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Author
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Topic: Resus macaque: evidence for non-random mutations
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David L. Hagen
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Member # 323
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posted 22. April 2007 21:57
adhitthana
Good questions.
Encourage you to read John Sanford's Genomic Entropy and the Mystery of the Genome. He gives a good popular discussion in the text, with summaries of technical studies in the appendix.
The dogma of natural selection posits selection based on beneficial/harmful mutations.
However Sandford shows how it is unusual that the mutations are preserved considering the how sexual reproduction preserves the genome.
More importantly, Sanford notes how it is difficult to distinguish and select between numerous mildly deliterous mutations. cf a princess distinguishing numerous tiny nucleotides beneath a pile of mattresses.
Thus I find it remarkable that such mutations would be purged. More remarkable would be to have them purged in one species and not in the other etc.
Michael Behe's Darwin's Black Box, and his upcoming book would also be good reading.
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nosivad
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posted 22. April 2007 23:50
"The struggle for existence and natural selection are not progressive agencies, but being, on the contrary, conservative, maintain the standard."
Leo Berg, Nomogenesis, page 406.
"Natural selection is a real factor in connection with mimicry, but its function is to preserve and render preponderant an ALREADY EXISTENT likeness, not to build up that likeness through the accumulation of small variations, as is do generally assumed.
Reginald C. Punnett, Mimicry in Butterflies, page 152, my emphasis.
Randomly generated mutations never had anything to do with the formation of species or of any of the higher taxonomic categories. In both ontogeny and phylogeny progress has resulted from within with the only role for the environment being to offer a stimulus for an endogenous predetermined potential. Selection, natural or artificial, can only produce intraspecifuc varieties, none of which are incipient species. Phylogeny, including true speciation, is now apparently finished and, in my opinion, will never resume.
"A past evolution is undeniable, a present evolution undemonstrable."
John A. Davison
[ 22. April 2007, 23:52: Message edited by: nosivad ]
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peter borger
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Member # 722
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posted 23. April 2007 09:07
Bruce,
"It is my understanding that common descent means that my great, great ... grandfather was a different species -- a non-human ape. Further, his great, great ... grandfather was a single-celled organism. I do not presume that "common descent" discusses how the species boundary, or how new organs, develop, only that these are produced out of preexisting species. If, for instance a designer creates a new designer siRNA, and injects it into a the egg of a non-human ape, causing that ape to birth a human, then common descent is maintained."
Why would the designer do so? If he is capable of designing and introducing novel unique genes, why would he not have reintroduced a functional GULO gene? This phylosophical question doesn't require addressing, as am not interested in phylosophy.
Let me illustrate it like this:
I have a question concerning my descent. There is some reason to doubt whether my parents are the persons I believe they are (my real biological ancestors). So, I go to see the doctor with some samples of blood (mine, mum's and dads') and it turns out I am having a gene that is not present in their genome. This observation qualifies as independent, objective biological evidence I am not their descendant. I can't be, because genes don't simply drop out of thin air.
That's why the unique human siRNA genes prove we did not descent from an ape-like ancestor, and the biological data that seem to point in that direction require re-interpretation.
"The only way that common descent is not maintained is if the designer begins from scratch, and forms each new species out of component atoms. However, if that is what happened, why did the designer also encode hundreds of identicle disease producing mutations in both the Rhesus and the Human. If we were reconfigured from scratch, then the only conclusion we can draw from these disease producing mutations is that they are the reasoned intention of the designer."
This is not how I see it. Initially, the functional genes in primate genomes may have been quasi-identical w.r.t. their sequence. Then, they have been subject to random and non-random mutations for a long time. The latter give an illusion of common descent, independent whether they are disease-producing or neutral.
"We can debate whether natural selection is capable of purging a disease producing mutation from a genepool, or whether each purged gene is the intentional act of a designer. I, for one, am content that disease producing mutations are the true product of chance, and that unguided natural selection is a powerful enough force to periodically remove the disease from the gene pool."
