Design debate:Coming soon to a theatre near you?

Disinherit the Wind: An Interview with Matt Chait About His Play
John G. West February 16, 2016 11:08 AM

I recently reviewed the intriguing new play Disinherit the Wind, which explodes many of the stereotypes about the current debate over Darwin and design. As a follow-up, I thought it would be interesting to talk with actor and playwright Matt Chait (pictured above right) about what inspired him to write and produce the play, which now can be watched on Vimeo and purchased as a book. Below is my interview with him.

Matt is interested in mounting the play again, so if you are interested in bringing it to your city, consider contacting him at complexhollywood@gmail.com.

John West: What is your background in the theater?

Matt Chait: I fell in love with acting during college and attended a wonderful acting conservatory right after graduation, the Neighborhood Playhouse. After the Playhouse I did acting work in New York and on tours, repertory companies, and summer stock. As much as I loved acting, the lifestyle of an actor was very difficult for me. I struggled with the insecurity of it, never knowing before hand if I would be working or where that work would take me. In an attempt to get more stability in my life, I got a masters degree in counseling psychology.

To support myself during this time I began working as an acting teacher at the American Academy of Dramatic Arts in their evening school. When I got my degree, the administrator of the evening school became the director of the entire Academy and offered me full time work teaching and directing. I did that for several years and then moved to Los Angeles where I taught acting at UCLA and began teaching private classes. My classes were successful and I bought the theater complex where I was renting space for my classes. I still own and operate that complex, called The Complex (catchy name), 25 years later. During all of this I have been acting, and producing and directing plays. Aside from a few sketches and adapting a British play for an American audience, however, I had never written a full-length play before Disinherit The Wind.

JW: What inspired you to write Disinherit the Wind? How did you get the idea?

MC: I was touring in a show in 1968 and was in the habit of calling my girlfriend back in New York about once a week (pay phones were much more expensive than cell phones, so daily calls were financially out of the question). During one of these calls she mentioned to me that she had begun doing exercises that "made you high." I couldn't imagine it. I was never fond of drugs -- acting being my drug of choice at the time -- but the notion that exercises could make you high really aroused my curiosity.

The exercises were called yoga (a word that I had never heard before) and I resolved to take some yoga classes as soon as I returned to New York. The classes that I found were taught by someone named Swami Satchidananda or by young people that had been studying with Swami, and they did make you high; at least for me they did. It was a kind of intoxication without toxins and I shortly found myself adapting a vegetarian diet, as Swami suggested, attending his lectures, and going on weekend yoga retreats that he ran from a place in upstate New York. This began a spiritual odyssey for me that lasted eight years and brought me in contact with a number of wonderful teachers.

At the end of this time I felt that I had a strong framework for understanding myself, my relationship to others, and to the universe and a strong sense of why we were here on this planet. I was very comfortable, within myself, with this framework, but not comfortable at all with sharing it with people that did not have a spiritual background.

When I met my wife and, especially, after we had children, we met a lot of people who had none of the spiritual background or experiences that I had had. Some of these people were scientists, as was my brother-in-law. They would say things casually in conversation regarding life and the body and the relationship between the two that made no sense to me at all. Sometimes when I interjected they would look at me as if I were delusional.

Evidently the things that I was saying were as nonsensical to them as their pronouncements were nonsensical to me. Not able to explain myself in a sound bite I held my peace, but as time went by it was not a very peaceful peace. I felt I was holding too much in and, although I was polite and friendly with these people, in a fairly shallow way, I wished that I could explain myself at a deeper level and have more open relationships with them.

I had a phone conversation once with a friend of mine who was a brain scientist. He was trying to explain to me the neo-Darwinian understanding of the beginning of life. It made no sense to me at all. I kept questioning him about it and he kept trying to put it to rest, since it was fairly late and well past his bedtime. I felt I just couldn't let him off the phone, however. I wanted my questions answered and everything that he said was just increasing my bewilderment.

Finally, as a last ditch effort to get me off the phone, he told me to read Richard Dawkins's The Selfish Gene, that Dawkins could explain it much better than he could, and before I had a chance to say anything else he said good night and quickly hung up the phone.

The Selfish Gene was the most infuriating piece of nonsense I had ever read. I could be silent no longer. I had heard about blogs and, although I had never read one, I thought that might be a good way to get my ideas out there in the open. One day I asked my assistant at work if he knew how I could go about starting a blog.

"Sure," he said, "you could start one right now."

"How long would it take?"

"About five minutes."

"You're kidding! How much would it cost?"

"It doesn't cost anything."

So, sure enough, within five minutes -- this was 2006, I believe -- I was the author of a blog. The title of the blog was, and still is, Beyond Evolution; Is There God After Dawkins? This is the origin of the following exchange in Disinherit the Wind, as Dr. Cates, acting as his own lawyer, questions the expert witness, Dr. Robert Hawkins:

CATES: It's a pleasure to meet you Robert. May I call you Robert?

HAWKINS: Not really.

CATES: Okay, Dr. Hawkins, then. It's still a pleasure. I'm familiar with many of your books, your lectures and interviews.

HAWKINS: And how did you find them?

CATES: Inspirational.

HAWKINS: Really? In what way?

CATES: Oh, much in the way that your King George inspired our Declaration of Independence or that Adolf Hitler inspired the United Nations Charter.

The more I wrote the blog, the more I discovered about the specific workings of science.

It really is remarkable how much you can learn, starting with almost no scientific background at all, just by using Google and Wikipedia. The first few years of writing this blog were a very fertile time for me. It wasn't just the excitement of learning all this new biological information but of finding ways to reframe it in a spiritual context.

It was a very natural step from this to Disinherit the Wind, which combined this new passion for writing about the relationship between spirituality and science with my old passion for theater.

JW: In the published script for your play, you thank "scientists Michael Denton, Michael Behe, Stephen C. Meyer, Jonathan Wells, and William Dembski both for their brilliance and for their indomitable courage to speak truth to power." I wondered if you could share with us how these scientists influenced you.

MC: As I said, in the beginning of writing my blog I was getting most of my scientific information from the Internet. I first heard of Discovery Institute when one reader commented that he was sure I was a member of it, with the same emotional intensity that one would accuse someone of being a member of the Nazi Party. I assured him, at that time, that not only was I not a member of DI, but that I had never heard of it until that moment. I don't think he believed me.

My readership was increasing and I was having a ball, fielding comments and expanding my knowledge of new areas of biology and physics. One reader introduced me to another blog with a wider readership called Michael Prescott's Blog: Occasional Thoughts on Matters of Life and Death. Michael became very enthused about my blog and published whole articles from it on his blog. I became an avid reader of Prescott's blog where I always found a lively discussion of important spiritual and scientific issues. Each week Michael had a feature article that first he discussed and then his readers continued to discuss. One week it was an excerpt from Michael Behe's book Darwin's Black Box.

