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Some testable predictions entailed by Dr. Kozulic’s model of Intelligent Design

In my last post, The Edge of Evolution?”, I drew readers’ attention to a 2011 paper by the Croatian biochemist Dr. Branko Kozulic, titled, Proteins and Genes, Singletons and Species, which argues that the presence of not one but literally hundreds of chemically unique proteins in each species is an event beyond the reach of chance, and that since these proteins exhibit specified complexity (as the amino acids which make up the polypeptide chain need to be in the correct order), each species must therefore be the result of intelligent planning. (A parallel argument can be made for de novo protein-coding genes.)

In this short post, I’d like to discuss a few falsifiable predictions which I believe are entailed by Dr. Kozulic’s hypothesis that Intelligent Design in Nature extends right down to the level of the species, in conjunction with his proposal that the concept of a species, which is defined in various ways in the field of biology, can best be defined in terms of the unique proteins and genes that characterize each species.

On a general level, the predictions made by Dr. Kozulic’s Intelligent Design model can be summed up in the following two propositions:

1. If two populations of organisms are known to share a common ancestry, and to have diverged from one another relatively recently, as a result of either unguided natural processes or human artificial selection, then there should not be any proteins or protein-coding genes that are unique to one of the two populations. (According to Dr. Kozulic’s Intelligent Design model, unguided processes are incapable of creating the hundreds of unique proteins and genes that characterize each species, within the time available; and of course, humans can’t accomplish this feat by selective breeding, either.)

2. If two populations of organisms are identified by biologists as distinct species on the basis of several independent criteria, then there should always be some proteins and protein-coding genes that are unique to each population. (According to Dr. Kozulic’s Intelligent Design model, each species of living organism can be characterized by proteins and genes that are unique to it.)

Falsification of proposition 1 would be absolutely fatal for Dr. Kozulic’s model of Intelligent Design. At the very least, it would mean that neither proteins nor protein-coding genes could be used to define the concept of a species, as he suggests. More importantly, it would also seem to imply that new proteins and protein-coding genes can originate as a result of unguided natural processes. (One might try to argue that perhaps the proteins and genes were originally present in both populations, but that some proteins and genes were subsequently lost from one population, but in my view, such an argument would be highly implausible. How could a population of organisms lose hundreds of proteins, as well as the genes that code for them?)

Falsification of proposition 2 would not be so serious: all it would mean is that the edge of evolution does not lie at the level of the species, as Dr. Kozulic hypothesizes, but at a higher taxonomic level – say, that of the genus. That should cause no alarm to Intelligent Design proponents, including those who profess to be old- or young-earth creationists. (Creationists entertain a wide variety of views as to what constitutes a “created kind”.)

Using Proposition 1, we can make the following predictions:

(a) If there are any genuine cases of ring species – and I say if because there are only four such species known in Nature, and some of the classic examples of ring species have recently been thrown into doubt – then there should be no proteins or genes which are unique to one population within that species;

(b) Domesticated animals should have the same proteins and protein-coding genes as their wild counterparts. For example, the domestic dog and its sole ancestor, the gray wolf (pictured above, courtesy of Wikipedia), should have the same proteins and genes.

(c) Man-made hybrid species, such as the mule, should not possess any proteins or protein-coding genes which are unique to that species.

Proposition 2 implies that any two species which are agreed by biologists to be genuinely distinct from one another should each possess (hundreds of) unique proteins and protein-coding genes.

The one case that I’d really like to see Intelligent Design biologists investigate is cichlid fish: a large family comprising up to 3,000 species, which are thought to have diverged within the last 10 million years. However, some of these species diverged much more recently, within the last few thousand years, making it very likely that their diversification was an unguided natural event. The question scientists need to examine is: which of these species possess unique proteins and protein-coding genes?

The following abstract by Barluenga et al. (“Sympatric speciation in Nicaraguan crater lake cichlid fish”, Nature, 2006 Feb 9; 439(7077): 719-723) illustrates what I’m getting at:

Sympatric speciation, the formation of species in the absence of geographical barriers, remains one of the most contentious concepts in evolutionary biology. Although speciation under sympatric conditions seems theoretically possible, empirical studies are scarce and only a few credible examples of sympatric speciation exist. Here we present a convincing case of sympatric speciation in the Midas cichlid species complex (Amphilophus sp.) in a young and small volcanic crater lake in Nicaragua. Our study includes phylogeographic, population-genetic (based on mitochondrial DNA, microsatellites and amplified fragment length polymorphisms), morphometric and ecological analyses. We find, first, that crater Lake Apoyo was seeded only once by the ancestral high-bodied benthic species Amphilophus citrinellus, the most common cichlid species in the area; second, that a new elongated limnetic species (Amphilophus zaliosus) evolved in Lake Apoyo from the ancestral species (A. citrinellus) within less than approximately 10,000 yr; third, that the two species in Lake Apoyo are reproductively isolated; and fourth, that the two species are eco-morphologically distinct.

