Saturday, May 28, 2011

Evolutionist: Larry Moran is Correct!

In my previous post I discussed Larry Moran’s undefendable claim that the vitamin C pseudogene is powerful evidence for evolution and common descent. In response an evolutionist in the know commented that I had it all wrong and Moran’s claim is quite correct:

We can calculate the likelihood of those mutations being shared via common ancestry. This likelihood is much higher than the likelihood you get under the hypothesis that the mutations were independently acquired by chance. This is strong support for the common ancestry model in the usual way that statistics are used to support hypotheses throughout all hypotheses in science.

It is worth elaborating on this argument to reveal the depths of evolutionary thinking. For this argument dates back centuries (at least to 1734 when Daniel Bernoulli used it) and hinges on, like all evolutionary arguments, deep metaphysics.

The term “likelihood” here refers to the probability of the evidence (the vitamin C pseudogene patterns in this case) we observe given a hypothesis of how they arose. So the likelihood of common descent, in this case, is the probability of the vitamin C pseudogene patterns given that they arose via the process of common descent.

Now the trick evolutionists use is to compare this likelihood of common descent with the likelihood of random design (or as our elite evolutionist puts it above, “independently acquired by chance”).

Don’t worry if you haven’t understood a word of this explanation. Here is the plain English version: Evolutionists claim that similarities (and in particular similarities that are harmful) between species are powerful evidence for their theory because it is obvious that such similarities did not arise by chance.

This certainly is the Mother of all false dichotomies. When put into plain English it is astonishing.

To be sure, who would disagree that most similarities between species—including the vitamin C pseudogene patterns—probably did not arise by chance? That seems reasonable enough.

But evolutionists then claim that, therefore, their unlikely theory is compelling.

In other words, simply put, it’s either evolution or chance. Those are your choices. That’s it. This argument is prima facie absurd and it is astonishing that evolutionists are serious. But they are, and that makes it important. Until you understand the depths of these fallacies you will not understand evolutionary thought.

Of course what evolutionists have actually shown is that their theory is better than origin by pure chance. That’s what their argument reveals—one silly theory is more likely than another silly theory. And they call this science? Sorry but this does not make evolution a fact. In fact, evolution and common descent still have all the monumental problems they had before evolutionists made the argument. None of those problems went away just because of the non random vitamin C pseudogene patterns.

But this argument is typical, and it speaks volumes. Evolutionary thought is not merely science gone wrong. It is not the consequence of a faulty experiment or flawed theorem. It is an utterly ridiculous mandate, tracing back to antiquity, that the universe and everything in it must have just happened to arise spontaneously. The scientific absurdity of the idea is exceeded only the evolutionist’s certainty it is true. Religion drives science, and it matters.

49 comments:

  1. Obviously no one should posit that it's either evolution or chance.

    It should be evolution, chance, or magicks. Right?

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  2. You forgot the fourth possibility: something that nobody has thought of yet.

    Hard to test statistically, though.

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  3. Cornelius Hunter: In other words, simply put, it’s either evolution or chance.

    You probably mean "common descent or chance."

    In any case, the observed nested hierarchy is not just any non-random pattern, but a highly specific prediction from the Theory of Common Descent.

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  4. Well, I knew it was too much to expect that CH would develop an honesty gland during his recent absence.

    Here we go again, back to stupid Creationist strawman city.

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  5. Scott, can we get you on record as saying all the "junk-dna" identified as pseudogenes are non-functional?

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  6. either the drug worked or the patients got better by pure chance

    either similar fossil assemblages are present along the coasts of different continents because the continents were once joined or by pure chance

    either jefferson's dna is present in sally hemming's children because he was the father or by pure chance.

    more false dichotomies? none of these make any of the hypotheses facts, but they do provide strong support for them, just as shared pseudogenes provide strong support for common descent.

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  7. Zach: "You probably mean "common descent or chance."

