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#21 BVZ

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Posted 11 November 2008 - 09:58 PM

Because of mutation.It´s expected that mutation, being a random process, leaves some garbage from ancient traits.And The bigger is the coding region, the greater is the genetic load.

For more details : Monkey-Man Hypothesis Thwarted by Mutation Rates

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I read the article.

Could you point out to me (in the article) where they explain why non-coding DNA with a function is a problem for evolution?

Even better, could you explain it yourself?

#22 jason777

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Posted 12 November 2008 - 12:13 AM

Hi BVZ,

Quote;I read the article.

Could you point out to me (in the article) where they explain why non-coding DNA with a function is a problem for evolution?

Even better, could you explain it yourself?


Theres never a problem for an evolutionist,but science makes predictions and when thousands of predictions over 150 years have all been proven wrong,should'nt it be a problem?

Thanks.

#23 BVZ

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Posted 12 November 2008 - 01:32 AM

Can you please answer the question?

How exactly is non-coding DNA with a function a problem for evolution?

If you want to use the article you provided, please specify where the article explains the problem, better yet, explain it yourself.

Thank you.

#24 deadlock

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Posted 12 November 2008 - 01:54 AM

I read the article.

Could you point out to me (in the article) where they explain why non-coding DNA with a function is a problem for evolution?

Even better, could you explain it yourself?

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Only with a 96% of non-coding region evolutionists have a solution for the deleterious mutation rates. Because 96% of mutation would be neutral.

Look at these posts on EvcForum :

"Let me briefly summarize. Fred has written an article claiming that estimated deleterious mutation rates are too high for man and chimpanzees to share a common ancestor".

"Fred, your 15 minutes are up. Your article is based on so much outdated information, it is no longer remotely accurate. In addition, I have been in contact with three of the people whose results/comments Fred uses to build his argument. These people are Dr. Adam Eyre-Walker, Dr. James Crow, and Dr. Michael Nachman. In the case of Dr. Nachman, Fred did not use his work in the article, but frequently uses a Nachman paper to justify his continued use of the argument."

"All three scientists told me the same thing. They said previous estimates of U, the deleterious mutation rate, were all based on gene estimates conducted prior to the Human Genome Project. These estimates were in the range of 60,000-100,000 genes. The actual count by the HGP is in the range of 30,000. All three scientists told me that this means their estimate of U was too high by about a factor of 2."

To quote Fred: ?What pray tell does this mean? What are the authors failing to make crystal clear?? It means that the number of conceptions (not offspring as Fred writes) would be less than 10 in order to maintain genetic equilibrium. This reduces the required number of surviving offspring down to somewhere between 2 and 5 in order to maintain equilibrium. Of course that?s not quite as compelling as writing ?40 births before we get one offspring that escapes a new defect!?, but that?s what can happen when one jumps to conclusions

FK: Hey, I know you. What you say was approximately stated by 2 of the 3 guys that I contacted. They said the genes were overestimated, but this would be partially compensated since the amount of functional noncoding DNA is higher than previously believed. However, they said that when both factors were accounted for, the overall deleterious mutation rate was certainly less than 3.

These posts are from 2003.Ever Since, the functional non-coding region is increasing in size making the evolutionary solution for deleterious mutation rate simply flawed.

EvcForum

#25 BVZ

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Posted 12 November 2008 - 03:17 AM

What does any of this have to do with non-coding DNA that also has a function?

I even read a bit from the thread on EvcForum. As far as I can tell, you are discussing mutation rates, and how deleterous mutations are weeded out or not weeded out. How is this relavent to non-coding DNA at all?

Can anyone explain how non-coding DNA with a function is a problem for the theory of evolution?

#26 deadlock

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Posted 12 November 2008 - 01:16 PM

What does any of this have to do with non-coding DNA that also has a function?

I even read a bit from the thread on EvcForum. As far as I can tell, you are discussing mutation rates, and how deleterous mutations are weeded out or not weeded out. How is this relavent to non-coding DNA at all?

Can anyone explain how non-coding DNA with a function is a problem for the theory of evolution?

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Because if non-coding DNA has a function it´s a target for harmful mutations and the U value will increase.

#27 BVZ

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Posted 12 November 2008 - 10:11 PM

Ah I think I am beginning to see what you are getting at.

Just to make sure I understand you correctly, I will explain it as I see it.

Basically what you are saying is that there are mutations, and most of them are neutral. But the way we determined if they are neutral or not is by simply checking if the mutations fall into non-coding or coding regions. If it fell in a non-coding region, we figured it must be a neutral mutation, and if it fell into a coding region, it might be deleterous or benificial, mostly deleterous.

