Of Hens Teeth and IDiots.

The literature published by the Discovery Institute often confuses me. I'm never quite sure if it should frustrate me or amuse me. Their constant mangling of science combined with their propensity for telling half-truths and distorting reality both makes me laugh (hah! They really think they have science on their side?) and makes me embittered (How dare they twist science to deceive and miseducate?). I guess this recent article by Discovery Institute crony Casey Luskin should be of no surprise, then. In the piece, titled Of Hen's Teeth and Neutral Mutations, Luskin attempts to dismantle a claim made by Stephen Jay Gould about hen's teeth (or the lack thereof):

"Evolutionists often cite an experiment which purportedly induced tooth growth in chickens, supposedly confirming that birds have genes for teeth and are descended from toothed reptilian ancestors. For example, in his book Hen's Teeth and Horse's Toes, Stephen Jay Gould discusses this experiment...But there's a problem with Gould's argument: as Sean Carroll explains, neo-Darwinism has a 'use-it-or-lose-it' rule. According to neo-Darwinism, if a trait is not used then the DNA which encodes it will accumulate neutral mutations, and eventually the trait will be lost forever. If supposed chicken genes for producing teeth haven't been used for 60+ million years, then that would strongly suggest that neutral mutations should have long-since destroyed their ability to function."

For those of you who might be unfamiliar with the experiment in question - and with Gould's discussion of it - it would be worth the while to go into detail.  In 1980, Gould published the book Hen's Teeth and Horse's Toes, a collection of articles he had written for various magazines (primarily for Natural History). Included was an article of the same name where he discussed atavisms - apparent reversions in individuals to an ancestral phenotype. Gould claimed that atavisms are a shining example of the evolutionary past of a species coming to the surface. He illustrated his point with two examples: polydactyl horses and chickens with teeth. It is this second example towards which Luskin has aimed his bow and launched forth a volley of ignorance.

On p.182¹, Gould explains a curious experiment performed by E.J. Kollar and C. Fisher: they devised a way to prompt chickens to develop teeth. If it's been a while since you took a good look in the mouth of your local avian friends, then it might interest you to know that birds don't have teeth. The most recent known fossil of toothed birds dates to around 80 million years ago, so somewhere in the intervening time, birds lost the ability to produce teeth. Odontogenesis in vertebrates is a complex process (then again, developmental programs always are!). It requires two different tissue types to occur: epithelial tissue and mesenchyme. The outer enamel layer of a tooth is formed by the epithelial tissue, while the inside dentin later of your tooth grows from the mesenchyme. But there's a catch: the mesenchyme cannot produce dentin by itself, it needs to be in contact with epithelium for dentin production to begin - that is to say, epithelium induces the production of dentin. This dentin, in turn, induces the production of enamel in the epithelium. Birds don't produce dentin, nor, consequently, enamel, so birds are born toothless. Kollar and Fisher's idea was brilliant but simple: what happens if you graft chick epithelium with murine (mouse) mesenchyne? Mice most definitely have teeth, so we know their mesenchyne is capable for producing dentin if prompted by epithelial tissue. What they found was astounding: when mouse mesenchyne was grafted to chick epithelium, teeth (dentin and all) were produced. This meant that avian epithelial tissue - despite the fact that birds have no teeth, and have not had teeth for as long as 80 million years - is still able to induce dentin production in the appropriate mesenchyne. Gould mused that this experimental result displayed the evolutionary history of birds. Why else would avian epithelial tissue have the latent ability to induce dentin production unless they had descended from toothed ancestors?

Luskin, however, thinks that Gould was completely wrong. Luskin argues that, if birds lost the ability to produce teeth 80 million years ago, then the genes for tooth production would have accumulated so many mutations that it would be impossible to revert back to the original toothed phenotype. The tooth production genes, he claims, would have since been destroyed beyond the ability to function. He bases this argument in something called Dollo's Law. Dollo's Law, put simply, states that evolution cannot reverse itself, and that genes which escape selection pressure will degrade fast enough that reverting to the original phenotype is tantamount to impossible. According to Luskin, the example of toothed hens is not the resurrection of a lost developmental pathway but the result of an experimental mistake.

