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Author Topic:   The "Logic" of the creationist....
Fedmahn Kassad
Inactive Member


Message 16 of 69 (15497)
08-15-2002 8:46 PM
Reply to: Message 13 by John Paul
08-15-2002 12:15 PM


quote:
Originally posted by John Paul:
quote:If we have millions of base pairs that are different, less than 2000 key genes, and some 225,000 coding positions that are different, that would tell me that more mutations took place than 1667. That said the ONLY way to get a human from some primitive ancestor in 1667 mutations would be to choose them. And by assuming common descent we are assuming that mutations can do the trick. Any evidence to support that assumption?

Where do these numbers come from, John Paul?

Regarding your last question, I am sure you saw this in the news:

http://www.cnn.com/2002/TECH/science/08/15/coolsc.speech/index.html

An interesting quote from the article: "There are not that many differences between the DNA of a human and a chimp, or even between a human and a whale. But, as knowledge of FOXP2 is revealing, even a tiny number of DNA mutations -- can lead to hugely important physical differences."

FK


This message is a reply to:
 Message 13 by John Paul, posted 08-15-2002 12:15 PM John Paul has responded

Replies to this message:
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Brad McFall
Member (Idle past 3144 days)
Posts: 3428
From: Ithaca,NY, USA
Joined: 12-20-2001


Message 17 of 69 (15539)
08-16-2002 2:01 PM
Reply to: Message 2 by TrueCreation
08-11-2002 2:53 PM


I am not ready to join this weave becasue I have finally been able to understand WHAT B. Russel thought of matter in so far as the changes he thought the predicative function could logically marshall the uncertainty of but since he looked for certainity and Pascal perfection I am not done reading. I hope to find this thread in good repairs when I return to the logic of Jacob etc.
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derwood
Member
Posts: 1457
Joined: 12-27-2001


Message 18 of 69 (15546)
08-16-2002 5:11 PM
Reply to: Message 13 by John Paul
08-15-2002 12:15 PM


quote:
Originally posted by John Paul:
SLP:
It, too, says nothing of the numbers of mutations required.

John Paul:
The links I posted were NOT supposed to discuss mutations. The context of the discussion was whether or not the alleged ancestor (10 million years ago) had any of the adaptations observed only in modern humans- language, speech & upright posture.
----------------------------------------------------------------------
Scott:
Then I have to wonder why they were presented as support for ReMine's claims re: 1667 fixed beneficial mutations... After all, ReMine's claims about posture and such are all premised on his unfounded and baseless assumption that 1667 fbms is too few...

John Paul:
What is your problem? Like I said the ONLY thing those articles were supposed to show is that our alleged primitive ancestor did NOT have the adaptations ReMine stated would have to come about in the time frame given.


And? For one, they don't really do that, either. How does ReMine know how many mutations were required to account for those adaptations? If he doesn't know (and he doesn't), then he has no rational or logical basis to claim that these adaptations - even if arising de novo, are too much to be accounted for (assuming - and I know how you hate assumptions - that ReMine's numbers are correct to begin with).

To borrow one of your new pet phrases - What is your objective test for this belief? Better yet, what is your evidence?

quote:

Scott:
Oh - and who said anything about 'choosing' the mutations?

John Paul:
You don’t get to choose the mutations.


AGAIN, who said anything about choosing mutations? If one looks back an event and discusses the probabilities and events surrounding the occurrance, would you warn them that they cannot choose what already happened?

quote:

In this method the criterion for selection is a long-range goal when in direct contrast the criterion for natural selection must be short-range.

What a bizarre statment! What 'method' are you talking about? There is no goal. Do you even have a beginner's grasp of evolutionary theory, or do you just blurt stuff out in an ad hoc fashion to suit your needs? Do you understand anything about the cumulative nature of evolution?

quote:

If we have millions of base pairs that are different, less than 2000 key genes, and some 225,000 coding positions that are different, that would tell me that more mutations took place than 1667. That said the ONLY way to get a human from some primitive ancestor in 1667 mutations would be to choose them.

