Survival of the Fittest?

DNA_Jock: Have been very busy, and have had to replace my modem. As to the improbability: the calculation is straightforward. It's 1 in 2^30. No problem. Nevertheless, it demonstrates the constraints that Darwinism labors under. It is possible, but not probable, that this worst case scenario could happen. IOW, the Darwinian mechanism is not robust. Behe demonstrates this in "The Edge of Evolution." But let's look at it from the neutral drift angle. Kimura calculates that it will take 4N_e generations to "fix" an allele in the population. With a population size of 800,000, that means 3.2 MILLION years for it to become fixed in that population. Now, what if 5 specific amino acid substitutions had to take place for some very minor "adaptation"? To be sure that this has taken place, we would need 20N_e generations, or, 16 million years. Now, you might say that due to these reductions in population--these collapses--N_e is half of the 800,000. This, then, would mean that for some simple, likely insignificant change to sweep through the population, 8 million years would be needed. What's the word which means the opposite of "robust"? That's the word I would attach to such a scenario. No fair-minded scientist can be persuaded by these numbers. PaV

Roy: IIRC, I got that number from Wikipedia. Maybe you can revoke their license to criticize population genetics. PaV

The genome size for mammals is 3.2 x 10^9 nucleotides.

That is not even wrong. Your license to criticise population genetics is hereby revoked. Understand then criticise. Roy

Arthur: It's intriguing what you say about cytochrome c. I just can't see how what you say is right. Can you expand? PaV

Earth to Arthur Hunt- Your position cannot account for any proteins. If you could then you would win a Nobel Prize. Virgil Cain

Arthur Hunt, your poster child protein turf13 was not produced by unguided material processes but was produced, in direct contradiction to 'random' neo-Darwinian thought, by the cell modifying its own genome.

De Novo Genes: - Cornelius Hunter - Nov. 2009 Excerpt: Cells have remarkable adaptation capabilities. They can precisely adjust which segments of the genome are copied for use in the cell. They can edit and regulate those DNA copies according to their needs. And they can even modify the DNA itself, such as with adaptive mutations,,,,One apparent de novo gene is T-urf13 which was found in certain varieties of corn. http://darwins-god.blogspot.com/2009/11/de-novo-genes-evolutionary-explanation.html Revisiting The Central Dogma (Of Evolution) In The 21st Century - James Shapiro - 2008 Excerpt: Genetic change is almost always the result of cellular action on the genome (not replication errors). (of interest - 12 methods of 'epigenetic' information transfer in the cell are noted in the paper) https://uncommondesc.wpengine.com/intelligent-design/central-dogma-revisited/

Moreover, TURF-13 is a constitutively transcribed mitochondrial gene that is derived from two already existing genes.

Genetic and molecular basis of cytoplasmic male sterility in maize - 2007 Excerpt page 51: The specific virulence of B. maydis towards CMS-T maize was found to be due to mitochondrial gene Turf 13, which is also responsible for the CMS phenotype in CMS-T. It is a constitutively transcribed gene which produces a 13 kd polypetide (Williams et al., 1992). Such a polypeptide is not found in CMS -S, CMS -C or normal maize cytoplasm. Turf 13 is a chimeric region gene which is a recombination product of 5’ region of the atp 6 gene and 3’ region of the 265 ribosomal gene (rrn 26). Its transcription is presumably under the control of the atp 6 promoter (Stamper et al., 1987). It is located in 3547-nucleotide mt DNA sequence that contains two open reading frames, one coding for urf 13 and the other for orf 221, which codes for a 25 kd polypeptide consisting of 221 amino acids and is 77 nucleotides downstream of urf 13 (Levings, 1990). The orf 221 encodes a membrane bound protein that has been identified as ATP4 (Heazlewood et al., 2003). http://agrobiol.sggw.waw.pl/~cbcs/articles/CBCS_2_1_7.pdf

As well, as if that was not bad enough, the adaptation was degenerative not constructive

