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  • #76
    Originally posted by TheLurch View Post
    That's not how the probabilities work. if an interacting sequence happens to be physically similar to a pre-existing sequence, then very few mutations would be needed.
    Let's start with a string of 50 zeroes. Then of all the random sequences of 50 1's and 0's, only 50 of them have a single "mutation", i.e. a 1 somewhere and the rest zeroes. That means that 250-51 sequences have two or more mutations! And the problem gets worse if you're working in base 4. So they are simulating a system which has a large number of average mutations, which is unrealistic.

    You can refute it that way, but the alternative — which Moran did successfully and you've been too dense to register, despite having it pointed out to you multiple times — is show that the assumptions behind Behe's numbers were wrong, and therefore the numbers could not possibly demonstrate what Behe tried to use them to demonstrate.
    What Moran said was that chloroquine resistance may have occurred with 4 mutations, not 2. But the paper he referenced said at least 2 mutations are needed, so Behe may still be right. But let's assume Moran is correct, then Behe's edge shifts to 4 new protein-protein interactions, which is not a great gain for evolution. So the assumptions behind Behe's numbers are essentially correct.

    Source: Larry Moran

    I do not deny that the observed routes to chloroquine resistance were highly improbable (10-20) but I account for this low probabilty by trusting the results of Summers et al. (2014) who showed that four separate mutations were required for effective chloroquine resistance and the mutations had to occur in a particular order. In addition, there are several other factors that contribute to the low overall probability; the most important is the demonstration that the particular combination of mutations are probably the only possible routes to resistance.

    © Copyright Original Source



    I explained in detail how Behe cherry picked his analysis of HIV to choose a period where it was not under much selective pressure, and therefore wouldn't fix many new mutations.
    And I responded that Behe picked where we have good numbers. And aren't anti-HIV drugs generating intense selective pressure?

    And then claimed that the probability applied to every case of protein interactions, in every single type of organism, under every single possible selective pressure. The probability he was left with is garbage not because his estimate of what happened in malaria is wrong, but because every single one of those claims — and again, more i haven't mentioned — are wrong.
    Source: Edge of Evolution

    Can we extrapolate from malaria and HIV to all of bacteria? To all of life? Sure. We do of course have to be cautious and keep in mind that we are indeed extrapolating, but science routinely extrapolates from what we see happening now to what happened in the past. The same laws of physics that work here and now are used to estimate broadly how the universe developed over billions of years. So we can also use current biology to infer generally what happened over the course of life on earth. Since we see no new protein-protein interactions developing in 1020 cells, we can be reasonably confident that, at the least, no new cellular systems needing two new protein-protein interactions would develop in 1040 cells—in the entire history of life, as illustrated in Figure 7.4. The principle we use to make the extrapolation—that the odds against two independent events is the multiple of the odds against each event—is very well tested.

    © Copyright Original Source



    Blessings,
    Lee
    "What I pray of you is, to keep your eye upon Him, for that is everything. Do you say, 'How am I to keep my eye on Him?' I reply, keep your eye off everything else, and you will soon see Him. All depends on the eye of faith being kept on Him. How simple it is!" (J.B. Stoney)

    Comment


    • #77
      Originally posted by lee_merrill View Post
      Let's start with a string of 50 zeroes. Then of all the random sequences of 50 1's and 0's, only 50 of them have a single "mutation", i.e. a 1 somewhere and the rest zeroes. That means that 250-51 sequences have two or more mutations! And the problem gets worse if you're working in base 4. So they are simulating a system which has a large number of average mutations, which is unrealistic.


      What Moran said was that chloroquine resistance may have occurred with 4 mutations, not 2. But the paper he referenced said at least 2 mutations are needed, so Behe may still be right. But let's assume Moran is correct, then Behe's edge shifts to 4 new protein-protein interactions, which is not a great gain for evolution. So the assumptions behind Behe's numbers are essentially correct.

      Source: Larry Moran

      I do not deny that the observed routes to chloroquine resistance were highly improbable (10-20) but I account for this low probabilty by trusting the results of Summers et al. (2014) who showed that four separate mutations were required for effective chloroquine resistance and the mutations had to occur in a particular order. In addition, there are several other factors that contribute to the low overall probability; the most important is the demonstration that the particular combination of mutations are probably the only possible routes to resistance.