Whaaa? Does ANYBODY here follow this supposed logic? Amazing - let me try, hopelessly, I am sure, to break this down.

The 1667 number stems from an application of a mathematical model to the evolution of humans from an unknown ancestor. The model has several constraints that make it inapplicable to many, probably most real-world populations (such as a constant population size - a growing population size, which is more realistic, negates the speed limit to a large extent).
As YOU claim, the numbers seem to be higher than that. These results are form DNA sequence analysis. Again, this is in contrast to a mathematical model.

The creationist chooses to reject actual data in favor of a largely inapplicable mathematical model, for the obvious reasons.

There is no need to 'choose' anything in this topic, any more than there is a need ot 'choose' the events that have taken place in one's life as one reminisces.

You should probably stop reading ReMine. He pollutes even the brightest [sic] creationist mind...

quote:

And by assuming common descent we are assuming that mutations can do the trick. Any evidence to support that assumption?


Yes.

Genomics 2002 May;79(5):657-62

Search for genes positively selected during primate evolution by 5'-end-sequence screening of cynomolgus monkey cDNAs.

Osada N, Kusuda J, Hirata M, Tanuma R, Hida M, Sugano S, Hirai M, Hashimoto K.

Division of Genetic Resources, National Institute of Infectious Diseases, Tokyo, Japan.osada@nih.go.jp

It is possible to assess positive selection by using the ratio of K(a) (nonsynonymous substitutions per plausible nonsynonymous sites) to K(s) (synonymous substitutions per plausible synonymous sites). We have searched candidate genes positively selected during primate evolution by using 5'-end sequences of 21,302 clones derived from cynomolgus monkey (Macaca fascicularis) brain cDNA libraries. Among these candidates, 10 genes that had not been shown by previous studies to undergo positive selection exhibited a K(a)/K(s) ratio > 1. Of the 10 candidate genes we found, 5 were included in the mitochondrial respiratory enzyme complexes, suggesting that these nuclear-encoded genes coevolved with mitochondrial-encoded genes, which have high mutation rates. The products of other candidate genes consisted of a cell-surface protein, a member of the lipocalin family, a nuclear transcription factor, and hypothetical proteins.

That is, mutations provide variation upon whihc selection acts.

Let me guess - this is not exactly precisely what you had in mind, so it does not count. Or there is no production of a new limb or something, so it doesn't count. or some such nonsense.

What, again, are your objective tests for divine creation?

What are your objective tests for in-kind variation and no more?

What is your evidence for anything you believe in?

[This message has been edited by SLPx, 08-16-2002]


This message is a reply to:
 Message 13 by John Paul, posted 08-15-2002 12:15 PM John Paul has responded

Replies to this message:
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derwood
Member
Posts: 1457
Joined: 12-27-2001


Message 19 of 69 (15547)
08-16-2002 5:12 PM
Reply to: Message 16 by Fedmahn Kassad
08-15-2002 8:46 PM


[QUOTE]Originally posted by Fedmahn Kassad:
"...even a tiny number of DNA mutations -- can lead to hugely important physical differences."

FK[/B][/QUOTE]

Silly FK - we cannot CHOOSE the mutations after the fact!


This message is a reply to:
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derwood
Member
Posts: 1457
Joined: 12-27-2001


Message 20 of 69 (15548)
08-16-2002 5:20 PM
Reply to: Message 14 by John Paul
08-15-2002 12:23 PM


quote:
Originally posted by John Paul:
Q:
BTW: Thanks for providing another example that refutes Tranquility Base's contention about the impossibility of novel gene evolution.

John Paul:
Taken in context Creationists state that is impossible only in the random mutation scenario. Directed mutations- by the designed genome's built-in ability to sense and react to environmental pressures- refutes the ToE. Actually it wouldn't. The ToE would just be re-written to accomodate directed mutations.


