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Book Review: Slaughter of the Dissidents

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I just got through reading Slaughter of the Dissidents, and I must say, it is fantastic. I was a little skeptical at first, simply because the title of the book was so extreme. After reading it, I still think that the title is extreme (there are real slaughters of people happening in different parts of the world), but I can see why it was chosen – the extent to which Darwin skeptics are being persecuted in academic environments is simply astonishing.

The first chapter, “A Context for Discrimination Against Darwin Skeptics” deserves special recognition. Kevin Wirth, who authored it, did an excellent job providing a background and context for this book, especially for those not familiar with the debate or why it generates so much controversy. It almost deserved to be an entire book unto itself. It described why (a) Darwin skeptics are skeptical, (b) Darwinists are skeptical of the skeptics, (c) why ID’ers and Creationists are often lumped together in a single category, even when completely inappropriate to the context, (d) the relationship between the source, the justification, and the effects of ideas (and why it matters), and (e) the relationship that religion has with this whole debate.

Honestly, if someone who wasn’t familiar with the issues asked for a short introduction to the whole issue, I would recommend that they buy the book if only to read the first chapter. That would give a good background on what the disagreement is over and why it is so heated.

Chapter 3 was emotionally tough to read – page after page after page of people being denied from academia precisely because they are Darwin skeptics. Bergman suggests that it is precisely this discrimination which causes there to be so few Darwin skeptics in academia. It was gut-wrenching to see, page after page, a veritable catalogue of good students being denied access to academia.

We’ve all heard about Carolyn Crocker and Guillermo Gonzalez, and some may have heard of Raymond Damadian and Dean Kenyon. All of these people’s stories are detailed and documented. But those only scratch the surface of the problem described by Bergman. Board after board, committee after committee, and court decision after court decision have ruled that it’s okay to single out a single range of views (skepticism of Darwinism) from consideration. In the Bishop case, the court actually ruled that the school has the right to censor any personal opinions of professors that it wants to (including tenured professors). In case after case, it is admitted by all parties that the teaching was not coercive, and the discussion was appreciated by the students, and it represented a tiny fraction of class time. But, since it was against Darwinism, it was alright for it to be censored.

This isn’t just happening in private schools – it’s happening in public schools (high school and college) which use public money for their operation. There is clearly a widespread problem of viewpoint discrimination, which your tax dollars are funding.

The last chapter asks what we should do now. The two which seem most relevant to the average Darwin skeptic (or even non-skeptic who disagrees with the discrimination) is to simply make your voice heard – whether it is a letter to the editor or speaking out at a school board meeting or writing your senator – make your voice heard. If you are a student, check out the academic freedom policy of your institution, and see what the limits are. If you are a non-tenured faculty member, Bergman suggests that you keep your head down and write pseudonymously. I disagree – I think everyone needs to be counted on this issue, though I know that some simply cannot because of the potential personal cost. For tenured faculty, it is imperative that you take students and younger faculty members under your wing and leverage your influence to help them come through the process unscathed. If we all stood up together, who knows what might be accomplished?

The book is great for anyone who is interested in the debate. It is informative to know what lengths people and groups will go to in order to eliminate discussion of the alternatives to Darwinism.

