Sunday, November 22, 2015

What do pseudogenes teach us about intelligent design?

The human genome has about 14,000 pseudogenes that are derived from protein-coding genes and an unknown number derived from genes that specify functional noncoding RNAs. There is abundant evidence that the vast majority of these pseudogenes are nonfunctional by all measurable criteria.
It would be perverse to deny the existence of pseudogenes. Almost all of them are junk DNA with no known function. Anyone who claims otherwise can be dismissed as a kook and it's not worth debating those people.

The presence of a single well-characterized pseudogene at the same locus in the genomes of different species is powerful evidence of common descent. For example, Ken Miller has long argued that the existence of common pseudogenes in chimpanzees and humans is solid evidence that the two species share a common ancestor. He uses the β-globin pseudogene and the gene for making vitamin C as examples in Only a Theory: Evolution and the Battle for America's Soul.
As we did for vitamin C, we might now ask how a designer cold have allowed this to happen. And our ID friends wold answer in the same way they did before; Our genome was originally designed with six working copies of the beta-globin genes, and therefore the loss of one of them from such molecular errors is no big deal. Therefore, all humans alive today are descended from individuals in which those mistakes first cropped up. Fair enough. But guess what: We're not the only organisms with a set of beta-globin genes, and we're not the only ones with a pseudogene right in the middle of that set.

Gorillas and chimpanzees have them, too, and they are arranged in exactly the same way—five working copies surrounding a single pseudogene, just as in humans—but here's where life gets truly interesting. The gorilla and chimpanzee pseudogenes have exactly the same set of molecular errors. Just like the two kids in my class, they have matching mistakes. [proving plagiarism] The student papers had a common source (the original essay), as do these two pseudgogenes—the original version of the pseudogene in the ancestor of all three species.

There's no escaping the implication of these matching mistakes, and there's no point in arguing that six identical mistakes could have turned up independently in the three unrelated species. The only sensible interpretation is tht the original errors developed at random in a single common ancestor of these three species. In a court of genetic copyright law, any motion that a designer could claim originality for the human genome would be tossed out in a flash. Our genome is a copy, an altered one to be sure, but a copy, nonetheless, of earlier genomes that preserve even the mistakes that our ancestors made in duplicating their DNA.

(p. 101-103)
Similar arguments have been made by Francis Collins, Richard Dawkins, and a host of other scientists. The details may vary, and some of the details may even be wrong, but the big picture is certainly correct. There are hundreds of pseudogenes shared by chimpanzees and humans and the only reasonable explanation is that chimps and humans share a common ancestor. This is just a tiny bit of the evidence for the history of life. It is so overwhelmingly supported by evidence that we consider it to be a scientific fact that humans and chimpanzees descend from a common ancestor. If you meet someone who denies this fact then it's probably not worth your time to debate with them about other issues concerning evolution and intelligent design. They are on a different planet.

The reason why shared pseudogenes are important is because they refute the idea of convergence and the idea of direct intelligent design. There's no reasonable way to explain common pseudogenes by invoking convergence on a common function and there's no reasonable way to advocate an intelligent designer that created chimpanzees and humans separately and stuck broken genes into their genome.

So, the evidence of pseudoegenes is not compatible with special creation and we can understand why Young Earth Creationists are upset. But we don't care about them. They are so wrong about so many things that their views can be dismissed out-of-hand except to point out, from time to time, that their ridiculous ideas are incompatible with science (and the real world).

But why are other ID proponents so bothered by pseudogenes? Many of them, like Michael Behe and Michael Denton, are perfectly comfortable with common descent. They aren't bothered in the least by the pseudogene argument advanced by Ken Miller. Their concern is to demonstrate evidence of guided evolution meaning that sometimes the gods tweak the results of evolution by introducing specific mutations in a background of random mutations.

Here's how Michael Behe deals with pseudogenes in The Edge of Evolution.
More compelling evidence for the shared ancestry of humans and other primates comes from their hemoglobin—not just their working hemoglobin, but a broken hemoglobin gene, too. In one region of our genomes humans have five genes for proteins that act at various stages of development (from embryo through adult) as the second (betalike) chain of hemoglobin. ... In that region between the two gamma genes and a gene that works after birth, human DNA contains a broken gene (called a "pseudogene") that closely resembles a working gene for a beta chain, but has features in its sequence that preclude it from coding successfully for a protein.