What is your evidence for the occurrance of 'directed mutations'?

What is your evidence that these mutations occur in multicellular eukaryotes?

What is your evidence that the 'information' already exists in the genomes?

What are your objective tests for these hypotheses? Keep in mind - phenotypic variation within species is not evidence for directed mutations.

Also, keep in mind that any objective test will need to have sequenced the genes in question in the origanisms prior to and after the application of phenotype altering stresses.


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derwood
Member
Posts: 1457
Joined: 12-27-2001


Message 21 of 69 (15549)
08-16-2002 5:22 PM
Reply to: Message 20 by derwood
08-16-2002 5:20 PM


Oh - one other thing. "Rewriting" a theory to accommodate new evidence is the hallmark of real science. Refusing to alter one's foundatinal premises (e.g., special creation of original kinds as is) regardless of what evidence indicates is quite antiscience, and quite irrational.
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derwood
Member
Posts: 1457
Joined: 12-27-2001


Message 22 of 69 (15550)
08-16-2002 5:25 PM
Reply to: Message 11 by peter borger
08-15-2002 12:52 AM


[QUOTE]Originally posted by peter borger:
[B]dear SLPx,

The article I refered to can be found in:
Nature 2001 Oct 4;413(6855),p514-9.

Let's have a carefull look at this gene family and whether a random non-directed mechanism can hold.

Positive selection of a gene family during the emergence of humans and African apes, by johnson ME et al.

Gene duplication followed by adaptive evolution is one of the primary forces for the emergence of new gene function. Here we describe the recent proliferation, transposition and selection of a 20-kilobase (kb) duplicated segment throughout 15 Mb of the short arm of human chromosome 16. The dispersal of this segment was accompanied by considerable variation in chromosomal-map location and copy number among hominoid species. In humans, we identified a gene family (morpheus) within the duplicated segment. ..Moreover, some genes emerge and evolve very rapidly, generating copies that bear little similarity to their ancestral precursors. Consequently, a small fraction of human genes may not possess discernible orthologues within the genomes of model organisms.

For your information:
PMID: 11586358 [PubMed - indexed for MEDLINE]

I recommend anyone who wants to participate in the discussion to read the article very carefully. I will soon send in my comments that demontrate where it clashes with NDT.

For now, focus your attention to the latter two sentences of the abstract. Will this paper provide a cover for future genes that will not be found in the great apes, but will be present in the human genome?

Best wishes,

Peter

[B][/QUOTE]

Can't wait to see your analysis. I suggest you read up on genomics before posting them, however.


This message is a reply to:
 Message 11 by peter borger, posted 08-15-2002 12:52 AM peter borger has responded

Replies to this message:
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John Paul
Inactive Member


Message 23 of 69 (15561)
08-17-2002 11:18 AM
Reply to: Message 18 by derwood
08-16-2002 5:11 PM


The goal would be humans and chimps from a common ancestor. That much should have been obvious. This method is akin to Dawkins' "weasel" program, which he admits isn't indicative of reality. It's a shame you can't see that.

Thanks to the article you posted about the FOXP2 gene we now know Walter's assumption about speech & language are very good. And if you can't see how the links I gave show that Walter's assumptions are good just tells me nothing would be good enough for you. I am sure you will try to spin out of the FOXP2 evidence that supports his assumption.

Also what you & Robert fail to realize is that if we use the chimp/ human comparison method that would bring the total number of possible beneficial mutations from 1667 in 10 million years down to 833 in 5 million or 1167 in 7 million (the alleged chimp/ human split coming in at 5-7 million years ago)

Then you would have to show that the "key" genes (1045 minimum) only took 1 mutation to make the changes required and that no other beneficial mutations outside of these key genes, remembering there are 222500 other coding positions that are different.

toodles


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John Paul
Inactive Member


Message 24 of 69 (15565)
08-17-2002 11:55 AM
Reply to: Message 16 by Fedmahn Kassad
08-15-2002 8:46 PM


FK:
Where do these numbers come from, John Paul?

