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Was Michael Behe Right?

An very interesting study has now made the press cycle. Susanne Dobler and Anurag Agrawal studied the genetic mechanism employed by monarch butterflies to resist cardenolides, a powerful toxin which binds the cell’s sodium pump, and which is common to milkweed and foxgloves.

They found that a single ” specific mutation — called N122H — of the Na,K-ATPase gene” was enough to confer resistance.

They then looked in other insect lines to see what genetic mechanism was employed by these other lines.

“Already knowing how monarchs deal with the toxin, we wanted to see if it was the same molecular solution used by beetles, flies and true bugs that are also resistant to cardenolides,” said Anurag Agrawal, a Cornell professor of ecology and evolutionary biology.

What did they discover?

By examining molecular changes in the sodium pump gene, the researchers found the mutation N122H in all four orders of insects studied. Furthermore, they discovered a second mutation in the same gene that also conferred resistance in 11 of the 18 species.

What do you know? Not just any old mutation worked. A very specific one. (So much for neutral drift coming to the rescue.) And, an second mutation conferred a higher level of resistance.

What do you know? Evolution at work, and what do we see? Two specific mutations in the gene involved with the cell’s sodium pump.

Doesn’t that sound familiar? Yes, it does. When Michael Behe studied the malarial parasite to see how it developed resistance to quinine, he found two specific mutations. And then he was roundly criticized by the evolutionists for his The Edge of Evolution.

Here we have it in spades!!!! Four different orders of insects, and the same, two mutations show up. And, one mutation generally suffices, with two being the maximum needed for development of resistance. Just as with the malarial parasite, faced with imminent death, evolution’s answer—that is, NS’ answer—was TWO mutations.

Read about it here.

Another day; another bad day for Darwinism.

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53 Responses to Was Michael Behe Right?

  1. Wasn’t Behe’s argument that Plasmodium falciparum needed both mutations for resistance, so only having one wouldn’t confer any advantage? But here, having one mutation is enough for resistance. So we’re a long way from Behe’s edge of evolution.

    If there’s a larger selective advantage to resistance, and this is the only mutation that would confer an advantage, I’m not surprised it repeatedly appears: that’s the power of natural selection.

  2. Behe’s edge of evolution is set at two new protein-to-protein binding sites.

  3. Joe:

    I was talking about the malarial parasite, not Behe’s limit on evolution—which is a generous lean towards evolution. I’ve had correspondence with him, and he is more generous than I am when it comes to conceding what evolution can do (which, of course, is not much).

  4. A Gene:

    If there’s a larger selective advantage to resistance, and this is the only mutation that would confer an advantage, I’m not surprised it repeatedly appears: that’s the power of natural selection.

    Well, may be it didn’t surprise you, but it sure surprised the experimenters.

    Four different orders of insects came up with the exact same mutation for resistance.

    Where’s the “random variation” part of this?

    ______________________
    In the case of the malarial parasite, again, the same thing. Now some what to crucify Behe over his use of 10^20 replications. From a simple population genetics point of view, it can easily be argued that a number of 10^16 should be used (the scientist studying the parasite found that, in practice, 10^12 replications were needed when only 10^8 would be needed per calculation via genome size and mutation rates).

    So, let’s use the figure a very conservative figure of 10^10 replications needed for two amino acids to change in ONE protein.

    The generation time for elephants is 35 years.

    Their population size is small. But let’s be generous. Let’s say you had a population size of one million. Then how many years would it take to come up with 10^10 replications: 35 x 10^4=350,000 years.

    This would be how long it would take for the mutation to show up. But what is the probability of this mutation taking hold in the entire population, i.e., becoming “fixed”?

    Well, per Kimura, it’s 1/2N. IOW, we would need 2 million generations, which would require 70 million years.

    So, let’s use a smaller population size. IIRC, the maximal population size for fixation given known mutation rates is around 50,000.

    Then, we would need only 1.75 million years. Added to the 350,000 years, a total of 2 million years would be needed for two amino acids to change.

    One wonders why Darwinists don’t give up.

    ________________

    [Well, it's because they try and fool themselves and everyone else by saying that these odds are only for "specific" amino acid changes. But the probability of some kind of mutation is quite high in each generation---the neutral drift approach. But, we can see here, that "specific" amino acid changes are required. Neutral drift can't help us out. Oh, alas and alack, another day, and another bad day for Darwinism!]

