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A simple calculation shows why evolution is impossible

Ophiolite

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from pitabread article:

"Work with the lambda repressor (Reidhaar-Olson and Sauer, 1990) yielded a “value” for the frequency of functional variants of 1 in 10^63 (roughly) for the 92-mer. Work with chorismate mutase (Taylor et al., PNAS 98, 10596-10601, 2001) gave a value of 1 in 10^24 for the 93 amino acid enzyme. Scaled for a similar size protein, Axe’s work gives a value of 1 in 10^59, which falls within the range established by previous work."

so its not a rare case.
And would you now like to identify the subsequent portion of the article that renders your claim misleading at best and dishonest at worst?
 
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mothcorrupteth

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And would you now like to identify the subsequent portion of the article that renders your claim misleading at best and dishonest at worst?
Be nice. I agree with your statements, but he's being nice, and English isn't his first language. He may not be catching all the nuance of our arguments. (I would have tried to simplify my own language, but I don't want to be condescending or risk simplifying the arguments.) And given his user name, I suspect being Jewish was/is not well received in his family's social network. So be nice, please.
 
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Ophiolite

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Be nice. I agree with your statements, but he's being nice, and English isn't his first language. He may not be catching all the nuance of our arguments. (I would have tried to simplify my own language, but I don't want to be condescending or risk simplifying the arguments.) And given his user name, I suspect being Jewish was/is not well received in his family's social network. So be nice, please.
That is a seemingly reasonable request and so it pains me to be unable to properly honour it. Xianghua has polluted thread after thread with oft refuted arguments based upon misunderstanding, misinterpretation and - all too often - misrepresentation of research. He has brazenly ignored gentle, careful, respectful attempts to educate him as to the nature of his errors, continuing to repeat the arguments. This is disrespectful to those who have sought to guide him and to those into whose threads he introduces his agenda, regardless of its relevance. There are thus. on record, hundreds of his posts in which he is anything but nice. So, while I appreciate and applaud your intervention I find myself unable to comply.
 
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pitabread

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again, from your own article:

"Work with the lambda repressor (Reidhaar-Olson and Sauer, 1990) yielded a “value” for the frequency of functional variants of 1 in 10^63 (roughly) for the 92-mer. Work with chorismate mutase (Taylor et al., PNAS 98, 10596-10601, 2001) gave a value of 1 in 10^24 for the 93 amino acid enzyme. Scaled for a similar size protein, Axe’s work gives a value of 1 in 10^59, which falls within the range established by previous work."

so its not just axe work and other papers give similar result.

First, those referenced papers were reportedly referenced in Axe's paper (you *did* read it didn't you?). Which is why they are specifically discussed in the article I linked.

Second, you appear to have completely ignored the following paragraph (which is what I specifically quoted) which discusses the relative methods for identifying and estimating rates of functional polymers. Here it is again:

Studies such as these involve what Axe calls a “reverse” approach – one starts with known, functional sequences, introduces semi-random mutants, and estimates the size of the functional sequence space from the numbers of “surviving” mutants. Studies involving the “forward” approach can and have been done as well. Briefly, this approach involves the synthesis of collections of random sequences and isolation of functional polymers (e.g., polypeptides or RNAs) from these collections. Historically, these studies have involved rather small oligomers (7-12 or so), owing to technical reasons (this is the size range that can be safely accommodated by the “tools” used). However, a relatively recent development, the so-called “mRNA display” technique, allows one to screen random sequences that are much larger (approaching 100 amino acids in length). What is interesting is that the forward approach typically yields a “success rate” in the 10^-10 to 10^-15 range – one usually need screen between 10^10 -> 10^15 random sequences to identify a functional polymer. This is true even for mRNA display. These numbers are a direct measurement of the proportion of functional sequences in a population of random polymers, and are estimates of the same parameter – density of sequences of minimal function in sequence space – that Axe is after.

(emphasis added)​

I suggest re-reading the article I linked and spending some time to try to digest it. It appears you merely skimmed it and consequently missed the entire point the author was making in reference to the experiment Axe performed.

and remember that axe paper is about a single domain.

Not even. Axe's experiment was based specifically on a variant of TEM-1 beta-lactamase. Which is primarily why the gross over-extrapolation of his results to all of molecular biology isn't warranted.

