On the evolution of Irreducible Complexity

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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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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... Read More

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

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.

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.

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.…

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!

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?

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.

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.

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.

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.

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!

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.

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.

Let’s not forget…

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

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?

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?

This must be an exampke of “poof” :-)

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.

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.

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?

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

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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[…]ble_com.html )

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.

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[…]ble_com.html )

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.

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

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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This page contains a single entry by Arthur Hunt published on May 1, 2007 9:55 PM.

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Science Blogging Conference ‘08 and The Open Laboratory 2007 is the next entry in this blog.

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