But now, since non-coding regions of DNA can also have a function, they can no longer simply be assumed to be neutral.

Is this a fair description of your position? If not, please explain.

EDITED TO ADD:

Since you don't think it is possible for deleterous mutations to become fixed in a population, why do you think that mutations in non-coding regions of DNA that also has a function is a problem for the theory of evolution?

If deleterous mutations cannot become fixed, it doesn't matter WHERE they occur right?

Also, I would like to know WHY you think it is impossible for deleterous mutations to become fixed?

#28 deadlock

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Posted 13 November 2008 - 02:20 AM

Ah I think I am beginning to see what you are getting at.

Just to make sure I understand you correctly, I will explain it as I see it.

Basically what you are saying is that there are mutations, and most of them are neutral. But the way we determined if they are neutral or not is by simply checking if the mutations fall into non-coding or coding regions. If it fell in a non-coding region, we figured it must be a neutral mutation, and if it fell into a coding region, it might be deleterous or benificial, mostly deleterous.

But now, since non-coding regions of DNA can also have a function, they can no longer simply be assumed to be neutral.

Is this a fair description of your position? If not, please explain.


Yes, except that mutations on the coding region can be neutral too not only beneficial and deleterious

Since you don't think it is possible for deleterous mutations to become fixed in a population, why do you think that mutations in non-coding regions of DNA that also has a function is a problem for the theory of evolution?


Because it needs excess of offspring to prevent genetic load

If deleterous mutations cannot become fixed, it doesn't matter WHERE they occur right?


Wrong

Also, I would like to know WHY you think it is impossible for deleterous mutations to become fixed?


Natural Selection, remeber ? it gets rid of bad mutations.

#29 BVZ

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Posted 13 November 2008 - 02:46 AM

Okay. So if non-coding DNA has a function, mutations to it might be deleterious. I understand that part.

Now... could you explain how this is a problem for the theory of evolution?

Could you walk me through your logic? Your responses so far have been pretty cryptic. Could you lay out your argument in detail?

#30 deadlock

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Posted 14 November 2008 - 03:52 PM

Okay. So if non-coding DNA has a function, mutations to it might be deleterious. I understand that part.

Now... could you explain how this is a problem for the theory of evolution?

Could you walk me through your logic? Your responses so far have been pretty cryptic. Could you lay out your argument in detail?

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Deleterious mutation rate:

KONDRASHOV and CROW 1993 suggested that it is possible to calculate the genomic deleterious mutation rate (U) from an estimate of the neutral mutation rate and an estimate of the fraction of the genome that is subject to constraint. Our estimate of the neutral mutation rate is 175 mutations per genome per generation (range 91–238). As a minimum estimate of the fraction of the genome under constraint, we consider only coding sequences. The human genome contains 70,000 genes (BIRD 1995 ) with an average length of 1500 bp (e.g., DUNHAM et al. 1999 ; EYRE-WALKER and KEIGHTLEY 1999 ) for a total of 2.1 x 108 bp of coding sequences and 1.6 x 108 nonsynonymous sites. What proportion of nonsynonymous changes are neutral and what proportion are deleterious? The fraction that are neutral, fo, can be calculated by comparing the total mutation rate, µt, with the substitution rate, o = foµt (KIMURA 1983A , KIMURA 1983B ). The proportion that are deleterious is 1 - fo. Using this approach, KIMURA 1983B estimated that 86% of nonsynonymous substitutions are deleterious. A more conservative estimate is obtained by assuming that silent substitutions are entirely neutral and thus reflect the total mutation rate. Then the ratio of nonsynonymous to silent substitutions (Ka/Ks) estimates fo. This will be an underestimate to the extent that silent mutations are deleterious. Data from Ohta indicate that the average = 0.27 among 49 genes in primates (OHTA 1995 ). This suggests that 1.7% of the genome is subject to constraint [ = 0.017]. The estimated genomic deleterious mutation rate, U, is thus 3 (U = 175 x 0.017), with a minimum value of 1.5 (U = 91 x 0.017) and a maximum value of 4 (U = 238 x 0.017), based on differences in divergence time, generation length, and ancestral effective population size. In fact, this range is likely to be biased downward because we have considered only nonsynonymous sites as potential targets for deleterious mutations. For example, a recent comparison of 100 kb of mostly noncoding DNA surrounding T cell receptor loci revealed striking conservation between humans and mice (KOOP and HOOD 1994 ), suggesting that much of this noncoding DNA may be functional and therefore includes targets for deleterious mutations.

