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And who that has understanding will suppose that the first, and second, and third day, and the evening and the morning, existed without a sun, and moon, and stars? - Origen, 215AD [De Principiis 4.1.16]
Cut him some slack, this is his first formal debate.
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“Gärtner, by the results of these transformation experiments, was led to oppose the opinion of those naturalists who dispute the stability of plant species and believe in a continuous evolution of vegetation. He perceives in the complete transformation of one species into another an indubitable proof that species are fixed with limits beyond which they cannot change.” (G. Mendel)
It was pretty good, about the same detail I would go into for a first post. In his future posts I hope he stresses the virus insertions more vigurously.
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A single psuedo gene and a couple of ERVs are not conclusive proof of evolution.
the point of the GLO pseudogene is not that it doesn't work, it is that it doesn't work in a particular way---see the common descent article on plagarism, and why courts accept deliberate error copying as proof of copyright infringements.
how many pseudogenes are there?
apparently they outnumber the functional genes.
just for cytochrome p450
There are over a thousand different CYPs, although the number in man is only about fifty (49 genes and 15 pseudogenes have been sequenced). It is likely that most of the human CYPs have already been discovered. Why are there so many varieties of CYP? The massive hetereogeneity of these oxidases is thought to reflect the complex interdependence {read: 'ongoing battle'} between plants and animals. Plants develop new alkaloids to limit their consumption by animals - the animals develop new enzymes to metabolise the plant toxins, and so it goes. It is possible to peer back in evolution by looking at similarities between CYP isoenzymes. When we do so, it appears that the number of CYP genes exploded at about the time when organisms moved from the oceans to dry land - around 400 million years ago!
__________________ i got a warning for flaming.
i find myself unable to participate here as a result.
this being the first of it's kind since i signed into FidoNet 20 years ago.
and am no longer posting to CF.
thanks to everyone who i have encountered over the years i spent here.
Looking at mark's reply I'm predicting this debate won't work, it's obvious that they are not shooting at each other, both wide of the mark and no real confrontation yet.
Mark's hung up on mechanismal / functionality issues while AEA is taking an analysis-of-evidence approach. Mark is completely missing the point that he needs to reexamine the auxiliary hypotheses surrounding his "intelligently-designed" presupposition (does an intelligent designer design pseudogenes that are deliberately non-functional with exactly homologous defects?) while AEA is probably going to sweep right past what he will (rightly) perceive as a plain "I-can't-believe-it's-brain" argument from incredulity.
But I'm a pessimist when it comes to debates so don't take my word for it.
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And who that has understanding will suppose that the first, and second, and third day, and the evening and the morning, existed without a sun, and moon, and stars? - Origen, 215AD [De Principiis 4.1.16]
I can't get Mark's ICR link to work. Does Daniel Criswell get his "less than 90%" claim from the same place Leubnow got his 700-2400 CC range for human cranial capacity?
__________________ (The Library of Alexandria) questioned the permanence of the stars, but did not question the justice of slavery - Carl Sagan in Cosmos
I can't get Mark's ICR link to work. Does Daniel Criswell get his "less than 90%" claim from the same place Leubnow got his 700-2400 CC range for human cranial capacity?
Link works for me. This one? http://www.icr.org/article/2324/ ... Criswell's source: However, preliminary research at ICR using genomic databases and the current literature indicates that the sequence homology between humans and chimpanzees may be less than 90%, as more genomic regions, such as heterochromatin (regions of condensed noncoding DNA) and unresolved alignment gaps are included in homology studies.
(emphases added)
We'll wait and see. The article goes on to use Haldane's Dilemma to "prove" that humans could not have evolved.
For all the talk about the homology going from 98% to 95% when indels are considered, creationists seem to shy away from the statistic in the opposite direction: when the most relevant mutations are considered, ie non-synonymous mutations in coding genes (i.e. mutations that actually do anything to change the sequence of a protein by changing an amino acid), the similarity is 99.4%, or only 0.6% of DNA actually coding for proteomic differences between chimp and human.
