FYI: I.D. IN DNA- Deciphering Design in the Genetic Code


By Fazale Rana http://www.reasons.org/resources/publications/facts-faith/2002issue08#deciphering_design

A pilot flying his plane over the South Pacific sees an uncharted island in the distance and circles downward to take a closer look. As the plane descends, the pilot spots large rocks on the island's shore arranged to spell out SOS. Beyond the reach of waves, he notices a grass hut. Without hesitation, the pilot radios for help.

Is this pilot behaving rationally? No one would question the point. He recognizes the improbability of wind and waves acting on the rocks along the shore to spell SOS.1 Experience has taught the pilot that intelligible messages must come from intelligent sources. SOS, though not a word in the English language, represents the code for the universal distress message. The island inhabitant spelled out not just a word, such as "help," but a special code, SOS, on the beach knowing that anyone seeing it from the air would recognize its meaning.

The grass hut also convinces the pilot to radio for help. It provides further evidence that the rocks' arrangement on the beach is not the effect of chance, but rather the work of someone stranded on the island. Encoded information coupled with additional evidence for intelligent activity provides support for design that goes beyond the mere presence of information. It requires an intelligent agent to choose and employ the code. And, encoded information carries an implied sense of purpose.

Over the last 40 years, scientists have found the same type of evidence inside the cell that prompted the pilot's radio call for help. They have discovered that the cell's biochemical machinery is an information-based system. Moreover, the chemical information inside the cell exists as encoded information. The genetic code (the rules used to encode the cell's information) defines the cell's biochemical information system.

By itself, the cell's encoded information offers powerful evidence for an Intelligent Designer. And, like the islander's grass hut, recent discoveries provide additional proof validating the premise. Molecular biologists studying the genetic code's origin have unwittingly stumbled across profound evidence for Intelligent Design—a type of fine-tuning in the rules that form the genetic code. These rules impart to the genetic code the surprising capacity to minimize errors.

Error-minimization properties in the genetic code allow the cell's biochemical information systems to make mistakes and still communicate critical information with high fidelity. It's as if the stranded island inhabitant could arrange the rocks as SSO or OSS and still communicate the need for help.

Biochemical Information
Proteins
Much as the islander's message began with the rocks, the description of cellular information begins with proteins. Proteins, the "workhorse" molecules of life, take part in essentially every cellular and extracellular structure and activity. They help form structures inside the cell and in the cell's surrounding matrix. Among other roles, proteins catalyze chemical reactions, harvest chemical energy, serve in the cell's defense systems, and store and transport molecules.2

Molecules called polypeptides make up proteins. One or more of the same and/or different polypeptides interact to form proteins. Polypeptides are chain-like molecules folded into precise three-dimensional structures. The polypeptide's three-dimensional architecture determines the way one polypeptide interacts with other polypeptides to form a protein. The structure of the polypeptide consequently dictates its function.3

Polypeptides form when the cellular machinery links together (in a head-to-tail fashion) smaller subunit molecules called amino acids.4 The cell employs 20 different amino acids to make polypeptides. The amino acids that make up the cell's polypeptide chains possess a variety of chemical and physical properties.5 In principle, the 20 amino acids can link up in any of the possible amino acid combinations and sequences to form a polypeptide.

Each amino acid sequence imparts the polypeptide with a unique chemical and physical profile along its chain. The chemical and physical profile determines how the polypeptide chain folds, and, therefore, how it interacts with other polypeptide chains to form a functional protein. Because structure determines the function of a polypeptide, the amino acid sequence ultimately defines the type of work the polypeptide performs.

A polypeptide's amino acid sequence contains information. Just as letters form words, amino acids strung together form the "words" of the cell, polypeptides.6 In language, some letter combinations produce meaningful words and others produce gibberish. Amino acid sequences do the same. Some produce functional polypeptides, whereas others produce gibberish polypeptides that serve no role inside the cell.7

Treating amino acid sequences as information has become a fruitful approach for researchers seeking to understand the origin of proteins.8 It has also helped them characterize the functional utility of different amino acid sequences.

DNA
DNA, like polypeptides, contains information. In fact, DNA's chief function is information storage.

Like proteins, DNA consists of chain-like molecules known as polynucleotides.9 Two polynucleotide chains align in an antiparallel fashion to form a DNA molecule. (The two strands are arranged parallel to one another with the starting point of one strand located next to the ending point of the other strand, and vice versa.) The paired polynucleotide chains twist around each other forming the well-known DNA double helix. The cell's machinery forms polynucleotide chains by linking together four different subunit molecules called nucleotides. The four nucleotides used to build DNA chains are adenosine, guanosine, cytidine, and thymidine, familiarly known as A, G, C, and T, respectively.