      © Copyright Original Source




      And I responded that Behe picked where we have good numbers. And aren't anti-HIV drugs generating intense selective pressure?


      Source: Edge of Evolution

      Can we extrapolate from malaria and HIV to all of bacteria? To all of life? Sure. We do of course have to be cautious and keep in mind that we are indeed extrapolating, but science routinely extrapolates from what we see happening now to what happened in the past. The same laws of physics that work here and now are used to estimate broadly how the universe developed over billions of years. So we can also use current biology to infer generally what happened over the course of life on earth. Since we see no new protein-protein interactions developing in 1020 cells, we can be reasonably confident that, at the least, no new cellular systems needing two new protein-protein interactions would develop in 1040 cells—in the entire history of life, as illustrated in Figure 7.4. The principle we use to make the extrapolation—that the odds against two independent events is the multiple of the odds against each event—is very well tested.

      © Copyright Original Source



      Blessings,
      Lee
      "Ground Hog Day" again and again . . . The Lurch, rogue 06 and I have trashed all of the above non-science dishonest ID arguments repeatedly including selective dishonest citations of Moran, and dishonest use of probability. I will wait to see if The Lurch has the patience to trash it again.

      Responding again and again with the same dishonest ID arguments does not help your case.
      Last edited by shunyadragon; 01-23-2021, 06:59 AM.
      Glendower: I can call spirits from the vasty deep.
      Hotspur: Why, so can I, or so can any man;
      But will they come when you do call for them? Shakespeare’s Henry IV, Part 1, Act III:

      go with the flow the river knows . . .

      Frank

      I do not know, therefore everything is in pencil.

      Comment


      • #78
        Getting the simple stuff out of the way first:
        Originally posted by lee_merrill View Post
        And I responded that Behe picked where we have good numbers. And aren't anti-HIV drugs generating intense selective pressure?
        No, Behe cherry picked. Why didn't he start with the relevant ancestor, SIV? Because his argument wouldn't work then. He's pretending to be reasonable while actually being dishonest by selecting his time period for consideration carefully.

        All effective HIV drugs target the active sites of enzymes. Resistance via new protein-protein interactions is pretty unlikely compared to changes in the active sites.

        Originally posted by lee_merrill View Post
        Let's start with a string of 50 zeroes. Then of all the random sequences of 50 1's and 0's, only 50 of them have a single "mutation", i.e. a 1 somewhere and the rest zeroes. That means that 250-51 sequences have two or more mutations! And the problem gets worse if you're working in base 4. So they are simulating a system which has a large number of average mutations, which is unrealistic.
        I get what you're trying to say; it's just wrong. You're assuming that any protein-protein reactions are a large distance from a starting protein, so, since randomized sequences are also a large distance from the protein, they're more likely to have protein-protein interactions.

        The problem isn't with your reasoning; it's with the assumptions you're basing that on. We have no idea whether a given protein is close to interacting with another or not. So, a single mutation may actually be more likely to produce interactions than randomizing a sequence.

        Originally posted by lee_merrill View Post
        What Moran said was that chloroquine resistance may have occurred with 4 mutations, not 2. But the paper he referenced said at least 2 mutations are needed, so Behe may still be right. But let's assume Moran is correct, then Behe's edge shifts to 4 new protein-protein interactions, which is not a great gain for evolution. So the assumptions behind Behe's numbers are essentially correct.
        You're focusing on Moran's arguments about the mutations. Pay more attention to his critique of Behe's assumptions.

        Think about both of the examples above. It's very possible to calculate the frequency of mutations in HIV, but it's the assumptions that dictate whether those numbers are relevant to a question. In the same way, you're right about the probability of mutations that cause a protein to adopt a very different configuration, but your assumptions - that a very different configuration is needed - is unfounded.

        You're acting like math is all that matters, and assumptions are irrelevant. That's very much wrong, and leading you badly astray.

        Originally posted by lee_merrill View Post
        Source: Edge of Evolution

        Can we extrapolate from malaria and HIV to all of bacteria? To all of life? Sure. We do of course have to be cautious and keep in mind that we are indeed extrapolating, but science routinely extrapolates from what we see happening now to what happened in the past. The same laws of physics that work here and now are used to estimate broadly how the universe developed over billions of years. So we can also use current biology to infer generally what happened over the course of life on earth.

