Saturday, October 28, 2017

Creationists questioning pseudogenes: the GULO pseudogene

This is the second post discussing creationist1 papers on pseudogenes. The first post addressed a paper by Jeffrey Tomkins on the β-globin pseudogene [Creationists questioning pseudogenes: the beta-globin pseudogene]. This post covers another paper by Tomkins claiming that the GULO pseudogenes in various primate species are not derived from a common ancestor but instead have been deactivated independently in each lineage.

The Tomkins' article was published in 2014 in Answers Research Journal, a publication that describes itself like this:
ARJ is a professional, peer-reviewed technical journal for the publication of interdisciplinary scientific and other relevant research from the perspective of the recent Creation and the global Flood within a biblical framework.
Tomkins explains two fundamental axioms of Young Earth Creationism.
  1. "An emerging theme from the continuing progression of genomics research across the spectrum of eukaryotic life is the widespread decay of pathways for vitamin-synthesis (Helliwell, Wheeler, and Smith 2013). This paradigm is of great importance to the creationist model of genetic entropy which postulates that genomes are in a continual state of degradation over time, not forward progressing evolution (Sanford 2010)."
  2. "Another important component of the creationist model of origins is the idea of molecular discontinuity between unrelated taxon (Tomkins and Bergman 2013). As will be demonstrated in this report, the enigma of the GULO pseudogene analyzed in the light of new genomic evidence most closely aligns with a creationist model incorporating both of these paradigms."
The idea here is that the loss of a gene for synthesizing vitamin C (GULO gene)2 is consistent with the YEC view of increasing loss and degradation of the genome. Such degradation must occur within species since the YEC model doesn't allow for shared ancestry. The main question Tomkins addresses is whether the pattern of GULO pseudogenes in various species is consistent with gene loss in an ancestral species and subsequent inheritance of a pseudogene in different lineages or whether the pattern is consistent with separate and independent loss in related species.

As you might have guessed, Tomkins argues that that the pattern is inconsistent with common ancestry and lends support to Young Earth Creationism. Here's the article ...
The Human GULO Pseudogene—Evidence for Evolutionary Discontinuity and Genetic Entropy
Jeffrey P. Tomkins, Institute for Creation research, Dallas, TX, USA
Answers in Genesis

Abstract: Modern genomics provides the ability to screen the DNA of a wide variety of organisms to scrutinize broken metabolic pathways. This wealth of data has revealed wide-spread genetic entropy in human and other genomes. Loss of the vitamin C pathway due to deletions in the GULO (L-gulonolactone oxidase) gene has been detected in humans, apes, guinea pigs, bats, mice, rats, pigs, and passerine birds. Contrary to the popularized claims of some evolutionists and neo-creationists, patterns of GULO degradation are taxonomically restricted and fail to support macroevolution. Current research and data reported here show that multiple GULO exon losses in human, chimpanzee, and gorilla occurred independently in each taxon and are associated with regions containing a wide variety of transposable element fragments. Thus, they are another example of sequence deletions occurring via unequal recombination associated with transposable element repeats. The 28,800 base human GULO region is only 84% and 87% identical compared to chimpanzee and gorilla, respectively. The 13,000 bases preceding the human GULO gene, which corresponds to the putative area of loss for at least two major exons, is only 68% and 73% identical to chimpanzee and gorilla, respectively. These DNA similarities are inconsistent with predictions of the common ancestry paradigm. Further, gorilla is considerably more similar to human in this region than chimpanzee—negating the inferred order of phylogeny. Taxonomically restricted gene degradation events are emerging as a common theme associated with genetic entropy and systematic discontinuity, not macroevolution.
The GULO gene encodes the enzyme L-glucono-γ-lactone oxidase, the terminal enzyme in the synthesis of ascorbic acid. Ascorbic acid is required in the synthesis of collagen and a few other processes in mammals. Mutations in the GULO gene can lead to loss of function but this is not lethal in many species because they get enough ascorbic acid in their diet.

The human gene is nonfunctional giving rise to a unitary pseudogene located on chromosome 8 at p21. As a result, ascorbic acid is now an essential component of the human diet. Because it has become essential, it is now called a vitamin (vitamin C) (see Helliwell et al., 2013) [Human GULOP Pseudogene].

The standard explanation for the origin of this pseudogene—and all other unitary pseudogenes—is that the original gene became inactivated by mutation at some time in the past. That null allele then became fixed in the population by random genetic drift. All descendants of that population inherited the pseudogene.

Tomkins takes a scattergun approach to the problem by bringing up all kinds of objections to the standard explanation. I don't have time to discuss all of his objections and I don't have enough knowledge of some of the issues to respond to his points. For example, I don't know enough about bird evolution to say whether the pattern of GULO gene loss is compatible with common ancestry or not.

Let's just look at the pseudogenes in primates to see which explanation is more reasonable. Lapachapelle and Drouin (2011) looked at the pattern of neutral substitutions in the primate lineages. All Haplorrhini3 primates (e.g. humans, chimpanzees, macaque, gibbon etc) have a pseudogene with certain shared characteristics, including a number of identical substitutions. This suggests that the ancestor of all Haplorrhini primates contained the pseudogene, which must have arisen shortly after the the split between Haplorrhini and Strepsirrhini (lemurs, galagos, etc.). According to the fossil record, the split occurred about 63 million years ago.

Lapachapelle and Drouin calculated that the pseudogene must have arisen about 61 Mya based on the neutral substitution rate. The fact that these values are so close lends support to the idea that all Haplorrhini species are derived from a common ancestor that lost the GULO gene.

The authors also looked at specific deletions to see if the results are consistent with common ancestry. All of the primate pseudogenes are missing exons 1 and 2 of the intact, functional, gene.4 They compared the sequences of the human, chimpanzee, and macaque genes to that of the galago gene. The result is shown in Figure 4 of their paper (see below).


Note that the large deletion of the two exons ("deletion") occurs at the same position in the human, chimpanzee, and macaque genomes. All three genomes also have two identical seven base pair indels in the upstream region preceding exon 1. This is evidence of common ancestry.

Lachapelle and Drouin were testing the hypothesis that large deletions in the GULO pseudogene were due to aberrant recombination between flanking transposable elements (TE). They mapped all surrounding transposons in the primate genes and concluded that TE's did not play a role in the deletion.

Tomkins discusses this paper in his creationist journal article. He ignores the evidence of common descent and focuses instead on the transposable elements. He points out that Lachapelle and Drouin failed to find evidence that TE's were responsible for the deletions. Here's what he wants his readers to conclude from a paper that strongly supports common descent ....
Despite the fact that TEs are apparently one of the main genomic drivers of deletion events in the genome, the researchers (Lachapelle and Drouin 2011) concluded that the lineage specific TE insertion patterns, which defied the standard inferred evolutionary model for primates, did not contribute to the loss of exons in the GULO gene. Thus, their evolutionary presuppositions caused the rejection of otherwise strong genomic data that implicated TE related unequal recombination at the GULO locus (resulting in exon deletion) that occurred in taxonomically restricted events.
I think it's disingenuous of Tomkins to focus on that aspect of the study while ignoring all the evidence for common descent.

The GULO pseudogene locus on human chromosome 8 is in a gene-rich region. Orthologous genes are present at the same site in all vertebrate species although the order of the surrounding genes has been repeatedly shuffled by microrearrangements (Yang, 2013).

The presence and order of the exons within the GULO gene/pseudogene in diverse vertebrates is consistent with several independent inactivations and descent from a common ancestor (Yang, 2013). One of them occurred in the primate lineage. All of the primate pseudogenes are missing exons 1 & 2 as well as exons 5, 7, and 10 as shown in the figure below.


The data is consistent with an ancestral pseudogene gene that was missing exons 1, 2, 5, 7, and 10. Exons 3 & 4 were subsequently lost in a separate events in the gibbon lineage. The orangutan and human pseudogenes are similar with respect to exon loss and the chimpanzee pseudogene is probably the same. (The 5′ region of the GULO pseudogene was not present in the chimp genome sequence.)

Tomkins doesn't discuss the evidence for the common ancestry of the primate pseudogenes and he doesn't try to explain the pattern according to a Young Earth Creationist worldview. Instead, he draws attention to another part of Yang's paper—the part where he documents the rearrangements of the genes surrounding the GULO locus. There's nothing unusual about such rearrangements. They are common between closely related species and even within a species. Over time, blocks of genes are shuffled and re-ordered so that distantly related vertebrates show very little synteny.

