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Author
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Topic: Wells' Molecular Phylogenies
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Ron Okimoto
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posted 05. December 2003 15:15
Peter:
Your last post is pretty useless for making the point that you are trying to make.
You have already given up the store because you claim that your model requires that more similar species have more similar genomes and would have more similar NRMs. I've asked you to try and generate the nesting found among all vertebrates. This was to get you to realize just what you have said. There must have been a nesting inherent in the genomes already before any of the NRMs mutated. What is the reason for the original nesting? Why do we group with primates, mammals, reptiles, amphibians, and fish in a nested pattern of similarity? It cannot be due to NRMs.
You can't explain the nesting even among the apes. You have to claim that fixation of NRMs is not dependent on their observed mutation rate. If you have 5 taxa and just 5 NRMs what is the probability that the NRMs are fixed in each population in just such a way that it looks like common descent happened. Gibbons would have the least similarity at these positions and humans and chimps would have the most similarity at the 5 NRMs. What is the probability that say chimps and humans had all the same mutations at the NRMS, gorrilas 4 out of 5 with humans and chimps, orangs with 3 out of 5 and gibbons with only one out of 5? Not only this, but they have to be nested similarities not just gross similarities. That one that the gibbons have similar to humans and chimps is also shared with gorillas and orangs. The three that the orangs have in common with chimps are found in the 4 that gorillas have in common. They form a nested similarity.
Sure it isn't as neat as this, but this is basically what you face. You have to generate a nested similarity, not just a gross similarity between all the extant species on earth.
You aren't going to do it by invoking Noah's ark. Because no matter how much more likely that you will get fixation of all those mutations that you require, you have to have those mutations occur in these small populations and you have to have them fixed in a nested similarity instead of a random similarity. Some preferred cites of mutation do mutate at frequencies as high as 1 in 10,000. Will you get just the right million or so genomic mutations in the survivors of the ark and get them all fixed in just the right pattern to do you any good? Just think how many mutations you are talking about in just the great apes? You have about a 5-7% difference in sequence between gibbons and humans. You are talking about 3 billion nucleotide positions in the genome. How many NRMs are you thinking about and how are you going to lay down the pattern that you need? This idea just will not fly. Say that gibbons were clean animals and that there were 12 or 14 of them on the ark. What is the probability that the right mutations would even occur in their population if the rate was as high as 1 in 10,000 let alone the ones that are occurring much less frequently. Humans and the other apes would also be mutating the NRM positions and you know you only had 4 pairs of humans, so what is the chance that just the right NRMs got mutated and fixed in the population to complement the gibbon, chimp, gorilla, and orang mutations to make it look like they all were derived from a common ancestor? Now add in each successive species until you account for all the life on earth.
The molecular nesting is the biggest reason that guys like Dembski have to admit that common descent is a fact of nature. It is the simplest means of generating what we observe and we have no problems determining that the mechanisms are alive and well and working in nature as we speak. You had parents, new species are derived from existing species. Molecular evolution is a frieght train that you can't stop, just neutral drift will change genomes with time.
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peter borger
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posted 08. December 2003 04:05
Thanks for the usual references. I read them ages ago, I know their content, and I know what assumptions are valse to come to such results. In a little chat with Dr Page (the self-acclaimed primatologist) on the EvC forum I already demonstrated that the evolutionary method of data analysis is invalid.
See:
http://www.evcforum.net/ubb/Forum5/HTML/000172-2.html
From your reference: "The patterns of point mutation are indistinguishable, suggesting considerable stability over evolutionary time (40–60 million years)."
