Mud-to-Mozart Atheology (Or, Who are the real skeptics?)

_{Gil Dodgen

October 22, 2011

Intelligent Design}

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I find the “skeptic” claim on the part of Darwinian materialists very interesting and equally illuminating. Darwinists exhibit no skepticism whatsoever about the thesis that physical stuff turned into Mozart by chance. (Don’t try to deny this, Darwinists, that is the essence of your claim. You can try to obfuscate with legion “peer-reviewed scientific papers,” but you’re not going to fool me and many others about what you are actually promoting and advocating.)

I choose Mozart not just because I am a classical concert pianist, but because his existence epitomizes everything that Darwinian theory is totally powerless to explain.

Darwinists, claiming to be skeptics, actually exhibit the antithesis of skepticism — making transparently ludicrous claims and providing a never-ending stream of unsupported extrapolations, based only on wildly imaginative speculation with no empirical support.

How is it that Darwinian atheists are the only ones who get to declare themselves legitimate skeptics? Is mud-to-Mozart-by-chance philosophy the only worldview immune to skeptical inquiry?

Comments

First: Is DrREC also DrBot? This gets a little confusing. So, I'll assume DrREC is not DrBot.
I can only conclude that you don’t know what an inference is. What other design have we observed as a basis of this inference?
And I can only conclude that your not careful about making proper distinctions. To make an inference "to human design" is to infer that humans are responsible for the design of life; which, of course is preposterous. Perhaps DrBot (DrREC?) meant to say "ID is based on what we know of human design", or, "ID is based on inference from human design". As to the quote from the UD website, it says that ID is based on "the empirical observation of the process of human design, and specific properties common to human design." Does this anywhere say that it is based on an "inference to human design"? No.
But SETI performs the search looking for halmarks of intelligent signals, based on what we think those would be from a human perspective.
This, really, is quite cheeky. Revelation tells us that we're made in the image of God. It would then be quite proper to understand our faculty of reason as being similar to that of God's. Thus, the "hallmarks" of human design can be reasonably taken to be similar to how God designs. (In fact, if one traces the whole history of modern science, it stems from an understanding of inertia inferred from the Biblical accounts of Creation. You might want to consult Stanley Jaki's "The Savior of Science.") But what reason have you to believe that human reason---leaving God and creation out of this for the moment---can be projected onto alien life forms (should they exist)? Further, if you believe that you can project these "hallmarks of intelligence" onto creatures you know nothing of, then this is to say that these "hallmarks" can be understood in an abstractly. And if they can be abstracted, then what prevents anyone from projecting, or detecting, them when it involves an unknown designer? ID posits that cellular organisms display all of the "hallmarks" of intelligent agency. It's not an "inference to human design". It's a scientific view that vastly different life-forms are best explained by the guiding hand of intelligent design---scientific in the very same sense as forensic science.PaV_{November 4, 2011
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68.1.2.1.4 PaV "ID is NOT based on inference to “HUMAN” design; it’s based on an inference to “DESIGN”." I can only conclude that you don't know what an inference is. What other design have we observed as a basis of this inference? Even this site disagrees with you: "Moreover, ID satisfies all the conditions usually required for scientific inquiry (i.e., observation, hypothesis, experiment, conclusion): "It is based on empirical data: the empirical observation of the process of human design, and specific properties common to human design....." https://uncommondescent.com/faq/ "This is pure silliness, as becomes evident when considering SETI, for example, which attempts to detect signs of an intelligence outside of our world that might easily (if not presumably) be “higher” than our own." But SETI performs the search looking for halmarks of intelligent signals, based on what we think those would be from a human perspective. "In sum, your statement that ID is based on inference to human design is completely off the mark." What is an inference, and what is the observation ID is based on, if not to human design? By the way, you could remove "human" from my post, and preserve the meaning. Those are not discernable indicators of design. Period.DrREC_{November 3, 2011
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DrBot:
No religion. Just design. ID is based on inference to human design.
