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Tuesday, August 26, 2014

Another stupid "prediction" by Intelligent Design Creationists

The IDiots are claiming to have "predicted" something that's been known for thirty years.

Let's start by reviewing some basic facts about codons.

Look at the standard genetic code (right). Notice that for some amino acids there are several codons. For example, There are four different codons for alanine (A): GCT (GCU), GCC, GCA, and GCG. These are called "synonymous" codons.

A lot of mutations in coding regions will change one codon into another without changing the amino acid encoded by the mRNA. These are presumably neutral mutations, since they occur frequently in populations and in comparisons between species. What this means is that it mostly doesn't matter which codons are being used.

Each of the codons is recognized by a particular tRNA molecule that carries an amino acid into the site on a ribosome where peptide bonds are made. There's a tRNAAla that recognizes alanine codons but it has a strange anticodon (IGC) that can interact with three different alanine codons. The third base of a codon is often called the "wobble" position since it's the one that seems less important in determining the correct amino acid. In the case of the alanyl-tRNA molecule, the "I" base (inosine) can form base pairs with U, C, and G so three different codons can specify alanine. There's a different alanyl-tRNA for the GCG codon.

It's important to keep in mind that there are 50 different tRNAs in most cells and most of them are expressed from multiple copies of their respective genes. There are about 500 tRNA genes in the human genome [Wikipedia: Transfer RNA]. There are many copies of the gene for the alanyl-tRNA with the IGC anticodon but there are also different alanyl-tRNAs with UGC, GGC, and CGC anticodons. The same variation is seen with synonymous codons for the other amino acids.

If you have lots of tRNAs for a particular codon then that codon is going to be translated relatively quickly during protein synthesis. (The rate of protein synthesis is about 20 amino acids per second.) Similarly, if there's a codon that can only be recognized by one of the minor tRNAs then synthesis will be slower. Normally this different isn't significant but there are times when it makes a difference.

In rapidly growing cells, for example, some proteins have to be synthesized at a high rate. The genes for these abundantly expressed proteins tend to be enriched for codons corresponding to the abundant tRNAs. This produces a bias in the codons that are used in a particular organism—the well-known codon usage tables that became popular about thirty years ago [Codon usage bias]. An example for Escherichia coli is shown on the left. (Codon bias can also be due to mutation bias and overall GC content of the genome.)

Note that the preferred alanine codon is GCG and the least preferred codon is GCU. This is a reflection of the fact that highly expressed genes tend to use GCG because there are more tRNAS for that codon. Keep in mind that there's only a three-fold difference because for most genes the GCU codon works just fine.

All this has been well known for decades. There have even been studies that measure the translation rate for different codons. I was able to dig from my files a paper that dates back to 1991 (Sørensen and Pedersen, 1991). Those authors showed that the GAA codon for glutamate (E) was translated at 21.6 codons per second while the GAG codon was only translated at 6.4 codons per second.

Long-held assumptions about "silent" genetic mutations have been torn down, challenging a fundamental evolutionary theory.

Lindsay Borthwick
March 2007
I blogged about this back in 2007 when I criticized an article in the now-defunct SEED magazine [Silent Mutations and Neutral Theory]. A reporter for SEED, Lindsay Bothwick, got all excited when a paper was published showing that rare codons slowed the rate of translation and this slow down could be detrimental because it leads to misfolding of the protein.

According to Lindsay Bothwick, this result conflicts with the idea that synonomous codons are "neutral." That was ridiculous back in 2007 and it's still ridiculous. We've known for decades that in some genes there are preferred codons. (But in most genes, it doesn't matter.) Most synonymous mutations are neutral, but some aren't.

Now there's another paper with the same result but a slight twist. D'Onofrio and Abel (2014) have shown that some bacterial genes have translational pause sites that assist protein folding. The idea is that pausing at some of the less preferred codons might actually be beneficial because it allows time for protein folding. There's nothing remarkable about this paper. It's pretty much confirming what we already knew.

But if you're an IDiot, like Casey Luskin, everything seems brand new because you are learning about it for the very first time. Furthermore, you assume that everyone else is as ignorant as you are. That leads you to make a fool out of yourself by posting this: Paper Finds Functional Reasons For "Redundant" Codons, Fulfilling a Prediction from Intelligent Design.
A new peer-reviewed paper in the journal Frontiers in Genetics, "Redundancy of the genetic code enables translational pausing," finds that so-called "redundant" codons may actually serve important functions in the genome. Redundant (also called "degenerate") codons are those triplets of nucleotides that encode the same amino acid. For example, in the genetic code, the codons GGU, GGC, GGA, and GGG all encode the amino acid glycine. While it has been shown (see here) that such redundancy is actually optimized to minimize the impact of mutations resulting in amino acid changes, it is generally assumed that synonymous codons are functionally equivalent. They just encode the same amino acid, and that's it.

