The Altenberg Sixteen

_{Paul Nelson

March 4, 2008

Intelligent Design}

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HT to Larry Moran’s Sandwalk for the link to this fascinating long piece by journalist Suzan Mazur about an upcoming (July 2008) evolution meeting at the Konrad Lorenz Institute in Altenberg, Austria.

“The Altenberg 16” is Mazur’s playful term for the sixteeen biologists and theoreticians invited by organizer Massimo Pigliucci. Most are on record as being, to greater and lesser degrees, dissatisfied with the current textbook theory of evolution. Surveying the group, I note that I’ve interacted with several of the people over the years, as have other ID theorists and assorted Bad Guys. This should be an exciting meeting, with the papers to be published in 2009 by MIT Press.

Mazur’s article is worth your attention. Evolutionary theory is in — and has been, for a long time — a period of great upheaval. Much of this upheaval is masked by the noise and smoke of the ID debate, and by the steady public rhetoric of major science organizations, concerned to tamp down ID-connected dissent. You know the lines: “Darwinian evolutionary theory is the foundation of biology,” et cetera.

But the upheaval is there, and increasing in amplitude and frequency.

[Note to Kevin Padian: journalists don’t like it when you do this to them. Mazur writes:

Curiously, when I called Kevin Padian, president of NCSE’s board of directors and a witness at the 2005 Kitzmiller v. Dover trial on Intelligent Design, to ask him about the evolution debate among scientists –- he said, “On some things there is not a debate.” He then hung up.

That hanging-up part…not so wise. If you’re going to say there’s no debate, explain why.]

Comments

DaveScot: Actually, many of the structures inside of eukaryotic cells bear a striking resemblance to complex crystals. For example, microtubules (which form much of the three-dimensional structure of eukaryotic cells), are formed of virtually identical repeated tubulin units, which spontaneously assemble into microtubules on the basis of a few simple binding rules (but only in the absence of free calcium ions in the cytosol, which disrupts this arrangement). The same is true for most if not all of the various components of cells. I would not be surprised if, in the near future, someone like Stuart Kaufman were to figure out one or more of the "assembly protocols" for such components, thereby rendering what appears to be a "magical confusion" into a "natural arrangement."Allen_MacNeill_{March 5, 2008
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Paul Nelson: Good to hear from you. I appreciated immensely our discussion following your "debate" with Will Provine (in which you two agreed much more than you disagreed). I hope you are working toward finally finishing that MS on common descent. Remember my rule: "The greatest enemy of accomplishment is the desire for perfection." You can't get it right if you don't get it written! As to the extended quote from Mazur, I have already commented on parts of it. To me, it simply expresses what most of us in evolutionary biology have known for a while: that the neo-Darwinian "modern synthesis" is showing its age, and is due for a major overhaul. I have commented on this repeatedly in my blog and elsewhere, and am currently writing a book on the subject for Wiley, entitled Evolution: The Darwinian Revolutions, in which I point out what is obvious to any historian of evolutionary biology: that the theory of evolution itself is evolving, and is currently passing through a Kuhnian paradigm shift, from gene-centered to phenotype/individual centered explanations for descent with modification and the origin of adaptations. I strongly recommend Jablonka and Lamb's book on this subject, Evolution in Four Dimensions, in which they survey the four main "evolutions", only one of which looks anything like the "modern synthesis." Looking forward to corresponding with you on this subject in the future. Keep writing!Allen_MacNeill_{March 5, 2008
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tyharris and gpuccio: I do not answer people who resort to insults, personal attacks, or ridicule (another reason why I rarely post at this site, BTW). I honestly attempt to answer people who are willing to accept that all conscientious people are interested in discovering as much as we can about how the universe works. If you are willing to reframe your questions in such a way as to indicate that you are willing to participate as members of a "community of scholars", then I will do my best. Otherwise, you have demonstrated just what kind of "scholar" you actually are, and do not deserve notice by me (or anyone else).Allen_MacNeill_{March 5, 2008
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Dear Allen, I am sorry to hear about your health problems. I hope you'll be doing better soon! A friend sent the following to me, to provoke further discussion here (I'll reply in a bit): ******************************* “Mazur’s article is worth your attention. Evolutionary theory is in — and has been, for a long time — a period of great upheaval.” Well, yes and no. The basics – universal common ancestry, descent with modification – are pretty unassailable. What may be interesting (if ironic) for the participants of UD is the debate regarding the reach of natural selection. Natural selection is, well, a fact – it happens, it shapes organisms and communities, it leaves its mark throughout biology. But the question as to how universal NS is remains an open one. The best way to understand the question is to consider a well-known case of evolution. The Hawaiian silverswords are a fantastically diverse group of plants that include several genera and undoubtedly share a common ancestry. This ancestry traces back to mainland North America, and the California tarweed (or something similar). This is a classic case of rapid