Tomkins thinks this is a serious problem for evolution ...
The GULO gene lies within a gene-dense region in all vertebrate genomes studied thus far (Yang 2013). Related to this fact is the evolutionary anomaly that the gene neighborhood surrounding the GULO locus is rearranged across the vertebrate spectrum of life, and the patterns cannot be readily resolved into the standard inferred evolutionary lineages (Yang 2013).
Once again, Tomkins is cherry-picking the data to focus on minor anomalies that don't fit with his strawman version of evolution. Once, again, he ignores the much more important data in the same paper that supports an ancient origin of an ancesral GULO pseudogene.

Let me close by mentioning one other "anomaly" that Tomkins raises. He questions whether the functional rat gene is an appropriate standard of comparison. You might be amused by his logic ...
Traditionally, the human GULO pseudogene has been compared to the functional rat GULO gene (Nishikimi, Kawai, and Yagi 1992; Nishikimi et al. 1994; Ohta and Nishikimi 1999). According to the UCSC genome browser (genome.ucsc.edu) and the Rat Genome Database (rgd.mcw.edu), the rat GULO gene (chr15, region p12) is oriented and transcribed on the minus strand. Interestingly, the human and ape GULO pseudogenes are oriented in the plus strand configuration (chr8, region p21.2 in human). While the rat GULO gene may serve as a general guide to exon presence and absence in degraded GULO genes in other mammals, the rat GULO is clearly in a different chromosomal configuration (compared to humans and apes) and represents a unique design pattern specific to rodents (mouse GULO is on chr15, minus strand).


1. In this case, Young Earth Creationist.

2. For more information on the GULO pseudogene see ...
How do Intelligent Design Creationists deal with pseudogenes and false claims?
Junk & Jonathan: Part 8—Chapter 5
Human GULOP Pseudogene

3. Also spelled Haplorhini.

4. Lachapelle and Drouin include a short 5′ exon (#1) that isn't present in most species. It's likely an artifact. I renumbered the exons according to Yang (2013).

Helliwell, K.E., Wheeler, G.L., and Smith, A.G. (2013) Widespread decay of vitamin-related pathways: coincidence or consequence? TRENDS in Genetics, 29:469-478. [doi: 10.1016/j.tig.2013.03.003]

Lachapelle, M.Y., and Drouin, G. (2011) Inactivation dates of the human and guinea pig vitamin C genes. Genetica, 139:199-207. [doi: 10.1007/s10709-010-9537-x]

Yang, H. (2013) Conserved or lost: molecular evolution of the key gene GULO in vertebrate vitamin C biosynthesis. Biochemical genetics, 51:413-425. [doi: 10.1007/s10528-013-9574-0]

135 comments :

  1. In one place in your post, poor Tomkins has suffered a deleterious insertion and become Tomlkins. In another, he has become Tompkins. Is this evidence that he is three people?

    ReplyDelete
  2. "...from the perspective of the recent Creation and the global Flood within a biblical framework."

    Which puts rather a large dent in the 'scientific' part of that.

    Dave Bailey

    ReplyDelete
    Replies
    1. Why don't they publish in mainstream scientific journals for God's sake. They keep forgetting that even if you end up falsifying evolution, it does not prove creationism.

      Delete
    2. Michael Okoko,

      Why don't they publish in mainstream scientific journals for God's sake. They keep forgetting that even if you end up falsifying evolution, it does not prove creationism.

      No? What would falsifying evolution prove? Panspermia?

      Delete
    3. "What would falsifying evolution prove?"

      Why do so many religious believers exhibit such painfully evident subnormal intelligence?

      Delete
    4. Jass,

      Falsifying evolution would definitely not prove creationism. That false dichotomy only exists in your mind and the rest of the creationists bandwagon.

      By the way panspermia doesn't address how things evolved, it addresses how the things we evolved from originated. I think a few articles would greatly help your misdirected proactive brain.

      Delete
    5. Michael Okoko,

      Unlike you, I rely on scientific, experimental evidence...

      Delete
    6. Jass,

      Hold your horses there, I thought YECs depend solely on the Bible and not scientific experimental evidence. Scientific experimental evidence tell us a Big Bang happened, but you don't believe that, scientific experimental evidence from radiometric dating tells us the earth is billions of years old (and that some plants are thousands of years old) but you don't believe that. Guess you have to revise your statement.

      Delete
    7. Assumptions... assumptions... assumptions...

      Delete
    8. "Unlike you, I rely on scientific, experimental evidence..."

      You are really jumping the gun on April 1 2018. But nobody would believe you when you say that anyway.

      Delete
  3. here is a very interesting argument:

    a) we know that a theoretical self replicating robot that made from organic components is evidence for design. because we know that any robot is evidence for design.

    b) from a physical perspective a walking creature (a penguin for instance) can be consider as a self replicating robot that made from organic components (without talking now about the free will question, i just talking now about the physical perspective).

    or in other words: if a robot that is identical to a penguin need a designer (including the ability to reproduce), then also penguin need, because they are identical in this case.

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    Replies
    1. Slight problem: Penguins aren't robots. Nice try, though. Part marks for originality.

      Delete
    2. dcscccc

      a) If you saw a self-replicating robot, wouldn't you search for the designer and contact him/her? Unfortunately, creationists and intelligent design proponents haven't done that. Science can accept the (a) part of your design argument, but if it can't test it, then it becomes irrelevant.

      b) A penguin is not a robot and it doesn't self replicate, it reproduces, to produce another penguin genetically (and maybe morphologically) different from it. DNA has the necessary information for it's self-replication and it does that through physical and chemical processes, you never see a "hand" telling polymerases or ligases what to do. Arguing for a designer is logical, but if you can't detect the designer then it's scientifically irrelevant.

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    3. why not michael? i think that we can detect design even without seeing the designer.

      "A penguin is not a robot and it doesn't self replicate, it reproduces,"-

      so change it into a robot that can reproduce. if you will see such a robot in a far planet, you cant detect design in this case? there is another problem: we know that there are is no stepwise way to evolve such a robot, so a self replicating material will not evolve into a self replicating robot.

      now about prof moran post. i found this paper very interesting:

      http://www.sciencedirect.com/science/article/pii/S2211124712002720#figs2

      according to the paper (fig s2) about 6 different exons loss are shared between marmoset and microbats. but surprisingly, without a common descent.so this finding prove that we can get the same exon loss without a common descent. therefore a shared exon loss cant be evidence for a common descent.interesting.

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    4. "i think that we can detect design..."

      How?

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    5. how you detect design when you see a robot?

      Delete
    6. "how you detect design when you see a robot?"

      And how is that?

      Delete
    7. "according to the paper (fig s2) about 6 different exons loss are shared between marmoset and microbats"

      You didn't check the figure carefully, did you? Check it again.

      The precision in deletions and shared mutations in the great apes is what betrays the common ancestry, not a gross look at exon deletions in common. Look at chimps, humans and gorillas in the same figure, for example. Do you see mere gross sharing of deletions?

      Delete
    8. dcscccc

      "why not michael? i think that we can detect design even without seeing the designer."

      Did I ever argue that you do not need a designer to detect design? If I did show me, if I didn't that means you need to read the arguments of the opposing party before you respond. There appears to be design in organisms, but how did it arrive, Evolution or Creation? If you claim its a designer, then where is the designer? There is enough empirical evidence for evolution. If a missile hits a military base, we don't need a designer to know it's a missile, but the next step is to detect the launcher of the missile (the designer) and IDists have not done this. In addition, there is ample evidence that evolution can generate molecular structures that appear designed.

      "so change it into a robot that can reproduce. if you will see such a robot in a far planet, you cant detect design in this case? there is another problem: we know that there are is no stepwise way to evolve such a robot, so a self replicating material will not evolve into a self replicating robot."

      A penguin cannot be a robot, neither can a robot be a penguin. Robots cannot reproduce and Penguins cannot self-replicate (why are you comparing plastic oranges to organic apples). A robot cannot evolve because it lacks DNA, RNA and other reproductive machinery that transmits heritable variation through generations of offspring. Do you even know what self-replication is? A self-replicating material like DNA (and probably prebiotic RNA) do not evolve, they simply accumulate mutations and cause the organisms which possess them to evolve (let this sink into your head). Lastly, robots do not self-replicate, they self-assemble (with the direct aid of humans, unfortunately for you, fatty acids and phospholipids can self-assemble into membranes purely through physico-chemical forces).

      Gabriel's post addresses your response to Larry's post. Don't forget that homology doesn't mean a one-to-one correspondence of content in genes or genomes, but rather a significant similarity in the content of the homologous genes. Also stop assuming that the molecular basis for figuring common ancestry rely on one criterion (there are usually two or three criteria). Yet again, this does not prove YEC, and neither disproves common descent.

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    9. Edit: Did I ever argue that you need a designer to detect design?