I let this go the first time; but since you want to take an aggressive tack, then let's talk about this a little bit. ID is NOT based on inference to "HUMAN" design; it's based on an inference to "DESIGN". The level of sophisticated programming evident in the eukaryotic cell is completely beyond anything a human designer can come up with---and, likely, could ever come up with (We'll see about that one down the line). Hence, we're dealing with a designer that far surpasses our intellects---humbling as that might seem to some. It is nothing but an intellectual distraction to claim that without our "human" experience of design and designers, this "inference" could not otherwise be made, and, that, therefore, ID can ONLY infer to a human design, and no more. This is pure silliness, as becomes evident when considering SETI, for example, which attempts to detect signs of an intelligence outside of our world that might easily (if not presumably) be "higher" than our own. IOW, to say that the design inference must be limited to what human designers can do, that otherwise we're impotent to detect it, is a bogus claim. In sum, your statement that ID is based on inference to human design is completely off the mark.PaV_{November 3, 2011
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DrBot: Yes, I'm struggling to try and understand your contentions---which, thus far, seem entirely unfounded. Arrogantly, you fail to see that the designs in nature surpass those of mere humans. Do you see this? How many times have we read in the paper that scientists were designing this, that or the other, based on the way that nature has solved the problem. What you also fail to see is that human design, indeed, has one goal in mind. OTOH, the Designer's goal is design something that can adapt to differing environments. Hence, different "solutions", if you will, are necessitated at different moments of time dependent on a whole hosts of variables. With such requirements, a certain open-endedness is unavoidable, and necessary. Now, can we claim that this is entirely so? No. But can the fact that "seeming" imperfections and adaptive dead-ends disprove the role of a Designer? Again, the answer is no. This is why, in posing the question to gpuccio, his answer was: "It could well be."PaV_{November 3, 2011
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Petrushka: The only test of functionality is reproductive success. ???? That is really big! So, I suppose, if I test the enzymatic activity of a protein in the lab, I am not testing a functionality? The exact nature of the rescue was not understood. But it could certainly be understood. Reproductive success is just one of all the functions that can be defined. Explain how a designer knows — absent selection — what the effect of a new sequence will be. First of all, a designer can well use selection: intelligent selection. And secodnly, it is perfectly possible to know in advance the effect by a thorough understanding of biochemical laws (that is the concept of top down protein engineering. It's not easy, but it can be done).gpuccio_{November 3, 2011
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A functional protein ia a functional item in the phenotype, whethet it affects reproductive fitness or not. A non functional protein is non functional. Period. It cannot implement any function. Sometimes it can be detrimental, but not always.
The only test of functionality is reproductive success. Recall the infamous study of "rescue" by "randomly" generated protein sequences. The exact nature of the rescue was not understood. Explain how a designer knows -- absent selection -- what the effect of a new sequence will be.Petrushka_{November 3, 2011
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Umm, PaV, you really seem to be struggling with this whole topic. Humans don't implement, as final solutions, designs that include modifications of an earlier design that are random with respect to need or impede an earlier function. What we do is implement systems that use stochastic variation and methods of automatically assessing functionality as a tool for generating final solutions. Unlike nature, we are only interested in the end result - if you are using a GA to design a circuit board you don't implement every design, only the best one you have generated at the end of the process.DrBot_{November 3, 2011
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DrREC:
I would say the following are not properties of human design: Utilizing mechanisms that are random with respect to need. Utilizing mechanisms that are open ended (no timeline) and not goal oriented. Utilizing mechanisms as likely to be deleterious to the design as beneficial.
Excuse me. Aren't you the one who wants to point out the utility of evolutionary algorithms as useful in other fields of human endeavor?
By the way, I didn’t think dualism (even in lighter forms) was popular these days. Burning at the stake and internal crusades and inquisitions and all…..
