Enclosed in this blog post is a poem that, for some reason, reminds me of the scientific community that is dominated by Darwinian thinking. Enjoy!
Their Way, by Bob Blues
I came with all my books, lived in dorms, followed directions. I worked, I studied hard, met lots of folks who had connections. I crammed, they gave me grades, and may I say not in a fair way. But more, much more than this, I did it their way.
I learned all sorts of things although I know I'll never use them.
The courses that I took were all required, I didn't choose them.
You'll find that to survive it's best to act the doctrinaire way.
And so I buckled down and did it their way.
Yes, there were times I wondered why
I had to crawl when I could fly.
I had my doubts, but after all,
I clipped my wings, and learned to crawl.
I had to bend, and in the end
I did it their way.
And so, my fine young friends, now that I'm a full professor
Where once I was oppressed, now I've become the cruel oppressor.
With me you'll learn to cope, you'll learn to climb life's golden stairway.
What can I do? What can I do? Open your books. Read chapter two. And if it seems a bit routine, Don't come to me, go see the dean. As long as they give me my pay I'll do it their way.
Seth Shostak of the SETI Institute has written an article on SETI and Intelligent Design, detailing the difference between SETI and Intelligent Design. He notes that intelligent design proponents have offered SETI’s methodology of detecting design as evidence that intelligent design is scientific. He then proceeds to respond to that claim.
There are several problems with his article, some of which I will address here, in quote-and-reply fashion.
As just about everyone is aware, these folks use similar logic to infer a "designer" behind such biological constructions as DNA or the human eye. The apparent complexity of the product is offered as proof of deliberate blueprinting by an unknown creator--conscious action, presumably from outside the universe itself.
Complexity (or, more specifically, linear complexity) may be defined as randomness [Li and Vitanyi; Yockey 1992].
To quote Abel (2009),
“A random string is the most complex because its sequence cannot be enumerated using any algorithmically compressive string shorter than itself. Notice that this precise definition of linear complexity has nothing to do with meaning or function.”
So, Seth Shostak is wrong when he claims that “the apparent complexity of the product is offered as proof of deliberate blueprinting by an unknown creator.”Complexity in itself is not offered as evidence of intelligent design in a given biological system. A random string of nucleotides is complex but it can be easily explained as the result of random mutations; in such a case, intelligence is not a more adequate explanation for the origin of that random string of nucleotides.
The way this happens is as follows. When ID advocates posit that DNA--which is a complicated, molecular blueprint--is solid evidence for a designer, most scientists are unconvinced. They counter that the structure of this biological building block is the result of self-organization via evolution, and not a proof of deliberate engineering. DNA, the researchers will protest, is no more a consciously constructed system than Jupiter's Great Red Spot. Organized complexity, in other words, is not enough to infer design.
The problem with this paragraph, of course, is that intelligent design proponents do not infer design on the basis of organized complexity. Complexity in itself really isn’t part of the equation in the detection of intelligent design. Nor is organization. A cube that is exactly 10 in. x 10 in. x 10 in. is not complex, and it is not organized either, but it is indicative of intelligent design (a la Dr. Sean Pitman). In brief, intelligent design proponents do not infer design on the basis of complexity or organization.
In fact, the signals actually sought by today's SETI searches are not complex, as the ID advocates assume.
We don’t assume that the signals SETI researchers are looking for are complex.
A SETI radio signal of the type we could actually find would be a persistent, narrow-band whistle…. And yet we still advertise that, were we to find such a signal, we could reasonably conclude that there was intelligence behind it. It sounds as if this strengthens the argument made by the ID proponents. Our sought-after signal is hardly complex, and yet we're still going to say that we've found extraterrestrials. If we can get away with that, why can't they? Well, it's because the credibility of the evidence is not predicated on its complexity.
In that last sentence lies the fatal flaw in Shostak’s line of argumentation. In the case of intelligent design, the credibility of the evidence is not predicated on its complexity. The word “straw-man” immediately comes to mind.
If SETI were to announce that we're not alone because it had detected a signal, it would be on the basis of artificiality. An endless, sinusoidal signal - adead simple tone - is not complex; it's artificial. Such a tone just doesn't seem to be generated by natural astrophysical processes.
We’re on to something now. Intelligent design proponents use the exact same methodology:
If intelligent design proponents were to announce that a certain biological system was intelligently designed, it would be on the basis of artificiality (whatever “artificiality” is supposed to mean). A biochemical system that cannot be explained by Darwinian processes is not necessarily complex (and let’s not forget how “complexity” is defined). Such a biological system just doesn't seem to be generated by Darwinian processes.
In addition, and unlike other radio emissions produced by the cosmos, such a signal is devoid of the appendages and inefficiencies nature always seems to add - for example, DNA's junk and redundancy.