On the non-evolution of Irreducible Complexity – How Arthur Hunt Fails To Refute Behe Excerpt: furthermore, T-urf 13 involves a kind of degradation of maize. In the case of the Texas maize–hence the T—the T-urf 13 was located by researchers because it was there that the toxin that decimated the corn grown in Texas in the late 60?s attached itself. So the “manufacturing” of this “de novo” gene proved to make the maize less fit. This is in keeping with Behe’s latest findings. https://uncommondesc.wpengine.com/intelligent-design/on-the-non-evolution-of-irreducible-complexity-how-arthur-hunt-fails-to-refute-behe/comment-page-3/#comment-373178

bornagain77

Arthur Hunt its funny that you guys always say that Axe is wrong, but you guys never actually demonstrate the origin of proteins by unguided material processes. Been there, done that. Arthur Hunt

Arthur Hunt its funny that you guys always say that Axe is wrong, but you guys never actually demonstrate the origin of proteins by unguided material processes. Don't you think you guys would have far more credibility, scientifically speaking, with the general public, as opposed to your atheistic cheerleaders, if you were to actually back up your grandiose claims for Darwinian evolution in the lab? Or is actual experimental evidence, that would physically substantiate your grandiose claims for how all life arose on earth, beneath the dignity of the Darwinian elites?

Show Me: A Challenge for Martin Poenie - Douglas Axe August 16, 2013 Excerpt: Poenie want to be free to appeal to evolutionary processes for explaining past events without shouldering any responsibility for demonstrating that these processes actually work in the present. That clearly isn't valid. Unless we want to rewrite the rules of science, we have to assume that what doesn't work (now) didn't work (then). It isn't valid to think that evolution did create new enzymes if it hasn't been demonstrated that it can create new enzymes. And if Poenie really thinks this has been done, then I'd like to present him with an opportunity to prove it. He says, "Recombination can do all the things that Axe thinks are impossible." Can it really? Please show me, Martin! I'll send you a strain of E. coli that lacks the bioF gene, and you show me how recombination, or any other natural process operating in that strain, can create a new gene that does the job of bioF within a few billion years. http://www.evolutionnews.org/2013/08/a_challenge_for075611.html Doug Axe PhD. on the Rarity and 'non-Evolvability' of Functional Proteins - video (notes in video description) https://www.youtube.com/watch?v=8ZiLsXO-dYo When Theory and Experiment Collide — April 16th, 2011 by Douglas Axe Excerpt: Based on our experimental observations and on calculations we made using a published population model [3], we estimated that Darwin’s mechanism would need a truly staggering amount of time—a trillion trillion years or more—to accomplish the seemingly subtle change in enzyme function that we studied. http://www.biologicinstitute.org/post/18022460402/when-theory-and-experiment-collide Can Even One Polymer Become a Protein in 13 billion Years? – Dr. Douglas Axe, Biologic Institute - June 20, 2013 - audio http://radiomaria.us/discoveringintelligentdesign/2013/06/20/june-20-2013-can-even-one-polymer-become-a-protein-in-13-billion-years-dr-douglas-axe-biologic-institute/ Correcting Four Misconceptions about my 2004 Article in JMB — May 4th, 2011 by Douglas Axe http://www.biologicinstitute.org/post/19310918874/correcting-four-misconceptions-about-my-2004-article-in The Hierarchy of Evolutionary Apologetics: Protein Evolution Case Study - Cornelius Hunter - January 2011 http://darwins-god.blogspot.com/2011/01/hierarchy-of-evolutionary-apologetics.html “The First Rule of Adaptive Evolution”: Break or blunt any functional coded element whose loss would yield a net fitness gain – Michael Behe – December 2010 Excerpt: In its most recent issue The Quarterly Review of Biology has published a review by myself of laboratory evolution experiments of microbes going back four decades.,,, The gist of the paper is that so far the overwhelming number of adaptive (that is, helpful) mutations seen in laboratory evolution experiments are either loss or modification of function. Of course we had already known that the great majority of mutations that have a visible effect on an organism are deleterious. Now, surprisingly, it seems that even the great majority of helpful mutations degrade the genome to a greater or lesser extent.,,, I dub it “The First Rule of Adaptive Evolution”: Break or blunt any functional coded element whose loss would yield a net fitness gain. http://behe.uncommondescent.com/2010/12/the-first-rule-of-adaptive-evolution/

