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Author Topic:   evidence that intelligent design can't explain
monkenstick
Inactive Member


Message 1 of 50 (13974)
07-23-2002 1:23 AM


DNA homology is supposedly due to intelligent design. Supposedly the similarity in gods creatures is due to god's reuse of genes (god's evidently fairly lazy, why build anything from scratch when you can take the easy path and just modify what you've got).
whenever I hear this argument, I post this link;
http://www.talkorigins.org/faqs/molgen/ (i'm sure some of you have already seen it)
then I ask them how intelligent design explains these types of homology. It usually just gets ignored
so, can an IDist explain to me why we and chimpanzees have identical errors in our GLO gene?
(another thing that puzzles me about the whole homology is due to design thing is why god uses virtually identical DNA sequence's in closely related species to encode for the same gene, especially when you consider the redundancy in the code and the fact that there are probably several (hundred? thousand?) possible aa sequences which could produce a gene with the same function. I guess god is fond of the copy/paste function in his DNA editor)

Replies to this message:
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peter borger
Member (Idle past 7665 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 2 of 50 (13979)
07-23-2002 2:43 AM
Reply to: Message 1 by monkenstick
07-23-2002 1:23 AM


Dear Monkenstick,
I already overthrew this fallacy, but for your updating I will show it once more. (As demonstarted in the thread: Pseudogenes & retrotransposons)
"In the evolutionary community the shared retroviruses are commonly regarded as evidence of common descent. However, this may only be superficial.
First there is the claim that they do not serve any purpose. That should be scientifically proven. Maybe their function cannot be deduced from knocking them out, but that does not say anything about their function, since you can knock out genes with an open reading frame without any effect on the organism (genetic redundancies). Secondly, I would like to see the complete DNA sequences within the species and between the species before jumping to conclusions.
I checked one claim about the GLO pseudogene (the gene that catalyses the final step in vitamin c synthesis) that has been inactivated in the same spot in primates and is taken as proof for common ancestry. And, indeed a superficial look would immediately convince any evolutionist. However, if you have a careful look at the presented sequences you will discover that the replacement of nucleotides is not at random between the distinct species. Secondly, you will discover that it does not make a difference for the mutation rate of this gene whether it is functional or not, in contrast to what evolution theory would predict. Thirdly, it violates population genetics: why would the inactivated gene become fixed in the entire population, while the active gene conveys longivity. In addition, evolution never compensated for vitamin C uptake in the gut, and, finally, the gene is redundant anyway since the third step in vit c synthesis already yields vitamin C by spontenaous oxidation and is sufficient to avoid vit c deficiency. Also not unimportant, at least 2 primates are able to synthesise vitamin c in the liver, indicating the presence of an intact GLO gene (I once had a discussion about this gene with Dr D. Theobald (Talk Origin) so I know a bit about pseudogenes).
However, at this level it is mostly speculation since we do not know a lot about it, yet.
In analogy to vestiges (appendix, tonsils) that shouldn't have a function according to evolution theory, it is far too early to say that this is proof for common descent. Show me the DNA sequences of these retroviruses in chimp and man, and I will respond in more detail.
Retrotransposons may have a function in epigenic regulation of gene expression (actually there is some proof for that. See: Dr. E. Max's website Talk Origin. Another one regulates the aghouti colour of fur in mice). It is thought that they may also play a role in eye colour (human), and some diseases like schizophrenia, and B.-W.-syndrome.
Evolutionists are free to claim these genes as evidence for common descent (as they did -- and still do -- for genetic redundancies, but which has actually contributed to the fall of natural selection as I will substantiate with scientific evidence in my forthcoming posting on genetic redundancy).
I foresee that ultimately there will be an unexpected (regulatory or stabilizing) function for these "vestiges".
Furthermore, read Spetner's book carefully on what he has to say on transposons. It makes sense. It will pay off to read opposite opinions. In summary, it is not an argument to take DNA sequences of which we do not know the function of as evidence for evolution. Our lack of knowledge described 98% of the DNA in the genome as "junk". This vision is increasingly proven to be wrong."
Best wishes,
Peter
Also read Dr Max's "rebuttal" to Spetner's book on the true-origin website.