This is also discussed in the article I linked. Here is the relevant quote:

Obviously, from these considerations, we can see that assertions that the tiny base of the “hill” in Figure 3 in any way reflects that of a normal enzyme are not appropriate. On this basis alone, we may conclude that the claims of ID proponents vis-a-vis Axe 2004 are exaggerated and wrong. Axe’s numbers tell us about the apparent isolation of the low-activity variant, but reveal little (nor can it be expected to) about the “isolation” or evolution of TEM-1 penicillinase. (Or any other enzyme, for that matter.)

when many biological systems (like the electric organ) contain many genes. so its not 10^60 but more like 10^200.

This isn't supported in the slightest by Axe's paper or anything else. You're just making this up.
 
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lasthero

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I know but they keep pushing the theory of evolution as fact. They have tried so hard to manipulate the genome of animals to produce an outcome that supports macro evolution but cannot. It's all a far fetched theory developed to discredit religion and God. It's been happening for a long time. Spontaneous regeneration was the accepted theory, as soon as it was discredited the theory of evolution was embraced. It's a shame because it actually holds back the advancement of science
Impressive.

Every single thing you wrote was incorrect.
 
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pitabread

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It's a shame because it actually holds back the advancement of science

How do you feel about the fact that the theory of evolution has practical applications and companies have even filed patents for practical techniques based on evolution in various fields of biological research?
 
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pitabread

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On a side note, I notice that per Research Gate that Axe's 2004 paper cited in the OP has a mere 53 citations. And a bunch of those citations are from other ID authors and even Axe himself.

If this paper really did refute all of biological evolution, you'd think it would be a bit more popular. :/
 
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mothcorrupteth

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That is a seemingly reasonable request and so it pains me to be unable to properly honour it. Xianghua has polluted thread after thread with oft refuted arguments based upon misunderstanding, misinterpretation and - all too often - misrepresentation of research. He has brazenly ignored gentle, careful, respectful attempts to educate him as to the nature of his errors, continuing to repeat the arguments. This is disrespectful to those who have sought to guide him and to those into whose threads he introduces his agenda, regardless of its relevance. There are thus. on record, hundreds of his posts in which he is anything but nice. So, while I appreciate and applaud your intervention I find myself unable to comply.
Thank you for filling me in on context I was not aware of. I still wish you would be kinder, though. He may not be Orthodox or even Christian, but it is a commandment of the Old Testament to treat foreigners among us with respect and sympathy, and so I am led to try to defend him insomuch as I have knowledge to do so. I don't see casting subtle taunts as likely to change his behavior, either. But I have no intention of trying to coerce you.
 
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Ophiolite

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Thank you for filling me in on context I was not aware of. I still wish you would be kinder, though. He may not be Orthodox or even Christian, but it is a commandment of the Old Testament to treat foreigners among us with respect and sympathy, and so I am led to try to defend him insomuch as I have knowledge to do so. I don't see casting subtle taunts as likely to change his behavior, either. But I have no intention of trying to coerce you.
Again, noble thoughts that I am somewhat in sympathy with. I simply note that, since this is a US based forum and most of the members appear to be American, I am also a foreigner. Respect and sympathy tend to evaporate when they are not returned in kind.

The unacceptability of his approach has been explained in a broad spectrum of ways by several members, themselves quite diverse. I can't cite the relevant research, but I strongly suspect his passive aggressive posting style has reduced my life span (through elevated blood pressure, acting on a heart troubled by an enlarged left ventricle and a pronounced arrhythmia) to a much greater extent than any openly hostile post or personal attack.

I wouldn't have characterised my post as a taunt. It was not intended as that; more a frustrated request.

I certainly don't feel coerced and on another day, with the wind blowing from the south and some Belgian chocolates on the sideboard I might well have defended him too. What I shall do, if and when I respond to him again, is to lay out my position and the reasons for it with as much clarity as I can muster. I fear the end result may still appear to you unkind, because my "attacks" are not on him, but on the contents of his posts. And they are objectively, objectionable. There is no way I know of to make that point in a kind way.
 
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Speedwell

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Be nice. I agree with your statements, but he's being nice, and English isn't his first language. He may not be catching all the nuance of our arguments. (I would have tried to simplify my own language, but I don't want to be condescending or risk simplifying the arguments.) And given his user name, I suspect being Jewish was/is not well received in his family's social network. So be nice, please.
He has repeated basically this same argument and ignored all serious responses in this forum for at least three years that I know of.
 
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mothcorrupteth

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I wouldn't have characterised my post as a taunt. It was not intended as that; more a frustrated request
Well, then, I apologize for misreading it, and I would change my request to, "Please show patience."

