Home » Intelligent Design » Signature in the Cell website now live

Signature in the Cell website now live

Steve Meyer’s new book from HarperOne, Signature in the Cell: DNA and the Evidence for Intelligent Design, will be in bookstores next week. The book’s companion website, www.signatureinthecell.com, is now live. Check it out.

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103 Responses to Signature in the Cell website now live

  1. 1
    Granville Sewell

    Looks very interesting, I just ordered my copy.

  2. I hope there’s an audio version coming. Only buy audio books now. Preferably it will be in the authors own voice.

  3. I love Steve- he is one of the most articulate people out there supporting ID.

    I did however notice that the “contact” part of the site is not working.

  4. 4
    CannuckianYankee

    There are some interesting videos in the “Media” section of the website. One particular one I found fascinating was Dr. Meyer’s “debate” with Michael Ruse on PBS’s “Think Tank” show. Dr. Ruse demonstrates how shallow some Darwinists think in relation to the ID movement. Of course the issue with ID Vs. DE is not in who can outflank who in debate, but in which argument is more cogent in light of current information. Meyer’s arguments seem a little more on the cogent side. Ruse merely demonstrates his ideological dislike for religion, and that’s pretty much it.

    This is perhaps Dr. Meyer’s greatest strength (apart from his education, apparent intellect and clear systematic thinking) – he engages only in the issues at hand, rather than try to deal with the motives or character of his opponents. From reading Dr. Meyers’ other works, this promises to be a groundbreaking work, which I believe will not disappoint.

  5. If Michael Ruse represents Darwinist best philosophical option against Design Theory, they are in trouble.

    I watched the videos earlier and was surprised at how vacuous his argument and reasoning were in the discussion.

    He all but called Meyers a liar nearly from the beginning. I think he said, “fibbing” to Meyers about his motives. He had nothing intellectually to rebut Meyers, so he lashed out in desperation it seemed.

    It was kinda sad to watch the cantankerous bearded Ruse become so uncomfortable at the realization he was getting whipped by Steve.

    It was like watching McCain get whipped in debates by Obama.

    Steve clearly wins the debate and was more approachable with integrity of his position, clearly open and limited his claims of ID theory.

  6. 6

    DATCG

    I watched the videos earlier and was surprised at how vacuous his argument and reasoning were in the discussion.

    Can you give an example of such vacous reasoning?

    I’d like to see what sort of thing you consider “vacuous”.

  7. The book’s Amazon blurb says “The first, major scientific argument for Intelligent Design by a leading spokesperson within the scientific community.”

    Since when is Steve Meyer “a leading spokesperson within the scientific community”? Such overweening puffery about Steve may lead readers of that sentence to question if other claims in that sentence are also false or inflated.

  8. I guess nobody is willing to name the signatory.

  9. Signature in the Cell is published by “HarperOne, a division of HarperCollinsPublishers, (which) strives to be the preeminent publisher of the most important books and authors across the full spectrum of religion, spirituality, and personal growth literature, adding to the wealth of the world’s wisdom by stirring the waters of reflection on the primary questions of life, while respecting all traditions.” – from their website.

    Signature in the Cell is also published by “Zondervan Publishing” – see http://www.zondervan.com/Cultu.....=Zondervan

    http://www.zondervan.com describes itself as an “Evangelical publisher of Bibles, Christian books for adults and children, audio books, videos, software.

    Are “HarperOne” and “Zondervan Publishing” the same organization operating under two different names?

  10. 10
    CannuckianYankee

    Me: “From reading Dr. Meyers’ other works, this promises to be a groundbreaking work, which I believe will not disappoint.”

    PaulBurnett #7 “Since when is Steve Meyer ‘a leading spokesperson within the scientific community’?’

    Ok, I take that back. Maybe for some it will disappoint.

    Paul, I think legitimately speaking, Dr. Meyer is a leading spokesperson for ID. Whether you want to admit that ID falls within science, is another debate altogether.

  11. 11
    CannuckianYankee

    Paul,

    The book is published by HarperOne, not by Zondervan. Zondervan carrys the book on its website perhaps as a publication of interest to Christians. I found this out simply by opening their “about the book” link. The two are completely separate entities, and I can find no link between the two. HarperOne is out of New York, and Zondervan is out of Grand Rapids.

  12. I hope I’m not out of line to discuss this here, and if I am…kindly do correct me. I’ve tried to find an example of an IC system arising, step by step…or even a model from the darwninist camp, or some substantial criticism of Dr. Behe’s Edge. Regarding IC, I’ve found nothing save one example (supposedly) of an IC system arising from scratch in nature. The gene in question, T-urf13, is mentioned in the Pandas Thumb blog, here:

    http://pandasthumb.org/archive......html#more

    I do not have the biochemical knowledge to observe what is actually going on with that system, but it does raise quite a few questions on my part…one of which is how much leeway does RMNS have…but I’ll leave my thoughts for now. For the experts on this blog, could you help me out here with figuring out how this fits in with Irreducible Complexity? How it came about? Whether its an exception, and if so, why?

    Thanks!

  13. 13
    CannuckianYankee

    Echidna.Levy:

    “Can you give an example of such vacous reasoning?

    I’d like to see what sort of thing you consider ‘vacuous’.”

    I spent considerable time on the content of this post, and I know it doesn’t show. I was going to post a large part of the transcript from the first video of PBS’s “Think Tank” show involving an interview with Dr. Meyer and Dr. Ruse. The problem with that, is it’s a very long transcript, and would take up far too much space. You can read the transcript for yourself, and I suggest that you do. It’s at the same linked webpage for the book, in the “media” section.

    The reason why Dr. Ruse appears vacuous in his arguments, is that he doesn’t engage any of the discussion from Dr. Meyer. He merely sidesteps all of Dr. Meyer’s discussion by accusing him essentially of being a “misguided Evangelical Christian with a religious agenda that is apart from science.” Dr. Meyer counters that accusation masterfully.

    Dr. Meyer goes to great length and clarity to state that his religious views are secondary issues, which are formed out of the implications of the evidence, and that the identity of the designer is therefore secondary from a scientific perspecive, to those implications. This is the best part of the “debate,” and Dr. Meyer runs circles around anything that Dr. Ruse has to say.

    The discussion towards the end delves into the teaching of ID in schools, which Dr. Meyer points out is not a position the DI favors; however, he ends the discussion with this:

    _________________________

    WATTENBERG (the moderator): But, Michael’s point seems reasonable that you teach that in comparative philosophy, in comparative religion, not necessarily biology.

    STEVE: Except that these arguments are in biological journals. There’s a tremendous amount of literature. Darwin had -– you were talking about the word theory –- Darwin had a more important word that he used in the origin. Talked about the origin of species being one long argument. And when I was in my doctoral studies in Britain, I had a tutor…

    WATTENBERG: Oxford?

    STEVE: Cambridge. He said, “beware the sound of one hand clapping.” And in biology like in every other field, any time you have an argument, there is a counter argument. And the discovery that I made was…

    WATTENBERG: And that’s how we advance.

    STEVE: That’s how science advances. And Michael has the idea that science is this pristine realm of endeavor that does not involve argumentation or differences of interpretation. And therefore, when you have a fundamental difference, then it must be philosophy or religion that should be sequestered off to the side. But scientists, like everyone else, argue about how to interpret things. And if we deprive students of those arguments, we’re depriving them of a scientific education… I don’t think it matters what you call it. I think we’re hung up on these science, philosophy, religion. These are categories of human thought. What we’re interested in is how do you explain the complexity that we see in life? And we think that design is the best explanation. If Michael wants to classify that as a philosophy hypothesis, then I would say that our philosophical hypothesis provides a better explanation than his currently popular Darwinian scientific hypothesis. What you call the inference or the hypothesis is not as important as whether or not it’s true.

    ______________________________

    What is disheartening about this is that Dr. Ruse is a Philosopher of Science, who teaches about these issues at the University level. I would hope that such an education in the differences between ID and Creationism, whould at least show the significant distinctions, which Dr. Ruse glosses over.

    I look forward to Dr. Meyer’s new book. He’s a masterfully clear thinker.

  14. 14

    “CannuckianYankee” (#11) wrote: “The book is published by HarperOne, not by Zondervan. Zondervan carrys the book on its website perhaps as a publication of interest to Christians. I found this out simply by opening their “about the book” link. The two are completely separate entities, and I can find no link between the two. HarperOne is out of New York, and Zondervan is out of Grand Rapids.

    Zondervan is an international Christian media and publishing company located in Grand Rapids, Michigan. Zondervan is a founding member of the Evangelical Christian Publishers Association (ECPA). … According to Zondervan’s website, the company was bought out by HarperRowCollins Publishing in 1988 and has continued to be its parent company’s Christian bookselling outlet.” – http://en.wikipedia.org/wiki/Zondervan_Publishing

    So it’s pretty clear who Signature in the Cell is aimed at, both in its primary religious publisher and its associated “Christian bookselling outlet” – i.e., it’s not intended for the mainstream science publishing market at all.

  15. 15
    CannuckianYankee

    Ok, here’s a few of the more significant things Dr. Ruse had to say:

    ___________________________________

    Well, I think Steve’s a really nice guy. I’ve known Steve for many years. I think he’s a bit of a sweetie, but as Winston Churchill once said, I think pretending that intelligent design theory has nothing to do with religion is what Churchill called, what was it, “a terminologically inexactitude.” In other words, it’s a great big fib.”

    And:

    “I think he’s not appealing to scientific ideas. I think he’s appealing to religious ideas for all that he’s saying that this is not religiously driven, I think that it is. But also, and I trust we’ll get into this, I think it’s also part of a general social cultural agenda which I would, in fact, link with the creationists.”

    and:

    “First of all, I don’t think your motives are dishonest. I think you know me well enough now to know that I don’t think that in dealing with you people at the Discovery Institute or indeed with the people at the Institute for Creation Research that I’m dealing with a bunch of crooks. Because I don’t think you are. I think you’re profoundly mistaken, I think you are often more religious than you let on, I think that you do try strategies to get around the separation of church and state, I think all of those things. But I think that you are deeply sincerely, if misguided evangelical Christians. So that is very much where I come from, and that’s where I feel at least we can meet there. Now let’s get back to the science.”

    ________________________

    So quite quickly after Dr. Meyer explained that he was not a Creationist, all Dr. Ruse does is reinforce this idea without an ounce of proof or reference. He does not at all engage anything that Dr. Meyer Stated.

  16. HarperOne and Zondervan are both publishing divisions of the News Corporation (Rupert Murdoch’s outfit).

  17. Blu,

    Turf-13 is found in maize- ie corn.

    Corn is a product of artificial selection, not natural selection.

    IC is an argument against natural selection and random mutations.

    Also Turf-13 leads to disease and male sterilization.

    Not quite the thing evos should hang their hat on.

    That they do just further exposes the desperation of their position.

  18. Blu,

    I am not sure they know for sure how Turf-13 came about but Art Hunter who comments here occasionally has written on it will know. I believe and he can correct me, that is arose from recombination. If this is so then they should be able to identify the origins of it. I would let Art or someone else familiar with plant biology describe it if they see your comment since I am in no way knowledgeable on this.

    The specific importance of Turf-13 is that is an ion channel between the inside and outside of the cell and that is not a trivial capability but does not rise to the level of an IC system. Again, someone with expertise could explain it better.

    Since it is found only in corn and corn is a recent phenomena due to natural selection, the origin of Turf-13 is relatively recent.