Note the phrase “nature always seems to add.” The intelligent designer(s), for example, could have designed the flagellum, and afterwards “nature” added other components which made it less efficient.
So that's one point: the signals SETI seeks are really not like other examples drawn from the bestiary of complex astrophysical phenomena. That speaks to their artificiality.
So that's one point: the biological systems with which intelligent design proponents infer design are really not like other examples drawn from the bestiary of complex Darwinian phenomena. That speaks to their artificiality.
In summary, SETI detects intelligence behind a radio signal on this basis,
(1)The signal is not known to be generated by natural astrophysical processes.
(2)The signal is produced by human intelligence.
(3)Also, context (i.e., where in the universe the signal is found). However, this is irrelevant to the field of intelligent design, since it would be difficult to imagine what would be an appropriate “context” to determine that the flagellum was intelligently designed.
Intelligent design proponents detect intelligent design in biological systems on this basis,
(1) The biological system is not known to be generated by mindless processes.
(2) The signal is known to be generated by human intelligence.
Why would a radio signal consisting of a string of the first 100 prime numbers be indicative of an intelligence, as suggested by Seth Shostak? It is because,
There is no known mindless process that can explain the origin of such a radio signal,
There is a known intelligent mechanism that can explain the origin of that radio signal.
And this is exactly the same methodology intelligent design uses to detect design in biological systems.
References:
Li, M.; Vitanyi, P. An Introduction to Kolmogorov Complexity and Its Applications, 2nd Ed.
Yockey, H.P. Information Theory and Molecular Biology. Cambridge University Press:
Cambridge, 1992; p. 408.
Abel, David L. The Capabilities of Chaos and Complexity. International Journal of Molecular Sciences, 10(1): 247-291(2009).
TheHumanApe’s blog is hardly deserving of attention, but nevertheless the job of shredding his ridiculous literature will be done.
He devotes a number of his blog posts to providing the evidence for evolution. For example, he quotes Jerry Coyne (author of “Why Evolution is True”) on why ERVs, embryology, et al., all demonstrate the validity of common descent. He describes how fossils and protein sequences provide confirmation of common descent. However, he makes the fatal error of equating evidence of common descent for evidence of a non-directed model of common descent. He cannot accept the prospect that evolution was guided. While I am not in anyway a theistic evolutionist, there is evidence in biology that certain parts of life were involved in a guided evolution. For example, a sequence analysis of the protein alpha-importin suggests that alpha-importin in unicellular organisms would guide the evolution of beta-canenin, and with the origin of beta-canenin, multicellular life forms would arise (see Mike Gene’s blog “The Design Matrix”). If TheHumanApe stubbornly clings to the belief that even a guided evolution is“magic,” then I’d love to hear his response to this.
TheHumanApe gives some treatment to chromosome 2, which he calls “undeniable evidence for evolution.” He is apparently ignorant of the possibility that Homo sapiens originally had 48 chromosomes, and then a fusion reduced that number to 46. The only thing chromosome 2 proves is that homo sapiens used to have 48 chromosomes.
He comes up with even more “undeniable evidence” for evolution – namely, the evidence from DNA sequences and molecular phylogenies. He is, of course, unaware of the fact molecular nested hierarchies can be explained by tissue constraints on protein sequences. A neutral substitution in one organism is not necessarily neutral in another, due to differences in the number of cell types. As such, the evidence from DNA sequences can hardly be considered “undeniable evidence.”
I found a particular portion of his blog amusing.
“Of course the idiot calls evolution ‘Darwinism’…. Again Christians, please read this carefully: Biologists are called ‘biologists’. It would help if you practiced saying the word "biologists" a few dozen times so you get it right next time.”
Right. It’s always difficult to get this point across to laymen like TheHumanApe: we use the term “Darwinian” to distinguish “Darwinian” evolution from Lamarckian evolution, saltationism, orthogenesis, et al. There are Darwinian biologists, there are Lamarckian biologists, etc. Biologists use the term ‘Darwinian’ to distinguish between the different evolutionary models. Of course, laymen like TheHumanApe still can’t get that straight.
Note that nowhere, absolutely nowhere, in his blog does he provide evidence against the following statement: certain features of the biological world are more adequately explained by an intelligence. He assumes that by providing a mountain of evidence for common descent, then this must mean that the flagellar motility system was not intelligently designed. One could provide all the proof in the world that humanity descended through a Darwinian process, but this would not prove that the same is true for the flagellar motility system.
One thing he said I found to be the most entertaining:
“I left the following comment for…an uneducated moron, a typical superstitious idiot.”
I.e., I am an uneducated moron and a typical, superstitious idiot. I find that to be, in short, hilarious.