DNA stores the information necessary to make all the polypeptides used by the cell. The sequence of nucleotides in the DNA strands specifies the sequence of amino acids in polypeptide chains. Scientists refer to the amino-acid-coding nucleotide sequence (for constructing polypeptides) along the DNA strand as a gene.10 Through the use of genes, DNA stores the information functionally expressed in the amino acid sequences of polypeptide chains. The DNA strands' nucleotides function as alphabet letters and the genes as words.

Central Dogma of Molecular Biology
No discussion of biochemical information systems would be complete without considering information "flow" inside the cell, known as the "central dogma of molecular biology."11 This concept describes how information stored in DNA becomes functionally expressed through the amino acid sequence and activity of polypeptide chains.

Found inside the nucleus of complex cells, DNA can be compared to the reference books found in a library. The information stored there cannot be removed but must be copied, or transcribed. DNA does not leave the nucleus to direct the synthesis of polypeptide chains. Rather the cellular machinery copies the gene's sequence by assembling another polynucleotide, messenger RNA (mRNA).12 This single-strand molecule is similar, but not identical, in composition to DNA. One of the most important differences between DNA and mRNA is the use of uridine (U) in place of thymidine (T) to form the mRNA chain. Scientists refer to the process of copying mRNA from DNA as transcription.

Once assembled, mRNA migrates from the nucleus of the cell into the cytoplasm. At the ribosome, mRNA directs the synthesis of polypeptide chains.13 The information content of the polynucleotide sequence is translated into the polypeptide amino acid sequence–– much like translating Spanish into English.

The analogical language used to describe the flow of information in biochemical systems is no accident. Biochemical systems are information systems.

The Genetic Code
Life's Encoded Information
One may wonder how the sequence of nucleotides in DNA translates into the sequence of amino acids in a polypeptide. There seems to be a mismatch between the storage and functional expression of information in the cell. A one-to-one relationship cannot exist between the four different nucleotides of DNA and the 20 different amino acids used to assemble polypeptides. The cell overcomes this mismatch by using a code comprised of groupings of three nucleotides to specify the 20 different amino acids.14

The cell uses a set of rules to relate these nucleotide triplet sequences to the 20 amino-comprising polypeptides. Molecular biologists refer to this set of rules as the genetic code. The nucleotide triplets, or "codons" as they are called, represent the fundamental communication units of the genetic code. In the same way that the stranded islander used three letters, SOS, to communicate his plight, the genetic code uses three nucleotide "characters" to signify an amino acid. The genetic code is essentially universal among all living organisms.

Sixty-four codons make up the genetic code. Because the genetic code only needs to encode 20 amino acids, some of the codons are redundant. That is, different codons code for the same amino acid. In fact, up to six different codons specify some amino acids. Others are specified by only one codon.

Interestingly, some codons, called stop codons or nonsense codons, code no amino acids. (For example, the codon UGA is a stop codon.) These codons always occur at the end of the gene, informing the cell where the polypeptide chain ends. Stop codons serve as a form of "punctuation" for the cell's information system.

Some coding triplets, called start codons, play a dual role in the genetic code. These codons not only encode amino acids, but also "tell" the cell where a polypeptide begins. For example, the codon GUG not only encodes the amino acid valine, it also specifies the starting point of the polypeptide chain. Start codons function as a sort of "capitalization" for the information system of the cell.

The Genetic Code and Intelligent Design
Observed information on the island leads the pilot to reasonably conclude that an intelligent agent designed it with a purpose. The information content of DNA and proteins, the molecules that ultimately define life's most fundamental structures and processes, leads to the inescapable conclusion that an Intelligent Designer with purpose in mind is responsible for life. This conclusion is as rational as the one made by the pilot when he spotted the message on the beach and radioed for help.

The genetic code, the set of rules that translate the stored information found in DNA into the functional information of proteins, provides further support for an Intelligent Designer. All codes require an intelligent agent to develop the set of rules defining the code.

The set of rules that define the genetic code, universal to all life, reveals still more amazing evidence for design. The genetic code displays a fascinating capacity to resist the errors that naturally occur as the cell uses information or transmits information from one generation to the next. Qualitative inspection of the code only partly exposes its fine-tuning. Recent studies employing methods to quantify error-minimization properties in the genetic code bring this new evidence for Intelligent Design squarely into focus.