If the two species Amphilophus citrinellus (pictured above, courtesy of Wikipedia and Omnitarian) and Amphilophus zaliosus are not only reproductively isolated but also eco-morphologically distinct, then we have multiple independent grounds for regarding them as bona fide species. In that case, Dr. Kozulic’s Intelligent Design model would predict that these species should each possess their own unique proteins and protein-coding genes. And if this turns out to be the case, then Kozulic’s model would imply that the daughter species did not arise as a result of ordinary natural processes, but as a result of intelligent manipulation of the ancestral species’ genome, less than 10,000 years ago. Obviously, there is a lot of research that needs to be done in this area.

Finally, I’d like to close with a brief discussion of Neanderthal man (depicted above, courtesy of UNiesert and Wikipedia), who is believed to have diverged from Homo sapiens somewhere between 350,000 and 700,000 years ago (when their presumed common ancestor, Heidelberg man, lived), but who is also thought to have interbred with modern human beings between 80,000 and 50,000 years ago, in Eurasia. (The skeleton of what is believed to have been a Neanderthal-Homo sapiens hybrid was found recently in Italy.) Neanderthal genes make up as much as 1 to 4% of the genome of Europeans living today. Despite his ability to inter-breed with modern man, many authorities classify Neanderthal man as a separate species, Homo neanderthalensis; however, others prefer to classify him as a subspecies, Homo sapiens neanderthalensis, placing modern man in the subspecies Homo sapiens sapiens. The ability to inter-breed does not necessarily indicate that Neanderthal man was the same species as we are; apparently, there are documented cases of two species hybridizing and producing fertile offspring and also of gene flow from one species into the gene pool of another by the repeated backcrossing of an interspecific hybrid with one of its parent species, so evidence of inter-breeding does not necessarily indicate that Neanderthal man was of the same species as we are.

Neanderthals had a brain the size of ours and are believed to have had a language, and they seem to have buried their dead with flowers, grave goods and ocher, although this remains controversial. On the other hand, the marked lack of innovation in their tool-making and the absence of conclusive evidence that Neanderthals created anything symbolic has led anthropologist Ian Tattersall, of the American Museum of Natural History, to doubt that they possessed the mental capacities that distinguish modern humans from other animals: “Burial in the simple Neanderthal style falls short of furnishing us with convincing proof of symbolic activity among these extinct hominids”, he declared in a recent interview. (Tattersall’s article, An Evolutionary Framework for the Acquisition of Symbolic Cognition by Homo sapiens, in Comparative Cognition and Behavior Reviews, 2008, Volume 3, pp 99-114, is also well worth reading.)

The question of whether Neanderthal man possessed unique proteins and genes is therefore one of vital importance for understanding who we are, and who this ancient human really was. As far as I can tell, he did possess a few unique genes. More information about Neanderthal genes can be found here, here, here and here. According to the study, A Draft Sequence of the Neandertal Genome by R. Green, D. Reich, S. Paabo et al. (Science, 7 May 2010: Vol. 328 no. 5979 pp. 710-722, DOI: 10.1126/science.1188021):

Features that occur in all present-day humans (i.e., have been fixed), although they were absent or variable in Neandertals, are of special interest. We found 78 nucleotide substitutions that change the protein-coding capacity of genes where modern humans are fixed for a derived state and where Neandertals carry the ancestral (chimpanzee-like) state (Table 2 and table S28). Thus, relatively few amino acid changes have become fixed in the last few hundred thousand years of human evolution; an observation consistent with a complementary study (57). We found only five genes with more than one fixed substitution changing the primary structure of the encoded proteins. One of these is SPAG17, which encodes a protein important for the axoneme, a structure responsible for the beating of the sperm flagellum (58). The second is PCD16, which encodes fibroblast cadherin-1, a calcium-dependent cell-cell adhesion molecule that may be involved in wound healing (59). The third is TTF1, a transcription termination factor that regulates ribosomal gene transcription (60). The fourth is CAN15, which encodes a protein of unknown function. The fifth is RPTN, which encodes repetin, an extracellular epidermal matrix protein (61) that is expressed in the epidermis and at high levels in eccrine sweat glands, the inner sheaths of hair roots, and the filiform papilli of the tongue.

