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Author
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Topic: The Other Flagellum II
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yersinia
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Member # 324
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posted 22. September 2003 02:24
Sorry for the delay folks, I've been away.
First, a correction: I meant to say "TPR" when I said "toprim". Wires crossed or something.
Random points:
Point 1:
Mike has still not explained the *sequence* similarity between the TPR motifs revealed by BLAST. The general rule with proteins is that structural similarity persists even if sequence similarity is zero. Ergo, *even if* it were true that one paper by Denton et al. disqualifies homology inferences based on domain similarity (a subject for another thread), said structural similarity does not explain the sequence similarity, which remains homology and evidence for common descent.
I think before rash ideas about designers re-using structures and just happening to copy the sequences also are tossed about, it might be worth reading articles like this:
quote:
Blatch GL, Lassle M. The tetratricopeptide repeat: a structural motif mediating protein-protein interactions. Bioessays. 1999 Nov;21(11):932-9.
Protein-Structure-Function Research Programme, Department of Cell Biology, University of the Witwatersrand, Johannesburg, South Africa.
The tetratricopeptide repeat (TPR) motif is a protein-protein interaction module found in multiple copies in a number of functionally different proteins that facilitates specific interactions with a partner protein(s). Three-dimensional structural data have shown that a TPR motif contains two antiparallel alpha-helices such that tandem arrays of TPR motifs generate a right-handed helical structure with an amphipathic channel that might accommodate the complementary region of a target protein. Most TPR-containing proteins are associated with multiprotein complexes, and there is extensive evidence indicating that TPR motifs are important to the functioning of chaperone, cell-cycle, transcription, and protein transport complexes. The TPR motif may represent an ancient protein-protein interaction module that has been recruited by different proteins and adapted for specific functions.
I haven't read it yet myself (no access), so who knows.
Point 2:
Regarding the apparently popular idea of measuring a "cooption frequency" -- here is a challenge for folks. Let's assume that what the above abstract suggests is true. Let's say that the TPR motif arose in some prokaryote ancestor of eukaryotes, and in eukaryotes the motif was extensively copied and spliced into proteins with all of the diverse functions described above. Now, which of these specific events get scored as cooption events:
1) The origin of the TPR motif
2) Each time the TPR motif is copied *within* a protein
3) Each time the TPR motif is transposed to a new protein
4) Each time a descendent of either #2 or #3 "changes function" binds to a new, but similar substrate protein
5) Each time a descendent of either #2 or #3 "changes function" binds to a new, significantly different protein
6) Each time a descendent of either #2 or #3 "changes function" binds to a new, significantly different substrate protein
7) Each time a TPR-containing protein maintains protein X as a substrate, but transports it to location Y instead of Z
8) After #7 occurs, the substrate protein duplicates and diverges to sub-specialize on its function in its new location.
9) Any of the above, except regulation is changed instead of substrate or substrate destination
10) Add alternative splicing
11) Add combinations
12) Add changes of function at the system level: e.g., if a cilium used for motility switches function to a feeding or sensory role, does every protein in the system get scored as a cooption?
13) Add changes of function at the cellular level: e.g., the currents induced by cilia that help determine left/right patterning in embryos
...etc. Simple cases, where a single protein family can be identified, that functions alone, not in a larger structure (e.g., an enzyme), no domain swapping occurred, and the different functions enumerated, *might* have some possibility of being tractable regarding a "cooption frequency," although this would still require decent dating, phylogeny, functional determinations, reasonable sampling, etc. This would be largely in prokaryotes probably. For the typical mix-n-match eukaryote protein, with all the variations on regulation, splicing, etc., plus the inherent ambiguity and fuzziness of "function", different organizational levels, etc., I don't see much prospect for deriving a "cooption frequency" that would be meaningful.
But perhaps Mike could tell us why this is so important anyhow, before we spend any more time contemplating this little exercise. If cooption is common, that's all that matters (to me) for whatever it is we were originally arguing about.
[ 22. September 2003, 02:36: Message edited by: yersinia ]
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gedanken
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posted 22. September 2003 23:17
I thought of a very rough analogy to help explain the issue of the "general" cooption frequency involving a specific gene, and the issue of probability in a particular circumstance of a cooption event.
