Arthur Hunt posted Entry 3087 on May 1, 2007 09:55 PM.
Trackback URL: http://www.pandasthumb.org/cgi-bin/mt/mt-tb.fcgi/3077

There has been a spate of interest in the blogosphere recently in the matter of protein evolution, and in particular the proposition that new protein function can evolve. Nick Matzke summarized a review (reference 1) on the subject here. Briefly, the various mechanisms discussed in the review include exon shuffling, gene duplication, retroposition, recruitment of mobile element sequences, lateral gene transfer, gene fusion, and de novo origination. Of all of these, the mechanism that received the least attention was the last – the de novo appearance of new protein-coding genes basically “from scratch”. A few examples are mentioned (such as antifreeze proteins, or AFGPs), and long-time followers of ev/cre discussions will recognize the players. However, what I would argue is the most impressive of such examples is not mentioned by Long et al. (1). Below the fold, I will describe an example of de novo appearance of a new protein-coding gene that should open one’s eyes as to the reach of evolutionary processes. To get readers to actually read below the fold, I’ll summarize – what we will learn of is a protein that is not merely a “simple” binding protein, or one with some novel physicochemical properties (like the AFGPs), but rather a gated ion channel. Specifically, a multimeric complex that: 1. permits passage of ions through membranes; 2. and binds a “trigger” that causes the gate to open (from what is otherwise a “closed” state). Recalling that Behe, in Darwin’s Black Box, explicitly calls gated ion channels IC systems, what the following amounts to is an example of the de novo appearance of a multifunctional, IC system.

An IC System From Scratch

The subject of this essay is a fascinating protein that I will call T-urf13 (see the first footnote). This protein, and its gene, was discovered in the mitochondrial genome of certain maize varieties that had been bred to be male-sterile (see footnote 2). There are many different cytoplasmic male sterility (or cms) “traits” in maize, and T-urf13 is found only in so-called cmsT maize (T stands for Texas). This protein was discovered, and studied, owing to an unfortunate circumstance in the 1969 and 1970 (see reference 2 for a review). Briefly, cmsT maize fields were devastated by the appearance of a fungal pathogen (Cochliobolus heterostrophus race T) that seemingly had a unique “taste” for cmsT plants. (The disease is known as Southern corn leaf blight.) After many years of genetic, molecular, and ultimately biochemical studies, it was found that disease was due to a unique susceptibility of cmsT maize to a toxin produced by the fungus (see reference 3 for a recent reviewon the biosynthesis of this toxin). It was also found that disease susceptibility, as well as male sterility, were due to rearrangements of the maize mitochondrial genome, resulting in a novel cmsT-specific locus (see the following paragraph; 4). Finally, it was found that this novel locus encoded a small protein, T-urf13, whose production correlated exactly with both male sterility and disease susceptibility (5).

(I apologize if the pathogen’s name is not familiar or current – I long ago gave up trying to keep pace with the taxonomy of fungi.)

The origins of the cmsT locus are fascinating. Several years ago, this locus was cloned and sequenced, and the sequence compared with normal maize mitochondrial DNA. This analysis revealed that the T-urf13 locus was the product of numerous recombination events (as many as seven different ones; along with reference 4, reference 6 has a nice overview of this). The consequence of these recombination events was the cobbling together of a number of disparate mitochondrial DNA (mtDNA) segments (I have tried to illustrate their origins in Figure 1) to yield a novel DNA segment in the cmsT mitochondrial genome.
———————————-

Turf13F1.png

Figure 1. I have superimposed two sections (colored circles) that have been brought together to form the unique region (2H3) in the mitochondrial genome of cmsT maize. For this, I have used the circular map of the maize NB mitochondrial genome (downloaded from Clifton, S. W., et al. Plant Physiol. 2004;136:3486-3503) to show the relative positions of the two major parts of the 2H3 region, as well as the location in the genome of the 2H3 region itself. Note that these circles, as well as the 2H3 region, are not drawn to scale. Also note that the NB genome map is being used for convenience (the paper has a nice figure that allows me to make the basic point). The actual genome from which cmsT was derived may differ in some ways from the NB genome, although not in the general features shown here. As shown in Figures 2 and 3, the T-urf13 gene lies within the green shaded portion of 2H3.
————————————

One consequence of these rearrangements was the protein-coding region for T-urf13. What is remarkable is that none of the T-urf13 protein coding region came from other protein-coding genes. This is illustrated in Figures 2 and 3. Briefly, this novel protein-coding” gene consists of a segment of the 3’-flanking region of the mitochondrial 26S ribosomal RNA gene, a much smaller (and not contiguous) part of the RNA-coding part of the same gene, and a number of bp that seemingly appeared from out of the blue (Figure 2).

Turf13F2a.png

Closer perusal of the sequences (Figure 3) reveals that the origination of this gene involved, not just the piecing together of two different parts of the mitochondrial genome, but several other mutational events (point mutations, small insertions and/or deletions).

Turf13F3a.png

The bottom line is that T-urf13 is a new protein, encoded by a gene that has no protein-coding antecedents; it is, bluntly, a new protein that arose “from scratch”, through a series of duplications, recombinations, and other mutations that occurred spontaneously in the course of the breeding process that gave rise to the cmsT line.

These points are already problematic for the assertion by ID proponents that new protein-coding information cannot arise by natural processes. But T-urf13 is more than a nondescript polypeptide that happens to affect male fertility in corn. It turns out that T-urf13 is a membrane protein, and in membranes it forms oligomeric structures (I am not sure if the stoichiometries have been firmly established, but that it is oligomeric is not in question). This is the first biochemical trait I would ask readers to file away – this protein is capable of protein-protein interactions, between like subunits. This means that the T-urf13 polypeptide must possess interfaces that mediate protein-protein interactions. (Readers may recall Behe and Snokes, who argued that such interfaces are very unlikely to occur by chance.)

T-urf13 also binds to the toxin produced by the fungal pathogen. But it does not just bind the toxin “passively” – upon binding, a non-selective ion channel is opened, leading to dissipation of transmembrane ion gradients, and all of the resulting events that accompany collapse of proton-motive force. (In mitochondria, this will lead to uncoupling and crippling of mitochondrial function; this is probably why cmsT plants are so devastated by the disease.) This is the second biochemical trait that readers should keep fresh in their minds – T-urf13 is a gated ion channel. (This an the other interesting biochemical properties of Turf13 are reviewed in reference 7.)

Those who have read Darwin’s Black Box might recall Behe’s description of a gated ion channel. On pp. 108-110, Behe describes the signal recognition particle (SRP)-mediated transport of proteins (footnote 3) as a gated transport process. In so doing, he asserts (among other things) that “(b)ecause gated transport requires a minimum of three separate components to function, it is irreducibly complex”. The three components he describes for SRP-mediated protein translocation are the signal peptide, SRP, and the transport channel. The T-urf13 gated ion channel also consists of three components – the fungal toxin (footnote 4) is analogous to the signal peptide, the toxin binding site is analogous to SRP, and the ion channel is analogous to the protein channel. In case this comparison has hidden the bottom line, it is this – T-urf13 is irreducibly complex in exactly the same way that Behe asserts for SRP-mediated protein transport.

The take-home message of all this is: portions of the maize mitochondrial genome that do not normally encode any protein were shuffled, extensively, so as to cobble together an expressed gene that encodes, not just any old polypeptide, but a multimeric gated ion channel. In other words, an irreducibly complex structure arose in one fell swoop, using DNA sequences that do not encode proteins. Basically, this is a case of IC from scratch.

