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Author | Topic: Explaining the pro-Evolution position | |||||||||||||||||||||||||||||||||
Dr Adequate Member (Idle past 311 days) Posts: 16113 Joined: |
The theory of evolution doesn't explain anything. It doesn't explain how rmns works, it doesn't explain how recombination works. The theory of evolution is mutation, selection, recombination, drift, lateral gene transfer, etc; basically, transmission genetics plus the law of natural selection. It is the theory of evolution because it is supposed to account for the facts of evolution --- from pathogens acquiring resistance to the descent of birds from dinosaurs. So far, it seems to be doing quite a good job.
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Admin Director Posts: 13038 From: EvC Forum Joined: Member Rating: 2.1 |
Rather than handing out reading or watching assignments, it is preferred that arguments be entered into the debate in one's own words and that links be used only as references.
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Pressie Member Posts: 2103 From: Pretoria, SA Joined: |
Kleiman writes: So, you're still avoiding the question. Are you a YEC?
I do think it is really weird to think that a T Rex red blood cell could last 70 million years.
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Pressie Member Posts: 2103 From: Pretoria, SA Joined: |
Kleiman writes: Ah, great. Now we're getting somewhere with a creationist. So did those dinosaurs have more or less genetic information than birds?
Last I checked, nobody has sequenced the dinosaur genome except in Jurrasic Park.
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bluegenes Member (Idle past 2504 days) Posts: 3119 From: U.K. Joined:
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Kleinman writes: If dinosaurs wanted to fly,... They didn't. Several extinct lineages may have evolved flight, and one species evolved into birds, but the overwhelming majority of dinosaur species remained terrestrial, and absolutely no species "wanted" to fly. Flight was not and is not a target at which evolution aims. There are no targets. Legend tells of how Robin Hood, on his deathbed, fired an arrow into the forest and asked to be buried wherever it chanced to fall. If a creationist came across the grave and heard the story he would, of course, wonder at the extraordinary improbability of Robin hitting the right spot!
Kleinman writes: ...they will need the alleles that would enable them to do this. And there are too many genetic loci needed to be transformed for scales to become feathers by rmns. How many is "too many"? On what time scale? What's the limit to the number of changes which can take place on a genome?
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Pressie Member Posts: 2103 From: Pretoria, SA Joined: |
Kleinman writes: Well, all modern birds have both scales and feathers. So, I'm not too sure why you asked that question. Do all modern reptiles also have genes for scales and feathers as well? I can't think of any modern reptiles having both scales and feathers. I'm not too sure why you asked the question. Edited by Pressie, : No reason given.
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JonF Member (Idle past 195 days) Posts: 6174 Joined: |
And, of course, no T. Rex blood cells have been found.
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Pressie Member Posts: 2103 From: Pretoria, SA Joined: |
The answers to this one from YEC's will be funny.
Apparently, from creationist sources, Dr Mary Schweitzer was supposed to have squeezed soft tissue out of those bones...
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Admin Director Posts: 13038 From: EvC Forum Joined: Member Rating: 2.1
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This thread, Kleinman's thread (I think it is safe to call it Kleinman's now), did not pass through the normal thread proposal process, but I think his claims are clear:
Normally I wouldn't request people to show the math, but the foundation for Kleinman's claims is that he's done the math that proves his claims, so therefore he should show the math. I find the rmns acronym rendered in lowercase a bit unreadable and suggest substituting any of RM/NS, RM-NS, RMNS. Please, no replies to this message, just take these requests into account during discussion.
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ringo Member (Idle past 439 days) Posts: 20940 From: frozen wasteland Joined: |
Kleinman writes:
It explains why we get a different strain of flu every year - the flu bugs mutate and the mutant strains that survive are the ones that survive.
The theory of evolution doesn't explain anything. It doesn't explain how rmns works, it doesn't explain how recombination works.
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Taq Member Posts: 10077 Joined: Member Rating: 5.1 |
Kleinman writes: What each of the different variants share in common is that they must amplify (increase in number) before there is a reasonable probability of another beneficial mutation occurring on a member of that lineage. And this is a problem how?
