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Author
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Topic: By what mechanism does the intelligent designer affect the physical world
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Zachriel
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Member # 1793
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posted 19. May 2006 07:38
peter borger: "There is no experimental test for creatons."
That statement was true to my knowledge as of this morning. If you wish to propose a scientifically valid test for 'creatons', please do.
[deleted snark]
Zachriel
http://zachriel.blogspot.com/
[ 19. May 2006, 09:47: Message edited by: Zachriel ]
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Bruce Fast
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posted 19. May 2006 12:44
Zachriel: quote:
peter borger: quote:
"There is no experimental test for creatons."
That statement was true to my knowledge as of this morning. If you wish to propose a scientifically valid test for 'creatons', please do.
This would certainly not be the first time that science has proposed an "unknown mechanism" and given it a name, only to find a test to vaildate/invalidate it years later, is it not. I present the example of ether. Ether, if I understand correctly was a proposed transport medium which allowed stuff like the travel of light to make sense. It was proposed, used, but never validated. When it was invalidated, science had to live with a "we don't have a clue" hole for a few years.
I, therefore, suggest it reasonable to propose a mythical "creaton" to help explain the phenomenon of biological development because the mechanism which currently is proposed - random mutation - is fundimentally inadequate.
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Zachriel
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posted 19. May 2006 13:34
Bruce Fast: "Ether, if I understand correctly was a proposed transport medium which allowed stuff like the travel of light to make sense."
Interesting that you would point to a failed hypothesis.
Light was a real observed phenomena and exhibited some wave properties. All known waves had a carrier, so the theory was developed along those lines. Luminous æther had specific empirical properties which led many scientists to doubt its physical reality. With Maxwell, it ceased to be a tenable theory.
Perhaps atoms would be a better example. Atoms were postulated to explain certain chemical properties of matter, e.g. mole ratios. They remained theoretical until Einstein demonstrated their physical existence (and estimated their mass) with his explanation of Brownian motion. However, again, atoms were posited to explain real observations.
Bruce Fast: "therefore, suggest it reasonable to propose a mythical "creaton" to help explain the phenomenon of biological development because the mechanism which currently is proposed - random mutation - is fundimentally inadequate."
Now, let's examine your own postulated particle. You find random mutation "fundamentally inadequate", even though random mutation, selection, and other aspects of genetic change can be directly observed.
But even if these mechanisms were inadequate, this is not positive evidence of a creator. So you posit a particle of force which has no observed effects, and no conceivable experiment which could detect them or their effects.
Maybe you'll find a pony in there somewhere — but I doubt it.
[corrected attribution]
Zachriel
http://zachriel.blogspot.com/
[ 20. May 2006, 09:03: Message edited by: Zachriel ]
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peter borger
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posted 19. May 2006 13:58
as particles equal energy lets call "creatons" virtual energy
[ 19. May 2006, 14:00: Message edited by: peter borger ]
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Scott
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posted 19. May 2006 22:12
quote:
You find random mutation "fundamentally inadequate", even though random mutation, selection, and other aspects of genetic change can be directly observed.
I have my doubts that these things can be "directly observed" as asserted.
However, since when is selection an aspect of genetic change? Selection operates to remove genetic diversity, not increase it. In order to operate, selection needs an absence of genetic change.
So what "other aspects of genetic change" did you have in mind?
How do you propose to establish that mutations are random? Not that it's all that important, but it does challenge one of the fundamental tenent of Darwinian evolutionary theory.
Now, here is the important question. Are random mutations sufficient to explain the history of life? IF mutations are important, why did systems evolve which have the effect of removing mutations? MET is at it's core incoherent, given what we know about life.
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Bruce Fast
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posted 19. May 2006 22:57
Zachriel: quote:
peter borger: "Ether, if I understand
You quoted me, not Peter.
quote:
You find random mutation "fundamentally inadequate", even though random mutation, selection, and other aspects of genetic change can be directly observed.
I, like (all of?) the others here, recognize that random mutation happens, and that selection happens. The question is not whether these are actual phenomenons, the question is whether they are "adequate". Show me experiments showing that RM+NS can produce complex organs, show me experiments showing that RM+NS can even produce biological speciation within a sexual organism (the "inability to produce fertile offspring" definition), show me a good explanation for PB's H1 gene puzzle, and show me a realistically plausible abiogenetic hypothes and I, for one, will happily become content that RM+NS (with its sub-theories including HGT) is adequate to explain the variety of life on earth.
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Zachriel
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posted 20. May 2006 11:37
Bruce Fast: "I, like (all of?) the others here, recognize that random mutation happens, and that selection happens. The question is not whether these are actual phenomenons, the question is whether they are 'adequate'."
That wasn't the issue raised, as I had accepted the premise for the purpose of making a different point.