Mutations
Why does the error-minimization capacity of the genetic code provide such a powerful indicator for Intelligent Design? Translating the stored information of DNA into the functional information of proteins is the genetic code's chief function. The genetic code's failure to transmit and translate information with high fidelity can be devastating to the cell. Briefly considering how mutations affect cells facilitates understanding.

A mutation refers to any change that takes place in the DNA nucleotide sequence.15 DNA can experience several different types of mutations. Substitution mutations are one common type. In a substitution mutation, one or more of the nucleotides in the DNA strand is replaced by another nucleotide. For example, an A may be replaced by a G, or a C may be replaced by a T. This substitution changes the codon that the nucleotide is part of. The amino acid specified by that codon changes, leading to an altered chemical and physical profile along the polypeptide chain. If the substituted amino acid possesses dramatically different physicochemical properties from the native amino acid, the polypeptide folds improperly. This improper folding impacts the polypeptide, and hence yields a protein with reduced or even lost function. Most mutations harm cellular health because they significantly and negatively impact protein structure and function.

Qualitative Design Evidence
The genetic code's redundancy appears to be well thought out rather than haphazard. Genetic code rules incorporate a design that allows the cell to avoid the harmful effects of substitution mutations. For example, six codons encode the amino acid leucine (Leu). If at a particular amino acid position in a polypeptide, Leu is encoded by 5' (pronounced five prime, a marker indicating the beginning of the codon). CUU, substitution mutations in the 3' position from U to C, A, or G produce three new codons, 5' CUC, 5' CUA, and 5' CUG, all of which code for Leu. The net effect produces no change in the amino acid sequence of the polypeptide. For this scenario, the cell successfully avoids the negative effects of a substitution mutation.

Likewise, a change of C in the 5' position to a U generates a new codon, 5'UUU, that specifies phenylalanine, an amino acid with similar physical and chemical properties to Leu. A change of C to an A or to a G produces codons that code for isoleucine and valine, respectively. These two amino acids also possess chemical and physical properties similar to leucine. Qualitatively, the genetic code appears constructed to minimize errors that result from substitution mutations.

Quantitative Design Evidence
Recently, scientists from the University of Bath (U.K.) and from Princeton University worked to quantify the error-minimization capacity of the genetic code. Early work indicated that the naturally occurring genetic code withstands the potentially harmful effects of substitution mutations better than all but 0.02 percent (1 out of 5000) of randomly generated genetic codes with codon assignments different from the universal genetic code.16

This initial work overlooked the fact that some types of substitution mutations occur more frequently than others in nature. For example, an A-to-G substitution occurs more frequently than does either an A-to-C or an A-to-T mutation. When researchers incorporated this correction into their analysis, they discovered that the naturally occurring genetic code performed better than one million randomly generated genetic codes. They also found that the genetic code in nature resides near the global optimum for all possible genetic codes with respect to its error-minimization capacity.17 Nature's universal genetic code is truly one in a million—or better!

The genetic code's error-minimization properties are actually more dramatic than these results indicate. When researchers calculated the error-minimization capacity of one million randomly generated genetic codes, they discovered that the error-minimization values formed a distribution where the naturally occurring genetic code's capacity occurred outside the distribution.18 Researchers estimate the existence of 1018 possible genetic codes possessing the same type and degree of redundancy as the universal genetic code. All of these codes fall within the error-minimization distribution. This finding means that of 1018 possible genetic codes, few, if any, have an error-minimization capacity that approaches the code found universally in nature.

Obviously concerned about the implications, some researchers have challenged the optimality of the genetic code.19 The teams from Bath, Princeton, and elsewhere, however, have effectively responded to these challenges.20

A Force Behind the Genetic Code
Based on their research results, the Bath and Princeton scientists concluded that the rules of the genetic code could not be a frozen accident. A genetic code assembled through random biochemical events would not possess near ideal error-minimization properties. These researchers argue that a "force" shaped the genetic code. Instead of looking to a supernatural explanation for the genetic code's origin, however, they appeal to natural selection. They believe random events operated on by "the forces of natural selection" over and over again produced the genetic code's error-minimization capacity.21

Can the Genetic Code Evolve?
Other scientific work questions the likelihood that the genetic code evolved. In 1968 Nobel Laureate Francis Crick, in a classic paper, convincingly argued that the genetic code could not have undergone significant evolution.22 The rationale for Crick's position is easy to understand. Any change in codon assignment leads to changes in amino acids in every polypeptide made by the cell. This wholesale change in polypeptide sequences would result in large numbers of defective proteins. Nearly any conceivable change to the genetic code would be lethal to the cell.