    Why not convergent evolution, like the 10 mutations in bats and dolphins for echolocation?

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  8. Tedford the Idiot said...

    Scott, can we get you on record as saying all the "junk-dna" identified as pseudogenes are non-functional?


    Why in the world would he say that Tedford? No one in science ever claimed ALL pseudogenes have been found to be 100% non-functional.

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  9. Blas said...

    Zach: "You probably mean "common descent or chance."

    Why not convergent evolution, like the 10 mutations in bats and dolphins for echolocation?


    Convergent evolution happens when similar environmental pressures drive evolutionary processes towards the same solution set in different, not closely related lineages.

    In cases like the echolocation you mention there are only a few solutions to make the gene 'work'. Alternately there are many many ways mutations can 'break' a gene and cause it to not function.

    What would the environmental pressure be that would independently select the same gene to be broken in the identical manner in different mammal species?

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  10. CH: Another good observation and explanation of evolutionist pseudo-logic.

    The amazing thing is that, judging by the responses, none of them got it. As usual.

    The acute cognitive dissonance generated by persistence in Darwinian "logic" short circuits the brain's ability to discern errors of reason.

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  11. I agree with Gary. Seems like most comments completely miss the point--that the argument for common descent is based on a false dichotomy. The evolutionist's only options are chance or chance called "common descent", i.e. chance mutations that resulted in an advantage that were then passed on, etc.. But the realistic options are common descent or common design. And the choice between those two option is based not on ANY physical evidence, but on one's metaphysical assumptions, i.e. either there is no designer or there is a designer.

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  12. "And the choice between those two option is based not on ANY physical evidence, but on one's metaphysical assumptions, i.e. either there is no designer or there is a designer. "

    would you feel comfortable if the authors of a clinical drug trial reported that their positive results were caused by an invisible gremlin?

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  13. Thorton:"What would the environmental pressure be that would independently select the same gene to be broken in the identical manner in different mammal species?"

    You tell me why NS allowed to survive the descents with the broken gene instead that with non broken gene?

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  14. "You tell me why NS allowed to survive the descents with the broken gene instead that with non broken gene? "

    perhaps because they could obtain a sufficient amount from their diet. this hypothesis is supported by the fact that most animals that can not synthesize vitamin c originate from the tropics, where fruit with vitamin c is plentiful.

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  15. Blas,
    and this paper suggests that normal expression of the vitamin c synthesis gene may inhibit cell growth: http://www.sciencedirect.com/science/article/pii/S0888754303002714

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  16. Blas said...

    Thorton:"What would the environmental pressure be that would independently select the same gene to be broken in the identical manner in different mammal species?"

    You tell me why NS allowed to survive the descents with the broken gene instead that with non broken gene?


    As was already pointed out, it's because the mammals with the broken gene had an alternative source of vitamin C from the fruit in their diet. As a result, the broken gene was not detrimental to their survival.

    Still waiting for your ID explanation as to why the identically broken gene is found in different mammalian species.

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  17. Blas: Why not convergent evolution, like the 10 mutations in bats and dolphins for echolocation?

    Dolphins also show convergence with fish in terms of their hydrodynamic shape. That's due to natural selection.

    Red Readers: Seems like most comments completely miss the point--that the argument for common descent is based on a false dichotomy.

    Well, how could we distinguish between the cases? Let's only consider non-synonymous substitutes, which usually have no effect on phenotype. With common descent, we would still expect the nested hierarchy. And that is what we find.

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  18. This comment has been removed by the author.

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  19. Cornelius, the point is not that a low probability explanation is better than an an even lower probability explanation, therefore the former simply must be true.

    Common descent is well supported by the evidence in the broken GULO gene (along with myriad other independent lines of evidence in the haplorhine primates). The fixed mutations in the broken gene form a nested hierarchy that matches phylogenies for functional genes. Interestingly, the susbtitutions differ from those in guinea pigs, which appear to have had an independent loss of GULO. These threads of evidence amount to more than claiming that common descent is only better than pure chance.