  19. Joseph, Jerry…thank you very much for your response.

    Joseph: As far as I understand, even though corn was the product of artificial breeding, the selection here was merely adding environmental selective pressure rather than genetic modification (correct me if I’m wrong here), so in that sense, one could imagine the plausible scenario where some environmental pressure led it to that direction (ok, highly unlikely…but what we’re trying to see is the internal capacity to generate an IC system from within, and if such minor exceptions exist what are they and where does one draw the line.)

    Jerry: I believe Art Hunter is Arthur Hunt, the person who wrote the article. If T-urf13 is the result of genetic recombination, can genetic recombination within certain systems result in an IC system? Again…just trying to draw a line here. To get as specific as I can in my own mind. I know a line exists for sure, I have a rough zone, but its not specified yet.

    You mention it doesn’t rise to the level of an IC system, could you kindly elaborate on that? What do you consider a proper IC system and how would we define one in relation to minor situations?

    Another point of interest, is in the fourth point in the footnotes, Art mentions:

    4. The toxin made by C. heterostrophus race T is a polyketide. It is beyond the scope of this essay to detail this class of compound, or the fascinating enzymes that synthesize them. Suffice to say that these enzymes add another layer of “complexity” to this subject, in that a rather complex set of activities had to evolve, along with the maize mitochondrial genome, to “assemble” the IC T-urf13 system.

    What I wonder is whether those enzymes too, arose “de novo”, or whether they were present in some dormant state before. If they did arise, what selective advantage existed that would confer the amount of successive mutations necessary (if I’m understanding the situation correctly), and if none was available is it due to the capacity of systems to retain some dormant combinatory possibilities in its underlying enzymes, or whether its something else?

    I would appreciate the input of the experts here on this! I believe its possible to clearly and definitively demarcate an edge if a contextual understanding arises (at least…for me!). I also have a few followup points and questions…so look forward to your response.

    PS. Does anyone know any other supposedly irreducible complex system that arose experimentally or even hypothetically? I’ve yet to find one. And I discount vague assertions that do not map to the details or subtleties of reality…and the difficulties that arise with them when one attempts to construct such systems.

  20. jerry,

    The specific importance of Turf-13 is that is an ion channel between the inside and outside of the cell and that is not a trivial capability but does not rise to the level of an IC system.

    if we compare it to an example used by Behe himself it is:
    (from the PT article)

    Those who have read Darwin’s Black Box might recall Behe’s description of a gated ion channel. On pp. 108-110, Behe describes the signal recognition particle (SRP)-mediated transport of proteins (footnote 3) as a gated transport process. In so doing, he asserts (among other things) that “(b)ecause gated transport requires a minimum of three separate components to function, it is irreducibly complex”. The three components he describes for SRP-mediated protein translocation are the signal peptide, SRP, and the transport channel. The T-urf13 gated ion channel also consists of three components – the fungal toxin (footnote 4) is analogous to the signal peptide, the toxin binding site is analogous to SRP, and the ion channel is analogous to the protein channel. In case this comparison has hidden the bottom line, it is this – T-urf13 is irreducibly complex in exactly the same way that Behe asserts for SRP-mediated protein transport.

  21. blu,

    joseph’s comments regarding T-Urf13 are misleading. He has been corrected on this before both by me and Art Hunt over on the ARN discussion board, yet inexplicably keeps repeating the argument here.

    Specifically, his comment about male sterilization leaves oiut a critical piece of information: maize plants are hermaphroditic, meaning each plant possesses both male and female reproductiuve organs. T-Urf13 does not make the entire plant sterile, it simply renders the male reproductive organs sterile. In other words, it turns the plant into a female. This has led some people (joseph especially) to declare T-Urf13 to be a deleterious mutation. Somehow, he has the idea that if the mutation were to become fixed in the population, then the population would become extinct. On the surface, this sounds like a reasonable argument. However, those familiar with basic evolutionary biology know that such a mutation would not become close to being fixed for the very same reason joseph thinks it is deleterious. However, that does not mean that it is reduces the fitness of the population (which is the definition of a deleterious gene) necessarily. It may be beneficial to the population if it remains at some frequency below fixation for two reasons: first, male sterility promotes outcrossing (prevents the plant from self-fertlizing), which reduces teh elevel of inbreeding, and second, maizet populations with male sterility genes (T-Urf13 is one of several that do this) show higher yields. The last thing one would expect a deleterious gene to do is increase yield of a population. Finally, T-Urf13 may confer a susceptibility to disease, but only under certain specific conditions. In niches where the disease isn’t present, the increased yield would grant populations polymorphic for T-Urf13 increased fitness.

    So, as you can see, the situation with T-URF13 is not as cut-and dried as joseph seems to think.

  22. Maybe Art Hunter can comment more when he gets a chance on this relationship to what Behe outlined in his book. It seems that a three element system is not one that should be described as irreducibly complex. I will have to get Behe’s book out to see just what he said.

  23. Hi blu,

    You asked:

    PS. Does anyone know any other supposedly irreducible complex system that arose experimentally or even hypothetically? I’ve yet to find one. And I discount vague assertions that do not map to the details or subtleties of reality…and the difficulties that arise with them when one attempts to construct such systems.

    One example that I have seen involves the process known as subfunctionalization. This is where a gene duplicates, and then both copiues undergo a series of complementary degenerative mutations such that each contributes an essential piece of the complete protein. That is, a protein that was once coded by one gene now relies on two (or more) genes to supply different elements of it before it can be fully functional. In other words, an IC system evoilved by Darwinian means. The process is described in this paper (which I believe is online) if you Google the title:

    Lynch M, M O’Hely, B Walsh & A Force (2001). The Probability of Preservation of a Newly Arisen Gene Duplicate. Genetics 158: 1789-1804.

  24. Hi Blu,

    Thanks for pointing out my essay. I think the comments by Khan and Dave are spot-on and don’t need any more commentary from me. If our ID friends seem stumped or have questions that others care not to address, maybe I will be able to move things along. (Sure would be easier if my comments didn’t languish in the moderation queue.)

    Along these lines, I would ask that if PaV is following this, (s)he might join in and recapitulate the gist of our conversation on Abbie Smith’s blog some time back.

    Maybe that Art Hunter guy will stop by …

  25. Hey Dave!

    Thanks for your response and the information regarding subfunctionlization. Thats interesting, I wonder if it would be a double edged sword in many instances though…I wouldn’t exactly count it as an IC system (according to what I’m looking for), as it is increasing the parts of an already functioning structure rather than accumulating components and information to generate a new structure. I wonder if it could be used as a step stone in that direction…it seems to me that it could both increase and decrease the specificity of a certain process. Giving it possible problematic status in the future (in the sense that it might increase redundancy, reducing the flexibility of the system: a part of it that binds to another future addition will cause the protein in question to be dysfunctional, etc.).

    Regarding whether T-urf13 is beneficial or not. I agree that what “beneficial” is, is based on context. Again, this is a double edged sword…but thats not the point here.

    What interests me is what are the specific changes that occured that led to T-urf13, and do they lie within what we know is possible for process X, where process X is what we know is the way RMNS works. Now, this might raise a few hackles from the darwinian camp, I’m not suggesting a “poof” argument or whatever, but it follows logically that if X is capable of Y and not of Z, and Z happened, either our understanding of X must change, or some other process resulted into the change. Simply observing the arisal of that system does not necessarily entail that the system arose by RMNS (and again, nor by any other system). What were the steps? Why were they selected? Why was information retained? Was it simply reshuffling preexisting potentiality within the system? When? Did steps occur that had to restructure the foundation of the system thereby making it impossible to have occured gradually? etc.

    I look forward to hearing your thoughts.

  26. And by the way, so far we have subfunctionlization, and t-urf13…both of which have a lot of subtle issues to deal with. Are there other examples of known IC systems that arose experimentally, or maps that result into a known IC system in a reasonable detailed manner?

    Thank you.

  27. Dave,

    Hm, I might have misunderstood. I’m reading the paper now, it isn’t quite specific on the actual mechanism by which such a process occurs in a gradual manner…they are mostly talking about the probability of its occurence and its fixation within a population that necessarily requires selection against parts of the duplicate gene. But isn’t it that during that process occuring, the primary gene encoding for the protein would stop functioning? Kindly correct me if I’m mistaken. Trying to wrap my head around this as best as I can.

  28. 28
    CannuckianYankee

    The Publisher Chronicles, Part:4?

    Mr. Burnett,

    Thanks for pointing out the connection between Zondervan and HarperOne. The important issue I see here is that the book is not published by the religious arm of the parent company, HarperCollins. That Zondervan features the book on its webpage seems a bit of a fluke, because I looked over the hundreds of publications on that site, and could find only a few that were not actually published by Zondervan. I have to stick with my original instinct that Zondervan features the book because of its possible interest to Christians.

    I don’t think that HarperCollins, however is at all a religiously oreinted publisher – despite The Collins company’s history as a publisher of Bibles and religious books. The merger of these companies suggests to me that the parent company desires to gain a niche in many different areas of publishing including religious, but not exclusively religious. The name of the game seems to be to earn a profit form various publishing ventures.

    I don’t think that you can easily make a case for the religious motivations of a publisher, which is involved in commissioning a “no-holds-barred” autobiography from George Micahel, or the many other secular works they publish. It’s a business, and as such, they need to diversify in order to survive – especially in this economy.

    What does that have to do with Dr. Meyer’s book? You tell me.

  29. 29

    This discussion with Blu regarding IC is fascinating, and I look forward to its continuation. However, I would like to introduce an idea I have been thinking about for some time of which I am reminded by Steve Meyer’s (and others’) characterization of the challenge to Darwinism as the problem of the origin of biological information.

    Not to belittle that; I agree that it is a major stumbling block for the Darwinian paradigm. But in my opinion there is another equally serious problem that arises from the nature of systems, although it is deucedly difficult to make rigorous. Fundamentally, the problem is that complex systems (and all living things from single cells to large multicellular creatures are extremely complex systems) simply cannot be changed in any major way by a series of small incremental steps if you impose the requirement that after each step the system must continue to function at least as well as it did prior to the change.

    I will give an example from technology, because we understand technology better than we do living systems, and then relate it back to living systems.

    Imagine a factory that produces the famous WWII fighter, the P51. Imagine further that the QA folks, rather than simply rejecting any aircraft that doesn’t match the specifications, always test it to see if it might perform better in some way than those that do. If it does, then they change the specifications so that future models incorporate the accidental change. In this way the P51 slowly evolves.

    Will this evolutionary process ever be capable of producing a jet aircraft? The answer is obviously no, because there is just no way you can change a piston engine into a jet engine by a series of small changes, each of which results in a functional engine. And even if you could, there are simultaneous changes that would have to occur in the aircraft as a whole to accommodate the vastly different engine: it would have to move from the front of the plane to the back, which would require re-positioning the wings to maintain proper balance; the air intakes would have to expand and a conduit for air into the front of the engine would have to be created, as well as a hole in the tail for the jet exhaust to escape; new cockpit instruments and controls would have to appear, etc., etc.

    Now the central dogma of Darwinian evolution is that many small, incremental changes to a species over geologic time will eventually produce genuinely new body plans, organs, organ systems, and processes (such as blood clotting or insect metamorphosis). But it seems to me that the same system problem that prevents a Rolls Royce Merlin engine from metamorphosing into a GE jet engine also prevents a reptilian bellows lung from metamorphosing into an avian circular one (for example), no matter for how many millions of years incremental changes keep occurring or even how directed the changes to the genome are, as long as the requirement that changes occur to only one or two (or even three) genes at a time is maintained.

