The last chapter was the first of a multi-chapter discussion on the origin of life. It described how living cells contain many circular systems that appear inexplicable in terms of step-by-step development. Evolutionists rely on the power of natural selection as the explanation for such circular paradoxes. However, can natural selection simply be assumed to explain how these chicken-or-egg systems originated?
Traditional science is based on the scientific method, which requires empirical evidence derived from observation. Unless a verifiable step-by-step procedure for the development of circular cellular systems is provided, invoking natural selection as an explanation is like invoking the power of a magic wand. If no experimental proof is ever required, natural selection can be invoked to explain anything and everything.
Complex biochemical systems with interlocking parts are found throughout the biological world. It would be practically impossible to overstate the case for biochemical complexity. In Human Physiology, Stuart Ira Fox, describes each human cell as a “highly organized molecular factory.”[1] This quote from Michael Denton’s Evolution: A Theory in Crisis provides an analogy that describes how complex such cellular factories are:
To grasp the reality of life as it has been revealed by molecular biology, we must magnify a cell a thousand million times until it is twenty kilometers [12.5 miles] in diameter and resembles a giant airship large enough to cover a great city like London or New York
A huge range of products and raw materials would shuttle along all the manifold conduits in a highly ordered fashion to and from all the various assembly plants in the outer region of the cell.[5]
The importance of precise protein shape to the function of molecular machines is emphasized in a Stanford University Power-Point Presentation entitled Protein folding is essential to life:
In order to carry out their function (for instance as enzymes or antibodies), proteins must take on a particular shape, also known as a "fold." Thus, proteins are truly amazing machines: before they do their work, they assemble themselves! This self-assembly is called "folding."[7]
Minor differences in protein folding can wreck their functionality. The Stanford publication describes how BSE (mad-cow disease) is transmitted by badly folded proteins inside nerve cells.[8] The shape of the normal proteins is altered when they touch the abnormally folded proteins. This shape change will eventually kill the nerve cells. This is just one example of how important precise protein folding is to proper cell functionality.
In an article for the Horizon Symposia (Nature Publishing Group), Joachim Pietzsch also emphasized the importance of precisely folded protein shapes:
Proteins are the biological workhorses that carry out vital functions in every cell. To carry out their task, proteins must fold into a complex three-dimensional structure — but what tells a protein which shape it should be and how does it achieve this?[9]
It is well known that the sequence of amino-acid components in a protein determine its precise 3-D shape.[10] However, the story is much more complicated than that. Pietzsch goes on to describe how an ordinary protein of 100 amino-acid units has perhaps 1030 theoretical 3-D shapes that it could fold into.[11] This amounts to a million times a trillion times a trillion possible shapes.
Empirical scientists have been working hard to identify why proteins fold into the precise shape that they do. Recent studies indicate that protein folding is controlled by complex interactions between the thousands of atoms in a protein:
After all, the folding of a protein is not a chemical reaction, with a bond breaking here and a new one forming there. It is more like the weaving of an intertwined molecular pattern, the stability of which is defined by innumerable forces between atoms.[12]
But cellular life is even more complicated than the atomic interactions that determine the shape of individual proteins. Biochemist Bruce Alberts has noted that, “every major process in a cell is carried out by assemblies of 10 or more protein molecules, comprising a ‘protein machine’.”[13] Assorted passages from Molecular Biology of the Cell (Alberts et al.) describe the immense complexity of cellular chemistry:
[Protein and DNA] are combined for use in marvelously subtle and complex ways, even in the simplest of organisms.[14]
… cell chemistry is enormously complex: even the simplest cell is vastly more complicated in its chemistry than any other chemical system known.[15]
The depths of biochemical complexity are hard to understand, even for the most brilliant of technical people. In an attempt to make such complexity understandable, biochemistry textbooks often contain simplified drawings. But even with the help of such simplifications, Molecular Biology of the Cell (Alberts et al.) acknowledges that it will be a long time before scientists truly understand the enormous complexity of cellular life:
These drawings cannot capture the enormous complexity of the networks of protein–protein interactions that are responsible for most intracellular processes, whose understanding will require new and more quantitative forms of analysis. Thus, we are no longer as confident as we were 18 years ago that simplicity will eventually emerge from the complexity. The extreme sophistication of cellular mechanisms will challenge cell biologists throughout the new century … [16]
Molecular Biology of the Cell (Alberts et al.) attempts to explain cellular complexity through its alleged evolutionary origin. But this quote honestly acknowledges that large gaps in our knowledge present a clear danger in relying on evolutionary speculation:
Clearly, there are dangers in introducing the cell through its evolution: the large gaps in our knowledge can be filled only by speculations that are liable to be wrong in many details.[17]
Many Evolutionists insist that Evolution is vital to understanding biological complexity. For example, according to Evolutionary Biologist Theodosius Dobzhansky, “nothing in biology makes sense except in the light of Evolution.”[18] But speculative stories about the origin of complex biological systems shed no light on the technical details of their modern day operation.