Our estimate of U = 3 is slightly higher than another recent estimate in humans based on a similar approach (U = 1.6; EYRE-WALKER and KEIGHTLEY 1999 ). The difference between these estimates of U is due in part to the different estimates of constraint . Eyre-Walker and Keightley's estimate of 1 - Ka/Ks = 0.38 is considerably lower than the value of 0.73 obtained by OHTA 1995 for a different set of genes. The genes analyzed by EYRE-WALKER and KEIGHTLEY 1999 appear to have an unusually low level of constraint and may not be representative of the genome as a whole. Our estimate of U = 3 is considerably higher than recent estimates from mutation accumulation experiments in Escherichia coli (U = 0.0002; KIBOTA and LYNCH 1996 ), Caenorhabditis elegans (U = 0.005; KEIGHTLEY and CABALLERO 1997 ), and Drosophila melanogaster (U = 0.02–1, MUKAI et al. 1972 ; KEIGHTLEY 1996 ; FRY et al. 1999 ). However, mutations of small effect may go undetected in these experiments. In general, organisms with larger genomes appear to have a greater number of deleterious mutations, although it does not appear that the deleterious mutation rate is constant per base pair across these organisms.

The high deleterious mutation rate in humans presents a paradox. If mutations interact multiplicatively, the genetic load associated with such a high U would be intolerable in species with a low rate of reproduction (MULLER 1950 ; WALLACE 1981 ; CROW 1993 ; KONDRASHOV 1995 ; EYRE-WALKER and KEIGHTLEY 1999 ). The reduction in fitness (i.e., the genetic load) due to deleterious mutations with multiplicative effects is given by 1 - e-U (KIMURA and MORUYAMA 1966 ). For U = 3, the average fitness is reduced to 0.05, or put differently, each female would need to produce 40 offspring for 2 to survive and maintain the population at constant size. This assumes that all mortality is due to selection and so the actual number of offspring required to maintain a constant population size is probably higher. The problem can be mitigated somewhat by soft selection (WALLACE 1991 ) or by selection early in development (e.g., in utero). However, many mutations are unconditionally deleterious and it is improbable that the reproductive potential on average for human females can approach 40 zygotes. This problem can be overcome if most deleterious mutations exhibit synergistic epistasis; that is, if each additional mutation leads to a larger decrease in relative fitness (KONDRASHOV 1995 ; CROW 1997 ; EYRE-WALKER and KEIGHTLEY 1999 ). In the extreme, this gives rise to truncation selection in which all individuals carrying more than a threshold number of mutations are eliminated from the population. While extreme truncation selection seems unrealistic, the results presented here indicate that some form of positive epistasis among deleterious mutations is likely
.

Estimate of the Mutation Rate per Nucleotide in Humans

So, The bigger the coding region the bigger the value of U.

#31 BVZ

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Posted 16 November 2008 - 10:54 PM

Thank you for your response.

Why did you leave out this part?

This problem can be overcome if most deleterious mutations exhibit synergistic epistasis; that is, if each additional mutation leads to a larger decrease in relative fitness (KONDRASHOV 1995 Down; CROW 1997 Down; EYRE-WALKER and KEIGHTLEY 1999 Down). In the extreme, this gives rise to truncation selection in which all individuals carrying more than a threshold number of mutations are eliminated from the population. While extreme truncation selection seems unrealistic, the results presented here indicate that some form of positive epistasis among deleterious mutations is likely.



#32 deadlock

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Posted 17 November 2008 - 02:05 AM

Thank you for your response.

Why did you leave out this part?

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Look carefully, I didnt leave out this part.It´s at the end in bold.

#33 BVZ

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Posted 17 November 2008 - 03:26 AM

Ah sorry, I missed it. Apologies!!

Now I feel foolish. :huh:

Now I have two questions:

1) Why do you find the solution to the problem unsatisfactory?
2) If you don't think deleterous mutations can become fixed in a population, why do you think a higher U value is a problem for the theory of evolution? (I think I know the answer, I just want you to explain a bit more. I just want to make sure we are on the same page.)

#34 deadlock

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Posted 17 November 2008 - 05:18 AM

Ah sorry, I missed it. Apologies!!

Now I feel foolish. :)

Now I have two questions:

1) Why do you find the solution to the problem unsatisfactory?


First, because the author himself admits it´s unrealistic but has no solution for the problem so accepts it by faith.Second, because there´s no empirical evidence that it happens.

2) If you don't think deleterous mutations can become fixed in a population, why do you think a higher U value is a problem for the theory of evolution? (I think I know the answer, I just want you to explain a bit more. I just want to make sure we are on the same page.)

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Because, all mammalians have low reproduction rate, so they cannot compensate the value of U.