Well, I think I’ll stop it there since I don’t want to waste anymore time on something that he won’t respond to. Cheers!
Last night, I took a look at the comments of my blog post “Bad Design Disproves Intelligent Design? Really?” As I was reading the comments there, the aroma of nuts wafted towards my eyes – roasted nuts. Except that this guy thinks I’m nutty.
A quick glance at his blog shook my confidence in human sanity (warning: this guy’s blog contains dozens and dozens of expletives). Of course, it’s obvious that he lacks even the most rudimentary knowledge and training in any of the biological sciences; and, for that matter, I am finding it difficult to believe that he even understands the basic methodology of science.
In this Monday evening blog post, I will do my best not to come down too hard on this deluded atheist. Normally I wouldn’t spend my time responding to an individual of his intellectual caliber, but for lack of something else to blog about, I will make a response to particular blog posts of this guy.
The first thing we notice when we go to his blog is his statement that,
“Evolution does not need defending because it's a basic scientific fact.”
He then proceeds to write scores upon scores of blog posts defending evolution as a scientific fact. The shear volume of his textual nonsense is a remarkable testimony to the amount of time he has on his hands – time that should perhaps be used to contribute to the advancement of science, instead of rantings and ravings that simply do nothing to add to science’s advancement. The bulk of his rhetoric consists of the argument “Darwin right. Intelligent Design magic. Christians bad. Darwin right.”
Now, before we eviscerate his blog, we will respond to the comment he left on my blog.
Let’s begin.
“Here's a translation of your gibberish that makes it more honest:
MAGIC as a scientific proposition, holds that certain features of the biological world are more adequately explained by a MAGIC MAN rather than a mindless process.”
Firstly, intelligent design does not invoke any magic. Intelligent design is a method of design detection, similar to SETI. Does SETI invoke magic? Or let me ask him the question in terms he might find more understandable:
(1)Does the method of detecting intelligence in SETI science invoke magic?
(2)Does the method of detecting intelligence in ID science invoke magic?
(3)Why or why not?
Also note that ID does not define the designer, so the phrase “magic man” is silly.
“By the way, Why Evolution is True by Jerry Coyne talks about "bad design" that makes perfect sense if evolution is true (it's true, evolution is a basic scientific fact).”
Please explain how the imperfect design of the flagellar motility system makes the origin of the flagellum more adequately explained in the light of evolution. This should be good.
“One more thing. Magic is NOT a scientific proposition.”
I agree. Magic is not science. Intelligent design is science.
“Scientists don't invoke magic…”
Intelligent design does not invoke magic either.
Now, we will respond to his blog with another post.
Supposedly, bad design is a refutation of intelligent design. How is bad design and intelligent design compatible? This is one of the most common arguments raised against intelligent design, albeit one of the more egregious ones. The argument goes like this: an intelligent designer would not have designed biological system X in this way, therefore Darwinian evolution dunnit.
I think one of the first things Darwinians need to learn when attacking intelligent design is exactly what it posits. Intelligent design, as a scientific proposition, holds that certain features of the biological world are more adequately explained by an intelligence rather than a mindless process.
So, we hold that only certain features in biology are more adequately explained by an intelligence. This alone is sufficient to overturn this argument against intelligent design. But what about flaws in the design of systems that are purported to be intelligently designed, such as the flagellum? First off, bad design is seen in objects that humans design. A broken down, badly-running watch does not indicate that it is not intelligently designed.Maybe the designer(s) of biological system X was having a bad day, and "it" made an error in designing that biological machine.
Now we come to the philosophical argument from bad design: namely, that bad design proves that the designer was not God. Proponents of this argument ask, "If God is perfect, then how could a perfect God made a bad design?"
I answer,
P1: God is perfect, and humans are not perfect. God is omnipotent, and you are not.
P2: An imperfect, non-omnipotent being is incapable of discerning poor designs of a perfect, omnipotent Being.
P3: Therefore, we cannot assert that the design of a perfect Being is imperfect, for we are not omnipotent.
I am expecting a response like "that's just special pleading" or "you are using the God-works-in-mysterious-ways argument." Obviously, these responses are only appeals to emotion, as they do not attack any of the premises in the above argument.
A new peer-reviewed paper has been published by BIO-Complexity, an intelligent design journal. Entitled A Vivisection of the ev Computer Organism: Identifying Sources of Active Information, this paper demonstrates that most of the success of the EV computer simulation in finding a target, is not due to the evolutionary algorithm, but rather "the success of ev is largely due to active information introduced by the Hamming oracle and from the perceptron structure."
And,
"It is not due to the evolutionary algorithm used to perform the search. Indeed, other algorithms are shown to mine active information more efficiently from the knowledge sources provided by ev."