This message is a reply to:
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Replies to this message:
 Message 3 by Peter, posted 07-23-2002 6:25 AM peter borger has not replied
 Message 4 by mark24, posted 07-23-2002 8:03 AM peter borger has replied
 Message 49 by Dr_Tazimus_maximus, posted 08-14-2002 11:38 AM peter borger has replied

  
Peter
Member (Idle past 1478 days)
Posts: 2161
From: Cambridgeshire, UK.
Joined: 02-05-2002


Message 3 of 50 (13992)
07-23-2002 6:25 AM
Reply to: Message 2 by peter borger
07-23-2002 2:43 AM


quote:
Originally posted by peter borger:

I checked one claim about the GLO pseudogene (the gene that catalyses the final step in vitamin c synthesis) that has been inactivated in the same spot in primates and is taken as proof for common ancestry. And, indeed a superficial look would immediately convince any evolutionist. However, if you have a careful look at the presented sequences you will discover that the replacement of nucleotides is not at random between the distinct species.

What do you mean by random ?
How can you know that the replacement is non-random ?
quote:
Originally posted by peter borger:

Secondly, you will discover that it does not make a difference for the mutation rate of this gene whether it is functional or not, in contrast to what evolution theory would predict.

Does evolutionary theory make any predictions about mutation
rates ? If so what are they ?
quote:
Originally posted by peter borger:

Thirdly, it violates population genetics: why would the inactivated gene become fixed in the entire population, while the active gene conveys longivity.

It depends on what other traits are expressed by alleles
on the same chromosome, surely.
Equally, elsewhere in your post you say that these sequences
may have as yet undiscovered functionality ... so you are making
the same jump-to-conclusion that you blame mainstream
evo's of.
quote:
Originally posted by peter borger:

In addition, evolution never compensated for vitamin C uptake in the gut,

The point being ... ?
quote:
Originally posted by peter borger:

and, finally, the gene is redundant anyway since the third step in vit c synthesis already yields vitamin C by spontenaous oxidation and is sufficient to avoid vit c deficiency.

So doesn't that answer your previous objection of how could
it be dropped ?
quote:
Originally posted by peter borger:

Also not unimportant, at least 2 primates are able to synthesise vitamin c in the liver, indicating the presence of an intact GLO gene (I once had a discussion about this gene with Dr D. Theobald (Talk Origin) so I know a bit about pseudogenes).
However, at this level it is mostly speculation since we do not know a lot about it, yet.

So why would a creator break the gene in all but two primates ?
I mean primate groups
Isn't the existence of an intact GLO gene in some primates, and
one broken in the same way in others support for branching of
the species in question ... i.e. for evolution ?

This message is a reply to:
 Message 2 by peter borger, posted 07-23-2002 2:43 AM peter borger has not replied

  
mark24
Member (Idle past 5194 days)
Posts: 3857
From: UK
Joined: 12-01-2001


Message 4 of 50 (13998)
07-23-2002 8:03 AM
Reply to: Message 2 by peter borger
07-23-2002 2:43 AM


Peter B,
quote:
Originally posted by peter borger:

"In the evolutionary community the shared retroviruses are commonly regarded as evidence of common descent. However, this may only be superficial.
First there is the claim that they do not serve any purpose. That should be scientifically proven. Maybe their function cannot be deduced from knocking them out, but that does not say anything about their function, since you can knock out genes with an open reading frame without any effect on the organism (genetic redundancies). Secondly, I would like to see the complete DNA sequences within the species and between the species before jumping to conclusions.

It’s a small number of transposons that are thought to have function, these are located near to functional genes. But, so what? We know how transposons replicate themselves through the genome, so homologous (between species) transposons are evidence of descent.
quote:
Originally posted by peter borger:

I checked one claim about the GLO pseudogene (the gene that catalyses the final step in vitamin c synthesis) that has been inactivated in the same spot in primates and is taken as proof for common ancestry. And, indeed a superficial look would immediately convince any evolutionist. However, if you have a careful look at the presented sequences you will discover that the replacement of nucleotides is not at random between the distinct species.