First we must recognize that if we discuss a specific event situation, we may know (or be able to learn) of differing constraints, ones that change probabilities of various occurrences in ways that are specific to the current situation and differ from other situations.
Now consider a "loaded" die. We move the load to the center, and roll the die. We get a random distribution of all the faces.
Then in sequence we "load" the die by moving the weight to opposite of each of the digit faces in sequence, 1 to 6. In each trial, we roll the die 100 times with the given position. We notice that after our trials, that the 6 digits have come up with similar frequencies! In fact the frequency of the "6" face is approximately 1/6 in our long sequence of trials.
Now finally we specifically load the die with the weight opposite of the 6 face. This is a specific situation--as opposed to the "general" frequency involving that specific die.
We roll the die in this specific situation. It seems to come up with 6 face with a very high frequency, a significant fraction of all rolls! How about that--the probability of an event does not necessarily relate to the "general" frequency of that event when measured under a sequence of different conditions.
So how does the "general" (with respect to presence of a specific gene) cooption frequency guide us in a specific case in which we have additional information about that situation?
Now of course in the case of a die, we have two separate and supporting bits of information to judge probability. First of all we know that if the die is properly balanced, there is no particular mechanism that would favor a particular face, thus each face would be favored equally, and the probability would by symmetry be 1 out of 6. Then we also have statistical knowledge from throwing the die itself.
But then (as above) we consider a specific situation. If we had complete knowledge, then we would know the probability of a particular face was either 1 or 0. But only by analyzing the situation to be similar to the other situations can we use the statistical "frequency" measurement as a reliable probability estimate. We need some basis for considering that the probability is equal to its relative frequency in other situations. So far I have seen nothing to suggest that any particular circumstance (e.g. "fan in" case to a "flagellum structure") has been analyzed to show that it is similar to general cases involving a specific gene.
Separately we have the issue of what is the “event” we are going to analyze. What is the “specification” we are dealing with? (And is it “independent of the event” in any way—because if it is not so it does not matter if meeting the specification is of low probability, as low probability combinatorial events happen all the time.) Once again, cooption frequency involving a specific gene (however estimated, from “general” frequencies of otherwise if that were useful) may have little to do with probability of meeting our “specification”. We would have to demonstrate that the specific gene had some reason to be involved very specifically in meeting our “specification”. By that I mean that it had to be involved, thus probabilities of meeting the event as specified have to involve that gene. Then to determine that the specification was not simply a fabrication, justify that the specification was “independent of the event”, even though the event was considered to so require that specific gene.
[ 23. September 2003, 00:11: Message edited by: gedanken ]
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yersinia
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posted 23. September 2003 16:34
Just came across something relevant to this argument by Mike Gene:
quote:
For example, if you search the entire genome of Arabidopsis or baker’s yeast, you don’t find ‘homologs’ anywhere. Such organisms have lost their flagella. But why would they also both just happen to lose the supposed flagellar precursors involved in “noncilial tubulin-based transport systems”?
It appears that Arabidopsis has *no* known dyneins whatsoever. Somehow higher plants have (apparently) dispensed with dynein entirely. Their mitosis and cell division is quite different due to the cell wall, so perhaps this is not surprising.
Yeast only has one identified dynein, in the "other" category (neither axonemal nor IFT), so presumably what exactly what it does is unknown.
It looks like there are some fairly substantial differences in transport systems between major eukaryote groups. Conservation of accessory transport proteins is a debatable assumption when the basic motor proteins are not conserved.
quote:
Cell. 2003 Feb 21;112(4):467-80.
The molecular motor toolbox for intracellular transport.
Vale RD.
Department of Cellular and Molecular Pharmacology, Howard Hughes Medical Institute, University of California, San Francisco, 513 Parnassus Avenue, San Francisco, CA 94143, USA. vale@phy.ucsf.edu
Eukaryotic cells create internal order by using protein motors to transport molecules and organelles along cytoskeletal tracks. Recent genomic and functional studies suggest that five cargo-carrying motors emerged in primitive eukaryotes and have been widely used throughout evolution. The complexity of these "Toolbox" motors expanded in higher eukaryotes through gene duplication, alternative splicing, and the addition of associated subunits, which enabled new cargoes to be transported. Remarkably, fungi, parasites, plants, and animals have distinct subsets of Toolbox motors in their genomes, suggesting an underlying diversity of strategies for intracellular transport.