I read Behe, then Denton, Stephen C. Meyer, etc. Each of these books was a revelation. Here was science explained in a way that made perfect sense to me. While Dawkins's writings undermined my spirituality, the writings of the scientists of Discovery Institute enhanced it. So I am greatly indebted to them for all the knowledge and insights that their wonderful, and wonderfully detailed and researched books have provided. They also exposed me to the role that politics plays in the world of science, particularly in the public face of science, and who gets to present that public face, especially in the area of evolution and the origin of life.

When I say that I honor the indomitable courage of the scientists of DI, I am not speaking hyperbolically. I have read enough to understand what happens. I can write whatever I want. I own theaters. No one is going to avoid any theater of mine because the owner does not believe in Darwinian evolution. Peer-reviewed journals will not publish my articles, but they wouldn't publish them anyway. Prestigious universities will not allow me to teach science or lecture there, but that was not part of the future that I envisioned for myself anyway. The scientists of Discovery Institute have put their careers, their financial futures, and their credibility at risk. I have no doubt that in twenty years' time their views will be the predominant ones and neo-Darwinian evolutionary biologists will be as rare as pay phones, but for the moment I believe that it is an act of enormous personal courage for a professional scientist to espouse any idea that challenges Darwinian orthodoxy.

JW: One of the intriguing things about your play is how it breaks stereotypes. For example, in our culture, people often think that there are no scientists who are skeptical of modern Darwinism. They also think that the only religious people are fundamentalist Christians. How does your play subvert those stereotypes?

MC: Before I ever started writing the play, my life experience itself had subverted all these stereotypes. The people that I have met whose words make the most sense to me and whose demeanor and bearing seem to reveal a deep understanding of life; all these wonderful people have deep concerns about neo-Darwinism and all reject materialist philosophy out of hand. I made sure to establish in my play that Dr. Cates and Howard Blair, both of whom present a scientific view in a spiritual context, were unquestionably brilliant scientists. Many religions are mentioned, but not Christian fundamentalism or any kind of fundamentalism.

There is one scene where Dr. Cates talks about some of his spiritual insights and experiences. In that scene I tried to turn the stereotype on its head. Here was the spiritual proponent making perfect sense and the "Darwinian" proponent incapable of hearing a word that the other one was saying. This inability to listen, to even consider another point of view is what we usually thing of as characteristic of fundamentalists. My point is that neo-Darwinism has become just as fundamentalist, just as resistant to change, just as fearful of new information, as the biblical orthodoxy that it replaced.

Discovery Institute is described on Wikipedia as " a non-profit public policy think tank ... best known for its advocacy of the pseudoscience intelligent design." Pseudoscience, indeed! People wonder how I can sustain an intensity of passion throughout the performance of this full-length and wordy play. It is precisely because of this kind of nonsense and all the acts of repression of anti-Darwinian information that I know of, and the demonizing of any one who questions Darwin, and the fraud committed by scientists in their attempts to prove Darwin's theories, and even the suppression before the public of the magnificent complexity of molecular biological life, for fear that it might engender wonder and awe, leading to a belief in design by a transcendent intelligence. All of this nonsense makes my blood boil. Just thinking about it before I perform keeps me razor-focused on unmasking the shallowness and inconsistencies of Hawkins (aka Dawkins) and the defense lawyer's neo-Darwinian thinking.

JW: You premiered the play in a six-week run in Los Angeles last year. What was the general reaction to the play?

MC: Amazing! There were a few fundamentalists, both religious and scientific, who literally could not hear the play. They were there to judge, not to listen. Even before the play began, someone refused to do technical work on it because it went against his neo-Darwinian views. On the other hand, an actor who auditioned for the play, and was effusive about the two pages that he had auditioned with, came back the next day to tell me that, now that he had read the whole thing, he realized that he couldn't do it because it went against his fundamentalist religious beliefs.

The argument of the play, however, is, I think, more compelling when you watch it than when you read it. So many people responded effusively, from atheists, who told me that the play had gotten them thinking and questioning in new ways, to religious people who told me that the play deepened their commitment and understanding of their own religious beliefs.

The biggest surprise was the number of people who told me that I was articulating and making more specific thoughts and feelings that they had entertained for years, but had never expressed. I think in our Darwinian/Freudian/Marxian environment, discussion of the deepest issues about the nature of ourselves and the universe rarely take place. We are under the false impression that omniscient "experts" have already answered these questions and our speculations might seem foolish or childish in a world in which we have been given the impression that these questions have already been answered and that we just don't know enough "scientific" or "psychological" or "economic" information to understand these answers. The "experts" are intentionally culpable, I believe, in giving this impression of omniscience. That is to the detriment of awe and wonder and the free discussion of these most profound issues, which, I think, are really part of our human birthright.

In the newest version of the play, Amanda, who is both the daughter of the chairman of the biology department and the love interest of Howard, the brilliant graduate student, is struck by the familiarity of Howard's ideas. She remembers that when she was a child she often thought about the connectivity of herself with others and the universe and about a sense of herself that was very distinct from her body. Rather than trusting in Howard's intelligence and background as an "expert," she accepts his ideas because they feel so right. They articulate thoughts and intimations that she had already had when she was a young girl, but never expressed in her "scientific" household, for fear that she would sound foolish.

JW: In watching the video of the play, I thought you were outstanding as Professor Bertram Cates. But I also loved the actor you had who played arch-Darwinist Robert Hawkins (above left), who was clearly a stand-in for Richard Dawkins. It's eerie just how much like Dawkins your actor was! Where did you find him?

MC: Two years earlier my friend and I were auditioning actors for a piece that he wrote based on hearings of the House Un-American Activities Committee. The two main roles were Whittaker Chambers, a staunch anti-Communist, who I was playing, and Alger Hiss, a statesman who worked with Roosevelt on the Yalta Agreements at the end of World War II and on the organization of the United Nations. Hiss was suspected of secretly being a Communist and of working to promote the interests of Joseph Stalin over our American interests. Like Dawkins, he was a real person and footage of him in interviews and hearings was available on the Internet. Although the project never got off the ground, there was one actor who made an indelible impression at his audition. He walked in as Alger Hiss; looked like him, talked like him, dressed like him, carried himself like him. It was really remarkable.