According to Molecular Biology of the Cell (Alberts et al.), “We now know there is nothing in living organisms that disobeys chemical and physical laws.”[19] Consequently, deciphering the operation of complex biochemical systems is dependent on the laws of physics and chemistry, and not on speculative stories of how natural selection could have used random genetic mutations to produce such complexity.
In order to understand how biological life functions, one has to understand how molecular machines operate. This requires intense empirical studies. One such empirical study was conducted by Keiichi Namba of Osaka University
Nature created a rotary motor with a diameter of 30 nm [about 0.0000012 inches]. … [The motion of bacteria] is driven by rapid rotation of a helical propeller by such a tiny little motor at its base. … [The flagellum] rotates at around 20,000 rpm, at energy consumption of only around 10-16 W and with energy conversion efficiency close to 100%.[20]
According to Namba, the motion of bacteria is driven by a “highly efficient flagellar motor that is far beyond the capabilities of artificial motors.”[21] In The Edge of Evolution, Biochemist Michael Behe provides this high-level description of the structure of a flagellum:
A flagellum can be conceptually broken down into three subsystems: the base (which contains the motor), the “hook” (which acts as a universal joint), and the filament (which is the propeller). Within each subsystem, however, are multiple precision-made parts.[22]
Additional details about the complexity of the self-assembly of a flagellum’s are given in an interview with Namba that was published in the Japan Nanonet Bulletin:
Individual atoms are used as functional parts, and this is the essential feature that makes biological macromolecules distinct from artificial machines at present.[23]
The flagellar motor … consists of various components, such as a rotor, stators, a drive shaft, a bushing, a rotation switch regulator, and so on.[24]
The flagellum is made by self-assembly of about 25 different proteins.[25]
After the motor has been formed, the flagellar filament, which functions as a helical propeller, is assembled.[26]
The flagellar filament is made of 20,000 to 30,000 copies of flagellin [a protein]... Flagellin molecules are transported through a long narrow central channel of the flagellum … where they self-assemble …[27]
Behe describes how the flagellum is assembled in a bottom-up fashion, starting with a base unit that lies within the cell.[28] The base is constructed of several ring layers, each constructed from multi-copies of their unique protein component. The layering of different quantities of unique proteins continues to the tip of the flagellum’s filament. This filament extends far outside the cell body (7 or more times the cell diameter).
An internet video shows the amazing auto-assembly process of a flagellum.[29] Namba’s group examined the atomic level interactions of the billions of atoms that comprise a flagellum to decipher its detailed structure and assembly. This detailed empirical analysis was required to understand complicated puzzles, such as how the direction of rotation for the flagellum’s can suddenly change (quite unlike an artificial motor).
The flagellum manufacturing process is like a modern construction site, except that it is fully automated. The automation includes a walking protein robot that lays down flagellin molecules as if it were a master bricklayer laying down bricks. The construction procedure is controlled by a Protein Export Apparatus that sends the correct sequence of proteins for each stage of construction to the growing end of the flagellum.
A scientific journal describes how assembling the long filament portion of the flagellum is “a much more sophisticated process than any of us could ever have envisioned”[30] Such sophisticated processes are constantly encountered in the cellular world. A 2008 New Scientist article by Dan Jones describes how scientists are actively debating the origin of complex molecular systems like the flagellum:
Biologists have been interested in the bacterial flagellum for decades, not least because it is a prime example of a complex molecular system – an intricate nanomachine beyond the craft of any human engineer. Explaining the origin of such systems is one of the most difficult and important challenges in evolutionary biology.
… The study of complex molecular systems has been given added impetus by the "intelligent design" (ID) movement … [To ID advocates], such systems are examples of "irreducible complexity", a concept that goes to the heart of their opposition to the theory of evolution.[31]
Leading advocates of the Intelligent Design movement claim that some biochemical systems are irreducibly complex – meaning that they can’t be built in step-by-step fashion, as suggested by the Fact of Evolution. Irreducible complexity implies that a complete set of core components need to be present before such systems are functional. Many Evolutionists deny that irreducible complexity exists in the biological world.
Intelligent design advocates claim that Evolutionists tend to echo the mantra that “Evolution created it,” no matter what complexity is revealed by empirical research. This quote from the 2008 New Scientist article by Jones emphasizes why ID-advocates make that claim:
The flagellum is certainly complex, but is it really too complex to have evolved through natural selection? Until recently it has been surprisingly hard for biologists to answer this question satisfactorily. … Kenneth Miller, a biochemist at Brown University University of Birmingham in the UK
If you look at this passage, Pallen’s quote implies that biologists often echo the mantra “Evolution created it,” even though they lack the knowledge of what exactly “Evolution has created.” Miller’s quote is even more revealing. It implies that biologists invent stories for the evolutionary origin of complex systems before anybody understands the details of how such systems work. Talk about putting the cart before the horse.