What does all this mean? A linchpin of ID thought is the notion that functional proteins, especially multifunctional ones, cannot arise de novo via natural processes. This proposition is one of Paul Nelson’s antievolutionary arguments that center on ORFans (briefly, the appearance of new function is one of Nelson’s alleged discontinuities), it is a part of the reason so many ID supporters retreat to the stage of the OOL when faced with other facts (presumably, they think that the origins of the first functioning proteins are beyond the grasp of natural mechanisms), it is ultimately where Behe’s ideas about irreducible complexity end up. The example discussed in this essay shows that even complex multifunctional proteins are well within the “reach” of normal, natural molecular processes.

Footnotes.

1. Veterans of the ARN boards will recognize this subject. One of the two threads that discussed T-urf13 has apparently been lost, but the other can still be accessed.

2. Male sterility is a trait used by plant breeders to promote outcrossing; in crops like maize, it is used in the production of hybrids, which increases yield through the phenomenon known as hybrid vigor. The trait is called “cytoplasmic male sterility” because it is inherited in a non-Mendelian fashion. Briefly, cms is maternally inherited, so that 100% of the progeny of a cross in which the mother is male sterile will also be cms. In animals, maternal inheritance is a hallmark of a mitochondrial gene; the same holds in plants, but maternal inheritance also applies for chloroplast genes.

3. SRP-mediated transport is the process by which proteins destined for vesicular transport and export out of the cell are synthesized. Briefly, proteins destined for transport possess N-terminal signal peptides that are recognized by the ribonucleoprotein Signal Recognition Particle; association of the SRP-nascent polypeptide peptide with the translating ribosome causes a pausing, which is released upon “docking” with the transport apparatus on the surface of the endoplasmic reticulum.

4. The toxin made by C. heterostrophus race T is a polyketide. It is beyond the scope of this essay to detail this class of compound, or the fascinating enzymes that synthesize them. Suffice to say that these enzymes add another layer of “complexity” to this subject, in that a rather complex set of activities had to evolve, along with the maize mitochondrial genome, to “assemble” the IC T-urf13 system.

References

1. Long M, Betran B, Thornton K, Wang W. 2003. The origin of new genes: Glimpses from the young and old. Nature Rev Genet. 4: 865-875. (a review, cited by Nick Matzke, on the origins of genes)

2. Levings CS 3rd. 1990. The Texas cytoplasm of maize: Cytoplasmic male sterility and disease susceptibility. Science 250, 942-947. (a nice summary of the phenomenon)

3. Turgeon BG, Baker SE. 2007. Genetic and genomic dissection of the Cochliobolus heterostrophus Tox1 locus controlling biosynthesis of the polyketide virulence factor T-toxin Adv Genet 57, 219-261. (a recent review of the synthesis of the T toxin)

4. Dewey RE, Levings CS 3rd, Timothy DH. 1986. Novel recombinations in the maize mitochondrial genome produce a unique transcriptional unit in the Texas male-sterile cytoplasm. Cell 44(3):439-49. (characterization of the T-urf13 locus in cmsT maize)

5. Dewey RE, Timothy DH, Levings CS 3rd. 1987. A mitochondrial protein associated with cytoplasmic male sterility in the T cytoplasm of maize. Proc Natl Acad Sci U S A 84(15):5374-5378. (links the T-urf13 protein with cms)

6. Hanson MR. 1991. Plant mitochondrial mutations and male sterility. Annu Rev Genet. 25:461-86. (A review that discusses cms in a broad context)

7. Rhoads DM, Levings CS 3rd, Siedow JN. 1995. URF13, a ligand-gated, pore-forming receptor for T-toxin in the inner membrane of cms-T mitochondria. J Bioenerg Biomembr. 27(4):437-45. (a review of the biochemical properties of T=urf13)

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Comment #172997

Posted by David B. Benson on May 1, 2007 9:14 PM (e)

Arthur Hunt — This is very well written. As a non-biologist, I thank you!

Comment #173001

Posted by Cowardly Disembodied Voice on May 1, 2007 10:31 PM (e)

Briefly, this novel protein-coding” gene consists of a segment of the 3’-flanking region of the mitochondrial 26S ribosomal RNA gene, a much smaller (and not contiguous) part of the RNA-coding part of the same gene, and a number of bp that seemingly appeared from out of the blue.

I suppose that makes enough room for the ID folk to fit in their designer.

And as to why He would go to such trouble to help a plant pathogen - those fungi have obviously been leading more virtuous lives than us humans; and He is sending us a biochemical message that He is NOT pleased with us.

Comment #173015

Posted by kay on May 2, 2007 1:09 AM (e)

I wonder if someone will make the case that 09 F9 11 02 9D 74 E3 5B DB 41 56 C5 63 56 88 C0 is irreducibly complex.

Comment #173034

Posted by Andrew on May 2, 2007 6:55 AM (e)

kay wrote:

I wonder if someone will make the case that 09 F9 11 02 9D 74 E3 5B DB 41 56 C5 63 56 88 C0 is irreducibly complex.

LOL - that is *everywhere*. I wonder how many DCMA takedown notices will need to be issued before they realise tha cat is already out of the bag….

Comment #173039

Posted by Vyoma on May 2, 2007 7:39 AM (e)

Cowardly Disembodied Voice wrote:

fungi have obviously been leading more virtuous lives than us humans

I would tend to agree with that, though I may be a bit biased!

Comment #173066

Posted by harold on May 2, 2007 9:49 AM (e)

Calling all ID advocates -

We all know you will ignore this article, yet wait for a chance to make the same philosophical-sounding claims. Or that you will wait for some trivial “mistake” on the part of some individual advocate of mainstream science and harp on it (eg “blah blah blah there is no record of anyone actually being quoted saying that a cartoon platypus proved that modern biomedical science is satanic, how dare they accuse us, blah blah blah blah blah”).

Here is some legitimate scientific work that directly rebuts the very foundation of your claims in a highly direct manner.

You have three choices -

1) Concede that you now realize that the whole “irreducible complexity” argument was wrong all along and that you now accept the overwhelming evidence in favor of biological evolution. This is the most honorable course, and the one I recommend.
2) Come up with some kind of experiment that could demonstrate that these findings actually demonstrate the work of a supernatural designer.
3) Concede that you can’t actually understand the science at issue, and concede that you shouldn’t be commenting on a scientific field which you lack the education to understand. This is an honest but rather lazy alternative; if you were so interested in evolution, you should educate yourself to the level of reading about it intelligently.

Or you could…

4) Hypocritically ignore this work, but make reference to the very claims that it refutes later, or raise patently irrelevant and illogical objections such as “the corn is still corn”.

Which will it be?

Comment #173071

Posted by David Stanton on May 2, 2007 10:21 AM (e)

If you worship the God of the Gaps, I guess your God just got a little bit smaller.

Still, Harold is right. If you still claim that the bacterial flagellum is irreducibly complex, if you still think there is no evidence that the human immune system could have evolved, if you still can’t believe that the human eye could ever “arise by chance”, there is a good bet that you won’t be convinced by this either.

After all, how can this “pathetic level of detail” ever convince someone who refuses to be convinced? All you have here is the sequence homology, the timing of events, a plausible mechanism and an entirely new function. Besides, even if this example is believable, I’m sure there must still be something out there you can’t explain to my satisfaction. Therefore, I’m not constrained to believe anything you say, so there.

I think Behe must have known that when he made predictions about specific examples that science would eventually catch up to him. He has had a lot of time to formulate a response to discoveries like this. Maybe the best he can do now is claim there is no evidence again.

Comment #173081

Posted by Frank J on May 2, 2007 11:22 AM (e)

Arthur Hunt wrote:

…it is a part of the reason so many ID supporters retreat to the stage of the OOL when faced with other facts…

If they did only that, and abandoned the original argument, then I could be persuaded that ID was based on honest, if mistaken, belief. But the fact that they keep moving the goal posts back and forth leaves no doubt that ID is a scam perpetrated by people who know exactly what they’re doing.

