Signature in the Cell website now live

_{Paul Nelson

June 15, 2009

Intelligent Design}

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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.

Comments

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?Joseph_{June 19, 2009
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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...Joseph_{June 19, 2009
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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.Dave Wisker_{June 19, 2009
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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.Joseph_{June 19, 2009
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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.Joseph_{June 19, 2009
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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.Dave Wisker_{June 19, 2009
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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.Joseph_{June 19, 2009
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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?Joseph_{June 19, 2009
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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: 37-52Dave Wisker_{June 19, 2009
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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).Blu_{June 19, 2009
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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.Dave Wisker_{June 19, 2009
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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.Bruce David_{June 19, 2009
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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.Blu_{June 19, 2009
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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.Blu_{June 19, 2009
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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.Blu_{June 19, 2009
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Mr Blu, In honor of your name, the Belgian Blue, a breed of cattle with a suppressor mutation.Nakashima_{June 19, 2009
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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.Nakashima_{June 19, 2009
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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.Dave Wisker_{June 19, 2009
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Edit: 9- a change of a part or -more- of an...Blu_{June 19, 2009
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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.Blu_{June 19, 2009
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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?Dave Wisker_{June 19, 2009
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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.Blu_{June 19, 2009
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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)?Blu_{June 19, 2009
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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.Dave Wisker_{June 19, 2009
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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.Dave Wisker_{June 19, 2009
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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.Dave Wisker_{June 19, 2009
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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...Joseph_{June 19, 2009
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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.Oramus_{June 19, 2009
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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)
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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.Joseph_{June 19, 2009
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