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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?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.
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.And would you now like to identify the subsequent portion of the article that renders your claim misleading at best and dishonest at worst?
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.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.
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.
and remember that axe paper is about a single domain.
when many biological systems (like the electric organ) contain many genes. so its not 10^60 but more like 10^200.
Impressive.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
It's a shame because it actually holds back the advancement of science
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.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.
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.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.
He has repeated basically this same argument and ignored all serious responses in this forum for at least three years that I know of.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.
Well, then, I apologize for misreading it, and I would change my request to, "Please show patience."I wouldn't have characterised my post as a taunt. It was not intended as that; more a frustrated request
Well, I shall make the effort to read as much kind intention in what emerges as I can.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.
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.
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.
And given his user name, I suspect being Jewish was/is not well received in his family's social network
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.
Attempting to redefine what constitutes a "functional protein" just seems like an exercise in moving the goal posts.
Correction - according to Axe's paper, a pre-specified functional active site in an enzyme will appear about one in every 10^77 sequences: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.
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.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.
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.first: it base on a scientific paper.
So generous. What is this premised on? Axe was looking for 'new' sequences that reproduced a specific enzymatic function.secondly: even if we will be generous and we will say that a functional part appear one in every billion mutations.
Are these 3 parts beta-lactamase active sites?if we need at least 3 new parts to evolve an electric organ
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.we are still talking about 10^27 mutations. that is still a huge number that evolution cant explain.
Yes, it is just like that.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.
Curious - have you ever looked at 'the numbers' regarding what you accept? Has Axe?take a look at the numbers we are talking about.
It seems like an out-of-the-rectum assumption.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.
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