Two years later, when I was casting Disinherit the Wind, I contacted Circus-Szalewski, the actor who had impressed me two years earlier, and told him that I would like him to audition for Robert Hawkins who was modeled after Richard Dawkins and that footage existed on the Internet of Dawkins giving lectures and interviews. When he came in for his audition he arrived as Richard Dawkins. Just like he did with Hiss, he walked like him, dressed like him, talked like him. I confessed to him later that I had already cast him in the part before he started the actual audition.

Circus is a great guy and a total pleasure to work with and he is also wonderfully eccentric. He changed his name to Circus because he felt that he embodied a whole circus full of characters within him. He even refers to himself as a circus. For instance, if you ask him how things are going, he will say something like, "The circus has been very busy lately."

He also spoke with an English accent through the entire rehearsal and performance of the play. We kept asking him if he really was from England but he refused to tell us. I did find out his true origins from a friend of his who attended the play and said he had known Circus from childhood. I hope he will forgive me if I let you know that Circus is from Indiana. He is also about one hundred pounds lighter than Dawkins and looks nothing like him. His resemblance to Dawkins is not really eerie as much as it is a product of Circus's skill and hard work.

JW: Did you have any scientists who responded to the play? If so, how did they react?

MC: I can only tell you about the scientists that I spoke with after the play. That may not be a fair sampling, because if there were scientists who did not like the play they probably wouldn't have hung around afterward to talk. But the ones that I do know loved it! It seemed to me like the more they knew about science, the more they appreciated the play. We had several people from Caltech and from the Jet Propulsion Lab who gave us standing ovations. I just had dinner at Caltech two weeks ago with someone who had seen the play and who wants to have it performed there, where it would most likely be viewed by the head of the Jet Propulsion Lab and NASA. Now wouldn't that be exciting!

I find it quite remarkable that the world of theoretical physics is so rich and imaginative and exciting, while the world of theoretical biology does not even exist, because we have been given the impression that Darwin has moved us past the theoretical stage. It seems that physicists are having none of that nonsense.

I should mention two different women who told me, both in tears, almost the identical story after seeing the play. In both cases, their fathers were prominent scientists who, in later life, began to put their scientific understanding in a spiritual framework. Both of them were condemned by the scientific community that had embraced them. The pain inflicted on both these gentlemen was evident in the emotion that their daughters experienced as they told their stories. What they discovered from watching the play and what I discovered from doing the play, is that these ideas are not so "weird" or "isolating" as we once thought. I no longer have any hesitancy in letting people know, if asked, that neo-Darwinian materialist philosophy is myopic nonsense in my opinion and I am happy to explain why.

JW: What are your hopes for the play for the future?

MC: Well, I do hope that it has a future. As I said, I have already rewritten it. We received a couple of sensational reviews that I think will help promote it. I, personally, cannot afford to mount another production, so hopefully I can find another person or some institution that would be interested in producing it. You had suggested, John, that I might rework it into the format of a radio or television debate. That way we would have a cast of three or four as opposed to ten and it would be a much easier play to tour with. It would also open up the possibility of an audio version. If there is anyone reading this who might be interested in mounting a production, please contact me. You can reach me at complexhollywood@gmail.com.

Thank you, John, for giving me this opportunity and thank you, readers, for hearing me out.

The challenge of floral networking to Darwin

Secrets of the Plant "Intranet" Are Coming to Light
Evolution News & Views February 17, 2016 3:09 AM

Most companies are on the Internet these days, but many also keep an internal network called an "intranet" for passing messages within the organization. In both respects, flowering plants and conifers are similarly equipped. They send and receive messages through the air in the form of volatile organic compounds, and through the soil by networks of fungal hyphae. A tree under attack by beetles, for instance, can send out distress calls that other trees in the forest can pick up, giving them time to shore up their defenses.

The plant "intranet" is where things really get interesting. When you think about it, a plant has to keep in touch with itself. The roots underground need to know how things are going up top. The leaves and branches, in turn, need to know if there will be enough water and nutrients in the soil to proceed with costly enterprises like flowering and fruit bearing. Plants have a remarkable communications system that allows rapid signaling and response, comparable to an automated email system.

The messages come in the form of molecules that travel through the vascular bundles in the stems and roots. A paper in Current Biology by Chinese scientists explains part of what happens. In effect, they opened a plant's email and read it. The message was in the form of a transcription factor named HY5, a protein that binds to a gene and controls its transcription rate. Wikigenes says that HY5 "binds directly to the promoters of light-inducible genes, promoting their expression and photomorphogenic development." The email says, "Turn up the heat, guys -- the economy is booming!"

But HY5 should not turn up the heat if the roots aren't ready in the supply room down below. Here's where long-distance communication comes in (long distance, that is, in the context of a small plant). The Chinese researchers found that HY5 migrates from the shoot to the root with its message. They list these four highlights of their findings:

HY5 is essential for light-responsive coordination of the growth of shoots and roots.

Shoot-to-root translocated HY5 mediate light-activated root growth and N uptake.

Carbohydrate photosynthate-induced NRT2.1 expression and N uptake depend upon HY5.

HY5 contributes to maintain balance of C and N metabolism at varying light fluence. [Emphasis added.]

Did you catch that word "translocated"? That's the email system. HY5 travels down the plant's phloem vessels from "shoot to root" -- from top to bottom. Watch for the intranet analogy in the summary of the paper. (Gene names are italicized; protein names are not.)

Coordination of shoot photosynthetic carbon fixation with root inorganic nitrogen uptake optimizes plant performance in a fluctuating environment. However, the molecular basis of this long-distance shoot-root coordination is little understood. Here we show that Arabidopsis ELONGATED HYPOCOTYL5 (HY5), a bZIP transcription factor that regulates growth in response to light, is a shoot-to-root mobile signal that mediates light promotion of root growth and nitrate uptake. Shoot-derived HY5 auto-activates root HY5 and also promotes root nitrate uptake by activating NRT2.1, a gene encoding a high-affinity nitrate transporter. In the shoot, HY5 promotes carbon assimilation and translocation, whereas in the root, HY5 activation of NRT2.1 expression and nitrate uptake is potentiated by increased carbon photoassimilate (sucrose) levels. We further show that HY5 function is fluence-rate modulated and enables homeostatic maintenance of carbon-nitrogen balance in different light environments. Thus, mobile HY5 coordinates light-responsive carbon and nitrogen metabolism, and hence shoot and root growth, in a whole-organismal response to ambient light fluctuations.

The key to any intranet is movement of information-bearing signals. In human email systems, each message has a "header" of metadata signifying the sender and receiver and other information, so that the router on the communications channel knows what to do with it. Then there is the body of the message. The plant's messages, of course, are different from human email written in alphabetic text; they're more like signals indicating "on/off" or "speed up/slow down." They are encoded, though, by molecular text -- the language of DNA. Notice that there's nothing about HY5 that looks like or smells like the meaning of the message. The meaning involves a pre-ordained convention about what the presence of the signal indicates.

