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Topic: Wells' Molecular Phylogenies
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peter borger
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posted 01. December 2003 05:46
Your discussion can easily be concluded as soon as you accept non random mutations (NRM).
It is now known that mutations are not only just random. (See also Lynn Caporales book and her discussion on this site.) Mutations can be independently introduced on the same spot, thus giving the impression of common descent. In bacteria it has been demonstrated that the context of the DNA determines the positions of mutations in integrated DNA sequences (Ann Rev Genetics, December 2002). If you are doing phylogenetic analyses, the context of the DNA sequences should also be taken into account.
Thus, (point)mutations in chimp and man genomes will be more likely to be on the same spot, than mutations in mouse and man. Why? Since the DNA context of their multipurpose genomes is more similar. I have discussed some mechanisms and provided the examples in the thread GUToB.
See also Nature 424: 197, 2003; Bergthorsson et al, Widespread horizontal transfer of mitochondrial genes in flowering plants.
Once these evolutionists realize that mutations in mitochondria genes (even for humans, as I have demonstrated previously) can also be NRM, such problems are easy to solve, and they do not have to invoke the ad hoc explanation HGT.
Peter
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Pim van Meurs
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posted 01. December 2003 17:13
It's important to understand the various meanings of the word random, especially as used in evolutionary theory.
When talking about random mutations, random refers to its immediate effect and as such Caporale's comments about fall well within the this meaning of randomness. When Caporale observes that some mutations are biased, this refers to the probability distribution function of said mutations. I doubt that Caporale is arguing that this is non randomness is wrt immediate effect.
Of course that mutations are non random in location, timing etc has been known for quite some time and in fact is often taken into consideration in theoretical applications.
I would certainly be interested in further pursuing Peter's ideas although I believe the original thread dealt sufficiently with some of his claims.
Then again the existance of non random mutations in location or timing is hardly shocking news to evolutionary science.
Rex Kerr captured it nicely
quote:
We need not necessarily know the mechanism of non-random mutation in order to detect its presence. The original claim was that nonrandom mutation was fooling phylogeny building to such a degree that we were assuming common descent where there was none. To support this claim, all we need to see is a demonstration that there are high levels of nonrandom mutation, and a demonstration that this nonrandom mutation significantly affects the standard phyolgenies we build.
So far, the ZFY data has been offered, and despite having relatively few mutations to work off of, I have demonstrated that phylogenies constructed off of the two halves of the gene produce essentially the same topology (certainly compatible topologies). So at this point there is absolutely no evidence that phylogenies are in any way mistaken.
[ 01. December 2003, 17:16: Message edited by: Pim van Meurs ]
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peter borger
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posted 02. December 2003 04:05
Non-random with respect to position and nucleotide. It has quite some implications for phylogenetics (as discussed). Furthermore,
Rex did not provide a tool to discriminate between a common mechanism and common descent. The common mechanism may as well give a the illusion of common descent. But the discrepancies (incongruencies) could be taken as proof for common mechanism. How do you discriminate between common mechanism and common descent? That would interest me. A lot.
And, as demonstrated by Rex the gorilla`s ZFX region demonstrates exactly the same mutations as in the hylobates ZFY region. I say that´s due to a common NRM mechanism, not common descent. Have a careful look at the sequences. The truth is always in the details.
PB
[ 02. December 2003, 04:15: Message edited by: peter borger ]
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Ron Okimoto
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posted 02. December 2003 11:18
quote:
Non-random with respect to position and nucleotide. It has quite some implications for phylogenetics (as discussed).
Furthermore,
Rex did not provide a tool to discriminate between a common mechanism and common descent. The common mechanism
may as well give a the illusion of common descent. But the discrepancies (incongruencies) could be taken as proof for
common mechanism. How do you discriminate between common mechanism and common descent? That would interest me.
A lot.
And, as demonstrated by Rex the gorilla`s ZFX region demonstrates exactly the same mutations as in the hylobates ZFY
region. I say that´s due to a common NRM mechanism, not common descent. Have a careful look at the sequences. The
truth is always in the details.
PB
This would be an interesting idea except for a very big problem. How are these NRMs supposed to be fixed in populations and how long will they take to be fixed? What time frame are you talking about to generate the massive amounts of sequence nesting seen in nature? How long ago would all the extant species have to have been designed in order to accumulate all these NRMs to make it look like common descent is true? Why would the NRMs show a nested pattern? If all apes have the same NRMs Why would the NRMs show a nested pattern among the apes? Why would we have more sequence in common with a chimp than a gibbon if gibbons have the same NRMs?