  5. 5

    Behe’s edge was meant to be two mutations where the first one which happened, be it in either order, was either neutral or deleterious.

    The argument about two protein-protein binding sites with six mutations was made on about two pages and seems like an afterthought. The central thrust of the book is the two mutation limit. But again, this is not just any two mutations. It’s two mutations that are both simultaneously required for the trait.

    That said, finding one mutation which does the trick doesn’t “break” the edge. It fits nicely within it, especially, as the OP emphasized, when four different species have the same one. It means these types of mutations, where one is enough, are so rare that only a very small number do the trick. Not nearly enough to provide a smooth Darwinian pathway from “ancestral” proteins to modern ones.

  6. Four different orders of insects came up with the exact same mutation for resistance.

    Where’s the “random variation” part of this?

    The random variation is in the mutation process.

    I’ve no idea why you brought up elephants, they’re not insects. Perhaps you meant to discuss blue whales?

  7. The random variation is in the mutation process.

    That is the propaganda. However with ID the mutations are not necessarily random.

  8. A Gene:

    The random variation is in the mutation process.

    Mutations are random. But here variation is not. It is the SAME mutation that occurs in four different orders of insects.

    I hope you appreciate the difference—which leads to:

    I’ve no idea why you brought up elephants, they’re not insects. Perhaps you meant to discuss blue whales?

    I discussed elephants because of their long generation times, which makes replicating take longer. The import of the insect experiment is that SPECIFIC SNPs are needed. And that requires a whole lot of replications. And I used the worst case scenario simply to highlight the problems for Darwinism. I’ll let you fill in the rest.

  9. Mutations are random. But here variation is not. It is the SAME mutation that occurs in four different orders of insects.

    Yes, which can still happen randomly. There are a lot of insects out there, so I think the probability of it happening is reasonable.

    I discussed elephants because of their long generation times, which makes replicating take longer.

    Yes, much longer than insects. And their population sizes are much smaller. So, why did you bring them up? How are they comparable to insects?

    (BTW, elephants have a higher mutation rate, because their testes remain in the body, so they have a higher temperature. Not really relevant, but a fun fact)

  10. A Gene:

    So, as an evolutionist, you assume common descent. We know that sponges have genes that are the same as those found in humans. But now you want to say: “Oh, well, other insects must do things differently; and, surely, elephants must do things differently.”

    How do we know that? Evolutionists were surprised by this finding. IOW, they weren’t expecting it.

    You’re simply say you don’t “expect” that other orders/classes of insects and other phyla will react this way. How do you know?

    If one assumes that ‘specific’ mutations are required, then neo-Darwinism is very, very, very limited. That’s what Behe pointed out. Do you think Behe was right? I do.

    Here’s more evidence vindicating Behe’s very conservative conclusions.

    Another day; another bad day for Darwinism.

  11. Mutation is not the only mechanism in evolution. Genetic drift is more important than mutation anyway… and also see the book Evolution–the Extended Synthesis and a few other recent books becuase theres a heck load more factors influencing evolution… evolution is far more complex than just mutation! Check out the extended synthesis including stuff like niche contruction .. nongenetic inheritance (jablonka et al), biological emergence & self-organization (Kauffman et al), field theories (goodwin et al) etc.. statis (Gould), saltation (Ryan et al) … phenotypic plasticity, gene regulation, internal selection (wallace authur) etc. Yet IDer’s ignore all of these and just talk about mutations.

  12. 12

    “Yet IDer’s ignore all of these and just talk about mutations.”

    IDers hardly ignore these things. At the same time, there could not possibly be a larger blind eye as the one turned by materialists towards the existence of recorded information. Except perhaps, the blind eye they turn towards the material requirements of that existence. “Life is matter controlled by symbols” Pattee 1968.

  13. So, as an evolutionist, you assume common descent. We know that sponges have genes that are the same as those found in humans. But now you want to say: “Oh, well, other insects must do things differently; and, surely, elephants must do things differently.”

    Well, that’s certainly putting words into my mouth. I said nothing of the sort.

    How do we know that? Evolutionists were surprised by this finding. IOW, they weren’t expecting it.

    They probably weren’t expecting to see exactly the same mutation in all orders. the usual pattern with convergent evolution is that as you look more closely at convergence, you find that there are differences in the details, e.g. in the evolution of flight in vertebrates. So I imagine they would have expected that different mutations would have arisen in different lineages. That they didn’t is a surprise, but suggests that there’s a strong evolutionary constraint.