Full article online at: http://valelab.ucsf.edu/publications/2003valecell.pdf
[ 23. September 2003, 16:39: Message edited by: yersinia ]
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Nel
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posted 23. September 2003 17:05
Ged writes:
quote:
I also apologize to Alonso for any lack of clarity causing him to waste his time debating other points that I did not make. For example my discussion of “missing distributions” is to be taken in the context of the thread that I referred to about that subject, called Does intelligence imply “motive”, which has several discussions of the effects of “missing distributions” in versions of the “Explanatory Filter”. This is specifically referred to by Dr. Dembski on page 67-68 of No Free Lunch, in the sentence “To be sure, this cannot be done with absolute finality since there is always the possibility that some crucial probability distribution was missed.” (Emphasis mine.) Some references to use of “motive” as a consideration of the “designer” that is not simply eliminative is also meant to refer to that thread for context. It is not my intention to debate the subject of that entire thread here, but rather just to make use of some of the results.
Actually, I'm not quite sure where I misinterpreted you. For example, your discussion of "missing distribution" in the motive thread is just a rehash of the same "we can explain it someday" argument coupled with an assertion that nature can mimic intelligent agency. Unfortunately, neither is relevant to either motive or co-option frequency.
I don't really see how you can reconcile your "general" claim with the "specific" situtations that I discussed with the Brachyury gene. There is nothing general about the specific example of obtaining that particular co-option frequency. As I mentioned, you attempted to categorize your problem with this excercize by differentiating between "possibilities" and "observed cases". There is no such thing as observed cases. However, since data constrains possibilities, this is not a problem.
Your quote from No Free Lunch basically supports my contention that 100% certainty is neither sought nor presents a problem as to the reliablility of things like EF (although seriously off-topic, I will return to co-option frequency in a moment). For example, in the very next sentence he states:
quote:
Nonethelesss, it is not enough for the design skeptic merely to note that adding a new chance explanation to the mix can upset a design inference. Instead, the design skeptic needs to explicitly propose a new chance explanation and argue for it's relevance to the case at hand.
This of course means that design inferences are falsifiable. Promises of future explanations are not.
Just a piece of advice, keep structuring your sentences like this: "are not simply not about certainty" and you will have provided a human example of how to front-load a particular result through intelligent design. Misinterpretation is almost inevitable.
Back to co-option frequency and to the pre-post points that Ged alludes to in his reply to me. I don't see how three levels of co-option would pose a problem in ascertaining co-option frequencies. I think as long as you have enough developmental genetic information (as I showed with my Brachyury example) then it should be fairly clear to discern whether each co-option event was a single gene or a multi gene circuit or a gene fragment.
Going back to convergence, I would be very interested in comparing similar co-optive adaptations that independently arose in different lineages. With respect to this, I've been thinking a lot about how I (speaking for myself) would calculate a co-option frequency that could illuminate a design inference based on convergence. So I decided to wake up my mathematical side and (maybe later my computer programming side) and figure out how I would go about calculating this. After obtaining phylogenetic data, if the data indicates that gene X was co-opted N independent times in a lineage that is Y years old, then the co-option rate for X is N/Y. If you could then look at an unrelated lineage and do the same thing, you might then be able to test whether co-option rates were similar across lineages, which might say something about the degree to which gene X is or is not constrained from being co-opted.
[ 23. September 2003, 19:05: Message edited by: Nelson-Alonso ]
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Nel
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posted 23. September 2003 17:11
Nic writes:
quote:
I think before rash ideas about designers re-using structures and just happening to copy the sequences also are tossed about, it might be worth reading articles like this:
The paper implies evolution from a common TPR motif, but it does not seem to exclude convergence.
Nic writes:
quote:
Let's say that the TPR motif arose in some prokaryote ancestor of eukaryotes, and in eukaryotes the motif was extensively copied and spliced into proteins with all of the diverse functions described above. Now, which of these specific events get scored as cooption events:
At the origin of eukaryotic cells and the emergence of multidomain proteins and multiprotein complexes, the TPR motif would have been pressurized to proliferate, spread and specialize. So I would think that your point 8 is the co-option event that forced the recruitment and spread of the TPR motif. (Notice that point 8 starts with a duplication, as Mike has noted that co-option usually begins with).