Not only by chance. It has been shown that mutations in p53 (protooncogene and gene of the year 1993) is subject to NRM as the result of regulatory hairpins.
Such hairpins are present in most regulatory genes and serve as docking sites for interacting and regulatory proteins. It is known these sites are more vurnerable to mutations. Many hotspots for mutations have been located in p53, which, in my opinion, qualifiy as non-random mutations since they line up in patienst having particular forms of cancer. Most likely, such mutations would not accumulate in the germline as they woudl be lethal before the reproductive age, but other non-lethal NRM in, for instance, redundant, non-essential genes would produce an illusion of common descent.
This is the only true explanation for the alignment of mutations in organisms that do not reproduce together.
Regards,
Peter
[ 23. April 2007, 09:22: Message edited by: peter borger ]
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nosivad
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posted 23. April 2007 14:33
Peter
Get it published.
John
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Bruce Fast
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Member # 924
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posted 24. April 2007 11:01
Peter Borger, "I can't be, because genes don't simply drop out of thin air."
I sit here eating a genetically modified tomato. I recognize that it is the same old kind of tomato that I ate yesterday, but it has an extra gene. That gene "dropped out of thin air" in some biologist's lab somewhere. We have a model that does exactly that, it seems reasonable to me that the designer would use a very similar mechanism.
Ultimately, I fail to grasp the validity of your argument. You suggest that "genes don't simply drop out of thin air" yet you suggest that an entire biological organism with all of its stunning complexity including a complete genome could drop out of thin air.
You then contend that the reason we have matching deleterious mutations to the Rhesus is because there are areas in our DNA that are more suseptible to mutation. (I doubt if any serious biologist would throw you out of the camp for suggesting so -- though there is something non-random about your position, it hardly brings the idea outside the precious fold of naturalistic thought.) While I am happy to contend that there are areas in the DNA that are more suseptible to mutation, I am betting that the areas that contain these identified mutations are not the complete set of vulnerable spots. If there are 10 vulnerable spots that are not mutated for each vulnerable spot that is mutated, then your hypothesis is toast. Is there not alread about 20 ways that each of these spots could be mutated? Seeing as these spots are identically mutated, does that not already toast the "weak spot" hypothesis?
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adhitthana
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Member # 2020
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posted 24. April 2007 14:03
quote:
While I am happy to contend that there are areas in the DNA that are more suseptible to mutation, I am betting that the areas that contain these identified mutations are not the complete set of vulnerable spots.
So it will be interesting to see the breakdown of the 84 versus the 97. How many of them are in common?
quote:
If there are 10 vulnerable spots that are not mutated for each vulnerable spot that is mutated, then your hypothesis is toast.
Although the question might arise, that if even one common mutation is the result of a common mecahnism, then how do we distinguish between common mechanism and common descent.
It would seem there at at least 13 instances of possible common mechanism , so all 13 must have been purged from one line for common descent to still hold (I would think), and the number may be higher.
Is this percentage possible, probable, improbable? I dont know. How can we say?
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peter borger
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Member # 722
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posted 25. April 2007 03:27
"I sit here eating a genetically modified tomato. I recognize that it is the same old kind of tomato that I ate yesterday, but it has an extra gene. That gene "dropped out of thin air" in some biologist's lab somewhere. We have a model that does exactly that, it seems reasonable to me that the designer would use a very similar mechanism."
If you look into the biome (the genomes of all known organisms) you will find the "alien" gene in your modified tomato.
Not so for the unique microRNA genes in humans/other organisms. You won't find them in the bioom. For me this, and other observations, is enough proof we've been specially created.
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adhitthana
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posted 25. April 2007 03:47
Peter, I wonder if you might be able to tell us the precise place or paper you got your figures from in the opening post.
I have obtained some more papers asscociated with the study but don't seem to have the paper which mentions the data you have brought up.
Can you tell us where you got it from?
Thank you.
