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Author Topic:   Arguments against evolution: are they valid?
Brad McFall
Member (Idle past 5033 days)
Posts: 3428
From: Ithaca,NY, USA
Joined: 12-20-2001


Message 16 of 23 (89815)
03-02-2004 3:09 PM
Reply to: Message 7 by KCdgw
02-18-2004 9:50 PM


Re: Genetic Homeostasis
But because Lerner left open the issue of how the locations the "drastic" selection were subsetted from opening on larger issues of interpretation in the terms I have the whole idea as useless. I was intrigued when I first ran across this one but if selection for chicken eggs in one farm in Penn can be drastically different than the comparision of a population on the farm and somewhere else the interesting application of the idea (to bound the effect as it is in Meso Evolution) fell a priori. It seems to remand the "new math" that Wright called down but has yet to appear.

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Saviourmachine
Member (Idle past 3554 days)
Posts: 113
From: Holland
Joined: 01-16-2004


Message 17 of 23 (89962)
03-03-2004 3:34 AM
Reply to: Message 13 by wj
02-29-2004 9:04 PM


Arguments => Questions
In the way I reformulated the points (except nr. 3) there are still problems to be solved by evolutionists. See post 6.
1) Beneficial mutations are still rare, mostly not tht beneficial at all, and happen mostly in the lab. (A lot beneficial mutations occur in articifial life)
2) Why should this blind process on the long term lead to current situation? Is nature able to select against slightly bad mutations, or select for slightly good ones? Are point mutations generally not filtered out? Can gene duplication lead to all known genes? What's the difference in enzyme space between them?
And so on, it aren't only creationists that have problems to solve. The word 'arguments' isn't cautious formulated, it are questions that need an answer.
- Edit - spelling errors
[This message has been edited by Saviourmachine, 03-03-2004]

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Replies to this message:
 Message 18 by JonF, posted 03-03-2004 9:13 AM Saviourmachine has replied

  
JonF
Member (Idle past 168 days)
Posts: 6174
Joined: 06-23-2003


Message 18 of 23 (89998)
03-03-2004 9:13 AM
Reply to: Message 17 by Saviourmachine
03-03-2004 3:34 AM


Re: Arguments => Questions
Beneficial mutations are still rare, mostly not tht beneficial at all ...
Yes. However, the mathematical analyses (on which I am not an expert) show that the observed beneficial mutation rates are more than sufficient (even though most mutations, beneficial or not, are not fixed in the population).
and happen mostly in the lab.
Huh? Do you have evidence for that? And, assuming it's true, so what? See my reply above.
Why should this blind process on the long term lead to current situation?
Because selection is a powerful filter. Note that selection does not lead to a predetermined situation; that is, the current situation is just one of many to which selection could have led. We can't predict in advance who will win the lottery, but someone's going to win; similarly, we couldn't have predicted the current state of life 4 billion years ago, but some current state of life was essentially guaranteed as of 4 billion years ago.
Is nature able to select against slightly bad mutations, or select for slightly good ones?
Yes. Population genetics is a large, rich, and well-studied field. See Introduction to Evolutionary Biology or, for lots of links to technical papers and software simulations, see Population Genetics Links (many of which are dead links, but there are some good live ones).
Are point mutations generally not filtered out?
Huh?
Can gene duplication lead to all known genes?
I don't know offhand. Since gene duplication is not the only observed mechanism of genetic variation, why do you ask the question?
What's the difference in enzyme space between them?
It varies widely, and there are different ways of defining "enzyme space". The analyses tell us that there's no reason to suspect that there are any unbridgeable gaps, the ID crowd's arm-waving arguments notwithstanding.

This message is a reply to:
 Message 17 by Saviourmachine, posted 03-03-2004 3:34 AM Saviourmachine has replied

Replies to this message:
 Message 19 by Saviourmachine, posted 03-05-2004 4:05 PM JonF has replied

  
Saviourmachine
Member (Idle past 3554 days)
Posts: 113
From: Holland
Joined: 01-16-2004


Message 19 of 23 (90614)
03-05-2004 4:05 PM
Reply to: Message 18 by JonF
03-03-2004 9:13 AM