etc.. etc.. etc.. bornagain77

Estimating the prevalence of protein sequences adopting functional enzyme folds: Doug Axe: Axe was (and is) wrong. Note that Axe has never responded to the core criticism in this piece, that his deliberate use of an enfeebled temperature-sensitive variant invalidates the use of sensitivity to mutation as any sort of measure of functional sequence space. Arthur Hunt

Art and wd400, seeing as you guys are into pop gen, perhaps you will enjoy this recent podcast interview of Richard Sternberg, who has a PhD in evolutionary biology. He seems to find a fairly large problem with the math of pop gen. Listen: Evolutionary Biologist Richard Sternberg on the Problem of Whale Origins - September 9, 2015 http://www.evolutionnews.org/2015/09/listen_richard099201.html Casey Luskin interviews Dr. Richard Sternberg, evolutionary biologist and CSC Senior Fellow, whose discussion of whale origins is featured in Illustra Media's new documentary, Living Waters: Intelligent Design in the Oceans of the Earth. bornagain77

Arthur Hunt, seeing as you have the math all figured out so that 'the probability, per Hoyle, comes out to be pretty close to 1', perhaps if you can do the same math trick for a naturally occurring code then you can toss your hat in the ring for this following prize (small caveat, they want to actually see you produce a code naturally)

The Origin of Information: How to Solve It Technology Prize for Origin of Information $100,000 For Initial Discovery $3 million USD if Patentable Non-Disclosure Agreements Required Natural Code LLC is a Private Equity Investment group formed to identify a naturally occurring code. Our mission is to discover, develop and commercialize core principles of nature which give rise to information, consciousness and intelligence. Natural Code LLC will pay the researcher $100,000 for the initial discovery of such a code. If the newly discovered process is defensibly patentable, we will secure the patent(s). Once patents are granted, we will pay the full prize amount to the discoverer in exchange for the rights. Our investment group will locate or develop commercial applications for the technology. The discoverer will retain a small percentage of ongoing ownership of the technology. http://cosmicfingerprints.com/solve/

bornagain77

"the probability, per Hoyle, comes out to be pretty close to 1." Just be sure never to ask a neo-Darwinist for an actual demonstration of that 100% probability of cytochrome c arising all by itself. Such as say how this post demonstrates the 100% probability of Intelligence generating functional information.

Estimating the prevalence of protein sequences adopting functional enzyme folds: Doug Axe: Excerpt: The prevalence of low-level function in four such experiments indicates that roughly one in 10^64 signature-consistent sequences forms a working domain. Combined with the estimated prevalence of plausible hydropathic patterns (for any fold) and of relevant folds for particular functions, this implies the overall prevalence of sequences performing a specific function by any domain-sized fold may be as low as 1 in 10^77, adding to the body of evidence that functional folds require highly extraordinary sequences. http://www.toriah.org/articles/axe-2004.pdf

bornagain77

No, the worst case scenario is the one I mentioned, where it takes all of 30 years for the tNM to appear, and then it is culled away; and, then this is repeated. That is the worst scenario, one for which I made the calculation.

It's kind of obvious now that you are making this up as you go along... but what possible relevance does this calculation have to anything? wd400

Fred Hoyle has done the calculation for you. It’s in his “The Mathematics of Evolution.” I mean, if were going to talk about improbabilities…. Actually, if you correct Hoyle's calculations, allowing for all of the amino acid substitutions that are seen in the universe of cyt C sequences, then the probability, per Hoyle, comes out to be pretty close to 1. Arthur Hunt

What are the odds of cytochrome c arising all by itself? Would you like to calculate those odds? Fred Hoyle has done the calculation for you. It's in his "The Mathematics of Evolution." I mean, if were going to talk about improbabilities.... PaV