Added in edit:
I found this reference to the 229 shared mutations in this paper, Evolutionary and Biomedical Insights from the Rhesus Macaque Genome
quote:
To identify the ancestral disease-associated alleles in human, we screened the macaque and chimpanzee assemblies for the presence of any of the 64,251 different disease-causing or disease-associated mutations collected in the Human Gene Mutation Database (63, 64). A total of 229 substitutions were identified for which the amino acid considered to be mutant in human corresponded to the wild-type amino acid present in macaque, chimpanzee, and/or a reconstructed ancestral genome (Table 6) (65) (see table S8.1 for a full list).
But I'm not sure where table S8.1 can be found (assumimng it has the rest of the data). can you help?
[ 25. April 2007, 04:16: Message edited by: adhitthana ]
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peter borger
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Member # 722
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posted 25. April 2007 08:32
Adhittana,
The data are online. Access requires subscription.
PB
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adhitthana
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Member # 2020
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posted 25. April 2007 17:34
quote:
Adhittana,
The data are online. Access requires subscription.
I can get access, can you tell me precisely where to look?
Thank you.
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peter borger
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Member # 722
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posted 26. April 2007 06:47
8.1 is a list of the disease-casuing mutations. You have to go to the online material, scroll down as far as you can en click this link:
choose1139247som_tables.zip (3.8 MB)
This will open a widno and you can now find all additoinal information. 8.1 is the file in the upper row, the bleu "word" e. Click and it opens.
The data are summarized in Penissi's article in the same issue of Science. That's where I found them.
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Bruce Fast
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Member # 924
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posted 26. April 2007 10:43
Peter Borger: If you look into the biome (the genomes of all known organisms) you will find the "alien" gene in your modified tomato.
Not so for the unique microRNA genes in humans/other organisms. You won't find them in the bioom. For me this, and other observations, is enough proof we've been specially created.
I agree with you that we seem to have some genes that were specially created to make us human -- thus we are the non-accidental intention of the designer. It still seems, however, more likely that the designer took an ape, which he had engineered with our end in mind, and edited that ape's gene-set to produce man. This acccounts for the evidence and respects occam's razor.
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peter borger
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Member # 722
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posted 27. April 2007 07:48
Bruce,
unique microRNA genes code for regulatory molceuales that have to recognize a motif in other genes. It is thus not just another unique gene, but it regulates other genes that must have such motifs. Add a gene and also introduce the motifs?
Why would a designer do that?
Why would he use an ape to let us be produced?
We can (almost) do that with our current techniques.
Is the designer human?
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adhitthana
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posted 28. April 2007 21:50
quote:
I am having some struggle interpreting your data, however. It seems that you are saying that common disease producing mutations have been identified as follows:
Rhesus and Chimp and Human = 200
Rhesus and Chimp, not Human = 97
Rhesus and Human, not Chimp = 84
Chimp and Human, not Rhesus = 48
Is this correct?
No that is not correct, as far as I can tell.
More than 200 sites were looked at, (presumably 229) where the "macaque had the same base at the same position as the diseased or at-risk human."
Rhesus and human, not Chimp =84
Rhesus Chimp and Human =97
Human and Chimp, not Rhesus =48
I looked here, Genomicists Tackle the Primate Tree
No data is given there for mutations shared by Chimps and Rhesus.
quote:
Hardison and his Pennsylvania State colleague Webb Miller found more than 200 sites where the macaque had the same base at the same position as the diseased or at-risk human. In 97 instances, both the chimp and the macaque matched the aberrant human base; in 48 cases it was just the chimp. And in 84 cases the rhesus, but not the chimp, matched the diseased human sequence, possibly because chimps also independently evolved away from the ancestral condition at those sites.
Unless I have misread this which is possible. ![[Wink]](wink.gif)
Added in edit:
I must have misunderstood the data though, as I can't see how humans and rhesus could share 229 mutations if Rhesus humans and not chimps share 84 and Rhesus humans and chimps share 97.
[ 28. April 2007, 22:01: Message edited by: adhitthana ]
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