It is no wonder that Miller describes developing such evolutionary explanations as a “very difficult” task. Such explanations are produced ahead of their scientific time – i.e., they claim to offer a scientific explanation for the detailed operation of complex biological systems, before scientists even understand how such systems work. Such a priori explanations are science done backwards. They are not reliable.
The concept that “Evolution created it” regardless of what it is that “Evolution has created” represents a scientific paradigm (guiding principle). In discussing the philosophy of science, Thomas Kuhn described how scientists seek to make everything fit to the currently reigning paradigm.[33] Those who oppose the reigning paradigm are normally classified as scientific heretics and treated with contempt.
In recent years, such contempt has been directed at scientists who back the concept of an intelligent designer. For example, the New Scientist article describes arguments for the irreducible complexity of the flagellum as a “focal point in science's ongoing struggle against unreason.”[34] In other words, if you fail to support the paradigm of Evolution created it, you are an enemy of science because you advocate “unreason.”
In a recent article claiming “the collapse of irreducible complexity,” Miller attacked the concept that the flagellum represents an irreducibly complex structure. Despite making this claim, Miller acknowledges that cells are filled with many complex structures whose evolutionary origins are unknown:
Living cells are filled, of course, with complex structures whose detailed evolutionary origins are not known. Therefore, in fashioning an argument against evolution one might pick nearly any cellular structure, the ribosome for example, and claim – correctly – that its origin has not been explained in detail by evolution.[35]
Because the intent of this book is to demonstrate that Evolution is not a fact, Miller’s quote raises an interesting question. If the evolutionary origin of “nearly any cellular structure” is not yet known, how could the evolutionary origins of such structures be classified as a fact? This ignorance is difficult to reconcile with the National Academy of Sciences description of a scientific fact, which requires repeated observation.[36]
Advocates for the Fact of Evolution have simply assumed it to be true – without providing details of why. Theories can lack details, but facts cannot. Promoting the Theory of Evolution in this way makes it a meaningless tautology: We know Evolution produced all the biological details we observe, so we know all the biological details we observe are due to Evolution. The details will be supplied later.
Moreover, intelligent design advocates seek to do more than demonstrate that Evolution is not a proven fact. For example, Behe has claimed that the irreducibly complexity of many biological systems has falsified the Fact of Evolution. The essence of Behe’s argument is that such biological systems can’t be created with a step-by-step process that modifies one system component at a time.
Behe has pointed out that Darwin himself suggested a collapse of his entire theory if one could demonstrate that such irreducibly complex systems exist.[37] Here is Darwin
If it could be demonstrated that any complex organ existed which could not possibly have been formed by numerous, successive, slight modifications, my theory would absolutely break down.[38]
Evolutionists like to point out that Darwin Darwin Darwin
Hence, whether or not Darwin Darwin Darwin Darwin
One claim often used in contempt of Intelligent Design is that it represents an argument based on ignorance. For example, consider this quote by Miller:
Nonetheless, until we have produced a step-by-step account for the evolutionary derivation of the flagellum, one may indeed invoke the argument from ignorance for this and every other complex biochemical machine.[41]
However, the paradigm of the Evolutionary tautology also represents an argument based on ignorance. By Miller’s own admission, the “detailed evolutionary origins” of many “complex [cellular] structures” are unknown. That represents ignorance – i.e., a lack of knowledge. But Miller considers it perfectly acceptable to fill this ignorance with potential evolutionary explanations that have yet to be discovered:
The lack of a detailed current explanation for a structure, organ, or process does not mean that science will never come up with one.[42]
Nobody can predict what will be discovered in the future, so Miller is correct. But conceding the possibility of a future explanation does not imply its certainty. With no certainty, there is no fact. If “Intelligent-Design-of-the-gaps” shows contempt for science, then “Evolution-of-the gap” with “details-to-be-named-later” shows similar contempt. Equating any form of ignorance with scientific fact is not in the interest of good science.
In fairness, Miller does put forth an argument for the “collapse of irreducible complexity.” He argues that the flagellum is not irreducibly complex because the Protein Export Apparatus of the flagellum may have evolved from another biochemical system called the TTSS (or T3SS). But Miller’s argument is bogus for a number of reasons. One reason is that the path for evolutionary development of the T3SS also lacks any certainty.
In the New Scientist article, Jones points out three different options that might explain the evolutionary relationship between a flagellum and a T3SS.[43] The first two possibilities mentioned by Jones are that either the flagellum or the T3SS may have originated first and then evolved into the other system. The other possibility mentioned by Jones is that both systems evolved in parallel from an unidentified common ancestor.
This description includes all possibilities, except for the possibility that neither the T3SS nor the Protein Export Machine have an evolutionary history. As evolutionary relationship is simply assumed because genetic comparisons indicate that the T3SS and Protein Export Machine have some similar protein components. But this assumption does not prove that the protein components of either system had an evolutionary origin.