        © Copyright Original Source

        I can't tell if Behe's being intentionally misleading, or truly is this stupid. But this is just fantastically mistaken. We can extrapolate in physics because we know the same behaviors occur under similar circumstances in all occasions. But we know this is not true in evolution. It often finds different solutions even under the same circumstances, as Lenski's experiments have shown. The sorts of mutations that lead to drug resistance are generally very different from those that occur during speciation, etc. etc. Behe's basically demanding that we ignore what we actually know about evolution in order to accept his extrapolation.

        Which, as i've said before, is garbage.
        "Any sufficiently advanced stupidity is indistinguishable from trolling."

        Comment


        • #79
          Originally posted by TheLurch View Post
          Getting the simple stuff out of the way first:

          No, Behe cherry picked. Why didn't he start with the relevant ancestor, SIV? Because his argument wouldn't work then. He's pretending to be reasonable while actually being dishonest by selecting his time period for consideration carefully.
          Behe cherry picking data? Being dishonest in order to fool his ignorant followers?

          Unfortunately Lee will continue to cite him and Evolution News because he's merely interested in being told what he wants to believe with absolutely no interest whatsoever in what is true.

          I'm always still in trouble again

          "You're by far the worst poster on TWeb" and "TWeb's biggest liar" --starlight (the guy who says Stalin was a right-winger)
          "Overall I would rate the withdrawal from Afghanistan as by far the best thing Biden's done" --Starlight
          "Of course, human life begins at fertilization that’s not the argument." --Tassman

          Comment


          • #80
            Originally posted by TheLurch View Post
            No, Behe cherry picked. Why didn't he start with the relevant ancestor, SIV? Because his argument wouldn't work then.
            One more protein-protein interaction is not going to destroy his argument (as I mentioned with Larry Moran's reply)

            All effective HIV drugs target the active sites of enzymes. Resistance via new protein-protein interactions is pretty unlikely compared to changes in the active sites.
            Yes, they are unlikely, but one new protein-protein interaction did occur. This gives us some idea of how often they can happen, which is what Behe is after.

            You're assuming that any protein-protein reactions are a large distance from a starting protein, so, since randomized sequences are also a large distance from the protein, they're more likely to have protein-protein interactions.
            No, I'm saying that randomized sequences are unrealistic, since they model a large number of mutations, on average. I believe a sequence of 50 random 1's and 0's would have an average of 25 "mutations" from an initial sequence of all zeroes.

            So, a single mutation may actually be more likely to produce interactions than randomizing a sequence.
            I think you just discounted the paper you quoted on randomized sequences. And we have numbers for what evolution actually did, so we don't need to speculate.

            Think about both of the examples above. It's very possible to calculate the frequency of mutations in HIV, but it's the assumptions that dictate whether those numbers are relevant to a question. In the same way, you're right about the probability of mutations that cause a protein to adopt a very different configuration, but your assumptions - that a very different configuration is needed - is unfounded.
            I'm not assuming anything about what configuration is needed, Behe just takes the number of interactions that evolution generated, and computes a rate from there.

            We can extrapolate in physics because we know the same behaviors occur under similar circumstances in all occasions. But we know this is not true in evolution. It often finds different solutions even under the same circumstances, as Lenski's experiments have shown. The sorts of mutations that lead to drug resistance are generally very different from those that occur during speciation, etc. etc.
            But Behe notes that HIV for instance, has the numbers to go through all combinations of six mutations! So the types of mutations have all been covered.

            Source: Edge of Evolution, pp. 154-155

            So to generate all possible six-nucleotide mutations in HIV would require only 1020 viruses, which have in fact appeared on earth in recent decades. In other words, while we have studied it, HIV has run the gamut of all the possible substitution mutations, a gamut that would require billions of years for cells to experience. Yet all those mutations have changed the virus very little. Our experience with HIV gives good reason to think that Darwinism doesn’t do much—even with billions of years and all the cells in the world at its disposal.

