Intro by Senior Editor Jim Stump: Our general goal for our blogs is to present information and arguments on the origins debate that can be understood by most any interested reader. The reality of the disagreements, though, is that they often hinge on technical details of the scientific literature which require some disciplinary background and experience to follow and understand fully. The current series probably falls into this category. But we think it is important for getting past the superficial and rhetorical claims (on both sides), and drilling down to the crux of the matter about DNA and information. Consider working through these posts carefully from the beginning.
In the previous post in this series, we examined evidence that strongly suggests that the genetic code had a natural origin. If this is correct, it undermines the Intelligent Design (ID) argument that the genetic code was designed apart from natural processes. To put it plainly, if the genetic code had an origin driven in part by chemical binding events, then it is not a “genuine code” in the sense we humans use the word—and further research might reveal plausible scenarios by which the entire code may have come to be.
When writing that last post, however, I had forgotten that ID proponent Stephen Meyer, along with his colleague Paul Nelson, had written a paper disputing the evidence for direct templating. They published their work in the in-house ID journal BIO-Complexity in 2011. Though I read it shortly after it was published (and I recall finding it unsatisfactory, even then) I did not remember it when writing that last post. This was indeed a mistake—I should have at least mentioned it, or better still addressed its claims. Failing to do so led to the Discovery Institute—the leading ID organization of which Meyer is a key member—calling me out for “recycling arguments refuted years ago”. Well, if nothing else, it made for a good headline I suppose. And yes, I have been using these arguments against Meyer’s position for several years—since in my view, they remain as valid now as they did in 2010 when I first raised them. So, they are “recycled” in that sense. But have Meyer and Nelson truly “refuted” the evidence for chemical interactions between amino acids and codons or anticodons? No, they have not—but it will take some effort to understand why. Since this claim is so important for the ID movement, it’s worth the effort to understand the science, as well as the inadequacy of the ID interpretation of it.
What’s at stake?
The ID movement in general, and Meyer in particular, has staked quite a lot on the assertion that the genetic code is a “genuine code”, in the sense that it represents arbitrary assignments of amino acids to codons. Because of this, advances in research that bear on this assertion are problematic for ID. If science eventually demonstrates a plausible mechanism for the natural origins of the genetic code, ID will lose a major argument of key apologetic importance. As such, it’s not surprising to see science in this area vigorously contested by the ID movement. For them, the genetic code is a code, and codes only come from intelligent coders, as it were.
As a kid, I used to be fond of making my own secret codes by drawing up a table of correspondences between symbols of my choosing and letters of the alphabet. Assigning correspondences between pairs of symbols and letters was of course arbitrary—there was nothing about the symbols and letters that chose themselves. In order to decode messages, the table was necessary, since it could not be worked out from examining the code itself. Meyer sees the genetic code in exactly this way—as a list of amino acids corresponding to certain codons, where in principle any amino acid could be assigned to any codon in an arbitrary fashion. For Meyer, calling the “genetic code” a code is not merely using an analogy to human-designed codes: he sees it as a genuine, symbolic code directly constructed by an agent rather than by a natural process. This thesis forms a major tenet of his 2009 book, Signature in the Cell.
As we have seen in Signature, Meyer claimed in support of his view that chemical interactions between amino acids and codons had never been found. If such interactions were known, so his argument goes, then there might be a case for some sort of natural, chemical process that led to the present-day genetic code. Since no interactions were known, Meyer claimed, there was no support for a natural process that could have formed the code. As such, he argued, the lack of a natural explanation for the genetic code shows that it was directly fashioned by an intelligent agent.
Meyer and Nelson respond to Yarus
In their paper disputing the evidence for amino acid binding, Meyer and Nelson make a series of claims about the work of Yarus and colleagues (who, as we have seen, are a major research group working on the direct templating hypothesis). Meyer and Nelson list their arguments as follows:
- Yarus et al.’s methods of selecting amino-acid-binding RNA sequences ignored aptamers that did not contain the sought-after codons or anticodons, biasing their statistical model in favor of the desired results.
- The DRT model Yarus et al. seek to prove is fundamentally flawed, since it would demonstrate a chemical attraction between amino acids and codons that does not form the basis of the modern code.
- The reported results exhibited a 79% failure rate, casting doubt on the legitimacy of the “correct” results.
- Having persuaded themselves that they explained far more than they actually had, Yarus et al. then simply assumed a naturalistic chemical origin for various complex biochemicals, even though there is no evidence at present for such abiotic pathways.
To summarize, Meyer and Nelson assert there is no need to abandon the claim made in Signature that the genetic code has no natural explanation (and thus, is the direct creation of a designer) for several reasons: the work of Yarus and colleagues is poorly done, and in reality does not show evidence of binding; amino acid binding is not a feature of the modern code, so these proposed mechanisms would not explain the origin of the code in any case; the results have a high rate of failure, so even the claimed positive results are suspect; and Yarus and colleagues do not account for other unexplained problems for hypotheses of abiogenesis in general.
Let’s examine these arguments in detail, starting with the first and third claims.
The first claim seeks to explain away the observed binding of amino acids to their codons or anticodons on short lengths of RNA (aptamers) as merely statistical artifacts of how Yarus and colleagues conducted their experiments. Meyer and Nelson liken the experimental design to fishing with a net, throwing back fish that are not wanted, and then declaring that almost only “wanted” fish were caught in the first place.