Chimp DNA has a very similar pseudogene at the same position. The beginning of the human pseudogene has two particular changes in two nucleotide letters that seem to deactivate the gene. The chimp pseudogene has the exact same changes. A bit further down in the human pseudogene is a deletion mutation, where one particular letter is missing. For technical reasons, the deletion irrevocably messes up the gene's coding. The very same letter is missing in the chimp gene. Toward the end of the human pseudogene another letter is missing. The chimp pseudogene is missing it, too.

The same mistakes in the same gene in the same positions of both human and chimp DNA. If a common ancestor first sustained the mutational mistakes and subsequently gave rise to those two modern species, that would very readily account for why both species have them now. It's hard to imagine how there could be stronger evidence for the common ancestry of chimps and humans.

That strong evidence from the pseudogene points well beyond the ancestry of humans. Despite the remaining puzzles, there's no reason to doubt that Darwin had this point right, that all creatures on earth are biological relatives.

The bottom line is this. Common descent is true; yet the explanation of common descent—even the common descent of humans and chimps—although fascinating, is in a profound sense trivial. It says merely that commonalities were there from the start, present in a common ancestor. It does not even begin to explain where those commonalities came from, or how humans subsequently acquired remarkable differences. Something that is nonrandom must account for the common descent of life.

(pp. 72-73)
This clear statement by Micheal Behe is a way of separating the kooks from the serious ID proponents. It's my new benchmark for debating them. If they reject Behe's argument for common descent then they are kooks and I'm not going to debate them.

But there's a problem. The ID proponents who remain upset about the pseudogene argument and common descent are often very coy about why it bothers them so much. They won't "come out" as kooks. For example, Casey Luskin doesn't like it at all and he's eager to jump on any evidence that a pseudogene isn't a pseudogene. Sometimes the irony of his argument is astonishing; like when he claims that the β-globin pseudogene isn't a pseudogene because a bit of the pseudogene in chimps and humans looks more conserved than they should be [Dover Revisited: With Beta-Globin Pseudogene Now Found to Be Functional, an Icon of the "Junk DNA" Argument Bites the Dust].

Casey Luskin loves the results of a recent paper that examined the evolution of the β-pseudogene in the chimpanzee and human genomes. The paper appeared in Genome Biology and Evolution (Moleirinho et al., 2013). The authors looked at diversity in the β-globin locus (1092 human genomes) and found lower than expected diversity in the pseudogene using standard evolutionary models and complex calculations based on modern evolutionary theory. They conclude that there might be a regulatory site within the pseudogene that determines chromatin structure for the entire locus. Presumably it arose after the pseudogene was created when that sequence became available for the evolution of a SAR. (Assuming the result is correct.)

The irony is that Casey Luskin has to rely on evolution and common descent to provide the evidence that some of the DNA in the β-globin pseudogene might have a function. But he's quite happy to use that evidence to challenge common descent and "Darwinism."

I don't know what goes on in the minds of Intelligent Design Creationists who oppose the idea of pseudogenes unless they're kooks who reject common descent. They desperately want to prove that pseudogenes are functional. Presumably they have in mind a scenario where the gods decide to break a functional gene and then create a new function from the broken gene. Who knows? It's impossible to get the ID proponents to explain anything.

You'll often come across ID proponents who claim that the common descent argument of Ken Miller et al. is the main argument for junk DNA. This is not correct. They may not be kooks—they may simply be confused. It's clear that pseudogenes are junk, if they are nonfunctional, so the argument takes that as a given. The reason for using pseudogenes to convince creationists isn't to prove junk DNA—that much is obvious—it's to show the absurdity of postulating an intelligent designer who would design species with common pseudogenes at the same location in their genomes. Micheal Behe gets it.

This is what a confused Casey Luskin says ...
Well, it's been Exhibit A—literally, offered as evidence in a court case—for critics of intelligent design who argue that our genome is full of useless, functionless junk, and therefore can't be a product of design.
Now, Casey Luskin may be skeptical about common descent (he's very coy about that) but here he's just confused. Pseudogenes make up only a tiny fraction of our genome (<1%) so they aren't ever being used as evidence that our genome is full of junk. There are other arguments that support lots of junk in our genome.