    I think there should be some sort of theorem stating that in systems above a certain level of complexity changes above a certain size or degree are impossible to achieve by a series of small incremental changes each of which results in a functioning system. As you can see, I don’t really know even how to frame such a theorem, much less prove it, but it does seem to me that when Darwinian theory proposes that an organism possessing a bellows lung can change into one possessing a circular lung via a series of small changes each of which enhances the fitness of the organism (to stick with our example), the burden of proof rests with Darwinism, not with those who point out that it appears to be quite impossible.

  30. Bruce…

    Yes! Yes!! That is -exactly- what I’m thinknig. And thats exactly where I think the line is ultimately drawn. Im pretty sure to state that the necessity of multiple beneficial mutations will actually weaken the evolutionary curve to a point where due to the specificity gained towards those functions, the system won’t even be able to backtrack or move in any serious way. I’m not sure if I’m clear, I agree with you that its hard to formula, but it is quite clear and definitive and I think you’d agree.

    Here is what I personally am trying to do. I think, that by definition, necessarily a limit to darwinian evolution exists. It actually must, due to the fact that…as you state, systems have a nature and structure, and to each system there exists an end to its combinatory/evolutionary potentiality. The limit is expanded the more steps you’re allowed at each stage (although, the more steps you’re allowed, the (considerably) higher the improbability of getting specifices steps at once).

    So, to formulate this, here is what I’m thinking (and even though some fo these points might be simple, I’d appreciate it if the people here could expand/correct/clarify):
    1- Define what a step is, and define its absolute limit. By absolute here I mean no matter how much time is given, you wouldn’t for example get…3 protein binding sites in a row by a triple mutation that isn’t extended from the combinatory possibilities of information already existing in a genome. So what I’m looking for here is the absolute limit of accumulating steps, not some probabilistic scenario (zapping radioactive slime from aliens in space excluded)
    2- Define, for any given structure all the combinatory possibilities coupled with what is defined in point 1. These include all known recombinations, shuffling, etc. coupled with what would increase the function of a system. This will actually exhaust all possibilities that the system can move towards, and will show the dead ends of a given system because of the following point.
    3- Define, at each stage when laying out the potentialities of a system’s evolution, the points at which it can’t step back. Where a particular change will not only be harmful, but fatal to the organism or to the particular system in question. The gradual accumulation will actually funnel the evolutionary pathway in a certain direction which it cannot gradually back up from to generate a higher structure. This isn’t only because it will be fatal, but its because it will reduce the efficiency of the system it has just arrived at. Moreover, it is because certain indirect changes will not (and this is case specific) translate into a particular function that will be reflected int he environment. This is specifically clear when it comes to morphological and structural changes, or attaining higher information networks for cognition (this also blends in changing of behaviour by species to their environment, and whether this would happen if the brain was a mere algorithmic neuronal network, which I’m pretty certain it isnt).
    4- Define, at each stage, the limits of the information accepting capacity from external sources through signalling out systems that would not/cannot change no matter how much information is derived from other sources by gradual means (lateral gene transfer, etc.) due to the same point in #3, and due to any factors that would resist particular insertions (and that, for certain systems, the information needs to be specific to the case, and is not generalizable, specifically considering the possibility space of biological systems this I believe is critical when it comes to developmental maps for multicellular morphologically novel organisms…if they exist at all).
    5- Define a limit for the accumulation of neutral/random components, this ties into #1, in the sense that its important to clarify that any addition whatsoever that can add to a (however improbable) step must be accounted for, the entire effort is to reach what is impossible given a certain method, not just what is improbable and it is rationally and logically achievable as far as I can tell.

    After doing the above, you exhaust all the possibilities of a given evolutionary pathway. If the possibilities are breached, then the process cannot account for that pathway. So you either see if the process assumed is faulty, or look for another explanation. Now, making such a possibility tree, if you’d allow me to call it that, is for one evolutionary pathway a daunting task. But, nonetheless…such pathways necessarily and logically must exist. The limit is defined by the maxiumum number of allowed steps by each stage, and the necessity of accumulating gradual benefit.

    Now, one might argue that indirect pathways always exist, and they might. But indirect pathways will also be limited by the necessity of them being A- gradual, B- one step at a time (or whatever the limit is) 3-the necessity of an indirect pathway to translate into an interaction with the environment that will be beneficial to the system. Two points to mention here, the nature of the systems accumulated by the gradual pathway will most likely differ from those that didn’t (at least theoretically, you can specifically backtrack and see what led to what), and that there will be zones where no gradual pathway can reach. These zones will be defined by a particular organizational/hierchical/regulatory structures that requires multiple connections to function, but with a few steps would do nothing at all and with a few steps will not translate into a change within the system’s fitness to get the ball going. Aka. fully irreducibly complex systems. (but here I’m not just talking about the systems themselves, but how systems fit together and can be integrated into a larger system). And again, the tendency of the step by step gradual benefit will create immense resistance to even an indirect pathway, since any evolutionary change that is beneficial must translate into a particular action that the organism activates and interacts with its environment. Limiting indirect pathways to pathways that must accumulate fitness and function.

    I think everyone who looks at the bacteria flagellum, intuitively senses that it lies within this boundary (especially if you consider the IFT, and who knows what else is lurking in the details). Or if someone looks at say…a mosquitos nervous system and its capacity for aerial navigation and pattern visual recognition, I believe something like that lies outside of the funnel.

    anyways, I’m writing too much already, the thought is still crystallizing within my mind, I have more thoughts about this, I look forward to hearing yours. I believe T-urf13 lies within the potential combinatory possibilities in question, and I’m not so certain that the information inherent therin arose by gradual accumulation that at one time translated into fitness (same with almost all organisms).

    (as a side note, irreducibly complex specified systems become not only hard to create, but hard to move away from)

  31. Can’t resist to add one more thing,

    What we have here are very specific driving factors, and they’re all interrelated.

    1- The number of steps allowed
    2- The point at which a structure of a system cannot change due to its interconnectivity with itself and its environment
    3- a gradual change that MUST translate into a change within the environment.

    The point I want to add is, the “number of steps allowed” is what allows the system to expand beyond its evolutionary funnel randomly. It is the free lunch so to speak to generate a particular multistep scenario that would allow the system to rise to a higher level of specificity/organization/function or to backtrack and create a restructuring shift that would in turn translate into fitness.

  32. And…one more thing:

    You don’t even need to observe the whole pathway, all that needs to be done is take any given system (within a larger system), define the maximum number of changes allowed/number of steps, observe the subsequent system, if there is no way to lead from A to B through creating to that system (where the limits and parameters are now being clearly defined due to the specific nature of the system and known allowable extentions).

    So you’d define all the things in the system that cannot be changed gradually, or at all. The structurally fixed points the change of which would cause the system to overload. then observe through those that you can change, out of those, you see whether given the number of steps allowed you can transfer any of those parts and their subsequent interaction that can affect the parts that cannot be changed. If the answer is no, then there’s the limit.

    I mean…I’m not saying anything new here, just trying to clarify my thoughts by discussing and expressing them. But it seems to me that the darwinian, instead of figuring out ways in which to make things work by laying explanations on top of data, should observe and define the limits, and move from there…I think we’d find those limits to the simplest systems pretty fast. (the more complex systems get, the more interconnected and interdependent, the harder the change, and if an irreducibly complex structure exists…we all know what happens if you try changing one part…you’d need another structure taking over its function while not overloading the system to fully arise before changing it. I think…).

  33. 33

    Hi Blu,

    Hm, I might have misunderstood. I’m reading the paper now, it isn’t quite specific on the actual mechanism by which such a process occurs in a gradual manner…they are mostly talking about the probability of its occurence and its fixation within a population that necessarily requires selection against parts of the duplicate gene. But isn’t it that during that process occuring, the primary gene encoding for the protein would stop functioning? Kindly correct me if I’m mistaken. Trying to wrap my head around this as best as I can.

    I have to apologize. The paper I cited was far more general, although it does discuss subfunctionalization. One focused on subfunctionalizatioin itself was published by two of the authors:

    Lynch M & A Force (2000). The Probability of Duplicate Gene Preservation by Subfunctionalization. Genetics 154: 459-473.

    Its available online as well (one of the great things about the journal Genetics. Figure 9 illustrates the process and paths very well. That <i.should answer your question, but if not feel free to ask for clarification.

  34. 34

    Hi Bruce,

    Imagine a factory that produces the famous WWII fighter, the P51. Imagine further that the QA folks, rather than simply rejecting any aircraft that doesn’t match the specifications, always test it to see if it might perform better in some way than those that do. If it does, then they change the specifications so that future models incorporate the accidental change. In this way the P51 slowly evolves.

    Will this evolutionary process ever be capable of producing a jet aircraft? The answer is obviously no, because there is just no way you can change a piston engine into a jet engine by a series of small changes, each of which results in a functional engine

    To use a biological example, are you saying a series of relatively small genetic changes could not produce an insect wing from a gill? The two structures have completely different, unrelated functions.

  35. Dave Wisker:

    To use a biological example, are you saying a series of relatively small genetic changes could not produce an insect wing from a gill?

    Do you have an example of an actual demonstration?

    Or are you just going to post the diatribe that speculates that such a thing happened?

    Speculation is meaningless without that demonstration.

    Gene duplication- again?

    In order for a duplicated gene to even get transcribed it must also have a binding site in its regulatory region.

    And yet we have a peer-reviewed paper that says just to get TWO specified mutations is close to impossible unless you have a very large population and they are fast reproducers.

  36. Dave Wisker:

    joseph’s comments regarding T-Urf13 are misleading. He has been corrected on this before both by me and Art Hunt over on the ARN discussion board, yet inexplicably keeps repeating the argument here.

    Wisker and Art are ignoranbt of ID’s claims.

    They think their ignorance is some sort if refutation.

    That they think they can continue that here is amazing to say the least.

    Artificial selection is NOT natural selection.

    IC is an argument against natural selection and random variation ONLY.

    That neither Dave nor Art understands that just further exposes their ignorance.

    And now Dave can’t even get my argument straight as he is continuing his lies.

    If lying is the best you have then why even bother posting?

  37. Dave Wisker:

    Specifically, his comment about male sterilization leaves oiut a critical piece of information: maize plants are hermaphroditic, meaning each plant possesses both male and female reproductiuve organs. T-Urf13 does not make the entire plant sterile, it simply renders the male reproductive organs sterile.

    Wisker leaves out a crucial piece of information- mainly that without males females will not reproduce.

  38. Mr Bruce David,

    Thank you for your thoughtful post. here are a few of the ideas it bring up for me.

    The mapping from genotype to phenotype is not linear. Small changes in the genotype can produce large changes in the phenotype. In large part this is caused by changing the pattern and timing of gene activation during development. This is the most basic challenge to any theory that demands that small changes must have small results.

    Thes kind of developmental changes are capable of opening and closing pathways between parts of the body, and these local changes can have a great change to the overall topology of the system.

    The comparative anatomy of all modern forms has to be taken carefully as a reading for what can and cannot have happened developmentally in the past. Birds are not the only animals with air sacs attached to the lungs. The feature appears in chameleons, some lizards, and snakes. This kind of wide distribution of a feature would argue that it is an old feature.