It is impossible to explain the DNA sequence data using this explanation. You will still be stuck with the fact that the designer must have used a more similar DNA template to create chimps and humans than he used to create gibbons and gorillas. How does this explain the nesting found amoung all vertebrates? How long would it take for each species to accumulate this nested similarity, and why would it show nesting that supports common descent instead of some top down nesting? If the nesting was due to NRMs you would expect mixed nested similarity, this is not observed. How are you going to regulate which NRMs are fixed in which populations? You have to explain why the NRMs that are fixed in your various species just happen to make it look like common descent happened. It is obvious from the data that not all NRMs have been fixed in all populations, so why would they be fixed in such a way that it looks like common descent.
Fixation is just when the vast majority of a population has inherited that allele. Simple definitions are when all individuals of a population are homozygous for that allele, but in large populations this doesn't happen very often because there are always mutants. So how are NRMs fixed in populations and how long would it have taken to fix enough NRMs to do the job you want them to do? You can't explain the data that we see using this simplistic explanation. Really, just try and make it work to explain the nesting among vertebrates.
If the NRMs were neutral, fixation rate would be the rate of mutation at that NRM. This just means that if the mutation rate were 10^-6. The probability of fixation would be 10^-6 for that mutation per generation. Squirrelly things happen when the populations are really small, but each mutation is less likely to exist in small populations. You can see that if you had a million such sites in the genome that you are going to get a random mess of fixations not a nested mess of fixations. For the nesting among the great apes (including humans) we are talking about millions of sites, so why would common descent be supported?
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Pim van Meurs
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posted 02. December 2003 14:28
Peter, you made some claims that non random wrt position and nucleotide would invalidate phylogeny but as Rex has shown, it didn't and you have not shown so far any evidence to the contrary.
Peter: And, as demonstrated by Rex the gorilla`s ZFX region demonstrates exactly the same mutations as in the hylobates ZFY region. I say that´s due to a common NRM mechanism, not common descent. Have a careful look at the sequences. The truth is always in the details.
Exactly the same mutations? So far the truth arising from the details does not lend credence to your claims.
So far you make claims about effects on phylogeny and as Rex has shown, these effects need yet to be demonstrated.
You claimed
quote:
If you have a careful look at the Kim et al paper you will find out that the studied region ZFX doe not show any polymorphism -NOT even on silent position:
Man – 99,7 – Hylobates agilis
Man – 99,7 – Siamang
Man – 99,7 – Orangutan
Man – 99,7 – Gorilla
Rex showed
quote:
99.7 is not 100. Also, gorilla and tamarin:
code:
Ggo 1 gaccagcaag gcagagaagg ccattgaatg cgatgagtgt gggaagcatt tctctcatgc
Str 1 taccagcaag gcagagaagg ccattgaatg cgatgagtgt gggaagcatt tctctcacgc
x x
Ggo 61 aggggctttg tttactcaca aaatggtgca taaggaaaaa ggagccaaca aaatgcacaa
Str 61 gggggctttg tttactcaca aaatggtgca taaggaaaaa ggagccaaca aaatgcacaa
x
Ggo 121 gtgtaaattc tgtgaatacg agacagctga acaagggtta ttgaatcgcc acctcttggc
Str 121 gtgtaaattc tgtgaatatg agacagctga acaagggcta ttgaatcgcc acctcttggc
x x
Ggo 181 ggtccacagc aagaactttc ctcatatttg tgtggagtgt ggtaagggtt ttcgtcaccc
Str 181 agtccacagc aagaactttc ctcatatttg tgtggagtgt ggtaagggtt ttcgtcaccc
x
Ggo 241 gtcagagctc aaaaagcaca tgagaatcca tactggggag aagccgtacc aatgccagta
Str 241 ctcagagctc aaaaagcaca tgagaatcca taccggggag aagccgtacc aatgtcagta
x x x
Ggo 301 ctgcgaatat aggtctgcag actcttctaa cttgaaaacg catgtcaaaa ctaagcatag
Str 301 ctgcgaatat aggtctgcag actcttctaa cttgaaaacg catgtaaaaa ctaagcatag
x
Ggo 361 taaagagatg ccattcaagt gtgacatttg tcttctg
Str 361 taaagagatg ccattcaagt gtgacatttg tcttctg
There are ten differences. Tamarins and gorillas are both primates.
Source
[ 02. December 2003, 14:36: Message edited by: Pim van Meurs ]
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peter borger
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posted 03. December 2003 03:46
Mutations are 1) random and 2) non random.
Differences between the two primates are due to the random mutations (I do not deny them) and shared mutations are due to a common mechanism, NOT common descent.