For those readers who (like myself) dislike jargon, here’s a less technical summary by the Smithsonian National Museum of Natural History (Ancient DNA and Neanderthals, page 3):

Researchers found 78 sequence differences that would have affected proteins in which Neanderthals had the ancestral state and modern humans had a newer, derived state. Five genes had more than one sequence change that affected the protein structure. These proteins include SPAG17, which is involved in the movement of sperm, PCD16, which may be involved in wound healing, TTF1, which is involved in ribosomal gene transcription, and RPTN, which is found in the skin, hair and sweat glands. Scientists do not know the function of the CAN15 protein, which was also one of the differences. Other changes may affect regulatory regions in the human sequence. Some changes are in regions that code for microRNA molecules that regulate protein manufacture.

As far as I can tell (and I’m not a scientist), most of the differences referred to above would have involved modifications in existing proteins, rather than brand new ones appearing, although apparently Neanderthals were missing the protein repetin, making them better adapted to the cold, but less so to disease. However, one swallow does not make a summer, and geneticist Jeff Tomkins writes: “Modern humans and Neanderthals are essentially genetically identical.” It seems, then, that on Dr. Kozulic’s Intelligent Design model, modern humans and Neanderthals constitute a single species, which means that their divergence could have occurred as a result of ordinary natural processes.

Before I finish, I’d like to thank bornagain77 for having alerted me to the existence of ‘species specific’ alternative splicing codes, which are described in an article entitled, Evolution by Splicing by Ruth Williams (The Scientist, December 20, 2012):

A major question in vertebrate evolutionary biology is “how do physical and behavioral differences arise if we have a very similar set of genes to that of the mouse, chicken, or frog?” said Ben Blencowe, a cell and molecular biology professor at the University of Toronto, who led one of the studies. A commonly discussed mechanism was variable levels of gene expression, but both Blencowe and Chris Burge, biology and biological engineering professor at Massachusetts Institute of Technology and lead author of the second paper, found that gene expression is relatively conserved among species.

On the other hand, the papers show that most alternative splicing events differ widely between even closely related species. “The alternative splicing patterns are very different even between humans and chimpanzees,” said Blencowe. “Alternative splicing is evolving faster than gene expression,” concluded Tom Cooper, professor of pathology at Baylor College of Medicine in Houston, Texas, who was not involved in the work.

It would be interesting to see if alternative splicing patterns “carve up” species of organisms in the same way as Dr. Kozulic’s proposed method of using unique proteins and protein-coding genes as defining characteristics of species.

I shall stop here and throw the discussion open to readers. Can anyone think of some other testable predictions of Dr. Kozulic’s model of Intelligent Design? Over to you.

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19 Responses to Some testable predictions entailed by Dr. Kozulic’s model of Intelligent Design

  1. 1
    Chance Ratcliff

    VJT, thanks for yet another informative article. I’m still working my way through it, but here are some things that caught my attention up front.

    “1. If two populations of organisms are known to share a common ancestry, and to have diverged from one another relatively recently, as a result of either unguided natural processes or human artificial selection, then there should not be any proteins or protein-coding genes that are unique to one of the two populations. (According to Dr. Kozulic’s Intelligent Design model, unguided processes are incapable of creating the hundreds of unique proteins and genes that characterize each species, within the time available; and of course, humans can’t accomplish this feat by selective breeding, either.)”

    (my emphasis)

    I think this is problematic. How do we test for unguided evolution. And if we’re open to a notion of guided evolution that is compatible with ID and universal common ancestry, why should we think that such diversification would only happen in the remote past, and not relatively recently?

    If a form of guided evolution suggests that the designer can act at any time in history to produce a new species, shouldn’t we expect to see singletons show up when these events occur, assuming that these singletons are crucial to the genesis of a new species, regardless of when the events occur?

    I hope I’m making sense here.

    “Falsification of proposition 1 would be absolutely fatal for Dr. Kozulic’s model[1] of Intelligent Design. At the very least, it would mean that neither proteins nor protein-coding genes could be used to define the concept of a species, as he suggests. More importantly, it would also seem to imply that new proteins and protein-coding genes can originate as a result of unguided natural processes.[2] (One might try to argue that perhaps the proteins and genes were originally present in both populations, but that some proteins and genes were subsequently lost from one population, but in my view, such an argument would be highly implausible. How could a population of organisms lose hundreds of proteins, as well as the genes that code for them?)”

    (my emphasis and annotation)

    [1] By model of Intelligent Design, do you mean the suggestion that singletons represent information that makes species distinct, and that they represent unbridgeable gaps too wide for unguided processes?

    [2] I’m not sure this follows. It would only imply that some process generated or transferred the information. We would still need an account of a law-like process capable of performing these feats to credit unguided evolution, imo.

    I’m not trying to be hypercritical, these things just stood out to me. Thanks in advance for any additional comments you might provide.

  2. 2
    Chance Ratcliff

    “It would be interesting to see if alternative splicing patterns “carve up” species of organisms in the same way as Dr. Kozulic’s proposed method of using unique proteins and protein-coding genes as defining characteristics of species.”