What determines if a mutation is beneficial or not is whether the variant can amplify (increase in number). In a very limited sense, amplification does not have to occur to improve the probability of a beneficial mutation occurring, a small number lineage which doesn't grow in size over the generations can have enough replications (the random trial) over many generations to improve the probability of another beneficial mutation occurring on a member of that lineage. I am still waiting for you to explain how this is a problem for rmns.
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Taq Member Posts: 10077 Joined: Member Rating: 5.1
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My mathematical model predicts the behavior of every real, measurable and repeatable example of rmns. Then please use that model on vertebrate genomes and show us which genetic differences between species could not be produced by rmns. If you can't do that, THEN WHAT ARE YOU GOING ON ABOUT?
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Kleinman Member (Idle past 362 days) Posts: 2142 From: United States Joined: |
There has been a call to see the mathematics of rmns. So let's do it. To make it a bit clearer, we will do this mathematics in the context of a real example of rmns measured in an experiment done by Weinreich and published here: icommons.harvard.edu In this experiment, he measured the mutations which would give e coli resistance to a particular antibiotic
What Weinreich el al found was that there were a variety of variants which evolved resistance to the antibiotic. It took 5 mutations to achieve high resistance to the drug but different combinations of mutations could accomplish this. What he found was that the first beneficial mutation determined what the other required mutations would be. So for one particular variant, you can label the set of 5 mutations to give resistance A1, B1, C1, D1 and E1, for another variant, you can label the mutations A2, B2, C2, D2 and E2 and for a third variant, you can label the mutations A3, B3, C3, D3 and E3 and so on What each of the variants have in common is that the sequence of mutations for a particular variant must always give improved fitness. So here is how you would do the mathematics for the general case of a variant getting mutations A, B, C, D, and E where each additional beneficial mutation in the evolutionary trajectory gives improved fitness to reproduce against the antibiotic selection pressure. There are two random trials in this problem, the principle random trial is the replication where there are two possible outcomes, either a mutation occurs at the particular site or a mutation does not occur at the particular site. The second random trial for this problem is the mutation itself. When a mutation occurs, it may not be the beneficial mutation, it could be a detrimental or neutral mutation, neither would contribute to improved fitness of that member. So to write out the possible outcomes for a mutation at a particular site, we can use the addition rule of probabilities for mutually exclusive event. P(−∞ < X < +∞) = P(Ad) + P(Cy) + P(Gu) + P(Th) + P(iAd) + P(iCy) + P(iGu)+ P(iTh) + P(del)+ = 1 Where Ad, Cy, Gu and Th are the bases, P(Ad) would indicate the probability that Ad was substituted and so on, P(iAd) would indicate that an Ad was inserted, P(del) would indicate that the base was deleted, and ... indicates any other mutation that could possibly occur. What can be said with mathematical certainty about each of the terms in this equation, the value for each of the terms ranges between 0 and 1. One of these terms also represents the beneficial mutation. So define a term, P(BeneficialA) such that if the substitution of Ad is the beneficial mutation, P(BeneficialA) = P(Ad). If the substitution of Cy is the beneficial mutation, P(BeneficialA) = P(Cy) and so on. Now, define a term, 𝜇, the mutation rate the probability (frequency) that an error in replication will occur at a particular site in a single member in one replication. With these definitions, we can compute the probability that mutation A will occur in a single replication of some member of the population. P(A) = P(BeneficialA)𝜇 We'll stop at this point for questions, comments, complaints... Edited by Admin, : Break up the large paragraph into smaller paragraphs and add a little additional spacing.
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Taq Member Posts: 10077 Joined: Member Rating: 5.1 |
Kleinman writes: So you have the genetic sequences for dinosaurs? We have plenty of living species whose genomes we can compare. For example, we have chimps and humans. When we use mutation rate, population size, and generation time to calculate the divergence time for genetic data you get 5-8 million years which matches the hominid fossil record.
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Taq Member Posts: 10077 Joined: Member Rating: 5.1
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Kleinman writes: It took 5 mutations to achieve high resistance to the drug but different combinations of mutations could accomplish this. Can you name a single beneficial difference between any two vertebrate species that required 5 simultaneous mutations? If not, THEN WHAT ARE YOU GOING ON ABOUT??????
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