[ 23. September 2003, 17:21: Message edited by: Nelson-Alonso ]
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gedanken
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posted 23. September 2003 17:50
quote:
Actually, I'm not quite sure where I misinterpreted you. For example, your discussion of "missing distribution" in the motive thread is just a rehash of the same "we can explain it someday" argument coupled with an assertion that nature can mimic intelligent agency.
I’m not sure where you got the part about “nature can mimic intelligent agency”, because that was not really in that thread. Rather the point was that nature can create events that might appear to match similar patterns to some we have a high probability of recognizing or picking out. I might agree that nature can mimic intelligent agency, but that was not in that thread. In fact it was very important to recognize that these were not mimicking intelligent agency, but that they were creating false impressions of low probability for the “specified” pattern in the rejection region—thus causing ID enthusiasts to falsely claim that the conditions for the EF were met! (No one claims that nature is mimicking intelligent agency when we see faces in clouds or ink blots. We are recognizing the high probability of our pattern recognition of certain patterns.)
The “missing distribution” is much more important that simply that there is something not known. It deals with a comparison of two “unknowns”. The EF, explicitly eliminative, also has an “unknown” of the “design” case. Where is explanation of the intelligent agent? ID itself seems to be a rehash of “we can explain the intelligent agent someday!”
But in fact the next presentation sets planned for that thread will demonstrate the mathematical reliability of the EF itself. It will show frequentist assumptions wherein the EF is highly unreliable. The main point is that the two missing pieces of information need to be compared, and whichever one outweighs the other points to the result—not the calculation of significance done in the EF. This is based on pure mathematics of Bayes Theorem. The EF, in its typical case, becomes only 50% “reliable” in terms of no false positives when the joint probability of the “missing distribution” causing the event is greater or equal to the joint probability of the intelligent agent causing the event in the rejection region. But without studying the intelligent agent’s probability of acting, you have no way of knowing if a small “missing distribution” is of overwhelming importance, or only a small and distant unknown. The key point is two unknowns—both agent activity and missing non-intelligent causes. Once again, when are you going to explain the missing probability of the intelligent agency in your case?
Then back to cooption frequency. Since you appear to ignore my points, I suggest that the reader go back and read my points about how different situations can easily have different known or knowable constraints. When you calculate the frequency (if you could do that) over all cases of the existence of a specific gene, you are not estimating the probability of that gene’s involvement in a specific case of possible cooption. You have not established that the conditions are similar. You need to establish why the situations are similar for any statistical significance to apply.
Then what is the “specification” that would be a result of any such specific study of the particular gene. I think it would be equivalent to the following:
Specification for explanatory filter: Flagellum structure, specifically involving Gene “x”.
(Fill in the blank “x”)
Now how is the probability of events in that particular class relevant? Just like the 500th coin toss after the last 499 tosses will produce a string of 500 bits that is very unlikely (10^-150), it could be very likely given the previous knowledge of the last 499 tosses (like 50%). That is why the EF requires an “independence” of the specification from the event. Does the specification above (or equivalent) look “independent of the event”?
It looks like you decided to take details out of the event, specific involvement of gene “x” (whatever that is) and call that your specification. It would be a “fabrication” in EF parlance. So either you have nothing of relevance to the explanatory filter, or you need to tell us what the “specification” would be.
[ 23. September 2003, 18:02: Message edited by: gedanken ]
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Nel
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posted 23. September 2003 18:07
Ged writes:
quote:
I’m not sure where you got the part about “nature can mimic intelligent agency”, because that was not really in that thread. Rather the point was that nature can create events that might appear to match similar patterns to those of intelligent agency.
You just said the same thing twice. Thats like saying I didn't say I killed my sister, I said I ended her life with a musical instrument.
Ged writes:
quote:
I might agree that nature can mimic intelligent agency, but that was not in that thread. In fact it was very important to recognize that these were not mimicking intelligent agency, but that they were creating false impressions of low probability for the “specified” pattern in the rejection region—thus causing ID enthusiasts to falsely claim that the conditions for the EF were met!
