14 February 2010

Signature in the Cell: Chapters 4 and 5 - errors and problems

Meyer's basic idea in chapters 4 and 5 is reasonably coherent. But I find further evidence in both chapters that Meyer is careless and underinformed on the subjects he addresses. (I explained before why I think this matters. If you think I'm not being nice enough to Meyer, consider providing me with the Rules of Engagement that apply when criticizing culture warriors who are proposing world-shifting new ideas.)

1. A bizarre paragraph in chapter 4 makes me wonder if Steve Meyer is terribly confused about bacterial transformation. On page 104, he writes:
Oswald Avery correctly determined it was DNA, not bacteria living or dead, that caused the mice to die. But when scientists established that DNA directs protein synthesis, Avery's results were viewed in a new light. DNA caused the mice to die, all right, but it did so by directing the production of proteins that were toxic to the mice (though, obviously, not to the bacteria from which the DNA was derived).
This is really strange talk. What Griffith had established was that one strain of bacteria could be converted – transformed – into another strain through direct contact. What Avery and colleagues showed was that DNA was the chemical agent that could transform bacteria. It was, in fact, living bacteria that killed the mice, and the key difference was not a toxic protein – it was a sugar-based coat called a capsule. I wonder if Meyer, portrayed as an eminent philosopher and historian of science, has actually read the work of Avery et al. If he had, he would know that those scientists wrote this on page 140 of their historic 1944 paper:
Transformation of types has never been observed to occur spontaneously and has been induced experimentally only by the special techniques outlined earlier in this paper. Under these conditions, the enzymatic synthesis of a chemically and immunologically different capsular polysaccharide is specifically oriented and selectively determined by the specific type of S cells used as source of the transforming agent.
Translation: we can induce one strain to transform into another, and we know that this occurs when a certain enzyme (a protein) creates a certain sugar-based capsule in the transformed strain. The enzyme appears when cells are exposed to the "transforming agent." And of course Avery et al. identified that transforming agent as DNA.

2. Meyer attempts to construct an analogy between CAD-CAM and protein synthesis on pages 120-121. It's a failure, because there's little analogy between the two processes, and Meyer wisely abandons the analogy after that. The main purpose seems to be a plug for Expelled and a pointer to free animations at the Signature in the Cell website.

3. On pages 125-126, Meyer briefly discusses introns and RNA splicing. In that paragraph, he does immense damage to his credibility as a scientific thinker or even commentator. There are two errors in the paragraph. One is merely embarrassing. The other is devastating. On page 126, Meyer writes this about the process of RNA splicing:
This process requires the existence of other specific enzymes – exonucleases, endonucleases, and splicesomes, for example – that can correctly identify and excise the nonprotein coding text from the initial RNA transcript and then splice together the resulting fragments of coding text in the correct order.
This statement shows that Meyer did not understand the two pages in Lodish's Molecular Cell Biology textbook that he cites there. RNA splicing is accomplished by a huge multi-part molecular machine called the spliceosome, which is made mostly of RNA and is not known to include either exonucleases or endonucleases. Meyer did mention the spliceosome, but spelled it wrong. (He got it right in the one other place he mentions splicing.) Did he not consider having a real biologist look at this book at some point before it was published? (I've seen the acknowledgements, and the answer appears to be "no" but I don't know all the folks mentioned there.) But the real mistake is on page 125:
...the original DNA text in eukaryotic organisms has long sections of text called "introns" that do not (typically) encode proteins. Although these introns were once thought to be nonfunctional "junk DNA," they are now known to play many important functional roles in the cell.
This is the discredited creationist "junk DNA" ploy. It signals the presence of some combination of ignorance, sloth, and duplicity. I've written elsewhere about the layers of dishonesty in the this ploy, and was hopeful that Meyer would either avoid using the tactic or would at least attempt to tell the truth about non-coding DNA. Here's a short explanation for why Meyer's statement is ludicrous.

The human genome contains at least 190,000 introns (though it's been recently estimated to contain almost 210,000). Together those introns comprise almost 1/4 of the human genome. One fourth. That's 768 million base pairs. And biologists have identified "important functional roles" for a handful of them. How many? Oh, probably a dozen, but let's be really generous. Let's say that a hundred introns in the human genome are known to have "important functional roles." Oh fine, let's make it a thousand. Well, guys, that leaves at least 189,000 introns without function, and gosh, they're snipped out of the transcripts and discarded before the darn things even leave the nucleus. We might return to this topic, since it's interesting and there are more layers of duplicity in the "junk DNA" fairy tale that Meyer has included in his book. But Meyer has done significant damage to his credibility by including it. In my view, he showed his cards. It looks to me like this isn't a book about science. It's a book using science to advance an agenda, and rigorous scientific truth-telling is secondary to that goal.


Hal said...

Might I suggest that the biologist who Meyer got to look through his book and to provide him with details was Jonathan Wells?

On junk DNA, it would seem that this recent article by Fuz Rana is more of the same.


The writings of ID advocates in these areas seem to be essentially indistinguishable from those at RTB, AIG, or ICR. Even Richard Sternberg, who Meyer hailed as a "genomics expert," made these arguments in their recent debate with Prothero and Shermer. He claimed "so-called pseudogenes" have important functions, as do ERVs, and Meyer said that "junk DNA is species specific" (whatever that means) and so is evidence against common descent.