You've showed your hand!PaV_{November 3, 2011
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DrREC: Design is a logical inference. We see the hallmarks of design, and we infer design. This is far different than saying I can make a rabbit appear out of thin air.PaV_{November 3, 2011
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That was supposed to be a backwards question mark-indicator or irony. Guess U+2E2E isn't supported here.DrREC_{November 2, 2011
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"It’s almost like magic. Which should give everyone pause." ?DrREC_{November 2, 2011
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Elizabeth: I don't know if you've looked at my response to your response on page 2? But let me pick out just this one point since I think it demonstrates quite clearly where we disagree.
Any changes to the original sequence aren’t going to do much for the phenotype, so the fitness landscape in that “gene space” (or let’s call it “sequence space, as it isn’t really even a gene yet) is flat. Any change will result in no change in phenotypic fitness. Then it hits a protein domain. Bingo – leap in fitness. That’s a continuous function – sure it’s got a big step in it, but that doesn’t matter. What does matter is how big the plain is at the foot, which may be pretty big.
FIRST: I can see why you disagree with Dawkins. You see no direction whatsoever in the biochemical changes taking place in the DNA template. For you, everything is neutral drift---until it isn't anymore (for selection now "selects"---excuse the "agency" language). SECOND: Your scenario should, I think, be called: "Taking A Lift Up Mount Improbable". Or, for Americans, "Taking An Elevator Up Mount Improbable". It's almost like magic. Which should give everyone pause. THIRD: While you talk about "how big the plain is at the foot", with, apparently the larger the plain the better, you don't apply a time-frame to this traverse; nor do you deal with deleterious mutations that are occurring far more frequently than anything called 'beneficial'. The larger (longer) the plain, the more time that will be needed; and the more opportunity, therefore, for harmful mutations to disrupt any possible future function. In my retort on page 2, I do a calculation demonstrating the importance of "fixation"---the importance of which you refuse to acknowledge. I invite you to take a look at that calculation. It's at 57.2.3.3.2.PaV_{November 2, 2011
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No religion. Just design. ID is based on inference to human design. I would say the following are not properties of human design: Utilizing mechanisms that are random with respect to need. Utilizing mechanisms that are open ended (no timeline) and not goal oriented. Utilizing mechanisms as likely to be deleterious to the design as beneficial. You're the one that jumped on the bad design=theology argument. Showed your hand there. By the way, I didn't think dualism (even in lighter forms) was popular these days. Burning at the stake and internal crusades and inquisitions and all.....DrREC_{November 2, 2011
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DrREC:
“DrREC: So gpuucio, you believe that a process spanning millions of year, using mechanisms that are demonstrably random with respect to need, and that often cause disease and infertility is “intelligent design?” gpuccio: “It could well be.” DrREC: "Unless you can demonstrate it IS, ID is just theistic evolution with a bad guess."
Have you ever had a cellphone go bad, DrREC? Would you then conclude that it wasn't designed? You're sneaking in theological considerations here, evident in your conclusion that ID is just "theistic evolution". If you want to talk theology, then do you want to talk about the reality of the devil? Do you want to talk about what the devil is able to do, or not do? If God can change an amino acid, can the devil? In the gospels we have Jesus talking about a woman who had a bleeding ulcer, and saying that it was the "devil" who had kept this daughter of Israel in this bondage for twenty years. So, if you want to talk theology, we can talk theology. But, otherwise, let's not just assume that only perfection is permissible in a world created by God. Revelation has a lot to say about all of this. God's foolishness is wiser than man's wisdom. That's just a sample.PaV_{November 2, 2011
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LOL. “the desisn inference can be made, based on the dFSCI of the protein.” Which you admit can't reasonably be calculated. Estimated, maybe. And if it could, any process, no matter what the mechanism, that exceeds the value you set, makes it designed. ANY potential falsification, by definition then=design. No problem there?DrREC_{November 2, 2011
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DrRec: See the problem? No.gpuccio_{November 2, 2011