      Delete
    10. " Look at chimps, humans and gorillas in the same figure, for example. Do you see mere gross sharing of deletions?"-

      of course they are more similar, since their genome is more similar. it doesnt change the fact that shared exon loss can happen without a common descent.

      Delete
    11. "it doesnt change the fact that shared exon loss can happen without a common descent."

      Yes. Almost any outcome can be assigned a probability that is greater than zero. So then it becomes a question of determining which is the more probable explanation for a given observation.

      For example, it could be that the number of eyes that a person possesses is determined entirely by chance, and it is just an incredible coincidence that almost everyone ends up with exactly two. The alternative explanation is that this didn't just happen by chance and that the number of eyes a person has is determined by genetics.

      Which explanation do you favour?

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    12. "so change it into a robot that can reproduce. if you will see such a robot in a far planet, you cant detect design in this case?"

      You've got it backwards. In order to determine it was a robot, you'd have to first determine it was designed. We do not believe the penguins here on earth are robots because they show no evidence of having been designed.

      Again, though, full credits for coming with a stupid argument that no creationist had thought up before. Unless they did think it up, but then realized it was too stupid to share.

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    13. " In order to determine it was a robot, you'd have to first determine it was designed. We do not believe the penguins here on earth are robots because they show no evidence of having been designed."-

      so if someone will create a penguin you will consider it as a robot? ok. so let me ask you this question: do you agree that an object that is identical to a robot is a robot?

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    14. dcscccc
      You have to realize that the paper you cited does not attempt to disprove evolution. I seriously don't how to show you all the info I have on this, but let me give you a few reasons why this doesn't contradict common descent.
      For one, marmosets, microbats and primates (humans, chimps, gorillas) are all mammals hence they descended from a last common ancestor who probably had a functional GLO gene. As divergence proceeded and the species formed could not interbreed, we would expect the GLO gene to undergo independent changes(and this can be used to detect parts of the genome responsible for a particular genotype-phenotype relationship, hence Forward Genomics). My point here is that microbats and marmosets have ancestors who descended from a common mammalian ancestor who probably had the GLO gene. Marmosets (New World Monkeys) and Hominidae(Humans etc.) have ancestors who descended from the common ancestor of Platyrrhines and Catarrhines respectively. So we expect independent actions on the GLO/GULO genes in either species.

      We know that loss of functional activity of particular genes can occur independently in different species, so it is not the only means of deciphering common ancestry. In science we rely on multiple lines of evidence to define common ancestry between species.


      Delete
    15. "so if someone will create a penguin you will consider it as a robot?"

      No. A robot is, by definition, something that was created and designed by an intelligent being. There is no such thing as a naturally occurring robot.

      However, it does not follow that everything created by an intelligent being is a robot.

      This is pretty elementary logic, so if you do not follow what I am saying, you just aren't intellectually capable of holding this discussion. You need to learn some logic first.

      "do you agree that an object that is identical to a robot is a robot?"

      No. Identical twins are not the same person.

      Delete
    16. but this isnt what you said here:

      "We do not believe the penguins here on earth are robots because they show no evidence of having been designed."

      so according to this criteria a designed penguin is a robot by definition.


      "No. Identical twins are not the same person."

      but they both still humans. right? so an object that its identical to a robot is a robot too.

      Delete
    17. "There appears to be design in organisms, but how did it arrive, Evolution or Creation?"-

      we know that a robot is evidence for design. so if we will find a robot with living traits like a replicating system and organic components, i think that we can conclude d esign even without seeing the designer. its simple logic to conclude design when we see something complex like a robot or a watch.

      Delete
    18. dcscccc

      Fallacy, fallacy, fallacy. We know that a robot is evidence of HUMAN DESIGN and not anything else. Can't you get it, we can't get a robot capable of self-replication and there are robots with organic parts (put there by humans). It's simple and FACTUALLY correct to conclude HUMAN DESIGN when we see watches or robots because we know HUMANS MADE IT. However, don't extrapolate it to everything in the universe, let it be restricted to human design, if I asked you to provide positive evidence for a designer, you can not and if you can't, just keep mute and let scientists do what they do jobs. Prior to the recognition of the mosquito as a malaria vector, what people knew was that malaria was caused by some disease agent. Tell me how the world would be if we didn't bother finding out the agent of malaria transmission, but simply satisfied with knowing the symptoms of malaria.

      Delete
    19. but this isnt what you said here:

      "We do not believe the penguins here on earth are robots because they show no evidence of having been designed."

      so according to this criteria a designed penguin is a robot by definition.


      Oh dear. You really don't understand logic. Let me try help:

      All ducks are birds.

      However, this does not mean that all birds are ducks.


      Do you agree with that? Are you able to follow the logic there? I hope so. Now, applying the same logic to your claim:

      All robots are designed.

      However, not everything that is designed would be a robot.

      Therefore, to say a penguin was "designed" does not mean the penguin is a robot.


      OTOH, since all robots are designed, then if a penguin was not designed, it is not a robot.

      Did I hit you with too much logic there all at once? I hope not.

      Delete
    20. Here's another thing to help you understand why your argument is so misguided, dcsccc.

      For many years people have been trying to make artificial diamonds, and we have reached the point where the best man-made diamonds can be distinguished from natural diamonds only by experts, and then only with some difficulty.

      Suppose some day we reach the point where an artificial diamond cannot possibly be distinguished from a real one. Would it then be correct to say that there is no such thing as a naturally occurring diamond, and that all diamonds in existence were the result of "design"?

      I don't think so. Do you?

      If you don't, then why do you believe that, if there were robot penguins that could not be differentiated from real penguins, that this would mean the real penguins were "designed"?

      Delete
    21. "No. Identical twins are not the same person."

      but they both still humans. right? so an object that its identical to a robot is a robot too.


      If a man made diamond is identical to a naturally occurring diamond, does that mean the naturally occurring diamond is not a naturally occurring diamond? (This involves the most basic law of logic, the law of non-contradiction. Let's see if you understand that one.)

      Delete
    22. dcscccc

      There is no evidence of conscious/intentional design in nature, we simply evolved. If you examine the structure of a snowflake ❄, it appears to be "designed" but we know it isn't, it is simply the product of mindless physical forces. Design in biological systems is an illusion, as everything arose through evolution. Mutations, recombination are agents of genetic change that allow living organisms develop new structures or functions, through the aid of natural selection or genetic drift. In a sense, evolution via natural selection is a "designer" (I sincerely hope you do not misunderstand my usage of that word) since it non-randomly furnishes animals with suitable adaptations to help cope in their environment. Lenski's experiment is a beautiful demonstration of this.

      You seem intelligent, so you should be smart enough to understand my argument above.

      Delete
    23. dcscccc,

      "of course they are more similar, since their genome is more similar. it doesnt change the fact that shared exon loss can happen without a common descent."

      You're not even trying. Since I doubt you can be that stupid, I suspect you're just trolling, so I leave it here.

      Delete
    24. If a man made diamond is identical to a naturally "occurring diamond, does that mean the naturally occurring diamond is not a naturally occurring diamond? "-

      no. but they both still diamonds. so let me ask you this: do you think that a robot thats is able to reproduce and made from organic components is evidence for design?

      note: english isnt my native. so i may not understand some of your words.

      Delete
    25. There is no evidence of conscious/intentional design in nature, we simply evolved. If you examine the "structure of a snowflake ❄, it appears to be "designed" but we know it isn't, it is simply the product of mindless physical forces. Design in biological systems is an illusion, as everything arose through evolution"-

      ok. but a snowflake isnt complex as a robot. so when we see a robot we know that someone designed it. even if it were no human but an alien for instance.

      the same with a theoretical robot with dna. if i will find such a robot i will conclude that its was designed.

      note: english isnt my native. so i may not understand some of your words.

      Delete
    26. no. but they both still diamonds.

      "No" Is the correct answer. Very good.

      so let me ask you this: do you think that a robot thats is able to reproduce and made from organic components is evidence for design?

      As I said, a robot is by definition something that was designed. So, the answer is "Yes."

      Now answer this question: Is a penguin that was not designed, and therefore not a robot, a robot?

      Delete
    27. the same with a theoretical robot with dna. if i will find such a robot i will conclude that its was designed.


      If you dig a diamond out of diamond mine, would you think it was created by someone and put there? Or would you think it was a natural diamond that was produced in the ground thru the usual processes that create diamonds?

      (BTW, your English seems fine. It's your logical thinking skills that need work.)

      Delete
    28. "(BTW, your English seems fine. It's your logical thinking skills that need work.)"

      More like the willingness to carefully consider the answers, rather than jumping around writing nonsense that shows that carefully considering the answers is last in the list of actions. I say either Poe or troll.