Perhaps this is a good place to show which processes you are talking about exactly?
Ged writes:
quote:
The “missing distribution” is much more important that simply that there is something not known. It deals with a comparison of two “unknowns”. The EF, explicitly eliminative, also has an “unknown” of the “design” case. Where is explanation of the intelligent agent? ID itself seems to be a rehash of “we can explain the intelligent agent someday!”
No we can explain the intelligent agent today. It is hypothesized that the intelligent agent is an advanced human-like intelligence. As to whats it's name, what does it like to eat, who cuts it's hair,here is a good discussion of how identifying design does not entail identifying the designer:
http://www.idthink.net/back/iden/index.html
This is all very basic stuff.
Ged writes:
quote:
But in fact the next presentation sets planned for that thread will demonstrate the mathematical reliability of the EF itself. It will show frequentist assumptions wherein the EF is highly unreliable.
I'm thinking of cross posting some of my points here into your thread (or a new one) unless I get bored. Basically, first things first, what the heck does it have to do with motive. But seriously, I would like to compare identifying the designer, hoping for future explanations, and the EF. I set out to show how the EF comes out as the most reliable tool to use when delineating design. Most likely I will respond to your new presentation there.
Ged writes:
quote:
The EF, in its typical case, becomes only 50% “reliable” in terms of no false positives when the joint probability of the “missing distribution” causing the event is greater or equal to the joint probability of the intelligent agent causing the event in the rejection region.
Basically I will focus on the major error of this logic, in this new thread, in that you could never identify the "missing distribution". That is a fatal error, I think, in your argument.
Ged writes:
quote:
But without studying the intelligent agent’s probability of acting, you have no way of knowing if a small “missing distribution” is of overwhelming importance, or only a small and distant unknown. The key point is two unknowns—both agent activity and missing non-intelligent causes. Once again, when are you going to explain the missing probability of the intelligent agency probability in your case?
In terms of identifying design, (i.e. actuallying finding a pattern indicative of intelligent agency), the probability of the intelligent agent acting is 1. As is the case for the designers of many things, including the builders of the pyramids.
Ged writes:
quote:
Then back to cooption frequency. Since you appear to ignore my points, I suggest that the reader go back and read my points about how different situations can easily have different known or knowable constraints.
Actually I have responded to each and every one of them. If you notice, there is no discussion of my brachyury example in any of Ged's replies.
Ged writes:
quote:
When you calculate the frequency (if you could do that) over all cases of the existence of a specific gene, you are not estimating the probability of that gene’s involvement in a specific case of possible cooption. You have not established that the conditions are similar. You need to establish why the situations are similar for any statistical significance to apply.
Actually, since co-option is say, changing that gene's cis-regulatory DNA or turning on a regulatory gene which turns on that gene, I am calculating the actual co-option event and the frequency of it. As well as comparing it to other co-option events.
Ged writes:
quote:
Now how is the probability of events in that particular class relevant. Just like the 500th coin toss after the last 499 tosses will produce a string of 500 bits that is very unlikely, it could be very likely given the previous knowledge of the last 499 tosses (like 50%). That is why the EF requires an “independence” of the specification from the event. Does the specification above (or equivalent) look “independent of the event”?
Calculating a co-option frequency doesn't require identfiying a pattern "independant of the event" except that the gene in question is performing differently in the descendant then it did in the ancestor. If we can see similar types of co-options in unrelated lineages, involving gene x, then we can get a feel for "co-optable genes".
Ged writes:
quote:
It looks like you decided to take details out of the event, specific involvement of gene “x” (whatever that is) and call that your specification. It would be a “fabrication” in EF parlance So either you have nothing of relevance to the explanatory filter, or you need to tell us what the “specification” would be.
The details are the actual functions of the gene in question. Same function across lineages implies conservation. Duplication events, followed by specialization or different function points to co-option.
[ 23. September 2003, 18:09: Message edited by: Nelson-Alonso ]
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Nel
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posted 23. September 2003 18:40
Nic writes:
quote:
It appears that Arabidopsis has *no* known dyneins whatsoever.