I see that you prefer to avoid my main issue:
The issue was and is how do you evolutionists discriminate between a common mechanism and common descent. Even if you split a sequence in two parts it will not give conclusive evidence about common descent, since both parts may as well be subject to non random mechanism, yielding similar results as common descent. So, Rex didnot show anything compelling. And, if he demonstrated anything with the ZFY and ZFX regions than it is that the same mutations can be found on the same spot, indepent of common descent. Apparently it depends on the context of the DNA where part of the mutations are introduced. Exactly these mutations line up in an interspecies sequence comparison and are taken as proof for common descent. I know, the part that does not line up are introduced after the split. Well, if so proof it. I have given several lines of evidence for NRM that give the illusion of common descent, so I have proofed my point.
Let me ask again. How do you discriminate between a common mechanism and common descent?
PB
[ 03. December 2003, 03:48: Message edited by: peter borger ]
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peter borger
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posted 03. December 2003 05:46
Comments to Ron:
First of all it simply depends upon from what DNA data you infer common descent from. For instance if you compare DNA sequences from primates common descent could be inferred from shared mutations that line up. However, primates have similar multipurpose genomes (same biochemistry, same DNA context) and from that stance I expect them to line up any way. That is what we see. As soon as you go further down the tree of life the line up is less and less supporting common descent. And the solution is HGT? This is not a solution, since we have no mechanism for it. How are mitochondria tranferred from the one to the other plant. This has to be inferred from recent data on sequence analysis (ref: Nature 2003 in my previous mail). How did it get in the germline of the plants? It is but an ad hoc hypothesis. NRM is as good as an explanation and since NRM has been observed (as discussed in GUToB) it is even better. An unbiased reanalysis of mtDNA will demonstrate NRM to be present everywhere.
Furthermore, common descent inferred from karyotyping in primates is much harder, unless you here too introfduce NRM. The chromosome bands (inversions and translocation) do not vary at random in primates. There is a pattern. In particular, when you include pan paniscus, which is usually left out (it doesnt fit the evolutionary random view). For a discussion do not hesitate to ask.
Evolution through a random mechanism is humbug.
[ 03. December 2003, 06:49: Message edited by: peter borger ]
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Ron Okimoto
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posted 03. December 2003 08:58
quote:
Peter wrote: Comments to Ron:
First of all it simply depends upon from what DNA data you infer common descent from.
No it doesn't. Take all the DNA evidence into consideration. It is that simple.
quote:
For instance if you compare DNA sequences from primates common descent could be inferred from shared mutations that line up. However, primates have similar multipurpose genomes (same biochemistry, same DNA context) and from that stance I expect them to line up any way.
This is where your model falls apart. Why should they have more similar genomes? Why should it matter about nonrandom mutations? You have to agree that if there is a designer he designed genomes sequentially. Fish genomes were designed before amphibian genomes and amphibian genomes were designed before reptile genomes and reptile genomes were designed before mammalian genomes and primate genomes were designed before human genomes. If this isn't the case just try and generate the pattern you propose using the nonrandom sites. The genomes that you start with already have to have the nested similarity to start with. How long would it take to generate the observed sequence similarity pattern if this was not the case?
quote:
That is what we see. As soon as you go further down the tree of life the line up is less and less supporting common descent. And the solution is HGT?
I'm a newbie, what is HGT? Is it horizontal gene transfer?
quote:
This is not a solution, since we have no mechanism for it. How are mitochondria tranferred from the one to the other plant. This has to be inferred from recent data on sequence analysis (ref: Nature 2003 in my previous mail). How did it get in the germline of the plants? It is but an ad hoc hypothesis. NRM is as good as an explanation and since NRM has been observed (as discussed in GUToB) it is even better. An unbiased reanalysis of mtDNA will demonstrate NRM to be present everywhere.
The probability of NRM being the mechanism is pretty small. You have to get just the right NRMs to change in the same organism. Why don't you expect a big mess? You can't control all the NRM positions and tell each one which is going to change. Even though you have hotspots of mutations the actual mutation can't be predicted for any given generation. You only have that probability of occurance for that site.