            © Copyright Original Source



            Blessings,
            Lee
            "What I pray of you is, to keep your eye upon Him, for that is everything. Do you say, 'How am I to keep my eye on Him?' I reply, keep your eye off everything else, and you will soon see Him. All depends on the eye of faith being kept on Him. How simple it is!" (J.B. Stoney)

            Comment


            • #81
              Originally posted by rogue06 View Post

              Unfortunately Lee will continue to cite him and Evolution News because he's merely interested in being told what he wants to believe with absolutely no interest whatsoever in what is true.
              Of course just a few hours after this observation Lee vomits up more of Behe's unsupported nonsense right on cue.

              Comment


              • #82
                Originally posted by lee_merrill View Post
                One more protein-protein interaction is not going to destroy his argument (as I mentioned with Larry Moran's reply)
                Yes, they are unlikely, but one new protein-protein interaction did occur. This gives us some idea of how often they can happen, which is what Behe is after.
                Let's go about this a different way. Behe chooses a handful of protein-protein interactions to make claims about the entirety of what's possible in life.

                Let's see what actual scientists know as a contrast. If you plug "evolution of protein-protein interaction" into google scholar, you get well over half a million hits. It's really clear from that that Behe has in no way come to grips with the extensive literature on what we actually know. He's making a rhetorical argument, not a scientific one, and his chosen examples are in no way representative of the full body of knowledge, because they simply can't be.

                But, of course, Behe's not much of a scholar, so let's just plug it into regular Google and pick a hit. I chose this:
                https://pubmed.ncbi.nlm.nih.gov/18753782/

                Which says, basically, that the rate of evolution of new interactions depends very heavily on the nature of the protein. So, if you don't pick a large number of proteins to examine, you'll run a very large risk of having an unrepresentative sample, making any statistics you derive from it meaningless.

                Behe's argument is utter garbage. It gives us no idea of how often they can happen, because he's chosen a sample size that's meaninglessly small and unrepresentative.

                You should be embarrassed to be repeating it, and you should apologize to us for wasting our time doing the work that you should have before repeating it.


                Originally posted by lee_merrill View Post
                No, I'm saying that randomized sequences are unrealistic, since they model a large number of mutations, on average. I believe a sequence of 50 random 1's and 0's would have an average of 25 "mutations" from an initial sequence of all zeroes.


                I think you just discounted the paper you quoted on randomized sequences. And we have numbers for what evolution actually did, so we don't need to speculate.
                You're clearly not getting my argument and, as detailed above, you clearly have some work to do in defending your own. So why don't you focus on that?

                "Any sufficiently advanced stupidity is indistinguishable from trolling."

                Comment


                • #83
                  Originally posted by lee_merrill View Post
                  He highlights chloroquine resistance, which occurred in about 1 in 1020 generations, whereas atovaquone resistance occurs in about 1 in 1010 generations.
                  1020 generations would take more than 100,000 times longer than the earth has been in existence.

                  You literally have no idea what you're talking about.
                  Jorge: Functional Complex Information is INFORMATION that is complex and functional.

                  MM: First of all, the Bible is a fixed document.
                  MM on covid-19: We're talking about an illness with a better than 99.9% rate of survival.

                  seer: I believe that so called 'compassion' [for starving Palestinian kids] maybe a cover for anti Semitism, ...

                  Comment


                  • #84
                    Originally posted by TheLurch View Post
                    Let's go about this a different way. Behe chooses a handful of protein-protein interactions to make claims about the entirety of what's possible in life.
                    You really should read his book, I spend most of my discussions about Behe here correcting misunderstandings. Behe states that about a half-a-dozen mutations are required for a new protein-protein interaction. He grants that all but two are neutral, and become fixed. He then evaluates the probability that two deleterious mutations will occur, so this sounds general, not specific to a few proteins.

                    Which says, basically, that the rate of evolution of new interactions depends very heavily on the nature of the protein. So, if you don't pick a large number of proteins to examine, you'll run a very large risk of having an unrepresentative sample, making any statistics you derive from it meaningless.
                    Source: PubMed

                    We focused on the evolutionary rates of proteins involved with PPIs, because it had been shown that for a given protein-coding gene the number of its PPIs in a biological network was one of the important factors in determining the evolutionary rate of the gene.

                    Source

                    © Copyright Original Source


                    So the dependency seems to be the number of PPIs in the network, not on the nature of the protein.