Perhaps, what Miller’s example actually demonstrates is that both the T3SS and the Protein Export Machine are irreducibly complex systems. Nothing in the definition of irreducible complexity precludes similar components from being used in two different irreducibly complex systems. Neither is an irreducibly complex system precluded from being a component in a second irreducibly complex system.
A macro-world example can clarify this concept. Imagine a hypothetical system that includes a mousetrap, a device that detects the odor of a dead mouse, and an IPod triggered to play a funeral march when a dead mouse is detected. It is clear that devices like mousetraps and IPod-like devices have other uses. But that doesn’t prove that they can be constructed piece-by-piece, with each new piece improving their functionality.
Arguments based on the similarities of system components cannot disprove irreducible complexity. For example, finding a laptop with a headphone similar to the IPod does not prove that neither laptops nor IPods are irreducibly complex systems. Similarly, the T3SS may be irreducibly complex even if shares a similar set of protein components with a flagellum’s Protein Export Machine.
Similarities of protein components may suggest evolution, but they don’t prove it. If biochemical systems with increasing functionality can be built one protein component at a time, then an empirical demonstration of this process should be theoretically possible. Such a demonstration would not prove that evolution used the same pathway, but it would demonstrate the feasibility of at least one evolutionary pathway.
An empirical proof of possibility would be much more believable than the just-so scenarios of evolutionary speculation. For example, evolutionary biologists speculate that T3SS proteins could be exchanged with those of the Protein Export Machine (or vice-versa). Science may be capable of empirically testing such scenarios. For example, it is possible to disable (or knockout) one gene and replace it with another.[44]
Would substituting an allegedly homologous gene of the T3SS into the Protein Export Machine wreck its functionality? Without empirical experiments, nobody could say for sure. It is one thing to imagine a hypothetical path of changing the T3SS into a Protein Export Machine. But an imaginative story lacks the certainty of an empirical experiment that slowly modifies each gene while examining its effect on system functionality.
It is common to assume that slight differences in genes imply an evolutionary relationship. But there are other possibilities. For example, some mutations could alter genes in a way that provide little functional change. With this class of relatively neutral mutations, genes that were originally the same (by virtue of design) could over time develop slight cosmetic differences that do not wreck their functionality.
But this is not the only non-evolutionary possibility. It is also possible that some slight genetic mutations have a major impact on functionality. Slightly different systems could have slightly different design constraints meaning they need slightly different genes. The nominal assumption of evolution is that slight genetic differences imply evolution. But it could be the case that even a slight genetic difference will alter system functionality.
For example, consider the walking protein robot that lays down flagellin proteins to form the flagellum’s filament.[45] The walking protein robot acts as a filament-cap with legs that fits in the creases between filament strands. However, a slight shape mismatch leaves a small opening that directs each flagellin molecule to its proper place. After placing each flagellin-molecule, the walking-robot moves to the new top of the filament.
Without empirical experiments that modify the gene for the filament-cap, nobody can say for certain what effect mutations to the filament-cap would have on system functionality. It is possible that any mutation to the filament-cap gene would wreck its system functionality. It is also possible that many mutations would be cosmetic only – i.e., they would not alter the critical functionality of the filament-cap.
The point is that empirical research is needed to understand the effect that specific genetic changes will have on key proteins. Without empirical research, the effect of any genetic mutation amounts to guesswork. To argue that genetic similarities always imply evolutionary development is to exclude other possibilities by a priori assumption. Such speculative arguments do not explain chicken-or-egg systems like the ribosome.
The ribosome is a circular paradox – i.e., it is built from proteins that are manufactured by a ribosome. What came first? Was it the proteins that form the ribosome, or the ribosome that forms proteins? Although our level of genetic knowledge is increasing rapidly, we still lack much knowledge. For example, in an Edge.org panel discussion, Geneticist Craig Venter described our current inability to make a ribosome:
… we tried to make synthetic ribosomes, starting with the genetic code and building them —The ribosome is such an incredibly beautiful complex entity, you can make synthetic ribosomes, but they don't function totally yet. Nobody knows how to get ones that can actually do protein synthesis. But starting with an intact ribosome is cheating anyway right? That is not building life from scratch … [46]
Similar ribosomes are found in a multitude of organisms. Although, such similarities may imply evolutionary origins, there is another possibility. For example, if all organisms have a similar complex component, where is the proof that it evolved gradually? In the same Edge.org panel discussion, George Church (Professor of Genetics at Harvard Medical School
The ribosome, both looking at the past and at the future, is a very significant structure — it's the most complicated thing that is present in all organisms. Craig [Venter] does comparative genomics, and you find that almost the only thing that's in common across all organisms is the ribosome. And it's recognizable; it's highly conserved. So the question is, how did that thing come to be? And if I were to be an intelligent design defender, that's what I would focus on; how did the ribosome come to be?[47]
As this quote from Molecular Biology of the Cell (Alberts et al.) declares, the details behind how evolution could have produced a ribosome are largely unknown:
Protein synthesis also relies heavily on a large number of proteins that are bound to the rRNAs in a ribosome … The complexity of a process with so many interacting components has made many biologists despair of ever understanding the pathway by which protein synthesis evolved.[48]
Although Molecular Biology of the Cell makes this statement, as NAS President, Alberts signed his name to a document that promotes the Fact of Evolution.[49] Miller and Alberts are both distinguished scientists that triumphantly proclaim that science has proven the Fact of Evolution. At the same time, they clearly admit that science lacks knowledge about evolutionary pathways. I find this stark contrast utterly mystifying.