Well, think again. The theory of intelligent design predicts that living organisms will be rich in information, and thus it encourages us to seek out new sources of functionally important information in the genome. This new paper fulfills an ID prediction by finding that synonymous codons can lead to different rates of translation that can ultimately impact protein folding and function.
Gee, I wonder where Casey Luskin was when I started teaching this stuff to undergraduates back in 1982? That was years before the modern Intelligent Design Movement produced the Wedge Document. Did he make his prediction before there ever was a "theory of intelligent design"?

I suppose anything is possible if you believe in gods.

But most of this (below) is not possible (or true) ...
It's this sort of sophisticated, information-rich control that is expected by intelligent design, in contrast to Darwinian biology which fails to anticipate it. On the contrary, Darwinian advocates publish mountains of papers banking upon the unquestioned assumption that there is no important, functional reason for the existence of "redundant" or "degenerate" features. Slowly but surely, the data are turning the tide in the evolution debate.
Do you still wonder why I call them "IDiots"?

D'Onofrio, D.J. and Abel, D.L. (2014) Redundancy of the genetic code enables translational pausing. Frontiers in Genetics, May 20, 2014. [doi: 10.3389/fgene.2014.00140]

Sørensen, M.A. and Pedersen, S. (1991) Absolute in Vivo Translation Rates of Individual Codons in Excherichia coli: The Two Glutamic Acid Codons GAA and GAG Are Translated with a Threefold Difference in Rate. J. Mol. Biol. 222:265-280.


  1. Let's pretend that codon usage was just discovered, and that Luskin has an actual argument to make instead of an imaginary, already falsified one.

    "The theory of intelligent design predicts that living organisms will be rich in information, and thus it encourages us to seek out new sources of functionally important information in the genome."

    This is why ID is not science and makes no scientifically testable predictions. How is "information-rich control" a logical hypothesis following from intelligent design? How could one rule out that naturalistic evolutionary processes did not produce this observation?

    Aside from failing to propose a hypothesis unique to ID, where does Luskin get the idea that an intelligently designed translation system will exhibit his vague "information-rich control". That doesn't logically follow from the starting point of ID. In order to get there, you have to claim special knowledge of the nature of this designer, such that you know that any system (s)he designs would necessarily exhibit information-rich control. Maybe information-rich control isn't appealing to the designer, and (s)he doesn't care to incorporate that into the system. How would ID know?

    1. Chris, I don't see how mere evolutionary theory could ever challenge the tight, economical logic of the following Intelligent Design prediction:

      "Most synonymous mutations are neutral, but some aren't" -> Therefore, God

    2. judmarc wrote:

      ""Most synonymous mutations are neutral, but some aren't" -> Therefore, God"

      No... Your theory is simply not holding up...You have to come up with a new one... or accept that some things are better explained by being intelligently design by God, gods or find a third alternative..

      It is as simple as that...

    3. No Quest, evolutionary theory is holding up very well, over the course of decades of scientific testing. How are things better explained by intelligent design? Name a single scientifically testable hypothesis unique to ID and show a definitive experiment providing evidence, any at all, for "intelligently designed by God". It's as simple as that.

    4. Chris B wrote:

      "No Quest, evolutionary theory is holding up very well, over the course of decades of scientific testing."


      Well..., if you say so.. why don't provide some of that scientific testing on say... how bacterial flagellum evolved...? Or how evolution has been tested to the point leading to replication.... or how cell membrane evolved without DNA or DNA with the cell... ?

    5. Quest,
      Yes, really.

      "Well..., if you say so.. why don't provide some of that scientific testing on say... how bacterial flagellum evolved...?"

      I don't say so, the scientific literature says so. I'm not going to do your work for you. If you want to know more about the bacterial flagellum, go look up some real scientific literature. Ignorance of the subject doesn't mean what you have been told about the flagellum is correct. The bacterial flagellum isn't irreducibly complex. Neither is blood clortting.

      "Or how evolution has been tested to the point leading to replication.... or how cell membrane evolved without DNA or DNA with the cell..."

      So now we're back to origins, Quest? How does evolutionary theory explain the origin of life on Earth? Here's your answer: we don't know (yet). Understand, though, that because evolutionary theory has not yet explained the origin of life a few billion years ago does not in any way invalidate the mountains of data accumulated over decades supporting evolutionary theory. That would be the equivalent of saying that if gravitational theory can't explain how and why the big bang occured, that this invalidates all gravitational theory.

      Resorting to 'origins' is just a god of the gaps argument. You have to keep retreating until you find some area that science doesn't yet explain. A place where god can magically poof life into existence by divine fiat. But you have zero evidence that is what happened. You have turned your god into nothing more than the embodiment of scientific ignorance.

    6. Well..., if you say so.. why don't provide some of that scientific testing on say... how bacterial flagellum evolved...?

      Compare the paper Matzke co-authored to the paper Jonathan Wells co-authored on the subject, and tell me which one is more scientific.