  14. A Gene,

    Well if the same random mutation can arise sperately in different populations then evos canNOT use genetic similarity as evidence for a common ancestry.

    You have just destroyed a MAJOR piece of evidence for universal common descent. Congratulations, nicely done.

  15. Joe – You>’re being naive. We don’t use a single mutation to infer ancestry, we use a lot. There’s a reasonable probability that two species will have the same base at one position. So we use many – hundreds to thousands – of bases. The probability of all of them being the same after mutation is vanishingly small.

  16. A Gene-

    If one mutation can arise spearately then so can “a lot”. So who is being naive?

    And given a common design then we would even expect more similarities…

  17. Nice job,Mayor

  18. Joe – the probability of “a lot” arising separately will be much less, as I indicated. With only 250 loci, the probability will be below the universal probability bound (assuming 4 equally likely bases).

    And given a common design then we would even expect more similarities…

    How many similarities would be expected given common design?

  19. A Gene- the probabilities are the same for each mutation. Once one happens the slate is wiped clean and the next one has a go at it. Just as with lotteries. Then, given a large enough population, the evolutionary eons of time and the limited number of choices, we can turn one identical mutation into hundreds or even thousands, especially given similar environmental pressures.

    And even more so given “built-in responses to environmental cues” ala Dr Spetner’s “non-random evolutionary hypothesis”.

    How many similarities would be expected given common design?

    As many as required.

  20. A Gene:

    Thank you for spelling out exactly how the Darwinist brain thinks (defectively):

    . . . the usual pattern with convergent evolution is that as you look more closely at convergence, you find that there are differences in the details . . .. So I imagine they would have expected that different mutations would have arisen in different lineages. That they didn’t is a surprise, but suggests that there’s a strong evolutionary constraint.

    But this is the entire point of my post: that it is the very same mutation across all four orders. This puts a “constraint” on neo-Darwinism. It puts a constraint on “neutral drift”. A very “specific” mutation is required. This requires that a multitude of replications is needed, which, as the elephant example demonstrates, might be just fine for insects—with large populations and small generation times—but not for elephants. Given reasonable population sizes and generation times for elephants, these “constraints” mean that almost nothing can have happened via putative neo-Darwinian mechanisms in the entire history of elephants.

    But, then, blithely, you just “hand-wave” it away: “That they didn’t is a surprise, but suggests that there’s a strong evolutionary constraint>”

    “No big thing.” Well, it is a big thing. Why do you think they invoke Stephen Gould.

    But this shouldn’t have come as a surprise to them. Why? Because if they had read Behe’s book, they would have known what to expect: a “specific” mutation arrived at at the cost of a very high number of replications.

  21. Well then elephant generation times were obvioulsy much quicker in the unseen past. Only when we started watching them did it slow down.

    ;)

  22. “if they had read Behe’s book”

    It’s not too late A gene:

    “The Edge of Evolution: The Search for the Limits of Darwinism”
    http://www.amazon.com/Edge-Evo.....0743296206

    The Edge Of Evolution – Michael Behe – Video Lecture
    http://www.c-spanvideo.org/program/199326-1

    A review of The Edge of Evolution: The Search for the Limits of Darwinism
    The numbers of Plasmodium and HIV in the last 50 years greatly exceeds the total number of mammals since their supposed evolutionary origin (several hundred million years ago), yet little has been achieved by evolution. This suggests that mammals could have “invented” little in their time frame. Behe: ‘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 that world at its disposal’ (p. 155).
    http://creation.com/review-mic.....-evolution

    Dr. Behe states in The Edge of Evolution on page 135:

    “Generating a single new cellular protein-protein binding site (in other words, generating a truly beneficial mutational event that would actually explain the generation of the complex molecular machinery we see in life) is of the same order of difficulty or worse than the development of chloroquine resistance in the malarial parasite.”