The origin of complex DNA sequences is as mysterious as the origin of complex protein machines. Not too long ago, it was assumed that DNA was like an information library.[50] It was thought that each protein had its own instruction manual in the library, and that each instruction manual contained a coded segment that determined the amino-acid sequence of a specified protein. Each of these coded segments was called a gene.
Much publicity has been given to claims that similarities of genes in different organisms prove Evolution (see Chapter 13 for a more detailed discussion). For example, even the genes of bananas are said to have a 50% similarity to human genes.[51] However, Molecular Biology is upsetting the classical view of “a gene as a discrete element.” This quote from a Genome Research article indicates how complex genes really are:
The molecular biology revolution changed this idea considerably. … the gene is [. . .] neither discrete [. . .], nor continuous, [. . .], nor does it have a constant location [. . .], nor a clearcut function [. . .], not even constant sequences [. . .] nor definite borderlines.[52]
It was previously thought that large portions of a genome had no function at all. DNA segments that coded for proteins were called Exons, while DNA segments that had no known coding function were called Introns.[53] Consequently, large DNA segments (up to 95% of Human DNA) were classified as Junk DNA.[54] But the ENCODE (ENCyclopedia Of DNA Elements) project has shaken the classical view of a gene.
An article published in Genome Research describes how highly complicated the coding structure of DNA actually is.[55] We now know that DNA coding has a lot of overlap. In some cases, a single DNA segment supplies code for manufacturing multiple proteins. This complexity has required a fundamental redefinition of what a gene is. Figure 5 of the Genome Research article illustrates the depth of genetic complexity.[56]
An article in Nature describes how the coding structure of the human genome is still very much a mystery. In particular, we have limited knowledge about gene expression – the process that controls which proteins a cell will make and how much of them it will make:
The human genome is an elegant but cryptic store of information. The roughly three billion bases encode, either directly or indirectly, the instructions for synthesizing nearly all the molecules that form each human cell, tissue and organ. … However, at present, we have an incomplete understanding of the protein-coding portions of the genome, and markedly less understanding of both non-protein-coding transcripts and genomic elements that temporally and spatially regulate gene expression.[57]
What we do know is that cells cleverly control the production schedule for proteins, through a cellular process called transcription:
Mathematical analysis suggests that this “just-in-time” transcription program (…) is optimal under constraints of rapidly reaching a production goal with minimal total enzyme [i.e., protein] production. Our findings suggest that … [the transcription program] can be understood using the engineering principles of production pipelines.[58]
Scientists originally thought that the “amount of protein in a cell was constant and proteins turned themselves off.” [59] However, we now know that genes are turned on and off by complicated control mechanisms. These control mechanisms are analogous to the control logic used in computer systems. Walter Gilbert, a Nobel Prize winning Chemist, has described the elaborate nature of the cellular logic that controls gene expression:
We now know that there are layers upon layers of control mechanisms, both ones that turn genes off and ones that turns genes on, and that the genes in our bodies are controlled by what we call combinatorial patterns of controls in which you have maybe ten or twenty molecules binding to the DNA near a gene to turn it off and on.[60]
Multi-cellular organisms add even more complication to gene expression. James Darnell, a Molecular Cell Biologist, has described how scientists once thought that the rates at which proteins were made was relatively static with only very slow changes to transcription rates.[61] As Darnell describes, we now know that cells have many complicated interactions that can rapidly change their level of protein production:
Because there are many, many other signaling pathways through which cells gain directions from outside and take these directions, interpret them, and activate different genes in the nucleus. There are by now at least 6 or 8 very well understood pathways, which can be operative simultaneously or sequentially, and the signals that finally reach the nucleus, and that effect gene transcription, can often be multiple for any given gene. So it is very seldom that a single signal from outside is in control of what happens to the cell. Rather, multiple signals are being sensed at all times. This of course leads to horrible complication.[62]
The control networks for regulating the development of multi-cellular organism add even further complication to gene expression. A visual representation of the logical complexity for one of the embryonic cell types in a sea urchin is available on the Internet.[63] If this represents the complexity for a single cell type in a relatively simple animal, the complexity for the development plan of a human being must be staggering.