Actually, it appears that Arabidopsis does encode dynein.
Traffic. 2002 Dec;3(12):930-1.
Dyneins motor on in plants.
King SM.
quote:
A recent report based on analysis of the Arabidopsis genome suggested that angiosperms do not contain the dynein microtubule motor. However, examination of the whole genome shotgun sequence for rice (Oryza sativa) has revealed that four dynein heavy chains are present in this monocot, indicating that the apparent lack of these sequences in Arabidopsis is not a general feature of angiosperm genomic organization. These observations also suggest that, in contrast to an earlier proposal, flowering plants may indeed use standard dynein-driven mechanisms to perform cellular transport activities that, in other organisms, employ the dynein motor
As there are a number of dynein-like gene products, I would bet there is a dynein involved in mitosis in higher plants. I havn't read the paper you referenced concerning transport motors yet.
[ 23. September 2003, 18:47: Message edited by: Nelson-Alonso ]
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gedanken
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posted 23. September 2003 19:34
I thought we weren’t supposed to do quote by quote replies as the major content?
Alonso said:
quote:
Perhaps this is a good place to show which processes you are talking about exactly?
Perhaps this is a good time to read the thread in question.
quote:
Basically I will focus on the major error of this logic, in this new thread, in that you could never identify the "missing distribution". That is a fatal error, I think, in your argument.
I’m glad “you think”, but I suggest that you wait for me to complete presentation of the mathematics. (I have it written in Word heavily laden equations format—trying to decide how to present on ISCID, may need to make a PDF.) Then of course I would not suggest disagreeing with one thread in yet another thread. (I would just have to give a link to where the answer appeared—most confusing to the readers.)
But the basics are simple: Consider a frequentist assumption. (Alonso, you are not going to disagree with an “assumption” being made, are you?) The assumption is, as Dr. Dembski recognized, that there is a “missing distribution”, and I give that distribution a probability. That is the joint probability of this missed non-intelligent cause of the event in the “rejection region”. You can argue all you want about whether a given case might have such a missed “cause” in the analysis, but you can’t argue with the consequences of the mathematics if it occurred unless there is an error in the math.
Then consider a given joint probability of the designer acting to create an event in the specified “rejection region”. This is also given as a frequentist assumption. You can’t disagree with an assumption, again, though you might disagree that the assumption could occur. That is a separate issue, and you have to document a basis for that.
Now if the natural-non-intelligent causes were analyzed to have an extremely low probability, you can see that these analyzed causes as analyzed are basically irrelevant if there are two other causes of significantly higher probabilities. We weigh these two other causes, the “missing distribution” and “intelligent agent”. If they were equally likely to cause the event, then you can see that over a sequence of trials in which those frequentist assumptions were held true that half of the time the EF would produce an incorrect or “false positive”. (Once again it is best to wait for formal symbolic presentation, but you can see this intuitively.)
Alonso, as to the assumption of “advanced human-like intelligence,” how is it acting, and what are its motives for creating things like “flagella”? (Motive, means, and opportunity!) Remember in my mathematical presentation on reliability of the EF, it depends on the joint probability that the agent caused an action in the rejection region, not just the probability of the agent causing some event. (That’s why “motive” is important, because if those “advanced human-like intelligences” have no motive to create a flagella, they would still have very low joint probability of existing AND causing an event in the specific rejection region!)
Alonso, I can’t wait for your paper to be published! I’m sure the Raleans will be very happy reading your paper. (Or perhaps you don’t think that something like that could ever be a “scientific” quality paper?) In any case, remember to document how you arrived at the joint probability of the ET existing, and having motive to create the events in the specified “rejection region”.
As to calculating the cooption frequency “independent of the event”—this is an interesting way of avoiding the question. But of course the question was “what is your specification”? That is what “independent of the event” is referring to. I’m trying to stick to topic of this thread. If one is to draw any sort of implication, one must use some form of inference, either comparative or eliminative. (Of course I deny the reliability of the “eliminative”) But without one or the other, no inference has been drawn at all, and I thought that was the intent of calculating the “frequency”.
So what is the specification?
(I think the readers will have to recognize the changes of subject by reading my post and Alonso’s response, I’ll leave most of that to them.)
