While my chapter in Signature of Controversy responding to Stephen Matheson’s review of Signature in the Cell deals with a variety of issues, I’d like to boil it down to two or three which I feel are the most important topics. Why are they the most important? Because it’s on these topics that Matheson engages in the most name-calling, and where Matheson also happens to be the most wrong. (Is there a reason why evolutionists so often increase the ad hominem attacks when their case is weak?) With that, here’s a condensed and abridged version of my response to Matheson:
What would you get if you crossed a snarky pro-evolution blog like Panda’s Thumb with a passionate defender of theistic evolution? You might get the critique of Stephen Meyer’s book Signature in the Cell (SITC) written by biology professor Steve Matheson of Calvin College. On his personal blog, Matheson has been reviewing SITC chapter by chapter, mixing frequent personal attacks on Meyer with exposés of occasional typos and the possible discovery of one minor error. That is not a bad track record for Meyer, considering that at the writing of this response, Matheson has reviewed nearly half the book.
Matheson is noteworthy because he at least gives every indication that he’s reading Signature in the Cell before attacking its author. It would have been preferable for Matheson to have read the book entirely before rendering judgment. But when it comes to many other critics of Signature in the Cell on the internet, this is progress.
Unfortunately, Matheson feels it necessary not just to critique SITC but to attack Meyer personally. Matheson smears the book as “not a serious work of scholarship,” not “serious science,” “awfully bloated,” potentially “a joke,” “disingenuous,” “sad,” “pathetic,” and “fluffy and vacuous, simplistic at best and not infrequently wrong or misleading.” In case you didn’t get the point, Matheson accuses Meyer of “some combination of ignorance, sloth, and duplicity,” using tactics that require “layers of dishonesty” that are “sufficient to justify a charge of deliberate dishonesty.”
In Chapters 4 and 5, Matheson thinks he finds multiple mistakes which he calls “embarrassing,” and “devastating,”perhaps even implying “dishonesty.” But close analysis shows he only finds one potential error — a minor one that in no way affects Meyer’s overall argument.
Matheson faults Meyer’s description of an experiment where Meyer wrote that mice died due to “proteins that were toxic” (p. 104), when in reality DNA transferred into the bacteria produced an enzyme that gave the bacteria a polysaccharide coating. This didn’t itself kill the mice, but rather prevented the mouse immune system from being able to detect and destroy the bacteria.
While Meyer could have made that point clearer, it was ultimately toxic proteins from the bacteria that killed the mice–most likely pneumolysin.38 So it’s not clear that Meyer was actually in error, although he could have clarified that the transferred DNA didn’t produce the toxic protein but rather merely enabled bacteria to evade the mouse immune system. But the mice still died, just as
Meyer says, due to “proteins that were toxic.”
Matheson goes on to obsess about another typo: Meyer’s misspelling of “spliceosome” as “splicesome” on one page of his book (the term is spelled correctly on two other pages). How this typo undercuts Meyer’s credibility is anybody’s guess, especially since PubMed reveals well over a dozen papers with the “splicesome” spelling in various science journals.39 For that matter, if perfect copy-editing is to be the test of scientific rigor, Matheson himself should watch out: There are typos on his own blog (in one instance he forgot to insert an “o” into the name of Dr. Russell “Dolittle,” much as Meyer forgot an “o” in “spliceosome”).
Matheson also faults Meyer for claiming that RNA splicing is accomplished using not just the spliceosome but also exonucleases and endonucleases. Matheson writes that Meyer is wrong because the spliceosome “is not known to include either exonucleases or endonucleases.” But Matheson didn’t read Meyer correctly. Meyer doesn’t say the spliceosome contains exonucleases or endonucleases. He just says that, along with the spliceosome, they are involved in the process of correctly identifying and excising introns. And in fact, there’s evidence that both endonucleases40 and exonucleases41 can be involved in the splicing process.
Since Matheson is so fastidious about scientific accuracy when it comes to the spliceosome, one should point out his own overstated claim that the spliceosome “is made mostly of RNA.” According to a 2009 paper in PNAS, “[t]he spliceosome is a massive assembly of 5 RNAs and many proteins”42–another paper suggests “300 distinct proteins”!43 So it seems the spliceosome is certainly made of RNA, but is not necessarily “made mostly of RNA.”