Here's another example of Casey Luskin's confusion about pseudogenes. Keep in mind that the vast majority of pseudogenes are not transcribed, according to ENCODE so there's no reason whatsoever to think they might have a function. The vast majority (>90%) are clearly junk. That makes it difficult to understand Casey Luskin's logic when he says ...
Pseudogenes serve as another good example of how Darwinian biologists have assumed that a type of non-coding DNA they didn't understand was functionless genetic junk, and thus ignored their functions. Indeed, the aforementioned paper in RNA Biology explains that one reason why evolutionists have been so slow to abandon the assumption that pseudogenes are junk is because their functions are difficult to detect. The authors observe that "almost all pseudogenes that exhibit significant biological activity are expressed in specific tissue or cell lines," meaning only specific tissues or cell lines may use a given pseudogene for some function. Additionally, it's difficult to detect function for pseudogenes because we have lacked the research tools to understand how they influence gene expression. The paper predicts that "more and more functional pseudogenes will be discovered as novel biological technologies are developed in the future," and concludes "The study of functional pseudogenes is just at the beginning." Indeed, two leading biologists writing in Annual Review of Genetics reported that "pseudogenes that have been suitably investigated often exhibit functional roles."
Problem 10: Neo-Darwinism's Long History of Inaccurate Predictions about Junk Organs and Junk DNA
No "leading biologist" would ever say that most pseudogenes have a function. Even the most vocal critics of junk DNA will admit that most pseudogenes are nonfunctional junk DNA.

ID proponents also claim that the common descent argument is used as proof of "Darwinism." But it's not. It's one bit of the evidence for common descent but there's lots and lots of other evidence. The existecne of pseudogenes just happens to pose a challenge to creationists who aren't comfortable with common descent.

Besides, in order to explain the existence of pseudogenes you have to invoke Neutral Theory and fixation by random genetic drift and those are decidedly non-Darwinian. I think this particular misunderstanding is at the heart of the objections of many ID proponents. They think that if they accept the existence of pseudogenes they will be accepting all of evolution and everything that it implies. That's why there's so much resistance.

Here's how Casey Luskin views it ...
But Ken Miller's argument for Darwinian evolution, and against ID, depends on the beta-globin pseudogene being "non-functional," implying as he does that the genetic differences between it and protein-coding beta-globin genes are errors. In light of this new evidence for the functionality of the beta-globin pseudogene, it seems that those genetic differences may not be errors at all. If so, then Miller's argument, his Exhibit A, collapses.
When I open a page of Darwin I immediately sense that I have been ushered into the presence of a great mind. ... When I read Phillip Johnson, I feel that I have been ushered into the presence of a lawyer.
Richard Dawkins, Biol. & Philos. 11:539-540. (1996)
Do you see the problem? Luskin thinks that the argument of Ken Miller and Michael Behe is not just an argument for common descent, it's an argument for "Darwinian evolution." That's much more threatening, even though it's an imaginary threat as Michael Behe explained in his latest book. Luskin also thinks that the β-globin pseudogene is the only example that supports the case for common descent. The truth is that there are thousands of pseudogenes common to chimps and humans.

Casey Luskin is a lawyer and lawyers are very good at making arguments in support of their clients. Truth is not the objective when arguing for your client. Winning in a court of law is the objective. But in science truth is the only objective. If you question common descent then you have abandoned the search for truth and you are just a lawyer.

Moleirinho, A., Seixas, S., Lopes, A.M., Bento, C., Prata, M.J., and Amorim, A. (2013) Evolutionary constraints in the β-globin cluster: the signature of purifying selection at the δ-globin (HBD) locus and its role in developmental gene regulation. Genome Biology and Evolution 5:559-571. [doi: 10.1093/gbe/evt029]


  1. Something that is nonrandom must account for the common descent of life.

    Not sure this statement you quote from Behe means what I think you think it means. I feel what Behe means by "nonrandom" is The Designer. I'm guessing that's not why you bolded this statement.

    1. Behe means that evolution is guided by the Intelligent Designer. This idea of nonrandom evolution (= guided evolution) is common among ID proponents.