As excellent, and necessary, as your article is, I’m sure you know that it just gives IDers more statements to mine and misrepresent.

Comment #173085

Posted by JohnK on May 2, 2007 11:40 AM (e)

While Art’s example of de novo origination of functional protein in a multiple component system is fascinating, far more important is the fact that Art presented this to the ID personages at ARN back in, I think, 1999 (the accessible ARN thread Art still can link to is his 2002 effort at a replay.)
Known to them all this time, but ignored, forgotten and sent down the Memory Hole. As I recall, they discounted it because it was associated with sterility and disease susceptibility. A creationist “OK, so irreducibly complex ‘degeneration’ can evolve, so what?” admission.

Comment #173088

Posted by CJO on May 2, 2007 12:14 PM (e)

Good stuff.
This goes further to show that every example of an attempt to formalize an ID concept (EF, IC, CSI ad nauseum) amounts to nothing more than a restatement of the question.

Of course the answer doesn’t change. And, also of course, it’s nothing but “courtroom theater” to point this out to them. Just more actual science that doesn’t exist if they pretend not to understand it.

Comment #173104

Posted by Dizzy on May 2, 2007 1:30 PM (e)

kay wrote:

I wonder if someone will make the case that 09 F9 11 02 9D 74 E3 5B DB 41 56 C5 63 56 88 C0 is irreducibly complex.

Hahahha. A friend of mine now has that in his forum signature.

Funny thing is, it *is* IC - take away any part of it and it ceases to work!

Comment #173105

Posted by rrt on May 2, 2007 1:30 PM (e)

As JohnK says, this won’t make a dent in the ID stalwarts. After all, this trait leads to sterility (evil) and susceptibility to a toxin (evil). Since evilution is the tool of Satan, and as everyone knows, Satan can never create, only corrupt and pervert, this gene is clearly the work of the devil, because harmful genes don’t constitute new “information.”

Silly as that is, I guarantee it’ll be argued in one form or another. I see it used all the time to explain antibiotic resistance: “See, the enzyme just degraded, it can’t do its job as well anymore, so it’s not ‘new information’ (translation: evil corruption vs. divine creation). Nevermind that in this case, no protein was degraded in order to cause “harm”, but rather a new one was created.

Oh, and of course this wasn’t REALLY new information, since most of the raw genetic material was borrowed from other pre-existing genes (nevermind their functions), and it was THOSE genes that the Designer made.

Comment #173110

Posted by David Stanton on May 2, 2007 1:51 PM (e)

So the argument was that no new information could be created by random mutation and selection. Now the argument is that no new beneficial functions can be created this way? If the mechanism operates to produce new proteins with new functions, what could possibly prevent it from creating a new protein that would have some beneficial function in some environment? Wasn’t the original argument that proteins of this type were IC and therefore couldn’t possibly evolve? What happened to that argument?

Man, if these guys were playing football the goal posts would be moving so fast that no one would even try to kick a field goal.

Harold,

I guess that a variant of number four is the response they actually went with. Of course it turns out that you predicted this possibility only after it actually happened. Oh well, to these guys that counts, remember.

Comment #173112

Posted by Ben (t.o.o.) on May 2, 2007 1:54 PM (e)

Let’s not forget…

“If the new function evolved from the ribosome, why are there still ribosomes?”

Comment #173117

Posted by Henry J on May 2, 2007 2:00 PM (e)

Re ““If the new function evolved from the ribosome, why are there still ribosomes?””

Or how about, If the panda’s thumb evolved from wrist bones, why do panda’s still have wrist bones?

Comment #173122

Posted by Scott on May 2, 2007 2:42 PM (e)

I suspect that the argument will be made that this isn’t “natural” selection at all, but was actually produced through “intelligent” intervention. This resulted from a human-directed breeding program, just like breeding dogs, and everyone knows that dog breeding isn’t “evilution”. Therefore, this “new” example is nothing new. It is not “evilution” but is yet another clear example of ID.

That is how the “It’s still corn” argument is supposed to work, isn’t it?

Comment #173124

Posted by Carl Hilton Jones on May 2, 2007 2:56 PM (e)

This must be an exampke of “poof” :-)

Comment #173127

Posted by David Stanton on May 2, 2007 3:22 PM (e)

There have been long discussions of what constitutes “natural” selection on other threads. The point is that even if the selection pressure was artificial this particular protein was not selected for. In fact, it took years of hard work to even find the genetic change responsible. If artificial selection can cause new information, new proteins and new functions to arise, then “natural” selection could obviously do the same thing given enough time. This is in fact some of the same type of reasoning that Darwin used when looking at pigeon breeding. The experiment may not tell us what actually occurrs in nature, but it tells us a lot about what could occur in nature. There is no theoretical reason why suposedly IC systems could not evolve, Behe and Dembski not withstanding. This study demonstrates that beyond a shadow of a doubt. If other “natural” systems are studied this intensely we are sure to find many more examples of exactly this type of thing. The age of genomics is upon us. Better be careful if you predict that genetics cannot do this or that.

OK, the kick is up, the kick is , , , wait a minute, somebody is trying to move the goal posts again. Darn.

Comment #173128

Posted by CJO on May 2, 2007 3:27 PM (e)

There is no theoretical reason why suposedly IC systems could not evolve, Behe and Dembski not withstanding.

You can take it even further: there are theoretical reasons why IC systems must evolve.

Comment #173192

Posted by Nick (Matzke) on May 2, 2007 9:20 PM (e)

Just to fill in one little gap for folks – the function of male sterility, i.e. pollen that doesn’t work, is to promote outcrossing. Basically, if the plant has sterile pollen then it is effectively a female plant, and will only be pollinated by pollen from other plants.

Plants (and animals…like humans) have all sorts of mechanisms to promote outcrossing, and the study of how natural selection produces outcrossing goes right back to Darwin.

I suspect there is a huge amount of literature on the question of male sterlity and under what situations it is favored by selection. I.e. I suspect it would be favored in situations where pollen from diverse sources is available, but the danger of self-pollination or pollination from very-near relatives is also high. Not sure what kind of spatial situation that would be – perhaps crops planted by American Indians?

Comment #173210

Posted by Henry J on May 2, 2007 10:40 PM (e)

Re “there are theoretical reasons why IC systems must evolve.”

Such as, if a part can be got along without, a mutation that gets rid of it is apt to save on the cost of making that part (and would therefore be beneficial)?

Henry

Comment #173225

Posted by Torbjörn Larsson on May 3, 2007 12:20 AM (e)

Syntax Error: mismatched tag 'kwickxml'

Comment #173226

Posted by Torbjörn Larsson on May 3, 2007 12:24 AM (e)

Henry J wrote:

Such as, if a part can be got along without, a mutation that gets rid of it is apt to save on the cost of making that part (and would therefore be beneficial)?

Around 80 years before ID caught up to the fact (or rather, dismissed it) Muller started to discuss reasons for interlocking complexity, which would be the biological term for reasons of priority.

This was discussed in a PT post where we can read:

Chris Ho Stuart wrote:

Muller’s definition of “interlocking complexity” is exactly the same as the definition of “irreducible complexity” – a system of mutually independent parts that requires all those parts to be present for the system to work. However, Muller’s claim is that this is an EXPECTED result of evolution.

PZ Myers wrote:

“‘Irreducible complexity’ is one of those things the ID people have gotten a lot mileage from, but every competent biologist immediately recognizes its antecedents: Muller’s ratchet.