John Paul:
The 1667 comes from 10 million years (divided by) 300 generations for 1 beneficial mutation to become fixed in a population (divided by) 20 years per generation.

The rest come from the debate I was having with an evolutionist on the Baptist Board: (read the uchicago article)

On to some numbers:

To further Helen’s point until we have finished the Human Genome Project and the Chimp Genome Project (some 70 genes (well less than 1%) have been compared with less than 1% difference found- 99.01% similar)

http://www.uchicago.edu/aff/mwc-amacad/biocomplexity/conference_papers/goodman.pdf [/b]*,

we won’t have the proper numbers to work with.
If we use 1% that would be a difference of 32 million base pairs (assuming both genomes are of 3.2 Gbp (Giga (= billion) base pairs)). However until we learn the loci of the differences and what those positions do to an organism all we have are numbers. IOW, in order to get the full effect we may have to wait until Human (chimp) Proteome Project (identifying all proteins) and then the Human (chimp) Physiome Project (how the proteins interact) are complete, or at least underway. But sometimes you work with what you have.

As you will read in the above article “However, there are also differences in the structure of the proteins encoded by genes, which undoubtedly account for some of the observed differences in phenotypes.” David Plaisted offers some insight as to the problems with changing the structure of a protein:

http://www.cs.unc.edu/~plaisted/ce/mutation.html and http://www.cs.unc.edu/~plaisted/ce/blocked.html

The basics of which is just how much change can a protein’s structure take and still be a functional part of the chain or function properly in its particular job? How many malfunctioning proteins can an organism handle?

[*from the article: “In order to analyze which amino acid replacements have occurred during the evolution of humans and apes, the evolutionary relationships among the species being studied must be inferred.” Which makes me wonder what happens when a Common Creator is inferred?]

quote:
--------------------------------------------------------------------------------

Just for reference:

From: http://imbs.massey.ac.nz/evo2.pdf

genetic differences, chimp/human:
- one chromosome fusion
- one enzyme lost (sialic acid)
- a couple of differences in copy number
- many small inversions
- transposable elements activated
- Many indels (insertions/deletions)
- many point mutations
- Some introns expanded/contracted

--------------------------------------------------------------------------------

Using just the numbers saying we have a 32 million base pair difference we would have to figure out the mutation accumulation rate of each branch. If we use Helen’s starting assumption of a 50/50 split that would be 16 million base pairs for each divergent branch. 16 million base pair differences/ 5 million years = 3 base pairs per year. We know that can’t be so we break it down into generations. A ten-year generation period would be 30 base pairs becoming fixed in a population every ten years. A twenty-year generation period would be 60, and so on. That is not to have 60 different base pairs in the population, but 60 bp that must become fixed (on average) per organism throughout the population. And if those organisms don’t take over, or get isolated from the population you add the risk of losing that 60 bp in the ensuing generations. One step forward, 2 steps back.

However the article on the chimp genome project estimates chimps & humans differ in 445,000 coding positions. 445,000/ 2 = 222,500, which amounts to just under 1 (.89) becoming fixed (per generation) in a population with a generation of 20 years. (Plus a number of non-coding mutations. this is considering a split of 5 million years ago).

The article then goes on to say ” Of these differences, the key ones at the nonsynonymous (nucleotide substitutions that change amino acids) sites are predicted to be found on between 2850 and 4000 genes.” So, still assuming a 50/50 split that would be between 1425 & 2000. If it takes much more than (an average of) 1 difference per gene to be one of the key ones, that would mean 1667 would be too few.


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Rationalist
Inactive Member


Message 25 of 69 (15566)
08-17-2002 12:09 PM


FK:
Where do these numbers come from, John Paul?

John Paul:
The 1667 comes from 10 million years (divided by) 300 generations for 1 beneficial mutation to become fixed in a population (divided by) 20 years per generation.

