has distinguishing traits (such as irreducible complexity) that we know require intelligent arrangement. (One formal analysis of how we come to a conclusion of design is presented by William Dembski in his recent monograph, The Design Inference (Dembski 1998).)

We can probe Orr's reasoning further by asking how we know that something was intelligently designed even if it indeed resulted from human activity. After all, humans engage in all sorts of activities which we would not ascribe to intelligence. For example, in walking through the woods a person might crush plants by his footsteps, accidentally break tree branches and so on. Why do we not ascribe those marks to purposeful activity? On the other hand, when we see a small snare (made of sticks and vines) in the woods, obviously designed to catch a rabbit, why do we unhesitatingly conclude the parts of the snare were purposely arranged by an intelligent agent? Why do we apprehend purpose in the snare but not in the tracks? As Thomas Reid argued in response to the skepticism of David Hume, intelligence is apprehended only by its effects; we cannot directly observe intelligence. (Dembski 1999) We know humans are intelligent by their outward actions. And we discriminate intelligent from non-intelligent human actions by external evidence. Intelligence, human or not, is evident only in its effects.

Michael Ruse in Boston Review raises another objection, saying that scientists qua scientists simply can't appeal to design.

Design is not something you add to science as an equal -- miracles or molecules, take your pick. Design is an interpretation which makes some kind of overall metaphysical or theological sense of experience. (Ruse 1997)
Contrary to Ruse's argument, however, many scientists already appeal to design. I mentioned the SETI program above; clearly those scientists think they can detect design (and nonhuman design at that.) Forensic scientists routinely make decisions of whether a death was designed (murder) or an accident. Archaeologists decide whether a stone is a designed artifact or just a chance shape. Cryptologists try to distinguish a coded message from random noise. It seems unlikely that any of those scientists view their work as trying to make "metaphysical or theological sense of experience." They are doing ordinary science.

Ruse probably meant that scientists can't specifically appeal to God or the supernatural. Evolutionary biologist Douglas Futuyma echoes Ruse's sentiment with rousing rhetoric:

When scientists invoke miracles, they cease to practice science....Behe, claiming a miracle in every molecule, would urge us to admit the defeat of reason, to despair of understanding, to rest content in ignorance. Even as biology daily grows in knowledge and insight, Behe counsels us to just give up. (Futuyma 1997)
In speaking of "miracles" -- relying for rhetorical effect on that word's pejorative connotations when used in a scientific context -- Ruse and Futuyma are ascribing to me a position I was scrupulous in my book to avoid. Although I acknowledged that most people (including myself) will attribute the design to God -- based in part on other, non-scientific judgments they have made -- I did not claim that the biochemical evidence leads ineluctably to a conclusion about who the designer is. In fact, I directly said that, from a scientific point of view, the question remains open. (Behe 1996, 245-250) In doing so I was not being coy, but only limiting my claims to what I think the evidence will support. To illustrate, Francis Crick has famously suggested that life on earth may have been deliberately seeded by space aliens (Crick and Orgel 1973). If Crick said he thought that the clotting cascade was designed by aliens, I could not point to a biochemical feature of that system to show he was wrong. The biochemical evidence strongly indicates design, but does not show who the designer was.

I should add that, even if one does think the designer is God, subscribing to a theory of intelligent design does not necessarily commit one to "miracles." At least no more than thinking that the laws of nature were designed by God -- a view, as we've seen, condoned by the National Academy of Sciences (National Academy of Sciences 1999). In either case one could hold that the information for the subsequent unfolding of life was present at the very start of the universe, with no subsequent "intervention" required from outside of nature. In one case, the information is present just in general laws. In the other case, in addition to general laws, information is present in other factors too. The difference might boil down simply to the question of whether there was more or less explicit design information present at the beginning -- hardly a point of principle.

While we're on the subject of God, another point should be made: A number of prominent scientists, some of whom fault me for suggesting design, have themselves argued for atheistic conclusions based on biological data. For example, Professor Futuyma has written: "Some shrink from the conclusion that the human species was not designed, has no purpose, and is the product of mere mechanical mechanisms -- but this seems to be the message of evolution." (Futuyma 1982) And Russell Doolittle remarks concerning the blood clotting cascade: ". . . no Creator would have designed such a circuitous and contrived system." (Doolittle 1997) It is rather disingenuous, however, for those who use biological data to argue that life shows no evidence of design, to complain when others use biological evidence to argue the opposing view.