    2. OK, reading back through your post and quote from Dr. Behe, you *did* interpret his quote as I did.

      So the best ID can do is say last common ancestors with broken, non-functional genes are somehow evidence of a Designer because common descent itself is somehow evidence of a Designer. Why this should necessarily be so escapes me. Perhaps Dr. Behe has said something about it?

  2. He uses the β-globin pseudogene and the gene for making vitamin C as examples in Only a Theory: Evolution and the Battle for America's Soul.
    Is the B-globin still considered a pseudogene?

  3. I think theres a subtle underappreciated reason why IDers are threatened by pseudogenes. Intelligent designers who go to the trouble of creating complex objects for a purpose aren't usually in the habit of letting random environmental influences destroy and degrade those objects - they repair and maintain those objects. That's part of our 'uniform and repeated experience' with designers.
    If the beta globin cluster was designed its reasonable to assume its designer wouldn't have allowed pseudogenes to persist. The fact they have is evidence against a designer.

    1. Intelligent ID proponents don't have a problem with pseudogenes.

      I wish the ID movement would purge itself of unintelligent ID proponents so we could have a serious debate. Problem is, there won't be many of them left to debate.

    2. Problem is, there won't be many of them left to debate.

      One "m" too many in that sentence. Can you find the typo?

    3. I guess the Intelligent Design movement is reluctant to purge itself of its unintelligent members because it so highly values open, uncensored discussion. We all know how rarely they ban people at Uncommon Descent, and how lively the discussion is in the comments section of Evolution News and Views.

  4. One aspect of IDiot thinking that all of us should be aware of, esp. where junk DNA is concerned, is their failure to understand basic logic. Consider the following two statements:

    1. "Most African-Americans are not president of the United States"

    2. "Barack Obama is President of the United States"

    If you were to think these two statements are mutually exclusive-- so, if someone says 1, you "prove them wrong" by citing 2-- you would be stupid. But that's the argument from most ID proponents, except Behe.

    Consider two statements about transposons:

    1. "Most transposons in the human genome are functionless junk"

    2. "Transposons have played a role in human evolution"

    Now most of *us* would immediately recognize that these two statements are not mutually exclusive. If 2 is proven, it does *not* disprove 1.

    However, almost no IDiots can grasp this logic (maybe Behe could, I suppose, but Luskin or Perry Marshall/ "Evolution 2.0" never could.)

    Thus, Perry Marshall's method for attacking Larry Moran at his Facebook page. Marshall quotes Larry Moran as saying: "'Transposons don't do anything, they just jump around". What Larry actually said was "They don't usually have any function other than replicating themselves and jumping around in the genome." Note the faking of quotes. Marshall substitutes what Larry wrote, which is basically correct, with "'Transposons don't do anything, they just jump around" and is probably not smart enough to realize that they don't mean the same thing.

    However, because of this substitution, Marshall believes that any proof of 2, above, "Transposons did something", logically disproves 1, "Most are junk." Thus, if 10 nucleotides out of all the 1+ billions of nucleotides in all transposons in the human genome are shown to have a function, Marshall says aha, I proved 2-- and therefore I disproved 1. What Marshall will never do, of course, is count up all the nucleotides in all transposons and divide the count of functionally-constrained nucleotides by the count of all nucleotides.

    And so it goes, also, with pseudogenes and Casey Luskin. Luskin believes these two statements are mutually exclusive:

    1. "Most pseudogenes in the human genome are functionless junk"

    2. "Many pseudogenes have small functional bits inside them"

    So if Luskin can find any example of 2, he thinks he's disproven 1. What he'll never do, of course, is count up all the nucleotides in all pseudogenes and divide the count of functionally-constrained nucleotides by the count of all nucleotides.

  5. Larry, for an IDea of what is needed (to teach us about intelligent design) follow this thread to where it leads. The next page required what you wrote about codons to be included in a biologically accurate model of brain cell origin and development:

    The future of ID is happening in places that don't know much or care about UD or the DI, but assimilating the controversial theory they are unable to properly scientifically develop is tempting. We only need to keep going on a never before programmed cognitive model the thread led to on its own, by there being a genuine need for such a thing in AI too.