Luskin cites a paper from Marshall, Raff and Raff² that seemingly supports his argument. In the paper, the authors devise an equation that determines the probability of a silenced gene's reversion as a function of time passed. They concluded that, for a gene that has been silenced for 10 million years, there is a near-zero probability for reactivation. How do they account for Kollar and Fisher's results? They state that "the classic example of the resurrection of "hen's teeth" is most likely an experimental artifact". Well, that settles it, right?

Well, no. Marshall, Raff and Raff's paper was published in 1994, and despite what Luskin might think, science has progressed in the two decades since. Perhaps if he had read through more recent literature he would have realized some problems with his argument and with Marshall et al's conclusion.

First, let's tackle the "experimental artifact" claim. When Kollar and Fisher's original paper was published, there was some skepticism about their results. There was controversy over whether or not the mouse mesenchyne they used was contaminated with mouse epithelial tissue. If this was the case, then their results would be invalid: it would be impossible to tell whether or not the formation of dentin was prompted by the chick epithelium or the mouse epithelium. Despite the experiment being repeated by other researchers, the possibility of contamination meant that many people wrote off their result as an "experimental artifact". This debate was put to rest, however, by an paper published by Cai et al in 2009³. In their paper, the team repeated the tissue graft experiment using mesenchyne from transgenic mice expressing the LacZ gene (LacZ is used in molecular biology as a reporter gene, because it produces a dark blue pigment when supplied the proper substrate). Like Kollar and Fisher, Cai et al's results showed the induction of dentin by chick epithelium. To prove that there was no contamination by mouse epithelium, they took cross sections of the graft and stained them. The transgenic mouse tissue, expressing the LacZ gene, stained a dark blue while the chick tissue remained unstained. What they found was that the entire epidermal tissue remained unstained, while only the mesenchyne stained blue, ruling out the possibility of contamination. Kollar and Fisher's original results, then, are still valid.

So if Kollar and Fisher were correct all along, then don't their findings go against Dollo's Law? Shouldn't the genes for tooth production, being free from selective pressures, have accumulated many mutations that would prevent the pathway from functioning at all? The answer, again, is no. Perhaps if Luskin had read the Marshall et al paper more closely (if, indeed, he had read it at all, since he only quotes the abstract) he would have gotten a hint. The authors mention in their discussion that "[r]eversals of long-lost structures do occur but evidently result from the cooption of genes that continue to survive in other roles". In other words, genes involved in traits no longer expressed can avoid the fate of accumulating mutations if they have other roles in development. The genes for tooth production most certainly fit this description. Work by West et al in 1998⁴ found that many of the genes required for odontogenesis are still expressed in the developing chick embryo, indicating that they still play important roles. BMP4, for example, plays important roles in muscle development and bone development as well as in the development of teeth. Members of the  Hedgehog family of proteins are involved in a whole slew of developmental processes, only one of which is odontogenesis. Toyosawa et al⁵, in 1999, looked at one protein in particular, Dentin Matrix Protein 1, or DMP1. Since birds don't produce dentin, what use would they have for such a gene? Toyosawa et al not only found that birds have this gene but found it was being expressed in the jaws of chickens. The case of hen's teeth escapes Dollo's Law because many of them are not silenced, and many of them have other functions in the developing embryo.

If you think about it, this really should come as no surprise. Dollo's Law describes what happens to single genes that control single phenotypes when they become silenced. Dollow's Law makes no claims about what happens to genes involved in complex developmental pathways. In order for Luskin to be correct, then it would require all the genes in a developmental pathway to have become silenced. Given the interconnected nature of developmental pathways, this simply is not a reality. One or two genes in the pathway may be lost, but the rest remain due to their involvement in other roles. If the missing genes are supplied, then the original, ancestral pathway is reconstructed and the ancestral phenotype is "resurrected". This is precisely what is going on in the example of hen's teeth. The tooth development pathway remains largely intact since many of the genes are involved in other roles. The genes in chick mesenchyne that respond to signals from the epithelial tissue have been lost, which is why birds do not develop teeth. But if you supply these genes in the form of mesenchyne from mice, then the lost pathway is reconstructed and teeth develop. This in no way violates Dollo's Law.