So, intelligent design has not contributed anything to the biological sciences, has it? I beg to differ. Undoubtedly, this paper has contributed something to science.
"Dr. Jackson Martin, Director and Professor of the Flagellum Project at the Hoboken Nature Institute, today announced completion of software that successfully demonstrates the evolution of the bacterial flagellum. Critics of evolution have claimed that the flagellum is too complex to evolve using the gradual changes required by natural selection.
'The flagellum is very complicated,' said Martin. 'Like a motor, it has a rotor, a stator, and complex control mechanisms.'
Martin and his students have demonstrated, however, that the complex flagellum can be easily created using the forces of natural selection.
'We have not only shown that the flagellum can be evolved, it’s hard not to evolve the flagellum.”
In simulation software called EvolFlag, Martin and his students carefully apply gradual modifications to an initial set of boundary conditions.
Martin’s most impressive demonstration was evolution of the bacterial flagellum from common table salt.
'Salt, of course, contains no biochemicals,' offered Martin. 'The ability to evolve a fully functional flagellum from simple table salt is a tribute to the miracle of evolution' . . ."
I've mentioned it before. That dreaded 29+ Evidences for Macroevolution by Dr. Douglas Theobald. I took the time to examine what has been pontificated as the "smoking-gun evidence for evolution" and the "irrefutable evidence." What many Darwinians believe is the most irrefutable argument for their views is the evidence from endogenous retrovirus insertion sites. I am petrified of this evidence. In fact, I am biting my nails. After gathering a few facts, I sent the following email to Dr. Douglas Theobald, concerning this astounding piece of evidence:
Dear Dr. Douglas Theobald,
In your 2004 article “29+ Evidences for Macroevolution” you write (Part 4: The Molecular Sequence Evidence, Prediction 4.5: Molecular evidence - Endogenous retroviruses):
“Endogenous retroviruses provide yet another example of molecular sequence evidence for universal common descent.”
You then go on to propose how this molecular sequence evidence for universal common descent could be potentially falsified:
“It would make no sense, macroevolutionarily, if certain other mammals (e.g. dogs, cows, platypi, etc.), had these same retrogenes in the exact same chromosomal locations. For instance, it would be incredibly unlikely for dogs to also carry the three HERV-K insertions that are unique to humans, as shown in the upper right of Figure 4.4.1, since none of the other primates have these retroviral sequences.”
Consider this molecular sequence evidence for universal common descent falsified. Essentially, in order to falsify this evidence, we must find an outgroup species that shares with a species of a certain clade the same retrogene or retrogenes insertions, but these insertion sites are not shared by the other species of that clade. This is what it boils down to.
Interestingly enough, Barbulescu et al. (2001) have identified “a human endogenous retrovirus K (HERV-K) provirus that is present at the orthologous position in the gorilla and chimpanzee genomes, but not in the human genome.”
What we have here is an outgroup species (gorilla) that shares a retrogene insertion site with a species (chimpanzee) of a certain clade (human-chimpanzee clade), but this insertion site is not shared by the other species of that clade. This alone, by your own criteria, falsifies the retrogene evidence for universal common descent you advance in your article.
Similarly, Bonner et al. (1982) report that the endogenous retrovirus colobus type C virus CPC-1 is shared by the chimpanzee and the gorilla but it is absent from the human genome.
Also note that certain classes of type C retroviruses are found in wooly monkeys and the gibbon ape, but it is not found in African great apes [Lieber et al. 1975].
Humans and Asian apes lack PTERV1 retroviruses, but they are present in African great apes and Old World monkeys [Yohn et al. 2005].
To quote Yohn et al. 2005:
“For example, only one interval is shared by gorilla and chimpanzee; however, two intervals are shared by gorilla and baboon; while three intervals are apparently shared by macaque and chimpanzee.…If these sites were truly orthologous and, thus, ancestral in the human/ape ancestor, it would require that at least six of these sites were deleted in the human lineage. Moreover, the same exact six sites would also have had to have been deleted in the orangutan lineage if the generally accepted phylogeny is correct. Such a series of independent deletion events at the same precise locations in the genome is unlikely.”
In summary, the very criteria that you stated would falsify this evidence for universal common descent has been met, and hence this evidence is effectively falsified. I am writing you so that you might add a correction to your article and realize that this evidence has been falsified.
Respectfully,
Livingstone Morford
References:
Barbulescu M, Turner G, Su M, Kim R, Jensen-Seaman MI, Deinard AS, Kidd KK, Lenz J. A HERV-K provirus in chimpanzees, bonobos and gorillas, but not humans. Curr. Biol. 11(10):779-83 (2001).
