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04-23-2003, 07:53 PM | #11 | ||||
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Re: Re: Re: Option three
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The design hypothesis can accomodate anything if it includes premises such as "designed to become broken." If you want to look at it from a design viewpoint, the cellular replicators are designed quite the opposite way -- to be very faithful to original. They work extremely well. This is often used as a support to the design hypothesis. In other words, the design hypothesis tells you nothing. "DNA replication is extremely good, therefore it was designed by a supreme being." "DNA replication fails (is broken), therefore a supreme being designed it as some sort of twisted punishment." Quote:
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But are viri"designed to be broken?" I think you are missing the point of the evidence: there is broken virus code in Human and other Ape DNA. This code is broken in the same way, and the code is at the same location the respective host's gene. The odds of this happening by chance are extremely remote, and get more remote with each such pseudogene discovered. We know the mechanisms by which a virus can insert itself into a host cell's DNA. We have observed it happening. It is not surprising to find virus code in our DNA and in other species. When the same virus is found in the same place in two different species, the obvious and logical conclusion is that they share an ancestor who experienced that virius parisitism. Quote:
That is not what the evidence is showing. The evidence is The same virus Located in the same place on the gene Containing the same errors which deactivate the virus. You could chalk it up to coincidence, yet when you build a family tree using this evidence you come up with results that are strikingly similar to family trees based entirely upon anatomy. hw |
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04-23-2003, 08:54 PM | #12 | |
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Re: Re: Re: Option three
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04-24-2003, 10:00 PM | #13 |
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And the odds are
Hi Rufus and happy wonderer!
HW:But are viri"designed to be broken?" I think you are missing the point of the evidence: there is broken virus code in Human and other Ape DNA. This code is broken in the same way, and the code is at the same location the respective host's gene. The odds of this happening by chance are extremely remote, and get more remote with each such pseudogene discovered. judge: Are you able to indicate exactly (or approximately if this is more appropriate ) how extremely remote this is? |
04-25-2003, 12:48 PM | #14 | |
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Re: And the odds are
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The typical mutation rate for a single nucleotide in creatures like humans vary between 10^-9 and 10^-10. I'll stick to the earlier number. Now, for a single population the probabily that a specific mutation occurs in a specific individual is 10^-9. Now if there are N individuals in that population, the rate of mutation is approximately N*10^-9. If a mutation is neither selected for nor selected against, it has 1 in N chance of becoming fixed in the population. Thus the probably of a single nucleotide mutation originating and becoming fixed in the population is N*10^-9*1/N = 10^-9. Similarity, the probability that the exact same mutation occurs in another population is 10^-9. Thus the probability that both occur is 10^-18. Off course that assumes that in both instances the pseudogene is neutral. If this is not the case, this probabilty is more likely to decrease rather than increase. Thus were left with the following probilities for a specific nucleotide mutation occuring and getting fixed in two populations. In two pops by common descent: 10^-9 In two pops by duplicated mutations: 10^-18 Clearly one is a more likely to be the explaination than the other. |
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04-25-2003, 01:34 PM | #15 | |
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Re: Re: And the odds are
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1: deletions of multiple nucleotides occur at a much lower rate than point mutations (somewhere on the order of 100 to 1000 fold lower if I remember correctly) and 2: you have to factor the probability that the exact same 8 nucleotides (in the steroid 21 hydroxylase gene for example) are deleted in both the human and chimp versions of the pseudogene. Anyone here care to do the math? |
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04-25-2003, 03:23 PM | #16 | |
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Re: Re: And the odds are
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04-25-2003, 04:30 PM | #17 |
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Average rate?
Thanks for the replies all.
So if we look at pseudogenes for the moment rather than retro-viruses. So if the typical mutation rate is between 10^-9 amd 10^-10, is this the average? What are the extremes (of rates of mutation) and do we know why extreme rates of mutation occur? If you can idulge me for a moment . I spose what I am getting at is what could possibly give us these mutations independently occurring? Conditions we don't observe? Thanks again for your time ALL! |
04-25-2003, 09:24 PM | #18 |
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Yes! It's a total retreat from the creationist side. Look at Socrates' latest obfuscation:
Blubba demands immediate responses to arcane questions by evolutionists or else creationists should give up and go home. But when creationists ask for remotely plausible scenarios for chemical evolution or explaining biological motors, they are told "we must look harder because a designer is not science". Heads, the evolutionists win; tails, the creationists lose. If creationists raise an insoluble problem, they are falsely accused of a "god of the gaps" argument, but there are plenty of "evolution of the gaps" style arguments. And to put these arguments in perspective, at the time of the Scopes trial, creationists apparently had no good answer to Piltdown Man, about 80 alleged vestigial organs, or embryonic recapitulation. Even earlier, Christians apparently had no answer to liberal archaeologists who thought that the Hittites were a biblical myth. Now, anyone would be laughed at for raising this sort of "evidence". So the moral of the story is, the history of science is full of theories being junked when more evidence comes in. Let's play a game of "Count the Red Herrings". |
04-26-2003, 10:32 AM | #19 | |
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