Re: Arguments => Questions
JonF writes:
However, the mathematical analyses (on which I am not an expert) show that the observed beneficial mutation rates are more than sufficient
If it's more than sufficient, then it's to much.
JonF writes:
Saviourmachine writes:
and happen mostly in the lab.
Huh? Do you have evidence for that? And, assuming it's true, so what? See my reply above.
Please, give me five beneficial mutations that happened in the open field (besides the famous 'nylon' digesting bacteria).
JonF writes:
Saviourmachine writes:
Is nature able to select against slightly bad mutations, or select for slightly good ones?
Yes. Population genetics is a large, rich, and well-studied field. See Introduction to Evolutionary Biology or, for lots of links to technical papers and software simulations, see Population Genetics Links (many of which are dead links, but there are some good live ones).
Natural selection is blind for slightly good or slightly bad mutations, the adaptive advantage is too small.
JonF writes:
Saviourmachine writes:
Are point mutations generally not filtered out?
Huh?
The antistreng is used as a backup.
JonF writes:
Saviourmachine writes:
Can gene duplication lead to all known genes?
I don't know offhand. Since gene duplication is not the only observed mechanism of genetic variation, why do you ask the question?
Some persons say that point-mutations can. Then you've to be very pre-justiced. But if you know some additional very clever mechanisms, tell me.
JonF writes:
It varies widely, and there are different ways of defining "enzyme space". The analyses tell us that there's no reason to suspect that there are any unbridgeable gaps, the ID crowd's arm-waving arguments notwithstanding.
Do you want to give me a few? Are they really saying that there are no unbridgeable gaps? How do they know that, how can you know that gaps you will encounter, won't be unbridgeable???

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 Message 18 by JonF, posted 03-03-2004 9:13 AM JonF has replied

Replies to this message:
 Message 20 by JonF, posted 03-05-2004 4:26 PM Saviourmachine has replied

  
JonF
Member (Idle past 168 days)
Posts: 6174
Joined: 06-23-2003


Message 20 of 23 (90623)
03-05-2004 4:26 PM
Reply to: Message 19 by Saviourmachine
03-05-2004 4:05 PM


Re: Arguments => Questions
However, the mathematical analyses (on which I am not an expert) show that the observed beneficial mutation rates are more than sufficient
If it's more than sufficient, then it's to much.
Only if one assumes a constant beneficial mutation rate ... remember that "beneficial" changes with the environment.
Please, give me five beneficial mutations that happened in the open field
Special today, half a dozen in humans:
  • polymorphism (4G/5G) of the PAI-1 gene.
  • two amino acid substitutions in LPL, the Asn291-Ser and the Asp9-Asn
  • a common mutation (Ser447-Ter) of the human LPL gene
  • heterozygotes for the Arg661 --> Stop mutation
  • C825T polymorphism in the gene encoding for the Gbeta3 subunit of heterotrimeric G proteins
  • polymorphisms involving R353Q and hypervariable region 4 of the factor VII gene

See The Mystery Village With No Heart Disease, Are Mutations Harmful?, and Examples of Beneficial Mutations in Humans.
Natural selection is blind for slightly good or slightly bad mutations, the adaptive advantage is too small.
Unsupported assertion. Please show your work. Population genetics has lots of known mathematics and theorems.
Are point mutations generally not filtered out?
Huh?
The antistreng is used as a backup
Huh?
You can't actually think that mutations that don't take place on both copies of a gene, or both sides of a DNA molecule, are cancelled out by the existence of the other gene or the other side of the DNA molecule? Can you?
Do you want to give me a few? Are they really saying that there are no unbridgeable gaps? How do they know that, how can you know that gaps you will encounter, won't be unbridgeable???
Give you a few what?
And no, nobody is really saying that there are no unbridgeable gaps, they are saying what I said already: "there's no reason to suspect that there are any unbridgeable gaps". IOW, we haven't encountered any, there is no well-supported theory that tells us that there should be any, and we might as well proceed as if there aren't any. If we come across any, we'll re-think.

This message is a reply to:
 Message 19 by Saviourmachine, posted 03-05-2004 4:05 PM Saviourmachine has replied

Replies to this message:
 Message 21 by Saviourmachine, posted 03-05-2004 5:05 PM JonF has replied

  
Saviourmachine
Member (Idle past 3554 days)
Posts: 113
From: Holland
Joined: 01-16-2004


Message 21 of 23 (90640)
03-05-2004 5:05 PM
Reply to: Message 20 by JonF
03-05-2004 4:26 PM


Re: Arguments => Questions
JohF writes:
Only if one assumes a constant beneficial mutation rate ... remember that "beneficial" changes with the environment.
So the beneficial mutation rate was lower in the past? Or do you want to say that you can't say anything about the past because we can't extrapolate the current rate?
The molecular clock gives a little bit older ages than the archeologic clock, so you may not be right about that the observed beneficial mutation rates are more than sufficient.
JonF writes:
Special today, half a dozen in humans:
  • polymorphism (4G/5G) of the PAI-1 gene.
  • two amino acid substitutions in LPL, the Asn291-Ser and the Asp9-Asn
  • a common mutation (Ser447-Ter) of the human LPL gene
  • heterozygotes for the Arg661 --> Stop mutation
  • C825T polymorphism in the gene encoding for the Gbeta3 subunit of heterotrimeric G proteins
  • polymorphisms involving R353Q and hypervariable region 4 of the factor VII gene
Apart from that site you mentioned, I didn't find the original papers. Do you have them? I tried to google for Asp9-Asn and Asn291-Ser substitution for example, and did find a lot of harmful mutations, increasing the progression of atherosclerosis (like here) but not the beneficial one.
Saviourmachine writes:
Natural selection is blind for slightly good or slightly bad mutations, the adaptive advantage is too small.
Seems reasonable, I don't see the need for numbers. If there is a lot of theory about this, would you explain this paradox in a few seconds? An argument I heard was that small differences in the genome can lead to big differences in the phenotype. Is there something more?
JonF writes:
You can't actually think that mutations that don't take place on both copies of a gene, or both sides of a DNA molecule, are cancelled out by the existence of the other gene or the other side of the DNA molecule? Can you?
The complementary streng with 'inverted' bases is just for correcting mistakes like point mutations.
JonF writes:
The analyses tell us that there's no reason to suspect that there are any unbridgeable gaps, the ID crowd's arm-waving arguments notwithstanding.
...
Give you a few what?
Can you provide me with an analyse regarding the nature of the remaining gaps?