  6. At the risk of being in the kook spectrum of humanity i say these little details are easily accommodated by the origin of mutations. In other words our bodies are copys of primates, though created separately, and upon the biblical story of the fall all our bodies had reactions to the new biology. A myual breakdown creating mutations , possibly for important reasons and not chance things, and then reaction to them.
    Why not like bodies react in like ways to like needs or like problems??
    I bet their is lots of genetic things in us/primates but not because of the only option of common descent.
    Again other options are not imagined.

    1. Then explain why 'like bodies' share similar genetic sequences even though the genetic code is redundant. Why are identical amino acids in a protein sequences specified by codons that demonstrate common descent? Also Australia has some pretty awesome examples of 'like bodies' reacting in very different ways to get to the same point again supporting common descent.

    2. The Lorax
      This stuff has every impression of being involved or complicated. Other options for how biology works must be a option.
      The original state for all like bodies could lead to like results for reasons that matter in those days.
      I see no reason that like bodies would react the same way. CD is not needed.
      Marsupials did and do have like bodies and the changes that brought the marsupialism, as i insist they are the same creatures as placentals, would be a factor in the genetics and not allow like genetics.
      No one actually ever saw genetic evolution. and with its nature being one of complex and mystery its wrong to insist only this or that could be the origin for like genetic details in unrelated beings.
      The conviction of CD for us/primates leads to a too quick convicyion of how to interpretate genetic convergence.

    3. Robert, what you've just said is one of the most insanely idiotic things I have read all day. At no point in your rambling, incoherent response were you even close to anything that could be considered a rational thought. Everyone in this thread is now dumber for having read it.

      What is "the new biology" and how could it possibly bring about hundreds of thousands of identical mutations in identical sequences in unrelated species?

      > Why not like bodies react in like ways to like needs or like problems

      Because mutations are stochastic. The vast majority of them happen randomly.

      > I bet their is lots of genetic things in us/primates but not because of the only option of common descent.

      Then suggest a reasonable alternative and provide the mechanism for how these common mistakes are highly targeted.

    4. Robert Byers last words were ...

      The conviction of CD for us/primates leads to a too quick convicyion of how to interpretate genetic convergence.

      Goodbye Robert.

      Take your meds.

    5. He will be missed. If only in the sense that his absence will be noticed.

    6. "Goodbye Robert."

      Larry, please don't ban Robert. If you do that, I fear that I will then be the stupidest person here. Well, except for Barry, and Beau, and...

    7. Three quick questions about the onions test, for anyone who'd care to answer them:

      1. In his book, "The Evolution of the Genome," T. Ryan Gregory argues for the existence of a causal relationship between genome size and cell size, and he goes on to say that cell size influences a number of key physiological parameters, although the manner in which it does so varies considerably between different classes of organisms. He also points out that cell size influences body size and organ (as opposed to organismal) complexity. It's my understanding that onions have very large cells. (I'm not sure why.) If onions require large cells for physiological reasons, then could one argue that the large amount of DNA in their genomes, which enables them to have large size, thereby serves a function? if not, why not?

      2. In his article on the onion test, T. Ryan Gregory writes that different onion species vary considerably in their genome sizes. Do they also vary in their cell sizes?

      3. An old article in the Harvard Gazette (see ) suggests that some organisms have more DNA because they faithfully copy everything when replicating their chromosomes, whereas organisms (such as fruit flies) which are careless about copying junk DNA when replicating will quickly lose it, and end up with smaller genomes in the process. Has this suggestion been borne out?

      Thanks very much to anyone who can help me with these questions.

    8. Sorry, that should be onion test, not onions test.

  7. Prof Moran

    I really enjoyed this article of yours but just two comments;

    I've stated before that I personally have no issue with CD but on the facts about it, I side with Dr Craig Venter. In addition Junk DNA and pseudogenes as per our discussion over at UD could very well mean that organisms started off in a pristine state but over time as with any system in operation accumulated garbage. I have no issue with that, and as I said if this is the case then there is no problem for me to accept Junk DNA as part of biological systems even from a design POV.

    We see systems accumulating, garbage, junk and rubbish all the time from an engine to an operating system. As stated to you before, once we know what that junk and garbage is and we strip it away what do we end up with? The very pristine system we'd expect it to be at the beginning of its operation. There is no escape that reverse engineering, like in the case of Dr Venter’s synthetic bacterial genome as you pointed out is a very strong indicator that we will recognise it as designed.