How do you know the replacement between species is not random?
At what GLO sites are the hotspots?
Also,
quote:
"Random nucleotide substitutions in primate nonfunctional gene for L-gulono-gamma-lactone oxidase, the missing enzyme in L-ascorbic acid biosynthesis."
Ohta Y, Nishikimi M
Abstract:
Humans and other primates have no functional gene for L-gulono-gamma-lactone oxidase that catalyzes the last step of L-ascorbic acid biosynthesis. The 164-nucleotide sequence of exon X of the gene was compared among human, chimpanzee, orangutan, and macaque, and it was found that nucleotide substitutions had occurred at random throughout the sequence with a single nucleotide deletion, indicating that the primate L-gulono-gamma-lactone oxidase genes are a typical example of pseudogene.
Interesting. Nishikimi thinks the substitutions are random in exon x of this pseudogene.
quote:
Originally posted by peter borger:
Secondly, you will discover that it does not make a difference for the mutation rate of this gene whether it is functional or not, in contrast to what evolution theory would predict.
Cite please.
quote:
Originally posted by peter borger:

Thirdly, it violates population genetics: why would the inactivated gene become fixed in the entire population, while the active gene conveys longivity. In addition, evolution never compensated for vitamin C uptake in the gut, and, finally, the gene is redundant anyway since the third step in vit c synthesis already yields vitamin C by spontenaous oxidation and is sufficient to avoid vit c deficiency.

Violates population genetics? I, & everyone else I know survives quite happily without being able to synthesise vitamin c. This shows that the inability to synthesise vit c doesn’t particularly affect fitness. As such, natural selection will have a very weak effect on the gene. If this is true, then the wrecked gene can be fixed by genetic drift.
quote:
Originally posted by peter borger:

Also not unimportant, at least 2 primates are able to synthesise vitamin c in the liver, indicating the presence of an intact GLO gene (I once had a discussion about this gene with Dr D. Theobald (Talk Origin) so I know a bit about pseudogenes).
However, at this level it is mostly speculation since we do not know a lot about it, yet.

Which two primates specifically? I'm willing to put money on that the two primates are "prosimian", & are placed low down the accepted primate phylogeny. Meaning that their divergence predates the vit c gene going tits-up. This is also at odds with your claim that hot spots wreck the genes at a specific location. Why haven't these primates vit c gene gone bang too, given that they are pre-programmed to?
Furthermore, & most importantly, in addition to the two primates, other orders & classes have fully functional vit c genes that haven’t been wrecked by your hot spot, why?
quote:
Originally posted by peter borger:

Retrotransposons may have a function in epigenic regulation of gene expression (actually there is some proof for that. See: Dr. E. Max's website Talk Origin. Another one regulates the aghouti colour of fur in mice). It is thought that they may also play a role in eye colour (human), and some diseases like schizophrenia, and B.-W.-syndrome.
Evolutionists are free to claim these genes as evidence for common descent (as they did -- and still do -- for genetic redundancies, but which has actually contributed to the fall of natural selection as I will substantiate with scientific evidence in my forthcoming posting on genetic redundancy).
I foresee that ultimately there will be an unexpected (regulatory or stabilizing) function for these "vestiges".
Furthermore, read Spetner's book carefully on what he has to say on transposons. It makes sense. It will pay off to read opposite opinions. In summary, it is not an argument to take DNA sequences of which we do not know the function of as evidence for evolution. Our lack of knowledge described 98% of the DNA in the genome as "junk". This vision is increasingly proven to be wrong."

Functioning transposons are just as good an evidence of common descent as functional gene sequences. Why does them having function represent a falsification?
Mark
------------------
Occam's razor is not for shaving with.
[This message has been edited by mark24, 07-23-2002]
[This message has been edited by mark24, 07-23-2002]

This message is a reply to:
 Message 2 by peter borger, posted 07-23-2002 2:43 AM peter borger has replied

Replies to this message:
 Message 5 by mark24, posted 07-23-2002 10:50 AM mark24 has not replied
 Message 6 by peter borger, posted 07-23-2002 8:19 PM mark24 has replied
 Message 14 by peter borger, posted 07-24-2002 2:40 AM mark24 has replied

  
mark24
Member (Idle past 5194 days)
Posts: 3857
From: UK
Joined: 12-01-2001


Message 5 of 50 (14002)
07-23-2002 10:50 AM
Reply to: Message 4 by mark24
07-23-2002 8:03 AM