Horizontal gene transfer of mitochondria has probably been observed. The example of the rare mule giving birth. They never checked the mitochondria, but they don't have to because it is maternally inherited. You can be pretty certain what the mitochondrial type is. The nuclear chromosomes are so scrambled between the two parent species that only the rare offspring that inherits all one parental chromosomes is viable. If the sire is a horse the resulting mule offspring has the chromosome complement of a horse, but it inherits the mitochondrial type of the maternal parent. This could be a donkey. So you get a horse with a donkey mitochondria. There is no reason that this same mechanism doesn't work for plants. A hybrid is made and the backcross to one species or the other horizontally transfers the maternally inherited mitochondria to that species. No magic or NRM involved.
quote:
Furthermore, common descent inferred from karyotyping in primates is much harder, unless you here too introfduce NRM. The chromosome bands (inversions and translocation) do not vary at random in primates. There is a pattern. In particular, when you include pan paniscus, which is usually left out (it doesnt fit the evolutionary random view). For a discussion do not hesitate to ask.
Evolution through a random mechanism is humbug.
This isn't a problem to common descent. You have to take all of the data not just a few odd examples. If you are correct why aren't the majority of examples odd? Inversions and translocations are not random in the fact that they are the result of abberrant recombination. Recombination usually occurrs between two similar DNA sequences. That there would be a nonrandom distribution of such events would not be unexpected. There are also weak spots in chromosome more susceptable to breakage and translocation events. The simple fact is that if you have 5 taxa with multiple such opportunities you do not expect a nice pattern reflecting common descent among the 5 taxa you expect a random mix of various events. We do not observe this. We observe the pattern consistent with common descent and we expect a distribution of events such that noise will occur in the system, but overall a random pattern does not appear. The chromosomes reflect the DNA sequence and the DNA sequence reflects the morphology and the fossil record supports the same pattern. Creationists are fond of calculating probabilities, why don't you calculate the probability of this all happening by chance due to a bunch of NRMs that you have no control over? Why would NRMs change in such a pattern that they would support common descent when they can change in any pattern in the 5 taxa? The more NRMs that you are talking about the less likely that the pattern that we observe would appear. How many NRMs does the human genome have? Why did they change in such a way as to make it look like we descended from an ape like ancestor? Take you model down to the nuts and bolts and try and make it work for even a simple case of say 3 taxa and just 10 NRM positions. How many patterns of NRM sequence can you make for those 10 positions in just 3 taxa? Now think about all the life on earth. Can your model possibly work?
This says nothing about the time scale. It would take so long to fix NRMs in the current pattern that you don't have to worry about common descent you have probably proven it. Remember you have to get nearly all the individuals in a species with the same NRM mutation either through descent or new mutation. How are you going to stop the back mutations at mutation hotspots?
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Pim van Meurs
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posted 03. December 2003 13:14
Peter : Let me ask again. How do you discriminate between a common mechanism and common descent?
Common descent is based on 'common mechanisms' so I am not sure what you are asking here. I think we are still waiting on your explanation that phylogeny would be confused by non random mutations. So far the evidence seems to contradict this.
In addition you claim that there is some common mechanism different from present evolutionary theory that explains the data. But you have yet to describe your ideas in any meaningful manner. Until then any conclusions seem to be somewhat premature.
A good example are pseudogenes which somehow, and not surprisingly, line up to indicate common descent. Are you saying that such pseudogenes share common mechanisms? Well I would agree in that they share the same common origin but if you argue that these deletetions happened separately in all affected lineages then there is somewhat of a problem.
[ 03. December 2003, 13:16: Message edited by: Pim van Meurs ]
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peter borger
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posted 04. December 2003 04:51
In response to "how do you discriminate between a common mechanism and common descent?" you say that
common descent is based on 'common mechanisms' so I am not sure what you are asking here. If you still do not understand what I mean with common mechanism vs common descent that you are either lacking the capacity to see the difference (which makes sense in the GUToB, since losses are easy to understand), or deliberately obtuse. I recommend you to read the thread "GUToB".
Than you ask me to explain why phylogeny would be confused by non random mutations and you state that the evidence seems to contradict this. However, I have already explained why NRM in similar genomes will give the impression of common descent.
I indeed claim that there is a common mechanism different from present evolutionary theory that explains the data. I have described my ideas in the thread GUToB, that deals with evolutionary theory and why it is wrong: selection can easily be demonstrated not to be valid at several levels of biology, in particual the redundancies. So, my conclusion are certainly not premature. It demonstrates that Neodarwian theory is wrong, common descent is false and the molecular data require a reinterpretation. That is what I do in GUToB.