    So let’s remove all the junk and see what we get.

    1. To make the case that there are multiple life forms here is a recent paper that shows quite possibly the discovery of a new life form in our gut.

    2. Way to go, Andre. Citing an article that relies on the existence of common ancestry to prove common ancestry does not exist.

      I'm sure Craig Venter is very happy to have you on his side.

    3. Andre, you have to do a lot better than that if you want to be taken seriously. If you have no problem with common descent and no problem with junk DNA, then what, exactly, is your problem? What evidence do you heve that a problem exists?

      I, also, agree with Craig Venter's position on evolution and the history of life and so do most evolutionary biologists. Why did you mention that you side with Venter? Does that mean you have left the ID movement?

    4. I do hope Andre Gross is able to elaborate on this idea of a "pristine" genome that existed some time in the past. Do we have any fossils of this "pristine" organism? Was it able to type things by computer on the internet? If not, why are you able to do this, Andre,with your genome in the decrepit and degraded state that it is?

    5. Most importantly, can it be reconstructed by simply stripping off "junk and garbage" as suggested by Andre?

    6. On one hand, IDists say that ID predicts no junk DNA. And on the other hand they say that it predicts junk DNA. And both of these hands belong to Barry Arrington.

    7. Most importantly, can it be reconstructed by simply stripping off "junk and garbage" as suggested by Andre?

      Just think. If we were to delete all our junk DNA, we'll be back with Adam and Eve in the garden of Eden, sinless and unblemished. But then what purpose would Jesus serve? I guess that's why the Designer left all that junk in there: To keep the churches in business.

    8. Wow a person offers his opinion and the Darwin trolls are on high alert. I am saying that Dr Venter does not agree with the standard narrative of CD but that there are multiple domains of life not derived from a single ULCA.

      Secondly To see if we can get to a.pristine genome we have to know what the junk is first. Litrally let's separate the wheat from the chaff.

    9. So whether it is designed or not the first living organism probably had no junk in its DNA. So strip the junk if we know what it is and them we can make an inference.

    10. Wow a person offers his opinion and the Darwin trolls are on high alert. I am saying that Dr Venter does not agree with the standard narrative of CD but that there are multiple domains of life not derived from a single ULCA.

      And that differs from "the standard narrative" - how, exactly? I'm not convinced you actually understand what you just typed there, TBH.

      Secondly To see if we can get to a.pristine genome we have to know what the junk is first. Litrally let's separate the wheat from the chaff.

      That doesn't really answer any of our questions. It certainly doesn't answer mine. Are you sure you understand what "junk DNA" is? If you do, then what do you expect would happen if it was all deleted from a genome?

      Also, you weren't talking about a "pristine genome" as something that could be caused to exist. You said it was something that actually has existed. Where? In what or whom?

      Sorry, you don't get to just spew stupid shit on a science blog and then, when people ask you elaborate on or substantiate what you've written, get all offended and call people "trolls." If you don't like being challenged on the stupid shit you write, then stop writing stupid shit.

    11. So whether it is designed or not the first living organism probably had no junk in its DNA. So strip the junk if we know what it is and them we can make an inference.

      So I guess Larry wasted his time explaining to you what a pseudogene is.

      Just what do you think that experiment would tell us about the first life form?

    12. Firstly stop with the you don't understand nonsense. Secondly two things.could happen if we stripped out all the junk, either the organism goes back into its pristine state as any new system is, or the system collapse because in the end it may not be junk. Who knows. That's why I'm saying identify the garbage, remove it and let's see what happens.

    13. What would it tell us?

      I think Prof Moran can answer that in his own words. A pristine system with a clean genome will in all like hood answer the question if it is designed or not. I have already said based on my conversation with Prof Moran at UD that acculturation of junk in systems in operation is what we do observe. That's not controversial on on that basis I accept that there is junk in the genome. But what happens if we can eliminate it do we get back to a pristine system? What will it tell us?

    14. Pro tip Andre: If you want people to "stop with the you don't understand nonsense," then don't spew another load of stupid shit that erases any lingering doubt that you don't understand.


