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Author | Topic: evidence that intelligent design can't explain | |||||||||||||||||||||||
peter borger Member (Idle past 7686 days) Posts: 965 From: australia Joined: |
Dear mark,
You write: "Your going to have to do better than a couple of mutations on the same spot. I've seen sequences where most sites have a couple of mutations, & one or two have hundreds." Show me the references. (And you weren't even surprised?) And:"They ARE hot spots. Such studies are concuded from thousands of mutations on particular genes." Than I expect thousands of references. More importantly, what do you think hotspots are? Best WishesPeter [This message has been edited by peter borger, 07-24-2002]
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mark24 Member (Idle past 5216 days) Posts: 3857 From: UK Joined: |
quote: Benzer, S. 1962 The Fine Structure Of The Gene from, An Introduction To Genetic Analysis, 7th Edition, Griffiths, Miller, Suzuki, Lewontin, Gelbart, Fig 9-26 p288 Showing an analysis of the distribution of 1,612 spontaneous mutations in the rII locus of phage T4. Over half of mutations were found to exist at two sites, furthermore, he (Benzer) identified 60 sites (total) that displayed non-random mutation, over the rest of the sites that displayed "one or two" occurrences. Benzer also notes that the hot spots change when mutagens are introduced. Ohta tested the extant x exon & found the mutations to be random.You are presuming to know that hot spots existed in the original stem primate vit c gene, & that they were responsible for wrecking the functionality of that gene. I would very much like to know how you know this, as your argument lives or dies on this point. Note, there is a difference between looking at homologous nucleotide sequences in primates, & testing extant ones for randomness of mutation. You are unable to tell the difference between a non-random mutation & random mutation in extant homologous sequences (retrospectively), because both may be carried to fixation & be evident in extant sequences. In other words, you cannot possibly know how many substitutions occurred at a single site before that particular allele was fixed, it might have been one (random), or 500 (non-random). This is especially true when you don’t know what mutagens individual primates had exposure to, & hot spot locations may have moved.
quote: That’s thousands of mutations, not thousands of studies! A hot spot is a site that exhibits a non-random occurrence of mutation. What do you think hot spots are? Mark ------------------Occam's razor is not for shaving with.
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peter borger Member (Idle past 7686 days) Posts: 965 From: australia Joined: |
dear mark,
You write:"A hot spot is a site that exhibits a NON-RANDOM occurrence of mutation." EXACTLY! Peter
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monkenstick Inactive Member |
okay, i'd like to thank mark for delving into peter's claims about this, I have to admit, I'm still getting my science degree, and some of this is above my head.
Here is the question I would really like answered Where does the intelligent designer fit in? did he create the GLO psuedogene, replete with a mistake in both chimpanzee's and humans? - is this what you believe an intelligent designer did?
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Peter Member (Idle past 1500 days) Posts: 2161 From: Cambridgeshire, UK. Joined: |
quote: I think the question raised was one of usage of the term'Random'. In terms of hot spots it appears (and I'm no expert) that the'non-randomness' refers to a statistically higher probability of one area exhibiting substitutions/deletions/insertions. Random in the sense of ToE means we cannot predict whenthe mutatation will occur i.e. it is not directed. They are different interpretations of the same word. Since you appear reasonably articulate, one has to questionwhether this is deliberate.
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mark24 Member (Idle past 5216 days) Posts: 3857 From: UK Joined: |
quote: Good grief, this isn’t in dispute!!! What is in dispute is ; 1/ That you are able to attribute alleged homologous hot spots to the wrecking of vit c synthesis by looking at extant sequences (see my last post), or even be able to attribute any of the extant pseudogene sequence to hotspots by looking at primate sequences. BECAUSE YOU CAN’T TELL WHERE THE HOT SPOTS WERE. The best you can tell is that a site has changed up to three times, eg from A, to either T,G, or C. That is, you can see the quality of mutation, but not the quantity. It is precisely the quantity you need to be able to divine in order to know whether a hot spot exists at that site. It cannot be done without having the original nucleotide sequence in the lab. Common descent & genetic drift remains the best explanation for non-vit c synthesis in primates, particularly given that the two prosimian primates that can synthesise vit c, fit in nicely at the bottom of the primate phylogeny, where they would be expected if evolution & common descent were responsible. That is, that vit c gene wrecking occurred after the prosimian divergence, leaving them unnaffected. A remarkable coincidence, don’t you think? 2/ That you are able to attribute the existence of hot spots to design, when the cause of hot spots is UNKNOWN. God-Of-The-Gaps. 3/ That non-random means directed, or pre-programmed in the sense of design, with regard to spontaneous mutations. If you think it does, rather than not-an-equal-chance-of-mutation-at-each-site, then you need to back this up. Remember, you have already told me you aren’t conflating the statistical & colloquial definitions of random/non-random. Mark ps Are you suggesting that no conclusions from transposons can be drawn regarding common descent, when the function of those transposons is unknown? And that before a conclusion can be drawn, absolute evidence must be available that shows this lack of function? ------------------Occam's razor is not for shaving with. [This message has been edited by mark24, 07-25-2002] [This message has been edited by mark24, 07-25-2002] [This message has been edited by mark24, 07-25-2002]
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mark24 Member (Idle past 5216 days) Posts: 3857 From: UK Joined: |
Bump.....