evolutionary diversification upon invasion of a new habitat. The relevant question for these genera is – how much of the diversification, the amazing range of morphologies and phenotypes that evolved after the “migration” of the original tarweed to the isles, may be attributed to natural selection, and how much is the result of genetic drift? Genomes leave some clues; thus, it seems likely that the diversification of flowers was driven in large part by natural selection (that’s the conclusion from studies of sequence variation in flowering genes). But many questions remain, and the depth to which NS reaches in the shaping of the complete organism is not known. It’s quite possible that the divergence that we see was framed partially, even largely by random genetic drift, rather than by selection for each and every trait at each and every step of the evolutionary trajectory. So where’s the irony? Reflect if one might – one aspect of the ”raging debate” is essentially “NS vs. random genetic drift”. This actually places Darwin and Nelson (that’s right - that Nelson) on the same side of the fence in this debate, arguing against “random chance”. That’s an interesting twist.Paul Nelson_{March 5, 2008
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Jerry: I'm not particularly well-versed in the class Aves (mammals are my preferred group), and so will address what I understand to be the situation with respect to mammals. Recent research indicates that the differences between individuals within species are close to the same order of magnitude as the differences between species. That is, there often is very little genetic difference between individuals of different species. However, this is compounded by the fact that one cannot simply look at particular genes and decide if the differences are significant. To give just one example, the main genetic differences between humans (Homo sapiens) and chimpanzees (Pan troglodytes)amount to changes in a few genes, mostly hox genes (including, but not limited to FOX2P). However, this ignores the fact that humans and chimps have different chromosome numbers. Humans have 23 pairs, whereas chimps have 24. There is convincing evidence that this is because human chromosome 2 is actually a fusion product of two of the chromosomes we share with chimps (you can find the fusion region in human chromosome 2 quite easily, if you know what you're looking for). Changes in chromosome number do not actually change genetic information at all. Consider J. R. R. Tolkein's The Lord of the Rings. Tolkein considered it to be a single volume (the "Red Book of Westmarch"), but divided it into six books (somewhat like the Bible). However, his publishers felt that dividing it into three volumes would make it more saleable, and so now you can buy it both ways: one volume or three volumes. However, none of the different ways of dividing up Tolkein's book changes anything in the text (except perhaps the numbering in the titles). The same can be the case for very closely related species with virtually identical genetic sequences, but different chromosome numbers. It has long been known that eukaryote species are generally distinguished by having different chromosome sequences or numbers, but not necessarily different genetic information. This dovetails nicely with the generally accepted definition of "species," which is based on reproductive isolation, not genetic composition. Clearly, genetic composition can be a component of reproductive isolation (for example, some species have genes that make hybrids with other species effectively sterile). However, it doesn't have to be. There are good examples of species (or near-species) that are virtually genetically identical, but virtually never interbreed as the result of behavioral differences, many of which are learned (i.e. inherited via Lamarkian, rather than Mendelian, mechanisms). Personally, I strongly suspect that the whole concept of "species" is mostly an artifact of our Platonically conditioned minds. As Lynn Margulis has repeatedly pointed out, bacteria do not have species at all, at least not as defined by the classical biological species concept. I have a post at my blog (http://evolutionlist.blogspot.com/) on this subject, entitled "Origin of the Specious."Allen_MacNeill_{March 5, 2008
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Snowflakes are a wonderful example of the organization that can be produced by chance and law. They're simple and no two are alike. They don't reproduce themselves, they contain no coded information, and they don't fit together with other snowflakes to form machines. In short, they're a great example of the upper end of the organization that law & chance can produce. The stupidity comes in when it's imagined that the laws governing crystal formation can produce cellular machinery which doesn't exhibit any crystalline properties at all. DaveScot_{March 5, 2008
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Looking at simple forms like the snowflake, he noted that its "delicate sixfold symmetry tells us that order can arise without the benefit of natural selection". How on Earth do you reason with people who (correctly) discard natural selection and then say, Hmm, I wonder what other unintelligent force can create brains? And point to snowflakes as evidence that order can arise on its own, ergo, so can brains. They're just too stupid to reason with.Granville Sewell_{March 5, 2008