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Me: "So gpuucio, you believe that a process spanning millions of year, using mechanisms that are demonstrably random with respect to need, and that often cause disease and infertility is “intelligent design?” "It could well be." Unless you can demonstrate it IS, ID is just theistic evolution with a bad guess. "And, obviously, the fact that transposons can behave randomly does not demonstrate that they always behave randomly. The same for mutations." LOL. Non-uniformity isn't the greatest thing in science, but when your science believes in miracles, guess you gotta go for it. "You have already computed the maximum dFSCI: 20^194 (if I remember well). The reald dFSCI is more difficult here, because it is a new protein, and the Durston method cannot be applied (it applies to protein families)." Ahh, see gpucio is too honest! Where others just cite the maximum dfisco, he realizes that is the calculation for the maximum! So what would the actual calculation be? Durston has an estimate, based on the number of sequences found in nature that perform the same function. (Of course, in this case there is only 1.) Taking known sequences with the same function substantially lowers the fits, to the point functional proteins and enzymes are below the some probability thresholds set here. But even that is just an estimate! Nature hasn't explored all of sequence space, and no one can make the entire sequence space of a protein and measure function. So you've got an estimate at best behind your 'design inference.' Which is odd, because in the same post you say: "the desisn inference can be made, based on the dFSCI of the protein." And how would you do that calculation again!?! You also have a circular non-falsifiability to it. I present something that has loads of what you call fisco, that developed over millions of years in processes known to be random with respect to need. Apparently natural. BUT, if it does have fscio, it is designed. See the problem?DrREC_{November 2, 2011
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Elizabeth: I am afraid you are really making a great confusion here. Genes are activated or deactivated all the time, that is true, but not in the sense that they are no more functional genes. The mechanisms of temporary activation or deactivation in individual transcriptomes are part of a complex regulatory network. They have nothing to do with the genes becoming non functional and no more appropriate for translation. A duplicated gene can become non functional in may different ways. A very simple event can be the appearance of stop codons in the gene, that interrupt transcription. I quote from Wikipedia: "The duplication of a gene results in an additional copy that is free from selective pressure. One kind of view is that this allows the new copy of the gene to mutate without deleterious consequence to the organism. This freedom from consequences allows for the mutation of novel genes that could potentially increase the fitness of the organism or code for a new function." So, the idea is, the duplicated gene in this model is not a gene that is transitorily non transcribed in a specific cell type. It is a gene that has become non coding in whole species, and for long evolutionary times. That's exactly what gives it the chance to accumulate free mutations, by definition "neutral". But not certainly the power to overcome probabilistic barriers. As DrBot has correctly pointed out, other problems remain: if the gene is not translated, how can NS "realize" at phenotypic level that some functional sequemce has been reached? I don't know, and really don't care. The model is bogus. But gradual remodeling of a non coding sequence, followed by a final repristination of its translation, is a very good model for design. And why do you go on saying that I am not referring to the phenotype? I am always referring to the phenotype. But, as I have said, the phenotype is not only reproductive fitness. It is a lot of other things. A functional protein ia a functional item in the phenotype, whethet it affects reproductive fitness or not. A non functional protein is non functional. Period. It cannot implement any function. Sometimes it can be detrimental, but not always. A non functional protein coding gene always implies a non functional protein, or the absence of a functional protein. We must reason on the whole system: genotype, biochemical phenotype, and all other levels of phenotype, including reproductive fitness. All are interrelated.gpuccio_{November 2, 2011
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In a design model, the inactive gene is prepared while remaining inactive, and only when it is ready, and everything else necessary has been prepared, it is shifted to translation.
But that makes no sense, gpuccio. Genes are switched on and off throughout the lifetime of the organism. If they weren't we wouldn't be differentiated multicellular creatures able to function in response to our environment. Every second of your life, genes are being activated and deactivated in your body, in different places, and in response to different inputs. "Frontloading" is a brave concept, but it's falsified by even a cursory glance at what genes actually do. And proteins in themselves are neither good not bad; what matters (from an evolutionary PoV) is whether they are expressed in a manner that enhances the reproductive success of the phenotype. A protein expressed by a gene in one part of the body, or at one time in development, may be highly beneficial; the same gene expressed later, or earlier, or elsewhere, may be highly deleterious. Or neutral. This is why it simply makes no sense to talk about evolutionary processes without reference to the phenotype. It's like saying "let's not complicate things by looking the left side of the equation, let's just concentrate on the right hand side". (This response is partly to PaV as well, but I'll try to get back later to be more specific).Elizabeth Liddle_{November 2, 2011
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What you are saying is the equavalent of microsoft loggin in to other peoples computers and tweaking the code directly and gradually over many years, then not testing it in any kind of sandbox but just switching the new function on when they think it is ready.
