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Signature in the Cell website now live
| June 15, 2009 | Posted by Paul Nelson under Intelligent Design |
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.
103 Responses to Signature in the Cell website now live
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Hi blu,
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.
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.
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)
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?
(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.)
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”.
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?
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.)
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.
Back to the book: “Signature in the Cell”- my copy arrived this morning.
I will dig in later today…
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.
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!
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.
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.