    If we were to reject common descent, is there some line of argument around common design being a better explanation for a shared, broken gene in a line of otherwise apparently closely related species? Why common changes to a pseudogene if not by descent? Why the presence of a broken gene at all, if by design? And why do other species (e.g. guinea pigs) that also have GULOP have different changes to the gene that indicate an independent loss, matching the exact predictions under common descent? Regardless of whether the design is directed by god or some other agent, under what model of common design are these patterns coherent (let alone likely)?

    One explanation is that these sequences are functional, and perform different functions in guinea pigs and primates. This leaves three problems for common design to address: firstly why re-use an apparently broken gene, located in the same place in the genome as a functional gene in other lineages to perform some function? What function could possibly be performed by it? And why is the sequence lacking conservation if it is functional?

    So many questions, yet all are answered by common descent. It is not merely some unlikely explanation as you claim.

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  20. That’s what their argument reveals—one silly theory is more likely than another silly theory.

    Assumption: Humans, gorillas and orangutans all share a pseudogene.

    The likelihood of finding the same pseudogene in chimps given common descent is not so low that it is silly.

    The likelihood of finding the same pseudogene in chimps given separate ancestry is so low that it is silly (in fact, the likelihood of the assumption under separate ancestry is so low that it is silly).

    The likelihood of finding the same pseudogene in chimps given ID can't even be estimated.

    Something here is silly, and it ain't common descent.

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  21. Thorton:"As was already pointed out, it's because the mammals with the broken gene had an alternative source of vitamin C from the fruit in their diet. As a result, the broken gene was not detrimental to their survival."

    Off course, something broke the gene leading to th lack of capacity of sintetise Vit C in the common ancestor of the primates. And that is an advantage for tha animals carryng the defect enough that this gene is selected over the unbroken gene.

    Magic!

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  22. Zachriel: Let's only consider non-synonymous substitutes,...

    That should read synonymous substitutes, of course.

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  23. Blas: Off course, something broke the gene leading to th lack of capacity of sintetise Vit C in the common ancestor of the primates. And that is an advantage for tha animals carryng the defect enough that this gene is selected over the unbroken gene.

    You seem to think a variant can only become fixed if it is selectively advantageous.

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  24. Zach:"You seem to think a variant can only become fixed if it is selectively advantageous."

    Ok then NS fix advantageous and non advantageous variants, then there is no selection at all!

    It si so problematic logic for darwinists?

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  25. Blas: Ok then NS fix advantageous and non advantageous variants, then there is no selection at all!

    The basic math for this was established nearly a century ago. It started with Hardy-Weinberg (1908), and culminated in Fisher's The Genetical Theory of Natural Selection (1930).

    Consider a simple situation, a population of 1000, and a single neutral mutation in a single individual. What is the chance of fixation? According to your naĂŻve position, it would be zero. Actually, if you think about it, the chance is actually one in a thousand. (Formally, we have to show that some variant or other will eventually become fixed.)

    Now what if we introduce a new neutral mutation every few generations. Over time, like continuously rolling a die, some of these will become fixed in the population. Turns out that the rate at which neutral mutations become fixed is equal to the rate of neutral mutation.

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  26. Zach:"Consider a simple situation, a population of 1000, and a single neutral mutation in a single individual. What is the chance of fixation? According to your naĂŻve position, it would be zero. Actually, if you think about it, the chance is actually one in a thousand. (Formally, we have to show that some variant or other will eventually become fixed.)

    Now what if we introduce a new neutral mutation every few generations. Over time, like continuously rolling a die, some of these will become fixed in the population. Turns out that the rate at which neutral mutations become fixed is equal to the rate of neutral mutation."

    I´m sorry Zach, but this is not a mathematical question is something about logical,¿what do you mean by selection? If any mutation has the same chance to be fixed no matter is benefitial or not there is no selection at all.
    Every non letal mutation, will occur and will be fixed.