You have to give the Designer credit for coming up with a process that is empirically compatible with mainstream biology. I have to apologize for using the word "poof" to describe the process. I might point out that in the reality we observe, the beta test code is online, and has actual effects on fitness.Petrushka_{November 2, 2011
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DrBot: No. I am analyzing two different scenarios (evolution of a translated functional gene and evolution in a non translated duplicate or a non coning DNA sequence). It’s not an error at all.
It is a major error, and the fact you can't see it is even more worrying! What is the difference between a translated gene sequence and a non translated gene sequence or just a sequence? The search space for a sequence includes anything that the sequence can be - all possible configurations. Some of those configurations produce proteins, others will not get translated. Fitness is the result of the sequence being in a specific configuration within the context of the whole genome and the environment. A gene sequence that is not expressed is not a search space, it is a specific configuration, a specific sequence. The search space is an n dimensional hypercube that incorporates an entire genome. Remember, gene sequences can vary in length so a search space for just a single gene has a variable number of dimensions and they are just a set of sub dimensions within the whole genome. Within that search space there may be many sequences that are not expressed, but also many that are.
In a design model, the inactive gene is prepared while remaining inactive, and only when it is ready, and everything else necessary has been prepared, it is shifted to translation.
That is very revealing in terms of the designers methods. The gene is taken 'off line' within an extant population and then adjusted via a sequence of steps before being re-activated. One could draw a few inferences from that. Firstly, the designer was not capable, or did not want, to make all the changes at once - if all the changes could have been made at once then there would be no need to take the gene off line. Secondly it indicates that members of the extant population were the only available entities in which to make these adjustments. In terms of observed design processes the normal approach would be to use a sandbox for development and testing before updating the actual system with the completed and tested new functions. It also indicates that the designer had some reason, or restriction in their operation, that required them to prepare the gene over such a long time period. If you think about it in terms of microsoft working on updates for windows: Normally Microsoft will have a set of test computers in their HQ, locked away from public view, and will use them for preparing and testing software patches. They will then publish the update. All the computers running windows will get the update - they will go from one version of a function to the new version in one step. What you are saying is the equavalent of microsoft loggin in to other peoples computers and tweaking the code directly and gradually over many years, then not testing it in any kind of sandbox but just switching the new function on when they think it is ready.
That is more or less what apparently happens in this case:
What emperical evidence have you got of the gene being intentionally prepared - how did the interactions between the designer and the organism occur?DrBot_{November 2, 2011
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DrRec: By the way, I was the one who first presented that paper on this thread, over a week ago. I know. Thank you. So gpuucio, you believe that a process spanning millions of year, using mechanisms that are demonstrably random with respect to need, and that often cause disease and infertility is “intelligent design?” It could well be. And, obviously, the fact that transposons can behave randomly does not demonstrate that they always behave randomly. The same for mutations. How did you determine this was a design process? I didn't. The following steps are missing: a) Confirmation and isolation of the protein b) Identification of its structure and biochemical function. If the protein is confirmed and analyzed, the desisn inference can be made, based on the dFSCI of the protein. I was curious if someone could calculate the gain in fciso for that de novo gene. You have already computed the maximum dFSCI: 20^194 (if I remember well). The reald dFSCI is more difficult here, because it is a new protein, and the Durston method cannot be applied (it applies to protein families). An analysis of the structure funtion relationship of the specific protein could help.gpuccio_{November 1, 2011
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By the way, I was the one who first presented that paper on this thread, over a week ago. I was curious if someone could calculate the gain in fciso for that de novo gene. Apparently not. This seems to be of no concern, and despite having quite tractable natural processed behind it, is now presented as an example of design. Remarkable.DrREC_{November 1, 2011