Deleted duplicate post.
[This message has been edited by mark24, 07-23-2002]

This message is a reply to:
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peter borger
Member (Idle past 7665 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 6 of 50 (14024)
07-23-2002 8:19 PM
Reply to: Message 4 by mark24
07-23-2002 8:03 AM


dear mark24,
The reference you have to study carefully is: Ohta et al Biochim Biophysica Acta 1472 (1999), 408-411. Study the presented DNA and protein sequences carefully with an unbiased mind. My biological intuitaion told me that something is wrong with the sequences. It took me months to figure out exactly what it was. If I were you I would calculate a bit on it.
If you have a close look you will see that the rate of change between rat and human, chimp, orang and macaque is almost constant 26/164, 25/164, 26/164 and 29/164, respectively. If we compare human with chimp, orang and macaque one finds 4/163, 7/163 and 15/163, respectively. However, if we compare chimp and orang, and chimp and macaque we find 9/163 and 15/163. Thus, while we observe 4/163 between human and chimp, human and chimp are equally similar to macaque. Thus if we reason from the macaque's position human and chimp coincide. Still, we "know" there is time difference of 6 million years.
If we assume 1% variation per million years (in primates this is reasonable), this implicates that the common ancestor for both human and chimp lived around 10 million years ago. Thus, this pseudogene example violates the descent of primates. (the authors choose their references so that it is in accord with the accepted vision, but there are references of neutral rates in primates that would support my vision). Even the authors admit that the orangutan does not fit in what they expected.
If it is allowed to compare these primates and assuming paleontological time scales to be right, the neutral rate observed in primates is actually 15/163:25 = 3.6exp-3= 0.36% per million years. Similarly, the change since the divergence of rats and primates is 26/164:50 = 0.31% per million years. Thus, it doesn't matter whether the gene has been inactivated or not, it still changes with the same rate. And so we have another violation.
Finally, it is no secret hat the GLO pseudogene violates Darwinian Evolution Theory (it is an example of non-darwinian evolution) and population genetics. I presume you know that.
Of course I agree with you on the common single nucleotide deletion, but it may have been directed.
Furthermore, you state:
"Furthermore, & most importantly, in addition to the two primates, other orders & classes have fully functional vit c genes that haven’t been wrecked by your hot spot, why?"
You are wrong. Throughout all orders and classed in the animal kingdom vit c synthesis has been inactivated randomly. For instance, the whole family of bats -- irrespective whether they are fruit eating or carnivorous -- do not synthesise vit c. It remains to be established which genes in the vit c biosynthesis have been inactivated, and where. Maybe there are several "hotspots".
You also wonder:
"Functioning transposons are just as good an evidence of common descent as functional gene sequences. Why does them having function represent a falsification?"
As mentioned before, you cannot take DNA sequences in the same spot of the chromosome that we do not know the function of as proof for common descent. Maybe it is not a falsification, but you are not allowed to do this. If you do that, than I will take alle homologue DNA sequences in human and chimp that are not in the same spot as proof against common descent. And, I think you will not like that since it is a tremendous amount.
Finally, "WHY-questions" are irrelevant in science, it is metaphysics.
Best wishes,
Peter

This message is a reply to:
 Message 4 by mark24, posted 07-23-2002 8:03 AM mark24 has replied

Replies to this message:
 Message 7 by mark24, posted 07-23-2002 9:06 PM peter borger has replied
 Message 8 by John, posted 07-23-2002 9:29 PM peter borger has not replied

  
mark24
Member (Idle past 5194 days)
Posts: 3857
From: UK
Joined: 12-01-2001


Message 7 of 50 (14027)
07-23-2002 9:06 PM
Reply to: Message 6 by peter borger
07-23-2002 8:19 PM


quote:
Originally posted by peter borger:

dear mark24,
The reference you have to study carefully is: Ohta et al Biochim Biophysica Acta 1472 (1999), 408-411. Study the presented DNA and protein sequences carefully with an unbiased mind. My biological intuitaion told me that something is wrong with the sequences. It took me months to figure out exactly what it was. If I were you I would calculate a bit on it.