Muller made the argument back around 1925 that genetic processes would naturally lead to increasing complexity; cycles of gene duplication and addition to pathways would unavoidably lead to more and more steps. Contrary to Behe, the phenomenon he describes is actually a prediction of 80 year old genetics.”

( http://www.pandasthumb.org/archives/2006/10/irre… )

There are links to some of Muller’s works. I haven’t checked this time around, but from the above quotes one gets the impression that the prediction is that interlocking complexity is highly likely and should be observed, in fact so likely it must be observed in some organisms. Not an uncommon description for contingent processes like evolution.

Comment #173243

Posted by Torbjörn Larsson on May 3, 2007 2:16 AM (e)

Henry J wrote:

Such as, if a part can be got along without, a mutation that gets rid of it is apt to save on the cost of making that part (and would therefore be beneficial)?

Around 80 years before ID caught up to the fact (or rather, dismissed it) Muller started to discuss reasons for interlocking complexity, which would be the biological term for reasons of priority.

This was discussed in a PT post where we can read:

Chris Ho Stuart wrote:

Muller’s definition of “interlocking complexity” is exactly the same as the definition of “irreducible complexity” – a system of mutually independent parts that requires all those parts to be present for the system to work. However, Muller’s claim is that this is an EXPECTED result of evolution.

PZ Myers wrote:

“‘Irreducible complexity’ is one of those things the ID people have gotten a lot mileage from, but every competent biologist immediately recognizes its antecedents: Muller’s ratchet.

Muller made the argument back around 1925 that genetic processes would naturally lead to increasing complexity; cycles of gene duplication and addition to pathways would unavoidably lead to more and more steps. Contrary to Behe, the phenomenon he describes is actually a prediction of 80 year old genetics.”

( http://www.pandasthumb.org/archives/2006/10/irre… )

There are links to some of Muller’s works. I haven’t checked them this time around, but from the above quotes one gets the impression that the prediction is that it is probable that interlocking complexity is observed, in fact that it is so likely it must be observed in some species.

Comment #173244

Posted by Torbjörn Larsson on May 3, 2007 2:19 AM (e)

Sorry about the double post, the PT comment queue is baffling.

Comment #173304

Posted by Arthur Hunt on May 3, 2007 8:18 AM (e)

I’d like to thank everyone for their comments so far, and especially David B. Benson for his very kind words.

I’ve seen, on another blog, that some think that Dembski has already dealt with these issues in NFL. Readers are invited to compare pp. 218-219 of NFL with my essay and make this judgment for themselves. Readers might also wade through the awfully-formatted ARN thread I mentioned in the first footnote, as it deals explicitly with pp 218-219 of NFL. To my knowledge, Dembski has never responded to the critique offered in the ARN forum, nor has he addressed the issues I raise in my essay here on PT.

Comment #173495

Posted by JoeG on May 4, 2007 10:22 AM (e)

CSI is information of 500 bits or greater. T-urf13 does not contain 500 bits.

CSI can also arise from existing CSI. T-urf13 can hardly be considered to have arisen from scratch seeing it required a perfectly viable organism before it could come into existence.

Next it is not ID’s position that IC can not evolve. ID says that IC can evolve it were designed to evolve.

And in the end this appears to nothing more than a re-shuffling of already existing information. IOW it could very well be “a built-in response to an environmental cue”. Please read “Not By Chance” by Dr Lee Spetner, for a better understanding of the biological information debate.

And yes Art, we have hashed this out on the ARN board. You were wrong then too.

Comment #173500

Posted by harold on May 4, 2007 11:19 AM (e)

Joe G. -

“CSI is information of 500 bits or greater. T-urf13 does not contain 500 bits.”

I assume that by CSI you mean “complex specified information” (an undefined and meaningless term), and not the popular televsion series.

First of all, the statement that a biological protein “does not contain 500 bits” is incorrect on a variety of levels. The use of the unit “bits” is naively inappropriate. But even if we use a grossly oversimplified model and say that each amino acid in a sequence represents the number of bits necessary to distinguish between over 16 choices - 5 bits - the molecular weight of the protein clearly indicates that it “contains over 500 bits”. (This might be, for example, the number of bits needed to model the sequence in a very simplistic computer program; it surely underestimates the “information” in a complex biological molecule by a massive factor).

What is magic about the arbitrary number 500?

Please answer this question - how did you measure the number of “bits” “contained” by the protein? You didn’t, did you? Not even in the crude, oversimplified, minimal way that I just did. You just parroted something that somebody told you and hoped that you would get away with it, didn’t you?

At any rate, this inappropriate unit choice indicates that you know very, very little about protein biochemistry or either major information theory.

“CSI can also arise from existing CSI. T-urf13 can hardly be considered to have arisen from scratch seeing it required a perfectly viable organism before it could come into existence.”

Putting aside the meaningless reference to CSI, this is an argument against creationism (which holds that things arise magically “from scratch”) and in favor of the theory of evolution

“Next it is not ID’s position that IC can not evolve.”

WHAT?????????? The whole POINT of the term “irreducible complexity”, as introduced by Behe, was to argue that irreducibly complex things could not evolve!!! (As is disproven by the post above, among many other things.)

“ID says that IC can evolve it were designed to evolve.”

WHAT??????? No, that’s what some (but not all) pro-science religious people who accept evolution say, more or less. Life evolved naturally, but a supreme being intended it to evolve.

“And in the end this appears to nothing more than a re-shuffling of already existing information.”

This irrelevant statement reflects, again, a total lack of understanding of either major information theory. It’s not really relevant here, but of course, if “existing” information is changed, “new” or “different” information is the result.

“IOW it could very well be “a built-in response to an environmental cue”.”

Explain this more clearly. What type of environmental cue? When and how was the “response” built in? Why would a supernatural designer “build” a vulnerability to fungus into corn? It doesn’t make sense.

“Please read “Not By Chance” by Dr Lee Spetner, for a better understanding of the biological information debate.”

Why don’t you read a legitimate science book?

“And yes Art, we have hashed this out on the ARN board. You were wrong then too.”

No comment.

Comment #173512

Posted by David Stanton on May 4, 2007 12:22 PM (e)

Well now the goal posts have been taken down and put into storage. No one is allowed to attempt to kick an extra point at all, ever.

The original argument was that IC structures cannot evolve and gated ion channels in particular could not evolve, therefore they must have been poofed into existence by some supernatural being, that is the only way they could have possibly come about.

The natural explanation using evolutionary theory showed how evolution tinkers with preexisting sequences to generate new functions and new proteins of eactly the type denied by the IC argument.

Now evolution doesn’t count if it occurs in a living organism? Now reshuffling of nucleotide sequences doesn’t count? Now there is an arbitrary boundry placed on what is complex enough to count? Now the only possible explanation is front loading of male sterility in corn? Bull loney! This is exactly how evolution works. Deal with it.

OK. No more goal posts. No more kicking extra points. From now on we’ll just have to go for two every time. Oh well, that just means more points for our team anyway.

Comment #173518

Posted by CJO on May 4, 2007 12:34 PM (e)

CSI is information of 500 bits or greater. T-urf13 does not contain 500 bits.

What an odd and arbitrary demarcation! So a complex, specified string containing 499 bits doesn’t cut it huh? Can I get a Whopper Junior?

Also, the article is about that other bogus restatement of the problem: Irreduceable Complexity. Who said anything about CSI?

CSI can also arise from existing CSI. T-urf13 can hardly be considered to have arisen from scratch seeing it required a perfectly viable organism before it could come into existence.

Holy Smokes, would you watch those goalposts MOVE!

Next it is not ID’s position that IC can not evolve. ID says that IC can evolve [if] it were designed to evolve.