      Delete
    29. "a) we know that a theoretical self replicating robot that made from organic components is evidence for design. because we know that any robot is evidence for design."

      Perhaps, if we lived in a different, creationist universe, where there actually are self-replicating penguin like robots made from organic material.

      In our universe, however, there is no such thing.
      Drawing conclusions from imaginary, unrealistic examples to the real world is not the way to get to the truth.

      Moreover: Suppose you was travelling on some distant planet, and saw something moving (not like anything we know back here on earth). Upon a closer examination, you find that this something is organic, and it's self replicating. At that point, would you assume it's a robot or a local, unknown life form?

      Please, if you want to make a point for creationism (or as most of you prefer to call it now - intelligent design) - try not to make a point that is so ridicules.

      Delete
    30. "As I said, a robot is by definition something that was designed. So, the answer is "Yes."-

      so a designed penguin can be consider as a robot sincne someone designed it too?


      Delete
    31. "If you dig a diamond out of diamond mine, would you think it was created by someone and put there?"-

      no, since there is a natural process that can create a diamond.

      Delete
    32. "In our universe, however, there is no such thing."-

      why not? a penguin can be consider as a self replicating robot.

      Delete
    33. This appeal-to-semantics argument dcscccc is making is ridiculous. You don't get to establish that life didn't evolve by simply CALLING it a robot.

      If organisms can be considered self-replicating meat-robots, then organisms are a counterexample to the claim that robots cannot evolve and need to be designed.

      In other words, if a penguin is a self-replicating robot, then that is proof that self replicating meat-robots can and do evolve, because penguins demonstrably evolved.

      If you argument is that robots can't evolve and that organisms are robots, then your argument is guilty of the fallacy of question-begging. If you insist that robots are by definition designed, then when you call an organism a robot, you are assuming your conclusion.

      Delete
    34. "In other words, if a penguin is a self-replicating robot, then that is proof that self replicating meat-robots can and do evolve, because penguins demonstrably evolved"-

      so a robot doest need a designer? ok. do you think its a logical conclusion? also: do you think there is a stepwise way from a self replicaiting material to a walking robot?

      Delete
    35. no, since there is a natural process that can create a diamond.

      Yes, that is correct. And since there is also a natural process that produces penguins, penguins cannot be considered robots.

      I don't know if you are actually as stupid as the things you write here would indicate you are. But if so then you're not worth wasting any more of time over.

      Delete
    36. "so a robot doest need a designer?"

      If you think a penguin qualifies as a robot, then yes a robot doesn't need a designer.

      "ok. do you think its a logical conclusion?"

      Yes, it is supported by evidence too.

      "also: do you think there is a stepwise way from a self replicaiting material to a walking robot?"

      You did it yourself in nine months. - J.B.S. Haldane

      Delete
    37. " And since there is also a natural process that produces penguins, penguins cannot be considered robots"

      prove it. lets take a specific example: a motion system. any motion system will need at least several parts to its minimal function. therefore a motion system cant evolve stepwise.

      Delete
    38. "Yes, it is supported by evidence too. "

      so a robot doesnt need a designer? ok.


      "You did it yourself in nine months."-

      im talking about evolution and not human developmant. see my example above about motion system.

      Delete
    39. The amazingly cool thing about evolution is that is shows a way to produce things that look designed without a designer. Once chemicals start replicating themselves, the ones that are best at replicating become more common. Again and again and again. Organisms are formed and each generation, ones that fit well in their environment succeed in reproducing and other die out. An inevitable, mindless process. A simple little process, again and again, but it can produce penguins and gulls and humans and all the other living things. Without planning to. Without actual design, without a designer.

      dc...c won't take the effort to understand that this makes sense. He/she is having too much fun with silly arguments from definitions.

      Delete
    40. @bwilson295

      The amazingly cool thing about evolution is that is shows a way to produce things that look designed without a designer.

      And the total failure of mutation breeding certainly proves your point... lol

      Evolution is not only smart it also has hidden the true mechanism of its miraculous actions to the point that intelligent scientists have no way or replicating the dumb luck...

      Whatta dumb luck! Such a cool idea though...

      Delete
    41. All breeding is "mutation breeding" Jass. All the domesticated life forms around us show that it's quite a success.

      I'm not surprised that you're so deeply misinformed though.

      Delete
    42. "dc...c won't take the effort to understand that this makes sense. He/she is having too much fun with silly arguments from definitions"-

      what realy make sense in evolution? if you will start with a self replicating matter you will never get a walking robot (penguin). since there is no stepwise from a self replicating matter to a walking robot.

      Delete
    43. @dcscccc:
      "why not? a penguin can be consider as a self replicating robot." The only way to consider any animal as a robot would be to ignore what an animal is, and what a robot is.
      That is, unless you can prove that nature is in fact artificial. (Does this makes more sense then a designer-less robot?)

      If your proof lies on animals considered as robots, that's a logical fallacy called called circular reasoning.
      What you are actually saying is that a penguin is a robot (false), and since all robots are designed (true) therefor nature has a designer (circular reasoning).

      There are two kinds of creationists - The first kind tells lies, and the second kind believes the lies told by the first kind. Which kind are you?

      Delete
  4. I find this part of his abstract interesting.

    "Further, gorilla is considerably more similar to human in this region than chimpanzee—negating the inferred order of phylogeny"

    Is Tomkins unaware that this is evidence of evolution. Even if it clashes with present phylogenetic pattern of divergence of chimpanzees and humans from a common ancestor, it presents gorillas as our divergent "mate" in the phylogenetic tree.

    By the way why would the YEC model predict genetic entropy when we know that the God of YECs is a God of order and not chaos (forgotten the verse in the Bible). If God made everything "good" or perfect, the YEC model should "predict" genetic stability instead of entropy. Doesn't Tomkins realize this?

    Going through some of the quotes on anomalies, it seems Tomkins imagines that evolutionists expect not to find deviations from the norm, or has he forgotten that science grows when we find something at odds with our expectations and we look into. I wish I was up to speed on the technicalities of Larry's critique and Tomkins paper so that I could offer a better review of both.

    ReplyDelete
    Replies
    1. I don't believe that anyone is ready to declare the gorilla our closest relative in light of this one finding. I don't know what Tomkins is referring to, but it is not unexpected that some parts of our genome would be more similar to gorillas. Our genome as a whole is still most similar to the chimp's.

      Look at it this way: Is it possible that you and your cousin could share an allele you inherited from your grandmother that your brother did not? Of course. But that would not mean you are more closely related to your cousin than to your brother, nor that your genomes would not show the correct relationship.

      Delete
    2. I completely agree with you lutesite. In fact, there are extreme cases where you could almost resemble a cousin far more than your parents or siblings but that doesn't detract your common ancestry from your parents.

      Delete
    3. Gorillas are only more similar to humans than are chimps in a few parts of the sequence and only if you use Tomkins's bogus measure of genetic distance, for which a 1-base indel part way through the sequence renders the rest of the sequence misaligned. Also, nobody determines phylogenetic relationships based on ordering of raw similarity.

      Delete
    4. Michael Okoko, many Christians figure that although God made the world good, humans messed it up when Adam and Eve ate the fruit of knowledge of good and evil, and therefore everything is going downhill. Therefore, the YEC idea of genetic entropy.

      You can argue with Christians about the Bible and its history and what it actually says (if you know enough about it), but you can't effectively argue theology with Christians. Interpretations are too many and various.

      Delete
    5. bwilson

      The Bible indicates that the only punishment meted out to Adam and Eve was death, it says nothing about their genes or genomes getting entropic. It is a man-made ASSUMPTION YECs make up that has no biblical support. Even if I allow it for humans, why should there be genetic entropy in the genome of animals, when we know that lions, gorillas did not do God any wrong? In addition, why should humans lose the function of the GULO gene when other creatures still have theirs being fully expressed, did God grant greater genetic stability to these animals than us?

      Delete
    6. Michael Okoko, I'm not trying to logically support the argument here. However, a fairly common theme in Christian interpretation of the Bible is that there was no evil, no death (of animals) before the Fall. One odd result of this is the argument one sometimes sees that Tyrannosaurus rex was an herbivore before the Fall. You can argue that this is extrapolating too far from the Biblical account, but a lot of people feel this is a reasonable conclusion.

      I personally am not defending this. I'm just trying to say that the logical argument you're attempting won't convince many of the people we might wish it would.