It's notable that the same signal can take on different meanings depending on context. The signal causes one reaction in the shoot, but a different reaction in the root. We also see a "To" and "CC" convention. HY5 lands on two genes: HY5 and NRT2.1. There's a unique aspect of this plant intranet in that it's "fluence-rate modulated," i.e., sensitive to message flow: the more signal, the more the response. Maybe that's like getting a flood of tweets.

Most importantly, the message is mobile and routable. HY5 has to carry its message over long distances and traverse numerous branching points to get to the intended recipient. As a result, just as with a corporate intranet, the plant benefits from "whole- organismal response" to what we might call the business environment. Just as a manufacturing plant needs to adjust its production to the availability of raw materials, a living plant must adjust its production to the availability of sunlight and soil nutrients.

The paper reads like a detective story. When they shined light of varying intensities on shoots, the roots grew. Intrigued by the rapid response of a distant part of the plant to the conditions at the top, they thought, Aha! -- "Shoot illumination promotes root growth, most likely via shoot-to-root signaling." It's no wonder that in the introduction to the paper, the scientists described it as "long-distance shoot-root communication." The hunt was on to find the emails.

Experiments honed in on the answer. Mutant plants that didn't grow stronger roots when illuminated were found to have a broken HY5 protein. Other tests confirmed that HY5 is the information-carrying molecule. But does it really travel long distance? To test that, they ran some experiments that first suggested "HY5 transcripts, HY5, or a HY5-dependent signal moves from shoot to root." Then they narrowed it down to HY5 itself. One clever test was fastening two other molecules onto HY5 in the shoots, and finding that none of them made it to the root. Why? "Most likely because its relatively large size prevents shoot-root mobility" -- i.e., the bigger emails clogged the communication channel.

But then, when they sent along a molecular scissors that cut off one of the hangers-on, the custom messages did arrive. Conclusion: "HY5 is a shoot-root phloem-mobile signal...." From there, they studied what the recipient of the "CC" email does (i.e., the gene NRT2.1). The second recipient, they found, promotes a gene that increases nitrate uptake.

In the conclusion, the authors recognized that what they were seeing was a case of real communications networking. The shoot is not just sending some sugar down the pipe for the roots to eat so they will work harder; sucrose is involved, but the HY5 protein transcription factor is a bearer of information. Here's how they express it in scientific jargon:

Although a previous study implicates phloem-mobile sucrose as a cotyledon-derived signal to control primary root elongation during early seedling development in Arabidopsis, the molecular mechanism of the shoot-root long-distance signaling regulating lateral root growth and N uptake remains unclear. Here, we show that HY5 is a shoot-root mobile signal that mediates light-regulated coupling of shoot growth and C assimilation with root growth and N uptake. This coupling is achieved via HY5 regulation of C fixation in the shoot and via sucrose-enhanced promotion of HY5-dependent N uptake in the root. In consequence, HY5 mediates homeostatic regulation of whole-plant C versus whole-plant N status. HY5 is already known to integrate multiple phytohormonal (e.g., abscisic acid) and environmental (e.g., low temperature) signaling inputs in the control of plant growth and development. Our discovery that HY5 is a mobile signal adds further dimension to this knowledge.


This is so cool; everyone should get a chill out of thinking that plants have email. They pass signals coded by a genetic language. They send them through communications channels to recipients. The recipients know what to do with that information. The resemblance to email is uncanny. When ID advocates see very similar concepts to email employed in living organisms like the humble rockcress, we have ample justification to celebrate. "You've got mail!"

Darwinism vs.the real world XXIX

Immune Defense: How Antibodies Work
Howard Glicksman February 16, 2016 4:08 PM

Editor's note: Physicians have a special place among the thinkers who have elaborated the argument for intelligent design. Perhaps that's because, more than evolutionary biologists, they are familiar with the challenges of maintaining a functioning complex system, the human body. With that in mind, Evolution News is delighted to offer this series, "The Designed Body." For the complete series,  see here. Dr. Glicksman practices palliative medicine for a hospice organization.

The body is constantly under attack from powerful microorganisms that, if given the chance, can cause serious infection and death. The body's first layer of defense is the skin and epithelium that lines the respiratory, gastrointestinal, and genitourinary tracts. If the microbes get past these barriers they come up against the body's immune system. The immune system can be divided into two parts.

The first is the innate immune system,which we have from birth and acts in the same way every time it encounters foreign matter. The second is the adaptive immune system, which develops over time and reacts in a specific way to the foreign matter it encounters. Without the first layer of defense or both components of the immune system, our earliest ancestors could not have lived long enough to reproduce.

In earlier articles I've shown how some of the immune cells and proteins of the innate system work together to defend the body from microbial attack. And in my immediately previous article I explored the immune cells of adaptive immunity: the lymphocytes, consisting of helper T-cells, which help other immune cells multiply and improve their killing ability; cytotoxic T-cells, which destroy infected host cells; and B-cells, each of whichproduces millions of identical antibodies. Now let's look at how antibodies -- the proteins of the adaptive immune system -- work to help the body's immune defense with extra intelligence, firepower, and precision accuracy.

Antibodies, also called immunoglobulins or gamma globulins,circulate in the blood as plasma proteins. When the first responders of innate immunity release chemicals to cause inflammation, this allows not only immune cells from the blood to come to the field of battle, but also proteins including immunoglobulins. Antibodies are good at helping other immune cells identify and kill bacteria, neutralizing toxins and limiting the effects of viruses before they can enter a cell. To understand how antibodies work, it is important to first look at their structure.

The antibody molecule consists of four chains of amino acids bonded to each other: two identical pairs of heavy and light chains joined together in the shape of a Y. The two connected heavy chains provide the basis of the Y-shaped structure while each light chain is connected to the outside of the branching portion of the heavy chain. The tips of the Y-shaped antibody molecule consist of the amino acids from the ends of each identical light and heavy chain. Together, they form a specific chemical pattern with a three-dimensional shape that is identical to the antigen receptors on the B-cell that produced them. These tips at the end of the antibody molecule act as antigen-binding sites and are known as the Fab portion (antigen binding fragment).