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"In a design model, the inactive gene is prepared while remaining inactive, and only when it is ready, and everything else necessary has been prepared, it is shifted to translation. That is more or less what apparently happens in this case: 63.1.2.1.2 gpuccio “A Human-Specific De Novo Protein-Coding Gene Associated with Human Brain Functions” http://www.ploscompbiol.org/ar.....bi.1000734" From the paper: "Insertion of repeat elements especially Alu contributed to the formation of the first coding exon and six standard splice junctions on the branch leading to humans and chimpanzees, and two subsequent substitutions in the human lineage escaped two stop codons and created an open reading frame of 194 amino acids." So gpuucio, you believe that a process spanning millions of year, using mechanisms that are demonstrably random with respect to need, and that often cause disease and infertility is "intelligent design?" How did you determine this was a design process?DrREC_{November 1, 2011
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drBot: But then you say “unless and until a new functional sequence is reached” – this is a direct contradiction in terms. The contradiction is not mine. It is in the darwinist duplication model I am tentatively discussing. Not my fault. It's the model that is inconsistent. In a design model, the inactive gene is prepared while remaining inactive, and only when it is ready, and everything else necessary has been prepared, it is shifted to translation. That is more or less what apparently happens in this case: "A Human-Specific De Novo Protein-Coding Gene Associated with Human Brain Functions" http://www.ploscompbiol.org/article/info%3Adoi%2F10.1371%2Fjournal.pcbi.1000734gpuccio_{November 1, 2011
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DrBot: No. I am analyzing two different scenarios (evolution of a translated functional gene and evolution in a non translated duplicate or a non coning DNA sequence). It's not an error at all.gpuccio_{November 1, 2011
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“You’re right that you absolutely cannot falsify someone’s belief that something is designed.”
Therefore, ID is not science. It is a belief tacked onto science.
You (intentionally?) spun my words. ID is not belief, it is the investigation of whether a phenomenon falls outside of the probabilistic resources of stochastic processes. If these can be empirically verified, the only other verified explanation left is design. Yes, I am restating the elementary definition of ID, but judging solely by this statement of yours, you do not grasp that yet.
“ID is defeated in this instance (even though it actually was designed!) because the inference to the best explanation results in a probabilistically viable natural explanation.”
Above, I reference a study showing a gene evolving by apparently natural processes, which are demonstrably random with respect to need. It creates a new functional protein. Is ID not defeated in this case because I’ve demonstrated a viable natural explanation for creation of new information? And secondly, where is the design inference? Is a long process, random with respect to need, comparable to human design?
I am a mechanical engineer, not a biochemist; I do not want to pretend to be something I'm not. I have looked at that paper but not enough to have a really serious conversation with you. My initial thoughts were there were several point mutations along with the rearrangement of lots of repeat elements which contributed to the formation of multiple introns, yet no mention of possible step-wise selectability of any of these changes. And if it was all needed for end functionality, there would need to be a huge island of functionality for this to drift to as all of these changes would easily go way beyond the probabilistic resources of the universe if they were all necessary and the only options. Also, you seem to contradict yourself: 24.1.1
No evolutionary process can be exhaustively proven to be “blind and undirected.”
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Above, I reference a study showing a gene evolving by apparently natural processes, which are demonstrably random with respect to need.
We know that it took multiple point mutations as well as complex rearrangement of repeat elements, and we know of no step-by-step selection increases (so we're assuming drift?) and don't know of the size of the "island of functionality", yet it is "demonstrably random"? I don't see that demonstration. Please point it out to me if it is there (not being sarcastic).
As I’ve said before, the design inference is without empirical support. Has anyone recorded the designer creating improbable amounts of information at once?