And you are not surprised? No variation on silent positions? No molecular evolution? You have to come up with better references, Pim. This is the opposite from compelling. It is NRM.
pb
[ 08. December 2003, 05:53: Message edited by: peter borger ]
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peter borger
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posted 08. December 2003 05:18
Ron, first I thought that you still do not get the point I am trying to make. But then you simply state that "your model requires that more similar species have more similar genomes and would have more similar NRMs." So I have to conclude that you indeed understand what I am trying to
say. The multipurpose genomes (MPG) have been designed so that they are able to change in order to adapt easily (adaptation is a prerequisite for life). Adaptation is achieved through shuffling or
duplication of existing DNA elements. It is on the level of gene expression, not on the level of DNA content. DNA content is not important for adaptive phenotypes. That is in a nutshell the first statement of GUToB.
Apparently the nesting found among all vertebrates has its origin in these MPG. Nesting of mutations in related MPG is a prediction of GUToB, since same (similar) DNA sequences and same (similar) biochemistry will spawn same (similar) mutations. So if we compare the same essential DNA sequence (say DNA elements coding for histons, or ubiquinin) than it is expected that part of the mutations will line up according to these rules. These are the socalled NRM, and may give the illusion of common descent. Of course these NRM are interspersed (sometimes) with random mutations. As should be known, I do not deny that RM occur, but they do not contribute to evolution. Usually the RM are neutral or detrimental. Even Kimura agrees with that. (And his ideas have recently been revived to get an grip on genetic redundancies, an observation in complete agreement with GUToB, not NDT).
Furthermore, the nesting can be a result of a biased evolutionary analysis. As I have demonstrated in the GUToB thread, the pseudogene globin --which is eagerly presented as proof for common descent-- does not at all show common descent if you consider the data from a different stance. Maybe the bias is already in the analysis programs. I would not be surprised. Alternatively NRMs in MPGs presents a elegant explanation.
If the probability that the NRMs are fixed in each population in just such a way that it looks like common descent would play a role in speciation I could agree with you that gibbons would have the least similarity at these positions and humans and chimps would have the most similarity at the 5 NRMs. However, chance does not play a role in the generation of new species so I do not see a role for your probability that chimps and humans had all the same mutations. It is all or none. You cannot have a bit of a species. It is either a human or a chimp, not a bit of both, or an in between. That is also why all assumed transition forms do not exist. Apparently we do not understand speciation with our 21st century knowledge. From the GUToB it is easy to explain since the MPGs have been designed. The rest of the observations are explained by NRM and shuffling. And the shuffling of the genomes is not nested, bur rather Non random (I mean the inversion and translocations). The position effects of transposable DNA elements determine the variation within the species, not the mutations.
Maybe I am going to do it by invoking Noah's ark, but you are going to do it by invoking bottlenecks. It is the same.
Over time fixation of NRM may occur anyway, since DNA will strive to the most favourable state. And will --due to entropy-- degenerate over time. No selection will work against that mechanism, since selection is always selection against and at the level of reproduction rate.
And you say that “the molecular nesting is the biggest reason that guys like Dembski have to admit that common descent is a fact of nature.” I do not mind what guys like Demski admit, they are mathematicians, not molecular biologists. And math --for all matter-- is a tautology.
[ 08. December 2003, 05:24: Message edited by: peter borger ]
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Ron Okimoto
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posted 08. December 2003 08:27
Peter:
You still do not get it. Generate your MPGs without resorting to common descent. It is really that simple. You can't do it. How do the MPGs just happen to fall into a pattern of similarity to make it look like common descent happened. Just do this for vertebrates. Why is the mammalian MPG nested within reptiles. Why is the reptile MPG nested within fish? It looks like your designer designed the fish MPG before he designed the amphibian MPG before he designed the reptile MPG etc. You have to make your model look so much like common descent that it doesn't matter.
Your ape example is still off. You still don't get the fact that your NRMs will not form the nested heirarchy among apes. What was the intitial sequences at these NRMs and how did just the ones mutate to get the nested similarity pattern. Just try it for 5 NRMs in the ape taxa. Start out with a sequence say there is an T at all 5 NRM positions (T T T T T). How do you get something like T T T T C for gibbons, T T T C C for orangs, T C C C C for gorillas and C C C C C for chimps and humans. Remember that these five sites are scattered around the genome. What is the chance that this pattern would occur rather than a non nested pattern? Multiply this by millions of positions in the genome and what do you get? Your idea just won't work even for something as simple as this example. You have to start invoking a different MPG for each species, and once you do that you might as well give up on NRMs because it is obvious that each MPG has to be nested in the same pattern that it is generating. This will not work for the apes and it definitely will not work for the massive nesting found among vertebrates.