    In all cases, inhalation and exhalation occur due to muscles attached to the skeleton changing the interior volumes of dead end air sacs. The great innovation in birds is to separate gas exchange functions and localize them away from these dead ends.

    I think your ideas on IC are closely related to several topics in evo-devo. thank you for sharing them.

  39. 39

    Dave Wisker:

    Specifically, his comment about male sterilization leaves oiut a critical piece of information: maize plants are hermaphroditic, meaning each plant possesses both male and female reproductiuve organs. T-Urf13 does not make the entire plant sterile, it simply renders the male reproductive organs sterile.

    Wisker leaves out a crucial piece of information- mainly that without males females will not reproduce

    And joseph fails to note that he has been coirrected on this point ad nauseum): populations polymorphic for cytoplasmic male sterility genes (like T-Urf13 have higher yields. Anyone with even a neophyte’s understanding of evolution can see that a gene which confers higher fitness for its population is not detrimental by definition.

    I and others can explain this to joseph, but what we cannot possibly do is understand it for him as well.

  40. 40

    joseph seems to think that T-Urf13 is detrimental because a population of all females couldn’t reproduce. There is only one possible scenario for this the T-Urf13 gene becomes fixed in the population (i.e., 100% frequency).

    So let us consider this possibility. Does evolutionary theory predict that a gene which confers male sterility would become fixed in a population via natural selection? Anyone with even a rudimentary knowledge of natural selection would laugh and say “of course not”.

    Would such a gene be eliminated from the population by natural selection? If it had no effect on fitness, probably. Natural selection would eliminate it fdrom the populatioin if it had a negative effect on fitness.

    So what are its effects on fitness? Well, we do know it leaves the plant with a heightened susceptibility to some diseases. But that is an environmentally dependent effect. But it also results in increased overall yields. That is an effect that <i.improves fitness by definition– a population polymorphic for the gene (that is, at some frequency under 100%) would have more offspring than one in which the gene is absent. So, evolutionary theory would never expect the gene to rise to 100% frequency, but would predict a rise to some lower frequency and evehntually reach an equilibrium .

    So, one can see joseph’s point about the population being all female is unrealistic, not what evolutionary theory would expect, and thus completely irrelevant. That he keeps bring it up shows very clearly that he has a scant understanding of the relevant biology.

  41. 41

    The third paragraph of my last comment should read:

    Would such a gene be eliminated from the population by natural selection? If it had no effect on fitness, it woukld probably eventually be eliminated by genetic drift. Natural selection would eliminate it from the population if it had an overall negative effect on fitness.

  42. 42

    One other thing: cytoplasmic male sterility also has another fitness advantage: it encourages outcrossing by preventing the plant from self-fertilization. It increases the overall variation of the population by driving down its level of inbreeding.

  43. Artificial selection is NOT natural selection.

    IC is an argument against natural selection and random variation only.

    Therefor to use a case of artificial selection as an argument against IC is dishonest at best and demonstrates ignorance of the debate,

    That Wisker keeps harping on this example demonstrtates the desperation of his position.

  44. Dave Wisker:

    Does evolutionary theory predict that a gene which confers male sterility would become fixed in a population via natural selection?

    LoL! The theory of evolution doesn’t make any predictions based on the proposed mechanisms.

    Also natural selection doesn’t have anything to do with this example.

    IOW you appear to have serious issues and should seek help.

  45. Dr Behe:

    How about Professor Coyne’s concern that, if one system were shown to be the result of natural selection, proponents of ID could just claim that some other system was designed? I think the objection has little force. If natural selection were shown to be capable of producing a system of a certain degree of complexity, then the assumption would be that it could produce any other system of an equal or lesser degree of complexity. If Coyne demonstrated that the flagellum (which requires approximately forty gene products) could be produced by selection, I would be rather foolish to then assert that the blood clotting system (which consists of about twenty proteins) required intelligent design.” (bold added)

  46. Bruce and Blu @ 32,

    I am thinking the same thing.

    I believe ID predicts a genomic adaptive landscape or threshold if you will that all organisms possess and cannot break through.

    An example I think would be the famous galpagos finch. Their beaks get bigger and smaller as the size of available seeds change. The question is, will finch beaks keep growing bigger and bigger if the seeds keep getting bigger and bigger.

    I suspect they will not. I think what would happen is that finches would die off in that envirornmental niche and another species like a parrot or other bird with beaks larger than the finches with the biggest beaks would eventually take over, once they happen to find the niche.

    If the parrots don’t find the niche and those super sized seeds don’t get eaten, then those trees that come from the big seeds with spread and they will attract other types of birds and eventually the parrot or like bird with oversized beak will find its way to the trees branches.

    The point being that the finch cannot keep increasing the size of its beak. In order to do so, it would have to change alot more than its beak as you allude to in your posts. Its not efficient as it would take too much time to make all the necessary changes. The finch would starve before it even got started that evolutionary path.

    Rather, the elastic nature of the biosphere does not require no desire an organism to break through their adaptive threshold. Instead, the biosphere simple shuffles the niches and organisms.

    So I think we would never see finches with oversized beaks. That is the limit of their adaptive landscape.

  47. One more thought- if a mutation or trait cannot become fixed in the population, just how beneficial could it be?

    Isn’t that the true test of benefit?

    But anyway…

  48. 48

    For those who find joseph’s montonous drumbeat of “Artificial Selection” convincing, some examples of cytoplasmic male sterility being maintained polymporphically in natural populations should render that objection irrelevant:

    Summer Savory (Satureia hortensis)

    Cabbage Thistle (Cirsium oleaceum)

    Perennial Ryegrass (Lolium
    perene
    )

    A paper discussing this is:

    Lewis D (1941). Male sterility in natural populations of hermaphroditic plants. New Phytologist 40(1): 56-63.

  49. 49

    One more thought- if a mutation or trait cannot become fixed in the population, just how beneficial could it be?

    Enough to increase fitness. That’s all it needs.

    Isn’t that the true test of benefit?

    No, of course not.

  50. 50

    joseph writes:

    LoL! The theory of evolution doesn’t make any predictions based on the proposed mechanisms.

    Basic population genetics predicts exactly what I wrote.

  51. Mr. Nakashima,

    I agree that movement from genotype to phenotype is not linear. But…how it got to be that way, and why it is that way, and how far changes can go is a critical question. Its very clear that we observe morphological/body plan constrictions on all empirical evidence of change in species, and some serious constriction on how much you can change an organism developmentally.

    More importantly, no one has a clear idea on how genotype actually maps to phenotype, we currently only can observe correlations between changing genotype and its effects on the organism as it grows. As far as my knowledge goes (and please correct me), most attempts to create some major morphological or structural change has lead to fatality in organisms save the example of snake coiling in an opposite direction.

    Personally, it is my intuition and belief that the darwinian scenario will face its ultimate challenge when it comes not to how genes correlate to phenotypes, but how forms arise to begin with. It sometimes surprises me (and I’m stating this generally) that the entire theory is based on the idea that genes react through regulatory reactive sequences and lead to the arisal of an organism. Nonetheless, we have no reason to believe that DNA and its subsequent reactions are the actual causal force responsible for the morphological and developmental structuring of an organsim. I say surprising because an entire academic culture has put its eggs in a basket that hasn’t even crossed the weaving stage (respectable opinion not withstanding). So in that regard, we are not very clear on what the limitations of such shifts are, and why a small shift in genotype leads to large shifts in phenotype and how far we can extrapolate that. Correct me if I’m wrong, but I believe they all reside within a definable limit.

    The points Mr. Bruce raised earleir and I tried to expand on, are critically important when it comes to the mapping out of an organism. Imagine the sensitivity to such a reactive map (if a reactive map exists), and how major requierments will require major remodeling due to the delays in targetting, timing, reactivity, function change, dependent correlations, etc.

    Oramus,

    I would actually take it a step further. I would say in some cases, as the seed size increases, in some cases, even if there weren’t finches with beaks that size in the population…ones would start appearing in response to the environmental change (not necessarily always, but I am saying its possible). Call me crazy, but thats how I think it happens. I personally do not take reality for an idiot (and we have quite a bit of evidence for rapid speciation and environmental triggered changes). I have quite a few reasons for that, but we can leave that for another discussion. For now, I have a question for the experts here…it might seem like a silly question but I ask your indulgence.

    How many steps can we expect to happen at once? Can we give a number. If there was no selective cleansing going on (where a mutation that wasn’t beneficial wouldn’t move forward) is there a limit to how many new steps/components an organism can have laying around? Or does the number increase indefinitely over time till something “clicks”(again, presuming that no selective cleansing pressure exists and the organism keeps reproducing)?

  52. Mr. Wisker,

    Regarding subfunctionlization, what interests me is the degree by which it can open up pathways…or possibility constrict them (due to the system requiring potential change to more parts due to the fact that it has become more specified). Even though its an important point to think about…according to the criteria I’m trying to arrive at…I wouldn’t -really- consider subfunctionlization an irreducibly complex system. Although I guess the technical definition might apply…to a certain extent.

    Thanks for sharing it again! I’ll read more about it and give it some thought.

  53. Hi blu,

    I’m glad the reference was of use. I do have one question, however. Given what you wrote:

    Even though its an important point to think about…according to the criteria I’m trying to arrive at…I wouldn’t -really- consider subfunctionlization an irreducibly complex system.

    What do you consider an IC system?

  54. Hey Dave,

    Here is what I look for: I consider an IC system a system that *requires* the generation of the following (or at least some of the following):
    1- Multiple components, the information of which is not already available in the combinatatory potentiality of a system, or ones which can be added to the combinatory potentiality of a system, but still requires components/steps/mutations beyond that of a number that surpasses the expected amount of steps allowable for an organism.
    2- Multiple components that must arise to manufacture the new components. These components would have the sole function of generating the new system…the IFT comes to mind.
    3- Integration within a pre-existing system that would affect the system’s function and therefore would require a hiearchical organizational shift due to the arisal of the new components
    4- Extendability and availability from a pre-existing system
    5- Specific synchronization and activation of the new parts for the new component to function
    6- multiple changes in the pre-existing development plan required to integrate the new component.
    7- multiple changes on a morphological and structural level that would be required, some of which would cause the organism to dead-end due to the necessity for beneficial gradual mutations.
    8- an absence of intermediate steps that would translate the new components into fitness.
    9- a change of a part or of an irreducible core of the larger system that contributes to some basic survival function of the entire organism.
    10- intersectability: a system that contains functions that would have interfered with the function of a larger system if they were activated one at a time, but not if they were all activated at once.

    I have some other subtle points, but thats what I generally look for.

  55. Edit:
    9- a change of a part or -more- of an…

  56. blu,

    Interesting list. Looking it iover quickly, I would think subfuntionalization fulfills:

    2) The multiple genes manufacture a component

    4)

    5) The sequence of mutations would have to be such that one copy was providing the functional protein until the final mutation(s). As seen in Figure 9.

    I don’t understand what you mean by 7 or 8.

    9 could apply if the protein in question was part of a pathway vital to survival or fertility of the organism.

  57. Mr Blu,

    Thinking about how suppressor genes work during development, changing suppressor function can let the corresponding productive gene effects continue to build the phenotype in ways that are hard to limit. Then you could get trees like redwoods growing to the limit of cellulose compression failure. Animals such as snakes or millipedes that have repeating units that can grow to hundreds of units in length. All because a small change stopped a suppressor during development.