Reagrding pseudogens. Pseudogenes (HERVs in particular) in known phylogenies do NOT give the known phylogeny in breeding experiments. The random (and non-random) mutations do, though. Furthermore, the mutations in pseudogenes can indeed be introduced by NRM mechanism. I have demonstrated this in the GUToB thread for a globin pseudogene. If you dismiss common ancestry in this DNA element, as I do, you will find out that there is no ancestry to be demonstrated by this sequence, but rather NRM in related MPGs (as demonstrated in the big apes). Even the GLO gene in primates can be shown to be subject to NRM. In exon X in the GLO gene we observe several mutations, including a 1 nt deletion. The deletion in the GLO gene is usually taken as the ultimate evidence for common descent. However, it is not common descent, but I demonstrated that one could as well take it as evidence for NRM. (Discussed in detail on the EvC forum)
By the way, what do you know about the function of such pseudogenes. You talk about them as if they are function less. A comparison between pseudogenes and protein coding genes does not demonstrate a significant difference between the mutation rate of both genetic elemenst (although exceptions can be found). This also accounts for the GLO gene: before and after the alleged inactivation that gave rise to this gene the matutions rate of the gene does not change. That must ring a bell, in particular in an evolutionists head, would be my guess.
You say that you would agree in that they share the same common origin but if you argue that these deletetions happened separately in all affected lineages then there is somewhat of a problem.
Such mechanism may sound implausible to you, a bit too non-random maybe, but that is why it is NRM (evidencing design and creative forces in the genome). I cannot help it that genomes have been designed to work like that in earth`s biogenic field. I also recommend you to read Margulis book Acquiring genomes, and you will see that she also advocates mechanism that go against the odds to explain speciation. And it happened before, and before. All great truths start as blasphemies.
PB
[ 04. December 2003, 05:28: Message edited by: peter borger ]
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peter borger
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posted 04. December 2003 05:25
To Ron,
You say that "the probability of NRM being the mechanism is pretty small." In fact this cannot be a problem. It should be noted that the probabilty of life from nonlife is a couple of magnitudes smaller, and this is accepted as scientific fact. So, I do not see a problem for NRM here. And as a newbee I recommend you to read my thread GUToB, where I explained what it holds. From GutoB it is easy to understand biology.
PB
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Ron Okimoto
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posted 04. December 2003 13:37
quote:
To Ron,
You say that "the probability of NRM being the mechanism is pretty small." In fact this cannot be a problem. It
should be noted that the probabilty of life from nonlife is a couple of magnitudes smaller, and this is accepted as
scientific fact. So, I do not see a problem for NRM here. And as a newbee I recommend you to read my thread
GUToB, where I explained what it holds. From GutoB it is easy to understand biology.
PB
This probability has not been determined. I'd contend that when you take all the sequence data from all the species extant on earth with the trillions of NRM sites possible that the probability of life arising by chance is greater than the chance that all these NRM just happen to mutate and be fixed in such a way to show common descent. We are talking about an unimaginable amount of data that indicates common descent, not just a few sequences here and there, but entire genomes. This means that abiogenesis by natural mechanisms is more likely to have happened than NRMs accounting for the sequence distribution that we observe.
Take the simple GLO example. It is possible that one deletion started this whole ball rolling back to our tarsier like ancestor. There have been hundreds, probably thousands of species of primates since this event. Just take the extant survivors and try and make the NRM model work for just this one case. What is the probability that all the apes (gibbons, orangs, gorillas, chimps and humans) would all have the same NRM just by chance? What is the probability that all the species of monkeys would just happen to have this NRM, but mammals like lemurs and mice and elephants don't? How long would it take for every member of every species of monkey and ape to become fixed for this NRM just by chance, esspecially when it probably was a detrimental mutation. Your model will not work. Outside of primates there probably isn't another species on earth with this exact mutation fixed in their population. There probably is no doubt that this mutation has occurred somewhere in nature in any given generation of all extant species, but fixation is not mutation. Remember fixation is when all or nearly all of the members of a population are homozygous for the allele.
The GLO example also shows other nested mutations that tell us the genetic history of the various primates with this defective gene. So you not only have to account for the initial NRM deletion, but all the other mutations that have occurred since that tell us common descent happened.
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Pim van Meurs
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posted 04. December 2003 23:48
Hi Peter,
quote:
Than you ask me to explain why phylogeny would be confused by non random mutations and you state that the evidence seems to contradict this. However, I have already explained why NRM in similar genomes will give the impression of common descent.
Okay I guess this means that you have dropped your original claim that NRM would confuse phylogenies. We are still left with your claim that NRM exists and that it would give the impression of common descent. In fact if it gives the impression of common descent, I would argue that there is no real issue. Common descent is infered despite NRM.
So far your claims of a 'mechanism different from evolutionary theory' to explain the data is interesting but seems to fail in its support from the data and theoretical support.
quote:
Peter: By the way, what do you know about the function of such pseudogenes. You talk about them as if they are function less.
