Friday, May 27, 2011

Larry Moran: Vitamin C Pseudogene is Powerful Evidence

In his on-going criticism of Jonathan Wells’ new book, The Myth of Junk DNA, evolutionist Larry Moran now asserts that the much discussed vitamin C pseudogene is powerful evidence for evolution and common descent:

The main argument of scientists like Ken Miller and Jerry Coyne is not that the GULOP pseudogene exists. It's that the GULOP gene and its pseudogene are at the same location in the genomes of all mammals. In the primate lineage this gene is non-functional due to a number of mutations that make it impossible to produce a functional protein. Some of the same deactivating mutations are found in related species such as humans and chimpanzees. This suggests strongly that the non-functional pseudogene was inherited from a common ancestor.

How did Moran arrive at such a conclusion? Why is the vitamin C pseudogene such strong evidence for inheritance via common descent? Unfortunately, Moran fails to explain his reasoning. He simply asserts this amazing claim.

Evolution and common descent have failed to explain how the original vitamin C gene could have arisen. In fact they fail to explain how any protein could have arisen. They have also failed to explain how all of biology could have arisen.

This is not a good start. So far this evidential claim of Moran’s seems unlikely. But let’s look at the pseudogene in particular. Perhaps there is something about this pseudogene that will make the evidence more obvious. For example, perhaps evolution made a strong, heroic prediction about this pseudogene.

In fact, evolution and common descent made no such prediction.

Well is there, at least, a powerful retrodiction? Again, no. Well perhaps evolution and common descent would absolutely be falsified if there were no such vitamin C pseudogene. Again, the answer is no.

No prediction, no retrodiction, and no falsification. Evolution and common descent do not predict the vitamin C pseudogene, and they are not harmed if there was no such thing. This in addition to the fact that evolution and common descent do not explain how the original gene could have arisen in the first place.

Moran’s assertion that the vitamin C pseudogene is powerful evidence for his unlikely idea appears to be just that, an empty assertion.

17 comments:

  1. clock is 2:43am here how are u guys

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  2. 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 is used to support hypotheses throughout all hypotheses in science.

    If you have an alternative hypothesis to explain the shared mutations, please present it, and show us a way to calculate the likelihood so that it might be statistically tested. We can use AIC to compare models if the models have different numbers of fit parameters.

    I just want you to be consistent and treat evolution, and whatever your alternative hypothesis is, with the same statistical standards that are used throughout the rest of science, e.g. in medicine, chemistry, etc.

    If you can't do this, well, too bad. You're not in the scientific running. You will be ignored as a crank, and you will deserve it.

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  3. Why does a loss of function support Darwinian Evolution?

    Can anyone help me here because 1 + 1 = 2 in base 10 the last I recall.

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  4. They have also failed to explain how all of biology could have arisen.

    As a layman who has been interested in the theory of evolution for quite some time, the referenced phrase caught my attention. In all the books and articles I have read, I don’t recall reading anything that would qualify as an explanation beyond the mantra of random variation and natural selection.

    Is there an article or paper available that describes an “evolutionary event?”

    The questions I have related to the evolutionary event are these. I define the evolutionary event as the event that is characterized by the phrase “random variation.”

    1. Where and when in the life cycle of an organism does the evolutionary event occur?
    2. What must the evolutionary event accomplish in order to be a step in the sequence of steps that eventually alters the morphology of the organism?

    It seems that an evolutionary sequence must accomplish three things, namely the alteration of parts, process, and plan.

    1. Parts - It must create a new part. What is the new part? Is it merely a protein?
    2. Process - It must provide “instructions” on where and when to place this part during the process of embryogenesis. The evolutionary event must therefore alter the assembly instructions in some way.
    3. Plan - Living organisms consist of a hierarchy of organs and tissues that are arranged according to a body plan. Is there a body plan stored in the organism somewhere? How is it altered during an evolutionary event?

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  5. @computerist29
    It doesn't. The GLO pseudogene is evidence for common ancestry because it is inactivated in closely related primates by the same mutations.

    It's more a problem for ID:

    "Why would a creator put a pathway for making vitamin C in all these species, and then inactivate it? Wouldn't it be easier simply to omit the whole pathway from the beginning? Why woul the sami inactivating mutation be present in all primates, and a different one in guinea pigs? Why would the sequences of the dead gene exactly mirror the pattern of resemblance predicted from the known ancestry of these species?"
    WEIT pg. 69

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  6. computerist29 said...

    Why does a loss of function support Darwinian Evolution?

    Can anyone help me here because 1 + 1 = 2 in base 10 the last I recall.


    Evolution doesn't always expect gain of function. Evolution only predicts that environmental pressure and the selection process will tend to optimize a species' chance for survival no matter what that change is. In some cases that means loss of function, like the loss of sight in a blind cave fish. Eyes are useless in the dark and cost lots of energy to maintain, so fish with degraded eyes and loss of function (= less energy expenditure) were selected for in the dark cave environment. There also exist blind cave salamanders and blind cave crickets that underwent the same selection pressure with the same results.

    What is ID's explanation for the eyes in these blind cave animals? The Designer was too lazy to take them out?