  58. Mr Blu,

    In honor of your name, the Belgian Blue, a breed of cattle with a suppressor mutation.

  59. Dave,

    Regarding 2, what I mean is something along the lines of IFT, where actual manufacturing that requires new protein structures/binding sites, etc. needs to exist. This would blend point 2 with the other points.

    Regarding 4, I would agree with you that subfunctionlization fulfills it, but what I’m alluding to more is the availability and extendability from a pre-existing structure. So say that an organism can already encode X proteins, and for the new component to arise, it has no existing structure/function to latch onto for extendability of the system as a whole.

    5- What I mean here is the necessary synchronization required for the building or functioning of an entire structure, like say…a motor, building sequence with other arising components from a protein secretion system, molecular machines, etc.

    By 7, I mean that some restructuring on say…the skeletal structure is required, coupled with muscular changes, shifts in nervous system and correlating shift in the brain to generate information for the newly arising function/structure. By the dead end…for a generalized scenario (I’m not being technical about the example, just using it for simplicities sake). Say you want to extend a pre-existing organism that led to the giraffe, to the giraffe’s neck. You can either increase the size, length, or angle of the neck to begin the motion. If you increase size or length, you will be putting some weight on the structure as a whole, and some support systems would need to arise, and some restructuring on the part of the vertebrae themselves, and the nervous system as a whole. If you change the angle (prior to elongation), where the angle starts shifting will be sharp, and this is early on…some restructuring will have to accommodate that too, a buffer zone at the angle coupled with curvature of vertebrae for support. So for each change, you’ll have a subsequent change that is required to support the entire structure (I’m ignoring that both need to happen at once here). The point is that from that point forward, the system becomes more rigid and resistant to change, since it has solidified the structure in response to a change, and a step backwards required for the flexbility and restructuring of the organism would be a negative rather than a positive. I’m sure there are better examples than this.

    By 8, I mean that the changes/components/steps that arise will not have an effect on the organism’s actions or survival, but if they accumulate in large numbers, then activate, would have a positive effect. In other words, I’m looking for beneficial changes that require multiple components with no intermediary beneficiaries in between (ina sense, just trying to get more specific on the definition of irreducible complexity).

    9, right…it has to do with integratability of larger systems in question.

    I guess the only reason I wouldn’t include subfunctionalization as an example is even though it might technically fit some definitions, I’m looking for something that can be extended into creating novel traits, machinery, cell types, organs, tissues, body plans, hiearchical organization structures that would unify/add information to a “lower” function. I’m not saying it doesn’t fit persay, just that I’m looking for something that would be constructive towards that direction. I am still trying to see hwo subfunctionlization can be constructive, not saying that it cannot.

    Hope that clarifies what I’m looking for better. The trick with this is that the issue is case specific. Mr. Nakashima earlier was talking about the lung, but change of a lung is a bit more subtle…I think. You don’t just “extend” a lung, systems don’t understand lungs. They understand highly integrated synchronized developmental maps, biomolecular pathways fixed to particular locations and functions, in relation to other ones. As the lung expands, its going to start pressing on a lot of things, deviate the balance structure that the organism is used to, perhaps add weight in certain areas. You have the blood circulation system, muscular system required to accommodate the new change, moving the neural wiring, adjusting the signals sent from the brain to allow for the proper expansion and constriction of the new position, adjusting any metabolic systems that require more/less energy to the new lung, repositioning an existing air pathway, etc. Each of these happening at a very minute scale…we know…the multicellular complex organisms that we are, that the slightest deviation in the slightest region will add immense load on the system and usually results in disease. Imagine the pain nerves signalling a response to an extending bone or shift of structure that starts occuring…or if the new organism, having aquired some different vocal chord structure or weird shape…would communicate with the other of his group…thinking he’s saying something while not even understanding what he’s saying. Nor they he. I’m saying this in a half-joking half serious way of course…but the point applies.

  60. As an extra (again, half-joking) point, has anyone felt the amount of pain associated with even the slightest deviation in spine structure? Poor giraffe.

  61. Mr. Nakashima,

    Thank you for the information. I didn’t say changes cannot occur, simply that we do not exactly know how things map out, or how they are organized. It seems to me in this case that the organization structure is still rolling but the corresponding “film” isn’t clicking the stop button at the right point. Nonetheless, we do not know how a 1000 or 2000 genes (correct me if I’m mistaken) code for an eye, or how a few genes can account for the growth and astounding synchronization and activation of the brain. We don’t know how very similar genes between different lines code for very different organisms. We don’t know how we can generate new novel body plans, organs, etc. rather than suppress/redirect existing mapping out to a certain extent.

    Actually, I’d go as far as to say that we -really- have no idea whats going on. The fact that embryos keep growing regardless of disturbing growth in different ways (and from different angles), as much as taking entire parts out…that development doesn’t seem to be very dependent on primacy of neighboring cells, on attaining some form of reactive equilibrium, that nervous systems extend in unpredictable fashions, and that morphological structure in general seem to be the force guiding the underlying cells in a specific direction rather than the other way around. Even the synchronization of information in organisms as a whole and something as simple as regeneration or cell duplication (when, why, how and what triggered it from a contextual perspective of the system). All systems that share features Cambrian forward are very vague in current understanding. As far as I know, there is still no theory accounting for morphology at all from a purely materialistic/reactive perspective. Usually you get the term “epigenetic”, but the problem is…if epigenetic factors are regulating the development of an embryo/organism, then shift to the epigenetic factors would result in the regulation being disturbed. But…what is regulated here, is what is doing the regulation (and, it arises from complementary genetic factors too), and affecting embryos in different ways (up to some serious disturbance) still maintains its growth. I actually don’t know of any concept in physics or chemistry that accounts for how this happens.

    Looking forward to hearing your response.

  62. I submitted my comment at 12:30 am California time before retiring last night, and when I checked this morning, the comment string has doubled in length while I was sleeping! I will attempt to respond to at least some of the posts regarding my comment, but I won’t be able to get to it until later today.

  63. blu,

    Have you read any of Sean Carroll’s books? Endless Forms Most Beautiful does a very nice layman’s job of explaining the interactions between genes, development, and form. At the very least, it might give you concrete paths to follow in your research.

  64. Dave,

    Yes, it was a good book. Although it still doesn’t address the serious challenges facing developmental biology and embryology, in the sense that it appears that DNA might not be the “regulating” agent, but might be like a group of bricks, metal bars, walls, etc. that are utilized by an underlying organization structure. Changing the shape (adding or removing) of the brick, a divider, or a wooden latch might affect things, but it still doesn’t address the generation of form itself which I believe requires more than what we currently possess. Caroll’s book is more of an overview of the current level of our knowledge.

    I personally preferred Brian Goodwin’s book, How the Leopard changed its Spots (although…he doesn’t actually mentions how it happens in the book!). He recognizes the difficulties faced by development and morphologies, and proposes mathematical fields of organization. I have two problems with his approach, the first is that mathematical structures that are generalizable across the board won’t reach the level of specificity required for the spatio-temporal development we observe today. Second, is that these mathematical structures aren’t fixed, but change from embryological stage to another…making them more of a sequence than a fixed field. Anyways, its a very good read…but I’ll leave that for another discussion, or for a later point of this discussion, save to say that our undrestanding of causality might be in need of some serious revision (or perhaps…completely getting rid of the concept all together, but I don’t think the naturalistic side is ready for that yet).

  65. 65

    Hi blu,

    Yes, it was a good book. Although it still doesn’t address the serious challenges facing developmental biology and embryology, in the sense that it appears that DNA might not be the “regulating” agent, but might be like a group of bricks, metal bars, walls, etc. that are utilized by an underlying organization structure. Changing the shape (adding or removing) of the brick, a divider, or a wooden latch might affect things, but it still doesn’t address the generation of form itself which I believe requires more than what we currently possess.

    Really? I’m not sure I agree with what you are saying. For example, we have examples of homeotic gene changes in plants (Aradopsis,specifically) triggering developmental changes that result in the following transformations of flower parts: stamens to petals; sepals to leaves; petals to sepals, stamens to carpels, to name a few. The genes control when and how cells begin differentiation into new tissues via chemical signalling.

    Are you saying the mutations may not be responsible for these fairly radical transformations?

    Reference:

    Bowman, JL, DR Smyth & EM Meyerowitz (1989). Genes directing flower development in Arabidopsis. The Plant Cell 1: 37-52

  66. And one more refutation- Turf 13 provides only ONE component.

    I don’t know any IDist who says that undirected processes cannot account for ONE component.

    And Wisker’s dismissal of “artificial selection” just demonstrates the desperation of his position.

    Bait-n-switch tactics further expose this fact.

    Basic population genetics predicts exactly what I wrote.

    Now you are moving the goalposts.

    Is that what you are reduced to?

  67. For those who find joseph’s montonous drumbeat of “Artificial Selection” convincing, some examples of cytoplasmic male sterility being maintained polymporphically in natural populations should render that objection irrelevant.

    Your whole “argument” is irrelevant.

    That said does this trait in any of your examples produce an IC system?

    THAT is the whole point.

  68. 68

    joseph, I refuted your artificial selection objection by citing examples of CMS being maintained in natural populations. T-Urf13 is a CMS gene.

    Your position has been thoroughly refuted with concrete examples. No bait-and-switch. It is now up to you to show that T-Urf13 is not a gene that confers cytoplasmic male sterility. Good luck with that.


    Basic population genetics predicts exactly what I wrote.

    Now you are moving the goalposts.

    Is that what you are reduced to?

    Joseph, I wrote that evolutionary theory predicts that a CMS gene will not become fixed in a population via natural selection, to which you replied:

    LoL! The theory of evolution doesn’t make any predictions based on the proposed mechanisms.

    Basic population genetics completely refutes your position. A gene for male sterility in a hermaproditic plant population will never reach 100% frequency via natural selection. That is as solid a prediction as you can get in population genetics. It is also intuitively obvious.

  69. Dave Wisker:

    joseph, I refuted your artificial selection objection by citing examples of CMS being maintained in natural populations. T-Urf13 is a CMS gene.

    LoL!!!

    This has NOTHING to do with CMS.

    It has EVERYTHING to do with IC.

    The IC system is the result of artificial selection.

    No artificial selection no IC system in corn with Turf-13.

    That you can’t even understand t6hat simple point is very telling.

    Joseph, I wrote that evolutionary theory predicts that a CMS gene will not become fixed in a population via natural selection, to which you replied-

    The theory of evolution and population genetics are not the same thing.

    A gene for male sterility in a hermaproditic plant population will never reach 100% frequency via natural selection.

    Natural selection is a result.

    And how the heck can unguided processes tell what percentage of the population has CMS and is male sterile?

    IOW you are once again grasping at straws.

  70. Dave Wisker,

    And one more refutation- Turf 13 provides only ONE component.

    I don’t know any IDist who says that undirected processes cannot account for ONE component.

  71. 71

    Joseph,

    <i.Natural selection is a result.

    And how the heck can unguided processes tell what percentage of the population has CMS and is male sterile?

    I suggest you actually learn the subject of population genetics and the concept of equilibrium. Your statement here tells me you are operating at a serious handicap and trying to talk about something about which you know practically nothing.

  72. Dave,

    Look in the mirror. It is obvious that you know nothing about ID and its claims.

    It is also obvious that you are conflating population genetics with the theory of evolution.

    And now you think your snide comment is another “refutation”.