As for Dollo's Law itself, there is mounting evidence that would indicate apparent exceptions to Dollo's Law might be the rule. In the last ten years, many examples of exceptions to Dollo's Law have been noted, including the evolution of  wings in stick insects⁶, the larval stage in salamanders⁷, digit loss in some lizards⁸, egg laying in sand boas⁹, teeth in frogs¹⁰ (which, by the way, have been toothless for 200 million years, more than twice as long as birds), shell coiling in limpets¹¹, and even the re-evolution of sexuality in Oribatid mites¹². As noted by Collin and Miglietta¹³:

"with the growing number of phylogenetic studies showing patterns consistent with re-evolution of characters, and genetic data showing that developmental pathways can be maintained for tens of millions of years, is it time to give up Dollo’s Law? Perhaps."

So what remains of Luskin's argument but smouldering rubble? Kollar and Fisher's experimental results were not due to experimental error, their results don't violate Dollo's Law, and Dollo's Law itself is on shaky ground. Gould was perfectly correct in referring to hen's teeth as an atavism hearkening back to a bygone day of toothed birds.

Once again, an argument put forth by the ID crowd has failed. Are they incapable of delivering a good argument? It sure seems hard to find one that is the least bit compelling. You might even say they're as scarce as hen's teeth.

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1. Stephen Jay Gould . Of Hen's Teeth and Horse's Toes. 1980

2  C. Marshall, E. Raff and R. Raff . Dollo's law and the death and resurrection of genes. Proceedings of the National Academy of Sciences. 1994. 91:12283-12287

3. Cai J, Cho S-W, Ishiyama M, Mikami M, Hosoya A, Kozawa Y, Ohshima H, Jung H-S. Chick tooth induction revisited. 2009. J. Exp. Zool. (Mol. Dev.Evol.) 312B:465–472.

4. Philippa Francis-West, Raj Ladher, Amanda Barlow, Ann Graveson, Signalling interactions during facial development. 1998. Mechanisms of Development. 75(1-2):3-28, DOI: 10.1016/S0925-4773(98)00082-3.

5. Satoru Toyosawa, Akie Sato, Colm O'hUigin, Herbert Tichy and Jan Klein. Expression of the Dentin Matrix Protein 1 Gene in Birds. 1999. Journal of Molecular Evolution. 50(1), 31-38, DOI: 10.1007/s002399910004

6. Whiting MF, Bradler S, and Maxwell T. Loss and recovery of wings in stick insects. Nature. 2003 421(6920):264-7.

7. Chippindale PT, Bonett RM, Baldwin AS, and Wiens JJ. Phylogenetic evidence for a major reversal of life-history evolution in plethodontid salamanders. 2004.  Evolution. 58(12):2809-22.

8. Kohlsdorf T, Wagner GP. Evidence for the reversibility of digit loss: a phylogenetic study of limb evolution in Bachia (Gymnophthalmidae: Squamata). 2006. Evolution. 60(9):1896-912

9.V. Lynch and G. Wagner. Did egg-laying boas break Dollo's Law? Phylogenetic evidence for reversal to oviparity in sand boas. 2010. Evolution. 64(1):207-216

10.Wiens JJ. Re-evolution of lost mandibular teeth in frogs after more than 200 million years, and re-evaluating Dollo's law. 2011 . Evolution. 65(5):1283-96.  doi: 10.1111/j.1558-5646.2011.01221.x

11. Collin R, and Cipriani R. Dollo's law and the re-evolution of shell coiling. 2002. Proceedings of the National Academy of Sciences. 270(1533):2551-5

12. Domes K, Norton RA, Maraun M, and Scheu S. Reevolution of sexuality breaks Dollo's law. 2007 . PNAS . 104(17):7139-44

13. Collin R, and Miglietta MP. Reversing opinions on Dollo's Law. 2008. Trends Ecol Evol. 23(11):602-9

Nephy's Nylonase Nonsense

Oh, Nephilimfree, you've done it again. You went and dragged genetics through the mud again, and I won't stand for it.