    15. Andre, they've done this with mice, and the mice were fine. Of course it's illegal to do such experimentation with humans.

      Living things starting in a pristine state and accumulating junk isn't what we uniformly observe. There are living things that have accumulated lots of junk and others that seem to have less. (See the "onion test.")

    16. Ah, but that's not quite what Andre is talking about. He's proposing that we first determine every single piece of junk DNA in a genome. Then, after we've shown that all this junk DNA is junk DNA, we take all the junk DNA out to see if the junk DNA is junk DNA.

      And, Andre says, this experiment will demonstrate if life was designed.

      Oh, and Andre doesn't need any tips from us. He understands all this stuff perfectly.

    17. Andre, evolution has involved the gain of "junk" DNA, the gain of new functional genes, and the loss of functional genes. Sometimes the gain in "junk" is a loss of a functional gene, for example when a gene necessary for producing vitamin C broke in primates and became a pseudogene. Therefore, simply removing the junk DNA cannot reveal the "pristine" genome of a common ancestor. It would be an interesting experiment, though!

      There is a the additional problem that the LUCA (last universal common ancestor) was a single-celled bacterium-like organism that lacked genes for many of the proteins we multicellular animals need. Therefore, removing the junk DNA from a modern multicellular organism wouldn't do much to reconstruct the LUCA genome.

    18. And, as you say, there are likely also genes that were possessed by the LUCA that were lost along the course of evolution.

      Andre was talking about "the first living organism", though, not the LUCA.

    19. Andre, read the following post and the 266 comments. Once you understand what Craig Venter meant, let me know is you still agree with him.

      Craig Venter Discusses the Tree of Life

    20. Lutesuite, you're right. I wrote about the LUCA because it seemed a better target than the no doubt sloppy genome of the first thing we could have called a living organism. But the first living thing fits better with Andre's argument.

    21. Actually, the comments section of the "Craig Venter Discusses the Tree of Life" article is an excellent reminder of why it's a waste of time trying to talk sense into Andre Gross.

    22. Haha, that thread man. Fuckin ell. There was this gemstone in there though:

      steve oberski Thursday, February 14, 2013 5:11:00 PM
      I think it's time to invoke Grey's Law:

      "Any sufficiently advanced incompetence is indistinguishable from malice."

    23. "Wow a person offers his opinion and the Darwin trolls are on high alert."

      You offered an opinion and other posters pointed out obvious flaws and problems with your scenario. This is not "trolling". If you are too thin skinned to take criticism, steer clear of areas like science and show business.

      Some questions for you:

      Why would the original pristine state of genomes contain no junk DNA?
      Why did the intelligent designer create a system that inexorably degrades over time?

      Are there examples of other organisms in Earth's history that went extinct because their genomes degraded to the point that they all died?

      How much time have we got before our genome has degraded to the point that we all die?

    24. ""Any sufficiently advanced incompetence is indistinguishable from malice."

      And its corollary: "Any sufficiently illogical and inarticulate argument is indistinguishable from ID."

    25. That link to Venter on Youtube does not work. The poster seems to be a serial violator of copyright. Do you have it somewhere else?

    26. That link to Venter on YouTube does not work.

      Thanks. Fixed.

    27. Speaking of gems from the old thread:

      Laurence A. MoranTuesday, February 12, 2013 9:13:00 PM

      Explain to me again where the bases come from? What about the ribose - where does that come from? Did someone "poof" it into existence? As for nucleotides .... not possible.

      Andre GrossWednesday, February 13, 2013 12:17:00 AM

      Yeah where did it come from?

      Andre's great moment of science: "Yeah, where?"

      OMG, LOL, etc., etc.

  8. What "pristine system" do you have in mind?

  9. I'm not entirely sure why, but this portion of quoted section of Behe's book really bothers me:

    "A bit further down in the human pseudogene is a deletion mutation, where one particular letter is missing. For technical reasons, the deletion irrevocably messes up the gene's coding."

    He had an opportunity to educate his audience about some really, really basic molecular biology, but apparently he decided that the concept of a frameshift mutation is just too "technical" for their minds, so he just elides right over the important information that would explain to his readers why this mutation has knocked out the function of the gene. I just find that to be especially aggravating.