Arthur Hunt said...

Hi Stephen,

To be as fair as possible, a central part of the spliceosome is an endonuclease of a sort - an enzyme (composed of RNA) that breaks the RNA chain so as to permit the removal of the intron.

And while I am sure that Meyer is unaware, the processing of ribosomal RNAs does involve exonucleases as well as endonucleases. Not that mixing up the different processing systems can restore any credibility to Meyer, but ...

Bill said...

Of course Meyer's book is written to advance his agenda. He may be an IDiot, but he's not an idiot. Nor is he woefully nor willfully ignorant. Meyer knows exactly what he's doing.

Consider what's failed for creationists: 2nd law of thermo., irreducible complexity, the explanatory filter, the "edge" of evolution. Nothing's working for them.

Now, they've latched on to something pretty obscure out of electrical engineering of all things: information theory. Unfortunately, that's not working out any better as they get messed up between Shannon and Kolmogorov definitions that apply to different things.

Specified information? Please! Why not just call it beautiful and really beautiful because, obviously, merely beautiful isn't good enough? Either way Meyer is trapped in subjectivity, and his thesis fails.

Whatever Meyer writes it's clear he started with the conclusion, the signature in the cell, and worked backwards to find support however tenuous. He's very careful to write and slant his writing only to things that support his conclusion. That's why it appears so much is missing and why there are so many errors. His target audience will neither care nor understand.

Ten years from now Meyer will still be touting "junk DNA" just as Behe touts "mousetrap."

Thank you for this continuing review. You're doing yeoman's work for the rest of us!

David said...

Hi Steve-
This series of posts has been quite amusing and enlightening, having not paid much attention to ID and creationism until recently. I haven't read SitC, but I've skimmed the parts available on amazon. A few things stood out in chapter 5:

To add to the list of errors-
On page 128, Meyer refers to a "protein within the ribosome known as a peptidyl transferase" performing the actual peptide bond formation reaction. Of course, this is a mistake, avoiding one of the key pieces of evidence for the RNA world: that the peptidyl transferase center of the ribosome is composed entirely of RNA- the ribosome is a ribozyme. It's not like this is a little known fact, it's one of the first major discoveries to come from the structure of the ribosome, which earned the Nobel Prize in Chemistry last year. It's hard to believe Meyer managed to miss it.

Considering one of Meyer's main points is the chicken/egg problem of translation, you think he might spend at least a little time discussing this point. As far as I can tell, Meyer never explicitly deals with it. The closest he comes is mentioning in the RNA world chapter (pg 304) that rRNA "promotes" peptide bond formation, citing very early biochemical work by Harry Noller from 1992 (long before the ribosome structure). Noller's biochemical work was critical early evidence for the role of RNA in the ribosome, but it was the structure that confirmed it. Meyer makes it sound like RNA is some cofactor, a claim that, prior to the structure, would still be something of a stretch, but was completely invalidated when the structure showed that RNA forms the entire PT active site.

And of course there are countless other problems. One other one that stood out-only a few pages after the peptidyl transferase protein, he claims the aminoacyl synthetases (aaRSs-the proteins that charge tRNAs with their cognate amino acids) all have distinct shapes. Although in some sense their active sites will differ to accommodate the different amino acids, all tRNAs share one of two common structures. There's a ton of work on tracing the evolutionary history of existing aaRS, suggesting they all descended from 2 common ancestor protein folds. Again, no discussion of this anywhere in the book as far as I can tell, just the assertion that all 20 had to emerge at once for translation to work.

Overall, my impression seems to be that Meyer has skimmed the literature, picked out points he has canned responses to, and ignored or managed to remain ignorant of vast swaths of other evidence.

Martin LaBar said...

Thanks for the series, again.

Gordon J. Glover said...

"Meyer attempts to construct an analogy between CAD-CAM and protein synthesis on pages 120-121. It's a failure, because there's little analogy between the two processes... "

This is so true. When I design a mechanical part to be fabricated, I can take my CAD output and export a data file that a CNC (computer numerical control) lathe or mill can read and translate into a part. Or I can export the model in a stereo-lithography file and have the part "printed" on an RP (rapid prototype) machine.

But in either case, if the data become corrupted, the process is terminated. Why? Because of the way the information is translated between formats, read, and interpreted, corrupt data necessarily become nonsensical during the process - which faults the sequence.

Now, if a corrupt data file cuased two features to be machined where I had only designed one, or if it swaped one feature with another or slightly modified a feature, then you would have something akin to protein synthesis. But as it stands now, CAD-CAM is absolutly nothing like DNA translation.

And like you, as soon as I ready the part about "junk DNA" I lost all interest in the book. And I was honestly enjoying it up to that point.

Bilbo said...

Hi Prof. Matheson,

You've got Mike Gene's attention:


Dan said...

WRT alternative splicing, it should be noted that a substantial percentage (at least 60%) of human genes are the result of intron fcnality in alternative splicing. (Molecular Cell Biology Sixth Edition pg. 126)

Multidomain protiens, for one example, are typical products of this process that play important roles in celluar function and many human disease are the result of mutations wrt to splice site selection. Molecular Cell Biology Sixth Edition pg. 126, pg. 334)