And it’s assertions like this that make it painfully obvious that ID is scientifically vacuous. Design is design, but –get this!– Evolution is design too! Heads you win and tails I lose, hmm? I bow to your superior schoolyard logic. Surely, also, you are rubber, and I am glue, no?

And in the end this appears to nothing more than a re-shuffling of already existing information. IOW it could very well be “a built-in response to an environmental cue”.

That sounds like “evolution,” but you were mumbling. Can you describe this “response”? It’s “built in”? Where?

Please read “Not By Chance” by Dr Lee Spetner, for a better understanding of the biological information debate.

“The biological information debate” consists of repeated attempts by creationists to muddy the waters by introducing obfuscatory concepts and generally cherry-picking definitions of “biological information” according to one’s convenience. It’s a thin shell of empty formalisms and wasted verbiage around a core of pure vacuity. Your blithering here is a case in point.

Comment #173530

Posted by Science Avenger on May 4, 2007 1:13 PM (e)

JoeG parroted:

And in the end this appears to nothing more than a re-shuffling of already existing information.

It is a testament to the willful ignorance of creationist/IDers that they can repeat this canard after being informed of gene duplication. Added genes is added information. Period.

Comment #173658

Posted by JoeG on May 5, 2007 6:32 AM (e)

So I see you guys are OK with a strawman argument. Fine.

The following demonstrates ID ignorance:

WHAT?????????? The whole POINT of the term “irreducible complexity”, as introduced by Behe, was to argue that irreducibly complex things could not evolve!!

That is not what Behe said. IC means it couldn’t have evolved via culled genetic accidents. Period.

And if you want to use gene duplications as evidence for anything then the onus is up to you to demonstrate they were the reult of a genetic accident as opposed to some built-in mechanism. THAT is what is being debated.

Also IC requires a system consisting of several parts. T-URF13 is only one component and you can’t even show how it arose. You can only assume it was via a genetic accident.

Also I don’t think it is wise to parade male sterility around as some kind of cool evolutionary inovation. It just exposes how desparate your position really is.

Comment #173659

Posted by JoeG on May 5, 2007 6:32 AM (e)

So I see you guys are OK with a strawman argument. Fine.

The following demonstrates ID ignorance:

WHAT?????????? The whole POINT of the term “irreducible complexity”, as introduced by Behe, was to argue that irreducibly complex things could not evolve!!

That is not what Behe said. IC means it couldn’t have evolved via culled genetic accidents. Period.

And if you want to use gene duplications as evidence for anything then the onus is up to you to demonstrate they were the reult of a genetic accident as opposed to some built-in mechanism. THAT is what is being debated.

Also IC requires a system consisting of several parts. T-URF13 is only one component and you can’t even show how it arose. You can only assume it was via a genetic accident.

Also I don’t think it is wise to parade male sterility around as some kind of cool evolutionary inovation. It just exposes how desparate your position really is.

Comment #173683

Posted by David Stanton on May 5, 2007 9:45 AM (e)

JoeG,

We know in great detail the molecular mechanisms that produce gene duplications. We also know in great detail the molecular mechanisms by which they can mutate to take on new functions. These are genetic accidents by any meaningful definition. They demonstrably create new genes, new functions and new information by any meaningful definition. There are many examples of this.

Behe did not place any arbitrary limits on the processes that would or would not count in producing IC systems, nor is it appropriate to do so. The only meaningful limitation would be that the processes must be naturally occuring instead of magically poofed into existence by some supernatural entity outside of the laws of nature. Behe claimed that gated ion channels were IC. He was wrong, admit it. It’s OK. He was wrong about the immune system, blood clotting and the bacterial flagellum as well. I’m sure he’ll come up with something else, eventually.

If you want to propose some front loading argument the onus is on you to demonstrate how the mechanism works and to demonstrate that it is not natural but depends on some supernatural intervention. Otherwise, I see no reason to presume that just because some sequences can randomly combine that they were always “meant” to do so. We know that that is how evolution works. How is your proposed mechanism any different?

As far a male steriltiy goes, Nick has already pointed out that it can be beneficial in certain environments. In fact, that is what was originally selected on by the researchers. If you are claiming front loading, you are the one who is saying it is a “cool innovation”. If you want to argue that it is “just devolving” then it is you who must show why such an undesirable trait must have been front loaded. Why not just make corn that didn’t have pollen production in the first place? Why not just make a pollen tube incompatability system that would still allow pollen to outcross and also enforce outcrossing in the pollen producer as seen in many other species? Why front load such a wasteful system when any number of more efficient systems could have been produced with only a little more planning? Why mimic exactly what would be produced by chance processes of mutation and selection?

By the way, I noticed you did not show your calculations for information content as requested. I notice you did not defend your arbitrary cut off point for information content as requested. Just thought I’d mention that before someone else does.

Comment #173702

Posted by Science Avenger on May 5, 2007 12:56 PM (e)

JoeG misstated:

IC means it couldn’t have evolved via culled genetic accidents. Period.

No. IC means it cannot evolve via step-by-step direct increments. It could be produced by an indirect evolutionary route, and Behe has said as much, which is another reason the whole argument is silly.

And if you want to use gene duplications as evidence for anything then the onus is up to you to demonstrate they were the reult of a genetic accident as opposed to some built-in mechanism.

So if a lamp falls in an empty room, and I say it was just an accident, whereas you claim a ghost pushed it over, the onus is on me to demonstrate it was the result of an accident? Surely you jest.

We know genetic accidents happen. We know gene duplication occurs. Therefore the most reasonable view is that gene duplications happen via genetic accident (though potentially deterministically explainable by a physicist), until YOU or someone who shares your views brings some evidence, not hand-waving rationalizations, that there is some built in mechanism to accomplish the task. You don’t get to shift the burdon of proof with mere speculation.

However, even if you did so, you haven’t really demonstrated much, because it makes perfect sense that if such mechanisms evolved randomly (evolution still being the only reasonable hypothesis), those creatures with them would be the ones most likely to end up with duplications in the first place. It is a biased sample. You simply cannot make any scientific headway as long as you play this game of pretending to not know or care about the nature of The Designer. And you expose yourself as totally unscientific every time you try.

So I see you guys are OK with a strawman argument. Fine.

You guys sound like you went to a school where you were taught to spit out the names of logical fallacies any time the going gets tough. You aren’t fooling anyone.

Comment #173729

Posted by David Stanton on May 5, 2007 3:10 PM (e)

Gene duplications are known to occur by many mechanisms. In each case, the exact mechanisms causing the duplications are well understood. In every case they are mistakes or accidents. There is no known mechanism whereby they can produce the exact duplications that are required for a certain phenotypic outcome and no known mechanism by which they could possibly anticipate future environmental selection pressures. Please feel free to add to the list.

(1) Polyploidy
(2) Anueploidy
(3) Unequal crossing over
(4) Replicative transposition
(5) Slipped strand mispairing

For those of you who are interested in the topic of where new genes come from, here is a short list of references. This is only the tip of the iceberg of course. Some major mechanisms include: gene duplication and divergence; pseudogenes; exon shuffling; alternative splicing; removal of stop codons and recruitment of 3’ UTR regions; transposition; lateral gene transfer; gene fusion; etc. Please feel free to add to the list with your favorite examples.

Nature Review Genetics 4:865-875 (2003)
Genome Research 15:1421-1430 (2005)
PNAS 103:9935-9939 (2006)
PNAS 104:882-886 (2007)
Molecular Biology and Evolution 24(2):457-464 (2007)
Gene 238:135-141 (1999)
Genetica 118:171-182 (2003)
Current Opinion in Genetics and Development 14:616-619 (2004)
Genetics 145:375-382 (1997)

Comment #173741

Posted by Torbjörn Larsson, OM on May 5, 2007 4:41 PM (e)

Joe wrote:

IC means it couldn’t have evolved via culled genetic accidents.