Comments
Kahn, kevinw, You said: "your book is awfully expensive ($27 for a paperback?). I didn’t see it on the website, but I assume a portion of the proceeds are going to a legal defense fund for the victims?" Funny man. Well, for starters, it's 450 pages, well researched, and wasn't written in a day. I'd say it could sell for more, but, you wouldn't believe it. Anyway, I'll be selling the e-book version soon for much less if paperback is too pricey for your pocketbook. " the connection is that, even in the absence of the claimed oppression, ID scientists are still unproductive. if you’re arguing that good science is being repressed, this fact certainly argues against that." Au contraire my friend, you are only seeing the glass half full. You still don't get it. Many Darwin skeptics are excellent scientists in a variety of scientific endeavors. Many of them are VERY productive in their chosen fields, and are recognized for their accomplishments and acievements UNTIL their skepticism of Darwinian ideas becomes known. Then, all of a sudden, they can't possibly be "good comrades" (as Ben Stein put it...) "I’m sure you’re aware of Axe’s paper in Plos One, a reasonably well-respected journal. Behe’s paper was accepted in Protein Science, a middling journal. Dembski apparently had a paper accepted somewhere, although he won’t say where. as to whether or not they would get accepted in nature or science, that’s all hypothetical until they actually submit there. even if they get rejected (as most of us do, boo hoo), if it’s exciting enough it will get published somewhere and noticed." True. But you are focusing on the guys that are front and center in the ID movement. Don't expect to see them get published in a Big Science journal near you anytime soon. When you shift your focus, what you find is a great many other scientists who are thought to be respectable and get published all over the place in highly respected science journals, UNTIL they are found out to be Darwin skeptics. "the biologic inst website lists at least 3 full-time staff, including two PIs. since salaries are the biggest expense of any scientific endeavor, that indicates to me they’re reasonably well-funded. but maybe you know better." WEll, let me put it this way. John West once asked Ken Miller what his annual budget was FOR HIS DEPARTMENT at Brown University. Miller popped up with a figure, to which West stated "I wish I had that kind of budget to work with - but I don't." And I believe West was referring to the ENTIRE budget for Discovery Institute (of which Biologic is just a part). I said: The problem that many Darwinians have is that they often seem to forget the fact that the imaginative bridges btwn the evidence is just that, and some of them have a tendency (after they co-mingle evidence with imagination) and call it all “evidence.” To which you responded "I would like to see a clear example of this from the peer-reviewed literature. i think you’re conflating what science writers do with what the scientists themselves do." Oh dear, you ARE kidding me, right? For starters, go read "Betrayers of the Truth" by Broad and Wade. Then do some research on confirmation bias. That ought to get you going down the path I'm thinking of. When every piece of evidence is viewed as evidence (by scientists) that must somehow fit into an evolutionary explantion, I'm not conflating anything here. It's a fact. Nearly all scientists do this (even if it's only lip service) when they report on the evidence: everything they look at is viewed in the light of evolution. When they don't understand how any evolutionary connection played a role in the development of a critter, they assume it did anyway, and they put up all kinds of stories about how they imageine it "must have", "most certainly", and "without question" had to have occurred (via evolution). Go read anything by Feduccia (on Birds), or Robert Carroll (vertebrate paleontology). These guys and others all talk about how we don't really understand how various fossil critters are related, but by their homology, we KNOW they must be related somehow. A MUST READ is Barbara Stahl's "Vertebrate History: Problems in Evolution." She was a trooper for evolution,but you won't find a more revealing account of what we don't know (and things haven't changed much since she wrote it)kevinw
January 14, 2009
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kevinw, your book is awfully expensive ($27 for a paperback?). I didn't see it on the website, but I assume a portion of the proceeds are going to a legal defense fund for the victims?
First of all, I don’t understand how or why you jump from my claim of discrimination to this question. There is no relevance I can see. What’s the connection here?
the connection is that, even in the absence of the claimed oppression, ID scientists are still unproductive. if you're arguing that good science is being repressed, this fact certainly argues against that.
Finally, I never argued that the reason they have not published stuff in their own journal is bc of oppression. I WOULD say that their research would not likely get published in many cream-of-the-crop refereed science journals if the authors were known ID sympathizers. Would not matter how good their science was.
I'm sure you're aware of Axe's paper in Plos One, a reasonably well-respected journal. Behe's paper was accepted in Protein Science, a middling journal. Dembski apparently had a paper accepted somewhere, although he won't say where. as to whether or not they would get accepted in nature or science, that's all hypothetical until they actually submit there. even if they get rejected (as most of us do, boo hoo), if it's exciting enough it will get published somewhere and noticed.
Secondly, ID certainly does NOT have a “well-funded research center” that I know of. What’s your source for that info? How well funded are they?
the biologic inst website lists at least 3 full-time staff, including two PIs. since salaries are the biggest expense of any scientific endeavor, that indicates to me they're reasonably well-funded. but maybe you know better.
The problem that many Darwinians have is that they often seem to forget the fact that the imaginative bridges btwn the evidence is just that, and some of them have a tendency (after they co-mingle evidence with imagination) and call it all “evidence.”