    Yes, exactly. If alternative splicing is significantly different between species, it might, like singletons might, represent an objective demarcation of species (a definition that appears to be somewhat controversial), but we should expect there to be strong correlation between the two. If this turns out to be the case, we would actually have a strong objective basis for defining a species, with two lines of converging evidence, and no obvious evolutionary pathway between differing species. Under this definition of species, I would also expect that we would not see hybridization events, but I’m just speculating.

  3. Dr. Torley, some of these notes are dated, but here is what I got thus far: These following studies and video, on Cichlid fishes, are evidence of the ‘limited and rapid variation from a parent kind’ predicted by the Genetic Entropy model:

    African cichlid fish: a model system in adaptive radiation research:
    “The African cichlid fish radiations are the most diverse extant animal radiations and provide a unique system to test predictions of speciation and adaptive radiation theory(of evolution).—-(surprising implication of the study?)—- the propensity to radiate was significantly higher in lineages whose precursors emerged from more ancient adaptive radiations than in other lineages”
    http://www.pubmedcentral.nih.g.....d=16846905

    Multiple Genes Permit Closely Related Fish Species To Mix And Match Their Color Vision – Oct. 2005
    Excerpt: In the new work, the researchers performed physiological and molecular genetic analyses of color vision in cichlid fish from Lake Malawi and demonstrated that differences in color vision between closely related species arise from individual species’ using different subsets of distinct visual pigments.
    http://www.sciencedaily.com/re.....072648.htm

    Cichlid Fish – Evolution or Variation Within Kind? – Dr. Arthur Jones – video
    http://www.metacafe.com/watch/4036852

    “For all the diversity of species, I found the cichlids to be an unmistakably natural group, a created kind. The more I worked with these fish the clearer my recognition of “cichlidness” became and the more distinct they seemed from all the “similar” fishes I studied. Conversations at conferences and literature searches confirmed that this was the common experience of experts in every area of systematic biology. Distinct kinds really are there and the experts know it to be so. – On a wider canvas, fossils provided no comfort to evolutionists. All fish, living and fossil, belong to distinct kinds; “links” are decidedly missing.”
    Dr. Arthur Jones – did his Ph.D. thesis in biology on cichlids

    What is Speciation? (Cichlids) – July 2012 – podcast
    http://intelligentdesign.podom.....1_12-07_00

    the entire spectrum of dog sub-species has been found to have less genetic diversity than the parent wolf species:

    ,,the mean sequence divergence in dogs, 2.06, was almost identical to the 2.10 (sequence divergence) found within wolves. (please note the sequence divergence is slightly smaller for the entire spectrum of dogs than for wolves)
    http://jhered.oxfordjournals.o.....0/1/71.pdf

    Genetic Evidence for an East Asian Origin of Domestic Dogs
    Abstract: The origin of the domestic dog from wolves has been established, but the number of founding events, as well as where and when these occurred, is not known. To address these questions, we examined the mitochondrial DNA (mtDNA) sequence variation among 654 domestic dogs representing all major dog populations worldwide. Although our data indicate several maternal origins from wolf, >95% of all sequences belonged to three phylogenetic groups universally represented at similar frequencies, suggesting a common origin from a single gene pool for all dog populations. A larger genetic variation in East Asia than in other regions and the pattern of phylogeographic variation suggest an East Asian origin for the domestic dog, ?15,000 years ago.
    http://www.sciencemag.org/content/298/5598/1610

    Caveman’s Best Friend, Evolution’s Newest Upset – October 2011
    Excerpt: Our view of domestication as a process has also begun to change, with recent research showing that, in dogs, alterations in only a small number of genes can have large effects in terms of size, shape and behavior.,,, It should be noted that dogs and wolves can interbreed,,,
    http://crev.info/content/20111.....est_friend

    podcast – On this episode of ID the Future, Casey Luskin talks with geneticist Dr. Wolf-Ekkehard Lönnig about his recent article on the evolution of dogs. Casey and Dr. Lönnig evaluate the claim that dogs somehow demonstrate macroevolution.
    http://intelligentdesign.podom.....1_14-08_00
    Part 2: Dog Breeds: Proof of Macroevolution?
    http://intelligentdesign.podom.....7_07-08_00

  4. If two populations of organisms are identified by biologists as distinct species on the basis of several independent criteria, then there should always be some proteins and protein-coding genes that are unique to each population. (According to Dr. Kozulic’s Intelligent Design model, each species of living organism can be characterized by proteins and genes that are unique to it.)