At this point, having dedicated a few posts to his inane ramblings, debunking Nephy's claims is beginning to feel like picking on the fat kid at the playground. He's a slow, lumbering target, and all the other kids on the playground keep picking on him because he's easy prey. But Nephy is so ripe with nonsense, so overflowing with vacuous crap like a bountiful cornucopia of bullshit, that it's hard to resist tearing his arguments apart when I'm looking for something to write about. And his silly website [Edit: 06/11/11: Looks like Nephy has let his registration of his domain lapse, so that link doesn't work any more. I tried to find an archived version, but had no luck] has no shortage of fodder for a creationist asskicking.

This week, I took a look at this article he wrote about the enzyme nylonase. You've probably heard about nylonase before, as it is often given as a great example of an evolutionary adaptation that has occurred in recent history. In 1975, a team of researchers from Osaka University in Japan got the idea to try and culture sludge obtained from the waste water outside of nylon factories¹. The samples they collected were used as inocula, and added to cultures which contained a form of nylon (6-aminohexanoic acid cyclic dimer) as the sole carbon and nitrogen source. Any bacteria that grew would have to rely on metabolizing nylon to survive. And grow they did. They designated the strain as KI72, and after isolating the bacteria, they identified it as a strain of Achromobacter guttatus, although later work by the same team reclassified the species as a strain of Flavobacterium². A few years later, the researchers identified two novel enzymes which allow the bacterium to metabolize nylon: 6-aminohexanoic acid cyclic dimer hydrolase and 6-aminohexanoixc linear oligomer hydrolase (6-AHA CDH and 6-AHA LOH, respectively)^3,4. Since nylon production began in the 1930s, these enzymes had to have originated in the time since then. After all, it doesn't make much sense for a bacterium to  have produced enzymes to specifically degrade nylon before nylon itself was invented. These genes, then, represent an example of a novel adaptation arising outside of the lab and within the past century.

But Nephy disagrees. He states, 

"Because the bacteria encountered nylon and developed an ability to digest it does not provide evidence of any kind of evolutionary change. This ability does not effect the form and structure (morphology) of the bacteria by introducing any new structural feature, nor does it transform any existing structural feature of the bacteria into a new kind of structure with a new physiological function."

Two paragraphs in, and he's already run into a major problem. He seems to have this odd idea that unless a change results in gross morphological alterations, it cannot be an evolutionary change. He simply discredits novel biochemical adaptation out of hand without any sort of justification. He simply wishes to define evolution as changes in "form and structure" and ONLY changes in "form and structure" - any other kind of change he refuses to acknowledge as evolutionary change. In essence, he's defining evolution in his own incredibly narrow terms, so that any actual evolutionary change can be shrugged off as "not evolution". If we were to narrowly define creationism as "the spontaneous formation of aardvarks from forest detritus", it would be pretty easy to discredit, too.

But beyond that, it is simply silly to only accept large changes in morphology as the only kind of evolutionary change. Morphological alterations cannot occur all at once. Any modification to an organism's body plan would require many not-so-obvious biochemical changes to occur first - the very type of changes that Nephy does not accept as "evolution". Evolution can only work with what it has available. No organism is going to mutate and grow wings de novo all in one shot, even if it would be advantageous. Such changes would require modifying the existing body plan, and this would require extensive biochemical changes to happen first.