    “The immediate, most important implication is that complexes with more than two different binding sites-ones that require three or more proteins-are beyond the edge of evolution, past what is biologically reasonable to expect Darwinian evolution to have accomplished in all of life in all of the billion-year history of the world. The reasoning is straightforward. The odds of getting two independent things right are the multiple of the odds of getting each right by itself. So, other things being equal, the likelihood of developing two binding sites in a protein complex would be the square of the probability for getting one: a double CCC, 10^20 times 10^20, which is 10^40. There have likely been fewer than 10^40 cells in the world in the last 4 billion years, so the odds are against a single event of this variety in the history of life. It is biologically unreasonable.”
    – Michael Behe – The Edge of Evolution – page 146

  23. Joe -

    How many similarities would be expected given common design?

    As many as required.

    Required for what? It’s not clear to me.

  24. PaV – I don’t see that this puts a constraint on evolution per se: as I pointed out, convergent evolution usually doesn’t involve exactly the same DNA changes: there’s more than one route to increased fitness. But here there’s apparently only one route, which is a surprise.

  25. A Gene- It all depends. For example many houses have the same structure- wall studs are 16″ apart on center, floor joists are 16″ apart on center, rafters 16″ apart, etc. Yet the floor plans can be entirely different.

    A computer and its printer will have some degree of common design and also many differences. All PCs have a great deal of common design and some differences. So it all depends on the requirements.

    If the requirement is to have a spinal column then there is no need to reinvent the sc for each organism that requires it.

  26. Fair enough, Joe. So for a biological problem, how would you decide what the requirements are?

  27. Customer wants/ desires vs design constraints, resources and costs

    :)

  28. Ah, so you’re saying the Designer has a customer, Joe? Who or what is this Intelligent Customer? I don’t recall Behe ever discussing this.

  29. Or the designer is the customer. And ID is not about the designer nor the customer, so why would Behe discuss it?

  30. If the ID is not about the designer, then how come it is about the customer?

    OK, but more seriously, how do you work out what the design constraints, resources and costs? In particular, how do you know what resources are available to the intelligent designer?

  31. A Gene:

    If the ID is not about the designer, then how come it is about the customer?

    I said it wasn’t. Can you read?

    OK, but more seriously, how do you work out what the design constraints, resources and costs?

    As a designer I know they exist and have to be dealt with.

    In particular, how do you know what resources are available to the intelligent designer?

    Well we know that the resources used have to be able to work in this universe governed by a set of laws.

  32. Joe – yes, we know that design constraints, resources and costs exist, but how do you know what they are? IOW, how do you know what it is that is required to lead to the similarities you are claiming would be more than we would see under evolution?

  33. 1- “Evolution” doesn’t say anything about similarities. It would be OK if everything were different.

    2- That is because “evolution” doesn’t say anything about origins which means there could be many different trees and “evolution” is OK with that as it is concerned with what happens AFTER.

    3- and finally “evolution” is an equivocation – what “evolution” are you talking about? Intelligent Design evolution, front-loaded evolution, blind watchmaker evolution, some other evolution? Please do tell

  34. A Gene:

    PaV – I don’t see that this puts a constraint on evolution per se: as I pointed out, convergent evolution usually doesn’t involve exactly the same DNA changes: there’s more than one route to increased fitness. But here there’s apparently only one route, which is a surprise.

    However, when evolutionists speak of convergent evolution, they’re usually talking about “phenotypic” convergence, not “genotypic” convergence. Here, we see constraints; and the natural question that flows is: is this typical, or this aberrant?

    You’re taking the position that it is aberrant; but I don’t share that view since this is something that is seen over four orders of insects.

    It is surprising; and, if further confirmed, severely undermines what evolutionists think can be arrived at via neo-Darwinian mechanisms.

    Why don’t these scientists start looking at more and more orders of insects, and then crossing over to different classes? I suspect they might; hope that they are.

  35. Joe – can you answer my question now, please. You made a claim about what ID says about similarity, and I’m interested in how you came to that claim.

  36. You’re taking the position that it is aberrant; but I don’t share that view since this is something that is seen over four orders of insects.

    We’re still talking about one trait – resistance to cardenolides. My argument is that it is this trait that is aberrant, because resistance can be conferred by only a very specific genotype. It’s different from other instances of convergent evolution, which involve different mutations in different species.

    I, too, hope that someone’s looking at more insects (assuming that there are more insects with this resistance, of course). It would also be interesting to investigate if there are other mutations that would give the same phenotype.

  37. A Gene-

    I said a common design says something about similarities and I gave examples. I know something about designs and how they sometimes have to play with other designs and that is where design standards come in- IEEE, for example. Building codes for another.