    You are a legend in your own mind…

  73. Dave Wisker:

    A gene for male sterility in a hermaproditic plant population will never reach 100% frequency via natural selection.

    But corn is the result of ARTIFICIAL selection.

    And via artificial selection male sterility in a hermaproditic plant population can most definitely occur.

    What part of that don’t you understand?

  74. 74

    Joseph,

    But corn is the result of ARTIFICIAL selection.

    And via artificial selection male sterility in a hermaproditic plant population can most definitely occur.

    What part of that don’t you understand

    It doesn’t matter one iota that maize is a cultivated plant. T-Urf13 arose naturally in maize. It wasn’t artificially introduced. T-Urf13 is a CMS gene. CMS can arise in natural populations and can be maintained in them. Thus your attempt to argue that T-Urf13 is a detrimental mutation is rendered impotent. Why did you try and argue that T-Urf13 is a detrimental gene, joseph? Why did YOU bring it up? That is what I am responding to– YOUR point. And when I do you divert the conversation by sudennly announcing its all about IC now. Why bring up the point about it being a detrimental mutation when all you REALLY want to talk about is IC?

  75. Dave Wisker:

    It doesn’t matter one iota that maize is a cultivated plant.

    Maybe not to you but to the IC argument it matters a great deal.

    T-Urf13 arose naturally in maize.

    No it didn’t. It arose due to artificial selection.

    T-Urf13 is a CMS gene.

    So what? That is irrelevant.

    This discussion is about IC not male sterility.

    The WHOLE point of Turf-13 is that it allegedly procuced an IC system.

    The part of it being detrimental is just a small part of that.

    Male sterility- more susceptible to fungal infections- yeah I would say it is more detrimental than beneficial.

    But again that is only a MINOR point.

    MY POINT has ALWAYS been that this (Turf-13) is NOT an example of IC being formed via RM and NS.

    And that much is obvious.

  76. And one more refutation- Turf 13 provides only ONE component.

    I don’t know any IDist who says that undirected processes cannot account for ONE component.

  77. Mr Blu,

    Thank you for inviting my further comments.

    Lets think about all the different cell types in the human body. The Wikipedia list of cell types is about 210 distinct types of cells. But to be safe from our own ignorance, lets double that, and round up to 500. Now lets double that again to cover all the cell types that might exist during development, but not in the final adult body. So human development takes 1000 cell types. Wow! How many gene switches would it take to regulate all those?

    10.

    2^10 = 1024.

    OK, our bodies might not be that efficient in terms of using switches, so double it.

    20.

    Maybe each signalling gene needs 3 other genes to work right.

    80.

    Lets round up and say that to be safe our original estimate of 10 was off by an order of magnitude.

    100.

    So the body uses 100 genes to build the eye. It uses the same 100 genes to build every other cell type.

    That is cool.

  78. Hi Nakashima,

    We can take your example one very impressive step further. If we assume a very simple model, whereby each and every cell in a human body (all 1 trillion of them) is specified by a unique combination of gene switches (say, transcription factors), the we would need only 40 or so such proteins to completely and uniquely define each and every cell.

  79. 79

    joseph,

    T-Urf13 arose naturally in maize.

    No it didn’t. It arose due to artificial selection.

    T-Urf13 had a natural origin in maize. How could it arise by artificial selection? Selection–artificial or otherwise— does not generate the variation.

    Male sterility- more susceptible to fungal infections- yeah I would say it is more detrimental than beneficial.

    Given your level of actual knowledge on the subject, and the evidence available to easily rebut it, your saying so doesn’t cut much ice.

    But again that is only a MINOR point.

    MY POINT has ALWAYS been that this (Turf-13) is NOT an example of IC being formed via RM and NS.

    Then don’t bring up minor points–especially if you cannot take correction of your errors on them gracefully.

  80. Hi Dave,

    Thanks for your response. Your example is a good example for the discussion, and perhaps might make me clarify my position further. Just like in the other examples Mr. Nakashima generously provided, the genes here act like a switch, press play, press stop. What I was referring to is the structure of the plant itself. Plants…are tricky. But, I believe you’d agree with me that all changes have maintained a plant’s inherent structure and form within a defined boundary. Consider the venus flytrap. The boundary I’m talking about is if you get a plant, and change its genes as much as you want, you’ll never get to a venus flytrap. The morphological form itself, and underlying structure requires additional factors. DNA, from my study and reflection, provides in multicellular organisms three components. (and again, plants are tricky…and as with all things…demarcation lines aren’t black and white). The first is the raw material, or more specifically an intersectional point of energetic transformation (from one kind of energy/chemical to another), the second is it provides the switches themselves. Note…I’m not saying it does the switching, I’m saying it contains switches that can be utilized to turn other things on and off. The third, is it might have a yet unknown property that functions as an organizational force in the cell, allowing it to be an intersectional point for that too. Now the last one might seem a bit woo-woo, but time will tell.

    Imagine a painter using a brush, palette and has a bunch of materials to make her canvas. If you change the kind of brush, its tip, its curve, or if you change the colours, or the material of the canvas she uses, the painting will come out different. Or if the painter needs some signals and ques to start painting one part or another, and those cues change…the result will differ. Nonetheless, none of these agents were the sole responsible factor for the generation of the painting.

    If you search the literature…you’ll find an immensely scarce supply of information on the generation of form and morphology. The best you can find are on plants, and its still not clear how things work. The critical point is: How does an organism recognize its spatio-temporal position in relation to the rest of the structure? The question’s difficulty becomes compounded when you realize that shifts done to the entire structure (whatever it is considered to be dependent upon), doesn’t change the direction of development nor the form taken, and that the same cell types take widely varying forms within the same organism. Its quite astounding and awe inspiring…if you look at for example, the development and branching out of the nervous system during development.

    To respond to Mr. Nakashima, I frankly have no idea how any number of control genes can direct any course of development to the degree of flexibility we observe. I am unable to generate or find a concept that applies. Multiple theories were provided in the past, cells get their developmental motion from the primacy of other cells. Ok…but if you change the other cells, everything goes fine, moreover if you change the angle of a developing embryo, it will contniue in its proper morphological trajectory. Cells attain a sort of chemical equilibrium: too general, doesn’t account for specificity of form or ist generation, and if you disturb the equilibrium in different ways you get the same result. Mathematical models account for the growth of cells, ok…but mathematical models would need to be highly specified and would change over developmental time…they don’t just accumulate one on top of another, and so on.

    So for now, I’ll choose silence. I think you’d both agree with me that the question: “How do forms arise?”…respectable opinion notwithstanding, is poorly answered. We understand -correlations- between the availability of switches in genes and their expressions. Gene controls in the past was actually used as a metaphor…now, its become the Word.

    Out of curiosity, did T-urf13, and the breeds before it undergo any artificial genetic modification? If it did, regarding what I mentioned earlier…a particular genetic change could have expanded its evolutionary funnel and allowed it to progress in a direction it otherwise couldnt’ve. This isn’t a point against the ICness of the system. And, as I mentioned earlier…I don’t think anyone has a clear idea on what the gradual changes leading to T-urf13 were, why they were retained, etc.

    And, a question to those who lean more to the side of the darwinian side of things. How do we deal with changes in organisms that require massive amounts of coordination, across multiple factors within the organism? Like what we spoke about before. See…the difficulty is, no one knows exactly how a neural network changes its structure, how a lung takes its shape…this is why there’s so little talk on these issues, and so much on how gene controls inhibit this, or activate that, and on how shifts on the reactive components of an organism result in others. But if a change in an organism required shifting its skeletal structure, muscular structure, neural networks, associated information in the brain, surpassing thresholds of pain to account for the transformation, change of weight and accustomed to balance, behaviour and habits, metabolic pathways and habits. Or something as radical as bats echolocation (imagine the first “random neuron” starting in the alleged pre-bat, making him see flashes whenever a sound arose…how useful would that be). 3D internal holographic generation from sound signals is something even we haven’t mastered!

    And when we say, skeletal, muscular, nervous, brain, etc. Imagine the amount of complexity required to carry those things out by subtle biochemical changes. When considering the necessity of coordinated change of this kind, how do we expect these changes to happen randomly again, and again, and again. And across different branches of species, numerous times. Across some very clear defined boundaries sometimes too, like insect metamorphosis, shifts in ways of oxygen intake, joint restructuring, cognitive maps, and many more (and joints are very location specific, slightest deviation will lead to a lock or a loose joint). Couple that with the fact that a lot of these features appear quite fully formed with all their information networks from the beginning (Cambrian), without any indication of a precursor…and I start getting pretty skeptical really fast.

    I look forward to hearing your response.

  81. Out of curiosity, did T-urf13, and the breeds before it undergo any artificial genetic modification?

    No.

    And, as I mentioned earlier…I don’t think anyone has a clear idea on what the gradual changes leading to T-urf13 were, why they were retained, etc.

    So what is it that is unclear about the figures and discussion in this essay?

  82. I don’t mean to reiterate, but I would really appreciate it if someone could aid me with this question. Its probably a very basic question for a lot of people here, and its important for me to get a clear answer:

    “For now, I have a question for the experts here…it might seem like a silly question but I ask your indulgence.

    How many steps can we expect to happen at once? Can we give a number. If there was no selective cleansing going on (where a mutation that wasn’t beneficial wouldn’t move forward) is there a limit to how many new steps/components an organism can have laying around? Or does the number increase indefinitely over time till something “clicks”(again, presuming that no selective cleansing pressure exists and the organism keeps reproducing)?”

  83. Hello Arthur,

    Good to hear your response! Would love it if you could join in on the other points in the discussion too if you have the desire. The essay was very well written, thank you for sharing it, and frankly provides the only IC system that I’m aware of that has been “observed” to arise live so to speak.

    What isn’t clear to me, as with most cases with studies of this sort. Is the following:
    1- The specific gradual changes that occured, their order and timing of their occurance
    2- Whether they were in fact gradual ( did the arisal happen with what we expect for how many “steps” are possible for this particular organism, and did it occur with what we probabalistically expect to be reasonable), or arose at once. And if they did arise gradually, why was each step selected.
    3- Whether the origin of the gene is recent or whether it was already present in the information and combinatory potentiality of the genome.
    4- Whether the gene was triggered by some environmental trigger, and existed within the combinatory potentiality of the genome.

    The main point is I’m trying to ask: Did it in fact arise randomly and gradually? I’m not saying it did or didn’t, simply asking what we do and do not know.

  84. I should also add the following, you mention in the last part of the essay that functional proteins are not difficult to attain, if I’m understandnig you correctly. Would you state that as a general rule? Are you saying achieving coherent functional proteins beyond specific combinatory potentialities within the organism’s already existing structure (how those potentialities came to be is another issue) isn’t difficult? And that it isn’t case specific?

  85. Moreover, (and this might be an ignorant statement on my part) isn’t the entire effort based on observing homologies between 2 parts with proteins in other corn genome, and the third part’s homology is not found?

    How much can we certainly and accurately extrapolate from that?

  86. And! (Finally, I promise), what is the basis for accurately and certainly stating that the origin of the gene is recent? (this doesn’t bear much, but it is nonetheless relevant)

  87. 87

    Hi blu,

    I’m off to work now, but I thought I’d at least acknowledge your comments. Given the nature of your questions, I’m reluctant to contribute much more, since developmental biology is way outside my area of expertise (I’m trained in Ecology, Population Biology, and Genetics). You seem to have done some research on the subject, so I think it would help if you gave some indication of what level of study in developmental biology (courses, textbooks, etc) you have taken. That way I’d know if I don’t have much to contribute to the discussion and should just shut up and listen ;)

  88. Hi Blu,

    Thanks for your interest.