Is there an actual paper title I could look up? I’m getting no joy with this Acta 1472 thang? Cheers.
quote:
Originally posted by peter borger:

Finally, it is no secret hat the GLO pseudogene violates Darwinian Evolution Theory (it is an example of non-darwinian evolution) and population genetics. I presume you know that.

Yup, drift must have played a part. Whats your point?
How does it violate population genetics?
You don’t even know that stem primates weren’t at an advantage in having their vit c synthesis ability switched off. Vit c is synthesised from glucose, if you already have an excellent source of vit c via your diet, then not having to lose valuable glucose to produce something you already have is an advantage, yes?
quote:
Originally posted by peter borger:

Of course I agree with you on the common single nucleotide deletion, but it may have been directed.

Directed in such a way as to appear random? How?
quote:
Originally posted by peter borger:

Furthermore, you state:
"Furthermore, & most importantly, in addition to the two primates, other orders & classes have fully functional vit c genes that haven’t been wrecked by your hot spot, why?"
You are wrong. Throughout all orders and classed in the animal kingdom vit c synthesis has been inactivated randomly. For instance, the whole family of bats -- irrespective whether they are fruit eating or carnivorous -- do not synthesise vit c. It remains to be established which genes in the vit c biosynthesis have been inactivated, and where. Maybe there are several "hotspots".

Excellent. Randomly inactivated.
I really don’t see the relevance of whether the wrecking site was on a hotspot or not, the point surely is that you couldn’t predict where the next mutation would occur, this is entirely a separate question as to the fixation of the gene. For your information, there was one family of the order Chiroptera (bats) that had at least one species that could produce trace amounts of vit c in the liver, the other 6 families tested were blank.
You have missed the point, the rest of the mammals, barring Guinea Pigs, can produce vit c. Why wasn’t their vit c gene wrecked by directed hot spots?
quote:
Originally posted by peter borger:

You also wonder:
"Functioning transposons are just as good an evidence of common descent as functional gene sequences. Why does them having function represent a falsification?"
As mentioned before, you cannot take DNA sequences in the same spot of the chromosome that we do not know the function of as proof for common descent. Maybe it is not a falsification, but you are not allowed to do this. If you do that, than I will take alle homologue DNA sequences in human and chimp that are not in the same spot as proof against common descent. And, I think you will not like that since it is a tremendous amount.

We are taking HOMOLOGOUS sequences, their function doesn’t need to be known, JUST THAT THEY ARE HOMOLOGOUS.
Now,
1/ How do you know the replacement between species is not random?
2/ At what GLO sites are the hotspots? You need to know this in order to attribute the wrecking to the hot spot(s) at all.
3/ Which two primates specifically CAN synthesise vit c?
Thanks,
Mark
------------------
Occam's razor is not for shaving with.

This message is a reply to:
 Message 6 by peter borger, posted 07-23-2002 8:19 PM peter borger has replied

Replies to this message:
 Message 9 by peter borger, posted 07-23-2002 10:09 PM mark24 has not replied

  
John
Inactive Member


Message 8 of 50 (14030)
07-23-2002 9:29 PM
Reply to: Message 6 by peter borger
07-23-2002 8:19 PM


quote:
Originally posted by peter borger:
If we assume 1% variation per million years (in primates this is reasonable), this implicates that the common ancestor for both human and chimp lived around 10 million years ago.
Isn't this about right? It on the high end of the range, but still just barely in there.
------------------
www.hells-handmaiden.com