#35 BVZ

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Posted 17 November 2008 - 10:30 PM

Okay, I think I understand where you are coming from.

But you do realise that any field in science will have a cutting edge, and at this edge, there will always be unanswered questions.

This is one of them.

Already there are scientists working on the problem, increasing thier knowledge. Here are two links I got from someone who knows a lot more about the topic than me:

http://www.ncbi.nlm....pubmed/16983079
http://www.ncbi.nlm....pubmed/18648534

So basically, this discussion is going nowhere before the research finds either that epistasis happens, or that it does not.

But I DO want to point out something interesting. I want to point out how you react to the situation. The author points out a problem, and a possible solution. You accuse him of accepting it on faith, where in reality, he is simply proposing a hypothesis.

You imediately assume that the hypothesis is INVALID, despite any evidence for or against it, where the scientific appraoch would be to see it as a possibility, until the evidence rolls in.

Now, this seems to be the crux of the problem.

Why do you imediately think the hypothesis (epistasis as a solution to the problem we are discussing) is INVALID, as opposed to simply waiting for the results to come in?

#36 deadlock

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Posted 18 November 2008 - 04:27 AM

Okay, I think I understand where you are coming from.

But you do realise that any field in science will have a cutting edge, and at this edge, there will always be unanswered questions.

This is one of them.

Already there are scientists working on the problem, increasing thier knowledge. Here are two links I got from someone who knows a lot more about the topic than me:

http://www.ncbi.nlm....pubmed/16983079
http://www.ncbi.nlm....pubmed/18648534

So basically, this discussion is going nowhere before the research finds either that epistasis happens, or that it does not.

But I DO want to point out something interesting. I want to point out how you react to the situation. The author points out a problem, and a possible solution. You accuse him of accepting it on faith, where in reality, he is simply proposing a hypothesis.

You imediately assume that the hypothesis is INVALID, despite any evidence for or against it, where the scientific appraoch would be to see it as a possibility, until the evidence rolls in.

Now, this seems to be the crux of the problem.

Why do you imediately think the hypothesis (epistasis as a solution to the problem we are discussing) is INVALID, as opposed to simply waiting for the results to come in?

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Why? Because HE are the one basing his entire argument on the ASSUMPTION that epistasis happens, the onus is on HIM to show that this is the case.

#37 BVZ

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Posted 18 November 2008 - 11:20 PM

I am not sure I know what you are talking about.

Could you point out the argument the author is basing on epistasis?

As far as I can tell, the author is simply offering epistasis as a possible solution to the problem. Can you show me where he is building an argument that uses epistasis as a premise?

The author identifies a problem (the one you are championing in this thread), and offers a possible explanation for it. Reasearch on epistasis is already underway.

Why exactly do you have a problem with someone offering a hypothesis that might solve a problem? You do realise that all scientific theories start out as a hypothesis right?

Edited to add:

Also, you did not answer the question.

Here it is again:

Why do you imediately think the hypothesis (epistasis as a solution to the problem we are discussing) is INVALID, as opposed to simply waiting for the results to come in?



#38 deadlock

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Posted 19 November 2008 - 05:29 AM

I am not sure I know what you are talking about.

Could you point out the argument the author is basing on epistasis?

As far as I can tell, the author is simply offering epistasis as a possible solution to the problem. Can you show me where he is building an argument that uses epistasis as a premise?

The author identifies a problem (the one you are championing in this thread), and offers a possible explanation for it. Reasearch on epistasis is already underway.

Why exactly do you have a problem with someone offering a hypothesis that might solve a problem? You do realise that all scientific theories start out as a hypothesis right?

Edited to add:

Also, you did not answer the question.

Here it is again:

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I'm only using your own logic http://www.evolution...opic=1786&st=40

His imagination is not enough

#39 BVZ

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Posted 19 November 2008 - 07:48 AM

Why are you not answering the question?

Here it is again (I will reword it a little, in case the wording is the problem).

Why do you think the epistasis hypothesis is not a valid hypothesis? There is only one way to invalidate or validate any hypothesis, and that is through evidence. What evidence did you consult to reach the conclusion that the hypothesis (epistasis) the author proposed is invalid?

#40 deadlock

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Posted 24 November 2008 - 01:33 AM

Why are you not answering the question?

Here it is again (I will reword it a little, in case the wording is the problem).

Why do you think the epistasis hypothesis is not a valid hypothesis? There is only one way to invalidate or validate any hypothesis, and that is through evidence. What evidence did you consult to reach the conclusion that the hypothesis (epistasis) the author proposed is invalid?

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Because I dont have to validate the hýpothesis.It´s his homework.




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