                    You're clearly not getting my argument and, as detailed above, you clearly have some work to do in defending your own. So why don't you focus on that?
                    Because your paper was proposing random sequences, with an average of 25 mutations! For strings of 1's and 0's, of length 50, and similarly in base 4. So this is clearly unrealistic, no wonder that they found a lot of new interactions.

                    Blessings,
                    Lee
                    "What I pray of you is, to keep your eye upon Him, for that is everything. Do you say, 'How am I to keep my eye on Him?' I reply, keep your eye off everything else, and you will soon see Him. All depends on the eye of faith being kept on Him. How simple it is!" (J.B. Stoney)

                    Comment


                    • #85
                      Originally posted by Roy View Post
                      1020 generations would take more than 100,000 times longer than the earth has been in existence.
                      There are about a trillion malarial cells in an infected person, and this requires 108 infected individuals to get to 1020 generations.

                      Blessings,
                      Lee
                      "What I pray of you is, to keep your eye upon Him, for that is everything. Do you say, 'How am I to keep my eye on Him?' I reply, keep your eye off everything else, and you will soon see Him. All depends on the eye of faith being kept on Him. How simple it is!" (J.B. Stoney)

                      Comment


                      • #86
                        Originally posted by lee_merrill View Post
                        You really should read his book, I spend most of my discussions about Behe here correcting misunderstandings.
                        And yet you started a thread to apologize for misunderstanding the basic premise of one of his books -- the entire concept behind the title -- after I corrected you several times about it. Funny that.

                        I'm always still in trouble again

                        "You're by far the worst poster on TWeb" and "TWeb's biggest liar" --starlight (the guy who says Stalin was a right-winger)
                        "Overall I would rate the withdrawal from Afghanistan as by far the best thing Biden's done" --Starlight
                        "Of course, human life begins at fertilization that’s not the argument." --Tassman

                        Comment


                        • #87
                          Originally posted by lee_merrill View Post
                          You really should read his book, I spend most of my discussions about Behe here correcting misunderstandings. Behe states that about a half-a-dozen mutations are required for a new protein-protein interaction. He grants that all but two are neutral, and become fixed. He then evaluates the probability that two deleterious mutations will occur, so this sounds general, not specific to a few proteins.
                          Why? I've read enough of Behe's writing to know he's a charlatan and, in my last post, clearly demonstrated how misleading he's being. Why should i financially support his fraud by buying his books?

                          In any case, "but Behe said" is not an argument when i've just shown that Behe has absolutely no grasp of the relevant scientific literature, and he's selecting his examples in a way that's completely misleading. Stop relying on Behe; start relying on biology. If you can't explain in biological terms why Behe isn't being misleading, then don't bother arguing.

                          Originally posted by lee_merrill View Post
                          Source: PubMed

                          We focused on the evolutionary rates of proteins involved with PPIs, because it had been shown that for a given protein-coding gene the number of its PPIs in a biological network was one of the important factors in determining the evolutionary rate of the gene.

                          Source

                          © Copyright Original Source


                          So the dependency seems to be the number of PPIs in the network, not on the nature of the protein.
                          Sure, that's a different way of viewing it, but the problem from Behe's perspective is the same: unless you look at enough proteins, you're not going to have a representative perspective on the the typical behavior. And Behe doesn't look at a lot of examples, so he's necessarily going to have an unrepresentative sample.

                          And remember - that was just one link i chose at random. Which indicates that, if i actually did an exhaustive search, i'd almost certainly find additional problems for his arguments.

                          Originally posted by lee_merrill View Post
                          Because your paper was proposing random sequences, with an average of 25 mutations!
                          Pay attention to what you're actually writing, please. The paper wasn't "proposing" anything - it actually did the tests. And there are no "mutations" in a randomized sequence, since there is no base sequence to compare them to. I don't know if you're being careless or really have that limited an understanding of biology, but just stop doing it, please. If you don't understand something, ask for an explanation first. I'm happy to explain; i'm getting quite fed up of correcting all the time.

                          Originally posted by lee_merrill View Post
                          For strings of 1's and 0's, of length 50, and similarly in base 4. So this is clearly unrealistic, no wonder that they found a lot of new interactions.
                          And here, you're just being stupid. They found a lot of new interactions because interactions are common. That's it, that's all you should be taking away from this. And if new interactions are common, we shouldn't be surprised to find them evolving.