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peter borger
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posted 08. December 2003 09:11
You ask "Why is the mammalian MPG nested within reptiles. Why is the reptile MPG nested within fish? But you already know the asnwer: "It looks like the designer designed the fish MPG before he designed the amphibian MPG before he designed the reptile MPG etc." That`s Genesis, mate.
Your ape example is still off. You still don't get the fact that your NRMs will not form the nested heirarchy among apes. What was the intitial sequences at these NRMs and how did just the ones mutate to get the nested similarity pattern. Just try it for 5 NRMs in the ape taxa. Start out with a sequence say there is an T at all 5 NRM positions (T T T T T). How do you get something like T T T T C for gibbons, T T T C C for orangs, T C C C C for gorillas and C C C C C for chimps and humans.
You will get this pattern through NRM as a function of time:
C C C C C C original sequence
C C T C C C original sequence (OS) after X time
C C T T C C OS after 2X time
C C T T T C OS after 3X time
C C T T T T OS after 4X time, etc
The chance that this pattern will occur is almost 1, since it is a non-random mechanism. In a MPG the mutations are determined by the sequence and not by chance. Subject to the laws of nature it is almost inevitable to arrive at the same sequences as time passes by. Selection is not involved. Pim`s Drosophilas example nicely demonstrates the power of NRM. After "40 - 60 million" years all NRM positions are saturated (and have mutated). It gives the impression as if no change occured during this tremendous amount of time. Howver, all NRM have changed to their most favorable state and therefore all mutations are on the same location. So, it gives the impression of a highly stable DNA sequence, kept in the genome through purifying selection (that is the evo explanation). But it is not, it is as unstable as the rest of the genome and this part is simply in ground state.
pb
[ 08. December 2003, 09:35: Message edited by: peter borger ]
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Ron Okimoto
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posted 08. December 2003 10:50
quote:
You ask "Why is the mammalian MPG nested within reptiles. Why is the reptile MPG nested within fish? But you already know the asnwer: "It looks like the designer designed the fish MPG before he designed the amphibian MPG before he designed the reptile MPG etc." That`s Genesis, mate.
Genesis doesn't fit the pattern. It has whales and birds coming before land vertebrates. That is not the correct order found in the genomes.
quote:
Your ape example is still off. You still don't get the fact that your NRMs will not form the nested heirarchy among apes. What was the intitial sequences at these NRMs and how did just the ones mutate to get the nested similarity pattern. Just try it for 5 NRMs in the ape taxa. Start out with a sequence say there is an T at all 5 NRM positions (T T T T T). How do you get something like T T T T C for gibbons, T T T C C for orangs, T C C C C for gorillas and C C C C C for chimps and humans.
You will get this pattern through NRM as a function of time:
C C C C C C original sequence
C C T C C C original sequence (OS) after X time
C C T T C C OS after 2X time
C C T T T C OS after 3X time
C C T T T T OS after 4X time, etc
The chance that this pattern will occur is almost 1, since it is a non-random mechanism. In a MPG the mutations are determined by the sequence and not by chance. Subject to the laws of nature it is almost inevitable to arrive at the same sequences as time passes by. Selection is not involved. Pim`s Drosophilas example nicely demonstrates the power of NRM. After "40 - 60 million" years all NRM positions are saturated (and have mutated). It gives the impression as if no change occured during this tremendous amount of time. Howver, all NRM have changed to their most favorable state and therefore all mutations are on the same location. So, it gives the impression of a highly stable DNA sequence, kept in the genome through purifying selection (that is the evo explanation). But it is not, it is as unstable as the rest of the genome and this part is simply in ground state.