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  27. Blas said...If any mutation has the same chance to be fixed no matter is benefitial or not there is no selection at all.

    All mutations don't have the same chance to be fixed. In each generation beneficial ones have a slightly greater than average chance of being passed on, neutral one have an average chance, deleterious ones have a less than average chance.

    That means in the long run most of the beneficial ones will become fixed, some (but not all) of the neutral ones will become fixed, most deleterious ones will tend to get weeded out.

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  28. Thorton:"All mutations don't have the same chance to be fixed. In each generation beneficial ones have a slightly greater than average chance of being passed on, neutral one have an average chance, deleterious ones have a less than average chance. "

    Well darwinist have to make his teory more coherent if want evolution to be believed as a fact.

    ¿deleterious mutation has a change to be fixed?
    ¿a benefitial mutation has more chance to be fixed than a non benefitial mutation?
    if the second answer is yes, why a broken gene that lead to the need of the Vit C get fixed against the normal gene?

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  29. Blas said...

    if the second answer is yes, why a broken gene that lead to the need of the Vit C get fixed against the normal gene?


    The broken gene didn't lead to the need of external vitamin C. The presence of external vitamin C in the diet led to the GULOP gene becoming not necessary for survival. Therefore when the gene 'broke' it was not a deleterious change but just another neutral one. And like all neutral mutations, it had a chance to go to fixation through genetic drift without the need for a selection pressure driver.

    BTW, I still haven't seen a single IDCer offer an ID explanation for the distribution of the broken gene. Well?

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  30. Thorton:"Therefore when the gene 'broke' it was not a deleterious change but just another neutral one. And like all neutral mutations, it had a chance to go to fixation through genetic drift without the need for a selection pressure driver."

    Well genetic drifting is not fixation, drifting as I understand is the survival of genes with no genetic pressure but cannot led to fixation, why should the broken GULOP rplace the GULOP. No matter what you eat better if you have not "need" to eat.

    But let that point appart, concede that the broke gene drifted and became fixed. Then, how this is a prove of common descent? How do you prove that the mutation did not happened in separated lineages and become fixed by drifting in humans and primates?

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  31. Blas said...

    Thorton:"Therefore when the gene 'broke' it was not a deleterious change but just another neutral one. And like all neutral mutations, it had a chance to go to fixation through genetic drift without the need for a selection pressure driver."

    Well genetic drifting is not fixation, drifting as I understand is the survival of genes with no genetic pressure but cannot led to fixation, why should the broken GULOP rplace the GULOP. No matter what you eat better if you have not "need" to eat.


    Wrong. Genetic drift can and does lead to fixation of a gene in a population.

    fixation - population genetics

    But let that point appart, concede that the broke gene drifted and became fixed. Then, how this is a prove of common descent? How do you prove that the mutation did not happened in separated lineages and become fixed by drifting in humans and primates?

    Not proof, evidence for common descent. One of just millions of pieces of consilient evidence. Just like if a teacher was grading term papers and found the same supposedly original identical paragraph with the same identical typos from a group of students. Such a situation is much more strongly an indication of cheating (i.e. a common origin of the passage) than each student writing the same passage with the same typos in the same place independently.

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  32. Thorton:"Such a situation is much more strongly an indication of cheating (i.e. a common origin of the passage) than each student writing the same passage with the same typos in the same place independently."

    But ypu call that situation cheating in one classroom (GULOP in humans and primates)and not cheating (echolocaation in bats and dolphins) in the other.
    But no matter of your double standard, the cheating situation should be common following your mechanism of evolution.
    Mutation occur and there are position were they have more chance to happened.
    Mutation get fixed no matter the advantage or not.
    So is expected to found the same mutation in the same loci with or without common descent.

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  33. @Blas

    Echolocation in bats and whales is an example of convergent evolution, while loss vitamin C production in primates was permissive.