Even if the genetic code could change gradually over time to yield a set of rules that allowed for maximum error-minimization capacity, is there enough time for this process to occur? Biophysicist Hubert Yockey has addressed this question.23 He calculates that natural selection would have to explore 1.40 x 1070 different genetic codes to hit upon the universal genetic code found in nature. Yockey estimates the maximum time available for the code to originate as 6.3 x 1015 seconds. Put simply, natural selection lacks adequate time to find the universal genetic code. It would have to evaluate about 1054 codes per second.

Other researchers suggest that the genetic code's origin coincides with the origin of life. Operating within the evolutionary paradigm, a team headed by renowned origin-of-life researcher Manfred Eigen estimated the age of the genetic code as 3.8 + 0.6 billion years.24 Current geochemical evidence places life's first appearance on Earth at 3.86 billion years ago.25

The Supernatural Origin of the Gentic Code
The genetic code—the set of rules used by the cell to translate information stored in DNA into the information used by polypeptides—possesses a virtually unique optimality in its capacity to resist errors caused by mutation. The genetic code in every way defies explanation as a frozen accident produced by random biochemical events, or as the fortuitous outcome of an evolutionary process directed by the blind forces of natural selection. Genetic code evolution would be catastrophic for the cell. Given the rapidity of life's origin, time is too short for natural selection to come across the well-designed universal genetic code found in nature. The genetic code seemingly originates at the time life first appears on Earth. All this evidence dictates the conclusion that an Intelligent Designer is responsible for the genetic code.

This conclusion becomes even more compelling when one considers that encoded information demands an intelligent agent not only to generate the information, but also to design and apply the set of rules that constitute the code. The remarkable fine-tuning of the genetic code provides cohesive corroborative evidence for the biblical Intelligent Designer. Like the SOS rock formation and the grass hut on the beach, the genetic code offers every indication that a Creator deliberately and purposefully shaped the message.

References:
Peter Kreeft, Fundamentals of the Faith: Essays in Christian Apologetics (San Francisco: Ignatius Press, 1988), 25-26.
Robert C. Bohinksi, Modern Concepts in Biochemistry, 4th ed. (Boston: Allyn and Bacon, 1983), 86-87.
Harvey Lodish et al., Molecular Cell Biology, 4th ed. (New York: W. H. Freeman, 2000), 54-60.
Lodish et al., 51-54.
Lodish et al., 52.
Michael Denton, Evolution: A Theory in Crisis (Bethesda, MD: Adler & Adler, 1986), 308-25; Walter L. Bradley and Charles B. Thaxton, "Information and the Origin of Life," in The Creation Hypothesis: Scientific Evidence for an Intelligent Designer, ed. J. P. Moreland (Downers Grove, IL: InterVaristy Press, 1994), 188-90.
Lodish et al., 257.
Hubert P. Yockey, Information Theory and Molecular Biology (Cambridge: Cambridge University Press, 1992); Charles B. Thaxton, Walter L. Bradley, and Roger L. Olsen, The Mystery of Life's Origin: Reassessing Current Theories (Dallas: Lewis and Stanley, 1984), 127-43; Bernd-Olaf Küppers, Information and the Origin of Life, (Cambridge, MA: The MIT Press, 1990).
Lodish et al., 101-05.
The gene structure is far more complex than portrayed here. Any biochemistry or molecular biology textbook can be consulted for a more thorough discussion of gene structure.
David Freifelder, Molecular Biology, 2d ed. (Boston, MA: Jones and Bartlett Publishers, 1987), 208.
Lodish et al., 111-116.
Lodish et al., 125-34.
Lodish et al., 117-20.
Lubert Stryer, Biochemistry, 3d ed. (New York: W. H. Freeman, 1988), 675-76.
David Haig and Laurence D. Hurst, "A Quantitative Measure of Error Minimization in the Genetic Code," Journal of Molecular Evolution 33 (1991): 412-17.
Gretchen Vogel, "Tracking the History of the Genetic Code," Science 281 (1998), 329-31; Stephen J. Freeland and Laurence D. Hurst, "The Genetic Code Is One in a Million," Journal of Molecular Evolution 47 (1998): 238-48; Stephen J. Freeland et al., "Early Fixation of an Optimal Genetic Code," Molecular Biology and Evolution 17 (2000): 511-18.
Freeland and Hurst, 238-48.
Massimo D. Giulio, "The Origin of the Genetic Code," Trends in Biochemical Sciences 25 (2000): 44.
Stephen J. Freeland, Robin D. Knight and Laura F. Landweber, "Measuring Adaptation within the Genetic Code," Trends in Biochemical Sciences 25 (2000): 44; Stephen J. Freeland and Laurence D. Hurst, "Load Minimization of the Genetic Code: History Does Not Explain the Pattern," Proceedings of the Royal Society of London B 265 (1998): 2111-19; Terres A. Ronneberg, Laura F. Landweber and Stephen J. Freeland, "Testing a Biosynthetic Theory of the Genetic Code: Fact or Artifact?" Proceedings of the National Academy of Sciences, USA 97 (2000): 13690-95; Ramin Amirnovin, "An Analysis of the Metabolic Theory of the Origin of the Genetic Code," Journal of Molecular Evolution 44 (1997): 473-76.
Robin D. Knight, Stephen J. Freeland and Laura F. Landweber, "Selection, History and Chemistry: The Three Faces of the Genetic Code," Trends in Biochemical Sciences 24 (1999): 241-47.
F. H. C. Crick, "The Origin of the Genetic Code," Journal of Molecular Biology 38 (1968): 367-79.
Yockey, 180-83.
Manfred Eigen et al., "How Old Is the Genetic Code? Statistical Geometry of tRNA Provides an Answer," Science 244 (1989), 673-79.
Fazale Rana, "Origin-of-Life Predictions Face Off: Evolution vs. Biblical Creation," Facts for Faith 6 (Q2 2001), 41-47.