                          All this confused stuff you're saying is just an attempt to avoid dealing with that fact.
                          "Any sufficiently advanced stupidity is indistinguishable from trolling."

                          Comment


                          • #88
                            Originally posted by TheLurch View Post
                            Why? I've read enough of Behe's writing to know he's a charlatan and, in my last post, clearly demonstrated how misleading he's being.
                            No, you misunderstood him.

                            Sure, that's a different way of viewing it, but the problem from Behe's perspective is the same: unless you look at enough proteins, you're not going to have a representative perspective on the the typical behavior. And Behe doesn't look at a lot of examples, so he's necessarily going to have an unrepresentative sample.
                            Again, you misunderstand Behe's argument, Behe states that about a half-a-dozen mutations are required for a new protein-protein interaction. He grants that all but two are neutral, and become fixed. He then evaluates the probability that two deleterious mutations will occur, so this sounds general, not specific to a few proteins.

                            And there are no "mutations" in a randomized sequence, since there is no base sequence to compare them to.
                            This is disingenuous, pick any sequence, and compare randomized sequences to it, and you'll find about 25 "mutations" in a sequence of 50. So of course they found interactions, with so much variability.

                            Blessings,
                            Lee

                            "What I pray of you is, to keep your eye upon Him, for that is everything. Do you say, 'How am I to keep my eye on Him?' I reply, keep your eye off everything else, and you will soon see Him. All depends on the eye of faith being kept on Him. How simple it is!" (J.B. Stoney)

                            Comment


                            • #89
                              Originally posted by lee_merrill View Post
                              No, you misunderstood him.
                              No, you don't like the fact that i do understand him.

                              Originally posted by lee_merrill View Post
                              Again, you misunderstand Behe's argument, Behe states that about a half-a-dozen mutations are required for a new protein-protein interaction.
                              He states that based on what? This isn't a game of Behe said - explain why that's true from the biology. Because we know from examples like sickle-cell hemoglobin that there are cases where a single mutation enables new protein-protein interactions, so it sounds like nonsense to me.

                              Originally posted by lee_merrill View Post
                              He grants that all but two are neutral, and become fixed. He then evaluates the probability that two deleterious mutations will occur, so this sounds general, not specific to a few proteins.
                              Again, if his probability is based on nonsense - and it is - then it's meaningless.

                              Originally posted by lee_merrill View Post
                              This is disingenuous, pick any sequence, and compare randomized sequences to it, and you'll find about 25 "mutations" in a sequence of 50. So of course they found interactions, with so much variability.
                              One, words have meanings. I'm using mutation according to its meaning. You're not.

                              And i'm mystified by your logic. They calculated a rate at which interactions were discovered. The rate indicated that interactions are relatively common. Unless you're trying to argue that their randomization wasn't actually random, then you've said absolutely nothing to challenge that.

                              (I'll also point out that there were probably other interactions within their randomized population that weren't detected here, since the assay was set up so that it could only identify regulatory interactions. So, there were probably some non-regulatory physical associations happening that didn't come out of the screen. But that's probably just going to confuse Lee's arguments even further, so i'm just sharing it for anybody else who wanders through here.)
                              "Any sufficiently advanced stupidity is indistinguishable from trolling."

                              Comment


                              • #90
                                Originally posted by TheLurch View Post
                                He states that based on what? This isn't a game of Behe said - explain why that's true from the biology. Because we know from examples like sickle-cell hemoglobin that there are cases where a single mutation enables new protein-protein interactions, so it sounds like nonsense to me.
                                I might complain here that you have not picked a representative sample.

                                And i'm mystified by your logic. They calculated a rate at which interactions were discovered. The rate indicated that interactions are relatively common.
                                Of course it is, since randomized sequences contain much more variation than can be expected in evolution.

                                Blessings,
                                Lee
                                "What I pray of you is, to keep your eye upon Him, for that is everything. Do you say, 'How am I to keep my eye on Him?' I reply, keep your eye off everything else, and you will soon see Him. All depends on the eye of faith being kept on Him. How simple it is!" (J.B. Stoney)

                                Comment

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