Bonner TI, Birkenmeier EH, Gonda MA, Mark GE, Searfoss GH, et al. Molecular cloning of a family of retroviral sequences found in chimpanzee but not human DNA. J. Virol. 43: 914–924 (1982).
Lieber MM, Sherr CJ, Todaro GJ, Benveniste RE, Callahan R, et al. Isolation from the Asian mouse Mus caroli of an endogenous type C virus related to infectious primate type C viruses. Proc. Natl. Acad. Sci., 72: 2315–2319 (1975).
Yohn CT, et al. Lineage-specific expansions of retroviral insertions within the genomes of African great apes but not humans and orangutans. PLoS Biol, 3:110 (2005).
There. Now I've gotten this load off my chest. That's some absolutely amazing piece of evidence.
Of late, my friend Chris has been blogging about the moral argument for the existence of God. Atheists typically respond to the moral argument by saying that morals evolved. While some very good refutations of that view are available, I wish to add my own comments regarding the atheist position. I'll tackle that position from the angle of genetics and not philosophy et al.
First off, is it morally acceptable for a member of the species homo sapiens to kill another homo sapiens without cause? Not at all, and most people, including atheists, will agree with me. So, here's another question: is it morally acceptable for humans to kill chimpanzees, for no reason other than, say for the chimpanzee's fur? If the answer is "no," then is it morally acceptable to kill (without cause other than profit) a gorilla? A lemur? To get to the meat of my argument, at what percent of DNA similarity to our DNA does it become morally acceptable to kill an animal for no real cause? Are we allowed to kill an animal whose DNA is say, 99.99% similar to our own DNA? Is it okay to kill an animal whose DNA is 98% similar to our own? 97%? You see, if morals evolved without any guiding intelligence, at what percentage of DNA similarity are we supposed to draw the line that separates those creatures that we may kill and those we may not kill? Something to ponder over. After all, we share 97.5% similarity to mice [Mural et al. 2002], and yet, intriguingly, tonight I am setting up some mice traps to catch those nasty pests. So, I would love to hear an atheist response to this.
References:
R. J. Mural et al. A Comparison of Whole-Genome Shotgun-Derived Mouse. Science 296: 1661 (2002).
The science journals appear to have come up with a clever strategy to keep papers critical of Darwinian evolution out of the peer-reviewed literature: simply reject the papers or letters to the editor on the grounds that "your response would not be of interest to our readers.” This is evidenced by the refusal to publish Michael Behe's responses to various papers. In short: if you're critical of a paper that attempts to explain a problem for Darwinian evolution, then your paper is not interesting, and hence it won't be published. It's a neat trick, and one that I suspect I fell for.
First off, I submitted a manuscript to the Journal of the Royal Society Interface. My paper was a critique of a paper by Dryden et al. 2008, "How much of protein sequence space has been explored by life on Earth?" In this paper, Dryden et al. argue that by reducing the functional amino acid repertoire, to, among others, a binary amino acid alphabet consisting of hydrophobic and hydrophilic amino acids, then evolutionary processes can easily navigate the whole of functional protein sequence space. Consider that for a protein only 100 amino acids in length, there are 20^100 potential amino acid combinations. By reducing the functional amino acid alphabet to one consisting of only hydrophobic and hydrophilic amino acids, then protein sequence space has a potential of only 2^100 functional sequences. Essentially, they argue that the only thing that matters for a protein to function is that the protein has the right sequence arrangement of hydrophobic and hydrophilic residues. They try to reduce the amino acid repertoire through other means, but the point is this: the paper is nonsense. There are many glaring errors in that paper, some of which I point out in the response I submitted to the Journal of the Royal Society Interface (I submitted the manuscript on August 28, 2010).
Well, gee, but ten days later I received the journal's decision regarding my paper. It shouldn't be hard to guess why they rejected my paper.
Here's a hint: it's not because the reviewers sent a rebuttal to my paper, and it's not because my paper made some error in biology.
So, anyway, here's why they rejected my paper:
"Thank you for submitting your manuscript entitled "On the Reduction of the Amino Acid Repertoire in Functional Protein Structures" to J. R. Soc. Interface.
...Many more good manuscripts are submitted to us than we have space to publish, and we give preference to those that present significant advances of broad interest. Unfortunately, your manuscript has been rejected at this stage, as it was not considered to have sufficient appeal for the general readership of J. R. Soc. Interface." [emphasis added]
Okay, I'll admit that my paper did not represent any real experimental research. But interestingly enough, Dryden et al.'s paper wasn't an experimental paper either, but purely theoretical. However, since I guess it had sufficient appeal for the general readership of the journal, it got published. No problem.
Oh, and I forgot to include this last line the journal sent me:
"Thank you for your paper and I hope that it will be published elsewhere." That makes me feel better.