And what about all of the other ambient mutations in the genome. Are we to believe that of all of the mutations that are introduced into the gene pool of a species, only one at a time can become fixed?

Is this based on Haldane's faulty replacement model by any chance?


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John Paul
Inactive Member


Message 26 of 69 (15568)
08-17-2002 12:34 PM
Reply to: Message 25 by Rationalist
08-17-2002 12:09 PM


Rationalist:
And what about all of the other ambient mutations in the genome. Are we to believe that of all of the mutations that are introduced into the gene pool of a species, only one at a time can become fixed?

John Paul:
A mutation, any mutation, has a better chance of getting lost in a population than it does becoming fixed. As we know most mutations are either harmful or neutral, why would these mutations even be selected? Beneficial is a relative word as there is no way to predict what would be selected for at any point in time. What may be beneficial for one generation may not be beneficial for future generations. However I am open to any evidence that shows that more than 1 beneficial mutation can become fixed in a population in a shorter timeframe. Also becoming fixed might not even be enough. What happens when an organism with this new mutation mates with an organism without it?

And yes the 1667 is derived using Haldane's dilemma. If you think it is faulty perhaps you should start a thread to explain why you think it is.


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Fedmahn Kassad
Inactive Member


Message 27 of 69 (15569)
08-17-2002 1:06 PM
Reply to: Message 26 by John Paul
08-17-2002 12:34 PM


quote:
Originally posted by John Paul:
Rationalist:
And what about all of the other ambient mutations in the genome. Are we to believe that of all of the mutations that are introduced into the gene pool of a species, only one at a time can become fixed?

John Paul:
A mutation, any mutation, has a better chance of getting lost in a population than it does becoming fixed. As we know most mutations are either harmful or neutral, why would these mutations even be selected? Beneficial is a relative word as there is no way to predict what would be selected for at any point in time. What may be beneficial for one generation may not be beneficial for future generations. However I am open to any evidence that shows that more than 1 beneficial mutation can become fixed in a population in a shorter timeframe. Also becoming fixed might not even be enough. What happens when an organism with this new mutation mates with an organism without it?

And yes the 1667 is derived using Haldane's dilemma. If you think it is faulty perhaps you should start a thread to explain why you think it is.


Thank you so much for your reply! Let me see if I have this correct. Please correct any errors. 1667 refers to beneficial alleles in the human line over the course of 10 million years. 225,000 refers to the coding difference between humans and the human-chimp ancestor. Is the relationship between the 1667 alleles and the number of coding differences known? I would assume that the majority of 1667 would be single base pair substitutions, but a transposon or two would allow many base pair differences. Does the 225,000 coding difference include neutral and harmful mutations?

Let me ask a hypothetical question. Assuming common ancestry for humans and chimps, how many beneficial alleles do you estimate it would take to create a modern human from this common ancestor? That seems to be a key question, but I am not sure how to answer it.

You also asked "What happens when an organism with this new mutation mates with an organism without it?"

I think the answer to this is that 50% of the offspring would receive the beneficial mutation. If it enabled them to survive better, it should in theory enable the offspring to more effectively compete for resources and have more offspring, and should allow the mutation to accumulate in the population.

One other thing. You said "This method is akin to Dawkins' "weasel" program, which he admits isn't indicative of reality."

It is important to note that Dawkins is merely demonstrating the concept of natural selection as opposed to blind chance. I have his book, and he is quite clear on this. This is related to your question above about mutations. Dawkins just showed that if selection is operating, selected mutations would accumulate.

Looking forward to your reply.

As-sallamu aleykum! (I was told that you are a fellow Muslim!)

FK

[This message has been edited by Fedmahn Kassad, 08-18-2002]


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Rationalist
Inactive Member


Message 28 of 69 (15603)
08-18-2002 10:38 AM


quote:
John Paul:
A mutation, any mutation, has a better chance of getting lost in a population than it does becoming fixed.