I would like to see a clear example of this from the peer-reviewed literature. i think you're conflating what science writers do with what the scientists themselves do.Khan
January 13, 2009
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And Khan, What is going to happen to that world-view when scientists finally figure out what IDists have been saying for years- that biological information is NOT reducible to the sequence. Rather it is very similar to the information on a computer disk- embedded on the DNA (and other structures) providing the assembly, editing, transcription, error correction and translation processes. BTW development is not an indication of evolution.Joseph
January 13, 2009
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Khan, Why osn't PAX6 evidence for a common design? Why must it be evidence for universal common descent when we don't even know whether or not thne transformations required are even possible via any amount of accumulating genetic mistakes? Then you say "be patient". That is not going to happen when one preaches a conclusion that has not been confirmed by anything but a world-view.Joseph
January 13, 2009
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Khan, I apologize for my rudeness at #42. Based upon the unexpectedness of the question and the phrasing of "do you know anything" made me expect you were about to launch into an attack on my person. I think your suggestion in #46 is a good place to start. Although I'd add that we should be looking for any foresighted mechanisms, as well. Also, I note that any changes in Pax-6 expression might need to occur simultaneously with changes in other genes, which makes this endeavor all the more difficult since we'd have to search for possible alternate (non-eye related) functionality as well. In any case, my point in all this discussion was to highlight how the grand claims of Darwinism (or whatever you want to call it) are largely unverified. This is the core of the theory yet supporting evidence only provides support for the smaller claims that ID proponents would expect to be true (although an exact "edge" is still a very rough estimate). Never mind OOL. We know that an intelligent agent is at least capable. But what remains to be researched is method (how did the actor act) and that is being tackled by ID-compatible hypotheses. Then of course there's the identity issue, although that remains to be seen whether we'll find any specific clues.Patrick
January 11, 2009
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Guys, Sorry I've been away for so long... Kahn said: "Kevinw,I read over the case studies that were on the web and I am not still not impressed." Not surprising. You don't sound like someone who would be (impressed). So read the book if you want a more robust perspective. I can't give it all away for free. What's on the SOD web site is intended to whet your appetite. Guess you don't have any. That's fine - you just go ahead and not be impressed. "Even if they are as bad as you say, I ask you this in return: ID has its own well-funded research center and its own journal. Nothing supporting ID has come out of the research center and the journal hasn’t published in 3 years. can you really argue this is bc of oppression?" First of all, I don't understand how or why you jump from my claim of discrimination to this question. There is no relevance I can see. What's the connection here? Secondly, ID certainly does NOT have a "well-funded research center" that I know of. What's your source for that info? How well funded are they? I know there's a lab (Biologic) and I've been there. But if that's what you're thinking is "well funded," I would think again. Finally, I never argued that the reason they have not published stuff in their own journal is bc of oppression. I WOULD say that their research would not likely get published in many cream-of-the-crop refereed science journals if the authors were known ID sympathizers. Would not matter how good their science was. Someone said: "I want real, empirical examples, just like you were asking of me. aren’t you the ones who accuse Darwinists of just “imagining” things?" Darwinists DO imagine stuff all the time. But let's be clear about something: imagination is an integral and legitimate part of building hypotheses when we don't have all the evidence we need. The problem that many Darwinians have is that they often seem to forget the fact that the imaginative bridges btwn the evidence is just that, and some of them have a tendency (after they co-mingle evidence with imagination) and call it all "evidence." That IS a huge problem. And I understand it - it comes from a strong desire to see what you want to see. That's what I call "confirmation bias." As far as I can tell, most Darwinians start with the assumption that all the evidence fits into an evolutionary scenario of one sort or another. There is little to know question that it could have been any other way. Not a truly objective approach to examining the evidence...would you say?kevinw
January 10, 2009