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Allen_Macneill (#15): "For that matter, the variations that are produced by the various mechanisms listed at my blog aren’t random either." I don't understand which mechanism generating "variation" is not random. Ah, yes, I know... design. NS is not a way to create variation, at best it is a way of eliminating and/or keeping it. But, again, variation has to be there, for NS to "act". Random variation is the only mechanism generating variation in darwinian theory, unless you invoke voodoo or magic (and I do think that some of the vague discourses of a few frustrated darwinists about "self-organization" and similar are really no more than that). "Think of it like shuffling and then dealing from a very large deck of cards." I am really something more than bored of all these "deck of card" analogies. I will not repeat here what I think of them just to stay polite. Here we are talking of proteins, molecular machines, complex regulation networks, and so on, not of cards. And, if you stick to your cards, please do the math, which is not encouraging... All the rest of your argument is a rather vahue discourse about the magic powers of NS. I dont't want here to address the NS problem in detail, because I have not the time, but I am ready to discuss it in details in future posts. For the moment, I will just say that: a) NS has to act on existing information, and cannot create it b) NS theory, even if not a theory of randomness, is a very vague conception, and in no way a theory from necessity. The theory has many ambiguities and inconsistencies, even in its use of language c) Even as it is, NS theory is completely inadequate to explain what it tries to explain. First of all, Dembski and Marks have shown that a search process, to really improve the results of random processes, has to incorporate active information about its target. Second, and most important, NS need a constant "step by step" deconstruction of any possible function, which is obviously abdurd, if it has to overcome the insurmpuntable probabilistic difficulties of the darwinian model. And, last but not least, NS is completely powerless versus the fundamental problem of Irreducible Complexity. As I have recently argued on this blog, IC is a complete "NS stopper". And, finally, NS can act only on information powerful enough to give a reproductive advantage, and anyway considerable time is needed to expand any new information, which, as you probably know, is a motive of very specific difficulties in the theory. Finally, you say: "To complete the model, of course, one also has to imagine that new cards are constantly being added (e.g. by modifying the remaining cards), again by mechanisms that appear entirely random." I am glad you admit that. That was exactly my original point in post #12, the one you never answered to, that random mechanisms absolutely have not the power to create the necessary new cards. That should be obvious, if you consider the math. And mathematical arguments "are" arguments from necessity! And, finally: "Once again, however, the continuous winnowing process that is the heart of natural selection reduces both the amount of possible variation and its “randomicity” over time." Magic and fairy tales all over again! How? Why? Please, let us discuss on real models, real math, real details. One last note: definitely, I am many things, but not one of your students.gpuccio_{March 5, 2008
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Allen_Macneill (#14): "Here is the misconception that consistently misleads most IDers: The whole point to natural selection is that the search isn’t random. Natural selection is no more random than is gravity, a point that a small fraction of my students consistently misunderstand." Here is the usual habit of darwinists, changing their arguments according to convenience, and never really answering a counter argument: 1) First of all, their is absolutely no misconception here. We are all well aware that NS is the "only" part of the darwinian fairy tale which "appears" to be not completely random. I have personally and recently defended exactly that point here, in another thread. But, as you should have understood, in my post (#12), I was exactly answering to your affirmations, very explicit, in post #8, about "variation": "my point was that so far we know about nearly fifty different mechanisms that produce a nearly incalculable amount of genetic and phenotypic variation (as shown by Kaufman’s calculations). Hence, there is absolutely no necessity to postulate the existance of other sources of variation unless and until there is empirical evidence that such mechanisms exist." My post #12 was very obviously trying to demonstrate (and, I thing, with good success) that what you were saying about "variation" was wrong. You say that there are a lot of causes fro variation, and that they more than enough to explain all the necessary variation. I very easily showed that nothing could be more distant from truth. So, why did you answer to my post with those self-sufficient arguments about "natural selection"? NS, be it random or not, is not a cause of variation. It has to act on variation after it was already generated. We can speak about NS and its ambiguity as long as you like, and indeed I have often done exactly that on this blog, but I would like that, if you answer to what I say, you really answered to what I say. 2)You say that NS is no more random than is gravity. I am afraid you don't have a detailed understanding of one or the other. Gravity (to be more correct, the theory of gravity, let's say for the sake of simplicity the newtonian one) is a theory which explains facts in terms of necessity, that is in detailed and non ambiguous mathematical form. It is a completely deterministic and explicit mathematical theory. If you believe that NS theory (let's not forget our epistemology, they "are" theories!) has the same properties, I would be very interested to hear your arguments. But you know, may be your students are wiser than you think.gpuccio_{March 4, 2008
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Dr. MacNeill, please allow me to defend my statement. I said above:
It was once he had published that statement that he acknowledged that the 47 sources, plus natural selection, did not provide an adequate explanation for the major adaptations that have occurred.