I certainly don't feel coerced and on another day, with the wind blowing from the south and some Belgian chocolates on the sideboard I might well have defended him too. What I shall do, if and when I respond to him again, is to lay out my position and the reasons for it with as much clarity as I can muster. I fear the end result may still appear to you unkind, because my "attacks" are not on him, but on the contents of his posts. And they are objectively, objectionable. There is no way I know of to make that point in a kind way.
Well, I shall make the effort to read as much kind intention in what emerges as I can.
 
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Gene2memE

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according to that paper a specific function (that is coded by a single gene) will appeare about one in every 10^77 sequences:

Estimating the prevalence of protein sequences adopting functional enzyme folds. - PubMed - NCBI

it means that to get the same function again we will need about 10^77 mutations. now, according to evolution many functions evolved at least several times. for instance: an eletric organ supposedly evolved about 6 times:

Genomic basis for the convergent evolution of electric organs

and remember that these organs are coded by about 30 different genes, so they suppose to be far more rare than the example above. it basically means that convergent evolution should be impossible, or at least nearly impossible. because there is not enough time.


I love these probabilistic arguments. What an abuse of statistics.

Here's a counter example:

There are between ten to the 78 and 10 to the 82 power atoms in the universe. There are 7 x 10 to the 27 power atoms in the human body.

Knowing this, calculate the probability of any two atoms in your body existing adjacent to each other. Then calculate the probability of your particular atomic make up existing.
 
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xianghua

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Second, you appear to have completely ignored the following paragraph (which is what I specifically quoted) which discusses the relative methods for identifying and estimating rates of functional polymers. Here it is again:

Studies such as these involve what Axe calls a “reverse” approach – one starts with known, functional sequences, introduces semi-random mutants, and estimates the size of the functional sequence space from the numbers of “surviving” mutants. Studies involving the “forward” approach can and have been done as well. Briefly, this approach involves the synthesis of collections of random sequences and isolation of functional polymers (e.g., polypeptides or RNAs) from these collections. Historically, these studies have involved rather small oligomers (7-12 or so), owing to technical reasons (this is the size range that can be safely accommodated by the “tools” used). However, a relatively recent development, the so-called “mRNA display” technique, allows one to screen random sequences that are much larger (approaching 100 amino acids in length). What is interesting is that the forward approach typically yields a “success rate” in the 10^-10 to 10^-15 range – one usually need screen between 10^10 -> 10^15 random sequences to identify a functional polymer. This is true even for mRNA display. These numbers are a direct measurement of the proportion of functional sequences in a population of random polymers, and are estimates of the same parameter – density of sequences of minimal function in sequence space – that Axe is after.

ok. lets take a deeper look at your article (note that its not a scientific paper but its ok). he gave no direct reference so i guess that he also refer to this paper by szostak:

Functional proteins from a random-sequence library

according to the paper the chance to get a functional protein that can bind an atp (or has the abillity to bind it strongly) is one to 10^12 sequences (by the “forward” approach). the problem with that is that its not even a functional protein. as far as i aware there is no even a single protein in nature that just bind an atp. any protein that bind an atp has at least one more site to make use of that atp. so its incorrect to say that this is a functionl protein.

the second problem is that the other papers still give us high numbers. so even if it was true that some proteins arent so rare in the sequence space it tell us nothing about the proteins that are indeed rare among the space.

tell me what do you think about that i we will continue.

And given his user name, I suspect being Jewish was/is not well received in his family's social network

its actually a nick of a video game figure. but thanks for the concern.
 
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pitabread

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ok. lets take a deeper look at your article (note that its not a scientific paper but its ok). he gave no direct reference so i guess that he also refer to this paper by szostak:

The reference is at the bottom of the article:

Cho et al., J Mol Biol 297, 309-319, 2000 (this describes one of the first successes in using mRNA display; Pubmed searches for “mRNA display” will yield many other papers)


Functional proteins from a random-sequence library

according to the paper the chance to get a functional protein that can bind an atp (or has the abillity to bind it strongly) is one to 10^12 sequences (by the “forward” approach). the problem with that is that its not even a functional protein. as far as i aware there is no even a single protein in nature that just bind an atp. any protein that bind an atp has at least one more site to make use of that atp. so its incorrect to say that this is a functionl protein.

Attempting to redefine what constitutes a "functional protein" just seems like an exercise in moving the goal posts.

the second problem is that the other papers still give us high numbers. so even if it was true that some proteins arent so rare in the sequence space it tell us nothing about the proteins that are indeed rare among the space.

Which goes back to the discussion of the relative methodologies used for estimation of these rarities in the first place.
 