The study of human physiology has revealed that there are many complicated feedback loops that maintain the state of the human body in a steady-state condition called homeostatis:
The concept of homeostasis has been of inestimable value in understanding human anatomy and physiology, because it allows diverse regulatory mechanisms to be understood in terms of their “why,” as well as their “how.” The concept of homeostasis also provides a major foundation for medical diagnostic procedures. When a particular measurement of the internal environment, such as blood measurements, deviates significantly from the normal range of values, it can be concluded that homeostasis is not maintained and the person is sick.[64]
The complicated control mechanisms that maintain homeostasis allow human beings to function the way they do. The complexity involved in maintaining this stability is staggering. Nobody doubts the value of empirical scientific research aimed at understanding how these complex control systems work. What evolutionary skeptics doubt is speculative stories about how Evolution created this complexity.
Acknowledgements
Endnotes are contained in the following section. The following shorthand notation connects the numbered endnotes to permission statements:
N(x, y, z, …) indicates endnotes numbered ‘x’, ‘y’, ‘z’.
I gratefully acknowledge permission to reproduce quotes from the following copyrighted material:
N(5, 10, 23): Michael Denton, Evolution: Theory in Crisis (Chevy Chase, MD: Adler and Adler, 1986). Used with the permission of Michael Denton.
N(2-6): Bruce Alberts, “Biology Past and Biology Future: Where have we been and where are we going?,” http://www.interacademies.net/?id=7642. Used with the permission of the author – Bruce Alberts.
N(31, 32, 34, 43): Dan Jones, “Uncovering the evolution of the bacterial flagellum,” 16 February 2008, New Scientist, http://www.newscientist.com/article/mg19726431.900-uncovering-the-evolution-of-the-bacterial-flagellum.html?full=true (accessed 2 February 2009). These quotes fall within the Fair Use guidelines of New Scientist: http://www.newscientist.com/contact/syndication.
N(36, 49): Science and Creationism: A View from the National Academy of Sciences, 2nd ed. (Washington, DC: National Academies Press, 1999), http://www.nap.edu/catalog/6024.html. Reprinted with permission from Science, Evolution, and Creationism, 2008 by the National Academy of Sciences, Courtesy of the National Academies Press, Washington , D.C.
N(46-47): John Brockman, ed., Life: What A Concept! (New York
N(57): Reprinted by permission from Macmillan Publishers Ltd: “Identification and analysis of functional elements in 1% of the human genome by the ENCODE pilot project,” The Encode Project Consortium, Nature 447:789-816, 14 June 2007, p. 799, http://www.nature.com/nature/journal/v447/n7146/pdf/nature05874.pdf, copyright © 2007.
N(58): Reprinted by permission from Macmillan Publishers Ltd: Alon Zaslaver et al., “Just-in-time transcription program in metabolic pathways,” Nature Genetics 36:486-91, 25 April 2004, http://www.nature.com/ng/journal/v36/n5/abs/ng1348.html, http://www.nature.com/ng/journal/v36/n5/pdf/ng1348.pdf, copyright © 2004.
Notes and References
[2]. Michael Denton, Evolution: A Theory in Crisis, (Chevy Chase, MD: Adler and Alder, 1986), p. 328.
[3]. Michael Denton, Evolution: A Theory in Crisis, (Chevy Chase, MD: Adler and Alder, 1986), p. 328.
[4]. Michael Denton, Evolution: A Theory in Crisis, (Chevy Chase, MD: Adler and Alder, 1986), p. 328.
[5]. Michael Denton, Evolution: A Theory in Crisis, (Chevy Chase, MD: Adler and Alder, 1986), p. 328.
[6]. Michael Denton, Evolution: A Theory in Crisis, (Chevy Chase, MD: Adler and Alder, 1986), p. 329.
[7]. “Protein folding is essential to life,”
[8]. Protein folding is essential to life,”
[9]. Joachim Pietzsch, “The Importance of Protein Folding,” Horizon Symposia, http://www.nature.com/horizon/proteinfolding/background/importance.html.
[10]. Joachim Pietzsch, “The Importance of Protein Folding,” Horizon Symposia, http://www.nature.com/horizon/proteinfolding/background/importance.html.
[11]. Joachim Pietzsch, “The Importance of Protein Folding,” Horizon Symposia, http://www.nature.com/horizon/proteinfolding/background/importance.html.
[12]. Joachim Pietzsch, “The Importance of Protein Folding,” Horizon Symposia, http://www.nature.com/horizon/proteinfolding/background/importance.html.
[13]. Bruce Alberts, “Biology Past and Biology Future: Where have we been and where are we going?” http://www.interacademies.net/?id=7642.
[14]. Bruce Alberts, Alexander Johnson, Julian Lewis, Martin Raff, Keith Roberts, and Peter Walter, Molecular Biology of the Cell, 4th ed. (
[15]. Bruce Alberts, Alexander Johnson, Julian Lewis, Martin Raff, Keith Roberts, and Peter Walter, Molecular Biology of the Cell, 4th ed. (
[16]. Bruce Alberts, Alexander Johnson, Julian Lewis, Martin Raff, Keith Roberts, and Peter Walter, Molecular Biology of the Cell, 4th ed. (
[17]. Bruce Alberts, Alexander Johnson, Julian Lewis, Martin Raff, Keith Roberts, and Peter Walter, Molecular Biology of the Cell, 4th ed. (
[18]. Theodosius Dobzhansky, “Nothing in Biology Makes Sense Except in the Light of Evolution,” The American Biology Teacher, March 1973, as quoted from the website: http://www.pbs.org/wgbh/evolution/library/10/2/text_pop/l_102_01.html.