      Delete
    7. bwilson

      Even if you are restating the position of YECs or OECs, I don't care, I am attacking their arguments and not you or them personally.
      The T-Rex is a super killing machine, whose dental structure is capable of ripping flesh apart and probably smashing bones quite easily. It was never a herbivore. There are herbivore dinosaurs, but the T-Rex is by all indications a full-fledged killer. Lions are also superb killers and the Creator must have really enjoyed designing the teeth of lions to kill deer's and antelope. Christian theologians may argue all they want about the mythological Adam and Eve story, but anatomy, genomics, biochemistry tell us a different story.
      Christians, Muslims and others make very remarkable statements for which they have no evidence for and they keep on arguing as if it has been proven. My annoyance is assuming the answer to a question before asking the question.

      Delete
    8. Michael Okoko, You're right. Showing people how to interpret the T-Rex anatomy can be an effective way to communicate about evolution.

      I'm just saying that basing an evolution vs. creation or young-earth vs. old-earth argument on the interpretation of the Adam and Eve story is a loosing game for scientists because all interpretations of this mythological story result more from what people want to believe than from logic. So that wasn't a useful argument above. The rest of what you're saying sounds great to me!

      Delete
    9. Tomkins's bogus measure of genetic distance, for which a 1-base indel part way through the sequence renders the rest of the sequence misaligned. Also, nobody determines phylogenetic relationships based on ordering of raw similarity.

      Thank you. Always nice to see a little science and sense in these discussions.

      Delete
  5. You are doing "a Tomkins", which here means to cherry pick some detail without really considering the bigger picture. Scroll up to Fig. 2D. The marmoset and microbat have each lost swaths of DNA at the GULO locus, and although the deletions extend to different lengths, consistent with their different origins, the large deleted areas overlap a bit and so some of lost exons happen to be the same exons. The bigger picture here happens to be shown in the previous figure.

    While you are at it, look at Fig. S1 which compares exon 2 across species. There are numerous base changes that are shown in exon 2 that line up nicely across sister taxons while differing in unrelated taxons.

    ReplyDelete
    Replies
    1. I mean, it's just staggering that anyone could be aware of that data and still have even the slightest doubt about common ancestry. There is just no other realistic explanation.

      Delete
  6. I suspect my question will get lost here. Despite being a medical geneticist, I can't follow all the technical details here. I'm not a creationist but my question is whether there are any valid points in this guy's article that are worth considering?

    ReplyDelete
    Replies
    1. Do you usually peruse "Answers Research Journal" when trying to keep up to date on the latest findings in medical genetics? That might give an indication of the value of this article.

      Delete
  7. If GULO gene is non-functional in so many species, like humans, apes, guinea pigs, bats, mice, rats, pigs, and passerine birds, why preserve it? Why natural selection has NOT been able to get rid of it for tens of millions of years in so many species?

    Non-random natural selection is apparently able to invoke strings of beneficial mutations that suffice to reshape one animal into the shape of another, and can't remove non functional junk from the genomes of so many species for millions of years...

    Impotence of NS vs the ability to achieve life structures human intelligence can only dream of...

    ReplyDelete
    Replies
    1. "and can't remove non functional junk from the genomes of so many species for millions of years... "

      That's because natural selection is not a magical being. It's a natural phenomenon. Natural selection does not work unless there's a survival-to-reproduction advantage or disadvantage to organisms carrying some feature. Since the GULO pseudogene does not disturb our survival and reproduction, the fixation of degraded alleles is expected to be mostly random.

      Delete
  8. "If GULO gene is non-functional in so many species, like humans, apes, guinea pigs, bats, mice, rats, pigs, and passerine birds, why preserve it? Why natural selection has NOT been able to get rid of it for tens of millions of years in so many species?"

    Jass, you're an ignorant man whose cognitive facilities are impaired by severe theopathy. If you understood even a little bit about what you have presumably read here, you could grasp how completely nonsensical your comment is.

    ReplyDelete
    Replies
    1. Really? I don't much value opinions, especially from ignorant trolls... So, unless you come up with some real answer, rather than you empty nonsense, you can consider your-self just an oxymoron that has not clue what this is about...

      You don't have to bother to answer...

      Delete
    2. Jass, it is in the process of decay. Exons 1, 2, 5, 7, and 10 have been lost. The remaining sequence has smaller deletions causing frameshift mutations and several substitution mutations. It's a dead and degrading gene. Not even Tomkins denies this.

      Delete
    3. If GULO gene is really non-functional, how come the experiments with animals on a diet devoid of vitamin c show normal or slightly below normal range vitamin c levels?

      Delete
    4. Mikkel Rumraket RasmussenMonday,

      Jass, it is in the process of decay. Exons 1, 2, 5, 7, and 10 have been lost. The remaining sequence has smaller deletions causing frameshift mutations and several substitution mutations. It's a dead and degrading gene. Not even Tomkins denies this.

      Doesn't Tomkins claim that those mutations arose independently? But then those mutations would have to be adaptive and non-random...but you don't like it either lol

      Delete
    5. "If GULO gene is really non-functional, how come the experiments with animals on a diet devoid of vitamin c show normal or slightly below normal range vitamin c levels?"

      References please.

      Delete
    6. "Doesn't Tomkins claim that those mutations arose independently?"

      Yes he does. He claims it is due to this "genetic entropy" nonsense. But that still means Tomkins agrees the protein coding gene is nonfunctional.

      "But then those mutations would have to be adaptive and non-random...but you don't like it either lol"

      Ask yourself: What is the probability that dusins of species of primates all happened to suffer the exact same exon-deleting mutations, in parallel, in the same gene? Unbelievably low.

      It is this very fact itself that implies common descent, rather than independent parallel losses.

      Tomkins tries to handwave this away by claiming the independent losses were due to the locus-specific activity of transposable elements in all primate lineages. Again, independently. Tomkins just stuffs together a lot of words to make it seem as if this is a reasonable inference to make.

      Delete
    7. "Ask yourself: What is the probability that dusins of species of primates all happened to suffer the exact same exon-deleting mutations, in parallel, in the same gene? Unbelievably low. "-

      actually not that low, since micro bat also shared about 6 exons deletions with marmoset, without a common descent. check also this paper about shared deletions as evidence for a common descent:

      https://utexas.influuent.utsystem.edu/en/publications/parallel-molecular-evolution-of-deletions-and-nonsense-mutations-

      the conclusion of the paper is that shared deletions arent good evidence for a common descent since its not rare to find shared deletions without a commondescent.

      Delete
    8. It is true enough that mechanisms are known that can cause parallel deletions due to the same underlying reaction taking place in different lineages. The problem is that Tomkins rejects the conclusion of a research article that explicitly tries to determine whether such a mechanism has been at work in primates deleting the GULOP exons. He just handwaves this away by calling it an evolutionary presuppostion, apparently oblivious that exact same line of reasoning can be turned right back against him: It is Tomkins' closed-minded a priori committment to creationism, that prevents him from accepting that there is no good evidence the exon losses in GULOP were due to parallel transposable element activity.

      If Tomkins can just invoke the "presuppositions" canard when scientists conclude things he doesn't like, then that very same thing can be said of himself.

      But suppose we took it at face value and agreed with Tomkins the exon deletions were parallel independent events. That just means we can't use the similar exon losses as evidence of common ancestry, but still using only the GULOP locus we have the patterns of substitution and other indels in the remaining introns and exons of the gene.

      It becomes rather difficult for Tomkins to extend his invoking a similar action of transposable elements as an explanation for parallel exon losses, to now also include parallel patterns in substitution and other indels. What new mechanism will Tomkins then appeal to? Notice how much ad-hoc reasoning Tomkins is forced to make to handwave away the simplest explanation: The locus is similar because the similarities are due to shared descent.

      And even then, it's not like the case for common descent of primates ever came down to a single pseudogene. Tomkins still has pretty much the entirety of the independent data sets from the genomes and morphology of all primates to try to pretend doesn't yield highly congruent phylogenetic trees. There is no sensible expanation for this fact that doesn't involve common descent.

      Delete
    9. "It is true enough that mechanisms are known that can cause parallel deletions due to the same underlying reaction taking place in different lineages. "-

      ok. so we cant conclude common descent base on exon loss.


      "Tomkins still has pretty much the entirety of the independent data sets from the genomes and morphology of all primates to try to pretend doesn't yield highly congruent phylogenetic trees. There is no sensible expanation for this fact that doesn't involve common descent. "

      first. im not sure that there are no problems with primates phylogeny. for instance:

      https://news.nationalgeographic.com/news/2009/06/090623-humans-chimps-related.html

      we also know that about 30% of gorila genes contradict the accepted phylogeny (when even scientific papers show us that even one gene should be enough to perform a correct phylogeny.

      we also know that about several ervs contradict the accepted phylogeny. so its not so easy. even if the current phylogeny is correct, how its suppose to be evidence for a comon descent?

      Delete
    10. "ok. so we cant conclude common descent base on exon loss."