Sidebar
The scientists from the University of Bath and Princeton University, fully aware of Francis Crick's work, still rely on evolution to explain the genetic code's optimal design because of the existence of nonuniversal genetic codes. While the genetic code in nature is generally regarded as universal, some nonuniversal genetic codes exist—genetic codes that employ slightly modified codon assignments. Presumably these nonuniversal genetic codes evolved from the universal genetic code. Therefore, researchers argue that genetic code evolution is possible. For the most part, however, the codon assignments of the nonuniversal genetic codes are identical to that of the universal genetic code with only one or two codon assignments being different. It is better to think of the nonuniversal genetic codes as deviants of the universal genetic code.

Does the existence of nonuniversal genetic codes imply that wholesale genetic code evolution is possible? The answer is no. Careful study reveals that codon changes in the nonuniversal genetic codes always occur in relatively small genomes, such as mitochondrial genomes, and involve either: (1) codons that occur at low frequencies in that particular genome; or (2) stop codons. Changes in assignment for these codons could occur without producing a lethal scenario, since only a small number of polypeptides in the cell or organelle would experience an altered amino acid sequence. Thus, it appears that limited evolution of the genetic code can take place, but only in special circumstances.1

Reference:
Syozo Osawa et al., "Evolution of the Mitochondrial Genetic Code I. Origin of AGR Serine and Stop Codons in Metazoan Mitochondria," Journal of Molecular Evolution 29 (1989): 202-7; Dennis W. Schultz and Michael Yarus, "On the Malleability in the Genetic Code," Journal of Molecular Evolution 42 (1996): 597-601; Eors Szathmary, "Codon Swapping as a Possible Evolutionary Mechanism," Journal of Molecular Evolution 32 (1991): 178-82.

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Comment by Dane on April 27, 2009 at 7:23pm
Chromosome 2 is widely accepted to be a result of an end-to-end fusion of two ancestral chromosomes. [3][4]
Fusion of ancestral chromosomes left distinctive remnants of telomeres, and a vestigial centromere


The evidence for this includes:

* The correspondence of chromosome 2 to two ape chromosomes. The closest human relative, the bonobo, has near-identical DNA sequences to human chromosome 2, but they are found in two separate chromosomes. The same is true of the more distant gorilla and orangutan. [5][6]
* The presence of a vestigial centromere. Normally a chromosome has just one centromere, but in chromosome 2 we see remnants of a second. [7]
* The presence of vestigial telomeres. These are normally found only at the ends of a chromosome, but in chromosome 2 we see additional telomere sequences in the middle. [8]

Taken From: http://en.wikipedia.org/wiki/Chromosome_2_(human)

"Chromosome 2 is thus strong evidence in favour of the common descent of humans and other apes. According to researcher J. W. IJdo, "We conclude that the locus cloned in cosmids c8.1 and c29B is the relic of an ancient telomere-telomere fusion and marks the point at which two ancestral ape chromosomes fused to give rise to human chromosome 2."[8]"

Also see Kitzmiller vs. Dover (latest court case (and a loss for I.D.) involving whether or no I.D. is science and should be in public school curriculum.)