Zachriel: But even if these mechanisms were inadequate, this is not positive evidence of a creator. So you posit a particle of force which has no observed effects, and no conceivable experiment which could detect them or their effects.
Scott: "I have my doubts that these things can be 'directly observed' as asserted."
By any reasonable definition of observation, mutation can be observed. They can even be induced.
Scott: "However, since when is selection an aspect of genetic change?"
Selection for heritable traits is a genetic change by definition. Ask any breeder.
Scott: "Selection operates to remove genetic diversity, not increase it."
Selection can remove diversity, or not. Ask any breeder.
Scott: "So what 'other aspects of genetic change' did you have in mind?"
Genetic drift would be such an example.
Scott: "How do you propose to establish that mutations are random?"
Luria and Delbrück, 1943.
Scott: "Are random mutations sufficient to explain the history of life?"
Of course not. It also requires selection, and other mechanisms such as drift and speciation.
Scott: "IF mutations are important, why did systems evolve which have the effect of removing mutations?"
Life requires an accurate copying mechanism. It provides a selective advantage by ensuring the quality of offspring and the continuation of the line. Even bacteria have such mechanisms.
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peter borger
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posted 31. May 2006 07:04
quote:
Scott: "How do you propose to establish that mutations are random?"
Luria and Delbrück, 1943.
There is a general but huge misconception about the L&B'43 experiments:
Luria and Max Delbrück conducted a series of experiments to prove that mutations are not related to the ENVIRONMENT. To this end they cultured strains of Escherichia coli, which they exposed to a lethal selective pressure – the bacterial virus T1. As this virus immediately kills non-resistant cells, the only bacteria to survive are those with a pre-existing specific mutation that renders immunity. Luria and Delbrück analyzed the number and distribution of surviving bacteria and concluded that the relevant mutations had occurred at random and had been present before they applied the selective pressure. The Luria-Delbrück experiments proved that a particular form of variation – that is the mutations that induced resistance to the T1 virus – was not induced by the ENVIRONMENT.
It is very important to realize that:
1) the resistance was present from the start otherwise none of bacteria would have survived the lethal exposure,
2) the L&B experiments did not reveal the nature of the pre-existing mutations. That is, where exactly had mutations been introduced? In what genes had changes occurred? And, how had they been introduced there?,
3) the experiments also did not address whether the resistance was the result of point-mutations in genes, or whether they resulted from gene inversions, gene duplications and losses, or simply reflected the reshuffling of the bacterial genome.
Nevertheless, the Luria-Delbrück experiments were interpreted as evidence that ALL mutations are random. ALL variation found in organisms is the result of random mutations in DNA sequences; mutations are unpredictable, not associated with behaviour or food; neither with social or environmental conditions. Mutations just happen and afterwards they are inherited.
That ALL mutations are random is merely a NON-SEQUITUR; a logical fallacy easy to see through.
I don't understand how the L&B'43 experiments can be taken as evidence that all mutations are random. We know now that mutations are modulated and largely predetermined by the DNA environment and context.
peebee
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Zachriel
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posted 31. May 2006 12:01
peter borger: "the resistance was present from the start otherwise none of bacteria would have survived the lethal exposure"
They started with clonal bacteria. As the bacteria multiplied, they mutated. (By chance alone, some bacteria had the beneficial mutation.) The experiment showed that the mutations were random with respect to the environment.
Also see Lederbergs' 1952 Experiment for a variation on the theme.
http://evolution.berkeley.edu/evosite/evo101/IIIC1bLederberg.shtml
These experiments only show that some mutations are random with respect to the environment. Nowadays, the process of mutation, and demonstrably decoupled from environmental conditions, can be directly observed in genomes. This is not a requirement of the original Theory of Evolution, but an empirical discovery of modern genetics.
[ 31. May 2006, 18:28: Message edited by: Zachriel ]
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peter borger
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posted 01. June 2006 08:00
quote:
They started with clonal bacteria. As the bacteria multiplied, they mutated. (By chance alone, some bacteria had the beneficial mutation.) The experiment showed that the mutations were random with respect to the environment.
Also see Lederbergs' 1952 Experiment for a variation on the theme.
http://evolution.berkeley.edu/evosite/evo101/IIIC1bLederberg.shtml
These experiments only show that some mutations are random with respect to the environment. Nowadays, the process of mutation, and demonstrably decoupled from environmental conditions, can be directly observed in genomes. This is not a requirement of the original Theory of Evolution, but an empirical discovery of modern genetics.
Yep, but do the experiments demonstrate whether:
1) the resistance was present from the start otherwise none of bacteria would have survived the lethal exposure?,
2) the L&B experiments did not reveal the nature of the pre-existing mutations. That is, where exactly had mutations been introduced? In what genes had changes occurred? And, how had they been introduced there?,
3) the experiments also did not address whether the resistance was the result of point-mutations in genes, or whether they resulted from gene inversions, gene duplications and losses, or simply reflected the reshuffling of the bacterial genome?.