Even if we would accept the straw man that the only observed mechanisms in evolutionary biology is the original theory of Darwin, it is selection on variation of hereditary characters. The only requirement on variation is that it is sufficiently independent from selection that the later actually selects.

Gene duplication is variation, independent of selection.

If you want to claim that evolution doesn’t work and can’t make interlocking complexity (which is the observed evolutionary phenomena), you must show why evolution doesn’t work, not your pitiful straw man. This is the goalposts of science - they only move when observations invalidates former theories, not on your say-so.

Joe wrote:

Also IC requires a system consisting of several parts. T-URF13 is only one component and you can’t even show how it arose.

Read the article again, it explains the various interlocking components and how they arose.

Comment #173744

Posted by Pete Dunkelberg on May 5, 2007 5:40 PM (e)

Behe, in _Darwin's Black Box_ p 39 wrote:

“By irreducibly complex I mean a single system
composed of several well-matched, interacting parts that
contribute to the basic function, wherein the removal of any one
of the parts causes the system to effectively cease functioning.”
[emphasis in original]

Comment #174070

Posted by James Collins on May 7, 2007 11:00 AM (e)

Evolutionists BUILD us a living cell.

If evolutionists want to end the arguments all they need do is, get their brilliant heads together and assemble a ‘simple’ living cell. This should be possible, because today they certainly have a very great amount of knowledge about the contents of the so-called ‘simple’ cell.

After all, shouldn’t all the combined Intelligence of all the worlds scientist be able the do what chance encounters with random chemicals, without a set of instructions, accomplished about 4 billion years ago, ‘according to the evolutionists,’ and having no intelligence at all available to help them along in their quest to become a living entity. Surely the evolutionists scientists of today should be able to make us a ‘simple’ cell.

If it weren’t so pitiful it would be humorous, that intelligent people have swallowed the evolution mythology.

Beyond doubt, the main reason people believe in evolution is that sources they admire, say it is so. It would pay for these people to do a thorough examination of all the evidence CONTRARY to evolution that is readily available: Try answersingenesis.org. The evolutionists should honestly examine the SUPPOSED evidence ‘FOR’ evolution for THEMSELVES.

Build us a cell, from scratch, with the required raw material, that is with NO cell material, just the ‘raw’ stuff, and the argument is over. But if the scientists are unsuccessful, perhaps they should try Mother Earth’s recipe, you know, the one they claim worked the first time about 4 billion years ago, so they say. All they need to do is to gather all the chemicals that we know are essential for life, pour them into a large clay pot and stir vigorously for a few billion years, and Walla, LIFE!

Oh, you don’t believe the ‘original’ Mother Earth recipe will work? You are NOT alone, Neither do I, and MILLIONS of others!

Comment #174074

Posted by David Stanton on May 7, 2007 12:01 PM (e)

James Collins,

End the argument once and for all. All you have to do is show us one miracle. For example, show a unique type of bacterial flagellum poofed into existence out of nothing. Show that it does not have any homologous sequences in the protein coding genes to any other genes. Show us an organism with a completely different genetic code that was just poofed into existence. Only one will do.

The burden of proof is on you. “All the worlds scientist” already have a natural explanation that MILLIONS find intellectually fulfilling. You are the one who calims a miraculous process that is not reproducible. YOu are the one who must produce a result in order to convince someone.

By the way, when we eventually find life on another planet, we will have another example of the processes that have occurred on earth creating an independent form of life. You however, are in the unenviable position of praying that this never happens. Good luck with that.

Comment #174493

Posted by Joe G on May 9, 2007 3:16 PM (e)

From Art’s article T-URF13 is a result of intentional breeding- ie ARTIFICIAL selection.

IC only argues against NATURAL selection.

Evolution and reproduction go hand in hand. Sterile males do not reproduce.

One component- the fungal toxin- is a pathogen. Meaning it is not created by the maize.

Without a membrane there isn’t a requirement for any type of channel. Therefore the membrane is also a component and must be accounted for via culled genetic accidents.

Comment #174496

Posted by GuyeFaux on May 9, 2007 3:25 PM (e)

IC only argues against NATURAL selection.

Actually, it doesn’t: see the quote above from Behe.

And what, do you think, is the difference between artificial and natural selection which allows the former to produce IC but not the latter?

Comment #174499

Posted by CJO on May 9, 2007 3:50 PM (e)

Scott said (#173122):

I suspect that the argument will be made that this isn’t “natural” selection at all, but was actually produced through “intelligent” intervention. This resulted from a human-directed breeding program, just like breeding dogs, and everyone knows that dog breeding isn’t “evilution”. Therefore, this “new” example is nothing new. It is not “evilution” but is yet another clear example of ID.

That is how the “It’s still corn” argument is supposed to work, isn’t it?

And gets a gold star, for “Correct Prediction of Specious Creationist Argumentation (Obfuscation Division)” Good work, Scott!

To Joe G:
Artificial Selection is just a subset of Natural Selection (at least in the absence of latter-day methods of genetic engineering). What I mean is, all the pathways to novel function are the same; it’s just that the selection pressure is skewed toward the traits the breeder is interested in. In principle it’s no different from the co-evolution of bees and flowering plants or any other commensual evoltionary relationship. So my question to you is how does the presence of a breeder make IC any more likely? After all, if the pathways aren’t available to “nature,” how do they become available to the breeder (who, clearly, need know nothing about the details of genetics)?

Anyway, the way I understand the IC argument, it doesn’t claim that a selection pressure could never exist favoring an IC structure, it claims that the pathways simply aren’t available to a step-wise process, regardless of the intensity (or origin) of the pressure.

Comment #174502

Posted by GuyeFaux on May 9, 2007 4:32 PM (e)

IC only argues against NATURAL selection.

Actually, Behe clearly does not make this distinction as is evidenced by what he said in court. Recall his suggested experiment to “test” whether IC structures can evolve: put a bunch of bacteria in still water, where they would be under artificial selective pressure for mobility. If the experiment can produce anything like a flagellum, ID is falsified. Therefore, his theory (in a nutshell, that IC systems can’t evolve) clearly does not care about natural versus artificial selection mechanisms.

Sorry Scott, Behe (who should know more about ID than you) rightly accepts that artificial selection is a good model of natural selection. I’ll try to dig up the link to his testimony. I don’t remember if he talked about it in cross or direct.

Comment #174503

Posted by CJO on May 9, 2007 4:45 PM (e)

Guye:
Scott’s name entered into this only because he predicted Joe’s argument, days ago.

Joe G is who, I believe, you meant to address (in “Sorry, Scott…”)

OT, heard from C Bass in awhile? Wonder why that is…

Comment #174507

Posted by GuyeFaux on May 9, 2007 4:57 PM (e)

I apologize for my aim. Sorry Scott, you were standing right next to Joe G.

Comment #174508

Posted by GuyeFaux on May 9, 2007 5:04 PM (e)

Re C Bass, he made an appearance on “The Pro-ID paper that wasn’t” thread a few days ago. He’s been since fisked there. To be honest, I think he’s one of the most direct pro-ID writers I’ve seen in a while. At least he tries and fails to answer questions posed at him.

On the other hand, I doubt I’ll receive a response from Goe J. with a semblance of coherence.

Comment #174516

Posted by Richard Simons on May 9, 2007 5:27 PM (e)

I did a Google on part of Jim Collins post and came up with 126 hits. I checked a number of these and as far as I can tell he has never reacted to any of the replies. I think that tells us all we need to know about him.