IV. "Giving Up" in "Ignorance"

Some scientific reviewers have dismissed the conclusion of design as an "argument from ignorance," or a "God of the gaps" argument. This can take several forms. One form of the objection is presented by University of London evolutionary biologist Andrew Pomiankowski, who writes:

Most biochemists have only a meagre understanding of, or interest in, evolution. As Behe points out, for the thousand-plus scholarly articles on the biochemistry of cilia, he could find only a handful that seriously addressed evolution. This indifference is universal. (Pomiankowski 1996)
So, Pomiankowski argues, we do not have answers because nobody has looked, and biochemists haven't looked because they have little interest in the subject.

Although initially plausible, this interpretation suffers from the fact that there is demonstrable interest in evolution among molecular bioscientists. (One doesn't have to officially call oneself a "biochemist" to address such problems. Molecular biologists, geneticists, immunologists, embryologists -- investigators in all of these disciplines are in a position to work on them.) The authors of the large number of books and papers listed on John Catalano's and David Ussery's web sites are clearly interested in evolution (see my discussion of the evolutionary literature on this web site), as are the authors of numerous other studies that involve sequence comparisons. Since many papers are published in the general area of molecular evolution, we have to ask why there are so few in the particular area of the Darwinian evolution of irreducibly complex systems. Pomiankowski proposes it is because the problem is so difficult (Pomiankowski 1996); I suggest it is difficult because irreducibly complex systems fit poorly within a gradualistic theory such as Darwinism.

A less reasonable form, I think, of the "ignorance" accusation is presented by Neil Blackstone. An evolutionary biologist at Northern Illinois University, Blackstone levels a formal charge at me of an error in logic -- the "argumentum ad ignorantium," as his review is titled (Blackstone 1997). He even cites a philosophy textbook by Irving Copi to give the charge authority. Those who chop logic to rule out a hypothesis, however, should make sure they are on very firm logical ground. Blackstone is not.

Copi defines the fallacy as follows: "The argumentum ad ignorantium is committed whenever it is argued that a proposition is true simply on the basis that it has not been proved false, or that it is false because it has not been proved true." (Copi 1953) But I certainly did not argue that the Darwinian evolution of biochemical complexity is false "simply on the basis" that it has not been proved true. Nor did I say that intelligent design is true "simply on the basis" that it has not been proved false. To lay the groundwork for a proposal of intelligent design I did argue extensively that the blood clotting cascade and other systems have not been explained by Darwinism. That, of course, was necessary because many people have the impression that Darwinian theory has already given a satisfactory account for virtually all aspects of life. My first task was to show the readership that that impression is not correct.

But my argument did not stop there. I spent many pages throughout the book showing that there is a structural reason -- irreducible complexity -- for thinking that Darwinian explanations are unlikely to succeed. Furthermore, I argued that irreducible complexity is a hallmark of intelligent design, took several chapters to explicate how we apprehend design, showed why some biochemical systems meet the criteria, and addressed objections to the design argument. Truncating my case for intelligent design and then saying I commit the fallacy of argumentum ad ignorantium is not, in my opinion, fair play.

Let's explore the intricacies of formal logic a little further. Although Blackstone didn't mention it, Copi has more to say on the argument from ignorance.

A qualification should be made at this point. In some circumstances it can be safely assumed that if a certain event had occurred, evidence of it could be discovered by qualified investigators. In such circumstances it is perfectly reasonable to take the absence of proof of its occurrence as positive proof of its non-occurrence. (Copi 1953)
Although I did not limit my argument to the lack of evidence for the Darwinian evolution of irreducibly complex biochemical systems, when qualified investigators (such as, say, those investigating blood clotting) come up empty, it is "perfectly reasonable" to weigh that against Darwinism. (By itself, of course, it is not positive evidence for design.) Although lack of progress is not "proof" of the failure of Darwinism, it certainly is a significant factor to consider.

In a milder variation of the "argument from ignorance" complaint, other scientific reviewers have objected that an appeal to intelligent design is tantamount to "giving up." For example, in the Forward Emory University evolutionary biologist Marc Lipsitch remarks:

[Behe] correctly suggests that a complete theory of evolution would include an account of how the intricate chemical systems inside our bodies arose (or might have arisen) from inanimate molecules, one step at a time. Mr. Behe's question is a fair one, but instead of suggesting a series of experiments that could address the question, he throws up his hands. (Lipsitch 1996)
Unfortunately, the point is made with circular logic: it depends on the presupposition that life is not designed, which is the point at issue. If life is not designed then, yes, a theory of intelligent design is ultimately a blind alley (if not quite "giving up"). However, if aspects of life are indeed designed, then the search for the putative unintelligent mechanisms that built them is the blind alley. But how do we decide ahead of time which is correct?

We can't decide the correct answer ahead of time. Science can only follow the data where they lead, as they become available.