Now for those of you interested in my critique of Dryden et al.'s paper, I will link to my response at the end of this post (too bad, but my paper didn't refer to some fairly recent work that further supports my paper).
Here's the abstract:
Abstract
It has been postulated by Dryden et al. [Dryden David T.F, Thomson Andrew R, White John H. How much of protein sequence space has been explored by life on Earth? J. R. Soc. Interface,5,25:953-956 (2008)] that the amino acid repertoire of functional protein structures may be reduced to a binary one consisting of hydrophobic and hydrophilic residues without affecting protein function. Moreover, they point to proteins with a low degree of functional complexity and posit that such structures demonstrate that the actual identity of most of the amino acids in a protein is irrelevant. They conclude that, as a result of such reduction there is no role for molecular contingency, and furthermore that potential functional protein sequence space is completely explorable.
Here, based on presented data and through a protein sequence alignment, it is shown that the stated postulate does not hold. For this reason, I conclude that there is a role for molecular contingency and not all of functional protein sequence space has been explored by life on earth.
Now I have to go and revise a paper that I'm having a little better luck with. And I have to go eat a sandwich because I actually am not a robot behind a computer screen, contrary to popular opinion.
The finishing touch to this will be two quotes from two different Darwinians:
"...at the molecular level, there is no role for contingency."
-Dryden et al. 2008, "How much of protein sequence space has been explored by life on Earth?"
"... historical contingency is especially important when it facilitates the evolution of key innovations that are not easily evolved by gradual, cumulative selection."
-Blount ZD, Borland CZ, Lenski RE (2008) Historical contingency and the evolution of a key innovation in an experimental population of Escherichia coli. Proc Natl Acad Sci U S A 105(23):7899-7906.
Addendum:
In my paper, one of the conserved residues in beta-tubulin is cys-12. Since this residue is conserved in all thirty organisms, one would predict that this residue is critical to beta-tubulin function. This prediction is confirmed by site-directed mutagenesis of this residue by Gupta et al. 2001:
"The results suggest that the C12 and C354 residues play important roles in the structure and function of tubulin."
Gupta ML, et al. Mutagenesis of beta-tubulin cysteine residues in Saccharomyces cerevisiae: mutation of cysteine 354 results in cold-stable microtubules. Cell Motil. Cytoskeleton, 49(2):67-77 (2001).
Unfortunately, Professor Larry Moran has been caught quote-mining in his blog post God Plays Bridge. And he doesn’t save the best for last: he quotes-mine right at the start. In case he accuses me of quote-mining, I will quote the Prof’s quote-mine (this blog post is not intended to be a tongue-twister regardless of what you might suspect):
“The creationists tell us that anything in biology with a probability of 10^39 or less is impossible.”
I searched and searched the web and didn’t find any sites saying that a biochemical system with a probability of origin less than 10^39 is more adequately explained by an intelligence, so I can confidently conclude that Prof. Moran is referring to what I said, and only to what I said (I suspect that in lieu of being caught quote-mining Prof. Moran will attempt to claim that he wasn’t referring to what I said per se’; we shall await further developments). So, where does he quote-mine me?
For starters, Prof. Moran confuses “impossible” with “intelligent design is a more adequate explanation.” What I said precisely was this,
“intelligent design proponents need only demonstrate that the odds of a particular biochemical system evolving are 10^-40 or less in order for intelligent design to be a more adequate explanation for the origin of such a biochemical system.”
Where did I say that if the odds of a particular biochemical system evolving is 10^-39 (or for that matter 10^-40) then it is impossible (to evolve I suppose is what Prof. Moran meant)? I did not say such a thing; I only said that in such a scenario intelligent design is a more adequate explanation for the origin of that system. Either I’m aging far sooner than I expected and Prof. Moran is seeing something I said that I can’t see or Prof. Moran is quote-mining. Take your pick.
This quote-mining business gets even more interesting when we see that Prof. Moran himself condemns quote-mining and has a lot to say about this dirty business (here, here, here, and here). Talk about double standards.
Anyway, Prof. Moran tries yet again to refute my argument regarding the probability of a Darwinian origin of biochemical systems, this time using a bridge game as an analogy (incidentally, I don’t play bridge). I believe I sufficiently responded to his analogies with a reference to a peer-reviewed paper, and once again I will remind our dear professor that his arguments contradict the very arguments advanced for common descent; namely, the argument from ERV insertion sites.
I wonder if Prof. Moran plays bridge? If he does, I wonder if that was when he thought up that lovely quote-mine?
I had the guts to make several comments on Professor Larry Moran’s blog, Sandwalk; he has responded to one of these comments with two blog posts (here and here). And now, I have the chutzpah to respond to Professor Larry Moran (to get the gist of what’s going on see my comments on Sandwalk) on BioTalk.