Arguably Matheson’s most vitriolic attacks on Meyer’s book come during his discussion of ” junk DNA,” a discussion that is out of date. In SITC Meyer writes that “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.” (p. 125) For making this argument, Matheson accuses Meyer of “some combination of ignorance, sloth, and duplicity” and “layers of dishonesty,” alleging, “This is the discredited creationist ‘ junk DNA’ ploy.”
Discredited? In 2003 Scientific American addressed a striking rebuke to those who claim introns are genetic junk: “The failure to recognize the importance of introns ‘may well go down as one of the biggest mistakes in the history of molecular biology.'”44
Matheson’s retort is that functions have been uncovered for only a “handful” of introns. But recent data shows evidence of mass functionality. An April 1, 2010, article in Nature reported that “Biology’s new glimpse at a universe of non-coding DNA–what used to be called ‘ junk’ DNA–has been fascinating and befuddling. Researchers from… ENCODE showed that in a selected portion of the genome containing just a few per cent of protein-coding sequence, between 74% and 93% of DNA was transcribed into RNA.”45 A variety of papers indicate that huge portions of DNA is being transcribed, hinting at function.46 Indeed, introns can affect gene expression even when they’re not transcribed.47 If Matheson ever finishes reading SITC, he’ll find a long list of functions discovered for non-coding DNA, citing over 45 papers from the mainstream scientific literature (p. 407). Even the journal Science stated that the ” junk DNA” mindset has “repelled mainstream researchers from studying noncoding DNA,”48 refuting Matheson’s claims to the contrary elsewhere.49
Are all these scientists part of a nefarious plot to promote, as Matheson calls it, a “discredited creationist ‘ junk DNA’ ploy”?
Matheson’s discussion of chapters 9 and 10 begins with another tedious parade of slurs: He claims the chapters “advance a straw man so idiotic that I wonder whether Meyer will be able to reclaim any significant intellectual integrity in the chapters that follow.” He charges Meyer with having “purely propagandistic aims,” which “do serious damage to the book’s credibility and to the author’s reputation.”
What disreputable blunder did Meyer make this time? Turns out Meyer’s crime is observing that some theorists attributed the origin of life to “chance,” a hypothesis Matheson doubts was ever actually put forth. You read that right.
Of course Meyer cites multiple authorities from the origin of life research community–giants such as Francis Crick or George Wald (see p. 195)–advancing the hypothesis that life arose by “chance” or “accident.” But this isn’t enough to convince Matheson. I’m sure that theorist David Deamer’s suggestion that “genetic information more or less came out of nowhere by chance assemblages of short polymers”50 wouldn’t convince Matheson either. How about the more charitable reader?
Had Meyer stopped SITC at chapter 10 then perhaps Matheson could say Meyer advocates a “straw man.” But these chapters are by no means Meyer’s entire argument. Meyer’s rhetorical structure is to first assess the “chance” hypothesis–but he fully acknowledges that there are more sophisticated theories to be dealt with later in the book which use various combinations of chance and law, including natural selection. Meyer thus writes at the close of chapter 10:
Some theorists, notably those proposing an initial “RNA world,” have sought to retain a role for chance by suggesting that natural selection might have played a key role in the origin of life, even before the origin of a fully functioning cell. They propose combining chance with natural selection (or other lawlike processes) as a way of explaining how the first cell arose. In doing so, they argue that random processes would have had to produce much less biological information by chance alone. Once a self-replicating molecule or a small system of molecules had arisen, natural selection would “kick in” to help produce the additional necessary information. In Chapter 14, I evaluate theories that have adopted this strategy. (pp. 227-228)
Meyer by no means leaves his readers hanging with the impression that materialists must believe an entire living cell appeared all-at-once by “chance,” directly negating Matheson’s criticism.
Matheson opens his review of chapters 9 and 10 by defining “straw man,” claiming that this is what Meyer puts forth. Like a judge who issues a verdict after only reviewing half the evidence, Matheson is prematurely accusing Meyer of misrepresenting origin of life thinking. What’s ironic is that by accusing Meyer of creating a straw man and ignoring SITC‘s much more comprehensive argument, it’s Matheson who is promoting the straw man.
Is this really the best critique possible from someone who is actually reading SITC?