pb
This doesn't explain the pattern. This explanation doesn't work for independently evolving "kinds." This explanation would only work if common descent were true. Think about it. If this is the pattern that humans have, what is to keep chimps from having this pattern:
C C C C C C Time period 0
T C C C C C Time 1
T C T C C C Time 2
T C T C T C Time 3
T T T C T C Time 4
And why would some species be stuck at some previous time period. Gibbons would be time 1, orangs would be time 2 and gorillas would be time 3. If all these species were created around the same time, why do they form the nested pattern of similarity?
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Pim van Meurs
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posted 08. December 2003 12:51
Peter:
quote:
You ask "Why is the mammalian MPG nested within reptiles. Why is the reptile MPG nested within fish? But you already know the asnwer: "It looks like the designer designed the fish MPG before he designed the amphibian MPG before he designed the reptile MPG etc." That`s Genesis, mate.
First of all Genesis seems to get the order wrong but then again, it's not a scientific text either so we should not put too much weight on its correctness. If the 'designer' designed the fish before the amphibian before the reptile, it seems to suggest that the designer had to do the following to get nested hierarchies:
1. Wait a few million years or more between design events
2. Use pre-existing genome and tinker with it to create the appearance of common descent.
As Ron has argued, without this, no appearance of common descent would arise.
Peter:
quote:
From your reference: "The patterns of point mutation are indistinguishable, suggesting considerable stability over evolutionary time (40–60 million years)."
And you are not surprised? No variation on silent positions? No molecular evolution? You have to come up with better references, Pim. This is the opposite from compelling. It is NRM.
Actually as the references show there IS molecular evolution. Did you read the paper?
It may be that you misinterpreted the meaning of "the patterns of point mutations are indistinguishable" to mean no variation on silent positions, no molecular evolution. The paper shows otherwise.
quote:
Relative Evolutionary Stability of Mutation Patterns. The D. virilis species group and the D. melanogaster species subgroup represent both parts of the two great subgenera in the Drosophila radiation. The D. melanogaster species subgroup is in the subgenus Sophophora, whereas the D. virilis species group is in the subgenus Drosophila. These subgenera are estimated to have diverged 40–60 million years ago (18), yet their patterns of point mutation are indistinguishable as judged from the relative frequencies of the six types of point mutation in the two Helena datasets. This finding is reassuring, because it indicates a certain stability in the point mutation pattern through time.
I doubt that you want to call this 'NRM'. What is interesting is that there is definitely a difference in the frequencies of different nucleotide substitutions.
quote:
This hypothesis would imply that the pattern of point mutation is adapted to the nature of the genetic code. An alternative hypothesis to explain a conserved pattern of point mutation is that the pattern is mainly determined by properties intrinsic to the chemical composition, structure, and metabolism of DNA, and less so by natural selection. This alternative would imply that the genetic code is adapted to the pattern of point mutation rather than the other way around.
See for instance here how such biases in substitution frequencies are used in phylogenetic analyses.
or this paper
Heterogeneity of nucleotide frequencies among evolutionary lineages and phylogenetic inference., Rosenberg MS, Kumar S.Mol Biol Evol. 2003 Apr;20(4):610-21.
quote:
A major assumption of many molecular phylogenetic methods is the homogeneity of nucleotide frequencies among taxa, which refers to the equality of the nucleotide frequency bias among species. Changes in nucleotide frequency among different lineages in a data set are thought to lead to erroneous phylogenetic inference because unrelated clades may appear similar because of evolutionarily unrelated similarities in nucleotide frequencies. We tested the effects of the heterogeneity of nucleotide frequency bias on phylogenetic inference, along with the interaction between this heterogeneity and stratified taxon sampling, by means of computer simulations using evolutionary parameters derived from genomic databases. We found that the phylogenetic trees inferred from data sets simulated under realistic, observed levels of heterogeneity for mammalian genes were reconstructed with accuracy comparable to those simulated with homogeneous nucleotide frequencies; the results hold for Neighbor-Joining, minimum evolution, maximum parsimony, and maximum-likelihood methods. The LogDet distance method, specifically designed to deal with heterogeneous nucleotide frequencies, does not perform better than distance methods that assume substitution pattern homogeneity among sequences. In these specific simulation conditions, we did not find a significant interaction between phylogenetic accuracy and substitution pattern heterogeneity among lineages, even when the taxon sampling is increased.