Here is a key witness in the case:

Comment by Jeff H on April 27, 2009 at 7:59pm
Alway a pleasure Dane,

And the Miller Told His Tale: Ken Miller's Cold (Chromosomal) Fusion (Updated)
by Casey Luskin (originally written in Oct. of 2005, some updates and changes added later.)

Dr. Kenneth Miller was the leadoff hitter for plaintiffs last week in the trial over ID in Dover. Amidst other things, Miller's testimony was aimed at making a case that the Neo-Darwinian hypothesis is as well-supported as gravitational theory. It was my understanding that this trial was about whether or not Dover had violated the First Amendment by mentioning to students that some book in the library advocated intelligent design. So I was a little confused as to why it was relevant for Miller to give us all a lesson in evolutionary biology. Nonetheless, this article will respond to Dr. Miller's arguments that evidence for fusion in human chromosome #2 demonstrates that humans share a common ancestor with living apes.

According to Neo-Darwinism, humans and extant apes supposedly share a common ancestor. During Dr. Miller's testimony supporting the theory of evolution, he discussed how human chromosome #2 has two centromeres, which are the central - attachment points used for pulling a chromosome to one end of a cell during mitosis. Chromosomes normally only have one centromere, but human chromosome # 2 looks like two chromosomes were fused together within its interior because it has two centromeres (or at least, it has one normal centromere, and another region that looks a lot like a centromere elsewhere within the chromosome). Miller further noted that human chromosome #2 has a section where there are two telomeres, structures normally at the tips of chromosomes, which are found in the middle of chromosome #2. Essentially, these two telomeres are oriented in a way that it looks, genetically speaking, like the ends of two chromosomes were fused together.

I am more than willing to acknowledge and affirm that Miller provided good direct empirical evidence for a chromosomal fusion event which created human chromosome #2. He claims this evidence strongly supports his view that humans and chimps share a common ancestor, because humans have two fewer chromosomes than chimp, and Darwinian evolution predicts this fusion evidence. But his argument raises two crucial questions:

(1) Is his chromosome fusion story good evidence for Neo-Darwinian common ancestry between humans and apes?

(2) Does Dr. Miller's hypothesis perhaps pose problems for a Neo-Darwinian account of human genetic history?

As will be discussed below, the answer to Question (1) is "No" and the answer to Question (2) is "Yes."

Evidence for Fusion in a Human Chromosome Tells you LITTLE TO NOTHING about whether Humans Share a Common Ancestor with Living Apes

Usually Darwinists argue for human-ape common ancestry based upon alleged "shared errors" in human DNA and ape DNA. But the chromosomal fusion evidence is not a “shared error” argument for human / ape common ancestry, because apes do not have a fused chromosome. The human chromosomal fusion argument focuses on a fusion event that is specific to the human line, and therefore provides a highly limited form of evidence for human / ape common ancestry.

All Miller has done is documented direct empirical evidence of a chromosomal fusion event in the human line. But evidence for a chromosomal fusion event is not evidence for when that event took place, nor is it evidence for the ancestry prior to that event.

To be more specific, the fusion-evidence implies that some of our ancestors likely had 48 chromosomes. But Miller has not provided any evidence that the individual with 48 chromosomes was historically related to modern apes. (I grant that our chromosome #2 has banding patterns similar to two ape chromosomes, but given that our chromosome structure is generally similar to that of apes anyways, it is not a stretch to assume that any 48 chromosome ancestor of modern humans might have also had a chromosomal scheme similar to that of apes, regardless of whether or not that individual was related to apes. Claiming that banding pattern similarities is evidence of common ancestry with apes simply invokes the “similarity = common ancestry” argument, and thus begs the question.) It is entirely possible that our genus Homo underwent a chromosomal fusion event within its own separate history.

Under Neo-Darwinism, the common ancestor of humans and apes is thought to have lived about six million years ago. But under Miller's account, it is entirely possible that this chromosomal fusion event happened in a human population only 10,000 years ago, in a population that has no relation to living apes. In such a case, this chromosomal fusion event thus needs not have anything to do with making us human-like as opposed to ape-like. Clearly this chromosomal fusion event could be extremely far removed from any alleged ancestry with apes.

In essence, we don't know that this chromosomal fusion event happened on a line which leads back to some alleged common ancestor of apes and humans. All we know is that this fusion event happened in the line that led to you and me. Whether that line has common ancestry with apes is a separate question which cannot be answered by this fusion evidence.