  2. Mr Moran, you have certainly been addressing a lot of ID arguments lately. I'm fairly new to reading your blog, is this common for you?

    1. I would think,Beau, if he is anything with respect to you it would be Professor Moran, and if you were simply a diligent reader you could check back through the blog to find the answer to your question

    2. You're right, my apologies Professor Moran. DGA I'm quite sure the good professor can answer for himself if he chooses. I have read some of the background and I'm under the impression Professor Moran might be intrigued by some ID arguments. I could be wrong I usually am.

    3. I bet Larry would be intrigued by ID arguments if they were both a) new and b) potentially valid. Actually, b would be enough, but a is a time-saver, as none of the old ID arguments are potentially valid.

    4. He doesn't waste his time with debunking ridiculous YEC claims, so every now and then when the IDiots get particularly proud of a "revelation" of theirs he steps in to show where they went wrong - and at the same time provides great scientific resources and information to learn while reading it. This combination is executed so well in his writing, it's one of the big reasons I follow Dr. Moran so closely. And the intellectual discussions in his comments (when they're not filled with trolls like Quest or Robert Byers) will often be as enlightening as Larry's writing. Contrast that with the echo-chamber (and discussionless) comment section present in a lot of other science and freethought blogs.

  3. It would be funny it it wasn't so sad.

    This 1995 paper by Paul Sharp et al (and several others by him, both earlier and later) focuses on selection acting on silent mutations:

    Interestingly, the above paper also addresses the issue of doublet mutations, which is relevant to recent posts on this blog discussing Behe's silly claims. There are a number of papers in the codon modelling literature of the last decade or so that make a case for the occurrence of doublet mutations at substantially higher rates than would be expected if they occurred independently.

  4. My IQ just dropped 20 points after reading Luskin's post.

  5. Luskin could have at least picked a legitimate paper on this topic. David Abel is a crank. He doesn't do any research, just pulls together a bunch of papers from other sources and adds his own gibberish. The "Institute" he works from is actually the garage of his home in suburban Maryland. PZM did a post on him years ago:

    I think someone determined that about 17% of the "peer-reviewed" papers that support ID on the DI website are actually from Abel.

    1. What's particularly awful about this is that there is a real problem with the the handling of this paper. The editor handling it, Firas H Kobeissy, is apparently a psychiatrist, not really an appropriate choice for this manuscript, and because the Frontiers series of journals has open peer review, you can see that one of the reviewers is Kobeissy himself (a conflict of interest).

    2. Frontiers in Genetics is one of the youngest members of the Frontiers family. It has no impact factor yet, and if the editors continue on the present course, they may steer the journal into the shoals.

  6. Larry Moran: The IDiots are claiming to have "predicted" something that's been known for thirty years.
    Look on the bright side Larry. It's something that's been known for thirty years.

    In this case I'm OK with just letting everyone have their science fun. Therefore I can also compliment how you are having yours by spreading the word of these basic facts about codons, few would otherwise have interest in reading.

    1. In this case I'm OK with just letting everyone have their science fun.

      Gee, thanks Gary. We were all trembling and afraid you'd destroy our arguments with the power of your scientific knowledge as you so often do.

    2. This is more fascinating than I at first thought.

      Could alanine store 4 state Confidence Data this way?

    3. Or in other words (for intelligence to exist) each addressable memory location (in this case for a three letter codon) must also contain (by storing or encoding) its "confidence level" in that being the correct action (correct amino acid for that location).

      Note in the circuit schematic there are two Data elements. The top one stores confidence level in that action, while the one shown below it is the (t-RNA) motor action (for adding the given amino acid to the sequence).

  7. Oh look, it's David L Abel, the young Earth creationist, of "Department of ProtoBioCybernetics/ProtoBioSemiotics, The Gene Emergence Project of The Origin of Life Science Foundation" fame.

    This is the website of this fancy-sounding "organization", in which they offer money to any one who can demonstrate the origin of life to their satisfaction:

  8. Luskin would find common cause with 'real' Darwinists (ie those of an adaptationist bent) with any of his ID 'predictions'. Adaptive reasons for codon usage or the arrangement of the codon matrix, like function for junk DNA, could as readily be retrodictively claimed by Darwinism sensu stricto. If something really is beneficial (all hail the Designer), that must be cashed in as reproductive success (all hail Having-More-Offspring!), else it's not really all that beneficial.

  9. I want to leave this here
    Protein Sci. 1996 Aug;5(8):1594-612.
    Ribosome-mediated translational pause and protein domain organization.
    Thanaraj TA, Argos P.

    and note that the result was well known at least 8 years earlier. There does remain a problem in that many still claim that proteins fold into a global free energy minima which is false. They fold into a trapped kinetic intermediate that sometimes is also the global minima. I wonder how the IDiots could reverse engineer that into a prediction of ID?

  10. I have read about how rare codons could make "pauses" and thus help folding since I started grad school back in the late 80s/early 90's. The papers were a tad older than that of course.