Peter; . Selection is not involved. Pim`s Drosophilas example nicely demonstrates the power of NRM. After "40 - 60 million" years all NRM positions are saturated (and have mutated). It gives the impression as if no change occured during this tremendous amount of time.
Peter, it seems you misread my drosophila example. Read beyond the abstract to realize that your conclusions do not seem to match the paper's data. No power of NRM was really demonstrated. So the question is, are there any examples of NRM that CAN be demonstrated? Especially NRM which affects phylogeny, somehow the biased nucleotide substitution rates do not seem to be enough to affect the common descent.
[ 08. December 2003, 13:16: Message edited by: Pim van Meurs ]
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peter borger
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posted 09. December 2003 04:00
You say that "It seems you misread my drosophila example. Read beyond the abstract to realize that your conclusions do not seem to match the paper's data."
Dear Pim, if the pattern of point mutations between species is indistinguishable that coud mean: common descent or common mechanism. Even if there is molecular evolution in this region it would not undo the phenomenon that the mutations are indisinguishable. You infer common descent from it. I infer a common mechanism from such --and other-- data. It should be noted that even the shared HERVs (for instnace HERV-K) seem to have aquired mutations independent of common descent on the same spot. (see Costas J et al, 2000). Why is it that over and over the same location in the DNA is involved? It is becasue they are reintegrated in the same location the DNA, This has been demosntraetd for integrated plasmids in bacteria. Why do I have to repeat myself over and over? NRM is a fact. It invalidates the best molecular argument for common descent.
And again you ask me for a examples of NRM. I already demonstrated (evidence beyond any doubt) that in Drosophila`s 1g5 gene the mutations are introduced on exactly the same spot and line up to give the impression of common descent. Thus far, you didnot comment on it (my final mail in the GUToB thread). I will try to get it published, so I can refer to it.
pb
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Pim van Meurs
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posted 10. December 2003 12:59
quote:
Pim: You say that "It seems you misread my drosophila example. Read beyond the abstract to realize that your conclusions do not seem to match the paper's data."
Peter:Dear Pim, if the pattern of point mutations between species is indistinguishable that coud mean: common descent or common mechanism. Even if there is molecular evolution in this region it would not undo the phenomenon that the mutations are indisinguishable. You infer common descent from it. I infer a common mechanism from such --and other-- data.
What I pointed out was that your conclusion based on reading a line in the abstract was erroneous.
In fact when you stated that And you are not surprised? No variation on silent positions? No molecular evolution? You have to come up with better references, Pim. This is the opposite from compelling. It is NRM. you seem to be arguing something NOT supported by the paper. In fact there IS molecular evolution.
What the paper shows is that the 'distribution' that is the statistical nature of these mutations are quite similar. I understand that you claim a common mechanism, as do I, namely variations combined with heritability. So far the evidence for your common mechanism seems to be lacking other than that you alternatively suggest the such common mechanism interferes with phylogeny or that it leads to the same phylogeny as expected from common descent.
Without further details on these 'non random' mutations and their mechanisms of how they achieve the observed distributions of nucleotides, I am afraid that NRM is not much of a scientific alternative.