References:

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

Behe, Michael J. The God of Science: The case for intelligent design. The Weekly Standard, 35-37. 6-7-1999.

Behe, Michael J. (2000). Self-organization and irreducibly complex systems: A reply to Shanks and Joplin. Philosophy of Science 67, 155-162.

Blackstone, N. W. (1997). Argumentum ad ignoratium. Quarterly Review of Biology 72, 445-447.

Bugge, T. H., Kombrinck, K. W., Flick, M. J., Daugherty, C. C., Danton, M. J., and Degen, J. L. (1996). Loss of fibrinogen rescues mice from the pleiotropic effects of plasminogen deficiency. Cell 87, 709-719.

Copi, I. M. (1953). Introduction to logic. (Macmillan: New York.)

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

Crick, Francis and Orgel, L. E. (1973). Directed panspermia. Icarus 19, 341-346.

Davies, P. C. W. (1999). The Fifth Miracle: The Search for the Origin and Meaning of Life. (Simon & Schuster: New York.)

Dembski, W. A. (1998). The design inference: eliminating chance through small probabilities. (Cambridge University Press: Cambridge.)

Dembski, W. A. (1999). Intelligent design: the bridge between science and theology. (Intervarsity Press: Dowbers Grove, Illinois.)

Denton, M. J. (1998). Nature's Destiny: How the Laws of Biology Reveal Purpose in the Universe. (Free Press: New York.)

Doolittle, R. F. A delicate balance. Boston Review [Feb/March], 28-29. 1997.

Flietstra, R. A response to Michael Behe. Books & Culture [Sept/Oct], 37-38. 1998.

Futuyma, D. J. (1982). Science on Trial. (Pantheon Books: New York.)

Futuyma, D. J. Miracles and molecules. Boston Review [Feb/March], 29-30. 1997.

Gross, P. R. The dissent of man. Wall Street Journal, A12. 7-30-1996. New York.

Hall, B. G. (1999). Experimental evolution of Ebg enzyme provides clues about the evolution of catalysis and to evolutionary potential. FEMS Microbiology Letters 174, 1-8.

Lipsitch, M. Fighting an evolutionary war. Forward 9. 10-25-1996.

Maddox, John (1989). Down with the Big Bang. Nature 340, 425.

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

National Academy of Sciences (1999). Science and creationism: a view from the National Academy of Sciences. (National Academy Press: Washington, DC.)

Orr, H. A. Darwin v. intelligent design (again). Boston Review [Dec/Jan], 28-31. 1996.

Orr, H. A. H. Allen Orr responds. Boston Review [Feb/March], 35-36. 1997.

Pennock, R. (1999). Tower of Babel: The evidence against the new creationism. (MIT Press: Cambridge, Massachusetts.)

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

Ruse, M. Enough speculation. Boston Review [Feb/March], 31-32. 1997.

Shanks, Niall and Joplin, Karl H. (1999). Redundant complexity: A critical analysis of intelligent design in biochemistry. Philosophy of Science 66, 268-282.

Shapiro, J. A. A third way. Boston Review [Feb/March], 32-33. 1997.

Ussery, David (1999). A biochemist's response to "The Biochemical Challenge to Evolution". Bios70, 40-45.

Weber, Bruce (1999). Irreducible complexity and the problem of biochemical emergence. Biology & Philosophy14, 593-605.

Notes:

(1) Kenneth Miller leads readers of Finding Darwin's God into thinking such a process would be very easy. He writes, "If microevolution can redesign one gene in fewer than two hundred generations (which in this case took only thirteen days!), what principles of biochemistry or molecular biology would prevent it from redesigning dozens or hundreds of genes over a few weeks or months to produce a distinctly new species? There are no such principles of course..." (Miller 1999, 108) Well, then, why doesn't he just take an appropriate bacterial species, knock out the genes for its flagellum, place the bacterium under selective pressure (for mobility, say), and experimentally produce a flagellum -- or any equally complex system -- in the laboratory? (A flagellum, after all, has only 30-40 genes, not the hundreds Miller claims would be easy for natural selection to rapidly redesign.) If he did that, my claims would be utterly falsified. But he won't even try it because he is grossly exaggerating the prospects of success.

(2) That the Big Bang theory has extra-scientific implications can be seen in the reaction of those who do not welcome the implications. For example, in a 1989 editorial in Nature with the intriguing title "Down with the Big Bang," John Maddox wrote "Creationists and those of similar persuasions seeking support for their theories have ample justification in the doctrine of the Big Bang. That, they might say, is when (and how) the Universe was created." (Maddox 1989)of Sciences 1999, 7)