    I’m not sure this counts as a prediction. It is more of a definitional issue. If two populations have different proteins then, by definition according to Kozulic, they are different species. Or is he really willing to say that every currently recognized species will have some unique proteins and protein-coding genes from every other recognized species? Even if we hypothesize that this is the case (on the idea that phenotypic variation must be reflected in genotype, or some similar idea), I’m not sure what principle of design it would follow from.

    Mind you, I think the idea of looking at unique proteins is very interesting and has some merit, perhaps as much merit as, say, phenotypic structures for defining species.

    But it is not clear on what principle of “intelligent design” we should expect to always see unique proteins and protein-coding genes. Particularly when there is a lot going on in organisms that isn’t necessarily dictated by protein-coding genes.

    So it is an interesting hypothesis, but I’m not very comfortable calling it a “model of intelligent design.” Particularly not if it is meant to be a proof of design.

  5. OK wait- Because of alternative gene splicing evolutionists can just claim that the novel proteins arose that way, they are the products of happenstance arrangements of alternatively spliced genes.

  6. How could a population of organisms lose hundreds of proteins, as well as the genes that code for them?

    I worry that prediction #1 is not a good prediction at all. Don’t some exons code for hundreds of proteins through alternate splicing? It’s common to observe deletions of hundreds of nucleotides in one go in a single mutational event–which could easily wipe out such an exon and its proteins with it. Or more likely (since this should be catastrophic), a dozen or so of these events taking out one or more less critical proteins at a time?

  7. Dr. Torley, another thing, along with ORFan/Singletons and Alternative Splicing Codes, that may be very useful for the differentiation of distinct species is what is termed Domain-Domain Interactions,,,

    A Top-Down Approach to Infer and Compare Domain-Domain Interactions across Eight Model Organisms
    Excerpt: Knowledge of specific domain-domain interactions (DDIs) is essential to understand the functional significance of protein interaction networks. Despite the availability of an enormous amount of data on protein-protein interactions (PPIs), very little is known about specific DDIs occurring in them.,,, Our results show that only 23% of these DDIs are conserved in at least two species and only 3.8% in at least 4 species, indicating a rather low conservation across species.,,,
    http://www.plosone.org/article.....ne.0005096

    Dr. Gauger relates why protein domains are not easily recombined into novel functional proteins here:

    Why Proteins (Protein Domains) Aren’t Easily Recombined – Ann Gauger – May 2012
    Excerpt: each particular helix or sheet has a distinct set of side chains sticking out from it, requiring a distinct set of chemical interactions with any nearby protein sequence. Thus, helices and sheets are sequence-dependent structural elements within protein folds. You can’t swap them around like lego bricks. This necessarily means that when you bring new secondary structure elements into contact by some sort of rearrangement, they will be unlikely to form a stable three dimensional fold without significant modification.
    http://www.biologicinstitute.o.....recombined

    “Why Proteins Aren’t Easily Recombined, Part 2″ – Ann Gauger – May 2012
    Excerpt: “So we have context-dependent effects on protein function at the level of primary sequence, secondary structure, and tertiary (domain-level) structure. This does not bode well for successful, random recombination of bits of sequence into functional, stable protein folds, or even for domain-level recombinations where significant interaction is required.”
    http://www.biologicinstitute.o.....ned-part-2

    Two Domain Protein – video (several binding sites required)
    http://www.facebook.com/photo......8024519477

    Dr. Torley, please note that this is at the domain level of proteins before the protein-protein interaction level is even considered. I couldn’t find any reliable numbers for comparing protein-protein interactions between species, but I did find this rather honest paper,,

    What Evidence Is There for the Homology of Protein-Protein Interactions? – 2012
    Excerpt: Protein-protein interactions appear to be very rarely conserved unless very high sequence similarity is observed. Consequently, inferred interactions should be used with care…
    Conclusion excerpt: Using this framework, we are able to estimate interactome sizes with a method that is different from others in the literature.
    Our estimates for the fraction of conserved interactions are very low for definitions of homology that are often associated with the transfer of functional annotations across species. We emphasise that our results will be overestimates due to the preferential investigation of homologous proteins in multiple species.,,,
    We urge extreme caution in interpreting interactions transferred across species unless the definition of homology employed is a strict one, and we believe that interactome incompleteness is not solely responsible for the lack of observed conservation of interactions.
    http://www.ploscompbiol.org/ar.....bi.1002645

    Dr. Torley, from what I can tell of the paper (being the novice I am), the protein-protein interaction networks may have been severely overestimated in the past. If this is so, then at the protein-protein interaction level we already have good data from Dr. Michael Behe as to extreme difficulty involved in achieving even a single novel protein-protein binding site. Thus, if this line of evidence pans out (i.e. that domain-domain and protein-protein interactions are widely divergent between species), then it will provide ID another clear demarcation for species:

    Notes:

    “The likelihood of developing two binding sites in a protein complex would be the square of the probability of developing one: a double CCC (chloroquine complexity cluster), 10^20 times 10^20, which is 10^40. There have likely been fewer than 10^40 cells in the entire world in the past 4 billion years, so the odds are against a single event of this variety (just 2 binding sites being generated by accident) in the history of life. It is biologically unreasonable.”
    Michael J. Behe PhD. (from page 146 of his book “Edge of Evolution”)

    Protein-Protein Interactions (PPI) Fine-Tune the Case for Intelligent Design – Article with video – April 2011
    Excerpt: The most recent work by the Harvard scientists indicates that the concentration of PPI-participating proteins in the cell is also carefully designed.
    http://www.reasons.org/protein.....ent-design

    Viral-Binding Protein Design Makes the Case for Intelligent Design Sick! (as in cool) – Fazale Rana – June 2011
    Excerpt: When considering this study, it is remarkable to note how much effort it took to design a protein that binds to a specific location on the hemagglutinin molecule. As biochemists Bryan Der and Brian Kuhlman point out while commenting on this work, the design of these proteins required:
    “…cutting-edge software developed by ~20 groups worldwide and 100,000 hours of highly parallel computing time. It also involved using a technique known as yeast display to screen candidate proteins and select those with high binding affinities, as well as x-ray crystallography to validate designs.2″
    If it takes this much work and intellectual input to create a single protein from scratch, is it really reasonable to think that undirected evolutionary processes could accomplish this task routinely?
    In other words, the researchers from the University of Washington and The Scripps Institute have unwittingly provided empirical evidence that the high-precision interactions required for PPIs requires intelligent agency to arise. Sick!
    http://www.reasons.org/viral-b.....-sick-cool

    Computer-designed proteins programmed to disarm variety of flu viruses – June 1, 2012
    Excerpt: The research efforts, akin to docking a space station but on a molecular level, are made possible by computers that can describe the landscapes of forces involved on the submicroscopic scale.,, These maps were used to reprogram the design to achieve a more precise interaction between the inhibitor protein and the virus molecule. It also enabled the scientists, they said, “to leapfrog over bottlenecks” to improve the activity of the binder.
    http://phys.org/news/2012-06-c.....ruses.html

  8. Dr. Torley,

    I believe that the cichlid fish are prime candidates for the research you recommend but a more interesting investigation that might have more clout would be birds, especially the famous Darwin finches.

    Several top apologists for Darwinian evolution gave lectures at Stanford in 2008 (including Daniel Dennett, Eugenie Scott, Niles Eldridge). Peter and Rosemary Grant specifically discuss species creation but made an amazing admission during their lecture. They discuss the finches in detail and at some place in the presentation said it would take 22 million years to create a new species. That was their estimate. It has been a few years since I watched the video but it should be easy enough to get the finches and do the analysis for their genes as well as suspected relatives on the mainland to see how they differ. It may take a few years to do all the work but the results would hopefully go round the world. Here is the link for the video

    http://www.youtube.com/watch?v=IMcVY__T3Ho

    The page for all the Stanford lectures are at

    http://www.richardprins.com/20.....-lectures/

    Another tack, would be to take all of Dawkins’ examples from his book, “Greatest Show”, and show just what happened to the examples, genetically. The strategy that will eventually work is to take all their examples and trivialize them. Of course all this takes money, and if Darwinists had any integrity they would do the research to show up the ID folks. They certainly have the money.

  9. Hi Chance Ratcliff,

    Thank you for your post. You asked:

    [1] By [Dr. Kozulic's] model of Intelligent Design, do you mean the suggestion that singletons represent information that makes species distinct, and that they represent unbridgeable gaps too wide for unguided processes?

    Yes.

    In response to my claim that if Dr. Kozulic’s Intelligent Design model is correct, then we can infer that:

    1. If two populations of organisms are known to share a common ancestry, and to have diverged from one another relatively recently, as a result of either unguided natural processes or human artificial selection, then there should not be any proteins or protein-coding genes that are unique to one of the two populations.

    you asked:

    How do we test for unguided evolution. And if we’re open to a notion of guided evolution that is compatible with ID and universal common ancestry, why should we think that such diversification would only happen in the remote past, and not relatively recently?

    If a form of guided evolution suggests that the designer can act at any time in history to produce a new species, shouldn’t we expect to see singletons show up when these events occur, assuming that these singletons are crucial to the genesis of a new species, regardless of when the events occur?

    That’s an excellent question. My answer to the question, “How do we test for unguided evolution?” would be: “Make a note of all the events you observe, and calculate their theoretical probabilities of occurring. If the observed probabilities roughly match the calculated ones over the course of time, then you can safely assume that the process you’re observing is an unguided one. But if you start seeing some very noticeable ‘blips’ in your graph, where very improbable events occur a lot more frequently than they should, then you might reasonably suspect that the events in question are the result of intentional guidance – just as you might reasonably suspect a die that kept turning up sixes of being loaded.”