Human DNA is programmed to produce about one million different heavy chains and about ten thousand different light chains, each with their own unique amino acid pattern. Each B-cell produces only one specific antibody, made up of two pairs of identical heavy and light chains. That means that the body is able of make, as an estimate, over ten billion (one million times ten thousand) different antibodies, each with its distinct combination of binding sites. This gives the body a wide array of specific blood-borne sentries that can detect specific chemical patterns on different invading microbes. The amino acid structure that makes up the base of the Y-shaped antibody molecule remains constant and is called the Fc piece (constant fragment). It is the Fc piece that becomes activated after the Fab portions attach to the specific antigen and makes the antibodies ready for action.

There are a few ways that activated antibodies help the immune system defend the body from infection. As you may recall, the neutrophils and macrophages of the innate immune system have their own receptors that attach to large parts of foreign proteins on invading microorganisms. However, many pathogenic microbes have developed ways to evade detection and destruction by these phagocytic immune cells. They can often make themselves invisible, allowing them to multiply and spread throughout the body. When antibodies' Fab portions attach to the specific antigens on the cell surface of the pathogens, they activate, and the pathogens lose the ability to evade and resist the neutrophils and macrophages. These immune cells have receptors on their surface that attach to the Fc piece of the antibody once it activates, allowing them to see and capture the pathogen. This activity is called enhanced attachment, or opsonization (opsonein, Greek: to buy food); the antibodies help phagocytes attach to microbes and literally make microbial food available to them.

Complement activation is another very important mechanism by which antibodies help kill microbes and infected host cells. As we saw previously, there are three different pathways that activate the complement system. The most efficient one requires a specific antibody to activate its Fc piece by attaching its Fab to a specific antigen on the cell surface of the microbe. Complement attaching to the activated Fc piece triggers the various other complement proteins. These swing into action and sometimes form the Membrane Attack Complex, which drills a hole in the membrane surrounding the microbe and kills it. Some of the fragments of activated complement (e.g., C3b) can attach themselves to microorganisms as well. Neutrophils and macrophages have receptors for C3b that allow them to identify and attach to the pathogen and kill it through opsonization.

In addition to enhanced attachment and complement activation, attaching antibodies to specific antigens on infected host cells activates NK (natural killer) cells.These attach to the activated Fc piece and, in a process called antibody-dependent cellular cytotoxicity (ADCC), release chemicals into the infected cell, causing its death. Moreover, both viruses and bacteria have specific structures on their outer surfaces that allow them to grab human cells and cause infection.

When antibodies attach to the specific antigens on these outer structures, they block the virus or bacteria from attaching to human cells and prevent infection. Furthermore, some bacteria release toxins that must attach to receptors on the surface of host cells to cause damage. When antibodies attach to the specific molecular patterns on these toxins, they block them from attaching to the host cell. Finally, microbes have structures, like flagella and cilia for mobility, which allow them to spread throughout the body. When antibodies attach to antigens on these structures, they cause them to malfunction and inhibit their ability to spread and do damage.

In prior articles I explained that the body's immune system is irreducibly complex, because not only are the innate and adaptive immune systems each needed for survival, but each of their respective components is as well. It also demonstrates natural survival capacity, for our earliest ancestors could never have survived long enough to reproduce if they hadn't had enough properly working first responder immune cells in their tissues, or neutrophils and complement in their blood, or T-cells in their lymphatic systems to prevent infection. So what about antibodies?

Primary immunodeficiencies are genetic conditions a person is born with that result in a poor immune response to infection. One example involves defective B-cell function and an almost total absence of antibodies, called Agammaglobulinemia. Infants receive temporary immunity from their mothers by antibodies crossing through the placenta into their bloodstream. However, after six months, they start to have infections which, if it weren't for modern medicine, would quickly lead to death. This shows that even if our earliest ancestors had had all of the other parts of the immune system working properly, without antibodies, they would never have survived.

Finally, it's important to realize that just like the coagulation cascade and the complement system, this system must turn on only when needed and stay or turn off when not. When antibodies cause the body to overreact to itself or to relatively harmless antigens, this can lead to major debility and even death. Some allergies, such as hay fever and asthma, are caused by certain antibody responses to pollens. When applied to venom from a bee sting, such overreactions can cause anaphylactic shock. When antibodies react inappropriately to normal tissue and turn on the immune system in what is called autoimmune disease, this leads to inflammation, injury, and destruction of different tissues and organs. It's vital not only that all of the components of the immune system be present, but that they be properly controlled.

On December 14, 1799, George Washington was suffering from a severe case of tonsillitis. The theory of the day was that infections were caused by the presence of ill humors in the blood that must be treated by bloodletting. Over several hours, in the midst of an acute infection, his medical attendants removed about five pints of blood. Modern medical practitioners know that infections are caused by germs, not ill humors, and that bleeding someone who has an acute infection is not only likely to cause further weakness but possibly even death.

Even though microbes had been observed under the microscope for almost two hundred years, it was not until the late 19th century that medical science began to recognize that specific germs cause specific diseases. And it was not until Louis Pasteur disproved the theory of spontaneous generation (the belief that life could originate from inanimate matter) that medical science realized that many infectious diseases were indeed preventable.

Clearly, when it came to the understanding of infections, the medical profession of George Washington's day was in error. Moreover, their misguided notions of what caused disease led them to apply the standard treatment of the day (bloodletting), which likely contributed to his death.

This demonstrates how a strongly held, but erroneous, idea can lead to certain assumptions and actions that are detrimental to human development and prosperity. In other words, ideas have consequences. As presented by today's evolutionary biologists, the dominant theory of how life came into being would appear to involve a type of spontaneous generation called abiogenesis. The current thinking is that inanimate matter (chemical elements), under the influence of chance and the laws of nature alone, eventually became multi-system organisms with complex body plans, like us. For vertebrates such as fish, birds, reptiles, amphibians, and mammals, this means that the immune response needed for survival, as described in previous articles, arose solely by these processes.The consequences of this strongly held, but erroneous, idea are pervasive within our culture and affect almost every aspect of human endeavor.


Next time, we'll begin to look at the digestive system and how the body acquires what it needs to live, grow, and work properly.

Religious liberty remains under assault in Russia

Out of Africa II

A brief history of the confederate battle banner

Electrons in slo mo?