This shows a misunderstanding of how Yarus and colleagues actually did their experiments. Sy Garte (who has written for BioLogos and is a biochemist) was quick to point this out to Nelson in the comment thread for the previous post in this series. Yarus and colleagues did indeed examine RNA sequences that did not bind to specific amino acids. As Garte wrote in response to Nelson:
Actually, Yarus in many of his papers, did exactly what you are asking of him here. As one example from his 2003 paper that I linked in my previous comment, he writes: "Of the remaining isolates sequenced, only one other repetitively isolated motif was prevalent, representing 18% of clones. Although it contained a possibly interesting conserved AUAUAUA sequence, this second isolate showed little specificity, having apparently similar affinity for isoleucine, alanine, valine, and methylamine." Note this second isolate (with no useful specificity) is also based on the ILE codon. In other words, he did look at other enriched sequences, and further evaluated them. He frequently admits that his technique isolates RNAs that are unrelated to amino acid-specific codons or anticodons.
As Garte rightly points out, the experiments that Yarus and colleagues have performed over the years have reported a number of RNA sequences that bind amino acids nonspecifically, or that bind amino acids without containing the codon or anticodon for that amino acid. So, contra to Meyer and Nelson’s claim, Yarus and colleagues did indeed examine a wide variety of RNA sequences that interact with amino acids. Meyer and Nelson are simply incorrect on this point—and as we will see in an upcoming post, these binding affinities have been confirmed by researchers in other groups, increasing our confidence that they are genuine, and not statistical artifacts arising out of biased, sloppy research.
Secondly, the binding results that Yarus and colleagues report are not based on trying to find “desired results” as Meyer and Nelson claim. The Yarus research group is interested in genuinely discovering what amino acids bind to their codons (or anticodons), and which do not. In fact, they fully expect that there are some amino acids which will not exhibit this sort of binding. They also expect that amino acids that do bind one of their codons (or anticodons) will not bind all of their possible codons or anticodons. Recall that the genetic code is partially redundant—most amino acids can be coded for by several codons. Rather, they expect that even the amino acids that were added to the code by chemical binding would later also “pick up” additional codons that they do not bind to. In other words, the direct templating hypothesis is not expected to explain the origin of the entire code, but only a more ancient subset within the current code. That the current code has a subset within it that exhibits specific binding affinities between amino acids and codons (or anticodons) is strong evidence that the current code passed through a stage where these affinities were important. As such, Meyer’s claim that the code is entirely arbitrary, and thus “designed”, fails. The genetic code is not like my childhood codes - some of the “symbols and letters” in the genetic code did seem to “pick themselves” - they paired together because they are chemically attracted to each other.
The idea that direct templating does not purport to explain the origins of the entire code is a point that Meyer and Nelson do not seem to understand. This is most obvious in their third objection in the list above, that "the reported results exhibited a 79% failure rate, casting doubt on the legitimacy of the ‘correct’ results.” In order to understand why Meyer and Nelson are mistaken, we need to understand where the “79%” figure comes from.
The work of the Yarus lab, summarized and discussed in their 2009 paper (PDF), examined eight amino acids (of the 20 found in the present-day code) for evidence of binding to their codons or anticodons. Their data reveal that six amino acids show strong evidence of binding to one or more of their codons or anticodons. These six amino acids, however, only show evidence for binding for a subset of their codons or anticodons (Table 1):
Table 1. Yarus et al., 2009 report that six amino acids show evidence of binding to their codons or anticodons. Glutamine and leucine showed no significant interactions in this study. Of the 24 possible codons (and their corresponding 24 possible anticodons) 79% show no evidence of binding.
Due to the redundancy of the genetic code, these eight amino acids have between them 24 possible codons, and thus 24 possible corresponding anticodons. For example, arginine can be coded for by six different codons (with six corresponding anticodons) in the modern code, but only three of those 12 possible sequences show evidence of binding to arginine directly. Thus, for these eight amino acids there are 48 possible sequences that may have shown binding to their amino acid. As you can see from the table, only 10 of the 48 show significant binding—or roughly 21%. That means that 79% of the possible codon or anticodon sequences do not show binding for this sample of eight amino acids. This is what Meyer and Nelson report as the “failure rate” for these experiments. But this is only a “failure rate” if one somehow expects that all 48 sequences should be shown to bind—and it would seem that Meyer and Nelson have exactly this expectation. But this is emphatically not what the direct templating model expects or predicts. Rather, as we have seen, the expectation is that only a subset of the code was established through chemical binding, and that later on other amino acids, codons and anticodons were added to the code. Whether they understand it or not, Meyer and Nelson are refuting a straw-man version of the direct templating model.
Moreover, the claim that the high “failure rate” casts doubt on the veracity of the bindings that were observed is puzzling. If Yarus and colleagues had reported binding affinities for all 24 codons and all 24 anticodons, that would be good reason to suspect that their experimental design was not able to distinguish between real binding and spurious binding. The fact that they observe differences—highly significant binding for some sequences, but not for others—indicates that their experimental design can in principle distinguish between binding and non-binding. So, far from being a problem for Yarus and colleagues—as Meyer and Nelson present it—this is evidence that their experimental design is appropriate and working correctly.
In the next post in this series, we’ll look at more problems with Meyer and Nelson’s response: how the work of Yarus and colleagues is profitably informing the research of other groups, and leading to new discoveries that bear on the direct templating hypothesis.