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Patrick, I asked the question bc I was going to suggest that you go to GenBank, collect all the sequence data and build a simple maximum parsimony gene tree. that would be a hypothesized pathway for the evolution of the Pax6 gene. then you could do a mutation-by-mutation analysis and see what you come up with. Or, you could just look at figures 2+3 from the Gehring paper I linked to. you would find that the evolutionary pathway is v simple, with a relatively small number of amino acid changes. however, the differences in eyes between those species is v great. of course, bc Pax6 controls so many genes, we can't simply say that small changes in Pax6 have led to large changes in phenotype. but it does suggest that of the key players in eye development had a single ancient origin and may have controlled the development of the first rhadobmeric photoreceptors (recruited into all eye types) from simple precursors. this is surprising bc it had been thought that eyes evolved independently many different times- but these data suggest a single common origin. these photoreceptors are hypothesized to have combined with pigment cells to form a prototype eye that then evolved into all the current forms. an example of how this diversification may have occurred can be found in ragworm eyes. as larvae, they have simple eyes composed of a photoreceptor and pigment cell. as adults, they have cup-shaped eyes that are composed of many larval eyes and constructed through repeated expression of the same Pax-6 and other genes used to construct the larval eye. Similarly, Pax-6 is differentially expressed during formation of all metazoan eyes, suggesting that the evolution of complex from simple eyes may have at least partially been driven by changes in Pax-6 expression. this work is still in progress, I urge you to be patient; after all, we still haven't found a cure for cancer despite orders of magnitude more scientists and funding. a promising avenue to get beyond just looking at Pax6 is to use microarrays to compare gene expression during eye development in different metazoans. this will allow us to get a handle on how the genes under Pax6's control have evolved. this was done for mice just this week: http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0004159 the other sources of info were "making of the fittest" and the review article by Gehring.Khan
January 10, 2009
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JohnnyB- If the mechanism "proves" correct, then academic freedom is a moot point. MY point is that academic freedom is not moot because the mechanism(s) cannot be objectively tested. Khan, Do YOU know anything about constructing a testable hypothesis? If so this would be a good time to present a testable hypothesis based on undirected processes. If you cannot do so then your digma trhreatens not only academic freedom but also critical thinking.Joseph
January 10, 2009
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Why is this all of a sudden focusing on the mechanism? Should we be insted focusing on academic freedom? We can debate the merits of ID in other, relevant threads. The point of the book is that academia is censoring opposing views by any means possible, and is doing quite an effective job of it. This is an outrage to anyone who cares about academic freedom.johnnyb
January 9, 2009
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I have a question and I don`t know if it is stupid to ask or anot.If a tree has a broken heart,can a tree hugger heal it?Dr. Time
January 9, 2009
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Yes, but I'm certainly not an expert. So I'm assuming you do not know of any better information or a potential hypothesis we could examine or are we now going to cover the five d-s? If so, spare me.Patrick
January 9, 2009
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Patrick, do you know anything about building phylogenetic trees?Khan
January 9, 2009
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The first link is not free. I could get hold of it later on, but does it develop the story with an information-based pathway or is it simply a vague generalization? If it's the former why don't you post the number of proposed steps in this pathway? Does it say anything at all about eyespots? The second link is more interesting as it does provide some research notes on what information may correspond to the eye:
Human PAX6 is transcribed as a 2.7kb mRNA and encodes a 422-amino-acid protein that includes the paired box, the homeo box, and a third possible DNA-binding motif, the PST domain (Proline, Serine, and Threonine-rich sequence; Glaser, et al. 1995. See Figure 1). Interestingly, PAX6 contains an alternative mRNA splice-site in the paired domain which can result in a 42-nucleotide insertion; the insertion allows the carboxy terminal subregion of the paired domain to recognize a novel DNA sequence, allowing PAX6 to regulate an expanded or restricted set of genes depending on how the mRNA is spliced (Epstein, et al. 1994). PAX6 extends over 22kb and contains 14 exons and intron sequences in the homeobox itself. In addition, a CCAGCATGC translation start site in exon 4, a TAA stop codon in exon 13, a transcription start site and promoter region with TATA, CAAT, and GC regulatory elements, and three possible polyadenylation signals have all been characterized in several converging lines of research. (Glaser, et al. 1992). Mutations in various positions within PAX6 give rise to gene dosage effects that support the hypothesis that PAX6 regulates gene expression during development by means of concentration gradients with other transcription factors. In one family, truncation of PAX6 in the PST domain by a point mutation in exon 12 led to cataracts and decreased visual acuity in the father; truncation of PAX6 in the paired domain by a point mutation in exon 6 led to iris absence, cataracts, severe decreased visual acuity, and other ocular malformations in the mother; and a