    So, we can rewrite my proposition 1 as follows:

    1. If two populations of organisms are known to share a common ancestry, and to have diverged from one another relatively recently, either as a result of either natural processes whose probability of occurrence roughly matches their calculated probability of occurrence over time, or human artificial selection [i.e. selective breeding, as opposed to genetic engineering], then there should not be any proteins or protein-coding genes that are unique to one of the two populations.

    How does that sound to you?

    I argued in my post that if proposition 1 were falsified, then “it would also seem to imply that new proteins and protein-coding genes can originate as a result of unguided natural processes.” You commented,

    [2] I’m not sure this follows. It would only imply that some process generated or transferred the information. We would still need an account of a law-like process capable of performing these feats to credit unguided evolution, imo.

    Referring back to my comments above on observed versus calculated probabilities, I would say that if the observed process in question conforms fairly closely to its calculated mathematical distribution, then it’s a lawlike one and therefore unguided.

    I hope that helps.

  10. Hi bornagain77,

    Thank you for the link to Dr. Arthur Jones’ Cichlid Fish – Evolution or Variation Within Kind? in which Dr. Jones claimed:

    For all the diversity of species, I found the cichlids to be an unmistakably natural group, a created kind. The more I worked with these fish the clearer my recognition of “cichlidness” became and the more distinct they seemed from all the “similar” fishes I studied. Conversations at conferences and literature searches confirmed that this was the common experience of experts in every area of systematic biology. Distinct kinds really are there and the experts know it to be so.

    The problem with this claim is that cichlids make up an entire family of fish, whereas Dr. Kozulic is saying that unguided evolution can’t go beyond the level of the species. If you compared one species of cichlid with one from another species or genus, you would almost certainly find some proteins or protein-coding genes that were unique to one of the two groups. According to Dr. Kozulic, nature is incapable of generating these genes. Hence most of the different species of cichlids should have been created separately, although two species that diverged within the last few thousand years as a result of sympatric speciation would presumably be an exception to this rule. In other words, I don’t think Dr. Kozulic would accept Dr. Jones’ view of created kinds.

  11. Hi Eric Anderson,

    Thank you for your post. In response to my claim that if Dr. Kozulic’s particular model of Intelligent Design is correct then we can infer:

    If two populations of organisms are identified by biologists as distinct species on the basis of several independent criteria, then there should always be some proteins and protein-coding genes that are unique to each population.

    you wrote:

    I’m not sure this counts as a prediction. It is more of a definitional issue. If two populations have different proteins then, by definition according to Kozulic, they are different species. Or is he really willing to say that every currently recognized species will have some unique proteins and protein-coding genes from every other recognized species?

    I think Dr. Kozulic is making the latter claim, at least in regard to species that are recognized as such on the basis of multiple independent criteria – e.g. reproductive isolation plus morphological distinction plus an ecologically distinct niche. If we found two species that were distinct on all three criteria which shared exactly the same proteins and protein-coding genes, then I think that would clearly falsify his claim that species can be defined in terms of their unique proteins and protein-coding genes.

    I agree with you that such a finding wouldn’t falsify Intelligent Design as such; all it would falsify is Dr. Kozulic’s particular model of Intelligent Design.

  12. Hi Joe Coder,

    Thank you for your comment. In response to my rhetorical question:

    How could a population of organisms lose hundreds of proteins, as well as the genes that code for them?

    you commented:

    I worry that prediction #1 is not a good prediction at all. Don’t some exons code for hundreds of proteins through alternate splicing? It’s common to observe deletions of hundreds of nucleotides in one go in a single mutational event–which could easily wipe out such an exon and its proteins with it. Or more likely (since this should be catastrophic), a dozen or so of these events taking out one or more less critical proteins at a time?

    My knowledge of genetics is limited, so I’m open to correction here, but as I understand it, while a mutation might deprive an individual of several – perhaps even hundreds of – proteins, such a mutation would be a highly deleterious one, and hence very unlikely to spread through an entire population.

    You then asked whether “a dozen or so of these events” might take out “one or more less critical proteins at a time.” I would answer that while I could imagine a population possibly losing a few proteins over time, the loss of hundreds is another matter. Perhaps I’m wrong here; if so, I’d be interested to hear of an example of this happening.

    I hope that clarifies things.