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yersinia
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posted 23. September 2003 19:37
Nelson writes,
quote:
As there are a number of dynein-like gene products, I would bet there is a dynein involved in mitosis in higher plants. I havn't read the paper you referenced concerning transport motors yet.
I was surprised that they hadn't found one myself. One would think it would be a tough thing to dispose of, since its involved in chromosome separation in mitosis. Your reference indicates that they still haven't found one in Arabidopsis as of 2002, mine as of 2003, although they have in other plants (monocots, a bit of a distance from Arabidopsis). Just goes to show that even fully sequenced genomes are not the end of the story with molecular homologs...particularly when the genomes are of model laboratory organisms, which are not really a random sample of biodiversity. E.g., short genomes are one preferred characteristic.
It's also possible that dynein exists but has diverged past ready identification via BLAST. This, again, would not be favorable for the prospects of retrieving sequence matches of accessory proteins.
[ 23. September 2003, 19:39: Message edited by: yersinia ]
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Nel
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posted 23. September 2003 19:44
Nic writes:
quote:
Your reference indicates that they still haven't found one in Arabidopsis as of 2002, mine as of 2003
Actually, it looks like they have been found, only some not published and some published:
quote:
Jellbauer,S., Scali,M., Vignani,R., Moscatelli,A. and Cresti,M.
TITLE Molecular cloning of PCR-fragments codifying for a putative
dynein
heavy chain in Arabidopsis thaliana
JOURNAL Unpublished
and
quote:
ACCESSION AAM63499 putative dynein light chain protein [Arabidopsis
thaliana].
AUTHORS Haas,B.J., Volfovsky,N., Town,C.D., Troukhan,M.,
Alexandrov,N.,
Feldmann,K.A., Flavell,R.B., White,O. and Salzberg,S.L.
TITLE Full-length messenger RNA sequences greatly improve genome
annotation
JOURNAL Genome Biol. 3 (6), RESEARCH0029 (2002)
[ 23. September 2003, 21:59: Message edited by: Nelson-Alonso ]
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Nel
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posted 23. September 2003 20:10
Ged writes:
quote:
Perhaps this is a good time to read the thread in question.
But I can't find any indication of a process that can mimic the low probability patterns of intelligent agency such that we would equally infer both (or neither).
Ged writes:
quote:
I’m glad “you think”, but I suggest that you wait for me to complete presentation of the mathematics. (I have it written in Word heavily laden equations format—trying to decide how to present on ISCID, may need to make a PDF.) Then of course I would not suggest disagreeing with one thread in yet another thread. (I would just have to give a link to where the answer appeared—most confusing to the readers.)
I don't see how you can rescue your "missing distribution" argument without first identifying them. Alluding to future ones doesn't quite cut it. All you are really doing is showing that the design inference is falsifiable.
Ged writes:
quote:
Alonso, as to the assumption of “advanced human-like intelligence,” how is it acting, and what are its motives for creating things like “flagella”? (Motive, means, and opportunity!)
These questions do not really detract from the actual delineation of design. Here is another article that explains this better than I can.
http://www.idthink.net/back/mech2/index.html
I don't really see how you connect, logically, motive in all of this. As to that question, I would say the motive is to evolve something humanoid. Although really, as Francis Crick has mentioned, how do we really know the motive behind any intelligent design, the atom bomb, science itself,etc.
Ged writes:
quote:
Alonso, I can’t wait for your paper to be published! I’m sure the Raleans will be very happy reading your paper. (Or perhaps you don’t think that something like that could ever be a “scientific” quality paper?) In any case, remember to document how you arrived at the joint probability of the ET existing, and having motive to create the events in the specified “rejection region”.
None of this is relevant, since any paper I write would be about how one can distinguish design from non-telic processes.
Ged writes:
quote:
As to calculating the cooption frequency “independent of the event”—this is an interesting way of avoiding the question. But of course the question was “what is your specification”? That is what “independent of the event” is referring to. I’m trying to stick to topic of this thread. If one is to draw any sort of implication, one must use some form of inference, either comparative or eliminative. (Of course I deny the reliability of the “eliminative”) But without one or the other, no inference has been drawn at all, and I thought that was the intent of calculating
the “frequency”.