daughter compound heterozygote with a copy of each of the parent's mutated PAX6 genes died eight days after birth with severe central nervous system and craniofacial defects and anopthalmia (Glaser, et al. 1994). ....... Later research, however, revealed that genes supposedly "downstream" of ey could also induce ectopic eyes. The products of Sine oculis (so), which encodes a homeobox-like domain, and eyes absent (eya), which encodes a novel nuclear protein, form a complex and can induce ectopic yes similar to those formed by ectopic ey expression (Pignoni, et al. 1997). More significantly, so and eya could together induce ey expression, which is not consistent with the idea of ey as the master regulatory of those genes. In addition, dachshund (dac), which encodes another novel nuclear protein and is induced by ey expression, and eya misexpression resulted in full ectopic eye production as well, while dac and eya alone could each weakly induce ectopic eye formation (Chen, et al. 1997). These gain-of-function experiments suggest that the protein products of ey and of its human homologue PAX6 operate not in a hierarchical linear pathway, but as a network with numerous feedback loops. A second possible hypothesis is that, because eye regulatory genes are activated several times during development, they are turned on in sequence at each stage. .... Research in several laboratories is directed towards characterizing the complex network of regulatory genes involved. Several PAX6 enhancer elements show promise as sites for upstream regulation of PAX6, and possibly even downstream products of eya, so, or dac may play a regulatory role. .... Research in several laboratories is directed towards characterizing the complex network of regulatory genes involved. Several PAX6 enhancer elements show promise as sites for upstream regulation of PAX6, and possibly even downstream products of eya, so, or dac may play a regulatory role.
It's been more than ten years since this article so I'd hope the information specific to the eye has been nailed down. And if that's been done then where is a hypothesis that provides a plausible scenario? Discussion of a potential "pathway" for evolving the eye was mostly limited to this statement:
The repeated use of the same regulatory genes during eye development has been explained in conjunction with the high degree of conservation of the genes: as eye formation progressed during evolution from simple photoreceptors to the complex visual systems in insects and vertebrates, the same regulatory genes were co-opted for each new developmental pathway (Desplan, 1997).
That's nice. Where's the information-based evidence that this story is plausible?
homology levels of 90-96% are clear indications that this gene has not evolved very much, and most of the changes involve recombination and loss/gain of parts of homeodomains and paired domains. hence, different parts have been shuffled around, lost and gained- classic evolutionary processes.
You're restating your assertion--not justifying it--and not saying anything all at the same time. Considering that this gene encodes for many other systems in a variety of very different vertebrate morphological features should we be surprised at the differences noted in sequence comparisons? What does your statement say at all about the evolution of the information specific to the eye? About the capabilities of undirected processes to pull off even an eyespot? Are you seriously claiming that merely noting similarities is evidence for your larger claim?Patrick
January 9, 2009
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What if evolution has been developing backwards and forwards at the same time?
It is a given that "evolution" does not have a direction.Joseph
January 9, 2009
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Khan, How about that testable hypothesis pertaining to un directed processes? That PAX6 is "highly conserved" is also evidence for common design. There isn't any known undirected processes that can put together a master switch which controls anything- nevermind 300+ other genes. However your avoidance of producing a testable hypothesis demonstrates a glaring weakness in your position.Joseph
January 9, 2009
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Hello folks.Kind of looking for an opinion of a theory I have been playing with for a while now and reading your comments and hopefully it will make you think if you thought about it much before. What if evolution has been developing backwards and forwards at the same time?We have alot of evolved or devolved species here on planet EARTH in many stages of real experimentation or maybe selection.Some are in other parts of the universe but as I mentioned before, many are here ,only in different sizes for storage and in starage programmed mode needing only the Master`s command to obey and transform/perform their along waited commands.If one can believe that a one cell life formed over time into us,for that source beyond,was it any more difficult to form either or,or and the top of and the bottom of{if we truly knew which was which}and,farmer talk,put every life form out to pasture to fend for themselves and hope that what is is noticed in time for a successful healthy balance? Please enjoy-hopefully proving/disproving.Thinking gives one life that they never knew they had before.Dr. Time
January 8, 2009
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Hmph. That’s annoying. There must be some sort of hypothesis out there we could examine. Know of anything?