    You asked:

    1- The specific gradual changes that occured, their order and timing of their occurance

    Several recombination events occurred (I don’t recall the exact number, but it was more than five). The order is not known. I don’t know what you mean by timing.

    2- Whether they were in fact gradual ( did the arisal happen with what we expect for how many “steps” are possible for this particular organism, and did it occur with what we probabalistically expect to be reasonable), or arose at once. And if they did arise gradually, why was each step selected.

    The series of recombinations was probably sequential (is this what you mean by gradual?). Plant mitochondria do this sort of “shuffling” of their genomes pretty regularly (relative to an evolutionary time scale).

    3- Whether the origin of the gene is recent or whether it was already present in the information and combinatory potentiality of the genome.

    The gene originated in the 20th century, as part of breeding programs focused on making new and improved corn hybrids.

    4- Whether the gene was triggered by some environmental trigger, and existed within the combinatory potentiality of the genome.

    ??? Are you asking if the gene itself is under regulatory control? Or if the recombination events were triggered by environmental signals? In any case, this gene came from sequences that have or had no protein-coding potential or history.

    I should also add the following, you mention in the last part of the essay that functional proteins are not difficult to attain, if I’m understandnig you correctly. Would you state that as a general rule?

    Yes.

    Are you saying achieving coherent functional proteins beyond specific combinatory potentialities within the organism’s already existing structure (how those potentialities came to be is another issue) isn’t difficult? And that it isn’t case specific?

    Yes. Of course, by “difficult” I would mean possible well within the limits places by population sizes, and the frequencies of occurrence of the many processes that contribute to the origination of new protein-coding genes. I discuss this here, here, here, and here.

    Moreover, (and this might be an ignorant statement on my part) isn’t the entire effort based on observing homologies between 2 parts with proteins in other corn genome, and the third part’s homology is not found?

    How much can we certainly and accurately extrapolate from that?

    The sequence similarities involve parts of the maize mt genome that do not encode protein. We know that plant mt genomes undergo all manner of recombinational shuffling, so we can be fairly certain as to how the T-urf13 gene came about.

    And! (Finally, I promise), what is the basis for accurately and certainly stating that the origin of the gene is recent? (this doesn’t bear much, but it is nonetheless relevant)

    It occurred (quite randomly) as a part of breeding directed at making new and improved corn hybrids. I don’t know exactly when the Texas cytoplasm was released, but this event was clearly a 20th century event, probably in the 40′s or 50′s.

  89. Dave Wisker:

    T-Urf13 had a natural origin in maize. How could it arise by artificial selection? Selection–artificial or otherwise— does not generate the variation.

    Artificial selection allowed for the development of the gene.

    Without artificial selection no corn no Turf-13.

    It’s pretty basic actually.

    MY POINT has ALWAYS been that this (Turf-13) is NOT an example of IC being formed via RM and NS.

    Then don’t bring up minor points–especially if you cannot take correction of your errors on them gracefully.

    Your point about Turf-13 being IC has been soundly refuted and neither you nor Art took the correction gracefully.

    As a matter of fact both of most likely still think it is an example of IC coming about via random mutations and natural selection.

  90. Hey Dave,

    I wouldn’t say I’m any kind of expert on the matter. You might even know more than I do! If I do have to contribute something to the discussion, its simply to state whats actually missing…and to state what my own personal reflections on the extents of any reactive system is…which I’ve done quite a bit of thinking and discussing on. Beyond correlations between control genes and expression in multicellular organisms, there is simply very little in the way of knowledge that anyone has on how genes map out into specified 3D shapes of -extreme- specificity along multiple stages (not just in terms of general morphology, but in terms of cell type X at point Y), and can regenerate/form regardless of the primacy of the cells neighbouring them, or any mapping hypothesis. What is even more disturbing is the fact that the same organs/limbs across different species (and lineages) arise developmentally from different areas during development.

    I’ve read quite a bit of books on the subject though, and a lot of articles. The books that, amongst others that come to mind are:

    From DNA to diversity and Endless forms most beautiful, Biological Physics of the Developing Embryo, How the Leopard changed its spots, Biased Embryos and Evolution, The Art of Genes, From Embryology to Evo Devo, Origination of Organismal Form…

    Sheldrake’s books, which I still consider scientifically worthy (and its always good to stir things up a bit) offer some very interesting points.

    In summary, evolution is the theory of how life came to be the way it is. Yet, we do not know how forms become the way they are, we do not exactly know how they stay the way they are and that they don’t Butterfly Effect apart from changes and spiral out of control. To imagine the sheer volume of the task, image a machine that generates itself, maintains itself, organizes itself, regulates itself…-to the nanobot-, in a way more complex than a Transformer would (and I do look forward to the second movie). And then imagine that it would have to do so reactively (and by chance, over time)…I don’t see how that can be possible, a regulating agent that has an informational blueprint of the structure as a whole (and this is just my personal view on thinsg) must exist. This presents a challenge to the current evolutionary paradigm. How does a cell know where it is? How does the body know where its components are? How does it maintain temperature regulation with such a varying degree of chemical reaction? How do cells split into daughter cells from a contextual perspective? When and how does the body know when to activate a component or another, and how does it regain equilibrium when the entire system is disturbed? How does an embryo or body regulate when its very organizational and regulatory features are themselves in constant regulation (even the brain is now known to continuously rewire itself).

    I’m rambling again…it is exciting stuff. But wouldn’t you say its important? Here we have an entire civilization stating something or another is a fact about how things came to be, when we haven’t even begun to understand what the thing in question -is-. Do you think forms of this degree of efficiency could come about by random mutation+chance?

    One last point I’d like to add, is that brain/informatino system’s evolution is also being currently ignored. This is another elephant in the room. Lets take the bat example. If someone had a computer program capable of even some complex coding features, could it ever arrive at a 3D layout from getting sound signals without having prior information on what 3D is, how to interpret the signals, how to understand relationships between them, how to signal out noise. -massive- amounts of information…we employ the same degree of complexity in our 3D hearing or seeing. I think most have an idea regarding cognition as a bunch of wiry nerves that randomly move about…step by step increase in complexity and then kind of…blllaaah…an emergent order arises. But out of my reflection on the matter, you can’t increase the information of a program by randomly putting strings in its code, nor by giving it feedback yes/no. It will reach a high degree of efficiency and refinement at its current level of information (if the noise isn’t strong), but won’t exceed that.

    I’m glad to be discussing this with you, I hope to hear your feedback soon. What would you say are the difficulties for the current evolutionary scenario? If you were to try to disprove it, where would you start and what would you find problems with?

  91. 91

    Hi blu,

    I’m rambling again…it is exciting stuff. But wouldn’t you say its important? Here we have an entire civilization stating something or another is a fact about how things came to be, when we haven’t even begun to understand what the thing in question -is-. Do you think forms of this degree of efficiency could come about by random mutation+chance?

    I am enjoying our conversation as well. I’ll start by making sure we are both clear about evolution not being just random mutation and chance. Variation has a chance element to its generation (and even then it isn’t random in the mathematical sense). Much of that randomness is constrained by natural selection, which is the antithesis of random.

    Beyond correlations between control genes and expression in multicellular organisms, there is simply very little in the way of knowledge that anyone has on how genes map out into specified 3D shapes of -extreme- specificity along multiple stages (not just in terms of general morphology, but in terms of cell type X at point Y), and can regenerate/form regardless of the primacy of the cells neighbouring them, or any mapping hypothesis. What is even more disturbing is the fact that the same organs/limbs across different species (and lineages) arise developmentally from different areas during development.

    Let me throw this out to start. Strictly speaking, genes do not “map out” into anything. They merely specify the structure (and resulting functionality) of the individual proteins for which they code. The morphology and control of the morphology is actually more a function of the interactions between the proteins coded by the genes. That is, the true complexity of an organism does not lie in the information carried by its genes, or even in the individual proteins themselves. Instead, the complexity lies in how those proteins interact not only with each other, but the environment as well. It is the biochemistry of the organism that is complex, not the information carried in its genome, and it is the biochemistry which determines morphology and form.

    That’s all I have time for at the moment. Take cae.

  92. Hey Dave,

    Right, when I said map out…I meant the extention of the interactions of the genetic material “out” into the organism. And I propose that the interactions themselves are not sufficient to explain the structure of organisms.

    And regarding randomness and chance, I understand that natural selection doesn’t make it random per say, but I was using the word in its strongest sense. That is…that these forms can arise without some underlying principle (whatever that may be) that is aware of the context of the organism as a whole, where its heading and how to get there. Just like if you input a string of data representing dots on a screen to a computer program, through trial and error the computer will be able to refine its existing code to perhaps simulate an organism moving right/left when dots appear on one side of the screen or another (even that would require quite a bit of information), but it would never reach a point where it recognizes what…say, a square is.

    I look forward to hearing your response. (and Mr. Nakashima’s, Arthur’s, Bruce’s and everyone else who might take interest)

  93. Arthur,

    Thank you for your response. I’ll give what you mentioned some thought and do some research. Whats your take on Dr. Behe’s Protein Science paper? From reading it, I understand arriving at multiple protein residues can be quite difficult. How would you suggest something requiring as many proteins and parts as the flagellum came about? And why would something as rapidly generating as E. Coli, Malaria or HIV not be able to generate constructive cellular functional proteins?

  94. (and as a side note, I’m not asking these questions in an argumentative manner. I’m genuinely asking for the answers, and really appreciate the time you take for your response. I think I kind of pulled the discussion in multiple angles, but I hope everyone here has the time and desire to continue with this conversation.)

  95. Mr Blu,

    First you hazarded a guess that the eye itself took 1000-2000 genes to build. I responded with an estimate based on cell types that was much lower. Now you say that you can’t even guess. There is no need to retreat into statements of complete ignorance.

    You may be interested in reading The Shape Of Life, by Rudolf Raff, or The Origin Of Animal Body Plans, by Wallace Arthur. Both are more technical than the popular evo-devo books like Carroll’s.

    i’m not sure why you have focused on plants, but sea urchins and fruit flies are very well studied models for development as well.

    With respect to the Venus Flytrap plant, I don’t know if it has had its genome sequenced. I’m not sure why you think it couldn’t be developed from modifying a more primitive plant. The trapping mechanism is not “irreducibly complex”.

  96. Mr. Nakashima,

    Heh, take it easy with the ignorance part. I gave the guess as the lowest concievable (on my part) estimate on what it would take, plus some of the numbers I recall from reading.

    If you disagree that you cannot make an estimate, and that it doesn’t have to do with cell types, could you tell me how the specific cells attain their specific location, merging into three dimensional form and organs and how many regulatory genes (if they were in fact responsible) it would take from early development till full expression for the expression of the eye?

    This doesn’t have to do with a cell type, it has to do with the where and the how. A bunch of cell types without specificed localization and organization and development isn’t the point. A form is exactly that, a full form. Be it on the level of genes or their “interactions” no one really knows how forms come to be the way they are. We can signal correlations, but we don’t know how it all fits together…and persume it to be one way or another.