[19]. Bruce Alberts, Alexander Johnson, Julian Lewis, Martin Raff, Keith Roberts, and Peter Walter, Molecular Biology of the Cell, 4th ed. (
[20]. Interview with Keiichi Namba, “Revealing the mystery of the bacterial flagellum – A self-assembling nanomachine with fine switching capability,” Japan Nanonet Bulletin, 11th Issue, 5 February 2004, http://www.nanonet.go.jp/english/mailmag/2004/011a.html. A PDF Version is available on this webpage: http://www.nanonet.go.jp/english/mailmag/pdf/011a.pdf, p. 3.
[21]. Interview with Keiichi Namba, “Revealing the mystery of the bacterial flagellum – A self-assembling nanomachine with fine switching capability,” Japan Nanonet Bulletin, 11th Issue, 5 February 2004, http://www.nanonet.go.jp/english/mailmag/2004/011a.html. A PDF Version is available at this website: http://www.nanonet.go.jp/english/mailmag/pdf/011a.pdf, p. 3.
[23]. Interview with Keiichi Namba, “Revealing the mystery of the bacterial flagellum – A self-assembling nanomachine with fine switching capability,” Japan Nanonet Bulletin, 11th Issue, 5 February 2004, http://www.nanonet.go.jp/english/mailmag/2004/011a.html. A PDF Version is available on this webpage: http://www.nanonet.go.jp/english/mailmag/pdf/011a.pdf, p. 5.
[24]. Interview with Keiichi Namba, “Revealing the mystery of the bacterial flagellum – A self-assembling nanomachine with fine switching capability,” Japan Nanonet Bulletin, 11th Issue, 5 February 2004, http://www.nanonet.go.jp/english/mailmag/2004/011a.html. A PDF Version is available on this webpage: http://www.nanonet.go.jp/english/mailmag/pdf/011a.pdf, p. 6.
[25]. Interview with Keiichi Namba, “Revealing the mystery of the bacterial flagellum – A self-assembling nanomachine with fine switching capability,” Japan Nanonet Bulletin, 11th Issue, 5 February 2004, http://www.nanonet.go.jp/english/mailmag/2004/011a.html. A PDF Version is available on this webpage: http://www.nanonet.go.jp/english/mailmag/pdf/011a.pdf, p. 3.
[26]. Interview with Keiichi Namba, “Revealing the mystery of the bacterial flagellum – A self-assembling nanomachine with fine switching capability,” Japan Nanonet Bulletin, 11th Issue, 5 February 2004, http://www.nanonet.go.jp/english/mailmag/2004/011a.html. A PDF Version is available on this webpage: http://www.nanonet.go.jp/english/mailmag/pdf/011a.pdf, p. 3.
[27]. Interview with Keiichi Namba, “Revealing the mystery of the bacterial flagellum – A self-assembling nanomachine with fine switching capability,” Japan Nanonet Bulletin, 11th Issue, 5 February 2004, http://www.nanonet.go.jp/english/mailmag/2004/011a.html. A PDF Version is available on this webpage: http://www.nanonet.go.jp/english/mailmag/pdf/011a.pdf, p. 3.
[29]. A video documenting the work done from Namba’s group can be downloaded from this website: http://www.nanonet.go.jp/english/mailmag/2004/files/011a.wmv. The video segment running from about 3:00-5:30 has fascinating pictures of a flagellum’s molecular construction. The video segment running from about 6:30-10:00 describes how Namba’s group unraveled the molecular components used in the flagellum’s construction. The video segment running from about 18:30-25:30 describes how detailed empirical study was used to uncover the complicated self-assembly process of the flagellum. Some short video clips of the flagellum are also available from this website: “Protonic Nanomachine Project,” Japan Science and Technology Corporation, http://www.fbs.osaka-u.ac.jp/labs/namba/npn/index.html.
[30]. A video documenting the work done from Namba’s group can be downloaded from this website: http://www.nanonet.go.jp/english/mailmag/2004/files/011a.wmv. See video segment at 25:30 for a photo of the article.
[31]. Dan Jones, “Uncovering the evolution of the bacterial flagellum,” New Scientist, 16 February 2008, http://www.newscientist.com/article/mg19726431.900-uncovering-the-evolution-of-the-bacterial-flagellum.html?full=true (accessed 2 February 2009). A subscription is now required.