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And who that has understanding will suppose that the first, and second, and third day, and the evening and the morning, existed without a sun, and moon, and stars? - Origen, 215AD [De Principiis 4.1.16]
The accompanying claim is that the large difference in ERV class 1 for humans and chimps is indicative of failure of the independent nested hierarchy given by ERVs. That is simply false; from the diagram the bulk of ERV class 1s in chimpanzees is given by PtERVs 1 and 2, which are recent germline invasions or horizontal transfers from other species ( http://biology.plosjournals.org/perl...l.pbio.0030110 ). Not only does this mean that we do not expect them to be found in human lineages, but that their recentness means that they will be very active and heavily replicating and transposing all over the genome - which is precisely what the large difference is.
This is nothing less than mishandling of the data, a proper understanding of PtERV 1 and 2 shows that it simply isn't the disproof of ERV phylogeny mark has been vainly seeking for so long.
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And who that has understanding will suppose that the first, and second, and third day, and the evening and the morning, existed without a sun, and moon, and stars? - Origen, 215AD [De Principiis 4.1.16]
... actually, that includes the evolutionists to a small extent. But largely just mark.
Originally Posted by mark kennedy
I understand it just fine, I just don't accept your conclusion since it's an assumption to begin with. I don't know what is so hard about this, GULO is a disfuntional gene. There is even reason to believe that it actually works in certain populations of Eskimos. These ERVs are showing up in psuedogenes a lot and I am starting to see how a person could make the connection between mutations in them and common ancestry. The problem is that the ERVs and mutations need not presuppose a common ancestor. What we can be sure of is the the GULO gene is disfuntional because selective pressure isn't acting on it because it's not vital.
The dead giveaway of sloppy, half-remembered work is the absence of a single corroborating link. Any variety of search along the lines of "Eskimo - GULO - pseudogene" quickly draws a blank. Instead, searching "Eskimo vitamin C" etc. quickly shows us what the real deal is:
Originally Posted by Wikipedia
In 1928 the arctic anthropologist and adventurer Vilhjalmur Stefansson attempted to prove his theory of how Eskimo (Inuit) people are able to avoid scurvy with almost no plant food in their diet. This had long been a puzzle because the disease had struck European Arctic explorers living on similar high-meat diets. Stefansson theorised that the native peoples of the Arctic got their vitamin C from fresh meat that was raw or minimally cooked. Starting in February 1928, for one year he and a colleague lived on an animal-flesh-only diet under medical supervision at New York's Bellevue Hospital; they remained healthy.
This is the most condensed version of the actual fact I can find. More detailed descriptions here:
Ironically, this example highlights the importance of the GULO pseudogene. Eskimos are able to derive vitamin C from fresh meat precisely because the animals they hunt have working GULO genes. (But since we normally eat our meat well cooked, it's not a useful source of vitamin C for nutrition for us.)
Having said that, let's get something out of the way. Humans, and primates, do synthesise vitamin C.
In humans, two separate gene mutations occurred to alter vitamin C synthesis from glucose (blood sugar) in humans.One mutation involves the enzyme that starts the vitamin C synthetic pathway (lactonase) and the other involves the enzyme that finishes the vitamin C synthetic pathway (lactone oxidase) [ie the GULO pseudogene]. In one mutation, the lactonase enzyme defect, no vitamin C can be formed at all and these are the people who develop scurvy (the vitamin C deficiency disease) if they do not have any vitamin C in their diet (at least 15 mg of vitamin C is needed each day to prevent scurvy). It’s estimated that 60 to 70% of the human race has this lactonase defect which prevents any formation of vitamin C at all. In the remainder of the population, a second gene mutation occurred, the lactone oxidase enzyme defect, which limited vitamin C synthesis but did not completely prevent it because even without the final enzyme which added oxygen to L-gulonolactone to form ascorbic acid, some vitamin C can still be formed from L-gulonolactone if oxygen is present. These people can still synthesize at least 15 mg of vitamin C each day, which is just enough to prevent the development of scurvy if their diet does not contain any vitamin C. These were the people who were not dying during long sea voyages when there was no food onboard vessels that contained vitamin C. It’s estimated that the lactone oxidase gene mutation occurred about 25 million years ago and that this initial gene mutation increased the gene mutation rate in Anthropoids (the ancestors to modern day primates) to give rise to Homo sapiens (humans). Vitamin C plays a major role in protecting DNA from oxidative damage that can lead to DNA mutations.Some of these mutations are beneficial and others are detrimental. According to the theory of evolution, gene mutations must occur for new species to evolve. This partial loss of vitamin C synthesis capability would have increased the DNA mutation rate without affecting survivability of the individuals with this particular genetic defect. A second gene defect then lead to the complete loss of vitamin C synthetic capability. In some populations of the world, people with the complete lack of vitamin C synthesis have been eliminated from the gene pool because the local food supply had little or no vitamin C (the Sahara nomads in Africa are an example of this phenomenon).