  13. Hi jerry,

    Thanks for your suggestion about Darwin’s finches. I agree with you that their genomes would be very interesting to examine. The following article should be of interest to you:

    Insights into the evolution of Darwin’s finches from comparative analysis of the Geospiza magnirostris genome sequence (Chris Rands et al., BMC Genomics 2013, 14:95 doi:10.1186/1471-2164-14-95)

    as well as this one:

    Comparative landscape genetics and the adaptive radiation of Darwin’s finches: the role of peripheral isolation (K. Petren et al., Mol Ecol. 2005 Sep; 14(10): 2943-57).

    Unfortunately, neither article seems to say anything about the existence of unique proteins or protein-coding genes in the different species of finches. The first one compares one species of finch with the zebra finch. This would be a very interesting field for a Ph.D. student to research.

    I completely agree with your comment:

    Another tack, would be to take all of Dawkins’ examples from his book, “Greatest Show”, and show just what happened to the examples, genetically. The strategy that will eventually work is to take all their examples and trivialize them. Of course all this takes money, and if Darwinists had any integrity they would do the research to show up the ID folks. They certainly have the money.

    That’s an excellent idea! By the way, thanks very much for the video links.

  14. 14
    Chance Ratcliff

    vjtorley @9,

    So, we can rewrite my proposition 1 as follows:

    1. If two populations of organisms are known to share a common ancestry, and to have diverged from one another relatively recently, either as a result of either natural processes whose probability of occurrence roughly matches their calculated probability of occurrence over time, or human artificial selection [i.e. selective breeding, as opposed to genetic engineering], then there should not be any proteins or protein-coding genes that are unique to one of the two populations.

    How does that sound to you?

    I think that’s helpful, thank you. Yet I wonder about an objective criteria for knowing if something was related by common ancestry. As it stands, the assumption is that all life is related by common ancestry, so independent criteria for evaluation is called for.

    Paul Nelson deals with this in the following video, from about 00:20:00 to around 00:50:00. What Ever Happened to Darwin’s Tree of Life?. I only mention this because proposition 1 begins with an inference to common ancestry. The entire video is of course worth watching. Paul Nelson’s presentations are informative and entertaining, and this one is no exception.

    Thanks again for your answers to my questions, and for providing the venue for discussing Dr. Kozulic’s paper.

  15. @Dr. Torley

    I am also not trained in biology, just an interested layman :P You should read Evidence for the design of life: part 1—genetic redundancy by Dr. Peter Borger (Journal of Creation, 2008). He opens with:

    Knockout strategies have demonstrated that the function of many genes cannot be studied by disrupting them in model organisms because the inactivation of these genes does not lead to a phenotypic effect. For living systems, this peculiar phenomenon of genetic redundancy seems to be the rule rather than the exception.

    The whole paper is worth reading.

  16. Some studies on essential genes:

    “To estimate the minimal gene set required to sustain bacterial life in nutritious conditions, we carried out a systematic inactivation of Bacillus subtilis [a gram negative bacteria] genes. Among approximately 4,100 genes of the organism, only 192 were shown to be indispensable by this or previous work. Another 79 genes were predicted to be essential. The vast majority of essential genes were categorized in relatively few domains of cell metabolism, with about half involved in information processing, one-fifth involved in the synthesis of cell envelope and the determination of cell shape and division, and one-tenth related to cell energetics. … Most essential genes are present throughout a wide range of Bacteria, and almost 70% can also be found in Archaea and Eucarya.” Essential Bacillus subtilis genes, PNAS, 2003

    “We have systematically made a set of precisely defined, single-gene deletions of all nonessential genes in Escherichia coli K-12. … Of 4288 genes targeted, mutants were obtained for 3985. … We were unable to disrupt 303 genes … which are candidates for essential genes.” Construction of e coli single-gene knockout mutants, Mol Syst Biol. 2006

    Doing the math that means only 6.6% and 7.6% were deemed essential.

  17. JoeCoder:

    Are they deleting one at a time, or multiple genes at once? This is important, because of redundancy.

    Also, do they show fidelity of reproduction and entire organismal lifecycle across multiple generations? This is important because there are likely many cellular processes (and, by extension, gene products) that are only used during certain portions of the lifecycle.

    The real demonstration of “essential” genes would not be to knock out a few here and there each time, but to replace all the existing DNA with a minimal genome containing just the gene sequences that they claim are essential and then see if the organism can indeed thrive over multiple generations.*

    —–

    * Even then, it would still not prove that the deleted genes have no function, but at least it would get us closer to answering which genes are “essential” in the sense of at least maintaining faithful lifecycle and reproduction over a few generations.

  18. 18
    Chance Ratcliff

    Eric @17, good point with regard to multiple knockouts. This is discussed by Denis Noble in the following video, beginning shortly before the 00:16:30 mark: Physiology and the Revolution in Evolutionary Biology.

  19. I’m not sure. I only read the abstracts.

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