    IOW my lifetime of experience dealing with designs is how I came to that claim.

  38. Joe, you specifically said “given a common design then we would even expect more similarities [than evolution]“. I just want to know how you come to that conclusion, and how many more. I’m not sure the IEEE are much help here, unless who (or whatever) is responsible for Intelligent Design is a member.

  39. A Gene-

    I have explained it for you. I cannot make you understand what I post. And IEEE is all about standards, which lead to a common design.

    Do you understand how examples work?

  40. Joe – I’m afraid you haven’t explained it. You’ve made vague statements, but haven’t given any substance. You mad ea quantitative statement, so either you were BSing or you actually made a quantitative assessment. I’m assuming it was the latter, so I just want to know how you made that assessment – what were the steps? What specific aspects did you assess and how?

  41. A Gene- You are afaraid, however that does not mean I didn’t explain it. I did:

    It all depends. For example many houses have the same structure- wall studs are 16? apart on center, floor joists are 16? apart on center, rafters 16? apart, etc. Yet the floor plans can be entirely different.

    A computer and its printer will have some degree of common design and also many differences. All PCs have a great deal of common design and some differences. So it all depends on the requirements.

    If the requirement is to have a spinal column then there is no need to reinvent the sc for each organism that requires it.

    and

    I said a common design says something about similarities and I gave examples. I know something about designs and how they sometimes have to play with other designs and that is where design standards come in- IEEE, for example. Building codes for another.

    IOW my lifetime of experience dealing with designs is how I came to that claim.

    That is how science works- observations and experiences

  42. The only one of those sentences that applies to biology is the one about the spinal column, so the rest are irrelevant. And that says nothing about mutations, which is what your original statement was about, so that’s irrelevant too.

    Care to try again?

  43. A Gene- you are confused. Common design extends beyond biology. And it the common design outside of biology that allows me to make the common design inference wrt biology.

    As for mutations, well your position’s claims is that they are all random, chance events. And it sez that due to total ignorance.

  44. But how does common design outside biology allow you to infer common design inside biology? You’re repeatedly dodging the question – how did you come to your conclusion? Give us the specifics.

  45. I said a common design says something about similarities and I gave examples. I know something about designs and how they sometimes have to play with other designs and that is where design standards come in- IEEE, for example. Building codes for another.

    IOW my lifetime of experience dealing with designs is how I came to that claim.

    I can’t help it if you can’t undersatnd that. perhaps you should not be discussing science.

  46. But how does common design outside biology allow you to infer common design inside biology?

    The observance of common design outside of biology tells us that common descent is not the only explanation for similarities. The observance of convergence within biology tells us that common design isn’t the only alternative to common descent wrt similarities.

    And all of that means is common descent is not the only explanation for similarities.

    Then there is a common mechanism which says that similar DNA sequences will tend to act, ie mutate/ change, similarly given similar environmental pressures. (feel free to sub identical with similar, makes no diff)

    how did you come to your conclusion?

    A lifetime of observances and experiences. For example- I have worked in carpentry, plumbing, auto mechanics and technology. In each there are standards that must be followed.

  47. I said a common design says something about similarities and I gave examples.

    You said more than that, though. You said that design would give more similarities than evolution. How did you come to that conclusion? You’re repeatedly ducking that question.

  48. 1- “Evolution” doesn’t say anything about similarities. It would be OK if everything were different.

    2- That is because “evolution” doesn’t say anything about origins which means there could be many different trees and “evolution” is OK with that as it is concerned with what happens AFTER.

    3- and finally “evolution” is an equivocation – what “evolution” are you talking about? Intelligent Design evolution, front-loaded evolution, blind watchmaker evolution, some other evolution? Please do tell

  49. Once more, Joe, you’re not answering my question. Why is it so difficult for you? Are you unable to support your assertion?

  50. I have answered your question. Again don’t blame me for your failure to comprehend my posts. OTOH you equivocate- see #3 above…

  51. Sorry, Joe. No you haven’t. You made a quantitative statement, but haven’t backed it up with any numbers. How many similarities would you expect under common design for cardenolides resistance?

  52. I backed it up with reasoning. And as I said apparently you have issues comprehending what I post. Not my fault.

  53. Arm waving is not reasoning. You made some general comments, which would support the contention that there would be some similarities under common design. But you’ve done nothing to show that there would be more similarities. And that is your fault.

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