You claim that NRM is a fact and I agree, mutations are not random in nature but your claim that it invalidates "the best molecular argument for common descent" seems to once again go against common knowledge. For instance I cited work which looked at non homogeneous nucleotide substitution rates and showed that "We found that the phylogenetic trees inferred from data sets simulated under realistic, observed levels of heterogeneity for mammalian genes were reconstructed with accuracy comparable to those simulated with homogeneous nucleotide frequencies"
So far I have to but conclude that the evidence supporting your claims, in whatever form, seem to be lacking and that despite various people requesting, you have yet to support that NRM "invalidates the best molecular argument for common descent".
So lets at least establish that Peter's quote from the abstract had no reference to NRM.
You reference a paper by Costas but perhaps you could provide us with more detailed references such as the title, or the publication?
I found the following paper "Characterization of the Intragenomic Spread of the Human Endogenous
Retrovirus Family HERV-W" Mol. Biol. Evol. 19(4):526–533. 2002
which seems to give little support to Peter's ideas.
Okay to the Costas 2000 paper which I interpret to be Evolutionary History of the Human Endogenous Retrovirus Family ERV9 by Javier Costas, and Horacio Naveira in Molecular Biology and Evolution 17:320-330 (2000)
quote:
In view of the extended period of ERV9 activity within primate genomes as well as its putative discontinuous transpositional dynamics, it is likely that some ERV9 elements retained its transpositional activity after the split of great apes. Thus, the presence of a functionally transposing subset of ERV9 in the human lineage, as described for HERV-K (Medstrand and Mager 1998 ), may be more probable than it is for other types of ERV sequences.
Other than a reference to other papers, Costas paper seems to not be relevant to HERV-K afaik.
But there is this paper 'Human-Specific Integrations of the HERV-K Endogenous Retrovirus Family by Patrik Medstrand and Dixie L. Mager in Journal of Virology, December 1998, p. 9782-9787, Vol. 72, No. 12
quote:
Several distinct families of endogenous retrovirus-like sequences (HERVs) exist in the genomes of humans and other primates. One of these families, the HERV-K group, contains members that encode functional proteins and that have been implicated in the etiology of insulin-dependent diabetes mellitus (IDDM). Because of potential functional and disease relevance, it is important to determine if there are HERV-K-associated genetic differences between individuals. In this study, we have investigated the divergence and evolutionary age of HERV-K long terminal repeats (LTRs). Thirty-seven LTRs, taken primarily from random human clones in GenBank, were aligned and grouped into nine clusters with decreasing sequence divergence. Cluster 1 sequences are 8.6% divergent, on average, whereas cluster 9 LTRs, represented by the LTRs of the fully sequenced HERV-K10 clone, show an average of only 1.1% divergence from each other. The evolutionary age of 18 LTRs from different clusters was then investigated by genomic PCR to determine presence or absence of the retroviral element in different primate species. LTRs from clusters of higher divergence were detected in monkeys and apes, whereas LTRs in clusters with lower divergence were acquired later in evolution. Notably, LTRs of cluster 9 were found only in humans at all nine loci examined. Genomic Southern analysis with an oligonucleotide probe specific for cluster 9 LTRs suggests that HERV-K elements with this type of LTR expanded independently in the genomes of humans and the great apes. This is the first report of endogenous retroviral integrations that are specific to humans and indicates that some HERVs have amplified much later than previously thought. These elements may still be actively transposing and may therefore represent a source of genetic variation linked to disease development
Perhaps Peter can provide a better reference to demonstrate his claims, perhaps with some examples that support his NRM scenario?
It should be noted that even the shared HERVs (for instnace HERV-K) seem to have aquired mutations independent of common descent on the same spot. (see Costas J et al, 2000). Why is it that over and over the same location in the DNA is involved? It is becasue they are reintegrated in the same location the DNA, This has been demosntraetd for integrated plasmids in bacteria. Why do I have to repeat myself over and over? NRM is a fact. It invalidates the best molecular argument for common descent.
I also looked at your GUTOB reference
quote:
Sequences from Schmidt and Tautz (PNAS 1997)
I had some problems finding this until I realized the misspelling in Schmid.