Scientists discover electrons moving like honey in graphene
February 12, 2016 by Ben Robinson

Electrons which act like slow-pouring honey have been observed for the first time in graphene, prompting a new approach to fundamental physics.
Electrons are known to move through metals like bullets being reflected only by imperfections, but in graphene they move like in a very viscous liquid, University of Manchester researchers have found.
The possibility of a highly viscous flow of electrons in metals was predicted several decades ago but despite numerous efforts never observed, until now as reported in the journal Science.
The observation and study of this effect allows better understanding of the counterintuitive behaviour of interacting particles, where the human knowledge and developed mathematical techniques are lacking.
One-atom thick material graphene, first explored a decade ago by a team at The University of Manchester, is renowned for its many superlative properties and, especially, exceptionally high electrical conductivity.
It is widely believed that electrons in graphene can move 'ballistically', like bullets or billiard balls scattering only at graphene boundaries or other imperfections.
The reality is not quite so simple, as found by a Manchester group led by Sir Andre Geim in collaboration with Italian researchers led by Prof Marco Polini.
They observed that the electric current in graphene did not flow along the applied electric field, as in other materials, but travelled backwards forming whirlpools where circular currents appeared.Such behaviour is familiar for conventional liquids such as water which makes whirlpools when flowing around obstacles, for example, in rivers.
The scientists measured the viscosity of this strange new liquid in graphene, which consists not of water molecules but electrons. To the researchers surprise, the electron fluid can be 100 times more viscous than honey, even at room temperature.
The scientific breakthrough is important for understanding of how materials work at increasing smaller sizes required by the semiconducting industry because such whirlpools are more likely to appear at micro and nanoscale.
The observation also questions our current understanding of the physics of highly conductive metals, especially graphene itself.
The simultaneous existence of such seemingly incompatible properties, with electrons behaving like bullets and a liquid in the same material prompts a fundamental rethinking about our understanding of materials properties.
Professor Polini commented: "Giving decades long efforts to find even minor signs of a viscous flow in metals, we were flabbergasted that graphene exhibited not just some small blip on an experimental curve but the clear qualitative effect, a large backflow of electric current."
Sir Andre Geim, who received a Nobel Prize for graphene, added: "Graphene cannot stop amazing us. Now we need to think long and hard how to connect such contradictory behaviour as ballistic motion of electrons, which is undoubtedly seen in graphene, with this new quantum weirdness arising from their collective motion. A strong adjustment of our understanding of the physics is due."

Civil War V :The Dino to Bird controversy.

Study challenges bird-from-dinosaur theory of evolution - was it the other way around?:
(PhysOrg.com) -- A new study just published in the Proceedings of the National Academy of Sciences provides yet more evidence that birds did not descend from ground-dwelling theropod dinosaurs, experts say, and continues to challenge decades of accepted theories about the evolution of flight.
A new analysis was done of an unusual fossil specimen discovered in 2003 called "microraptor," in which three-dimensional models were used to study its possible flight potential, and it concluded this small, feathered species must have been a "glider" that came down from trees. The research is well done and consistent with a string of studies in recent years that pose increasing challenge to the birds-from-dinosaurs theory, said John Ruben, a professor of zoology at Oregon State University who authored a commentary in PNAS on the new research.
The weight of the evidence is now suggesting that not only did birds not descend from dinosaurs, Ruben said, but that some species now believed to be dinosaurs may have descended from birds.
"We're finally breaking out of the conventional wisdom of the last 20 years, which insisted that birds evolved from dinosaurs and that the debate is all over and done with," Ruben said. "This issue isn't resolved at all. There are just too many inconsistencies with the idea that birds had dinosaur ancestors, and this newest study adds to that."
Almost 20 years of research at OSU on the morphology of birds and dinosaurs, along with other studies and the newest PNAS research, Ruben said, are actually much more consistent with a different premise - that birds may have had an ancient common ancestor with dinosaurs, but they evolved separately on their own path, and after millions of years of separate evolution birds also gave rise to the raptors. Small animals such as velociraptor that have generally been thought to be dinosaurs are more likely flightless birds, he said.
"Raptors look quite a bit like dinosaurs but they have much more in common with birds than they do with other theropod dinosaurs such as Tyrannosaurus," Ruben said. "We think the evidence is finally showing that these animals which are usually considered dinosaurs were actually descended from birds, not the other way around."


Another study last year from Florida State University raised similar doubts, Ruben said.
In the newest PNAS study, scientists examined a remarkable fossil specimen that had feathers on all four limbs, somewhat resembling a bi-plane. Glide tests based on its structure concluded it would not have been practical for it to have flown from the ground up, but it could have glided from the trees down, somewhat like a modern-day flying squirrel. Many researchers have long believed that gliders such as this were the ancestors of modern birds.
"This model was not consistent with successful flight from the ground up, and that makes it pretty difficult to make a case for a ground-dwelling theropod dinosaur to have developed wings and flown away," Ruben said. "On the other hand, it would have been quite possible for birds to have evolved and then, at some point, have various species lose their flight capabilities and become ground-dwelling, flightless animals - the raptors. This may be hugely upsetting to a lot of people, but it makes perfect sense."
In their own research, including one study just last year in the Journal of Morphology, OSU scientists found that the position of the thigh bone and muscles in birds is critical to their ability to have adequate lung capacity for sustained long-distance flight, a fundamental aspect of bird biology. Theropod dinosaurs did not share this feature. Other morphological features have also been identified that are inconsistent with a bird-from-dinosaur theory. And perhaps most significant, birds were already found in the fossil record before the elaboration of the dinosaurs they supposedly descended from. That would be consistent with raptors descending from birds, Ruben said, but not the reverse.
OSU research on avian biology and physiology has been raising questions on this issue since the 1990s, often in isolation. More scientists and other studies are now challenging the same premise, Ruben said. The old theories were popular, had public appeal and "many people saw what they wanted to see" instead of carefully interpreting the data, he said.
"Pesky new fossils...sharply at odds with conventional wisdom never seem to cease popping up," Ruben wrote in his PNAS commentary. "Given the vagaries of the fossil record, current notions of near resolution of many of the most basic questions about long-extinct forms should probably be regarded with caution."

The Crisis continues II

Denton, Still a Theory in Crisis, Part 2:


February 16, 2016 Posted by Barry Arrington 

This is the second of a series of posts reviewing Michael Denton’s new book Evolution: Still a Theory in Crisis.

“Gaps among known species are sporadic and often small.  Gaps among known orders, classes, and phyla are systematic and almost always large.”  George Gaylord Simpson, “The History of Life,” in ed. Sol Tax, Evolution After Darwin (Chicago:  University of Chicago Press, 1960), 1:149.

“Unfortunately, the origins of most higher categories are shrouded in mystery; commonly new higher categories appear abruptly in the fossil record without evidence of transitional ancestral forms.”  D.M. Raup and Steven M. Stanley, Principles of Paleontology (San Francisco:  W.H. Freeman and Co., 1971), 306.

“The known fossil record fails to document a single example of phyletic evolution accomplishing a major morphologic transition and hence offers no evidence that the gradualistic model can be valid.”  Steven M. Stanley, Macroevolution:  Pattern and Process (San Francisco: W. H. Freeman, 1979), 39.

