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Author
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Topic: Peter Borger: Shared mutations: Common descent or common mechanism?
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peter borger
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Member # 722
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posted 24. July 2006 03:39
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Jehu, these genes are not phylogenetically incongruent - if you compared them with their gorilla equivalent, you'd find that all human genes were still closer to their chimp homologue than to the gorilla copy.
This is simply untrue. It seems Dr McArthur "MESK" is delibetately obtuse or ignorant.
Since the sequencing of the genomes of the big apes it has become clear that a considerable part of the genes of man are more closely related to gorilla than they are to chimp. It instantly falsifies common descent.
GUToB:
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This observation has made it necessary that the estimated time to the common ancestor of human and chimpanzee now coincides with that of gorilla and the line that gave rise to chimpanzees and man. The word is now the human lineage split off from that of chimpanzees around 4-6 million years before present and from gorilla 6-8 million years ago. Evolutionists such as Jared Diamond have argued man is the third chimpanzee. The portion of human DNA that is more closely related to gorilla strongly challenges this idea. The genetics of the primates show humans are not “solely chimpanzee”; rather the human genome was built of the same genetic elements as the other primate lineages were created from.
Originaly, the genetic elements of the distinct primate multipurpose genomes (MPG) had the same functional sequences. Over time they have accumulated both non-random mutations (NRM) and random mutations. The NRM line up and give an illusion of common descent. The details of the primates' genomic data, however, show there is no common descent. GUToB is the only reasonable explanation for these observations (GUToB = MPG + NRM).
peebee
[ 24. July 2006, 03:41: Message edited by: peter borger ]
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John A. Davison
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posted 24. July 2006 07:26
ALL the primates including man were built out of a common block of original genetic information. There is no need to postulate the introduction of any new information to account for that common ancestry. It was all "prescribed" and probably predestined as well with Homo sapiens determined to be the terminal product. All primates share a common ancestor. To assume otherwise is without tangible foundation.
What we see in the genomes of all organisms is only what is not silenced.
"Everything is determined... by fores over which we have no control."
Albert Einstein
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peter borger
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posted 24. July 2006 10:09
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ALL the primates including man were built out of a common block of original genetic information. There is no need to postulate the introduction of any new information to account for that common ancestry. It was all "prescribed" and probably predestined as well with Homo sapiens determined to be the terminal product. All primates share a common ancestor. To assume otherwise is without tangible foundation.
John,
A few years ago, with the then available biological data, I was also inclined to argue as you do now. Back in 2002, I independently arrived at your conclusion of prescribed evolutionary changes. Then I discovered your manifesto on the net. You may remeber that we had email exchange several times. To you, I pointed out the evidence in the primate genome for a non-random mechanism. I have send you the karyotypic evidence from Folia Primatol. (Basel) published in 1979 where they showed the translocations and inversions of the primate genomes, including the Bonobo. The latter was actualy very revealing as it shows the same NRM as homo sapiens and must have been independentaly acquired. So far so good.
However, over the past few years, with the finishing of all these mega sequencing project, it has become clear to me: NO common descent. Although I agree with you that all the primates including man were built out of a common block of original genetic information, we do not share a common ancestor with primates through a reproductive mechanism.
I agree that if the prescribed evolutionary hypothesis were true, there is no need to postulate the introduction of any new information to account for that common ancestry. However, we see in the human genome 36 genes, which are completely absent from the chimpanzee's genome. (I could not find data yet on novel chimpanzee genes.)
We also see single copy genes that required a few very specific point mutations and cannot be the result of a prescription (or you must postulate a molecular mechanism that can do so), neither can they be understood from a gradual darwinian mechanism. Currently, I think these functional point mutations can only be understood invoking immediate creation events (of MPG) or as non-random mutations (NRM).
peebee
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John A. Davison
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posted 24. July 2006 14:25
Peter
Assuming just for the heck of it, because I do not believe for one instant that we have not had a common ancestor with all other primates, just where, in your opinion, did Homo sapiens come from and what was the cytogenetic and reproductive mechanism by which he got here?
Surely you must have some ideas on this. I offer you this opportunity to present them.
My own opinion is that we are the direct descendent of Neanderthal for the simple reason there was no other humanoid around at the time of our debut around 100,000 years ago.
Which genes are shared with which other organisms is of little importance since these may be shut off or activated as part of the evolutionary scenario and may be nothing more than position effects. They may have little or nothing to do with the reproductive history of the lineage.