Comment #174596

Posted by Joe G on May 10, 2007 7:01 AM (e)

Artificial selection is not a subset of natural selection. Artificial selection can do things that NS would not do- poodles for example would never arise without AS.

The debate is all about NATURAL selection and genetic accidents- that is what are they capable of. That is what IC agrues against. That is where the goalposts have ALWAYS been.

And Behe does make the distinction in all of his writings on the subject.

Here is a sample:

“How about Professor Coyne’s concern that, if one system were shown to be the result of natural selection, proponents of ID could just claim that some other system was designed? I think the objection has little force. If natural selection were shown to be capable of producing a system of a certain degree of complexity, then the assumption would be that it could produce any other system of an equal or lesser degree of complexity. If Coyne demonstrated that the flagellum (which requires approximately forty gene products) could be produced by selection, I would be rather foolish to then assert that the blood clotting system (which consists of about twenty proteins) required intelligent design.”- Dr Behe

“Darwin knew that his theory of gradual evolution by natural selection carried a heavy burden.” DBB page 39

“Since natural selection can only choose systems that are already working, then if a biological system cannot be produced gradually it would have to arise as an integrated unit, in one fell swwop, for natural selection to have anything to act on.”- Dr Behe page 39 DBB

“In order to be a candidate for natural selection a system must have minimal function“… page 45 of DBB

And it still remains that the fungal toxin, one of Art’s components is not even derived by the maize. It is an external factor.

You guys should really learn about ID by reading pro-ID literature. Trying to understand ID just by reading anti-ID propaganda is a sure way to set up nothing but strawman arguments- just like Art has done. And your collective ID ignorance has you following along like sheep. Baaaah, baaah….

Comment #174616

Posted by GuyeFaux on May 10, 2007 9:18 AM (e)

Joe G. wrote:

And Behe does make the distinction in all of his writings on the subject.

In all the things you quote, artificial selection isn’t even mentioned. So how can he be making a distinction?

And anyhow, you didn’t answer my question: why, if Behe thinks that artificial selection can do things natural selection cannot, would he propose a falsifying experiment of ID using artificial selection?

Comment #174638

Posted by CJO on May 10, 2007 11:18 AM (e)

You guys should really learn about ID by reading pro-ID literature. Trying to understand ID just by reading anti-ID propaganda is a sure way to set up nothing but strawman arguments- just like Art has done. And your collective ID ignorance has you following along like sheep. Baaaah, baaah….

I’ve read plenty of pro-ID literature; what you should do is bring an iota of critical thinking to your evidently naive and sycophantic attitude toward the authors of that literature and their foregone conclusions. I know and understand the writings of Behe and Dembski, for instance, and they simply do not show what they claim to show. The sheep are those incapable of or unwiling to exaimine the claims of ID and the supporting arguments with a skeptical eye. If you don’t do this, you are caught in the trap of simply accepting on their say-so that their arguments prove what they claim to prove.

Furthermore, you’re not addressing the arguments here, you’re just barking “strawman” like a trained poodle. Answer the questions posed. Why would Behe suggest that his claim that IC can’t evolve would be falsified by an excercise in artificial selection? What pathways to novel function are available to a breeder that are not available to natural selection? And, that’s “pathways” not “selection pressure.” Don’t understand the difference? Well, then, perhaps it is you who is ignorant of the position you wish to argue against. Something to think about before you get too cocky.

Comment #174658

Posted by Joe G on May 10, 2007 12:41 PM (e)

“Why would Behe suggest that his claim that IC can’t evolve would be falsified by an excercise in artificial selection?”

He didn’t. Or at least I have never heard him make such a claim. Do you have a reference?

“What pathways to novel function are available to a breeder that are not available to natural selection?”

The point is what is kept, ie preserved. Breeders can preserve traits that nature would not.

As for accepting someone’s “say so” take a look in the mirror.

Ya see it’s all about the selction. And just how would a sterile male pass on its genes? IOW you are missing the basic concept, regardless of anything else.

GF chimes in with:
“In all the things you quote, artificial selection isn’t even mentioned. So how can he be making a distinction?”

Umm Behe only considers IC to be an obstacle for natural selection. THAT is the point. He, just like every other educated person, knows that artificial selection can do things that NS cannot. Artificial selection is a design mechanism. (there isn’t an ID argument against AS)

IOW you don’t know what you’re talking about and use that ignorance as some sort of refutation. Strange…

And on gene duplication- a duplicated gene does not convey new or an increase in information any more than duplicating a word out of a dictionary conveys new or an increase of information to that dictionary.

Comment #174662

Posted by Joe G on May 10, 2007 12:54 PM (e)

http://beepbeepitsme.blogspot.com/2006/11/natura…

2. Natural selection describes a biological process by which individual organisms with unfavorable traits are less likely to survive and reproduce than those with favorable traits. Natural selection works on the whole individual, but only the heritable component of a trait will be passed on to the offspring, with the result that favorable, heritable traits become more common in the next generation. Given enough time, this passive process can result in adaptations and speciation. Natural selection is the “engine” of evolution.

3. Artificial selection describes the deliberate human manipulation of a biological process. It is driven by a human agenda. It is the process where intentional or unintentional modification of a species through human actions will encourage the breeding of certain traits over others. It was originally defined by Charles Darwin in contrast to the process of natural selection, in which the differential reproduction of organisms with certain traits is attributed to improved survival and reproductive ability in the natural habitat of the organism. Artifial selection is the OPPOSITE of natural selection.

IOW “survival of the fittest” vs “survival of the desired”

Comment #174663

Posted by GuyeFaux on May 10, 2007 1:16 PM (e)

Why would Behe suggest that his claim that IC can’t evolve would be falsified by an excercise in artificial selection?

He didn’t. Or at least I have never heard him make such a claim. Do you have a reference?

From Behe, quote on Uncommon Descent. The Dover transcripts are more definitive.

I claim, for example, that the bacterial flagellum could not be produced by natural selection; it needed to be deliberately intelligently designed. Well, all a scientist has to do to prove me wrong is to take a bacterium without a flagellum, or knock out the genes for the flagellum in a bacterium, go into his lab and grow that bug for a long time and see if it produces anything resembling a flagellum.

Comment #174665

Posted by GuyeFaux on May 10, 2007 1:21 PM (e)

From Behe’s cross, day 12:

Q. And you said, To falsify such a claim, a scientist could go into the laboratory, place a bacterial species lacking a flagellum under some selective pressure, for mobility, say, grow it for 10,000 generations, and see if a flagellum, or any
equally complex system, was produced. If that happened, my claims would be neatly disproven. Now the test you’ve described, that would falsify the claim, your claim that the bacterial flagellum is irreducibly complex in the way you’ve described it, and could, in fact, evolve from pre-cursors, right, if that was successful?