Nevertheless, the discovery of novel nylon-degrading enzymes is indisputable. Musing over the origins of these enzymes, Nephy declares that these proteins, or any protein, could not have simply evolved. No, he says, statistical analysis says otherwise:

"The field of sicence [sic] called Statistical Ananlysis [sic] which is employed to determine probability in various fields of science, has determined that the formation of proteins by random molecular interactions is on the order of 10^950, which is 1 to a number for which no name exists; a number greater than all of the paticles [sic] of matter in the speculated universe. In other words, according to science itself, the chance of a single, medium-sized protien [sic] arising by purely materialistic molecular interactions is considered impossible to science because it is considered impossible times impossible times impossible. The evolutionist would have you believe that random mutation is capable of producing novel protiens [sic] which have specific function, but this is not only unfounded but exceedingly irrational."

This is a typical creationist talking point: whipping out statistics to churn out large numbers and proclaim "See! It's statistically impossible for evolution to occur!"  It is also typical, as Nephy demonstrates quite well, for creationists not to cite the source of these statistical calculations. The problem with Nephy's argument is that he does not take into account the process of selection during evolution. Forming a protein "randomly" and all at once is incredibly unlikely (though not entirely impossible), but if you factor selection into the equation, it becomes an incredibly likely phenomenon. Richard Dawkins illustrates this beautifully in his book The Blind Watchmaker, where he likens evolution to monkeys banging away at typewriters. If you were to wait for a monkey to type out the sentence "Methinks it is like a weasel", you'd be waiting for eons for it to "randomly" happen. But suppose you were to use cumulative selection to pick and keep the letters that work. Dawkins wrote a computer program to do just this (as computer programs are much cheaper and easier to work with than hordes of monkeys). Starting with a string of gibberish and then changing one letter per generation, the computer program "evolved" the correct sentence is about 40 generations⁵. It took only a few minutes for the computer program to complete this task, whereas single-step selection (waiting for the correct sentence to happen randomly, and all at once) would have taken the computer "a million million million million million years"⁶. Obviously, selection gets past the staggering statistical improbability that creationists argue.

But Nephy continues. He tells us that it was discovered that the nylonase genes originated from a frameshift mutation, resulting in an alternate reading frame which produced a novel enzyme⁷. This may be true, but recent work by Negoro et al indicates that the origin of the genes might be due to base substitutions after an ancestral gene duplication⁸. Nephy proceeds to tell us that there are only two ways that such a frameshift can occur: a random mutation or by a "Programmed Translational Frameshift Mutation".

At last, we come to the crux of Nehpy's argument. According to him, random frameshift mutations are invariably bad and the idea of a random frameshift mutation is a cop-out employed by "evolutionists" to ignore the reality of intelligent design. The origin of nylonase must be due to "Programmed Translational Frameshift Mutation", a process, he claims, is divinely inspired..

At this point I feel I should clear something up. Nephy, I hope you're reading. There is no such thing as "Programmed Translational Frameshift Mutation". Programmed Translational Frameshift (PTF) is a very real process, but it is not a mutation. PTF actually describes a variety of complex, but similar, processes. The essence of the idea is this: under normal circumstances, a protein is produced when a ribosome translates a strand of mRNA. Usually, the ribosome translates in a linear fashion, starting at the 5' end of the strand and reading the length of the strand until it comes to a stop codon at the 3' end. But in certain cases, the ribosome can be induced to "skip" or "hop" over a number of nucleotides in the sequence. The result is that the ribosome is shifted out of frame, and the resulting gene product is unlike the original⁹. With PTF, one gene sequence can produce multiple gene products: the original, unshifted, product and the second, shifted, gene product. This process is not a mutation. Mutations are changes to the genetic sequence itself, and such changes do not occur during PTF.

Perhaps Nephy's mistake stems from him being unable to comprehend the scientific literature. In his article, he describes PTF as "the modification of the arrangement of amino acids in a chain caused by information in the DNA which programs the event to occur", which is inaccurate, to say the least. This is further evidenced by the fact that he chooses to illustrate PTF with a diagram of alternative splicing, which is an entirely different process altogether! These errors would indicate that he simply did not understand what PTF is. I get the feeling that Nephy just skims through paper abstracts, pulling out words to form misshapen ideas, rather than taking the time to actually read any scientific papers.