On 11/10/2007 in post: https://uncommondescent.com/intelligent-design/future-risk-assessment-in-the-genome/ you said:
As for macroevolution, I agree that at the present time we have little or no formal theory predicting the observed patterns of change in deep evolutionary time. This is one reason why I have asserted that the so-called “modern evolutionary synthesis” of the mid-20th century is “dead” – it’s theoretical predictions have either been superceded (e.g. by evo-devo) or shown to be inadequate.
I am puzzled that you now say that I was in error.bFast_{March 4, 2008
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Regarding gpuccio's comments in #5 on gene-protien dogma and probability.... Here's a link to a relevant article on the Encode Project, which, ( unfortunately for darwinist true-believers ) has determined that human biological complexity appears to be even MORE insanely complicated than we originally thought. ( apparently the "junk DNA" wasn't junk after all...) http://www.boston.com/news/globe/health_science/articles/2007/09/24/dna_unraveled/ To quote briefly - "Cellular processes long assumed to be genetic appear quite often to be the result of highly complex interactions occuring in reigons of DNA void of genes."..."It's a radical concept, one that a lot of scientists aren't very happy with", said Francis S. Collins, director of the national Human Genome Research Institute". So basically, even given our CURRENT, incomplete specification of biological complexity, the odds of the genetic information present in even the SIMPLEST known life form self-assembling, exceeds the actual number of fundamental particles that exist in the universe? ... and now the odds have just gotten worse? I wonder just how deep this rabbit hole goes, and I wonder at what point will darwinists simply have to look around at the probabilistic ground upon which they are standing and finally admit to themselves that there has to be SOME limit of SOME kind as to what is realistically plausible in a finite universe? The more complex and non-linear ( what "small sucessive steps" of RM+NS created these non-genetic "complex interactions"?) our model of human biology becomes, the closer we also have to come to a realization of actual irreducible complexity being present here. Regarding Mr. MacNeill's lecturing to ID'er's about their misled misconceptions ( #14 )... I would like to hear fewer condescending assertions, and fewer hypothetical guesses about how it all "might " have happened, and instead see more specific details and observable, duplicatable EVIDENCE from darwinists. Could Mr. MacNeill please specify the EXACT RM+NS sequence of small, linear, succesive steps that got us from the first life forms to the kind of complexity the Encode project is talking about? Regarding Mr. MacNeill's apparent belief that universal probability bounds don't apply to biological information because "natural selection isn't random", may I ask how his naturalistic theories overcome the improbabable series of allegedly un-guided steps that got us from a pile of rocks to abiogenesis, before RM+NS could have even been called into play? By what means did the first self-replicating information processor create itself and then proceed to write upon itself the minimum information neccesary to begin synthesizing proteins in the first functioning cell? EXACTLY how did it occur? By what method did it occur, if not by random chance? And if it WAS random chance, then what do you figure the odds are of THAT all coming about? How does RM+NS get you out of THAT probabilistic jam, mister Smarty-MacSmarty-pants ? It would seem that naturalistic theories of life have exceeded dembski's UPB ( and many other UPB calculations that I have heard thrown about here at uncommon descent ), before RM+NS even has a chance to function. I mean, come on MacNeill, naturalistic theory strains credulity at best, and with NO explanation whatsoever for abiogenesis, and NO specification of the precise RM+NS steps that allegedly got us from THAT mysterious point to our current specification of biological information complexity, why should critical minds accept this nonsense? It doesnt surprise me that your students repeat your "NS is not random" mantra back to you like sheep,and are willing to accept all of this unsubstantiated naturalistic rubbbish as though it were unquestionable fact. Most students these days are just empty heads full of mush, ready to believe whatever they are told. That's why all the kids are for Obama. he tells them he belives in"change", in "hope" and in "the future". Like darwinism, obama-ism sounds good, but it lacks any actual realistic or specific mechanism to acheive what it claims to be able to deliver. Intellectual courage is about as rare as intellectual objectivity these days ( ie. the willingness to see what you see, not what you want to see...) Jerry Maguire said " Show me the Money!" Now I say " Show me the proof!"tyharris_{March 4, 2008
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Allen We all know natural selection is non-random. Our position is bascially that non-random natural selection isn't sufficient to generate all the complexity of life if its only input is random mutations. If we were playing poker I'd say "I see your non-random natural selection and raise you non-random mutations." I don't think any of the mechanisms you propose generate non-random variation before they are run through a selection filtern unless you're trying to resurrect Lamarck. The thing about all the combinatorial mechanisms you list is they are all reactionary as selection can't operate on unexpressed characters. It can only react like a movie critic AFTER seeing the movie. We assert that a proactive process must be in play now and/or in the past. DaveScot_{March 4, 2008