The comment to which Prof. Moran responded to was pretty straightforward. Namely, I argued that “intelligent design proponents need only demonstrate that the odds of a particular biochemical system evolving are 10^-40 or less in order for intelligent design to be a more adequate explanation for the origin of such a biochemical system. This is because there have been no more than 10^39 bacterial cells in the history of life on earth.”
Prof. Moran contends that the above argument cannot possibly hold much water, and he attempts to substantiate that assertion by bringing up the following argument:
That the odds of a specified sperm uniting with an egg is deplorably low, and as a result, through various calculations he does, he concludes that the probability of his four great-grandparents being born is lower than 10^-64 – a probability significantly lower than my stated 10^-40.
Unfortunately by arguing thusly our dear professor is opening a can of worms for the entire common descent framework in that he is tacitly “refuting” the evidence for common descent. One of the oft-cited evidences for common descent are the shared insertion sites of endogenous retroviruses between humans and chimpanzees. However, if we are to accept Prof. Moran’s dictum that something having a probability of occurring of 10^-64 is in fact perfectly plausible, then we must accept that it is perfectly plausible that the shared ERV insertion sites between humans and chimpanzees may be the result of mere coincidence. Prof. Moran is trying to have it both ways but that is a of course a blatant contradiction.
Moreover, I would like to ask Prof. Moran to please explain to me in terms of probability, why precisely polyvalent antimalarial treatments are more effective than standard treatments? It seems as if Prof. Moran is wishing to go against the peer-reviewed literature, where we see that White (2004) says,
"If two drugs are used with different modes of action, and therefore different resistance mechanisms, then the per-parasite probability of developing resistance to both drugs is the product of their individual per-parasite probabilities. This is particularly powerful in malaria, because there are only about 1017 malaria parasites in the entire world. For example, if the per-parasite probabilities of developing resistance to drug A and drug B are both 1 in 1012, then a simultaneously resistant mutant will arise spontaneously every 1 in 1024 parasites. As there is a cumulative total of less than 1020 malaria parasites in existence in one year, such a simultaneously resistant parasite would arise spontaneously roughly once every 10,000 years — provided the drugs always confronted the parasites in combination. Thus the lower the de novo per-parasite probability of developing resistance, the greater the delay in the emergence of resistance.”
Now, to support my assertion that it is implausible to expect Darwinian processes to produce a biochemical system having a probability of origin less than 10^40, we must merely use a little logic.
If the per-E.coli probability of evolving biochemical system A is 10^40, then a mutant E. coli with this biochemical system will arise every 1 in 10^40 cells. As there is a cumulative total of about 10^30 bacterial cells in existence in one year [Whitman et al. 1998], such a mutant E. coli would arise roughly once every 3.55 billion years.
Sound familiar? I’m using the exact same math that White 2004 is using, yet amusingly I don’t see Prof. Moran talking about how the referee(s) of White’s paper messed up in their review of his paper; nor for that matter do I see him criticizing N.J. White’s work; nor for that matter have I seen a letter from Prof. Moran to the Journal of Clinical Investigation correcting White’s work. I wonder why that could be? Oh right, I forgot, I’m advocating intelligent design so only I can be wrong when I use the same reasoning a peer-reviewed paper uses. Neat, isn’t it?
References:
1. White, Nicholas J. Antimalarial drug resistance. J. Clin. Invest, 113(8):1084–1092 (2004).
2. WhitmanW.B, ColemanD.C, WiebeW.J.Prokaryotes: the unseen majority Proc. Natl Acad. Sci. 95(12): 6578-6583 (1998).
Addendum:I said that, "If the per-E.coli probability of evolving biochemical system A is 10^40, then a mutant E. coli with this biochemical system will arise every 1 in 10^40 cells. As there is a cumulative total of about 10^30 bacterial cells in existence in one year [Whitman et al. 1998], such a mutant E. coli would arise roughly once every 3.55 billion years."
I might add that " thus the lower the per-E.coli probability of developing biochemical system A the greater the delay in the emergence of biochemical system A", a statement consistent with White's paper.
It has long been assumed in Darwinian circles that a neutral substitution in a protein is neutral in any given organism. In other words, a neutral substitution in a protein will be neutral in the human variant of that protein as well as the yeast variant of that protein, and in the amoeba variant of that protein, etc. So how did I found out that there is this assumption in Darwinian thinking? I peeked. Actually, I peeked a long time ago at Dr. Douglas Theobald's "29+ Evidences For Macroevolution (please do not ask me where he came up with the fascination with the number '29')." One of the things he said is telling of the assumption I described above. And this assumption is echoed by none other than Mr. Randy Crum! Since Mr. Crum actually describes it in more audience-friendly prose, I will quote Carumbas Blog yet again (click here to see Dr. Theobald's own words).