    I wasn’t focusing on plants, I was just responding to David’s example to clarify what I mean by morphological development. If you know of a way that the venus flytrap’s -shape- can arise from another organism (any other organism, evolution aside…even through genetic engineering), I’d be interested to hear it. The fact of the matter is…there are is no real theory of morphology, and generalizations simply won’t do.

    Regarding the books, I did read Wallace’s book, and if you noted the list I wrote to David earlier, you’ll find that a few of those are technical.

    Finally, I invite your response to the other points…I do apologize as there were quite a few of them, but your response would be appreciated when you have the time. Specifically (and amongst them), if you were to try to disprove neo-darwinian theory, how would you do it and where would you start? What do you find weaknesses with?

  97. And regarding your mention of fruit-flies (and any other experiments on the development of animals in general). You’ll find that all major changes have been quite limited in morphological scope, and any attempt to create a major change has led to fatality. We know the same genes are used for the development of different organs, we know same organs use different genes and we know same organs embryologically develop from different parts of the embryo between different species, and when I say the same organs…I mean the exact patterns not some generalized similarity, Gavin de Beer raised this issue all the way back in the mid-late nineties. (and I don’t want to get technical here to name an extra wing major, I mean new body plan major/serious change in size and shape that still makes the organism coherent, and isn’t merely replacing an antenna with a leg. etc.)

  98. Hi blu,

    And I propose that the interactions themselves are not sufficient to explain the structure of organisms.

    What specifically leads you to this conclusion?

    (I’m now quoting from your other post)

    You’ll find that all major changes have been quite limited in morphological scope, and any attempt to create a major change has led to fatality.

    Is this problematic? Most mutations of large effect can be expected to be lethal. Ronald Fisher was pointing this out in the 1920’s. I’m not sure what your point is here.

    I mean new body plan major/serious change in size and shape that still makes the organism coherent, and isn’t merely replacing an antenna with a leg. etc.)

    Again, I’m not sure what you are getting at (I admit, it’s late, and I may just be too tired for the relevance to make it through). So I’ll quit while I’m behind.

  99. Back to the book: “Signature in the Cell”- my copy arrived this morning.

    I will dig in later today…

  100. Mr Blu,

    Let me focus on the following:

    If you disagree that you cannot make an estimate, and that it doesn’t have to do with cell types, could you tell me how the specific cells attain their specific location, merging into three dimensional form and organs and how many regulatory genes (if they were in fact responsible) it would take from early development till full expression for the expression of the eye?

    We, first I should apologize if I caused any offense. I’m very sorry.

    My estimate of the number of genes remains the same – 100 or less.

    Every cell doesn’t come with a fixed 3D street address. it is better known by the sequence of cell types it has gone through before becoming fully specific. There are patterning factors such as noggin and chordin that establish the basic 3d axes of the embryo, but once the organogenesis stage is reached, all the overlaying morphogen fields become quite complex as the interact with the cell types. Some cells also are developed in one place, then migrate to another (a process which can be interfered with by the mother drinking alcohol during pregnancy, FAS).

    i’ll take up your question of disproving NDE in another post.

  101. Mr Blu,

    To prepare to answer your question, I want to share my little folk typology of anti-evolution claims.

    1 – Evolution doesn’t happen. This can either be the Genetic Entropy argument of BA77 quoting Dr Sanford or simply the flat denialism of Gil Dodgen. Often paired with frontloading to explain real world variety.

    2 – Evolution is resource starved. The resource usually chosen is time. This is the one that bothered Darwin, because then current estimates of the age of the Earth were too low, he felt, to allow evolution enough time to work. Often displayed on UD by KairosFocus. Inverted by creationists who assume a short time period and therefore must have very rapid evolution instead of none.

    3 – Evolution works, but only because of X. Not really a disproof of evolution, but a relabelling of what is important. This is unlikely to be cast as Newtonian angels pushing molecules around to cause mutation. More likely to be:
    – Evolution works but OOL doesn’t (help at the start).
    – Alfred Russell Wallace’s help at specific stages.
    – Evolution is like three card monte. Don’t watch the cups, watch the ball (FSCI).

    4 – Evolution might work in the abstract but there is no evidence for it here in the real world. Here on UD, often argued by Joseph until a Google search or Wikipedia article deflects into a demand for a pathetic level of detail.

    5 – Micro-evolution, but not macro-evolution. The limited modified hangout option. Be magnanimous about anti-biotic resistance, but attack macro-evolution using one of the arguments above.

    6 – Sure evolution works, but no civilized person would want to use that kind of thinking.

    7 – Evolution is a social construct of a privileged elite.

    8 – Evolution is a religion, but can be attacked for not being the right religion, or for claiming a privileged place in a supposedly religion neutral society.

    As I said, purely my own taxonomy, and probably incomplete. But it should help frame my thinking in the next post!

  102. Hey Dave!

    What leads me to that conclusion is the high morphological specificity aquired by the organism, that same cell types in different organisms contain different morphological fields, its capacity for specified regeneration post development, and the fact that disturbing embryonic development in different way through different angels does not cause it to stop…but it continues regardless of its disturbing of equilibrium.

    There are other reasons I have, but they’re not what you’d call currently academically acceptable. But they’re strong nonetheless, I’d be happy to share them if you want. But they’re just side points from personal experience.

    Regarding the rest, yes…its problematic, I think over time it will be found that most developmental sequences (don’t really want to call them maps anymore) will be found to be highly polymorphic (I believe thats the conclusion reached for our genome in general), and that any distrubance prevents large scale evolution due to the interdependent, specified, and interconnected nature of the organism. Its problematic because it poses as a problem for how gradual structural changes occur over time.

    Mr. Nakashima, thank you for your posts. No offense taken! We’re all (I think) trying to learn something here or expand in one way or another.

    You said:

    Every cell doesn’t come with a fixed 3D street address. it is better known by the sequence of cell types it has gone through before becoming fully specific. There are patterning factors such as noggin and chordin that establish the basic 3d axes of the embryo, but once the organogenesis stage is reached, all the overlaying morphogen fields become quite complex as the interact with the cell types. Some cells also are developed in one place, then migrate to another (a process which can be interfered with by the mother drinking alcohol during pregnancy, FAS).

    Alright, this is a rough sketch of the parts of some theories for how things work. But it hasn’t been fully nor emperically tested, it gets very fuzzy at the “complex interactions” and “morphogens” stage, and even way before that. Anything we say now is merely speculation. The point I’m disagreeing with is that cells have a kind of 3D pattern, one of the reasons being if it was simply a cascade of interaction between cell types…the slightest disturbance in the process or prevention of a certain cell type to interact with its “preceding” sequence would cause cascade failure. And, because I do not believe that it is mathematically possible any interactions between cell types or underlying tissues or factors will specify the layered sequence due to the high degree of specificity found.

    To illustrate my thinking better. If you had a solid dot, and you placed in an equidistant manner some gell around it in suspended state. You’d get a sphere. But if you did that, and got a dot with equidistant spikes, and all that was underneath was the iron ball, you’d suspect something else is acting. Now if you got a 3D smiley face, you’d really start wondering. As the smiley face grows, you cut off a part -under- the growing gell, and the part regenerates and the growing gell continues to grow. You use a ruler to prevent one side of the gell interacting with another…and the form uses another side to grow the same structure. Highly flexible. These are all the marks of a system where the target or goal are primary, and the factors leading to them are secondary. I hope that illustrates what I (and many other embryologists) believe to be the problem.

    All underlying factors from that point are used not as the causal root, but as the tools utilized to bring the structure about. Noggin and chordin and the axis notwithstanding. (and I have to say…the idea of axis as developing the 3D structure has not been verified, they form a solid core for the structure to build on…kind of like metal wiring in a building, but I know of no empirical evidence to state that they result into the 3D form we observe.)

    This level of morphological stability and detail, and fields of organization that run through the body can be verified with our own bodies…in a sense. If you get a cut on your arm that scrapes a large portion off (hope that doesn’t happen), and prevent the “primacy” sequence of different parts by placing an obstruction, the body will develop and heal the area from any angle possible. Moreover, the skin will return along with the exact same hair spacing and will be just like new. You might disagree, but this process, to this day…has not been fully defined nor settled. Now consider the same things happen in an embryo during development, when its overall structure hasn’t even had a chance to settle yet…and, supposedly, the developmental process uses itself for its own development, making any effect in the regulator affect the regulated…and here the regulator and regulated are one and the same. Therefore the dilemma.

    Regarding your little folk anti-evolutionary claims list. I’m interested to hearing your next post before responding to the whole thing. Its an interesting list, but I think we both agree that the real difficulties are far more to the core…and perhaps with how much we can really know, regardless of what we can possibly find out.

    Looking forward to your next post

    PS. Arthur, I am still awaiting your response, would appreciate it when you have the time. Have a few thoughts and questions on T-urf13 too that I’d like to ask.

  103. Hey Arthur,

    I’ve been thinking about the content and articles you wrote, and would appreciate your response on the following (plus the questions I asked earlier).

    What I’m having trouble with, is it seems that you’re generalizing specific cases where a particular change “triggers” a possible combinatory sequence in an organism, but nonetheless…I don’t see how this is generalizable to state that the addition of information in organisms is not difficult. While maize might reshuffle its mitochondrial genome and might be able to attain a protein coding gene (and I still don’t see how you can make the speculation that it DID in fact happen sequentially and randomly, we have no epistemic ground to make that claim unless we emperically track down the probability of maize attaining a functional protein sequence and protein binding sites through direct observation…not secondary inference through homology studies. Only then we can we infer whether this is soemthign that generally happens or not)even considering the different protein sites required as you mention in your second essay as well as the underlying construction agent…which I will not profess to understand and would appreciate your clarification on. What worries me is that you seem to generalize certain cases across all organisms. So whereas an already information rich organism can contain combinatory/triggered changes within its already existing structure (to a certain limit), how does this extend to an organism like E Coli? Or a complex multifunctional integrated cell? Or a multicellular organism from a cellular organism? On what -empirical- grounds, across multiple species of the same “genre”, are we making that extention?

    Moreover, it is clear that many changes require change within the developmental plan for the organism. If something like bacteria flagellum, excluding the new parts and IFT, was co-opted, a change would happen at the developmental level too. So how are we moving from the above, to the attainment of -functional- (as in, functional when other multiple changes occur) proteins is not difficult?

    If you could point me to a few empirical studies regarding maize, its probability of attaining a protein binding site, its probability of attaining a protein coding gene, and the extendability of those processes to create say…a new cell type. I’d appreciate it. And if could point me to empirical studies regarding the attainment of -multiple- sequential protein components in a simple organism that has added up over time to create a novel complex structure composed of multiple matching (and perhaps, irreducible) components…I’d appreciate that too.

    My difficulty isn’t with attaining -a- protein, my difficulty arises when it comes to the building of a complex cell with thousands of proteins working together at multiple levels to generate one function. And to the limitations of a protein being functional and fixed -within the context of- a particular organism. If, for example, you require 20 proteins none of which are available within an organism, to have a function that would be beneficial and would only then remain fixed, and whereby there is no combinatory “room” within the organism to shuffle pre-existing structures (not talking about genome shuffling) in a slight direction here or there. On what basis are we claiming that is not difficult?

    What still bugs me is, how come E Coli, bacteria and malaria and even HIV still remain within clear boundaries regarding their internal structure and machinery. With HIV (-disputably-) attaining one viral protein site in its entire course of relationship with human history, with no constructive evolution to speak of. We can’t simply dismiss that as negligble.

    I hope I was able to express myself properly.

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