If this were not true, the genetic load of mutations would become somewhat of a problem.

quote:
As we know most mutations are either harmful or neutral, why would these mutations even be selected?

Neutral mutations aren't, and negative mutations are actively removed from the population through the disproportionate death of those indivudals who have them.

quote:
Beneficial is a relative word as there is no way to predict what would be selected for at any point in time.

Certainly there is. A change in the survival traits of an organism which gives it an advantage relative to its peers will be selected. These can include features such as better camoflage, smaller size to avoid detection of predators, larger size to discourage predators, etc. etc.

quote:
What may be beneficial for one generation may not be beneficial for future generations

And conversely, what may be beneficial for one generation will commonly be beneficial for future generations.

quote:
However I am open to any evidence that shows that more than 1 beneficial mutation can become fixed in a population in a shorter timeframe.

http://www.gate.net/~rwms/haldane.html#solutions

The basic criticism of Haldane's supposed "dilemma" is that it is an outdated and basically invalid model of how population genetics works.

The specific problem with it is that it posits a 'replacement cost' that assumes that for each mutation to be fixed in a population, the rest of the individuals in the population with the existing version of the gene must be eliminated.

This scenario, however, is only valid in instances where the selection pressure on a particular gene is very very high, as in the case of rapid environmental change.

The more common scenario is that of a large number of mutations entering the genome, being winnowed to a very small number first by sexual selection and natural selection, and becoming fixed in "pipeline" fashion over the course of a few dozen generations. In this manner, each generation fixes a new set of mutations which are the end product of a much larger set of raw mutations which entered the genome many generations ago.

This is how real ordinary population genetics works, and it is the basis for the modern theory of evolutionary genetics, and results in a vastly larger number of differences than Haldane's faulty model.

quote:
Also becoming fixed might not even be enough. What happens when an organism with this new mutation mates with an organism without it?

This is a non-sequitur. A fixed gene is one in which only one version of a particular nucleotide in a population exists.

quote:
And yes the 1667 is derived using Haldane's dilemma. If you think it is faulty perhaps you should start a thread to explain why you think it is.

Haldane's model is kept alive only by creationists. Why don't you spend some time making the argument as to why creationists seem to ignore the rest of the body of population genetics since Haldane, and the obvious problems with his early model.

[This message has been edited by Rationalist, 08-18-2002]


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degreed
Inactive Member


Message 29 of 69 (15606)
08-18-2002 12:26 PM
Reply to: Message 28 by Rationalist
08-18-2002 10:38 AM


I must have missed an incredibly important part of this thread. Please thrash me if i have. Isn't most of this overshadowed by what i thought was a widely read paper by Whitfield et al, "Sequence Variation of the Human Y Chromosome" in Nature 378? How many other hominid species were around 50,000 years ago? 1 - Neandertals. How many of us think that Neandertals make a good origin for Homo Sapiens? --don't answer that--

Shouldn't we discuss the bigger point? We can toss our respective educations around all we want, but first tell me that this study (which, as studies go, seems to have been fairly simple once the sample population was reached) was full of crap. Then all of the talk about mutation rates becomes relevant, not before.


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John
Inactive Member


Message 30 of 69 (15607)
08-18-2002 5:00 PM
Reply to: Message 29 by degreed
08-18-2002 12:26 PM


quote:
Originally posted by degreed:
How many other hominid species were around 50,000 years ago?

homo sapiens, homo erectus and homo neandarthalensis -- three species up until about 30,000 years ago.

quote:
Shouldn't we discuss the bigger point? We can toss our respective educations around all we want, but first tell me that this study (which, as studies go, seems to have been fairly simple once the sample population was reached) was full of crap. Then all of the talk about mutation rates becomes relevant, not before.

I couldn't find this article when searching Nature. Do you have a link for it?

------------------
www.hells-handmaiden.com

[This message has been edited by John, 08-18-2002]


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