      Purely on exon loss alone (if all we knew was that gene X is missing four exons in ten different species), then no. But that isn't all we know, because the mechanism that is responsible for parallel exon losses is simply not in evidence has having been responsible for the exon losse in question. So it is prima facie evidence of common descent.

      "first. im not sure that there are no problems with primates phylogeny. for instance:

      https://news.nationalgeographic.com/news/2009/06/090623-humans-chimps-related.html"


      How is any of this a response to what I wrote? If orangutan happens to be the most closely related primate to humans, then it is the most closely related primate to humans. There can be ambiguity in the data that makes it difficult to determine the correct branching order of taxons (if branchings events were close together in time, for example), but this is very different from saying that we can't be highly certain that they share common descent.

      We can make a direct analogy here to human family relationships. Twins might be very difficult to establish which one was born first, so difficult that it might even be practically impossible. What isn't difficult is figuring out that they really are twins, as in share parents. We can make it easier and have two siblings, 50 and 52 years old. In this case it might also be very very difficult if we aren't told which one is the oldest, yet again it would be trivial to show with a genetic test that they are siblings sharing at least one parent.

      It is basically like that with the branching order of many taxons. There is no doubt they are related by common descent, but the exact branching order, because they have been close together in evolutionary time scales, is more difficult to determine.

      That said, the branching order the great apes (Orangutan, Gorilla, Chimp+Bonobo, and Humans) really isn't in doubt either.

      "we also know that about 30% of gorila genes contradict the accepted phylogeny"

      They simply show incomplete lineage sorting. Which by the way is an unavoidable consequence of a splitting non-clonal population, meaning the creationist charge of "ad hoc" reasoning is demonstrably false.

      "we also know that about several ervs contradict the accepted phylogeny. so its not so easy."

      I wouldn't be surprised since we know some viruses can move between closely related species. Why can they do that, by the way? Because they evolve, and because the species they infect are closely related.

      "even if the current phylogeny is correct, how its suppose to be evidence for a comon descent?"

      A phylogeny is not itself evidence for common descent. It is the statistical significance of the congruence between the phylogenetic trees drawn from multiple independent data sets, that is evidence for common descent.

      Delete
    11. Creationist debaters will try to bamboozle you with a handful of examples of genetic loci which show branching orders that conflict the accepted phylogenetic tree. This is a rhetorical trick (or the creationists just don't understand how phylogenetics work). Cherrypicking a handful of examples of minor incongruent trees does nothing to take away from the unfathomable level of support for the tree of shared descent. Douglas Theobald wrote about this in his 29 Evidences for macroevolution article:
      "When two independently determined trees mismatch by some branches, they are called "incongruent". In general, phylogenetic trees may be very incongruent and still match with an extremely high degree of statistical significance (Hendy et al. 1984; Penny et al. 1982; Penny and Hendy 1986; Steel and Penny 1993). Even for a phylogeny with a small number of organisms, the total number of possible trees is extremely large. For example, there are about a thousand different possible phylogenies for only six organisms; for nine organisms, there are millions of possible phylogenies; for 12 organisms, there are nearly 14 trillion different possible phylogenies (Table 1.3.1; Felsenstein 1982; Li 1997, p. 102). Thus, the probability of finding two similar trees by chance via two independent methods is extremely small in most cases. In fact, two different trees of 16 organisms that mismatch by as many as 10 branches still match with high statistical significance (Hendy et al. 1984, Table 4; Steel and Penny 1993). For more information on the statistical significance of trees that do not match exactly, see "Statistics of Incongruent Phylogenetic Trees".

      The stunning degree of match between even the most incongruent phylogenetic trees found in the biological literature is widely unappreciated, mainly because most people (including many biologists) are unaware of the mathematics involved (Bryant et al. 2002; Penny et al. 1982; Penny and Hendy 1986). Penny and Hendy have performed a series of detailed statistical analyses of the significance of incongruent phylogenetic trees, and here is their conclusion:
      "Biologists seem to seek the 'The One Tree' and appear not to be satisfied by a range of options. However, there is no logical difficulty in having a range of trees. There are 34,459,425 possible [unrooted] trees for 11 taxa (Penny et al. 1982), and to reduce this to the order of 10-50 trees is analogous to an accuracy of measurement of approximately one part in 10^6." (Penny and Hendy 1986, p. 414)"


      Read that whole article.

      Delete
    12. "But that isn't all we know, because the mechanism that is responsible for parallel exon losses is simply not in evidence has having been responsible for the exon losse in question."

      why not actually?


      "It is basically like that with the branching order of many taxons. There is no doubt they are related by common descent,"-

      actually there is a huge doubt. think about this analogy: what if we will have a self replicating car (even with DNA). do you think its possible to such a car to evolve into an airplane by small steps? also: do you think that such a car is evidence for evolution or design in this case?


      "Creationist debaters will try to bamboozle you with a handful of examples of genetic loci which show branching orders that conflict the accepted phylogenetic tree. This is a rhetorical trick (or the creationists just don't understand how phylogenetics work). Cherrypicking a handful of examples of minor incongruent trees does nothing to take away from the unfathomable level of support for the tree of shared descent. Douglas Theobald wrote about this in his"

      ok fine. kets assume that this is true for a moment.lets focus in my main points above.

      by the way: english isnt my native. so i may not understand some of your words.

      Delete
    13. actually there is a huge doubt. think about this analogy: what if we will have a self replicating car (even with DNA). do you think its possible to such a car to evolve into an airplane by small steps?

      Sure. Why not?

      Delete
    14. dcscccc is not even trying to understand your answers. It's not that English is not her native language. It's mere trolling.

      Delete
    15. Rum,

      Differential Regulation of the Ascorbic Acid Transporter SVCT2 during Development and in Response to Ascorbic Acid Depletion

      https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3210393/

      Regulation of Vitamin C Homeostasis during Deficiency

      https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3775232/#B29-nutrients-05-02860

      In vivo vitamin C deficiency in guinea pigs increases ascorbate transporters in liver but not kidney and brain.

      https://www.ncbi.nlm.nih.gov/pubmed/25150123

      Have you heard about the Inuit/Eskimo vitamin C paradox Rum? You should have since you are a Viking...

      They ate no vegetables of fruits for 9 months out of 12 per year and they didn't die...

      Delete
    16. @Jass,
      Your publications don't say what you think they say. They don't show the GULOP pseudogene to be functional, they simply show that vitamin c transporter gene is upregulated in periods of vitamin C depletion, which makes sense since when vitamin C sources are low, the physiological response is to try to absorb as much as possible if any should exist in the evironment. In other words, the metabolic cost of upregulating transporter protein synthesis is outweighed by the importance of getting whatever little vitamin C there might be in the diet, into the cells. This is the exact type of response you'd expect in an organism that can't make it's own vitamin c.

      Regarding your eskimoes, they eat internal organs (like livers and some times kidneys) of animals that make their own vitamin C. That's where they get it from.

      Sorry to break it to you but GULOP is nonfunctional and even creationist Tomkins agrees.

      Delete
    17. "Sure. Why not?"-

      because there is no stepwise way from a car into an airplane. so a self replicating c ar will not evolve into an airplane.

      Delete
    18. @dcscccc: Where did you get the idea that you can look at electro-mechanical contrivances to predict the behavior of biological entities? Did you go to an auto mechanic when you needed your appendix removed?

      Delete
    19. because there is no stepwise way from a car into an airplane. so a self replicating c ar will not evolve into an airplane.

      I don't see how you can justify that claim. There are transitional forms between cars and planes that exist at this very moment:

      https://www.youtube.com/watch?v=VRZNLBL7Px4&t=133s

      Delete
    20. @Milkkel

      You didn't read the papers carefully enough or you omitted the important stuff...as I expected...

      "Protective mechanisms exist to preserve ASC in critical organs, including preferential retention in brain and ASC recycling, but the regulation of these is not yet understood."

      So what's that mechanism Mikkel?

      Same with the Inuits: Studies have shown that there organ base diet can provide at best up 10% of the daily requirement of Vit C which is not be enough... Inuits are known for their great health almost cancer free...
      So, if GULO gene is non-functional, by what mechanism can mammals synthesize vit c to survive?

      Delete
    21. Studies have shown that there organ base diet can provide at best up 10% of the daily requirement of Vit C which is not be enough

      Mid-20th century studies conducted on Inuits who lived in larger settlements and no longer ate a traditional diet showed that the Westernized diet they were eating didn't provide sufficient vitamin C. Studies conducted since then on smaller settlements where Inuits eat the more traditional diet Mikkel was talking about show that diet provides minimum daily requirements of vitamin C, and sometimes far more.