[38.] See J. B. Rubins et al., “Distinct roles for pneumolysin’s cytotoxic and complement activities in the pathogenesis of pneumococcal pneumonia,” American Journal of Respiratory and Critical Care Medicine, Vol. 153(4):1339-1346 (April, 1996) or Pneumolysin entry at: http://www.uniprot.org/uniprot/P0C2J9
[39.] For some examples, see M. Hieda et al., “Nuclear Import of the U1A Splicesome Protein Is Mediated by Importin α/β and Ran in Living Mammalian Cells,” The Journal of Biological Chemistry, Vol. 276:16824-16832 (2001); Kristy B. Lidie & Frances M. Van Dolah, “Spliced Leader RNA-Mediated trans-Splicing in a Dinoflagellate, Karenia brevis,” Journal of Eukaryotic Microbiology, Vol. 54(5):427-435 (2007); Leo Lester, Andrew Meade, and Mark Pagel, “The slow road to the eukaryotic genome,” BioEssays, Vol. 28(1):57-64 (2005).
[40.] See Song Xue, Kate Calvin, Hong Li, “RNA Recognition and Cleavage by a Splicing Endonuclease,” Science, Vol. 312(5775):906-910 (May 12, 2006).
[41.] See Jonathan P Staley and John L Woolford Jr, “Assembly of ribosomes and spliceosomes: complex ribonucleoprotein machines,” Current Opinion in Cell Biology, Vol. 21(1):109–118 (February, 2009).
[42.] Samuel E. Butcher, “The spliceosome as ribozyme hypothesis takes a second step,” Proceedings of the U.S. National Academy of Sciences, Vol. 106(30):12211–12212 (July 28, 2009).
[43.] Timothy W. Nilsen, “The spliceosome: the most complex macromolecular machine in the cell?,” BioEssays, Vol. 25:1147–1149 (2003).
[44.] Wayt T. Gibbs, “The Unseen Genome: Gems among the Junk,” Scientific American (Nov., 2003).
[45.] Erika Check Hayden, “Life Is Complicated,” Nature, Vol. 464:664-667 (April 1, 2010).
[46.] See John S. Mattick & Igor V. Makunin, “Non-coding RNA,” Human Molecular Genetics, Vol. 15: R17–R29 (2006); Shao-Yao Ying, Donald C. Chang & Shi-Lung Lin, “MicroRNA (miRNA): Overview of the RNA Genes that Modulate Gene Function,” Molecular Biotechnology, Vol. 38:257-268 (2008); Marcel E. Dinger, Paulo P. Amaral, Timothy R. Mercer & John S. Mattick, “Pervasive transcription of the eukaryotic genome: functional indices and conceptual implications,” Briefings in Functional Genomics and Proteomics, Vol. 8: 407-423 (2009); Aristotelis Tsirigos & Isidore Rigoutsos, “Alu and B1 Repeats Have Been Selectively Retained in the Upstream and Intronic Regions of Genes of Specific Functional Classes,” Vol. 5(12):e1000610 (December 2009); Rodrigo Louro, Anna S. Smirnova & Sergio Verjovski-Almeida, “Long intronic noncoding RNA transcription: Expression noise or expression choice?, Genomics, Vol. 93: 291-298 (2009); Noam Shomron & Carmit Levy, “MicroRNA-Biogenesis and Pre-mRNA Splicing Crosstalk,” Journal of Biomedicine and Biotechnology, Vol. 2009: 594678 (2009).
[47.] Ian A. Swinburne & Pamela A. Silver, “Intron Delays and Transcriptional Timing during Development,” Developmental Cell, Vol. 14: 324- 330 (2008).
[48.] See Wojciech Makalowski, “Not Junk After All,” Science, Vol. 300(5623) (May 23, 2003).
[49.] See Talking trash about “junk DNA”: lies about “function” (part I). For a further rebuttal to Matheson, see also Cornelius Hunter’s blog, “Stephen Matheson: Talking Trash About Junk DNA,” (October 3, 2009). (Matheson responds to Hunter merely by calling him “a poorly-equipped ID demagogue.”)
[50.] David Deamer, quoted in Susan Mazur, The Altenberg 16: An Expose of the Evolution Industry, p. 180 (Scoop Media, 2009).