As I noted in part one of this series, Dr. Denton has no doubt that Darwinian evolution occurs.  Nor should he.  The term “bauplan” comes from the German “building plan” or “building scheme,” and is often translated in biology as “body plan.”  In chapter 2 (entitled Galápagos), Denton explains that the biosphere is replete with examples of minor variations of bauplans – such as the beaks of the finches of the Galápagos islands made famous by Darwin – that are doubtless due to purely Darwinian processes.  These minor variations of bauplans are often classified under the term “microevolution.”

Before we go any further, let us anticipate an objection.  Darwinists who post in these pages often howl in indignation over the term “microevolution.”  They say the term is never used by “real” biologists.  Perhaps they do not consider George Gaylord Simpson to be a “real” biologist:

“Micro-evolution involves mainly changes within potentially continuous populations, and there is little doubt that its materials are those revealed by genetic experimentation.  Macro-evolution involves the rise and divergence of discontinuous groups, and it is still debatable whether it differs in kind or only in degree from microevolution.”  George Gaylord Simpson, Tempo and Mode in Evolution (New York: Columbia University Press, 1944), 97

Or Stephen Jay Gould:

“As a Darwinian, I wish to defend Goldschmidt’s postulate that macroevolution is not simply microevolution extrapolated . . .”  Stephen Jay Gould, The Return of Hopeful Monsters, Natural History, 86 (June/July 1977), 24, 30

Or Douglas H. Erwin and James W. Valentine:

“Explanations of the Cambrian radiation of invertebrate marine phyla and classes have focused on species selection or traditional microevolutonary processes.”  Douglas H. Erwin and James W. Valentine, “‘Hopeful Monsters,’ Transposons, and the Metazoan Radiation,” Proceedings of the National Academy of Sciences, USA 81 (September 1984): 5482-5483

Eminent biologists have recognized and referred to the distinction between microevolution and macroevolution for nearly one hundred years.  Let us hope that we can dispense with the “real biologists don’t use the term ‘microevolution’” canard once and for all.

Denton uses the Galápagos finch beaks as an example of microevolution.  The finches of the various islands are closely related in terms of nest architecture, egg coloration and DNA.  Yet in other respects, including their beak morphology, they can be quite different.  Denton quotes Darwin’s correct inference regarding the origin of these differences: “Seeing this gradation and diversity of structure in one small, intimately related group of birds, one might really fancy that from an original paucity of birds in this archipelago, one species had been taken and modified for different ends.”  Darwin was also correct about the causal mechanism that resulted in these changes: “Darwin also inferred (again rightly, as the work of subsequent researchers on Galápagos has amply confirmed) that the major causal mechanism responsible for their adaptive divergence—the shaping of their beaks for example—is the simple mechanism of natural selection.”

Denton concludes that evolution on this scale is caused by purely Darwinian mechanisms:

As far as the evolution of finch beaks is concerned, there is no need either at the morphological or genetic level to call for any causal agency other than cumulative selection. Here I concur with classic Darwinism. The beaks are clearly adaptations and their evolution is entirely explicable within a classic functionalist framework. . . . The lesson of the Galápagos, and one of the repeated mantras of Evolution: A Theory in Crisis (see Chapters 2 and 4) is simply this: Cumulative selection will work its magic as long as the novelty of interest is adaptive and there is a functional continuum (at the morphological or genetic level) leading from a putative ancestor species or structure A to a descendant species or structure B.

(emphasis in the original)

In summary, Denton has absolutely no problem with attributing evolutionary change to Darwinian mechanisms so long as the two conditions Darwin himself asserted are necessary are in place:  (1) the novelty is adaptive (otherwise there is nothing for natural selection to “select” for); and (2) there is a functional continuum – there can be no “gaps” in functional intermediates.

This brings us to another  important term: “saltation.”   In Origin of Species Darwin quoted six times the Latin sentence natura non facit saltus.  It means “nature does not take jumps.”  The word saltus means “leap” or “jump,” and in evolutionary theory a drastic or sudden change in an a line of organisms (a “jump”) is called a “saltation.”  Thus, Darwin himself asserted that his theory does not allow for saltations. Stephen Jay Gould added in his 2002 The Structure of Evolutionary Theory  that Darwinian evolution requires variation for natural selection to act upon, AND that variation must, by definition, be very small.  Otherwise, it would be the variation itself, and not natural selection, that would account for the evolutionary change.

Thus Darwinists, beginning with Darwin himself, have always insisted that the theory absolutely requires the “functional continuum” to which Denton alludes.  Saltations are not possible under the theory.  Gould goes so far as to say “For this reason . . . saltationist (or macromutational) theories have always been viewed as anti-Darwinian.”  Stephen Jay Gould, The Structure of Evolutionary Theory (Cambridge, MA: Belknap Press [Harvard], 2002), 111.

Functionalist evolutionary theory demands a continuous chain of functional intermediates for natural selection to work at all:

Darwin’s interminable series of transitional forms is necessary for straightforward mechanistic reasons (how else can one get from A to B by cumulative selection?), but it is also essential if the sole agency of change is to be natural selection.  Where a complex adaptation—no matter how complex—can be reached in a series of tiny adaptive steps, then natural selection can indeed function, in Dawkins’s description, as a blind watchmaker and change A into B no matter how complex the transition, without any other causal agency being involved.

But what if the continuous chain of functional intermediates is missing?  Here we get to the nub of the matter, because Denton claims that

many of the taxa-defining homologs actualized during the course of evolution have never been shown to be adaptive and even in the case of those homologs which are apparently adaptive, functional continuums are either unknown or very hard to envisage.

And if this is the case, certain conclusions follow ineluctably:

To acknowledge their absence [i.e., the absence of a continuous chain of functional intermediates] is to acknowledge that the paths of evolution must have been ordered and directed by additional causal factors, i.e., that cumulative selection is not the sole or even the major directive agency.

Denton writes that this “need for adaptive continuums brings us to the nub of the problem, the core contention of Evolution: A Theory in Crisis, and the major point defended here: Practically all the novel, taxa-defining homologs of all the main taxa are not led up to via adaptive continuums.  Moreover, as argued later in this book, many of these novel Bauplans do not convey any obvious impression of being adaptive . . .”

Denton concludes the chapter with this delightful observation of fine irony:


It is ironic that the very evidence for believing that microevolution has indeed occurred in cases like the finches—an empirically known or readily envisaged continuum of forms leading from an ancestral form A to descendant form B—is precisely the evidence that is lacking when attempting to account for macroevolution and the origin of the defining features (feathers, hands, mammary glands, hair, the placenta, flowers, body plan, etc.) of the major taxa.