      Delete
    22. @Jass
      Again, they don't synthesize new Vitamin C, they have coping mechanisms that increase how effectively the body takes up and uses the available vitamin C in the diet. That what the papers you link show.

      Sorry, no matter how much you blather about this the GULOP gene is and remains a nonfunctional pseudogene in primates. It is you who fail to understand the significance of the papers.

      Your last question is nonsensical, because it is not ALL mammals that can't make vitamin C. There are mammals that can. Those that can have a functional L-Gulono-Y-Lactone-oxidase (GULO) gene. Those that can't make vitamin C, like all humans, have to eat other organisms that can and therefore contain it. The fact that some humans have adapted to low-vitamin C diets by apparently having evolved increased efficiency of retention and recycling of vitamin C is further evidence that their GULOP gene really is a nonfunctional pseudogene, and that the retention and recycling functions are adaptations to the combination of low vit-c diets and a GULO pseudogene (GULOP).

      Think Jass, think!

      Delete
    23. @Judmark
      Interesting. Another fact for Jass to pretend doesn't exist.

      Delete
    24. "Protective mechanisms exist to preserve ASC in critical organs, including preferential retention in brain and ASC recycling, but the regulation of these is not yet understood."

      I'd never guessed that "preserve," "retention" and "recycling" meant "synthesize." We learn something new everyday.

      Delete
    25. "I don't see how you can justify that claim. There are transitional forms between cars and planes that exist at this very moment:"-

      actually this video support my claim. since you cant add one part to a car and make it fly. you will need at least several parts at once to do that.so this "transitional car" need a big jump from a regular car.

      Delete
    26. @dcscccc

      You said:

      "because there is no stepwise way from a car into an airplane. so a self replicating c ar will not evolve into an airplane."

      Then later you said:

      "actually this video support my claim. since you cant add one part to a car and make it fly. you will need at least several parts at once to do that.so this "transitional car" need a big jump from a regular car."

      Go look up "stepwise" , then lookup "moving the goalposts" because that is what you just did.

      Delete
    27. since you cant add one part to a car and make it fly. you will need at least several parts at once to do that.

      Are you really this ignorant? Do you think that is how evolution works? That, e.g., you "add one part" to a fish and it becomes an animal that can live on land?

      Delete
    28. ok. i will continue this discussion above...

      Delete
    29. @Mikkel

      "Significantly, mice that lack the SVCT2 die at birth, despite the ability to synthesize their own ASC (Vit C) by embryonic day 15. "

      https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3210393/#R15

      So, mice die at birth if they lack SVCT2 transporter but the paper clearly states that embryonic mice can synthesize their own Vit C. So, how could mice be able to make vit c as developing embryos if their GULO gene is defective?

      Same with Inuits/Eskomos; they are Vit c deprived by 90% according to the health requirements for 9 months per year...

      Both mice and humans have a defective gene GULO and yet evolution didn't get rid of it for 63 million years...

      Delete
    30. @Jass
      The mice GULO gene isn't defective, that's why they can synthetize it.

      Delete
    31. In the study you link they compare mice on diets that contain vitamin C, to mice on diets without it. They have several different test groups. Both with and without the transporter gene, with and without functional GULO gene, and with and without vitamin c supplemented diets. I recommend you read the papers you link in full before you post.

      Delete
    32. The Human GULO Pseudogene—Evidence for Evolutionary Discontinuity and Genetic Entropy

      by Jeffrey P. Tomkins on April 2, 2014
      Abstract
      Modern genomics provides the ability to screen the DNA of a wide variety of organisms to scrutinize broken metabolic pathways. This wealth of data has revealed wide-spread genetic entropy in human and other genomes. Loss of the vitamin C pathway due to deletions in the GULO (L-gulonolactone oxidase) gene has been detected in humans, apes, guinea pigs, bats, mice, rats, pigs, and passerine birds. Contrary to the popularized claims of some evolutionists and neo-creationists, patterns of GULO degradation are taxonomically restricted and fail to support macroevolution. Current research and data reported here show that multiple GULO exon losses in human, chimpanzee, and gorilla occurred independently in each taxon and are associated with regions containing a wide variety of transposable element fragments. Thus, they are another example of sequence deletions occurring via unequal recombination associated with transposable element repeats. The 28,800 base human GULO region is only 84% and 87% identical compared to chimpanzee and gorilla, respectively. The 13,000 bases preceding the human GULO gene, which corresponds to the putative area of loss for at least two major exons, is only 68% and 73% identical to chimpanzee and gorilla, respectively. These DNA similarities are inconsistent with predictions of the common ancestry paradigm. Further, gorilla is considerably more similar to human in this region than chimpanzee—negating the inferred order of phylogeny. Taxonomically restricted gene degradation events are emerging as a common theme associated with genetic entropy and systematic discontinuity, not macroevolution.

      Delete
    33. Jass, could it be that a mere abstract does not clarify the full circumstances of how, where, and when, mice have defective GULO genes?

      I must repeat myself. Read the papers you quote in full. Stop quoting me these tiny snippets, start reading for comprehension.

      Delete
    34. Here Jass:
      https://www.ncbi.nlm.nih.gov/pmc/articles/PMC15418/

      Nobuyo Maeda, Hiroyuki Hagihara, Yukiko Nakata, Sylvia Hiller, Jennifer Wilder, and Robert Reddick.: Aortic wall damage in mice unable to synthesize ascorbic acid. Proc Natl Acad Sci U S A. 2000 Jan 18; 97(2): 841–846.

      "ABSTRACT
      By inactivating the gene for l-gulono-γ-lactone oxidase, a key enzyme in ascorbic acid synthesis, we have generated mice that, like humans, depend on dietary vitamin C. Regular chow, containing about 110 mg/kg of vitamin C, is unable to support the growth of the mutant mice, which require l-ascorbic acid supplemented in their drinking water (330 mg/liter). Upon withdrawal of supplementation, plasma and tissue ascorbic acid levels decreased to 10–15% of normal within 2 weeks, and after 5 weeks the mutants became anemic, began to lose weight, and die. Plasma total antioxidative capacities were approximately 37% normal in homozygotes after feeding the unsupplemented diet for 3–5 weeks. As plasma ascorbic acid decreased, small, but significant, increases in total cholesterol and decreases in high density lipoprotein cholesterol were observed. The most striking effects of the marginal dietary vitamin C were alterations in the wall of aorta, evidenced by the disruption of elastic laminae, smooth muscle cell proliferation, and focal endothelial desquamation of the luminal surface. Thus, marginal vitamin C deficiency affects the vascular integrity of mice unable to synthesize ascorbic acid, with potentially profound effects on the pathogenesis of vascular diseases. Breeding the vitamin C-dependent mice with mice carrying defined genetic mutations will provide numerous opportunities for systematic studies of the role of antioxidants in health and disease."


      Here's the introduction:
      "Studies of the pathogenesis of human diseases have benefited from the availability of small laboratory animal models for many years. Mutant mice are particularly useful for investigating the interplay of genetic and environmental factors in the pathogenesis of common, but multifactorial, diseases (5). However, there is a major handicap for studies involving the endogenous redox systems of humans and mice: humans (and other primates) lack the ability to synthesize ascorbic acid because of a loss of function in the gene (Gulo) coding for a key synthetic enzyme, l-gulono-γ-lactone oxidase (6), whereas mice have the functional gene. As a consequence, mouse tissues generally have high levels of ascorbic acid, which are only slightly influenced by exogenous vitamin C. In contrast, humans depend entirely on vitamin C derived from the diet. Guinea pigs also have lost this enzyme function and depend on dietary vitamin C (7). Hence severe deficiency of vitamin C causes disease (scurvy) in both primates and guinea pigs. A strain of rats (ODS, Osteogenic Disorder Sionogi, ref. 8) also has a defect in the same gene (9). No mouse strain is known with this deficiency, yet such mice, in which vitamin C intake can be controlled by diet, would be particularly valuable for investigating the interplay between endogenous and exogenous redox systems, genetic factors, and various diseases. To this end, we have generated Gulo −/− mutant mice, and we here describe the effects of vitamin C deficiency on three factors influential in vascular disease: plasma antioxidative capacity, plasma lipoprotein levels, and vascular integrity."

      I need say no more.

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    35. I need say no more.

      For anyone with an ounce of sense who actually wants to learn about reality, you are correct.

      Delete
    36. Jass,

      Had I been caught mistaking transportation, preservation, and recycling for synthesis, I'd be very worried and working hard to improve my reading comprehension abilities. I truly don't understand how you can go on using the very same careless "methodology" and expect a different result.

      Well, unless you're just trolling, which wouldn't be too surprising.

      Delete
    37. Did Jass really just cite an article by Jeffrey Tomkins as his main source of evidence? For real?