All that evolutionists have claimed is that this fusion event occurred after the split that led to humans, so it occurs only in the human lineage. Evidence of a chromosomal fusion event is not evidence that our line leads all the way back to apes.

Given that we had a 48-chromosome ancestor, we don't know if our 48-chromosome ancestor was an ape or not. For all we know, our 48-chromosome ancestor was a part of a separately designed species, as fully human as any person you might meet on the street today. There is no good reason to think that going from a 46-chromosome individual to a 48-chromosome individual would make our species more ape-like.

This is explained in figure 1 below:



Figure 1. This animated gif shows how even if the empirical genetic evidence mandates a chromosomal fusion event, this doesn't tell you anything about whether or not humans share ancestry with apes. The "Separate Ancestry" slide shows that the chromosomal fusion event may have simply taken place in a separately-designed basic type which, initially, had 48 chromosomes. The "Common Ancestry" slide shows how the chromosomal fusion event may have also taken place in a line which led back to a hypothetical common ancestor of humans and modern apes. The point is that all we have is evidence for a fusion event, but that fusion event is equally compatible with either separate ancestry from apes, or common ancestry with apes. The fusion event itself does not provide any independent evidence for common ancestry with apes. To argue that it is evidence for common ancestry requires special pleading.


Miller's "prediction" of Neo-Darwinian evolution is not a hard prediction of his theory: if common ancestry is true, Miller predicts that there must have been a fusion event. But the converse is not true. The presence of this fusion event in no way requires that common ancestry is true.

It only gets worse for Neo-Darwinism
Under Neo-Darwinism, genetic mutation events (including chromosomal aberrations) are generally assumed to be random and unguided. Miller's Cold-Fusion tale becomes more suspicious when one starts to ask harder questions like "how could a fusion event get fixed into a population via random and unguided processes, or how could it result in viable offspring?" Miller's account must overcome two potential obstacles:

(1) In most of our experience, individuals with randomly-fused chromosomes or extra chromosomes can be normal, but it is very likely that their offspring will ultimately have a genetic disease. A classic example of such is a cause of Down syndrome, where an individual has an extra chromosome #21.

(2) One way around the problem in (1) is to find a mate that also had an identical chromosomal fusion event or chromosomal splitting event. But this would require a rare mutant finding a mate with identical traits. Valentine and Erwin explain that the odds of rare-mutants finding mates with identical traits are highly unlikely:
"[T]he chance of two identical rare mutant individuals arising in sufficient propinquity to produce offspring seems too small to consider as a significant evolutionary event."

(Erwin, D..H., and Valentine, J.W. "'Hopeful monsters,' transposons, and the Metazoan radiation", Proc. Natl. Acad. Sci USA, 81:5482-5483, Sept 1984)
In other words, Miller has to explain why a random chromosomal fusion event which, in our experience ultimately results in offspring with genetic diseases, didn’t result in a genetic disease and was thus advantageous enough to get fixed into the entire population of our ancestors. Given the lack of empirical evidence that random chromosomal fusion events are not disadvantageous, perhaps the presence of a chromosomal fusion event is not good evidence for a Neo-Darwinian history for humans.

Miller may have found good empirical evidence for a chromosomal fusion event. But our experience with mammalian genetics tells us that such a chromosomal aberration could have created a non-viable mutant, or a normal individual who could not produce viable offspring. Thus, Neo-Darwinism has a hard time explaining why such a random fusion event was somehow advantageous.

If it were to turn out that the fusion of two chromosomes can only result in a viable individual if the fusion event takes place in a highly unlikely and highly specified manner, then we may actually be looking at a case for a non-Darwinian intelligent design event in the history of the human genus.
Comment by Jeff H on April 27, 2009 at 7:59pm
sorry... source above http://www.ideacenter.org/contentmgr/showdetails.php/id/1392
Comment by Dane on April 27, 2009 at 9:09pm
Perhaps some of those fine folks from the Discovery Institute such as Mr. Luskin should have been witnesses in Kitzmiller vs. Dover, they certainly could have helped promote the ideology central to the Institute, which is creationism, I mean creation science, er, I mean Intelligent Design. He also fails to recognize in his writing that central to the court case was the issue of whether or not 'Intelligent Design' was science and could be taught as such. A secondary portion of the case focused on the Textbook that the Dover schoolboard wanted to introduce, which was called 'Of People and Pandas'. This was a book developed by the Foundation for Thoughts and Ethics (notice, not a professor of biology or a scientific academy of some sort), and was the subject of much criticism for it's obvious religious agenda and pseudo-science content.