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peter borger
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posted 25. July 2006 03:40
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My own opinion is that we are the direct descendent of Neanderthal for the simple reason there was no other humanoid around at the time of our debut around 100,000 years ago.
I am also inclined to believe the neandertaler is a product of the same MPG as man. Furthermore, reproducing organisms were created as MPG with an built-in ability to 'evolve'. Only reproducing MPG are able to evolve, but because it is controlled by a limited number of genetic elements it is non-random and finite.
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Which genes are shared with which other organisms is of little importance since these may be shut off or activated as part of the evolutionary scenario and may be nothing more than position effects. They may have little or nothing to do with the reproductive history of the lineage.
If so, we should find the same genes in pan and homo. We don't. Homo has three dozen novel genes; No trace of them to be found in the chimp genome. All one can argue now is that they have recombined out of the genome, not leaving a trace. I do not believe naturalistic stories that cannot be tested. For this reason I don't believe we are merely higher evolved apes. For the same reason I also do not believe the big bang ever happened for no reason. It is merely human inventions so they not have to accept the Creator.
peebee
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John A. Davison
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posted 25. July 2006 06:18
Peter
I don't think genes have much to do with evolution. I am willing to bet that if we and chimps were identical at the gene level, that we would still be chimp and human respectively. It is the chromosome, not the gene, that is the mediator of evolution. Goldschmodt claimed the same thing 66 years ago. It is our chromosomes that make us what we are.
I still want to know where we came from if not from Neanderthal. We sure didn't come from nothing, like the big bang for example. I share your skepticism about the Big Bang.
"A past evolution is undeniable, a present evolution undemonstrable."
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peter borger
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posted 25. July 2006 08:57
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I don't think genes have much to do with evolution. I am willing to bet that if we and chimps were identical at the gene level, that we would still be chimp and human respectively. It is the chromosome, not the gene, that is the mediator of evolution. Goldschmodt claimed the same thing 66 years ago. It is our chromosomes that make us what we are.
Genes are the tools. We can do without many tools, as demonstrated by genetic redundancyies.
The arrangement of the chromosomes is the blueprint how to build a three-dimensional body in which the tools can operate to let it function as a whole. Typical morphology is due to the position effect induced by rearrangements, and resulst from differential gene expression. The variation we see within MPG is due to jumping genetic elements (VIGEs), formally known as retroviral elements, LINES, SINES, Alus and the like. Still there are human specific genes not present in chimps. Question is are these genes present in other primates? It would support yxour stance. If not, it would support mine.
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I still want to know where we came from if not from Neanderthal. We sure didn't come from nothing, like the big bang for example. I share your skepticism about the Big Bang.
Created ex nihilo...
peebee
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John A. Davison
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posted 25. July 2006 19:46
Peter
Do not publish your last statement as it will be used against you. Trust me.
Best, John
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adhitthana
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Member # 2020
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posted 25. July 2006 23:00
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We also see single copy genes that required a few very specific point mutations and cannot be the result of a prescription (or you must postulate a molecular mechanism that can do so), neither can they be understood from a gradual darwinian mechanism. Currently, I think these functional point mutations can only be understood invoking immediate creation events (of MPG) or as non-random mutations (NRM).
Hi Peter, can you explain this a bit further for the layman?
John , do you have any response or thoughts on this?
Thank you both for your time. ![[Smile]](smile.gif)
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peter borger
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posted 26. July 2006 06:41
Adhitthana,
The FOXP2 transcription factor is an example. The FOXP2 protein is identical in chimp, gorilla and rhesus monkey, while that of orangutan and mouse differ by only one amino acid. In contrast to these sequences, the sequence found in humans differs by two positions. The two amino acid variations are present in all 226 examined human chromosomes, a clear indication that they are fixed. It has been concluded that the two amino acid substitutions in the human sequence were selected during the last five or six million years of human evolution, and fixed in the entire population between 0 and 120 thousand years ago, as a result of an adaptive selective sweep [Enard et al, Nature 2002; Zhang et al, Genetics 2002].
It should be noted that because the human FOXP2 gene differs by two amino acid positions from chimpanzees, at least two selective sweeps are required to explain the two fixed amino acids in human FOXP2 protein.