Here's a somewhat dated, but reasonable place to start: http://www.cell.com/trends/genetics/abstract/S0168-9525(99)01776-X again, it's an idea that has some evidence supporting it, but not that much. and people are working on it. However, the evolution of Pax6 itself is reasonably well known, as is reviewed briefly in the above paper and in http://www.jyi.org/volumes/volume1/issue1/articles/friedman.html homology levels of 90-96% are clear indications that this gene has not evolved very much, and most of the changes involve recombination and loss/gain of parts of homeodomains and paired domains. hence, different parts have been shuffled around, lost and gained- classic evolutionary processes.Khan
January 8, 2009
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The important point is that all the information pertaining to each type of vision system is apparently not directly encoded into Pax6 or its non-vertebrate homologs.. of course not.
You say "of course not" but how does that square with your earlier statement of "complex eyes arising from repeated expression of the Pax6 gene that controls the formation of simple eyes"? That's the only reason I said that.
c) that all of the (v little) evolution it has undergone has come through cobbling together of other bits of genes, i.e. well-knwon evolutionary processes.
How can you justify this assertion?
as for the other 371 genes, as you can imagine sorting that out is a bit more complex, but once again we can say “we don’t know.”
That's why I suggested starting with a simpler system like the light-sensing ocelli or a simple eyespot to see if there any plausible pathways for even that. I just ran a quick search looking for a simulation or at least a hypothesis and didn't have much luck. Apparently I'm not the only ID proponent who has not heard of such research. Luskin wrote this just a couple days ago:
Humes cites a “computer program” which he claims explains "the plausibility of eye evolution by natural selection with a virtual organism possessed of a flat, three-layer eyespot similar to the sensory organ on many simple microscopic creatures.” (pg. 125.) First we must ask, where did these first "three-layer eyspots" come from? Humes gives no explanation. But evolutionary biologist Sean B. Carroll admitted that it is inappropriate to assume that such early eyes were simple, writing, “do not be fooled by these eyes’ simple construction and appearance. They are built with and use many of the ingredients used in fancier eyes.” Humes' most egregious error with regards to eye evolution is that Humes apparently didn't know that there is no such computer program as he cites, and that these claims are a Darwinist urban legend promoted by Richard Dawkins. The real study’s math and the notion that it used a computer program were refuted by Darwin-skeptic and mathematician David Berlinski. For details, see by David Berlinski's "The Vampire’s Heart."
Hmph. That's annoying. There must be some sort of hypothesis out there we could examine. Know of anything?Patrick
January 8, 2009
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Patrick,
So, to sum up: we have a “minimal” transcriptome search space of 2^25,000, which, according to Kaufmann (I have not checked) is equivalent to 10^7,000, which is quite a number,
I'm sorry, what exactly are you calculating here? the probability of PAX6 controlling transcription of any given gene? did something get cut off above that in your comment? In Drosophila, Pax6 causes expression of 371 genes, if that helps you in your calculation.
The important point is that all the information pertaining to each type of vision system is apparently not directly encoded into Pax6 or its non-vertebrate homologs..
of course not. but let's focus on what we do know, which is the master control gene. We know a) that it is expressed during eye development in all metazoans b) it is highly conserved among those metazoans, to the extent that genes from one species can stimulate eye formation in other species and c) that all of the (v little) evolution it has undergone has come through cobbling together of other bits of genes, i.e. well-knwon evolutionary processes. as for the other 371 genes, as you can imagine sorting that out is a bit more complex, but once again we can say "we don't know."Khan
January 8, 2009
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I did not read #30 and #31 before writing #32.
I read Behe. And even he doesn’t know whether or not anti-freeze arose via design or via an accumulation of genetic accidents.
For certain, no. I'm just saying that their story based upon undirected processes is at least plausible in this case. gpuccio made this good point:
Behe concludes that this example is in the range of what unguided evolution can do. But I will cite here the last words in the abstract of the paper, which are indeed revealing: “The notothenioid trypsinogen to AFGP conversion is the first clear example of how an old protein gene spawned a new gene for an entirely new protein with a new function. It also represents a rare instance in which protein evolution, organismal adaptation, and environmental conditions can be linked directly.” Interesting, isn’t it? I would add “the first ‘and only’ clear example”. And Behe shows the reasons why it is not a real example of emergence of complexity (in the sense of CSI). The first example: how does that ring for a theory which, in the minds of most, is considered “a fact”?