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Allen The whole point to natural selection is that the search isn’t random. You need to learn something about search algorithms. Of course natural selection isn't random, but it doesn't produce anything, it doesn't create anything -- it just throws stuff out. Throwing stuff out is a destructive process at worst and a conservative process at best, not a creative process. It continues to boggle my mind that Darwinists can't see this. All the random variation in the world, no matter the variety of the variation and no matter how many failed attempts are thrown out, won't turn a Hello World computer program into a grandmaster chess or checkers program. But this is what Darwinists claim happened in the history of life. Just do the math. The combinatorial explosion is so huge that orders of magnitude must be expressed with exponents that must be expressed in orders of magnitude. In addition, there is no hard or even soft empirical evidence that these fantastic Darwinian speculations have any basis in reality when it comes to extrapolating them to explain all of life's complexity, diversity, information content, and functionally integrated machinery, not to mention consciousness, morality, human artistic creativity and much more. The only "evidence" that the mechanisms you propose can accomplish that with which they have been credited is that the alternative is philosophically unacceptable.GilDodgen_{March 4, 2008
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Edit SMTP should read SNRP. {DLH corrected SMTP to SNRP in 17}.bFast_{March 4, 2008
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How many of these mechanisms of variation led to the first self-replicating lifeform? (Snicker)mike1962_{March 4, 2008
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Dr. MacNeill, nice to see you are back. I am sorry for misunderstanding you on the last UD thread where you became chatty. (I would love it if someone could find the thread to see what Dr. MacNeill actually said, and what I misunderstood as: “couldn’t provide an adequate explanation for the major adaptations that have occurred.”) Thanks for the information about SNRPs. I have heard that there are actually hundreds of thousands of protein products despite there being only 25,000 coding genes. I know that Denton discusses some of the mechanisms that produce multiple protein products from single genes. However, I don't believe that he discusses SNRPs. As a software developer (aren't about half of us on this site?) I find the concept of a single gene coding for multiple proteins to be a challenging concept for evolution. Once a gene begins to code for more than two or three protein variants, especially if more than one of these variants plays a vital role, it should become immutable. It should become ultra-conserved. Failure of that being the case would be seem unevolvable from the prospective of a computer nerd who recognizes that intolerance of error that is the result of any data compression technology -- this is data compression technology. Dr. MacNeill:
So, like my students, repeat after me: natural selection is not random.
I think you would be surprised at just how few IDers suffer from this misunderstanding.bFast_{March 4, 2008
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Allen MacNeill, I have a question for you. If you take a class such as birds or aves with about 10,000 species and look at their genomes would you expect to find major differences or minor differences separating the various species. Now I realize that penguins and humming birds are quite different but would the difference be just in a series of minor differences in the proteins or would there be major structural variation between them that would represent creation of new complexity or maybe loss of some original complexity. I may not be expressing it clearly but what could we expect the differences be that cause these very different phenotypes? And if we were to examine all the bird species would we find that most of them just represent minor changes in the genomes of each. I realize you may not know much in particular about birds per se so if you want to pick another class, order or family of species and comment it would be appreciated. I only used birds since we have been discussing them here recently and while they have some very unique species, most are quite similar. It seems to me that natural selection would have taken various gene pools or an original gene pool and refined them to smaller gene pools and thus over deep time led to all the variety we see in birds. And as many of these sub population gene pools came about after a time many wouldn't be able to inter breed. So the card deck generated numerous smaller card decks and these smaller card decks occasionally get augmented by occasional mutations. If so then it would seem possible to examine the nature of these mutations by comparing genomes. I realize that the data for such research probably does not exist today but maybe in the near future such a project could be possible. In other words what speculation/knowledge could you provide that would probably explain how the aves class developed over deep time or some other population that you are more familiar with? I look forward to your comments and any thing you can add to clear up my rambling and muddled questions.jerry_{March 4, 2008
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For that matter, the variations that are produced by the various mechanisms listed at my blog aren't random either. Yes, in many cases (but not all), the underlying combinatorial processes that produce the variations (such as Mendelian independent assortment, which is mechanism #32 in my list) are random for all intents and purposes. However, when one combines these processes, the results are anything but random. Think of it like shuffling and then dealing from a very large deck of cards. At first, there are a huge number of possible combinations. However, if you start selectively removing cards from the deck (which is essentially what natural selection does), the number of possible combinations steadily drops. Also, the remaining possible combinations are not a random sample of all of the combinations that were originally possible. On the contrary, as selection continues to winnow down the deck, the amount of variation available in the remaining combinations of cards steadily declines as well. And, this decline is not random; only the cards that don't get eliminated continue to be shuffled and dealt. To complete the model, of course, one also has to imagine that new cards are constantly being added (e.g. by modifying the remaining cards), again by mechanisms that appear entirely random. Once again, however, the continuous winnowing process that is the heart of natural selection reduces both the amount of possible variation and its "randomicity" over time.Allen_MacNeill_{March 4, 2008