    Do you agree that mutations occur randomly? It can concluded that GLU is evidence for common descent because the genes share inactivating mutations. Because mutations occur randomly, the best explanation for shared mutations is that they inherited them from a common source. The same can be said of the phylogenetic analysis of one of the genes involved in echolocation in bats and whales.

    Are you asserting that mutations in GLU are not random? Then why do we see different inactivating mutations in other, unrelated species? Please explain.

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  34. Blas said...

    Thorton:"Such a situation is much more strongly an indication of cheating (i.e. a common origin of the passage) than each student writing the same passage with the same typos in the same place independently."

    But ypu call that situation cheating in one classroom (GULOP in humans and primates)and not cheating (echolocaation in bats and dolphins) in the other. But no matter of your double standard, the cheating situation should be common following your mechanism of evolution.


    Wrong again. The situations are very different. The convergent evolution in bats and dolphins was driven by strong selection pressure, and the fact there are a very limited number of ways to produce high frequency sensitivity in mammalian hearing. The non-functional GULO gene on the other hand had no selection pressure, so there is no logical reason for it to be found in so many different mammalian species except through common descent.

    Mutation get fixed no matter the advantage or not.

    No, that is not true, and we've been over why it is not true. There is more than one mechanism for fixation, and SOME neutral mutations get fixed. But like a typical IDCer you have to misrepresent the evidence when your nonsense gets you backed into a corner.

    I'm still waiting for the ID explanation for the distribution of the non-functional GULO genes. Why won't you or any of the other ID pushers provide one?

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  35. sciencehole:"Echolocation in bats and whales is an example of convergent evolution"

    Ok, the same mutation occur in different species and different times and are selected by natural selection.

    "while loss vitamin C production in primates was permissive."

    The same mutation, not advantage then cannot be selected by natural selection, then could only happened once, then it is evidence of CD.

    The problem with this is:

    Why get fixed a non advantage mutation? Why the population without GULOP prevailed over the population with GULOP?

    Thorton and Zach answered there is no need of advantage to get selected then the mutation could happened more than once in different species at different times then it is the same case of convergent evolution not evidence for CD.

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  36. Thorton:"The convergent evolution in bats and dolphins was driven by strong selection pressure, and the fact there are a very limited number of ways to produce high frequency sensitivity in mammalian hearing."

    Yes, but mutation do not know they are building an echolocation system, so the probability that the mutation for the echolocation occur is the the same for the mutation for broke GULOP no matter selective pressure or not.

    "There is more than one mechanism for fixation, and SOME neutral mutations get fixed"

    Ok, I got it. Then why lost of GULOP should happened only once?

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  37. Blas said...

    Thorton:"The convergent evolution in bats and dolphins was driven by strong selection pressure, and the fact there are a very limited number of ways to produce high frequency sensitivity in mammalian hearing."

    Yes, but mutation do not know they are building an echolocation system, so the probability that the mutation for the echolocation occur is the the same for the mutation for broke GULOP no matter selective pressure or not.


    But the probability and pressure for fixation is not. The echolocation convergence was filtered and driven by selection pressure. Not so for the GULO genes.

    T: "There is more than one mechanism for fixation, and SOME neutral mutations get fixed"

    Ok, I got it. Then why lost of GULOP should happened only once?


    It did happen more than once, by different ways in different mammalian lineages.

    Gulonolactone oxidase deficiency

    The loss of activity of the gene for L-gulonolactone oxidase (GULO) has occurred separately in the history of several species. The loss of this enzyme activity is responsible for the inability of guinea pigs to enzymatically synthesize vitamin C, but this event happened independently of the loss in the haplorrhini suborder of primates, including humans. The remains of this non-functional gene with many mutations, is however still present in the genome of the guinea pigs and in humans.[4] The function of GULO appears to have been lost several times, and possibly re-acquired, in several lines of passerine birds, where ability to make vitamin C varies from species to species. In addition, GULO activity has also been lost in all types of bats, regardless of diet

    Why won't you give us the ID explanation for the distribution of the nonfunctional gene? Why are you avoiding the question?