What makes you say that? I merely argue that the appearance of pseudogenes with deletions in similar places for lets say primates and other locations for guinnea pigs would seem to undermine your ideas? Also the appearance of these pseudogenes supports phylogenies infered from other data suggesting once again strong support for common descent.
quote:
.
Such mechanism may sound implausible to you, a bit too non-random maybe, but that is why it is NRM (evidencing design and creative forces in the genome). I cannot help it that genomes have been designed to work like that in earth`s biogenic field. I also recommend you to read Margulis book Acquiring genomes, and you will see that she also advocates mechanism that go against the odds to explain speciation. And it happened before, and before. All great truths start as blasphemies.
Yes, I remember N-rays or cold fusion, which at least seemed to have some empirical data to support its claims and yet these 'blasphemies' started as such and became 'great truths' of science. Just not perhaps in the meaning envisioned by you.
It is not what sounds implausible to me but what you can deliver in support of NRM and your claims. So far the evidence supporting common descent, not just from gene data, is just overwhelming and you have yet to show that NRM or whatever else can do equally well or even better. Until then, you may have an interesting idea but lacking in empirical and theoretical foundations and certainly overshadowed by a theory which does much better at explaining the observations.
quote:
Furthermore, the mutations in pseudogenes can indeed be introduced by NRM mechanism.
What NRM mechanism are we talking about. Could you show some examples of these somewhat elusive mechanisms?
As far as your claims of pseudogenes are concerned they also seem to go against common knowledge
quote:
You talk about them as if they are function less. A comparison between pseudogenes and protein coding genes does not demonstrate a significant difference between the mutation rate of both genetic elemenst (although exceptions can be found).
versus some of the facts
quote:
4) Pseudogenes evolve fast.
-We'll need to explain what pseudogenes are.
-Pseudogenes are evolving fast. "Replacement" and "silent" sites in pseudogenes are evolving at the same rate. Once again, using the logic of above, this shows that stabilizing selection influeneces rates more than positive selection.
-So, increases in rate of evolution are often correlated with loss of constraint, not with gain in constraint.
-Interestingly, pseudogene sites are evolving faster than even synonymous sites (this leads us to the next section); the mutation rate at pseudogenes may be our best indicator of the actual mutation rate.
In fact pseudogene mutations tend to be similar to neutral mutation rates. Much higher than the mutation rates of genes under selection.
See also
Nature. 1981 Jul 16;292(5820):237-9.
Pseudogenes as a paradigm of neutral evolution.
Li WH, Gojobori T, Nei M.
quote:
On the neutral mutation hypothesis, the rate of nucleotide substitution is expected to be higher for functionally less important genes or parts of genes than for functionally more important genes, as the latter would be subject to stronger purifying (negative) selectio. On the other hand, selectionists believe that most nucleotide substitutions are caused by positive darwinian selection, in which case the rate of nucleotide substitution in functionally unimportant genes or parts of genes is expected to be relatively lower because the mutations in these regions of DNA would not produce any significant selective advantages. Kimura and Jukes have argued that the higher substitution rate observed at the third positions of codons than at the first two positions supports the neutral mutation hypothesis, as most third-position substitutions are synonymous and do not change the amino acids encoded, although others have discussed the possibility that third-position substitutions are subject to positive darwinian selection. Recently, Kimura noted that the mouse globin pseudogene, psi alpha 3, evolved faster than the normal mouse alpha 1 gene, although he did not compute the substitution rate. Here, we present a method of computing the rate of nucleotide substitution for pseudogenes, and report that the three recently discovered pseudogenes show an extremely high rate of nucleotide substitution. As these pseudogenes apparently have no function, this finding strongly supports the neutral mutation hypothesis.
As far as HERVs are concerned here is a good example
quote:
Figure 4.4.1. Human endogenous retrovirus K (HERV-K) insertions in identical chromosomal locations in various primates (Reprinted from Lebedev et al. 2000, © 2000, with permission from Elsevier Science).
[quote]
Beautiful examples which strengthen the common descent hypothesis.
And more
Mutation Pattern Variation Among Regions of the Primate Genome D. Casane,* S. Boissinot, B.H.-J. Chang,** L.C. Shimmin, W.-H. Li J Mol Evol (1997) 45:216–226
shows phylogenies for primates as infered from three different pseudogenes which seemed 'remarkably' similar.
[ 05. December 2003, 00:24: Message edited by: Pim van Meurs ]
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peter borger
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posted 05. December 2003 09:11
So, you are going to tell me that the probablity of life from non life is bigger than NRM to explain phylogeny?