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Here is the misconception that consistently misleads most IDers: "I have to remark again here that Dembski’s UPB of 10^150 is a level of complexity so high that it could never be exhaustively explored by random search even if the whole universe had done nothing else, in its whole existence, than using all its bits to calculate the possibilities." The whole point to natural selection is that the search isn't random. Natural selection is no more random than is gravity, a point that a small fraction of my students consistently misunderstand. As Daniel Dennett pointed out in Darwin's Dangerous Idea, natural selection constrains the pathways that variation can take through "variation space", winnowing down an almost unimaginable number of possible pathways to a surprisingly small number (which grow smaller in umber, rather than larger, with time). So, like my students, repeat after me: natural selection is not random.Allen_MacNeill_{March 4, 2008
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Allen_MacNeill (#11): "Actually, it seems likely that the primary source of information determining what proteins (and therefore what traits) a cell will produce is the location of the cell, especially the cells it is touching and the cells that are nearby." That's exactly the kind of fairy tales I was referring to. To think that such a complex and integrated process like cellular differentiation and organization may take place "only" as a mechanical response to outer stimuli, without being guided by complex information procedures "inside" the cell, is pure folly. Again, I affirm that we have not the slightest idea of where the code which stores the real important information is located. Protein coding genes are only the "effectors" of the program of life. The true program of life is elsewhere to be found.gpuccio_{March 4, 2008
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Allen_MacNeill: First of all, I am well aware of transcriptional and post-transcriptional variations, and I had explicitily mentioned them in my post. Moreover, I think you are grossly underestimating the search space of possibilities which has to be faced by the nechanisms of variation you cite. I have to remark again here that Dembski's UPB of 10^150 is a level of complexity so high that it could never be exhaustively explored by random search even if the whole universe had done nothing else, in its whole existence, than using all its bits to calculate the possibilities. Enough for your idea of variation! The complexity of even the smallest genome is well beyond that, and of thousands of orders of magnitude. So, I am not impressed at all by your mechanisms of random variation, be they mutation, alternative splicing, duplication, or anything else, be they 50 or 500. They are completely powerless to accomplish the task that darwinists have given them.gpuccio_{March 4, 2008
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Actually, it seems likely that the primary source of information determining what proteins (and therefore what traits) a cell will produce is the location of the cell, especially the cells it is touching and the cells that are nearby. Cells that touch each other exchange their contents (via gap junctions) and modify the expression of each other's genes via signal transduction pathways that have their start in the cell membrane. Cells that are near each other send each other a myriad of chemical messages, which bind to cell sruface receptors (and, in the case of lipid-soluble molecules, to cytoplasmic receptors), both of which have the capacity to modify the expression of genes inside the cells. Furthermore, the similarities and differences between the specific pathways currently identified for these processes are entirely consistent with the hypothesis that they have evolved via descent with modification from a set of common ancestral pathways which have their origin somewhere in the deep evolutionary past (i.e. probably about 1 billion years ago or more - that is, somewhere coincident with the origin of eukaryotic cells). Far from "exposing the fairy tails of the Darwinists", the discovery and elucidation of these pathways has paved the way for the new evolutionary synthesis, soon to be celebrated at Altenberg. And the reason I'm not going is that I'm already committed to teaching yet another upper-level evolution seminar course at Cornell in July. The topic this year will be "Evolution and Ethics: Is Morality Natural," and will feature readings from such authors as T. H. Huxley, David Sloan Wilson, and Edward O. Wilson, among others. Check my blog for more information as it becomes available.Allen_MacNeill_{March 4, 2008