A. That would show that my claim that it required design — required intelligent design was incorrect.

Comment #174668

Posted by CJO on May 10, 2007 1:39 PM (e)

Day 12, Kitzmiller Trial transscripts
Eric Rothschild’s cross of Michael Behe:

Q. Right. Okay. You’ve taken the position in this
courtroom that intelligent design is open to direct
experimental rebuttal, correct?
A. Yes.
Q. And you stated that very clearly in your article
Reply to my Critics?
A. Yes.
Q. And the way you said this could be done, and why
don’t we turn to that document, which is Exhibit 718.
If you could turn to page 697. Matt, if you could
highlight in the second paragraph the passage that
starts, To falsify such a claim, and go to the bottom of
the paragraph.
And you’re asking the question here, or stating,
intelligent design is open to direct experimental
rebuttal, correct?
A. Yes.
Q. And you said, To falsify such a claim, a
scientist could go into the laboratory, place a
bacterial species lacking a flagellum under some
selective pressure, for mobility, say, grow it for
10,000 generations, and see if a flagellum, or any
equally complex system, was produced.
If that happened, my claims would be neatly
disproven. Now the test you’ve described, that would
falsify the claim, your claim that the bacterial
flagellum is irreducibly complex in the way you’ve
described it, and could, in fact, evolve from
pre-cursors, right, if that was successful?
A. That would show that my claim that it required
design – required intelligent design was incorrect.
Q. Let’s break that down. You have this concept of
irreducible complexity, right?
A. Yes.
Q. And you stated that the bacterial flagellum is
irreducibly complex, right?
A. That’s correct.
Q. And this test would, if it was successful,
demonstrate that the bacterial flagellum is not
irreducibly complex. We can, in fact, put a bacterial
species lacking a flagellum under some selective
pressure, and eventually it’s going to get that
flagellum, right?
A. Well, just a distinction. It wouldn’t
demonstrate that it wasn’t irreducibly complex. It
would demonstrate though that random mutation and
natural selection could produce irreducibly complex
systems.

Comment #174670

Posted by GuyeFaux on May 10, 2007 1:43 PM (e)

For the previous post, I should add emphasis mine.

GuyeFaux wrote:

In all the things you quote, artificial selection isn’t even mentioned. So how can he be making a distinction?

Umm Behe only considers IC to be an obstacle for natural selection. THAT is the point. He, just like every other educated person, knows that artificial selection can do things that NS cannot. Artificial selection is a design mechanism. (there isn’t an ID argument against AS)

This is proved wrong by Behe’s test of ID (described above), which is a clear case of artificial selection.

And I repeat our plea for you to describe to us genetic pathways which are open for artificial selection but are not open to natural selection. You said something vague about preserving traits, but once again these to me sound like you’re talking about selection as opposed to a genetic pathway.

And why the hell are you quoting some blog from some guy who calls himself “BEEP BEEP”?

Comment #174674

Posted by CJO on May 10, 2007 1:50 PM (e)

Joe’s got some ‘splainin’ to do.

Comment #174697

Posted by Joe G on May 10, 2007 3:20 PM (e)

The Court here speaks of “evidence for evolution”. Throughout the trial I carefully distinguished between the various meanings of the word “evolution”, and I made it abundantly clear that I was challenging Darwin’s proposed mechanism of random mutation coupled to natural selection. Unfortunately, the Court here, as in many other places in its opinion, ignores the distinction between evolution and Darwinism.- Dr Behe responding to Judge Jones’ ruling

And CJO posts this from Behe:

It would demonstrate though that random mutation and natural selection could produce irreducibly complex.

IOW his proposed test is not an example of artificial selection- at least not in his opinion.

GF quotes Behe:

I claim, for example, that the bacterial flagellum could not be produced by natural selection;

Again NATURAL selection.

Natural selection is about the survival of the fittest and artificial selection is about the survival of the desired. Huge difference between the two.

Why did I quote “beepbeep”? Because that definition of both AS & NS is correct. AS is the opposite of NS. Can you use a search engine? Or is “argument from ignorance” the best you have to offer?

Comment #174698

Posted by Joe G on May 10, 2007 3:27 PM (e)

GF has reading issues:

“And I repeat our plea for you to describe to us genetic pathways which are open for artificial selection but are not open to natural selection.”

Because natural selection would eliminate that which artificial selection would keep. IOW natural selection only works on what exists. When one artificially preserves certain traits others ride along too. And if you continue to artificially select the offspring those traits that otherwise would not have survived are now available for selection.

For example the genetic pathways that led to toy poodles would never be available to natural selection.

Comment #174706

Posted by CJO on May 10, 2007 4:03 PM (e)

his proposed test is not an example of artificial selection- at least not in his opinion.

There are at least two other, more plausible, explanations:
1) Behe is a lying sack of turds and his “opinion” about what he’s said is worth less than squat, since we have to hand his exact words,
or
2) Behe understands, as do I and Guye Faux, that artificial selection, properly understood, is a subset of natural selection with the interesting property that the fitness landscape is strongly skewed toward the desires of human agents.

And you still haven’t figured out the import of the other question you keep dodging. The pathways to novel function are decoupled from selection, so to keep insisting on what no one has denied, that the process of artificial selection often preserves forms that “nature” wouldn’t, doesn’t explain how certain pathways magically become available to human breeders. “Preserving” them doesn’t address this. They have to exist in the first place to be preserved.

Comment #174765

Posted by GuyeFaux on May 10, 2007 6:43 PM (e)

So a scientist placing a population of bacteria under selective pressure is not an instance of artificial selection?

For example the genetic pathways that led to toy poodles would never be available to natural selection.

Why not? If you say that it’s because “nature would never select for the traits of a toy-poodle”, you will not have answered the question.

Comment #174768

Posted by GuyeFaux on May 10, 2007 7:00 PM (e)

I claim, for example, that the bacterial flagellum could not be produced by natural selection;

Again NATURAL selection.

Natural selection is about the survival of the fittest and artificial selection is about the survival of the desired. Huge difference between the two.

Then why, in the next sentence, would Behe propose an experiment involving artificial selection to test his claim? Here it is:

Well, all a scientist has to do to prove me wrong is to take a bacterium without a flagellum, or knock out the genes for the flagellum in a bacterium, go into his lab and grow that bug for a long time and see if it produces anything resembling a flagellum.

Comment #174779

Posted by Richard Simons on May 10, 2007 7:28 PM (e)

Natural selection is about the survival of the fittest and artificial selection is about the survival of the desired. Huge difference between the two.

What I don’t understand is how the bacterium knows whether the environment that is doing the selection is natural or a result of human interference.

It seems to me that the whole argument is based on the arrogant assumption that humans are not part of the natural world (half way to gods, perhaps?) plus muddled thinking about the relationship between genetic variation and selection.

Comment #174781

Posted by Science Avenger on May 10, 2007 7:43 PM (e)

Joe G dissembled thusly:

The point is what is kept, ie preserved. Breeders can preserve traits that nature would not.

True but irrelevant. The point is that breeders can’t preserve traits that nature CANNOT. Anything that COULD be produced by breeders COULD, however improbably, be preserved by nature, and vice versa. Your question of how a sterile man could reproduce actually argues against your point, because he fails to do so whether by breeder or nature.

You are also guilty of playing the game of pretending that selective breeding is ID. It isn’t. ID is concerned with IC items, those that can’t be produced by step-by-step mutation, REGARDLESS of whether those mutations are selected by nature or a breeder. IC items supposedly have to be assembled all at once, thus the anti-evolution force of the argument.

Comment #174790

Posted by Arthur Hunt on May 10, 2007 9:18 PM (e)

I think it’s useful to recall that the two phenotypic traits of interest in this thread - cms and susceptibility to toxins - can and do arise (evolve) in the wild, through natural selection acting on randomly-occurring variation in populations of plants and microorganisms.

Also, Joe G’s arguments would seem to carry the claim that plant breeders in some way deliberately designed the cmsT mitochondrial genome to possess the T-urf13 open reading frame. This is absurd, once one realizes that no one today - no breeder, molecular biologist, or biochemist - could possibly produce, using any and all of the predictive and wet-bench tools that constitute the state of the art, what random variation and natural selection has wrought.

Trackback: Natural Production of New Information

Posted by Threads from Henry's Web on May 2, 2007 8:15 AM

One of the key arguments for Intelligent Design (ID) is that new information cannot be produced by natural processes, and thus there must be intervention by an intelligent designer for this new information to appear. That’s a crude statement, bu...