We have plenty of empirical support of intelligence designing things, like this very comment. We do not have any evidence of a specific designer creating biological information. No ID advocate has asserted this (to my knowledge). So if someone is trying to use the design inference to prove the existence of the God of the Old Testament, then your argument is valid. If they are trying to use it to argue that at least some of life was designed, your argument means nothing. Analogy: ME: Someone murdered this man. It was no accident. See ______ as evidence. YOU: Do you have any evidence or direct observation of John Doe murdering him? If not then your inference is invalid. ME: I didn't say that this evidence proves John Doe did it, just that someone did it, intentionally. Out of time, can't get to the rest of your comment right now.uoflcard_{November 1, 2011
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If you have, for example, a duplication event, then a mutation to the duplicate will not destroy the function that exists in the original. The search space for the copy includes the existing function (a protein domain), other new functions (other protein domains), neutral and advantageous non coding sequences, non expressed sequences and deleterious sequences.
Exactly. The whole search space is neutral in that case, unless and until a new functional sequence is reached, transcribed and translated (and integrated in the existing scenario).
If the whole search space for this gene is neutral then no mutation of any kind will cause the sequence to become deleterious or to become advantageous, to loose expression or gain it. You are basically saying that the gene can be anything - any possible gene - and it will not affect fitness because it is a duplicate. But then you say "unless and until a new functional sequence is reached" - this is a direct contradiction in terms. If the entire search space is neutral then by definition it contains NO advantageous functional sequences and NO deleterious ones. Now of course if you limit your enquiry to ONLY the parts of a sequence that do not control expression, and assume it is not expressed, then your entire search space from this frame of reference is neutral. What you have to remember is that the search space is ultimately for the whole genome, individual sequences can be viewed as sets of axis within that space. Changes from expression to non-expression are part of the space of possibilities therefore the search space is not flat with respect to fitness. A duplication event gives you two genes, one of which can potentially change without a loss of function (because the original retains the function) - the fitness landscape for the duplicate is defined in part by the fact that there is an identical sequence.
Again the same error. No move is deleterious, until the sequence is translated. And no move is advantageous.
Any unexpressed gene exists on a neutral area, yes. If a single mutation event will cause it to be expressed then it will step into an area of the search space where selection will operate.
If you want to analyse the probabilities of getting from A to B in an evolutionary system you need to have a good understanding of the topology of the fitness landscape
I have. And you?
You are analysing the same search space and assuming that there are two different fitness landscapes - one neutral and one not. This is a major error!DrBot_{November 1, 2011
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57.2.3.3.2 PaV, "I’d rather base my thinking on what nature is known to have done than on undemonstrated “assumptions”." Absolutely. Behe keeps saying that (i) it is highly improbable rather than impossible (ii) the current evolutionary models are way to simple and, consequently, imprecise. In other words, just guesswork. As soon as the talk touches the details, their machinery grinds to a halt. With every next necessary mutation, probability plummets while complexity rockets up. But one thing that is certain is that neo-Darwinists do have fruitful imaginations.Eugene S_{November 1, 2011
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DrBot: Of course NS has a role – thats what EL and I keep saying – neutrality is DEFINED by NS acting on the search space. NS acts to keep a sequence neutral when there is no hill to climb but flat areas exist You are palying with words, and falling heavily into the trap of agency language, so feared by Elizabeth. You want to say that NS has the role of non existing when variationis neutral? that's fine for me. What changes. The point remains that, if variation is neutral, it is not selected in any way. In the case of a non transcribed or non translated gene, the landscape is flat. No selection applies to the variation (more on that later). Neutral variation cannot easily reach any target – how could a sequence of neutral mutations reach a target in the middle of a sea of deleterious function? That's exactly why existing functional genes don't reach any distant target. Variation can occur only inside the functional island, or at most as minor tweaking at the active side level (as said many times). New genes are derived from non coding DNA, be it a duplicated non translated gene, or simply a repetitive sequence. Topology refers to the shapes of the surfaces in the landscape. What you are talking about is just the distances between two points. As said, in the case of a non