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jerry: the genome is the same in all single cells of a multicellular organism, the only exception being the cells of the immune system, where specific rearrangements take place in the course of ontogenesis to generate the repertoire on antibodies and T cell receptors. Another possible exception could be random mutations in single cells or clones, and obviously neoplastic cells. For the rest, all cell types share the same genome. Promoters are just genes, or anyway DNA segments, which, like the protein coding genes, can be activated or not according to cell type, differentiation and functional state. That's exactly what I meant in my post. Nobody knows where the information is coded that allows billions of cells to differentiate in different tissues, cell types, and so on, and to respond to any kind of stimuili, selecting the appropriate transcriptome from the almost infinitely varied possibilities. What makes a cell what it is, and not another type of cell, is, as far as we know, mainly its transcriptome. The set of possible transcriptomes is the set of all possible combinations of all possible states of all the genes in the genome. It is absolutely huge. How cells apparently know, each differently from the others, which genes to transcribe, how and how much, in each single moment of their life, and in harmony with the general plan of the organism, is one of the greatest mysteries of biology. Transcriptomes are being studied, now, mainly through the technology of micro-arrays, which allow to test which genes are transcribed in a cell population at a certain moments. The quantity of information which is being gathered through this technique is huge, but at present very poorly understood. We are just scratching the surface of the complexity of cell life. It's only the beginning. And the more we know, the more the fairy tales of darwinism and reductionism will be exposed.gpuccio_{March 4, 2008
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Yet another mechanism for producing variation (which no one has mentioned here yet) is the editing of mRNA transcripts by spliceosomes (also referred to as SNRPs, for Small Nuclear Ribonucleo Proteins). These objects, which are structurally related to ribosomes in some ways, cut out segments of primary RNA transcripts prior to translation in riobosomes in eukaryotic cells (prokaryotes apparently don't have them). The activity of SNRPs can produce hundreds (and in some case thousands) of different proteins from a single nucleotide sequence in DNA. SNRPs are themselves coded for by DNA, as are the proteins that make up part of their structure, which means that genes in eukaryotes massively modify the expression of other genes in eukaryotes. Therefore, the current estimate of the number of genes in the human genome (i.e. somewhere between 25,000 and 30,000) is really only an estimate of the number of different DNA sequences, not the number of different gene products produced by protein synthesis in the ribosomes. This number is at least 100 times larger, and may be thousands of times larger. Multiply that times the number of different cell types, and modify that product by the number of different environments that such cells can respond to, and the amount of "variation space" potentially available to eukaryotes is so massively large that the real problem is not "is there enough variation to produce all the things we see", but rather "how is it that out of all that variation, we only see a relatively small subset?" Again, the best answer is natural selection, combined with random genetic drift (which allows for the "colonization" of parts of the "variation space" that selection alone effectively prohibits). Also, for the curious, the reason I haven't been posting of late (nor updating my blog) is that I have been recovering from a fairly serious medical condition, which has only now (after many months) allowed me to do more than meet the minimum responsibilities of my position as husband, father, and teacher at Cornell. I plan on posting about my experiences at my blog (http://evolutionlist.blogspot.com) within the next couple of weeks. The title will be "On Pain" - watch for it.Allen_MacNeill_{March 4, 2008
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Actually, I never admitted that the huge variety mechanisms listed in the post at my blog "couldn't provide an adequate explanation for the major adaptations that have occurred." On the contrary, my point was that so far we know about nearly fifty different mechanisms that produce a nearly incalculable amount of genetic and phenotypic variation (as shown by Kaufman's calculations). Hence, there is absolutely no necessity to postulate the existance of other sources of variation unless and until there is empirical evidence that such mechanisms exist. Proposing that some new source of variation is needed (when clearly it is not, if the calculations cited above are within 1000 orders of magnitude), isn't science, it's pure wishful thinking. As to what could possibly winnow down the almost mind-numbing amount of genetic variation produced by the processes Kaufman cites, perhaps one might cite the same one proposed by Charles Darwin - natural selection? That is the whole point to the mechanism of natural selection as proposed by Darwin: variety (for which he didn't propose a mechanism, but for which we now know about at least 47 major mechanisms, heredity (for which Darwin once again did not propose a mechanism, but which now comprises the fields of genetics, genomics, and proteomics, just to mention a few), and fecundity (the implications of which were first pointed out by Malthus, and which virtually no one disputes today), all of which together have the effect of producing unequal, non-random survival and reproduction; evolution, in a word.Allen_MacNeill_{March 4, 2008
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gpuccio, There is another issue and that is cell type. Apparently the promoters of the various genes are different in the different cell types. At least that is what I thought I heard in one lecture of many on genetics that I just watched. So that is why cells in the bone marrow don't produce hair but red blood cells and hair cells do not produce red blood cells but hair cells. The promoters in each are different. If this is true then each cell's DNA is not quite the same but has different promoters for the appropriate genes. If anyone has information on this, I would be curious because I always thought each cell is the same in terms of DNA. And if it is true, what determines these differences during gestation.jerry_{March 4, 2008
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Jerry:
It is hard to separate out all the various ideas in this article. But like MacNeill’s 47 sources of variation it might be worthwhile looking at each to see what they really mean.