It just isn't synthesized anywhere at all near the level at which other organisms synthesize it.
Conclusion: no humans have a working copy of the GULO pseudogene, Eskimos notwithstanding. If Mark had done his research (it took me less than ten minutes to draw a complete blank on Eskimo-GULO connections via Google and Wikipedia) he would have known this.
Allright, I'll tell you what. I would be willing to give you this point under one condition. If we are talking about the same disfuntion in the same loci then the inverse logic has to be valid. If we are looking at unique traits fixed with specific loci then 'special creation' logically follows. I'm not saying you have to accept my conclusion, only that you recognize the logic and concede that it is valid and reasonable. Now back to your regularly scheduled arguement:
No, the point of common pseudogenes is that they form a nested hierarchy that independently confirms the nested hierarchies constructed from taxonomy - and not only that, they do so in a way that contradicts the auxiliary assumption of common design (namely that the designer designs for optimal function).
The unique traits of humans don't in any way disprove the nested hierarchies given by pseudogenes and taxonomy (and of course ERVs, but knowing you ). But I'll leave that to those more familiar with nested hierarchies.
It seems like the debate is proceeding as projected: AEA's approach is evidential, mark's mechanismal.
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And who that has understanding will suppose that the first, and second, and third day, and the evening and the morning, existed without a sun, and moon, and stars? - Origen, 215AD [De Principiis 4.1.16]
Last edited by shernren; 27th October 2006 at 01:22 PM.
Reason: making the conclusion clear.
The sad part is that Mark can't understand how we know that it is a disfunctional gene in the first place. Perhaps a better description for the gene is "vestigial" in the same way that an ostrich wing is vestigial. Any function that the GULO psuedogene may have is rudimentary to the activity of the homologous gene in other species. An ostrich may use it's wings to cool itself off, but this function is plainly a rudimentary function for a wing.
The second problem is that Mark thinks that lineage specific insertions, deletions, and point mutations somehow evidence special creation. The first problem he runs into is that all life uses DNA. There is no reason that separate creations would use the same genetic molecule, or the same codon triplets, or even triplets at all. Why don't we find organisms that use codon quadruplets, or couplets, or quintuplets? The second problem is that we see lineage specific insertions, deletions, point mutations, and even chromosomal rearrangements happen naturally all the time. Mark needs to explain why this could not happen in the past, and why his deity is the only possible explanation.
Another annoyingly obvious problem is Mark's "Big Brain/Big Problem" argument. Mark claims that science does not know what changes in which genes are responsible for larger brains in humans. Mark then says that the fixation of mutations is too high. Wait a minute. In order for Mark to claim that the fixation rate is too high in genes controlling brain size he must first tell us which genes control brain size which he claims is unknown. Oops. Somehow, a high fixation rate in unknown genes is reason to believe in a deity. Might as well claim that there are too many craters on the moon, so Invisible Moon Bunnies are real.
__________________ "Since YAC [Young-Age Creation] epistemology accepts Biblical claims over physical evidence and human reason, logical or evidential arguments for evolution and/or against YAC are likely to be ineffective in converting most YACists."--Kurt Wise
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