This message is a reply to:
 Message 6 by peter borger, posted 07-23-2002 8:19 PM peter borger has not replied

  
peter borger
Member (Idle past 7665 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 9 of 50 (14032)
07-23-2002 10:09 PM
Reply to: Message 7 by mark24
07-23-2002 9:06 PM


dear mark,
You say:
"I really don’t see the relevance of whether the wrecking site was on a hotspot or not, the point surely is that you couldn’t predict where the next mutation would occur, this is entirely a separate question as to the fixation of the gene. For your information, there was one family of the order Chiroptera (bats) that had at least one species that could produce trace amounts of vit c in the liver, the other 6 families tested were blank."
This is not significant. Vit c synthesis requires the activity of four proteins. Thus, theoretically four gene defects can give rise to vitamin C deficiency. In human we see two genetic defects. A defective lactonase gene completely abolishes vitamin C synthesis. Defects in L-gulonolactone oxidase, which is the final step in vitamin C synthesis does not completely abolish vitamin C synthesis (your bat example shows trace amounts vit c), because the substrate, L-gulonolactone, spontaneously decomposes to 2-keto-gulono-gamma-lactone (=vitamin C) in the presence of oxygen. Remember that there was a considerable amount of sailors who survived the long 16th century overseas voyages. The survivors were still able to synthesise vitamin C, albeit in very low concentrations through the action of lactonase, and they did not have to take vit c. (In some human populations, for instance the desert nomads of the Sahara the non-synthesisers are completely removed from the gene pool.)
Question remains how this (redundant) enzyme evolved, while it was not absolutely required for survival (lactonase is already sufficient to produce the amount of vit c to survive)?
The GLO enzyme ensures longevity. Why than was selected for non-producing primates (=non-darwinian evolution)? It is obvious that the longevity must have been a redundant trait. It is an evolutionary riddle how a defective gene improved reproductive success: it was spread throughout the complete population of primates.
If the GLO enzyme was inactivated 25 million years ago there was ample opportunity to improve vit c uptake in the gut. Still, humans are very lousy uptakers. (Levels of vit C uptake reach levels that can also be generated by lactonase activity alone).
Your questions:
1/ How do you know the replacement between species is not random?
Have a look at the predicted protein sequence in the article I refered to.
2/ At what GLO sites are the hotspots? You need to know this in order to attribute the wrecking to the hot spot(s) at all.
We do not know yet, since the mechanism is not known. There may be several hotspots. Have a close look at the 1g5 gene in Drosophila.
3/ Which two primates specifically CAN synthesise vit c?
Two prosimians, don't know what species. Maybe you can look it up.
best wishes
Peter

This message is a reply to:
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Replies to this message:
 Message 10 by John, posted 07-23-2002 10:38 PM peter borger has replied

  
John
Inactive Member


Message 10 of 50 (14034)
07-23-2002 10:38 PM
Reply to: Message 9 by peter borger
07-23-2002 10:09 PM


[QUOTE]Originally posted by peter borger:
[b]Remember that there was a considerable amount of sailors who survived the long 16th century overseas voyages.[/QUOTE]
[/b]
Wasn't scurvey a huge problem though?
quote:
In some human populations, for instance the desert nomads of the Sahara the non-synthesisers are completely removed from the gene pool.
I'm curious. Do you mean that there are nomads with no non-synthesisers? Or that the nomadic populations are cut off from the gene pool?
------------------
www.hells-handmaiden.com

This message is a reply to:
 Message 9 by peter borger, posted 07-23-2002 10:09 PM peter borger has replied

Replies to this message:
 Message 11 by peter borger, posted 07-23-2002 11:46 PM John has replied

  
peter borger
Member (Idle past 7665 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 11 of 50 (14037)
07-23-2002 11:46 PM
Reply to: Message 10 by John
07-23-2002 10:38 PM


Dear john,
Indeed scurvy was a huge problem, but not everyone died during these voyages. It is reasonable to assume that the vit c synthesizer (via sponteneous oxydation) were the survivers. Thus, there was selection during these voyages for the intact galactonase enzyme. Similarly, desertnomads all have this intact gene. Do a search on internet and you will find the answer to your questions.
best wishes
Peter

This message is a reply to:
 Message 10 by John, posted 07-23-2002 10:38 PM John has replied

Replies to this message:
 Message 12 by John, posted 07-24-2002 12:06 AM peter borger has replied