------------------Occam's razor is not for shaving with.
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mark24 Member (Idle past 5216 days) Posts: 3857 From: UK Joined: |
Bump.....
------------------Occam's razor is not for shaving with.
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mark24 Member (Idle past 5216 days) Posts: 3857 From: UK Joined: |
C'mon Peter B, I only mention what I do in the postscript of the last post, because, if you are claiming that we need to know function of alleged "junk" DNA in order to apply phylogenetic analysis (or anything else), then you can't make ANY judgements yourself about vit c pseudogenes & any inherent sequences therein.
Why? Because you have to "scientifically" show that said pseudogenes have no function. If you can't do this, then vit c redundancy cannot falsify evolution BY YOUR OWN STANDARDS!!!!! More specifically, you need to show that their is neutral rate mutation in said sequences BECAUSE they are functionless. I only ask you apply the same standards to evolution, as you apply against it. Mark ------------------Occam's razor is not for shaving with.
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peter borger Member (Idle past 7686 days) Posts: 965 From: australia Joined: |
dear Mark,
You say: "C'mon Peter B, I only mention what I do in the postscript of the last post, because, if you are claiming that we need to know function of alleged "junk" DNA in order to apply phylogenetic analysis (or anything else), then you can't make ANY judgements yourself about vit c pseudogenes & any inherent sequences therein." Ultimately, we are not able to make judgements. The only thing we can do is to have faith in a paradigm. Whether it should include design and/or a creator or not is up to you. best wishesPeter
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John Inactive Member |
quote: Interesting Peter B. how deep does this idea run in your thoughts. Are you contending that we can't come to any knowledge at all? ------------------http://www.hells-handmaiden.com
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peter borger Member (Idle past 7686 days) Posts: 965 From: australia Joined: |
Dear Peter,
You write:"Random in the sense of ToE means we cannot predict when the mutatation will occur i.e. it is not directed." If we do not know the mechanism how can you speak of "not directed". If the mutation is induced by the environment it is reasonable to expect a non-random mechanism. Since we do not know the mechanism the introduction of mutations seems to be at random. I think we might compare it to immunoglobulin-antigen affinity improvement. Here, it seems that a random mechanism introduces the mutations. At present we do not know all ins and outs about this process, but it might well be non-random. As soon as we elucidate the underlying mechanism(s) we may also discover that the introduction of mutations is non-random (or maybe semi-random). Maybe we are even able to predict the exact location of mutations.(It should be noted that not all mutations are directed, but I already mentioned that in previous mails.) Best wishes Peter
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Peter Member (Idle past 1500 days) Posts: 2161 From: Cambridgeshire, UK. Joined: |
You are mixing and mis-matching definitions of random
again. Non-random in the sense you appear to be using it issaying that there is a mechanism which promotes/provokes mutations at some sites and not others. Random in the sense of ToE means we don't know when it willhappen. It is not a direct response to the environment, but a happy circumstance if it's a benefit. Whether there is a mechanims (naturalistic) behind mutationor not, it IS a leap to claim that it is directed.
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mark24 Member (Idle past 5216 days) Posts: 3857 From: UK Joined: |
quote: Absolute nonsense! John got there first, but how can we have any knowledge whatsoever if this is true? You have been hypocritical in how you apply standards. We’re not allowed to make any judgements on transposons because we cannot be sure of function, but you make judgements in spite of not knowing function. You have contradicted your own statement, above. Please answer points 1-3 in post 21. Thanks, Mark ------------------Occam's razor is not for shaving with. [This message has been edited by mark24, 07-29-2002]
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mark24 Member (Idle past 5216 days) Posts: 3857 From: UK Joined: |
Bump......
------------------Occam's razor is not for shaving with.
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