On the scientific method.

Bacteria:Known troublemakers for design deniers

Derbyshire VI: Behe's Bacterial Flagellum--Still Stirring Up Trouble for Darwin's Defenders:
Jonathan Witt February 18, 2005 2:50 PM

John Derbyshire is on The Corner arguing that we can never safely infer that certain biological structures were designed. To a reader who asserted that organizational complexity cannot arise from impersonal processes, Derbyshire replies, "How do you know it can't? It is true that the genesis of organizational complexity is not currently well understood; but to leap from that to telling me we shall NEVER be able to find a natural-law explanation for it is just dogma."

Derbyshire's argument is worth confronting because it represents the opinion of leading Darwinists. Biologist Kenneth Miller, for instance, routinely makes just such an argument. Design theorist William Dembski responds thus:

Miller claims that the problem with anti-evolutionists like Michael Behe and me is a failure of imagination -- that we personally cannot "imagine how evolutionary mechanisms might have produced a certain species, organ, or structure." He then emphasizes that such claims are "personal," merely pointing up the limitations of those who make them. Let's get real. The problem is not that we in the intelligent design community, whom Miller incorrectly calls "anti-evolutionists," just can't imagine how those systems arose.
The problem is that Ken Miller and the entire biological community haven't figured out how those systems arose. It's not a question of personal incredulity but of global disciplinary failure (the discipline here being biology) and gross theoretical inadequacy (the theory here being Darwin's).

The particular mechanism Miller has in view here is the bacterial flagellum. Click here and scroll down for a good, brief description and animation of the bacterial flagellum, and here for an enlarged view with its parts labeled. Biochemist Michael Behe made this little engine that could famous by showing that it was irreducibly complex, like a mouse trap: "If any one of the components of the mousetrap (the base, hammer, spring, catch, or holding bar) is removed, then the trap does not function." With even four of these parts, it's utterly useless. The mousetrap is irreducibly complex.

What does irreducible complexity have to do with Darwinian evolution? Evolution by mutation and natural selection must proceed by one slight, functional improvement at a time. So how can it build an irreducibly complex propeller motor one step at a time if the motor can't propel at all until all of its parts are in place? It can't. Something else built it.

Behe's argument doesn't assume that none of the other parts could ever be used for anything else. The spring on a mousetrap could be taken and used in some other device. The base with cheese on it could feed a mouse. Several but not all of the parts of a bacterial flagellum--while completely useless as a rotary propulsion machine--can be used to transport proteins across a membrane. But this hardly provides a credible Darwinian pathway.

Imagine if a boy told a girl he could climb to Mars because there supposedly existed a natural ladder stretching from one planet to the other? The girl is skeptical, pointing out that nobody on earth has ever found such a ladder. The boy screams, "That's an argument from ignorance! Scientists are finding all sorts of new things all the time. Look! The moon! The moon is one step along the way. You see, everything is falling into place." The Darwinists' desperate efforts to spin away the clear significance of the bacterial flagellum is strangely akin to this sort of reasoning. Dembski explains:

Darwin's theory, without which nothing in biology is supposed to make sense, in fact offers no insight into how the flagellum arose. If the biological community had even an inkling of how such systems arose by naturalistic mechanisms, Miller would not -- a full six years after the publication of Darwin's Black Box by Michael Behe -- be lamely gesturing at the type three secretory system as a possible evolutionary precursor to the flagellum.
Miller and Derbyshire are like the boy convinced of the natural ladder to Mars, who finds the moon and yells "Ah ha! Now who dares to play the skeptic!" Well, design theorists do. Consider this passage from a peer-edited paper by biologist Scott Minnich and philosopher of science Stephen Meyer, in which they discuss recent evidence for the delicately orchestrated and information-rich proteins of the bacterial flagellum:

[I]f anything, TTSSs [Type Three Secretory Systems] generate more complications than solutions to this question. As shown here, possessing multiple TTSSs causes interference. If not segregated one or both systems are lost. Additionally, the other thirty proteins in the flagellar motor (that are not present in the TTSS) are unique to the motor and are not found in any other living system. From whence, then were these protein parts co-opted?
Also, even if all the protein parts were somehow available to make a flagellar motor during the evolution of life, the parts would need to be assembled in the correct temporal sequence similar to the way an automobile is assembled in factory. Yet, to choreograph the assembly of the parts of the flagellar motor, present-day bacteria need an elaborate system of genetic instructions as well as many other protein machines to time the expression of those assembly instructions. Arguably, this system is itself irreducibly complex. In any case, the co-option argument tacitly presupposes the need for the very thing it seeks to explain--a functionally interdependent system of proteins.

Now one letter writer, responding to Behe's column in The New York Times, complained that we only describe the bacterial flagellum as an outboard motor because we have no better analogy, not because it is an outboard motor. The letter writer argues that believing this molecular motor was designed is like the astronomer Percival Lowell mistaking Martian canyons for canals. The suggestion is that false design inferences have been made, so surely all of the design inferences in the natural sciences are false. In this case, the fallacious argument--a favorite among Darwinists--is doubly silly because the Martian canyons turned out to be far simpler, far less specified, than engineered canals; while the bacterial flagellum has turned out to be far more sophisticated than our outboard motors.

As Minnich and Meyer note, the discovery of molecular motors is opening a whole new field, where biology and engineering meet:

To paraphrase the original rendition of the Department of Energy's Genomes to Life web site, "the molecular machines present in the simplest cells, produced by evolution, dwarf the engineering feats of the 20th century." The dissection of the complexity and sophistication of ... machines like the bacterial flagellum are indeed a testimony to the power of modern molecular biological techniques. Yet, the elegant structural properties, efficiency, and the highly controlled genetic programming to produce these machines was neither anticipated nor predicted. The potential applications of this knowledge are legion and have spawned a new discipline focused on nanotechnology.
One needn't go far for examples. Here at Physics Today, well trained physicists are standing around this astonishing little machine, the bacterial flagellum, like neighborhood mechanics getting a chance to take apart and learn from a NASCAR racing engine.
Derbyshire, Miller and other Darwinists are mixed up about the direction of things. The more we KNOW about the bacterial flagellum, the less and less it is anything the Darwninian mechanism could produce. Moreover, there are strongly affirmative grounds for inferring design from the presence of irreducibly complex machines and circuits. Every time we know the causal history of an irreducibly complex system (like the NASCAR racing engine or an electronic circuit), it always turn out to have been the product of an intelligent cause.


Finally, the list of known biological mechanisms that appear irreducibly complex isn't shrinking, it's growing.