Peter argued elsewhere
quote:
1) the gene does not change fast (most mutations are in the introns). It is almost stable within the D mel population.
Things get a bit confusing since their figure 1 is a random subsample of intron/exon data. Starting at position 141 and ending at 922.
To understand the polymorphism argument, I refer to for instance This paper
To see the theoretical foundations link
[ 11. December 2003, 01:42: Message edited by: Pim van Meurs ]
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peter borger
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posted 15. December 2003 07:03
O I see,
the selective bottleneck sweep thing again.
Nice try and Thanks.
pb
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peter borger
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posted 15. December 2003 07:30
quote:
What I pointed out was that your conclusion based on reading a line in the abstract was erroneous.
In fact when you stated that And you are not surprised? No variation on silent positions? No molecular evolution? You have to come up with better references, Pim. This is the opposite from compelling. It is NRM. you seem to be arguing something NOT supported by the paper. In fact there IS molecular evolution.
Pim, you should realise that changes at the molecular level in DNA is not equivalent with molecular evolution. I agree that there is genetic change in these regions: It is non-random genetic change in approx 50% of mutations and that will give the impression of common descent. And as long as you cannot provide a tool to discriminate between common descent and common mechanism, I take such examples as evidence of a common mechanism.
For a sequences analysis of Herv-W sequences see Costas, J. Mol Biol Evol 2002, 19(4):526-33. Of course you have to do it yourself, since the discussion is subject to standard ET. However, you will find that almost all polymorphisms involve exactly the same positions, while the nucleotides and/or type of mutations vary (point or indels). That is quite compelling for NRM2. Don`t you think so?
pb
[ 15. December 2003, 07:36: Message edited by: peter borger ]
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Ron Okimoto
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posted 15. December 2003 10:45
quote:
Peter wrote: Pim, you should realise that changes at the molecular level in DNA is not equivalent with molecular evolution. I agree that there is genetic change in these regions: It is non-random genetic change in approx 50% of mutations and that will give the impression of common descent. And as long as you cannot provide a tool to discriminate between common descent and common mechanism, I take such examples as evidence of a common mechanism.
For a sequences analysis of Herv-W sequences see Costas, J. Mol Biol Evol 2002, 19(4):526-33. Of course you have to do it yourself, since the discussion is subject to standard ET. However, you will find that almost all polymorphisms involve exactly the same positions, while the nucleotides and/or type of mutations vary (point or indels). That is quite compelling for NRM2. Don`t you think so?
pb
You keep missing the point that this will not generate the observed nested similarity. Two lineages may evolve at these sites in one direction, but a third outgroup species will tell you that the direction is random in relation to the pattern. You can't predict which NRM will be fixed in what lineage. You only know that certain ones are more likely. The simple ape example should tell you that your NRMs are not going to work to explain all the taxa that exist. Not only that, but you have to allow for the time it takes to fix these NRMs in the particular pattern that you need them in. Do you have enough time for the millions of NRMs that you would predict to be in just the ape group (humans, chimps, gorillas, orangs, and gibbons)?
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Pim van Meurs
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posted 15. December 2003 12:17
Peter: Pim, you should realise that changes at the molecular level in DNA is not equivalent with molecular evolution. I agree that there is genetic change in these regions: It is non-random genetic change in approx 50% of mutations and that will give the impression of common descent. And as long as you cannot provide a tool to discriminate between common descent and common mechanism, I take such examples as evidence of a common mechanism.
As I have shown non randomness in mutations did not make a difference for the inference of common descent. But Peter's comments show that his common mechanism is nothing different from common descent UNTIL he can propose why these common mechanisms would lead to erroneous common descent inferences. As Ron and others have so clearly shown, common mechanisms do NOT explain the observed data.
So until Peter can show some supporting evidence all we have is his claim, unsupported so far, that NRM exist which would lead to erroneous inferences of common descent. Until Peter can explain all the data, we will have to reject his claims.