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  38. Thorton:"It did happen more than once, by different ways in different mammalian lineages."

    Why it is then evidence of CD.

    "Why won't you give us the ID explanation for the distribution of the nonfunctional gene? Why are you avoiding the question?"

    I´m not an ID supporter, I do not know what the theory says about that so I can´t answer.

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  39. Blas said...

    Thorton:"It did happen more than once, by different ways in different mammalian lineages."

    Why it is then evidence of CD.


    It's evidence of common descent in the Haplorrhini suborder of primates which included humans) because the identical gene is rendered non-functional in the identical location.

    The fact that it broke in different ways in different lineages is evidence that the gene had many ways to become non critical in mammals due to diet.

    To recap. Common descent offers a logical and coherent explanation explanation for the observed sequences that is consistent and consilient with all the other genetic evidence.

    ID offers not a damn thing.

    Which should we go with?

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  40. Blas: I´m sorry Zach{rie}, but this is not a mathematical question is something about logical,¿what do you mean by selection?

    The previous discussion didn't include selection. Even without selection, variants can become fixed in a population, which is something you didn't seem to understand.

    Blas: If any mutation has the same chance to be fixed no matter is benefitial or not there is no selection at all.

    That's right. The previous discussion concerned neutral mutations, those without any selective benefit or detriment. Do you understand the previous discussion?

    Blas: Every non letal mutation, will occur and will be fixed.

    Not at all. If it is beneficial, then it is more likely to be fixed. If it is deleterious, then it is less likely to be fixed.

    Blas: if the second answer is yes, why a broken gene that lead to the need of the Vit C get fixed against the normal gene?

    A broken gene for Vitamin C is normally highly deleterious, and is quickly weeded out of a population. The exception is when there is plenty of Vitamin C in the diet, such as in primitive primates. Then the mutation is *neutral*. And as you should now know, there is a finite chance of fixation of a neutral mutation.

    Blas: So is expected to found the same mutation in the same loci with or without common descent.

    That is not correct. When the gene is no longer under selection, then it will mutate randomly along its length. Any mutation is a likely as another. If the mutations were independent, then we would not expect a nested hierarchy in different lineages, but a random relationship. Instead, we do see a nested hierarchy. This is clearly due to common descent.

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  41. Thorton:"Common descent offers a logical and coherent explanation explanation for the observed sequences that is consistent and consilient with all the other genetic evidence."

    That is the point, CD has an explanation. But having an explanation is not evidence. As you can explain the same facts by the ramdon mutation and fixation by drift also in a non CD model like a orchard model.

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  42. Blas said...

    Thorton:"Common descent offers a logical and coherent explanation explanation for the observed sequences that is consistent and consilient with all the other genetic evidence."

    That is the point, CD has an explanation. But having an explanation is not evidence.


    Wrong again. CD is an explanation based on the large amount of consilient evidence.

    As you can explain the same facts by the ramdon mutation and fixation by drift also in a non CD model like a orchard model.

    Then do do. Please explain the distribution of identical non-functional GULO genes in the Haplorrhini suborder of primates by using the 'orchard' model.

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  43. Zachriel: “ previous discussion didn't include selection. Even without selection, variants can become fixed in a population, which is something you didn't seem to understand.”

    That's right. The previous discussion concerned neutral mutations, those without any selective benefit or detriment. Do you understand the previous discussion?

    You are right, I do not understand selection that sometimes select sometimes do not select.


    Not at all. If it is beneficial, then it is more likely to be fixed. If it is deleterious, then it is less likely to be fixed.

    A broken gene for Vitamin C is normally highly deleterious, and is quickly weeded out of a population. The exception is when there is plenty of Vitamin C in the diet, such as in primitive primates. Then the mutation is *neutral*. And as you should now know, there is a finite chance of fixation of a neutral mutation.