But, regardless of whether or not PTF counts as mutation, Nephy's argument that nylonase originated due to PTF, rather than a simple frameshift mutation, doesn't hold much water. What we know about nylonase - the gene's sequence, how it is regulated, etc - would indicate that PTF is NOT at play here. As mentioned above, PTF occurs when a single transcript is read in two different reading frames, resulting in two different gene products. But in the case of nylonase, there is only ONE reading frame. It is always read by the ribosome in the same fashion. At no point is the ribosome prompted to switch to a new reading frame during translation - a hallmark of PTF. In many cases, this switch is induced by particular sequence elements, but the nylonase gene does not contain any such sequence elements. All evidence points to an ancestral gene that underwent a frameshift mutation that permanently altered it's reading frame, rather than two different and active reading frames from a single sequence. The original frameshift alteration was likely transcriptional in nature rather than translational.

Nephy's claim that random frameshift mutations are always harmful is nonsense as well.  In any case where a mutation is deleterious, creationists are quick to say "See! Random mutations are bad!"; any case where a mutation proves to be beneficial, they shout "That didn't count! That was Intelligent Design!". This amounts to little more than special pleading. Nephy does not see it this way. He states 

"The problem for evolutionists is that we have discovered that random frameshift mutations produce novel proteins which do not have a function in the cell, and when produced in great numbers, are causes of diseases such as Alzheimers and Tay-Sachs."

But how are deleterious mutations and non-functional proteins a problem for evolution? On the contrary, they are a huge problem for Creationists! After all, why would God allow for non-functional proteins to cause deadly conditions? Why would God allow for mutations to begin with? Pretty sloppy work for a Creator who is supposedly "perfect".

Another issue with his argument is how he ascribes PTF as an "intelligent design process". What evidence does he have that PTF is not a naturally occurring process? Why does he call it intelligent design? He gives no reason. He simply slaps the ID label on and announces "Hah! PTF proves intelligent design!" with no justification whatsoever. One could just as easily label espresso brewing "intelligent design" and proclaim that Starbucks baristas are evidence of divine creation. It is nonsensical. 

Nephy proceeds with a few paragraphs of rambling spew about DNA being a "computer code". I have already talked at length about why DNA is not a code, so I will not go into it here. Needless to say, it makes little sense.

So what it all comes down to is this: the nylonase gene is a product of a frameshift mutation and not programmed translational frameshift; programmed translational frameshift is not a mutation, nor is it evidence of Intelligent Design; biochemical adaptations do count as evolution; and nylonase still illustrates a wonderful example of evolution occurring within recent memory.  Once again, Nephilimfree abuses genetics to form a murky mire of distorted truth, and once again, his claims do not stand up to the scrutiny of critical thought.

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1. Kinoshita, S.; Kageyama, S., Iba, K., Yamada, Y. and Okada, H. (1975). "Utilization of a cyclic dimer and linear oligomers of e-aminocaproic acid by Achromobacter guttatus". Agricultural & Biological Chemistry 39(6): 1219−23

2. Negoro, S.; Shinagawa, H.; Nakata, A.; Kinoshita, s.; Hatozaki, T. and Okada, H. (1980). "Plasmid control of 6-aminohexanoic acid cyclic dimer degradation enzymes of Flavobacterium sp. KI72".  Journal of Bacteriology 43(1): 238-245

3. Kinoshita, S.; Negoro, S.; Murayama, M.; Bisaria, V. S.; Sawada, S. amd Okada, H. (1977). "6-aminohexanoic acid cyclic dimer hydrolase . A new cyclic amide hydrolase produced by Achronobacter guttatus KI72" European Journal of Biochemistry. 80: 489-495.