[32]. Dan Jones, “Uncovering the evolution of the bacterial flagellum,” New Scientist, 16 February 2008, http://www.newscientist.com/article/mg19726431.900-uncovering-the-evolution-of-the-bacterial-flagellum.html?full=true (accessed 2 February 2009). A subscription is now required.
[33]. Phillip E. Johnson, Darwin on Trial, 2nd ed. (Downers Grove, IL: Intervarsity Press, 1993), pp. 120-124.
[34]. Dan Jones, “Uncovering the evolution of the bacterial flagellum,” New Scientist, 16 February 2008, http://www.newscientist.com/article/mg19726431.900-uncovering-the-evolution-of-the-bacterial-flagellum.html?full=true (accessed 2 February 2009). A subscription is now required.
[35]. Kenneth Miller, “The Flagellum Unspun: The Collapse of Irreducible Complexity,” http://www.millerandlevine.com/km/evol/design2/article.html.
[36]. Science and Creationism: A View from the
[38]. Charles Darwin, On The Origin of Species by Means of Natural Selection, 6th ed., Chapter 6, http://www.literature.org/authors/darwin-charles/the-origin-of-species-6th-edition/chapter-06.html.
[39]. For one example, see this website: “Didn’t
[41]. Kenneth Miller, “The Flagellum Unspun: The Collapse of Irreducible Complexity,” http://www.millerandlevine.com/km/evol/design2/article.html.
[42]. Kenneth Miller, “The Flagellum Unspun: The Collapse of Irreducible Complexity," http://www.millerandlevine.com/km/evol/design2/article.html.
[43]. Dan Jones, “Uncovering the evolution of the bacterial flagellum,” New Scientist, 16 February 2008, http://www.newscientist.com/article/mg19726431.900-uncovering-the-evolution-of-the-bacterial-flagellum.html?full=true (accessed 2 February 2009). A subscription is now required.
[44]. Anthony J.F. Griffiths, Jeffrey H. Miller, David T. Suzuki, Richard C. Lewontin, and William M. Gelbart, Introduction to Genetic Analysis, 7th ed. (
[46]. John Brockman, ed., Life: What A Concept! (
[47]. John Brockman, ed., Life: What A Concept! (
[48]. Bruce Alberts, Alexander Johnson, Julian Lewis, Martin Raff, Keith Roberts, and Peter Walter, Molecular Biology of the Cell, 4th ed. (
[49]. Science and Creationism: A View from the
[51]. "Cracking the Code of Life" Nova, PBS Airdate: 17 April 2001, http://www.pbs.org/wgbh/nova/transcripts/2809genome.html.
[52]. Mark B. Gerstein et al., “What is a gene, post-ENCODE?” Genome Research 17: 669-681, 2007, p. 679, http://genome.cshlp.org/cgi/reprint/17/6/669.pdf.
[55]. Mark B. Gerstein et al., “What is a gene, post-ENCODE?” Genome Research 17: 669-681, 2007, http://genome.cshlp.org/cgi/reprint/17/6/669.pdf.
[56]. Mark B. Gerstein et al., “What is a gene, post-ENCODE?” Genome Research 17: 669-681, 2007, Figure 5, p. 678, http://genome.cshlp.org/cgi/reprint/17/6/669.pdf.
[57]. “Identification and analysis of functional elements in 1% of the human genome by the ENCODE pilot project,” The Encode Project Consortium, Nature 447:789-816, 14 June 2007, p. 799, http://www.nature.com/nature/journal/v447/n7146/pdf/nature05874.pdf.
[58]. Alon Zaslaver et al., “Just-in-time transcription program in metabolic pathways,” Nature Genetics 36:486-91, 25 April 2004, http://www.nature.com/ng/journal/v36/n5/abs/ng1348.html, http://www.nature.com/ng/journal/v36/n5/pdf/ng1348.pdf.
[59]. “Genes can be turned on and off,” DNA From The Beginning – Segment 33, http://www.dnaftb.org/dnaftb/33/concept/index.html. Quote is from text description in Video Interviews Tab – Clip 1.
[60]. “Genes can be turned on and off,” DNA From The Beginning – Segment 33, http://www.dnaftb.org/dnaftb/33/concept/index.html. Quote is an unofficial transcript of part of the Video Interview with Walter Gilbert – Clip 6.
[61]. “DNA Responds to Signals from outside the cell,” DNA From The Beginning – Segment 35, http://www.dnaftb.org/dnaftb/35/concept/index.html. This is a summary of the Video Interview with James Darnell – Clip 1.
[62]. “DNA Responds to Signals from outside the cell,” DNA From The Beginning – Segment 35, http://www.dnaftb.org/dnaftb/35/concept/index.html. Quote is an unofficial transcript of the Video Interview with James Darnell – Clip 6.
[63]. Eric Davidson Laboratory, “Endomesoderm Network: Overview Up To 30 Hours,” http://sugp.caltech.edu/endomes/#UpTo30NetworkDiagram. I originally viewed a version of this diagram in the book: Michael Behe, The Edge of Evolution (
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