    So, can you explain my question:” Why the population without GULOP prevailed over the population with GULOP?”


    That is not correct. When the gene is no longer under selection, then it will mutate randomly along its length. Any mutation is a likely as another. If the mutations were independent, then we would not expect a nested hierarchy in different lineages, but a random relationship. Instead, we do see a nested hierarchy. This is clearly due to common descent.

    Wich nested hierarchy you sre talking about? If thorton says:” It did happen more than once, by different ways in different mammalian lineages.”

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  44. Blas said...

    You are right, I do not understand selection that sometimes select sometimes do not select.


    Genetic drift is not driven by selection. You've already had that explained to you about half a dozen times now.

    So, can you explain my question:” Why the population without GULOP prevailed over the population with GULOP?

    You've already had that explained to you about half a dozen times now too.

    Wich nested hierarchy you sre talking about? If thorton says:” It did happen more than once, by different ways in different mammalian lineages.”

    Are you just playing disingenuous and dumb on the web for kicks, or are you really disingenuous and dumb?

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  45. "or are you really disingenuous and dumb?"

    At least I am not a darwinist.

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  46. Blas said...

    "or are you really disingenuous and dumb?"

    At least I am not a darwinist.


    So you're not a 'darwinist', and you're not an ID supporter. What are you then? Loki troll?

    How are you coming with that explanation for the distribution of identical non-functional GULO genes in the Haplorrhini suborder of primates by using the 'orchard' model?

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  47. Blas: You are right, I do not understand selection that sometimes select sometimes do not select.

    The discussion concerned differences that have no selective benefit or detriment. For instance, a synonymous substitution normally has no benefit or detriment because it doesn't change the phenotype.

    Blas: Why the population without GULOP prevailed over the population with GULOP?

    It would help if you tried to understand the general case discussed above. If you won't or can't, then it's unlikely you will quite understand the following.

    As there was ample Vitamin C in the primate diet, there was no benefit to a working Vitamin C gene. If any mutation occurs to the gene, it will be a neutral mutation because the gene is extraneous and of no benefit to the primate. Now, if you remember from above, the rate of fixation of neutral mutations is equal to the neutral mutation rate. The gene sequence will drift.

    Blas: Wich nested hierarchy you sre talking about? If thorton says:” It did happen more than once, by different ways in different mammalian lineages.”

    That's right. If it occurred independently, then we wouldn't expect it to fit the nested hierarchy. And that's what we see when comparing guinea pigs and primates.

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  48. Zach:" If any mutation occurs to the gene, it will be a neutral mutation because the gene is extraneous and of no benefit to the primate. Now, if you remember from above, the rate of fixation of neutral mutations is equal to the neutral mutation rate. The gene sequence will drift. "

    Sorry for mu dumb question, we have some individuals with GOLUP and others with GOLUP broken. why is fixed by drift the GOLUP broken
    and not the GOLUP? And no see any reason for GOLUP broken replace GOLUP in all the population of the following generations.

    "That's right. If it occurred independently, then we wouldn't expect it to fit the nested hierarchy. And that's what we see when comparing guinea pigs and primates"

    If they occurred independently, the mutation is not passed trough CD, then why they fit the nested hierarchy?
    If the mutatons are independents, the occurrence is random, so they fit nested hierarchy just ny chance. Am I wrong?

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  49. Blas: we have some individuals with GOLUP and others with GOLUP broken. why is fixed by drift the GOLUP broken

    Let's break it down into pieces:

    Do you understand that in the case of an organism with ample supplies of Vitamin C in its diet, that it doesn't matter whether the GULOP gene works or not?

    And that this would make changes to the GULOP gene selectively neutral, neither a benefit or a detriment?

    Do you understand that in a finite population there is a non-zero probability of a neutral variant becoming fixed?

    Do you understand that in the case of neutral mutations, the rate of fixation is equal to the rate of mutation?

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