I also admit I cannot remember whether the Trichromatic Color Vision scenario was based experimental evidence or by examining sequence similarities. It's been a while since I've read up on the subject. So perhaps I may be too hasty in agreeing that it's plausible. In any case, I'll be gone for the day. I just cleared the moderation queue and Khan has not responded on anything yet.Patrick
January 8, 2009
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I'll make some general comments on the pax6 gene and eye development. First off, genes encode for multiple functions so information pertaining to eyes is not the only thing encoded into it. Moreover, as it is well known today, the “one gene - one protein” dogma is completely false. We know that one gene can, through various mechanisms (introne regulation, post transcriptional regulation, and many others), really code for many different proteins (in theory, even thousands of them, in practice certainly more than one). Indeed, Darwinists, with their usual short-sightedness, seem to be very fond of this “one gene - many proteins” fact, apparently not understanding the terrible pitfalls which await them there. So, to sum up: we have a “minimal” transcriptome search space of 2^25,000, which, according to Kaufmann (I have not checked) is equivalent to 10^7,000, which is quite a number, if we remember that 10^150 is “just” Dembski’s UPB. That number has certainly to be increased of many, many orders of magnitude(nobody can say how many), if we take into account the different “levels” of transcription of each single gene plus the different “types” of transcription of each single gene. Second, since it's a master control gene during development it's merely controlling the expression of data encoded elsewhere. I note that this Pax6 gene from a mouse can be used to express eyes in Drosophila. Its homolog within Drosophila, if expressed elsewhere, can also switch switch on development of eyes throughout the body. A more thorough report is here. The important point is that all the information pertaining to each type of vision system is apparently not directly encoded into Pax6 or its non-vertebrate homologs (on a side note, I wonder if calling them "homologs" is accurate). In order to examine a potential scenario we need to know the information content that defines a system in total. Since it's now claimed that all eyes share a simple precursor the work is made a bit easier. So it's probably best to start with a simple light-sensing system, and see what pathways could potentially develop it and whether they're plausible. Then we can move onto the more complex systems. The problem is, if we do not know what information content defines intermediate systems then we cannot determine whether there exists plausible pathways (although obviously identifying small variations within types has been done). So this discussion may go nowhere based upon that point alone, since we do not want to be discussing arguments based upon ignorance. There's also the fact that the visions systems are very complex. That's why many people choose to focus on the flagellum since it's a. relatively "simple" b. well-studied and c. the information content is known. There's also arguments related to common design, common descent, convergent evolution, incorrect predictions, etc. but I don't want to distract from the main topic.Patrick
January 8, 2009
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trichromatic vision arising through duplication and modification of three aminto acids (each modification slightly beneficial in its own right) in an opsin gene.
This we should be able to test- from The Evolution of Trichromatic Color Vision:
Trichromacy in all Old World primates is dependent on separate X-linked MW and LW opsin genes that are organized into a head-to-tail tandem array flanked on the upstream side by a locus control region (LCR).
Also with gene duplication, in order to do anything, the new gene requires a promoter. It is also required to be in a position that is accesible- ie not tightly wound around a histone or via methylation- so that it can be transcribed. Now if evolutionists want to use copying errors, ie point mutations, to make their case, that is fine. But when they start talking about gene duplication then that is another story altogether- see Dr Spetner's "Not By Chance"- gene dupications are part of his non-random evolutionary hypothesis.Joseph
January 8, 2009
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Patrick, I read Behe. And even he doesn't know whether or not anti-freeze arose via design or via an accumulation of genetic accidents. Cumulative selection does not equal undireceted processes. My point is one needs a testable hypothesis for the proposed mechanisms, ie UNDIRECTED PROCESSES. IOW a hypothesis which would demonstrate the "power" of the mechanisms. PAX6 is just a master switch. When the PAX6 of a mouse is put into a fly with a missing or damaged gene, the fly develops FLY eyes. IOW no one knows where the information for the TYPE of eye resides. And no one knows if said information can arise via an accumulation of genetic accidents.Joseph
January 8, 2009
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Shameless plug for Sanford's Genetic Entropy book: http://www.godtube.com/view_video.php?viewkey=273bd8d07d99f4016636bornagain77
January 7, 2009
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Evidence: antifreeze genes in Antarctic fish arising from motif multiplication of a portion of an existing digesive enzyme gene Was that by design or via an accumulation of genetic accidents?