4.  Kinoshita, S.; Terada, T.; Taniguchi, T.; Takene, Y.; Masuda, S.; Matsunaga, N. and Okada, H. (1981). "Purification and characterization of 6-aminohexanoic-acid-oligimer hydrolase of Flavobacterium sp. KI72". European Journal of Biochemistry. 116(3): 547-551

5. Dawkins, R. (1986). The Blind Watchmaker, p. 48

6. Ibid. p. 49

7. Ohno, S. (1984). "Birth of a unique enzyme from an alternate reading frame of the preexisted, internally repititious coding sequence".  Proceedings of the National Academy of Sciences. 81: 2421-2425

8. Negoro, S.; Ohki, T.; Shibata, N.; Sasa, K.; Hayashi, H.; Nakano, H.; Yasuhira, K.; Kato, D; Takeo, M. and Higuchi, Y. (2007). "Nylon-oligomer degrading enzyme/substrate complex: catalytic mechanism of 6-aminohexanoate-dimer hydrolase". Journal of Molecular Biology. 370: 142-156

9. Farabaugh, P. (1996) "Programmed Translational Frameshifting". Microbiological Reviews. 60(1): 103-134 

Shall we write Chapters a letter?

There is a reason why I don't shop at popular music stores: they don't seem to be able to get their genres right. I'm a bit of a "genre Nazi", and it annoys me to see breakcore albums placed under "techno" or albums by pop groups placed under "punk" (HMV is the worst for this kind of thing), so I do my music shopping online. This goes for books as well as music. One place where I'm satisfied with the sorting of the stock, though, is Chapters. Chapters usually does a good job. Usually.

I was browsing at Chapters yesterday when I noticed something a bit disheartening. They had a table with a pile of books on it, under the header "Ideas and Opinions". They had Christopher Hitchens' God is Not Great, along with Harris' Letter to a Christian Nation and some Christian apologetics books, which is fine. A lot of those matters are ideas that need to be shared and some of them boil down to personal opinions. But what really irked me was their inclusion of On the Origin of Species.

Darwin's seminal work is not merely an "idea" or "opinion". It is the genesis of the foundations for all of modern biology. To call it an idea does not do it any justice, and to call it an opinion is to do it an incredible disservice! Yes, the book was built upon ideas that Darwin had while journeying on the Beagle, but calling it simply an idea has the connotation that it's something unsupported by evidence; it's tantamount to saying evolution is a mere hypothesis rather than a scientific theory. Calling it an opinion is blatantly wrong; there is a fine distinction between fact and opinion, and evolution is as much of a scientific fact as you can get.

What's more is that, upon looking through Chapters' science section (where Chapters usually puts On the Origin of Species), I came across copies of Michael Behe's IDiotic Darwin's Black Box and The Edge of Evolution. Perhaps the bigwigs at Chapter's are unfamiliar with the Dover trial, but Intelligent Design is certainly not science and should not be found under the Science section. If any book should be found under "Idea's and Opinions" then Behe's trash would be it. The girlfriend and I just happened to have a pen and a sticky note on us, so we left a message for the Chapters staff, asking them to move it to a more appropriate section, like philosophy or religion.

Alas, I think it will go ignored.

Perhaps we should write Chapters a letter. I can understand their wanting to be impartial in the current culture war over evolution and putting Origin in a neutral category, but it's simply wrong. Evolution is science. Evolution is not "just a theory" or "idea" or "opinion". Writing a letter will probably do nothing - and maybe I'm just being a "genre Nazi" again - but maybe it's something we, the secular and scientific community, should consider.

Couldn't Have Said it Better Myself

Here's a clip from Henry Rollins' show, where he discusses the evolution vs Intelligent Design 'debate'. Rollins has such a way with words.

I couldn't have said it any better myself.

Answers in Genesis tries to play with the big boys, fails epically.

One of the things that is often used to laugh at how silly Creationists and, more specifically, Intelligent Design, is, is that it makes no predictions, no testable hypotheses, and porponents lack published papers in scientific journals. Some time ago, Answers in Genesis tried to address these criticisms by starting their own journal (Sorry, AiG, but it doesnt count when you need to start your own journal to publish your own papers, and the peer-review process only works when people outside of your own little group review your science). Nevertheless, we all still chuckled because their papers were non-technical drivel with faulty reasoning and laughable conclusions. Now, the folks over at AiG have tried to remedy this by attempting real 'semi-technial' research. In their article, they compare the fitness of an antibiotic resistant strain of Serratia marcescens to a suseptible strain, in an attempt to discredit evolution of antibiotic resistance (and thus, micro- and macroevolution). But, as the folks over at The Panda's Thumb point out, they fail majorly.

