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Author | Topic: Rebuttal To Creationists - "Since We Can't Directly Observe Evolution..." | |||||||||||||||||||||||||||||||||||||||
dwise1 Member Posts: 5952 Joined: Member Rating: 5.2 |
Taq writes:
You are a whiner and you are stupid. Why do you lie when you claim to have done the mathematics of descent with modification? You are not only stupid, but you are also a liar. If all you can do is call people stupid then you have no argument. Says the creationist who is rubbish without his script. OK, actually you're also rubbish even with your script.
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Kleinman Member (Idle past 364 days) Posts: 2142 From: United States Joined: |
Kleinman:You aren't thinking about this very clearly. Changing environments changes the reproductive fitness of members in that environment. An adaptive allele in one environment may very well be neutral or detrimental in a different environment. That's why Lenski's experiment initially had drug-resistant variants in his populations but they were selected out because there were no drugs in the environment. And why don't you give examples of mutations that are beneficial in more than a single environment? Or is all that you can do is speculate? Kleinman:Is that the best you can come up with? You are stupid and you lie, that's all you can do unless you want to add in speculate.
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Kleinman Member (Idle past 364 days) Posts: 2142 From: United States Joined: |
Taq:I can do descent with modification for the Kishony and Lenski experiments. And what can dwise1 do? Nothing. He can't explain why it takes a billion replications for each adaptive mutation in the Kishony and Lenski experiments. Not so wise for dwise1.
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Taq Member Posts: 10085 Joined: Member Rating: 5.1 |
Kleinman writes: You aren't thinking about this very clearly. Changing environments changes the reproductive fitness of members in that environment. An adaptive allele in one environment may very well be neutral or detrimental in a different environment. It may very well be beneficial in a different environment.
And why don't you give examples of mutations that are beneficial in more than a single environment? Mutations that confer increased intelligence would be beneficial in humans since it could increase the efficiency of tool use in many different environments.
Is that the best you can come up with? You are stupid and you lie, that's all you can do unless you want to add in speculate. Insults are for those who can't deal with the evidence.
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Tanypteryx Member Posts: 4451 From: Oregon, USA Joined: Member Rating: 5.0
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Just tell me who hurt you. Biologists and other smart people.Stop Tzar Vladimir the Condemned! What if Eleanor Roosevelt had wings? -- Monty Python One important characteristic of a theory is that is has survived repeated attempts to falsify it. Contrary to your understanding, all available evidence confirms it. --Subbie If evolution is shown to be false, it will be at the hands of things that are true, not made up. --percy The reason that we have the scientific method is because common sense isn't reliable. -- Taq
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Taq Member Posts: 10085 Joined: Member Rating: 5.1
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Kleinman writes: I can do descent with modification for the Kishony and Lenski experiments. Apparently, you can't do "descent with modification" in the Lederberg experiment. Joshua and Esther Lederberg published a hallmark paper in 1951 titled, "Replica Plating and Indirect Selection of Bacterial Mutants", which can be found here: REPLICA PLATING AND INDIRECT SELECTION OF BACTERIAL MUTANTS - PMC Luria and Delbruck went on to explain the processes that undergirded the Lederberg's results which later won Luria and Delbruck a Nobel Prize. There is one interesting observation in the Lederberg paper: "The culutre is fully sensitive to the phage T-1, as well as to streptomycin, and like most E. coli strains gives rise to resistant mutants at rates of approximately 10E-7 and 10E-10 per division, respectively." In this example we saw a beneficial mutation rate of 1 in 10 million and 1 in 10 billion to two different selection pressures using the same strain of E. coli. Kleinman is telling us that one beneficial adaptation every billion divisions is some universal constant, or something of the like. It is so universal that it can even be applied to human evolution. However, in another experiment using E. coli we see beneficial mutation rates that are quite different than what Kleinman claims. If Kleinman's math can't even apply universally to evolution in E. coli, what hope does it have of applying to any other species?