The only pattern I really need to show is that the gene is acting differently in the ancestor then in the descendant. I don't really see how this is hard to glean from my posts, since I specifically showed an example of how one would do it.
[ 23. September 2003, 20:11: Message edited by: Nelson-Alonso ]
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gedanken
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posted 23. September 2003 20:20
Alonso, what are the “processes” of construction of a cloud face, if we should happen to look into the sky and remark “I see a face”? I think they are implicit, even if not explicitly demonstrated, and likewise for random geological processes making a structure that happens to match a human form in some regard.
My point in that thread may have some relevance here as well. The point was that the “specification” could not be given in such a way that it did not have high probability of being met. That was not a “false positive”. If you read the thread, you would know that over and over I pointed out that certain cases were failures of a different type, not a failure of a “false positive”. (The notes are repeated multiple times.)
The failure was that there was a high probability of meeting the “specification”. Thus the EF does NOT “infer design”. (A false negative). Yet the ID enthusiasts were touting the example as one in which one could infer design? (And presuming that the EF did so!!!!) (And you can search for multiple exclamations there to see when I said about the same thing.)
I think it may have relevance here as well. The point would be that there is no “inference” even by “Explanatory Filter” standards to be had. So don’t claim that an inference has been drawn.
However, in that thread, if you think that the terms of the EF have been met, show the calculations. Likewise here, show the calculations. Do so even with preliminary numbers, and show how one could justify them in the future. But show the mathematics of inference as well—show what is inferred.
With regard to my assumptions I find this very odd coming from someone who just suggested that I could assume intelligent agents processes creating a flagellum. I assume that you are throwing my own request for details back in my face, so to speak, as opposed to actually meaning that I can’t make the assumption.
But in my case I am not trying to develop a new method of inferring design that I am certain will be useful. I am first simply cataloging how and when the existing procedure fails to be reliable—it fails to be reliable under the specified conditions. That does not need “rescue”, it is a mathematical derivation. After that, we can see if modifications will improve it, but even such modifications may fail to be useful.
[ 23. September 2003, 22:12: Message edited by: gedanken ]
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Nel
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posted 23. September 2003 20:24
Ged writes:
quote:
Alonso, what are the “processes” of construction of a cloud face, if we should happen to look into the sky and remark “I see a face”? I think they are implicit, even if not explicitly demonstrated, and likewise for random geological processes making a structure that happens to match a human form in some regard.
There is a difference between seeing a cloud face (perhaps specified but not complex) and seeing "Happy Birthday Ged!" written across the sky (with the plane long gone mind you). I would certainly not infer intelligent design from the former, definitely from the latter.
Ged wrote:
quote:
My point in that thread may have some relevance here as well. The point was that the “specification” could not be given in such a way that it did not have high probability of being met. That was not a “false positive”. If you read the thread, you would know that over and over I pointed out that certain cases were failures of a different type, not a failure of a “false positive”. (The notes are repeated multiple times.)
But what I'm interested in is those processes that would cause things like motors. Why is the design inference equal to a non-design inference in this case? Would you really infer design from an ambigious cloud face?
I'm perfectly comfortable with false negatives.
[ 23. September 2003, 20:39: Message edited by: Nelson-Alonso ]
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gedanken
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posted 23. September 2003 20:41
I believe that I have far exceeded my allotment for posting, and may be in trouble for answering this.
But if you read that thread, you will see that I fully accept that one can “infer design”. I accept fully that one can infer design of the Easter Island figures—and also of “Happy Birthday Ged!”. (If you had read the thread, you would realize that. Why not actually read it?)
I too am interested in how one could actually differentiate a human or even other-worldly construction. My point in that thread is that the strict conditions of the EF were not being met—not that the cases could not be differentiated. So the EF fails to be reliable in various ways. One of the failures is ID enthusiasts claiming that the conditions of the EF have been met, when in fact they have not.
(Then as a different condition, under different circumstances, the EF was producing false positives—but this was a different case!)
The same problem occurs in this thread. The “frequency” measurement has not been justified as being statistically significant with regard to anything that anyone is trying to infer. Working out the actual probability theory will show unexpected results if you don’t understand it.
[ 23. September 2003, 20:42: Message edited by: gedanken ]
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