Here is a copy of the judge's conclusion and ruling in the case. It speaks for itself.

H. Conclusion

The proper application of both the endorsement and Lemon tests to the facts of this case makes it abundantly clear that the Board's ID Policy violates the Establishment Clause. In making this determination, we have addressed the seminal question of whether ID is science. We have concluded that it is not, and moreover that ID cannot uncouple itself from its creationist, and thus religious, antecedents.

Both Defendants and many of the leading proponents of ID make a bedrock assumption which is utterly false. Their presupposition is that evolutionary theory is antithetical to a belief in the existence of a supreme being and to religion in general. Repeatedly in this trial, Plaintiffs' scientific experts testified that the theory of evolution represents good science, is overwhelmingly accepted by the scientific community, and that it in no way conflicts with, nor does it deny, the existence of a divine creator.

To be sure, Darwin's theory of evolution is imperfect. However, the fact that a scientific theory cannot yet render an explanation on every point should not be used as a pretext to thrust an untestable alternative hypothesis grounded in religion into the science classroom or to misrepresent well-established scientific propositions.

The citizens of the Dover area were poorly served by the members of the Board who voted for the ID Policy. It is ironic that several of these individuals, who so staunchly and proudly touted their religious convictions in public, would time and again lie to cover their tracks and disguise the real purpose behind the ID Policy.

With that said, we do not question that many of the leading advocates of ID have bona fide and deeply held beliefs which drive their scholarly endeavors. Nor do we controvert that ID should continue to be studied, debated, and discussed. As stated, our conclusion today is that it is unconstitutional to teach ID as an alternative to evolution in a public school science classroom.

Those who disagree with our holding will likely mark it as the product of an activist judge. If so, they will have erred as this is manifestly not an activist Court. Rather, this case came to us as the result of the activism of an ill-informed faction on a school board, aided by a national public interest law firm eager to find a constitutional test case on ID, who in combination drove the Board to adopt an imprudent and ultimately unconstitutional policy. The breathtaking inanity of the Board's decision is evident when considered against the factual backdrop which has now been fully revealed through this trial. The students, parents, and teachers of the Dover Area School District deserved better than to be dragged into this legal maelstrom, with its resulting utter waste of monetary and personal resources.

To preserve the separation of church and state mandated by the Establishment Clause of the First Amendment to the United States Constitution, and Art. I, § 3 of the Pennsylvania Constitution, we will enter an order permanently enjoining Defendants from maintaining the ID Policy in any school within the Dover Area School District, from requiring teachers to denigrate or disparage the scientific theory of evolution, and from requiring teachers to refer to a religious, alternative theory known as ID. We will also issue a declaratory judgment that Plaintiffs' rights under the Constitutions of the United States and the Commonwealth of Pennsylvania have been violated by Defendants' actions. Defendants' actions in violation of Plaintiffs' civil rights as guaranteed to them by the Constitution of the United States and 42 U.S.C. § 1983 subject Defendants to liability with respect to injunctive and declaratory relief, but also for nominal damages and the reasonable value of Plaintiffs' attorneys' services and costs incurred in vindicating Plaintiffs' constitutional rights.

NOW, THEREFORE, IT IS ORDERED THAT:

1. A declaratory judgment is hereby issued in favor of Plaintiffs pursuant to 28 U.S.C. §§ 2201, 2202, and 42 U.S.C. § 1983 such that Defendants' ID Policy violates the Establishment Clause of the First Amendment of the Constitution of the United States and Art. I, § 3 of the Constitution of the Commonwealth of Pennsylvania.
2. Pursuant to Fed.R.Civ.P. 65, Defendants are permanently enjoined from maintaining the ID Policy in any school within the Dover Area School District.
3. Because Plaintiffs seek nominal damages, Plaintiffs shall file with the Court and serve on Defendants, their claim for damages and a verified statement of any fees and/or costs to which they claim entitlement. Defendants shall have the right to object to any such fees and costs to the extent provided in the applicable statutes and court rules

s/John E. Jones III
John E. Jones III
United States District Judge
Comment by Dane on April 27, 2009 at 9:12pm
And a second response dealing with human chromosome #2. Chromosome #2 shows a definite fusion between two chromosomes at some point in the past, giving modern humans 46 chromosomes instead of 48 like a good number of other primates very similar to ourselves. I'd like to know - what's the other, valid, sensible, explanation for this fusion of chromosomes happening other than a fusion of two primate chromosomes at some point in an evolutionary process?

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