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Kleinman Member (Idle past 364 days) Posts: 2142 From: United States Joined: |
Kleinman:So you speculate. I give you real examples where this doesn't happen in the Lenski experiment or PaulK's example of the sickle cell trait. Why doesn't Desai do this experiment, showing that different alleles are adaptive in different environments? Kleinman:Again you speculate, why couldn't chimps have the same mutations? Kleinman:When are you going to deal with evidence, all I've seen is your speculations. I'm the only one dealing with the evidence, the Kishony and Lenski experiments. You lie about the fact that you have done descent with modification for either of these experiments.
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Kleinman Member (Idle past 364 days) Posts: 2142 From: United States Joined: |
Kleinman:Here's your big chance, do the mathematics of the Lederberg experiment and prove me wrong.
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Taq Member Posts: 10085 Joined: Member Rating: 5.1
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Since Kleinman seems to like his probabilities, let's see how that works out for endogenous retroviruses (ERV's).
Retroviruses insert themselves into the host genome as part of their normal lifecycle. These insertions can become hereditary if they occur in a germline cell (i.e. sperm or egg). These are called endogenous retroviruses. Claiming that these are not from retroviral insertions is like claiming that a fingerprint on a doorknob at a crime scene isn't evidence because it could have been put there by God, or that it's just "part of the doorknob" and doesn't mean anything. We can observe retroviruses creating insertions both in the lab and in the wild, so the cause isn't under question. The human genome paper found ~200,000 of these hereditary retroviral insertions. The chimp genome paper found about the same amount. Interestingly, only ~300 of the chimp ERV's were not at the same base in the human genome, and only ~100 of the human ERV's were not at the same base in the chimp genome paper. This means that nearly all of the ERV's in each genome are at the same base in each species. We can observe that retroviral insertion is largely random. There is some preference for different genomic features, but these features are made up of many, many bases. For example:
quote: While HIV prefers transcription units, the number of bases that HIV prefers is still in the billions. So for our figures, let's go on the conservative side. Let's say that retroviruses have about 500 million bases that they prefer. What are the chances that two retroviruses will insert at the same base in independent events? That would be 1 in 500 million. What about 200,000 insertions? That would be 1 in 500 million to the 200,000th power. That's a big number. Therefore, the best explanation for the observation of 99+% of ERV's occurring at the same base in the genomes of two species is that the insertion happened once in a common ancestor. This is the very same mechanism that produces shared ERV's between humans.
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Taq Member Posts: 10085 Joined: Member Rating: 5.1 |
Kleinman writes: Here's your big chance, do the mathematics of the Lederberg experiment and prove me wrong. My whole point is that you can't have a set equation for the beneficial mutation rate in E. coli, contrary to your claims. There is no equation that can predict the beneficial mutation rate. The best we can do is calculate the mutation rate.
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Kleinman Member (Idle past 364 days) Posts: 2142 From: United States Joined: |
Taq:Why should I do all the math? It's your turn, you do the math (if you can). You certainly can't do the math for the Lederberg experiment.
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Taq Member Posts: 10085 Joined: Member Rating: 5.1 |
Kleinman writes: It's your turn, you do the math (if you can). I did the math. From the previous post: So for our figures, let's go on the conservative side. Let's say that retroviruses have about 500 million bases that they prefer. What are the chances that two retroviruses will insert at the same base in independent events? That would be 1 in 500 million. What about 200,000 insertions? That would be 1 in 500 million to the 200,000th power. That's a big number. Therefore, the best explanation for the observation of 99+% of ERV's occurring at the same base in the genomes of two species is that the insertion happened once in a common ancestor. This is the very same mechanism that produces shared ERV's between humans.
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Kleinman Member (Idle past 364 days) Posts: 2142 From: United States Joined: |
Kleinman:So do the mathematics and prove me wrong. Don't just babble on like the idiot you are.
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Taq Member Posts: 10085 Joined: Member Rating: 5.1
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Kleinman writes: So do the mathematics and prove me wrong. The observations prove you wrong. The rate of beneficial mutations differred by a factor of 1,000 in two different environments when using genetically identical E. coli.
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Kleinman Member (Idle past 364 days) Posts: 2142 From: United States Joined: |
Kleinman:Go ahead and cherry-pick your data, I'm sure it will impress the mathematically incompetent like Tany.
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