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  7. This comment has been removed by the author.

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  8. Doublee said...

    They have also failed to explain how all of biology could have arisen.

    As a layman who has been interested in the theory of evolution for quite some time, the referenced phrase caught my attention. In all the books and articles I have read, I don’t recall reading anything that would qualify as an explanation beyond the mantra of random variation and natural selection.

    Is there an article or paper available that describes an “evolutionary event?”


    Doublee, go read Endless Forms Most Beautiful and The Making Of The Fittest by Sean B. Carroll and Your Inner Fish by Neil Shubin.

    They should give you a good leg up in understanding how body plans develop and are modified.

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  9. Thorton, you misunderstood me.

    I already know all about the NS & RM mantra.

    What I am curious about is why there is more examples of Darwinian Evolution via loss of function than a gain and when an example of gain in function should have been presented, a loss is chosen as its replacement. What is it about these gains of function by RM & NS Darwinian Evolutionists are not so sure of as sure as they are that a loss was caused by the exact same mechanism?

    It is far easier to lose function than it is to gain it. To use an example of inactivation to support your position is one thing, to state that you have a case against ID is ridiculous, even if common ancestry is involved.

    Common ancestry is a process. Processes are governed by mechanisms.

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  10. computerist29 said...

    Thorton, you misunderstood me.

    I already know all about the NS & RM mantra.


    You may know the words but you certainly don't understand the concepts.

    What I am curious about is why there is more examples of Darwinian Evolution via loss of function than a gain and when an example of gain in function should have been presented, a loss is chosen as its replacement. What is it about these gains of function by RM & NS Darwinian Evolutionists are not so sure of as sure as they are that a loss was caused by the exact same mechanism?

    The biggest reason loss is easier to demonstrate than gain is that loss often leaves an easily visible physical vestige on the extant animals. Any layman can see the degenerated eyes on a cave fish, or the vestigial legs bone on the skeleton of an extant whale. You can't point to an extant cetacean and show 'that used to be a non-fluke", or "those used to be non blowhole". To make those determinations you have to do a detailed study of the fossil and genetic records, and use the consilient data to draw relevant conclusions. Scientists have indeed done this and the evidence for gain is just as scientifically strong at that of loss.

    It is far easier to lose function than it is to gain it. To use an example of inactivation to support your position is one thing, to state that you have a case against ID is ridiculous, even if common ancestry is involved.

    I don't need to make a case against ID because ID has no positive case to begin with. I have a theory that explains the empirical evidence quite well in no small amount of detail. What does ID have?

    Common ancestry is a process. Processes are governed by mechanisms.

    Yep. ToE has the mechanisms of genetic variation produced by imperfect copying, sexual recombination, genetic drift, LGT. It has the mechanism of differential reproductive success acting as a filter. It has the two mechanisms combined into one iterative feedback loop.

    What are ID's mechanisms again?

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  11. The inability of humans and other closely related primates to synthesize Vitamin C is due to the inactivation of the GLO gene. This gene is 'broken' in the same way in each species. The explanation for this is that this gene mutated in an ancestral species, which was subsequently inherited down the primate lineage that lead to the great apes and us. This is explained well in light of common ancestry. What is the alternative explanation on offer?

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  12. Nick M...here is the problem with your line of reasoning.

    The question isn't the probability of shared mutations given common descent. The question is the probability of common descent by Darwinian mechanism.

    Your question is similar to asking the probability of a pig's nose getting cold given that pigs could fly. Yes, it is highly probable that a pig's nose would get cold during flight, but the real question is what is the probability that pigs can fly.

    Check out the following work by Doug Axe and Ann Gauger. It suggests that the probabilities are not in your favor.

    "When Theory and Experiment Collide"

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  13. Thorton,

    "The biggest reason loss is easier to demonstrate than gain is that loss often leaves an easily visible physical vestige on the extant animals."

    My point is that what you and Darwinian Evolutionists are implying is that a gain is derived through the same mechanism a loss is derived.

    Selected-in == selected-out

    Is this correct?

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  14. computerist29 said...

    Thorton,

    "The biggest reason loss is easier to demonstrate than gain is that loss often leaves an easily visible physical vestige on the extant animals."

    My point is that what you and Darwinian Evolutionists are implying is that a gain is derived through the same mechanism a loss is derived.

    Selected-in == selected-out

    Is this correct?


    That's what the evidence shows.

    You forgot to list the mechanisms of ID. Please correct this oversight, thanks!

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  15. Methinks that Cornelius understands very little about how predictions are made. He is TRIVIALLY correct when he says that evolution doesn't predict the existence of the pseudogene in question. But if one adds some assumptions when making a prediction (which Cornelius totally failed to do here), the situation changes. For example, given that humans, gorillas and orangutans all have this pseudogene, common descent predicts that chimps will also have it. Or, to paraphrase, the likelihood of the existence of the pseudogene in chimps is high given common descent (and previously mentioned assumptions).

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  16. For any ID supporters out there:

    Given that humans, gorillas and orangutans all have the pseudogene in question, what does ID predict about the chimp genome?

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  17. When I was a boy I always wanted to be a monkey.

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