The first problem with their research is breaking one of the golden rules of research: if you are examining a particular variable, everything else needs to remain constant. For example, if you are trying to determine if regular or supreme gasoline gives you a better fuel mileage, you have to compare the two types in the same car, or at least the same model of car. You cant put regular in a Civic, put supreme in a Prius and then declare that supreme is better because the Prius goes further. There is no way to determine if the difference was caused by the gasoline itself of if other factors that differ between the two cars were the cause. You'd have to do the experiment in the same (type of) car. Everything except the variable you are testing needs to remain the same. The same thing goes with working with bacteria. If you are going to compare two strains - one resistant to Ampicilin, the other not - then both strains need to be genetically identical sans the resistance gene. This is one of the most basic, common sense rules about research. Its also the first rule that Answers in Genesis breaks in their 'research'. They compared an S. marcescens Amp resistant strain (it's never explicitly stated where they obtained it, but they allude to Dr. Robert Williams at the Texas Medical Center who has aparently kept the strain going) to a "wild type" that they, get this, isolated from a random sample of pond water. They have no way (short of sequencing the entire genome of each strain) if both strains are genetically identical. One is resistant to ampicilin, the other isnt. But is that the only difference? Most likely not. How can they conclude with any certainty that any fitness difference between the two were because of the resistance gene? They can't. It's as simple as that. They cannot make such a conclusion because they used grossly improper research technique; their findings are absolutely worthless.

The second big problem with their research is that they dont understand what the heck "fitness" means. They define fitness as as ‘growth rate and colony “robustness” in minimal media’ (What the heck is a "robust" colony? That's a pretty subjective qualifier). Unfirtunatley, because of their lousy techniques mentioned above, they can't tell if a smaller colony is less fit (by their definition) because of the resistance gene or some other factor they did not controll. Not only that but the figure they use to describe the growth curves has no error bars, so you cannot tell how accurate their numbers are and whether or not the difference between the two strains is statistically significant (it likely isn't). They then go on to conclude that the resistant strain is "less fit" than the wild type. This makes little sense, considering 92% of Serratia marcescens infections in hospitals are antibiotic restistant (which they state in their own paper). If such strains were less fit then why are they more common than the wild type strain? Because hospitals use antibiotics and the resistance provides a reproductive (fitness) advantage. But because they use a lousy definitation of fitness, they conclude that resistant strains are less fit.

The third big problem is that they dont seem to know the difference between "compete" and "compare". What they did in their paper was compare the two strains. They plated one on minimal media and counted the colonies. Then they plated the second on minimal media and counted the colonies. They compared the numbers, etc. Nevertheless, they constantly refer to the bacteria "competing". There is a big difference. Let's imagine we have two cages, each with a mouse. You feed Mouse A ten pieces of cheese, and it eats all of them. You feed Mouse B ten pieces of cheese, and it eats all of them. Comparitively, both mouse seem the same. But put both mice together and feed them some cheese, and mouse A eats 90% of it, while mouse B only gets 10% of it. This is because Mouse A outcompetes Mouse B. This is not what AiG did. They compared the two strains. They didn't make them compete. So how could they conclude that the non-resistant strain of Serratia marcescens outcompetes the resistant strain? They can't.

And even if all this was forgiven, if they had used proper technique, they had made the strains compete, used a proper definition of fitness....their conclusions are still wrong. If they had bothered to look, this exact experiment had been done before (properly), and the authors concluded the exact opposite of what AiG found.

Nice try, Answers in Genesis, but you're not cut out for this kind of thing. Leave the research to the people who know how to do it. Leave the science to the scientists.