    1. As a teacher, I'd say that Dr. Moran made the right decision here. Frameshift mutations are very interesting and worth a post, for sure. But the point of this post was what the way pseudogenes are used by those trying to support the hypothesis of intelligent design.

      Explaining frameshift mutations to people who don't know about them already is harder than you may realize. It requires explaining the genetic code and giving at least one example of the translation of the original code and of the mutated version.

      I suspect that Dr. Moran figured that either his readers would know about frameshift mutations and be able to figure out what he meant (as you did!), or explaining this point would double the length of the post and hide the point he was trying to make.

    2. Oh, I wasn't criticizing Dr. Moran's post. I'm pretty confident he has explained frameshifts elsewhere. I was criticizing Behe for not taking an opportunity to educate his audience, who are, in my experience, sorely in need of more basic biological knowledge.

  10. Larry,

    What do you make of this:

    1. The first sentence of the abstract already contains a lie (or, using a more generous interpretation, proof that the author has a reading problem), and the rest of the paper elaborates on it. Dr Tomkins is the Black Knight of the ID movement.

    2. It is my understanding that the vitellogenin pseudogene is over 20,000 base pairs in length. Where does Tomkins get this 150 number? And why doesn't he refer to the VIT1, VIT2, and VIT3 genes by name? And why is this "research" not published in a recognized journal? This smells like a very detailed strawman to me.

    3. If you search Brawand, Wahli & Kaessmann (2008) for "150", you'll get zilch. But their "Supporting Information" incluldes Figure S2: Sequence Alignment of the VIT1 Exon 3 from Human (Homo sapiens), Dog (Canis familiaris), Armadillo (Dasypus novemcinctus), and Chicken (Gallus gallus). That's where "a mere 150 base fragment of alleged similarity" comes from. As for what made Tomkins think it was the only matching fragment, I haven't the foggiest. Didn't he have a look at Figure 2 in the article and read the accompanying text? The autors say there what Fig. S2 illustrates (boldface added):

      Exon 3 of VIT1 reveals shared indels between human and dog (Figure S2), which indicates that VIT1 was inactivated before the separation of the human and dog lineages (representing the eutherian superorders Laurasiatheria and Euarchontoglires) ∼90–100 Mya.

      They also say clearly that they

      identified a few VIT pseudogenic coding sequence remnants (mainly from VIT1 and VIT3) with premature stop codons and frame-shifting insertion/deletions (indels) in regions syntenic to those containing these VIT genes in chicken (Figure 2 and Figure S1).

      So either Tomkins honestly believes the fragment of VIT1 Exon 3 shown in Fig. S2 is the only remnant of the whole VIT complex identifiable in humans (which means that he has a serious reading issue) or he is deliberately trying to mislead his readers (or, in plain English, he's lying).

    4. PS Compare this nice post by Aceofspades25: LINK

    5. It is my understanding that the vitellogenin pseudogene is over 20,000 base pairs in length.

      That's the chicken gene, not the human pseudogene fragment. The combined length of the 35 exons in chickens is 5,787 bp, or at least so they say here:

    6. Sorry, the first paragraph above is a quotation from Fair Witness's comment and should have been italicised.

  11. Also, what exactly is the GAM (genomic address manager) gene Tomkins talks about? I can't find much about it in the literature. The reference he links to (Bentwich 2007) is a patent, not a paper.

    1. And it's worth noting that GAMs are supposed to be miRNAs (and the patent has sequences for download, most of which are 22nt in lenght). Long noncloding micro-RNAs seem like a novel idea of Tomkins and a patently silly one at that...

    2. It seems to be a ghost gene, but Tomkins makes an interesting use of it: he proposes that the synteny argument is "null and void to begin with" because the sequence sits inside an active functional gene. This summary rejection apparently frees him from the obligation to address any details of the question of synteny (never mind the remaining pseudogene fragments). He has played this trick before, so it isn't a new weapon in his arsenal:

      My analysis confirms that the site is located inside a gene called DDX11L2 on human chromosome 2. Furthermore, the alleged fusion sequence contains a functional genetic feature called a “transcription factor binding site”... -- Sounds familiar, doesn't it?

      New research debunks human chromosome fusion