If so, it wouldnot be hard for you to provide several documented examples demonstrating your claim, since I already demonstrated were NRM can be found in the scientific literature. (See my last letters in the GUToB thread. As you will find out the NRM line up in Drosophilas Ig5 gene and give the impression of common descent, while we now it is not.)
Exon X in the GLO gene demonstrates at least three NR positions, and that wouldnot be expected for a pseudogene. Why would the same spot be involved several times? The gene is a pseudogene and to conventional knowledge it would not matter where it mutates, because mutations are introduced at random. Apparently, they are not introduced at random and only a close up scrutiny reveals the non random positions. But, since these NRM are present in exon X, why cannot the deletion be a NRM. Deletions can be introduced on the same spot over and over, and this has been demonstrated in T4. Before such positions are taken as evidence for common descent, it should be exluded that a common mechanism is involved. That would be the scientific approach.
You say that there may have been hundreds, probably thousands of species of primates. There may also have been hundreds or thousands of spacealiens that initiated life on earth, but lets keep it scientific. From the evidence (fossil record) we know that there have only been a handful of primates, that did not change over time, but went extinct with only minor changes to the phenotype. We could easily list them, it would only take a couple of sentences.
So, I would rather take the extant survivors because that is the material we can directly work with and subject to molecular biological techniques. And it can be demonstrated that in these extant organisms mutations can be non random. Caporale wrote a book on it, and NRM implies that Darwin made an unwarranted extrapolation, since all the information to genarate variation for adaptive phenotypes is already present in the genomes. Apparently, organsim have been geared with multipurpose genomes. That also explains why organism are able to invade new environments. The source is already there.
You ask "What is the probability that all the apes (gibbons, orangs, gorillas, chimps and humans) would all have the same NRM just by chance?"
It depends on what type of NRM mechanism is involved. And on the context of the DNA. Since the primates have the same deletion in exon X of the GLO gene I would expect that the chances are fairly high for this position. But science did NOT exclude the possibility that ALL primates have the deletion on this spot. Usually, these studies are n=1 studies since it is quite an effort to obtain the material. n=1 is not really compelling in science. Or maybe these organisms were on Noahs ark (I mean only these organsims survived a bottle neck).
Why would a NRM become fixed in a population? Probably because the mechanism is an irreversibel mechanism. I envion that there are several mechanism, either utter physical or protein driven. It requires a lot of intraspecies comparison to get an idea about the amount of NRM in the population, would be my guess.
You claim that outside of primates there probably isn't another species on earth with this exact mutation fixed in their population. In GUToB this could have two explanation. Firstly, the (genetic) make up of primates is thus that only in primate the deletion can be introduced in exon X (probably depends upon the coiling of the DNA during replication and the formation of imperfect hairpins). You should know that the sequences in primates are more similar than between primates and other mammals, so it makes sense. Secondly, longevity that is conveyed by the GLO gene has been selected against.
pb
[ 05. December 2003, 09:18: Message edited by: peter borger ]
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Pim van Meurs
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posted 05. December 2003 13:07
Peter: If so, it wouldnot be hard for you to provide several documented examples demonstrating your claim, since I already demonstrated were NRM can be found in the scientific literature.
You have argued that NRM can be found in the scientific literature but 1) you have not provided any in depth analysis that shows the existence of NRM, certainly not to the extent as argued by you 2) you have not shown how this NRM can give the impression of common descent.
Peter: The gene is a pseudogene and to conventional knowledge it would not matter where it mutates, because mutations are introduced at random.
Actually the nucleotide replacement probabilities are known to be biased but once again I ask Peter to show how this would give the impression of common descent and where the evidence of NRM can be found?
Peter: From the evidence (fossil record) we know that there have only been a handful of primates, that did not change over time, but went extinct with only minor changes to the phenotype. We could easily list them, it would only take a couple of sentences.
From the fossil record and other data, although limited we know how primates show the same phylogenies over and over again strongly pointing to common descent.
Peter: And it can be demonstrated that in these extant organisms mutations can be non random. Caporale wrote a book on it.
Yes, her comments on mutations and selection are on the record and I do not think they give much support to Peter's claims. Of course the issue is not the existence of evolved biases in mutations but rather the effect of such biases. As shown by Rex and others, the evidence of common descent remains strong.
Peter: Why would a NRM become fixed in a population? Probably because the mechanism is an irreversibel mechanism. I envion that there are several mechanism, either utter physical or protein driven. It requires a lot of intraspecies comparison to get an idea about the amount of NRM in the population, would be my guess.
Or even a likely mechanism?
Peter: You claim that outside of primates there probably isn't another species on earth with this exact mutation fixed in their population.
Of course not that would be a silly claim.