I loved the discussions going on w/ MacNeill around the time when he published his 47 sources of variation. It was once he had published that statement that he acknowledged that the 47 sources, plus natural selection, did not provide an adequate explanation for the major adaptations that have occurred. I actually think that MacNeill would be an excellent asset at the meeting. I seem him to be an honest biologist, who honestly sees that NDE doesn't have it in the bag.bFast_{March 4, 2008
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I found this passage by biologist Stuart Kaufmann very interesting: ""Well there's 25,000 genes, so each could be on or off. So there's 2 x 2 x 2 x 25,000 times. Well that's 2 to the 25,000th. Right? Which is something like 10 to the 7,000th. Okay? There's only 10 to the 80th particles in the whole universe. Are you stunned?" A couple of comments. First, it seems that someone is beginning to do the math, which is comforting. Second, Kaufmann here is pointing to an aspect which is often overlooked, even in the ID debate, and which instead is, in my opinion, fundamental. It is the problem of how transcriptomes are "selected" in each single cell from the bulk of available genes. That's very intriguing, because we really don't have the slightest idea of how it happens. As Kaufmann correctly points out, if we have 25,000 protein coding genes in the human genome (and that should not be very far from truth), and if we consider two possible states for each gene (transcripted - not transcripted),in each cell we have a search space of 2^25,000 possible transcriptomes, which Kaufmann justly finds stunning. But the reality is much worse than that, even with the little knowledge we have of the process of transcription. Indeed, we must consider a couple of other things: a) Each gene has not only two possible states, but many more. Indeed, the "quantity" of gene transcription is of fundamental importance, and that is a continuous variable, rather than a binary one. b) Moreover, as it is well known today, the "one gene - one protein" dogma is completely false. We know that one gene can, through various mechanisms (introne regulation, post transcriptional regulation, and many others), really code for many different proteins (in theory, even thousands of them, in practice certainly more than one). Indeed, darwinists, with their usual short-sightedness, seem to be very fond of this "one gene - many proteins" fact, apparently not understanding the terrible pitfalls which await them there. So, to sum up: we have a "minimal" transcriptome search space of 2^25,000, which, according to Kaufmann (I have not checked) is equivalent to 10^7,000, which is quite a number, if we remember that 10^150 is "just" Dembski's UPB. That number has certainly to be increased of many, many orders of magnitude(nobody can say how many), if we take into account the different "levels" of transcription of each single gene plus the different "types" of transcription of each single gene. So, a very simple question: how can each cell, in each specific moment of its individual life, choose the right transcriptome in that almost infinite search space? And be careful, that question is really two different, and equally problematic, questions: 1) How did all that information pertaining to the right trancriptomes evolve? 2) Where, and how is it written? Well, darwinists seem to ignore both those questions. Maybe they already have too many other unsolved questions to deal with (CSI, IC, and similar). But we here in the ID field, who, I hope, can sleep with greater tranquility and a more serene cognitive consciousness, what answers can we suggest?gpuccio_{March 4, 2008
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Mazur:
Pigliucci cites epigenetic inheritance as one of the mechanisms that Darwin knew nothing about....these kinds of phenomena are part of what's loosely being called self-organization , in short a spontaneous organization of systems.
Um, I thought this was touched upon years before by none other than the much maligned Dean Kenyon in his Biochemical Predestination monograph. I wonder if his name or his work will ever come up in these upcoming discussions.
Snowflakes, a drop of water, a hurricane are all such spontaneously organized examples.
I hope these scientists are kidding when nonchalantly throwing about such superfluous analogies. And I just wonder how they are going to bridge the connection between snowflakes that exhibit repeatable patterns with the highly specified functions of DNA.
These systems grow more complex in form as a result of a process of attraction and repulsion.
Right. Like the wind of a hurricane acting against snow-making forces and blowing through a garden to create a lovely and tasty Piña Colada.JPCollado_{March 4, 2008
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No one from Cornell was invited. Allen MacNeill and Will Provine are not included nor interviewed by Mazur. It is hard to separate out all the various ideas in this article. But like MacNeill's 47 sources of variation it might be worthwhile looking at each to see what they really mean. I am getting the impression that natural selection is still a very viable construct but that it isn't everything. This is exactly what ID is saying. There doesn't seem to be any discernment over the separation of variation and genetics and how the current theory would be modified. Behe made this distinction and has pointed to the variation side of Darwinian ideas as the real achilles heel to the modern synthesis. These people in this article would never admit an intelligent input but I am not getting any feeling as to what they actually believe. None of the 16 were interviewed except Pigliucci. Most of the interviews were with people not invited. The papers have already been written so I wonder if any of their ideas will be available before next year.jerry_{March 4, 2008
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