active gene, the topology is simply flat. The distance remains the only pertinent topologic parameter. Instead, in the case of a functional gene, the topology is simply against any complex transition. Even separtated islands with the same function are impossible to reach, as shown in this paper about the ragged landscape model: "Experimental Rugged Fitness Landscape in Protein Sequence Space" A quote from the discussion: "In practice, the maximum library size that can be prepared is about 1013 [28,29]. Even with a huge library size, adaptive walking could increase the fitness, ~W, up to only 0.55. The question remains regarding how large a population is required to reach the fitness of the wild-type phage. The relative fitness of the wild-type phage, or rather the native D2 domain, is almost equivalent to the global peak of the fitness landscape. By extrapolation, we estimated that adaptive walking requires a library size of 10^70 with 35 substitutions to reach comparable fitness." Get the idea? Your examples: 1) If there exists a series of steps from A to B, and each confers an advantage, then an evolutionary ‘search’ can ‘climb the hill’ OK. That is positive NS. Then there are intermediates. Then there are functional steps. Nothing of that is true for protein domains. Falsified. 2) If there exists a series of steps from A to B, and each confers no advantage or disadvantage, then an evolutionary ‘search’ can ‘cross the ridge’ It can, but it will not, because the proibabilities are too low. What do you think the dFSCI discussion is about? We are not talking of "possibility", but of empirical credibility. 3) If there exists a series of steps from A to B, and each is seriously harmful, then an evolutionary ‘search’ will never take more than one step in that direction. Agreed. That's why functional genes remain as they are, and change only in sequence, while retaining their function. And so? Your error is in point 2. You attribute to neutral mutation a power it has not. Empirically. Therefore the probability of getting from A to B in the three examples is different in each case (1 is the highest, 3 is the lowest) despite the distance between A and B being the same. Yes, and in 2), that is the only alternative left to reach new unrelated domains, it is almost zero. So we know that darwinian evolution can wrok in a scenario that is not true, can maintain existing functions, and can never create new protein domains. That was my initial point, exactly. The sequence space includes sequences that code for proteins, that are not expressed, that are non coding and that are deleterious. Either I don't understand what you are saying, or this is really nonsense. By what mechanism a sequence that is not expressed should be deleterious? Please, elucidate. Only those areas of the sequence space where a point mutation will not cause a change in selective potential are neutral, the rest are not – the rest are areas of sequence space upon which NS will act. Again, could you explain how a point mutation in a gene that is not expressed, or in non functional non coding DNA, could be non neutral, and dealed with by NS? The entire sequence space encompasses neutral, deleterious and advantageous areas, some of these areas do not form part of the searchable space All the space is searchable for non expressed sequences. Practically none of it is searchable for functional sequences, constrained by negative NS (except the functional island they are in). If you want to analyse the probabilities of getting from A to B in an evolutionary system you need to have a good understanding of the topology of the fitness landscape I have. And you? you need to take into account how much of the sequence space is not searchable, how much of it is neutral, and how much of it confers some advantage. I have discussed that. I think the error you seem to be making is in thinking that neutrality refers to a different search space than non neutral – it doesn’t, it is just a feature of the fitness landscape for the entire search space of the sequence. A neutral mutation does not render the entire search space neutral. No. Neutrality for an existing function is one scenario. As said, it creates constraint to change. Neutrality, instead, is the normal condition for variation in a non expressed, non functional sequence. They are two different scenarios, two different concepts. If you have, for example, a duplication event, then a mutation to the duplicate will not destroy the function that exists in the original. The search space for the copy includes the existing function (a protein domain), other new functions (other protein domains), neutral and advantageous non coding sequences, non expressed sequences and deleterious sequences. Exactly. The whole search space is neutral in that case, unless and until a new functional sequence is reached, transcribed and translated (and integrated in the existing scenario). The question here is whether there exists a route through sequence space for the duplicate from its starting state to a new functional state that does not require a move into deleterious function. Again the same error. No move is deleterious, until the sequence is translated. And no move is advantageous. You confound the potential advantage or damage in the genotipic sequence with a true phenotypic advantage (or damage).gpuccio_{November 1, 2011
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