      Delete
    38. Not just "an article by Jeffrey Tomkins"; the article by Jeffrey Tomkins, the very one Larry demolishes above. This is evidence that Jass doesn't read what he's supposedly responding to, and I suspect he doesn't read the quotes he posts either.

      Delete
  9. @Rum, judmarc, Gab

    I need say no more

    What?

    Are you telling me that there is just no way that GULO gene is functional in most mammals, like humans, chimps, primates, etc?

    ReplyDelete
    Replies
    1. It's kind of a shame you're too stupid to realize how hilarious your posts here have been.

      Delete
    2. "Are you telling me that there is just no way that GULO gene is functional in most mammals, like humans, chimps, primates, etc?"

      No, I'm not telling you there is "no way" the GULOP pseudogene is functional. I'm telling you that it doesn't make the enzyme L-gulono-Y-lactone oxidase, which is the last step in the vitamin C biosynthesis pathway, and which used to be it's function over 60 million years ago.

      The locus could have some other function today, I can't claim to know it does not with an absolute certainty. But it doesn't make a functional enzyme as it used to. That much I can say.

      Delete
    3. Mikkel,

      So, if natural selection is a non-random process, as any Darwinist would sacrifice his life to prove it, why would it preserve a non-functional gene; a burden to so many organisms, in the process of evolution for 60 million years? Why?

      But, is natural selection a non-random process? The GULO non-functional gene is just another evidence that natural selection is impotent and proves what many scientists have questioned it's non-randomness...

      If that's the case, then it is a different story...but you ain't going to like this fact either...

      This is what happens when one gets married to a virtual reality; you can get a double edge sword shoved up your a.s...
      I'm just the one delivering it... lol

      Delete
    4. "So, if natural selection is a non-random process, as any Darwinist would sacrifice his life to prove it, why would it preserve a non-functional gene; a burden to so many organisms, in the process of evolution for 60 million years? Why?"

      But it has not preserved it for fucks sake. The gene is broken, large pieces of it are missing because they have been deleted. The rest is mutated so even if the missing pieces weren't gone it still wouldn't function.

      Get it?

      And it isn't much of a burden, it is a single gene of a few thousand bases out of three billion. The cost of having this degraded gene around is practically invisible to selection.

      I will have no part in your sticking "swords" up anyone's ass-fantasy.

      Delete
    5. "Out of 120,000 fertilized eggs of the green frog only two individuals survive. Are we to conclude that these two frogs out of 120,000 were selected by nature because they were the fittest ones; or rather - as Cuenot said - that natural selection is nothing but blind mortality which selects nothing at all?"-Litynski

      Natural selection can't remove defective genes or even can't select nothing at all... ;-)

      Delete
    6. Jass is finally beginning to accept the role of genetic drift in evolution. Larry must be so happy that his teachings are starting to sink in at long last.

      Delete
    7. He's stuck in black-and-white thinking. It has to be all or nothing in his head. He can't seem to comprehend that there is a spectrum between fully protected by natural selection, and protected against by natural selection. Or that it takes time for genes to get erased, they don't have to disappear instantly.

      So this gene has not been fully erased by deletions, so Jass now thinks that means natural selection can't at all remove it, or any genes under any circumstances. The quintessential creationist false dichotomy.

      Delete
    8. @lutesuite,

      Jass is finally beginning to accept the role of genetic drift in evolution. Larry must be so happy that his teachings are starting to sink in at long last.

      I know that random generic drift is Larry's god, so I have done my homework on it

      Will random genetic drift save neo-Darwinism or what's left of it? Oh yeah!

      "Considering genetic drift.. Griffith and colleagues state in agreement with these authors (1999, p. 564):

      Even a new mutation that is slightly favorable will usually be lost in the first few generations after it appears in the population, a victim of genetic drift. If a new mutation has a selective advantage of S in the heterozygote in which it appears, then the chance is only 2S that the mutation will ever succeed in taking over the population. So a mutation that is 1 percent better in fitness than the standard allele in the population will be lost 98 percent of the time by genetic drift."

      lol

      Delete
    9. If latesuite had at least a half of brain of natural selection, he wouldn't fall into this trap... lol

      Delete
    10. "Be suspicious of a theory if more and more hypotheses are needed to support it as new facts become available, or as new considerations are brought to bear."-Sir Fred Hoyle
      lol

      Delete
    11. "Be suspicious of a theory if more and more hypotheses are needed to support it as new facts become available, or as new considerations are brought to bear."-Sir Fred Hoyle.

      However, that doesn't seem to apply here, where "genetic drift" and "selection" are just different parts of a continuum. Understanding of evolution was actually simplified when changes in allele frequencies in populations were summarized in simple equations that used a "selection coefficient" (s) that can have any value from 0 to 1. At zero, the alleles don't matter. There is no advantage or disadvantage to them. At 1 (or -1), all the individuals with one of the alleles die. We can explore all the situations when s = 0 or 1 or an intermediate value.

      We give the name "genetic drift" to the situation where s = 0. Situations where s is greater than 1 are called selection. They're examples of a more general idea.

      Delete
    12. "Out of 120,000 fertilized eggs of the green frog only two individuals survive. Are we to conclude that these two frogs out of 120,000 were selected by nature because they were the fittest ones; or rather - as Cuenot said - that natural selection is nothing but blind mortality which selects nothing at all?"-Jas quoting Litynski

      Actually, out of 120,000 eggs of an adult green frog, and AVERAGE of 2 survive to become reproducing adults (if the population is stable). Some adult frogs produce 10 reproducing offspring, others produce 100 or even more. Many adult frogs produce no offspring at all).

      That difference may be random, but usually it is due to the genetic advantages or disadvantages that those adult frogs have in that environment -- what we call selection.

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    13. "So a mutation that is 1 percent better in fitness than the standard allele in the population will be lost 98 percent of the time by genetic drift."

      Exactly. So what is your point? Other than demonstrating yet again your utter cluelessness, that is?

      Helpful hint: How rare or common are non-lethal mutations?

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    14. Yet another helpful hint, Jass: What is "Neo-Darwinism"? Is it still a viable hypothesis? If you've been paying attention to this blog, that should be a give away question.

      Delete
    15. I am reasonably sure by the time we are done here, Jass will have "established" a function for GULOP related to quantum coherence as decreed by the Father, the Son, and the Holy Quantum Radiation Source.

      Delete
    16. Jass mistakes transportation, preservation, and recycling for synthesis. Jass then mistakes a comment about the need to avoid mistaking those terms for "GULO could not possibly have a function." Now Jass thinks that (s)he's making devastating remarks about evolution and natural selection, despite numerous attempts at explaining her/his complete lack of understanding. I don't see how more explanations will help. Jass would have to be willing to read for understanding, and that's just not going to happen.

      Delete
    17. "... so I have done my homework on it"

      Sure you did Jass. Sure you did. You cannot understand the difference between recycling and synthesis, but you have done your homework on genetic drift. Sure.

      Delete
    18. What regulates mutations in overlapping genes?

      Does anybody know how many overlapping genes are there in human genome?

      Delete
    19. Would it kill evolution theory if natural selection had an element of randomness and mutations an element of non-randomness?

      Delete
    20. Well...what's to kill if mutation breeding failed miserably...but speculative copulation genetics keeps it alive...somehow... lol

      Delete
    21. Jass, "What regulates mutations in overlapping genes?"

      The same things that regulate mutations in all genes and all junk DNA. There is a difference, though in the consequence of mutations. As you know, mutations in some positions in a gene have no effect, but other positions may cause a significant effect or even death. Where two genes overlap, a mutation that has no effect on one gene may cause a harmful effect on the other. Therefore, areas of DNA where two genes overlap tend, in general, to demonstrate slower change overall than areas where genes don't overlap.

      "Does anybody know how many overlapping genes are there in human genome?"

      Somebody may, but I certainly don't.

      "Would it kill evolution theory if natural selection had an element of randomness . . . ?"

      No. Natural selection does have some randomness. Individuals with superior genetics may die for one reason or another. This is not a problem for evolution theory.

      "Would it kill evolution theory if . . . mutations an element of non-randomness?"

      That depends on what you mean by "non-randomness." Mutations do have some non-randomness. There are places in DNA that are mutation "hot-spots," prone to mutate for some chemical reason, and other areas that mutate much less often. That's no problem for evolution theory.

      What would be a problem for evolution theory would be if organisms always got the mutations that would help them. For example, if plants facing drought always got mutations that help them conserve water, and not mutations that would waste water. However, that doesn't happen, as far as I can tell.

      As for your third November 10 question just above, it's not clear to me that the question makes sense to me, so I can't answer it.

      Delete