  
John
Inactive Member


Message 12 of 50 (14039)
07-24-2002 12:06 AM
Reply to: Message 11 by peter borger
07-23-2002 11:46 PM


quote:
Originally posted by peter borger:
Dear john,
Indeed scurvy was a huge problem, but not everyone died during these voyages. It is reasonable to assume that the vit c synthesizer (via sponteneous oxydation) were the survivers. Thus, there was selection during these voyages for the intact galactonase enzyme. Similarly, desertnomads all have this intact gene. Do a search on internet and you will find the answer to your questions.
best wishes
Peter

Actually a web search isn't helping, and I am good at finding things online.
Can you provide some links or other info?
------------------
www.hells-handmaiden.com

This message is a reply to:
 Message 11 by peter borger, posted 07-23-2002 11:46 PM peter borger has replied

Replies to this message:
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peter borger
Member (Idle past 7665 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 13 of 50 (14041)
07-24-2002 12:10 AM
Reply to: Message 12 by John
07-24-2002 12:06 AM


Dear John, Don't give up so fast.
It took me along time to find all relevant information. But here I have a link for you:
http://yarchive.net/med/vitamin_c.html
Have a good one,
Peter

This message is a reply to:
 Message 12 by John, posted 07-24-2002 12:06 AM John has not replied

  
peter borger
Member (Idle past 7665 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 14 of 50 (14052)
07-24-2002 2:40 AM
Reply to: Message 4 by mark24
07-23-2002 8:03 AM


Dear Mark,
In response to:
"Interesting. Nishikimi thinks the substitutions are random in exon x of this pseudogene."
If you have a very careful look at the protein sequence you will discover that they do not change at random. The article of Ohta and Nishikimi is discussed according to the paradigm of common descent.
If you objectively study the presented sequences, i.e without this paradigm in mind, you will see that some changes are non-random. In the presented protein sequence this is most obvious. From orangutan to chimp 2 aa changed, and 2 aa changed afterwards (from chimp to human). I find it very surprising that the aa at position 11 (from the righthand side) was two times involved, since it is a non-functional protein. I wouldn't have expected that by chance alone. So I think there is a (non-random) mechanism involved.
Cleared things up?
Best wishes,
Peter

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 Message 4 by mark24, posted 07-23-2002 8:03 AM mark24 has replied

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 Message 15 by mark24, posted 07-24-2002 10:28 AM peter borger has replied

  
mark24
Member (Idle past 5194 days)
Posts: 3857
From: UK
Joined: 12-01-2001


Message 15 of 50 (14058)
07-24-2002 10:28 AM
Reply to: Message 14 by peter borger
07-24-2002 2:40 AM


quote:
Originally posted by peter borger:
Dear Mark,
In response to:
"Interesting. Nishikimi thinks the substitutions are random in exon x of this pseudogene."
If you have a very careful look at the protein sequence you will discover that they do not change at random. The article of Ohta and Nishikimi is discussed according to the paradigm of common descent.
If you objectively study the presented sequences, i.e without this paradigm in mind, you will see that some changes are non-random. In the presented protein sequence this is most obvious. From orangutan to chimp 2 aa changed, and 2 aa changed afterwards (from chimp to human). I find it very surprising that the aa at position 11 (from the righthand side) was two times involved, since it is a non-functional protein. I wouldn't have expected that by chance alone. So I think there is a (non-random) mechanism involved.
Cleared things up?
Best wishes,
Peter

Your going to have to do better than a couple of mutations on the same spot. I've seen sequences where most sites have a couple of mutations, & one or two have hundreds. They ARE hot spots. Such studies are concuded from thousands of mutations on particular genes.
If you are going to say with any certainty that these sites are hot spots, then you need a much larger sample. Your problem is, that unlike extant sequences where we can directly test the likelyhood of mutations at particular sites, you don't possess the original gene with which to test.
You are also going to have to do better than "the article of Ohta and Nishikimi is discussed according to the paradigm of common descent". If you are going to dismiss their conclusion that mutations on exon x are random, then you need to show the opposite. Hand waving won't work.
Mark
------------------
Occam's razor is not for shaving with.

This message is a reply to:
 Message 14 by peter borger, posted 07-24-2002 2:40 AM peter borger has replied

Replies to this message:
 Message 16 by peter borger, posted 07-24-2002 8:01 PM mark24 has replied

  
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