Joseph, Behe wrote about this in EoE but I'd agree that it's probably a good example of cumulative selection and the reasons for why I've explained here and here. gpuccio also commented on it. Heh, sometimes I feel like I could hold a whole conversation by back-linking. Anyway, I need to get other things done now, but I think you should focus on discussing vision systems or the "complex eyes arising from repeated expression of the Pax6 gene that controls the formation of simple eyes". Outside references: 1 2 3 4 While some variation within the functionality of some types of vision systems should be plausible (like the trichromatic vision example) this does not consider the whole picture for reasons give here.Patrick
January 7, 2009
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Classical Darwinian theory predicts that evolution will occur by the accumulation of beneficial mutations, so the pathway you propose in another post w mostly deleterious mutations would be just the opposite.
1) That is nonsense because 2) "Beneficial" is relative, and 3) Evolution can occur without an accumulation and 4) Without beneficial changes In reality A) There is no way to predict what mutations will occur at any point in time. And B) There is no way to predict what will be selected for at any point in time.Joseph
January 7, 2009
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Hypothesis: Novel genes will evolve through slight modifications of existing genes.
Strike one- NOTHING about a mechanism.
Evidence: antifreeze genes in Antarctic fish arising from motif multiplication of a portion of an existing digesive enzyme gene
Was that by design or via an accumulation of genetic accidents?
trichromatic vision arising through duplication and modification of three aminto acids (each modification slightly beneficial in its own right) in an opsin gene.
By design or an accumulation of genetic accidents?
melanic coat coloration in some populations of pocket mice arising from a single mutation in a melanocortin receptor gene
Same question.
complex eyes arising from repeated expression of the Pax6 gene that controls the formation of simple eyes
Again you have FAILED to test the mechanism. I would also love to see the experimental test that demonstrates that complex vision systems can arise given our lack of understanding pertaining to cellular differentiation.
Care to counter w any similar ID findings?
It appears you don't know what is being debated. hint- "Evolution" is NOT being debated. Please use undirected processes in a testable hypothesis. UNDIRECTED PROCESSES.Joseph
January 7, 2009
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Oh, you mean I just need to merely calculate every single potential indirect stepwise pathway? How extremely generous of you I hope you realize this is exactly what you are asking evolutionary biologists to do.
Not at all. A single plausible pathway will do, which does not require analyzing ALL possibilities. And if this pathway happens to consist of processes that act uniformly in regards to other biological objects, then a large chunk of most design hypotheses would be falsified. But if you plan on verifying whether a plausible pathway does not exist at all, then indeed we'd need to calculate every single potential pathway. We are merely asking that the grand claims be verified in ANY manner. Essentially, you're asking us to accept as an article of faith that pathways of hundreds and thousands of informational bits leading to an irreducible core are as easily achieved as pathways consisting of less than 50 informational bits (and IC is often not an issue at all).Patrick
January 7, 2009
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critter #19, Probably the lack of purported funding. Seriously, if the ID community has all this money then where is it? This website is not funded and I've never been paid for my efforts. The majority of ID proponents I know of hold day jobs that have nothing to do with ID research. And when they do attempt to get funding it's usually an uphill battle. For one example, Dembski had his funding taken away at least twice. I think it humorous, no hypocritical, that Darwinists often demand more research of ID proponents yet at the same time support any action to prevent such research from ever taking place. As such, ID proponents are typically limited to cheap options. For example, analyzing research accomplished by others and writing books is relatively cheap. Although, I sometimes wonder why the Discovery Institute spends a relatively small percent of its budget on research. My guess is that they're hoping to break down barriers to getting more funding for research. But what if the means for doing this might be research in itself? The good news is that the equipment costs keep going down. So now it's largely down to salaries...unless you expect people to keep ID research a hobby or something.Patrick
January 7, 2009
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ps saying "I don't know, and neither does anyone else" is hardly a dodge and brush off. it's a statement of fact. you can do all the probability calculations you want and it doesn't change the fact that we don't know. (try calculating the probability of your own birth sometime. it's extremely low, but it happened.) and we won't know until someone does the hard work of figuring it out.my guess is it won't be anyone from ID, bc they haven't produced any empirical work at all. it won't be me, bc i have lots of grant money to do other things (including your favorite, nanoscience). but until they do, using it as argument against evolution is extremely weak.Khan
January 7, 2009
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