Thus sayeth Mr. Randy Crum (I will try to make this the last blog post where Mr. Crum takes flack, in case any of you are feeling sorry for him):
"In the last few decades, scientists have been able to sequence DNA and determine the specific amino acid sequences that make up proteins. Some of these proteins are very important and are present in all living things. But in many cases not every amino acid is necessary. Evolution predicts that differences will be explicable through evolutionary history.
The best way to explain this is through an example. The prototypical example is cytochrome-c.
Cytochrome c is an absolutely essential protein found in all organisms, including eukaryotes (organisms with cells that have a nucleus) and bacteria. It is necessary for life in all organisms because it allows mitochondria - the energy fuel of cells - to function.
Much of the cytochrome c protein is not needed (it is “functionally silent”). That part varies from organism to organism. Human cytochrome c has been confirmed to work in yeast - a single-celled organism - despite the fact that the naturally occurring cytochrome c found in yeast is very different from that found in humans (sharing only 38 amino acids)."
Okay I'll have to digress for a bit here. Mitochondria actually isn't the "energy fuel of cells" as Mr. Crum claims, but rather the ATP molecules are.
Anyway this assumption I spoke of earlier is very prevalent in Darwinian circles. And what's wrong with this assumption? Well, to put it in terms that you would all understand, this assumption is simply wrong.
The evidence from protein sequences convinces me of this. The error in this assumption is that it does not take into account organismal complexity, i.e. the number of different cell types in an organism. A yeast cell for example has only one type of cell, but the human organism has many different types of cells, from neurons to fat cells to erythrocytes. And this has rather profound implications. A neutral mutation in a yeast protein may not be neutral in humans. Here's why:
An ontogenic amino acid substitution in a human protein must be compatible with every one of the different cells found in the human organism (every cell, that is, that contains the protein; actin is prevalent in most human tissues, to name one example, while hemoglobin is found only in erythrocytes), while an amino acid substitution in a yeast protein must be compatible with only one cell type.
An analogy may (in a theoretical sense) be useful here. Say you have protein A. And you have cell type X, Y, and Z. Any substitution mutation in protein A must be compatible with all three cell types. Meanwhile, if you only have cell type X, then protein A needs only to compatible with X (analogy a la Dr. Shi Huang).
Now, the idea that a neutral mutation in yeast is not necessarily neutral in say, humans, is consistent with observations from cytochrome c sequences.
I compared the cytochrome c sequence of two unicellular organisms: Naegleria gruberi and Dictyostelium discoideum. To guard against any deletions, insertions, and what-not that might influence my sequence alignment I used the dot-matrix approach (Figure 1) as well as using ClustalX for the alignment.
The dot-matrix method found nothing that would significantly influence the alignment, although after correcting for gaps I achieved what I believe is the best alignment of the cytochrome c sequence of the two unicellular organisms (Figure 2).
Next, I aligned the cytochrome c sequence of two organisms as distant as the tuna and humans. The dot-matrix approach revealed a deletion as well as a higher degree of sequence similarity (Figure 3) than that between the two unicellular organisms. For a more quantifiable degree of sequence similarity between tuna and human cytochrome c, see Figure 4.
From the dot-matrix alignment and the ClustalX alignment one can see that there is obviously more sequence conservation in human and tuna cytochrome c than in the cytochrome c of the two unicellular organisms. This is what would be expected if a substitution in a unicellular organism was not necessarily neutral for a multicellular organism. I will add here that while human cytochrome c functions perfectly fine in yeast, no experiments have proven the reverse: I highly doubt that yeast cytochrome c would function in humans. I would predict that any protein from a multicellular organism would also function in a unicellular organism, but not vice versa.
Indeed, throughout the biological world we see conservation of protein sequences in multicellular organisms while there might often be a lack of conservation in unicellular organisms. Also, if one found a protein sequence that was conserved in unicellular organisms but not conserved in multicellular organisms then the entire idea I am proposing here would be proven utterly wrong. But there's not a single example of that, which would seem to validate this idea (an idea first proposed by Dr. Shi Huang I believe).
I suspect the Darwinians would respond with something like this: unicellular organisms reproduce faster than humans and tuna so they have had more time to accumulate neutral mutations. This however contradicts the notion of a constant clock, opening a can of worms for the Darwinian hypothesis.
So what are the implications of this? Namely, that one cannot really arbitrarily argue for a Darwinian origin of life forms on the basis of functional redundancy in proteins, since what is functionally redundant in one organism may not be in another.
I guess I'd better sit down and start working on a technical paper along these lines. And try not to feel sorry for you-know-who.