But the example of the GULO gene in primates versus guinnea pigs shows evidence against NRM since the guinnea pig line has deletions in different nucleotides.
Peter: and NRM implies that Darwin made an unwarranted extrapolation, since all the information to genarate variation for adaptive phenotypes is already present in the genomes
Perhaps Peter can give us an example of an unwarranted extrapolation by Darwin since Darwin's ideas seem to be quite compatible with Caporale's ideas. I assume that Peter is aware that Darwin had no idea about the mechanism(s) of heritable transmission?
Peter: Exon X in the GLO gene demonstrates at least three NR positions, and that wouldnot be expected for a pseudogene. Why would the same spot be involved several times?
Common descent? I urge Peter to support his case of NR and that such would not be expected from a pseudogene. Some clear well argued examples would be helpful in furthering his interesting ideas. So far their support in data and theoretical foundations seems minimal.
Some additional relevant information
quote:
Mol Cells 2000 Oct 31;10(5):512-8
Evolution of the X-linked zinc finger gene and the Y-linked zinc finger gene in primates.
Kim HS, Takenaka O.
Division of Biological Sciences, College of Natural Sciences, Pusan National University, Korea. khs307@hyowon.cc.pusan.ac.kr
We have sequenced the partial exon of the zinc finger genes (ZFX and ZFY) in 5 hominoids, 2 Old World monkeys, 1 New World monkey, and 1 prosimian. Among these primate species, the percentage similarities of the nucleotide sequence of the ZFX gene were 96-100% and 91.2-99.7% for the ZFY gene. Of 397 sites in the ZFX and ZFY gene sequences, 20 for ZFX gene and 42 for ZFY gene were found to be variable. Substitution causes 1 amino acid change in ZFX, and 5 in ZFY, among 132 amino acids. The numbers of synonymous substitutions per site (Ks) between human and the chimpanzee, gorilla and orangutan for ZFY gene were 0.026, 0.033, and 0.085, respectively. *In contrast, the Ks value between human and hominoid primates for the ZFX gene was 0.008 for each comparison. Comparison of the ZFX and ZFY genes revealed that the synonymous substitution levels were higher in hominoids than in other primates. The rates of synonymous substitution per site per year were higher in the ZFY exon than in the SRY exon, and higher in the ZFY exon than in the ZFY intron, in hominoid primates.
Peter argued elsewhere:
quote:
The sequence shown in the paper is the sequence of exon X. It is of interest since it demonstrates a non-sense mutation (introduction of a stop codon). Since the protein is not expressed at all, all positions in the DNA are completely neutral. This means that natural selection does not act on the sequence since the protein is not expressed. So, mutations should be introduced completely at random according to NDT.
Actuall NDT does not state anything about randomnes in location only about its immediate effects. It may be helpful to distinguish between all positions are neutral and the mutation rates at varying positions. NDT and Darwinism can very well include non-randomness in location, timing of mutations etc. And in fact they do when incorporating nucleotide transition probabilities.
Examples can be found throughout the scientific literature
Patterns of nucleotide substitution in Drosophila and mammalian genomes
quote:
To estimate patterns of molecular evolution of unconstrained DNA sequences, we used maximum parsimony to separate phylogenetic trees of a non-long terminal repeat retrotransposable element into either internal branches, representing mainly the constrained evolution of active lineages, or into terminal branches, representing mainly nonfunctional “dead-on-arrival” copies that are unconstrained by selection and evolve as pseudogenes. The pattern of nucleotide substitutions in unconstrained sequences is expected to be congruent with the pattern of point mutation. We examined the retrotransposon Helena in the Drosophila virilis species group (subgenus Drosophila) and the Drosophila melanogaster species subgroup (subgenus Sophophora). The patterns of point mutation are indistinguishable, suggesting considerable stability over evolutionary time (40–60 million years). The relative frequencies of different point mutations are unequal, but the “transition bias” results largely from an ≈2-fold excess of G·C to A·T substitutions. Spontaneous mutation is biased toward A·T base pairs, with an expected mutational equilibrium of ≈65% A + T (quite similar to that of long introns). These data also enable the first detailed comparison of patterns of point mutations in Drosophila and mammals. Although the patterns are different, all of the statistical significance comes from a much greater rate of G·C to A·T substitution in mammals, probably because of methylated cytosine “hotspots.” When the G·C to A·T substitutions are discounted, the remaining differences are considerably reduced and not statistically significant.
and
Chapter 4 : Rates and Patterns of Nucleotide Substitution
[ 05. December 2003, 13:19: Message edited by: Pim van Meurs ]
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