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xianghua

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Attempting to redefine what constitutes a "functional protein" just seems like an exercise in moving the goal posts.

not at all. it is actually shows that the punda's thumb article is incorrect since its not even a functional protein. and even if it was true its still irrelevant since if the chance to get a functional protein (according to your article) is about 10^10 then the chance to get a multiprotein system (that contain 3 proteins) is about one to 10^30. using panda's thumb own calculations.
 
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SLP

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according to that paper a specific function (that is coded by a single gene) will appeare about one in every 10^77 sequences:

Estimating the prevalence of protein sequences adopting functional enzyme folds. - PubMed - NCBI
Correction - according to Axe's paper, a pre-specified functional active site in an enzyme will appear about one in every 10^77 sequences:

"Using these simplifications, the difficulty of specifying a working beta-lactamase domain is assessed here. An alignment of homologous domain sequences is used to deduce the pattern of hydropathic constraints along chains that form the domain fold. Starting with a weakly functional sequence carrying this signature, clusters of ten side-chains within the fold are replaced randomly, within the boundaries of the signature, and tested for function. The prevalence of low-level function in four such experiments indicates that roughly one in 10(64) signature-consistent sequences forms a working domain. Combined with the estimated prevalence of plausible hydropathic patterns (for any fold) and of relevant folds for particular functions, this implies the overall prevalence of sequences performing a specific function by any domain-sized fold may be as low as 1 in 10(77), adding to the body of evidence that functional folds require highly extraordinary sequences."

it means that to get the same function again we will need about 10^77 mutations.

First, this does not follow. Second, all Axe is doing is chasing a pre-specified functional domain. This is essentially what Behe did with his CCC thing. It is smoke in mirrors for the easily duped.

now, according to evolution many functions evolved at least several times. for instance: an eletric organ supposedly evolved about 6 times:

Genomic basis for the convergent evolution of electric organs

and remember that these organs are coded by about 30 different genes, so they suppose to be far more rare than the example above.
Did you read the paper? All of the proteins involved are modified already-existing proteins (i.e., coded for by modified pre-existing genes; i.e., evolution). I found another paper that found 2 homologs in humans, so not only are these not 'brand new' proteins, they are not even unique to these fish.

From your perspective, this means a creator deity was bound to haphazardly allow some fish to produce these electric organs, and the overwhelming majority just got plain old muscles. Such chaos.
 
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SLP

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first: it base on a scientific paper.
So your position is that if something is in a scientific paper it is necessarily true and correct? I'm betting this position has a very proscriptive distribution.
secondly: even if we will be generous and we will say that a functional part appear one in every billion mutations.
So generous. What is this premised on? Axe was looking for 'new' sequences that reproduced a specific enzymatic function.
if we need at least 3 new parts to evolve an electric organ
Are these 3 parts beta-lactamase active sites?
we are still talking about 10^27 mutations. that is still a huge number that evolution cant explain.
What is the mutation rate of the genetic loci in question? How many such gametes are produced in these fish? I could not find clutch sizes for these fish specifically, but fish in general lay 10s to 100s of thousands of eggs at a time. From a brief perusal of fish genetics (not a lot on them), I guess a rough estimate of mutation rates in sperm is about 1.8x10^-5 (higher than in humans). Bottom line, these assertions about things being 'impossible' usually do not take scale, rates, etc. into consideration.

and remember that i reduce 30 genes into only 3. far from reality. its like saying that we can reduce a cell-phone from 30-40 parts into 3-4 and it will still work.
Yes, it is just like that.

:doh:
 
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SLP

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take a look at the numbers we are talking about.
Curious - have you ever looked at 'the numbers' regarding what you accept? Has Axe?

What, for example, are the odds that the deity that you ascribe to exists? And how was that calculated? What is the probability that this deity created these fish using these specific DNA sequences, and how was that calculated?

Isn't is something - how those claiming evolution is 'mathematically impossible' never seem to mathematically assess their contrarian position.
 
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SLP

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ok. so lets go a step by step. first lets deal with the initial claim. do you agree for instance that a tipical new anatomical part will appear one in a billion mutations? im not talking about a specific trait but any trait that is new: like new vision part or a new ear part etc. it seems to be a very generous assumption.
It seems like an out-of-the-rectum assumption.

Define "new". Define "anatomical part". "Vision part" is a bit too... vague.

One of the foundational flaws of this line of argumentation is that hose using them seem to think that 'parts' arise de novo from thin air, rather than how they actually do form - as modifications/duplications of previous 'parts.'
 
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