Peter:
For a sequences analysis of Herv-W sequences see Costas, J. Mol Biol Evol 2002, 19(4):526-33. Of course you have to do it yourself, since the discussion is subject to standard ET. However, you will find that almost all polymorphisms involve exactly the same positions, while the nucleotides and/or type of mutations vary (point or indels). That is quite compelling for NRM2. Don`t you think so?
If NRM2 is polymorphisms and selection then that would explain exactly the same positions. I fail to see how Peter thinks polymorphism is relevant to the discussion since their mechanisms seem to be quite well understood. What Peter sees here is the effect of selection in action. And before Peter points out that selection does not play role in these neutral areas let me point out that polymorphisms combined with selection in other parts of the genome help understand the spread of these 'neutral' mutations.
Lets say there are two polymorphisms and in one of them a benficial mutation arises in another part of the genome. This variant will spread quickly through the population and with it the mutations in the neutral area. Sort of a hitchhiking.
Nothing really about NRM or no real problems for common descent here.
And really no evidence that Peter's common mechanism, whatever that may be, has any relevance here. Unless of course the common mechanism is common descent.
Common descent is the logical outcome of hereditary changes, even at the species scale we all have our grandparents and great-grandparents. Common descent is not an illusion but a fact strengthened beyond the species level (and with polymorphisms we are looking at the species) by molecular data, fossil records and other data. All of which strongly support common descent.
I am looking forward to a better explanation of these data by Peter though.
[ 15. December 2003, 12:21: Message edited by: Pim van Meurs ]
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peter borger
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posted 16. December 2003 04:42
From your reference (Clark AG, PNAS USA 1997), about a theoretical model for shared polymorphisms:
"Formally, shared polymorphisms may arise either when there was a polymorphism in the population ancestral to the two species examined today, and that polymorphism has been maintained through the two distinct species` lineages, or by more recent parallel generation of similar alleles"
In other words, the author says that either it has a common origin through common descent or through common mechanism (=NRM). Next he says that it may be "extremely unlikely" that multiple parallel mutations occur. It should be noted, however, that it is only extremely unlikely under his evolutionary (outdated) assumption that mutations are introduced at random only. As I have demonstrated in several organisms now, mutations are not random, and commonly the same locations are involved. As a matter of fact I can substantiate that for almost all discussed sequences.
A close look at his model demonstrates that it assumes randomness and neutrality of mutations. And, the long lived polymorphism suppose to have been maintained by natural selection (page 7730). Neutral selection? Neutral selection is nothing but an oxymoron and like the 1g5 gene (that also involved neutral selection to explain it in an evolutionary way) demonstrates the NDT to be false. Even Clarks model is not able to save the day for the NDT, since observed and expected polymorphism are not superimposed. Nice try, but it doesn`t work.
So, still you cannot discriminate between a common mechanism or common descent. I was expecting such data anyway, since closely related organisms (where you find this phenomenon) have closely related MPGs.
pb
[ 16. December 2003, 04:48: Message edited by: peter borger ]
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peter borger
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posted 16. December 2003 05:00
Ron says that I "keep missing the point that this will not generate the observed nested similarity". But of course I do not agree with that, since the observed nested similarities is only nested in closely related MPGs. A reanalyis of the globin pseudogene (see GUTOB thread) demonstrtaes that the great apes have a similar MPG and thus also have similar NRM (that line up and give the impression of common descent). The monkeys, though, do not share a MPG and there is now sign of common descent and mutations do not line up. From Colobus (spp) we see a line up of shared non ranodm mutations again to give the (false) impression of common descent.
I already discussed that here:
http://www.iscid.org/boards/ubb-get_topic-f-6-t-000345-p-8.html
Retrospectively, it is absolutely clear which of the locations in the DNA sequence represent NR positions, since mutations on these spots line up and give the impression of common descent. And this pertains a pseudogene with unknown function (but assumed functionless), and thus is even more evidence for my view.
pb
[ 16. December 2003, 05:04: Message edited by: peter borger ]
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