Alignment of DNA and/or amino acid sequences of several species reveal where changes occurred, reveal which nucleotides are different, and whether pieces of DNA were added or deleted. The substitution of two amino acids in the FOXP2 protein, to be precise on position 303 and 325, is due to two independent mutations in the corresponding gene sequence. The two mutations specific for the human sequence are 1) T303 --> N303, which requires A-C-N (with N = U, C, A, G) --> A-A-N (with N = U or C), and 2) N325 --> S325, which requires U-C-N (with N = U, C, A, G) --> A-G-N (with N = U or C). The second mutation must have happened in one individual or in a direct descendant of the individual with the first mutation. This is because a recombination event between the two mutations can be excluded.
These mutations were very specific events, since the sequence in humans has been positively selected and is now subject to purifying selection (the Darwinian's word). In fact, the probability that these two independently mutations occurred on exactly these positions of the FOXP2 gene is roughly 10exp-19 (0.3 x 10exp-9 for the first specific mutation and also for the second specific mutation). This very remote possibility tells me that the genetic changes cannot have happened by chance alone, as it would require an effective population size of (unrealistic) billions of individuals. The alternative is that the genetic changes must have been internally driven as the result of a non-random phenomenon ("created" if you wish).
The molecular biology of FOXP2 thus shows that the transition from primates to humans cannot have come into existence by a gradual evolutionary process, as it involved two non-random mutations and two selective sweeps. Rather the amino acid substitutions in the human FOXP2 gene must have been the result of a rapid, saltational evolutionary process (creation, if you wish),
peebee
[ 26. July 2006, 10:48: Message edited by: peter borger ]
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John A. Davison
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posted 26. July 2006 20:12
Sure
I will stick to my guns. Allelic mutations and selection never had anything to do with the emergence of any true species or any of the higher taxonomic categories. The only conceivable role for point mutations was to ensure ultimate extinction, thereby making way for the next preprogrammed event in the evolutionary scenario, a scenario no longer in progress.
"A past evolution is undeniable, a present evolution is undemonstrable."
John A. Davison
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John A. Davison
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posted 26. July 2006 20:17
There is nothing in my reposne in conflict with what Peter has presented. The only thing is the denial of any role for chance. It was all "prescribed."
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peter borger
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posted 27. July 2006 03:39
A survey of the amino acid sequence of the FOXP2 proteins shows the gene is subject to two forms of non-random mutations. First, there is s repetitive sequence of glutamines. Here, mouse and chimpanzee have independently acquired a glutamine. This underlies a NRM mechanism. Glutamines are specified by the protein code as the triplets GAG or GAA. Duplication of DNA during cell division requires the action of DNA polymerases that make the complementary DNA strand from the template. During cell division the double stranded DNA helix is transiently single stranded and the DNA polymerase uses the single strand as the template to synthesize the complementary strand. In a long stretch of repeating nucleotides such as found in the FOXP2 gene the DNA polymerase sometimes looses track and slips back or forward. In a repeating stretch of identical DNA units the enzyme cannot remember which triplet was duplicated and which was not. When the polymerase slips back it adds a triplet and the repeat units grow; when it slips forward the stretch of repeat units decreases. This way variation is introduced in a non-random manner. The repeat units often form palindromes, sequences that can read back and forth with same meaning. In DNA sequences palindromes in repeat units may stick together and the stretch of DNA that separated them may delete entirely. Stretches of repeating DNA units are subject to non random genetic changes and this is indeed what frequently and independently happened.
Second, a comparison of the FOXP2 genes in 29 mammals and one bird (chicken) revealed that the amino acid on position 325 may either be an asparagine (Asn) or a Serine (Ser). Remarkably, both the meat eaters and humans independently acquired serine on this spot in the protein.
Selection? NO!
NRM? Yeah!
It is clear: The DNA is subject to NR mutations.
peebee
[ 27. July 2006, 04:08: Message edited by: peter borger ]
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Albert Voie
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posted 27. July 2006 06:22
Peter,
Has anyone tried to insert the human protein in a mouse to see what happens? What do the point mutations do, and are they both required?
Is it possible to have a copy of your paper on this issue?
Albert
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peter borger
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posted 27. July 2006 07:06
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Has anyone tried to insert the human protein in a mouse to see what happens? What do the point mutations do, and are they both required?
Not that I know of. Probably nothing happens in the knock-in as the protein is largely redundant in humans. SLI is speech disorder that runs in some human families and known to be related to mutations in the FOXP2 gene, but it does not contribute to seriously diminished fitness (=reproductive succes. Otherwise it would not run in families, would it?
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Is it possible to have a copy of your paper on this issue?
The paper I wrote on the topic is currently under review.
peebee
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