No, they did not. The process of stochastic accumulation of debilitating mutations (this is RM) is sufficient to induce the resistant phenotype, as all it requires is blocking the entry to invading the bacterium. As the entry-protein makes up only about 1/5000 part of the genes it is reasonable to expect many resistant bacteria only due to this disabling mechanism. I don't see how it can be concluded from this one experiment that ALL mutations are random? How does it address my three points?
peebee
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peter borger
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posted 01. June 2006 08:06
BTW, although the bacteria may have been clonal (derived from one single bacterium), the mutations that render immunity must have been preexisting mutations (in the expanding clonal population). How else can the organism withstand lethal viral infection?
Prediction from GUToB: the resistance was at the cost of reproduction rate.
peebee
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Zachriel
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posted 01. June 2006 08:27
peter borger: "BTW, although the bacteria may have been clonal (derived from one single bacterium), the mutations that render immunity must have been preexisting mutations (in the expanding clonal population). How else can the organism withstand lethal viral infection?"
You got it. That's the point of the experiment. Mutations happen randomly whether the clonal bacteria are exposed to antibiotics or not. There is no mechanism that converts the genome when exposed to the antibiotic. Mutations happen regardless of any possible benefit. But in certain environments, certain mutations are beneficial.
http://nobelprize.org/medicine/laureates/1958/
peter borger: "the resistance was at the cost of reproduction rate"
In fact, the bacteria without the mutation died when exposed to the antibiotic. They had (near) zero reproductive rate. The bacteria with the mutation survived and reproduced.
[ 01. June 2006, 08:29: Message edited by: Zachriel ]
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peter borger
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posted 01. June 2006 09:42
quote:
peter borger: "BTW, although the bacteria may have been clonal (derived from one single bacterium), the mutations that render immunity must have been preexisting mutations (in the expanding clonal population). How else can the organism withstand lethal viral infection?"
You got it. That's the point of the experiment. Mutations happen randomly whether the clonal bacteria are exposed to antibiotics or not. There is no mechanism that converts the genome when exposed to the antibiotic. Mutations happen regardless of any possible benefit. But in certain environments, certain mutations are beneficial.
Randomly with respect to environment (so not induced by the environment), and beneficial in regard to reproduction. The mutant bacterium is still able to replicate, while the WT cannot.
Most darwinains would say they had an increased fitness. But an increased fitness is just another way of saying they are able to reproduce faster (in a particular environment). The resistant bacteria are able to reproduce in an environment where the WT cannot due to the permanent selective constraint (the virus). I explained why and why we might expect this in individuals of a clonal population due to disabling mutations. We do not disagree here. I fail to see, however, how such mutations help Darwinian (upward) evolution.
quote:
peter borger: "the resistance was at the cost of reproduction rate"
In fact, the bacteria without the mutation died when exposed to the antibiotic. They had (near) zero reproductive rate. The bacteria with the mutation survived and reproduced.
I believe we have a misunderstanding here. The L&B experiments were performed with E.coli in the presence of the lethal T1 virus. If the WT E. coli has a reproduction rate of 1 cycle every 20 minutes under control situations, the resistant variety will have had one that is longer under the same conditions. Of course, the wild type's cycle in the presence of the constraint is endless, as it cannot replicate (actually they are lysed).
peebee
[ 01. June 2006, 09:45: Message edited by: peter borger ]
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Zachriel
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posted 02. June 2006 06:53
peter borger: "I believe we have a misunderstanding here. The L&B experiments were performed with E.coli in the presence of the lethal T1 virus."
That comment immediately followed my cite to the Lederbergs experiment. Please note that now we have two different experiments, one with viruses and one with antibiotics. The detailed statistical analysis of the experiments shows that the mutations were of a random distribution. And later genetic studies have largely confirmed this.
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peter borger
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posted 02. June 2006 11:38
quote:
The detailed statistical analysis of the experiments shows that the mutations were of a random distribution. And later genetic studies have largely confirmed this.
If random means unrelated to the environment, yes. The experiments did not address whether or not a mutational mechanism is at work or not, they did not address where the mutations were introduced. The genetic location. It turns out that the mutations are often found on the exact same spot. Known as hot spots they are determined by the DNA context. Many mutations can be predicted because of their DNA context and thus cannot qualify as randomly introduced mutations (although they are independet of the environment).
My argument was -- and still is -- that these mutations give the illusion of common descent, while in actuality they are the result of a common mechanism operating in similar genomes. Bottom line is, we cannot discriminate between mutations introduced by either common descent or a common mechanism. It explains why many point mutations are in linkage disequilibrium.
peebee
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