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 Message 20 by JonF, posted 03-05-2004 4:26 PM JonF has replied

Replies to this message:
 Message 22 by JonF, posted 03-05-2004 6:13 PM Saviourmachine has replied

  
JonF
Member (Idle past 168 days)
Posts: 6174
Joined: 06-23-2003


Message 22 of 23 (90670)
03-05-2004 6:13 PM
Reply to: Message 21 by Saviourmachine
03-05-2004 5:05 PM


Re: Arguments => Questions
So the beneficial mutation rate was lower in the past?
Perhaps. The benefical mutation rate is a function of the mutation rate (which may change somewhat) and what is beneficial (which changes as the environment changes). And, of course, the fixation rate changes too.
Natural selection is blind for slightly good or slightly bad mutations, the adaptive advantage is too small.
Seems reasonable, I don't see the need for numbers.
Doesn't seem reasonable, only numbers will resolve the disagreement. You have made an assertion, support it or abandon it.
If there is a lot of theory about this, would you explain this paradox in a few seconds?
What paradox? I haven't seen mention of any paradox.
If you want me to teach you the math of population genetics in this forum, no thanks; the medium is too limited and I don't know it well enough to teach it. You can look at things like A formal mathematical treatment of natural selection, or the links I posted already, or go to a library.
I didn't find the original papers. Do you have them?
No. Go to a library or, if you are willing to spend a little money, yo can get anything from the MIT Library
The complementary streng with 'inverted' bases is just for correcting mistakes like point mutations.
Indeed? Would you explain this in a few seconds, paying particular attention to evidence for how this process works and how effective it is.
Can you provide me with an analyse regarding the nature of the remaining gaps?
No. Again this is a terrible medium, and again I don't know it well enough to teach it.
I find it very interesting that you made several assertions and are now asking fundamental questions about the subjects of your assertions, revealing that you don't know much of anything about what you've claimed.

This message is a reply to:
 Message 21 by Saviourmachine, posted 03-05-2004 5:05 PM Saviourmachine has replied

Replies to this message:
 Message 23 by Saviourmachine, posted 03-06-2004 5:18 PM JonF has not replied

  
Saviourmachine
Member (Idle past 3554 days)
Posts: 113
From: Holland
Joined: 01-16-2004


Message 23 of 23 (90831)
03-06-2004 5:18 PM
Reply to: Message 22 by JonF
03-05-2004 6:13 PM


Re: Arguments => Questions
Current mutation rates in human lineage compared to old world monkeys seemed to have slowed down (see this study). But I don't have a clue about a general trend of molecular clocks slowing down or speeding up. It don't see any reason for that.
JonF writes:
I find it very interesting that you made several assertions and are now asking fundamental questions about the subjects of your assertions, revealing that you don't know much of anything about what you've claimed.
It wasn't my aim to claim certain truths, I've only some questions, see title.
I don't bother about knowing little, but I want to learn, that's why I'm asking questions.
Natural selection is blind for slightly good or slightly bad mutations, the adaptive advantage is too small.
Doesn't seem reasonable, only numbers will resolve the disagreement. You have made an assertion, support it or abandon it.
I do not see why the mutation that prevent atherosclerosis (in Asn291-Ser and Asp9-Asn) would conquer the world (for example). The advantage is so small, I'm wondering if their offspring would be more than average. Strange, that you never asked this question yourself.
You can think it will (conquer the world), by genetic drift. You think that that accounts for almost every small beneficial mutation? I'm just asking your opinion. Don't be offended.
What I'm thinking is that if small beneficial mutations spread with almost the same rate as neutral mutations, it's maybe not fast enough. That's why it seems me difficult to explain.
Take a look to the work of Motoo Kimura for example. He wrote 'The neutral theory of molecular evolution'.
The complementary streng with 'inverted' bases is just for correcting mistakes like point mutations.
Indeed? Would you explain this in a few seconds, paying particular attention to evidence for how this process works and how effective it is.
Here you can find something about error correction, possible due to the existence of the parallel strand. Why are you asking this? Everybody knows.
- Edit: Added Motoo Kimura
[This message has been edited by Saviourmachine, 03-06-2004]

This message is a reply to:
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