Oh dear. Even if we go along with your deranged insistence that the tNM only ever arises in the generation immediately preceding a cull, you are now arguing that it is culled every single time. So out of 60 cullings, it is present (at only one copy, wtf?) at 30 cullings, right? The probability that tNM survives at least one culling is 1 - 0.5^30, that is 99.9999999% Yikes. DNA_Jock

No, the worst case scenario is the one I mentioned, where it takes all of 30 years for the tNM to appear, and then it is culled away; and, then this is repeated. That is the worst scenario, one for which I made the calculation. PaV

PaV, the calculation that is hopelessly wrong is the one you offered in comment 38. Here you calculated that, thanks to the 50% culls that you reckon occur every 33 years, any (particular) favorable allele would have a 1 in 2^60 ( i.e. 1 in 10^18) chance of surviving 2,000 years, i.e. through 60 successive culls. This calculation assumes that allele X arose only once, 2,000 years ago, and is present at precisely one copy immediately preceding every one of the 60 culls. That's hilarious. In comment 57, you introduce a different calculation, wherein you calculate that the "needed" mutation only has a 50% chance of arising in 33 years. Ignoring (for now) the error inherent in "the needed mutation" (tNM), your math is still hopelessly wrong. In the worst case scenario, tNM occured immediately preceding the cull, and has a 50% chance of surviving the cull, giving a 25% chance (50% * 50% = 25%) of being present post-cull. But most of the time tNM will have occurred somewhere 5 to 25 generations prior to the cull, and be present in, say, ten or more different animals, and thus have 49.95% chance (50% * (1 - 2^10)) of being present post-cull. IOW the intermittent culls don't have the earth-shattering effect you think. Annual culls would merely reduce the effective population size by 50%, and thus make drift more important, relatively speaking. But we should master basic math before moving on to pop-gen, amirite? DNA_Jock

No wd400, the 2.4/(3.2 x 1.5) calculation is a separate calculation, that just happens to yield exactly the same value as PaV was using for the effect of the cull. What are the chances? Perhaps we can borrow a design detector from one of the denizens at UD... DNA_Jock

Yo are (incorrectly as far as I can tell, what is 2.4/(3.2 x 1.5) ?) trying to calculate the probability of a specific mutation arising once, staying a frequency 1/2N then surviving a halving of the population? And you think this biologically relevant? wd400

DNA-Jock: Point out where it is "hopelessly" wrong. I've already done one calculation. Through the limitations that the die-offs represent, there is only a 50% chance that the needed mutation would occur in the thirty year period. If it never 'arises,' then how does it 'spread' through the population. You can argue that statistically, given enough chances, it will reach that point. Then, and only then, would the math falter. But let's look at the big picture: we're talking about ONE amino acid change. That's the whole argument of Behe's "Edge of Evolution." It appears, based on the malarial parasite example, that the most one can expect of "evolution" is two two-amino-acid changes. This is "hopelessly" inadequate, wouldn't you agree? PaV

Poperian: Again, it seems as if your strategy to deny evolution is true is to only accept misconceptions of it. Read Michael Denton's, "Evolution: A Theory in Crisis," or Behe's "The Edge of Evolution." There are problems with Darwinian theory. And, in "Darwin's Doubt," Meyer argues forcefully that Darwinian theory does not have the "explanatory" power necessary to explain the Cambrian Explosion. PaV

No PaV, post 38 (which is about drift), contains math that is hopelessly wrong, whatever prism you try to squint through. But if you want to talk about the OP, sure: What is the evidence that supports your claim that the 1988 die-off led to "hardly any change"? Careful though, it's a trap... DNA_Jock

PaV:

The OP was meant to underscore problems with common analyses used in population genetics. If you have a problem with NS, take it up with them. I’m afraid that I am not interested in having the discussion.

The OP is titled: "Survival of the Fittest?" This underlies the entire premise of the OP. For example, you wrote....

(1) How do we define the “fittest”? Are they the “strongest”, the “fastest”, the most “aggressive”? What are they? Maybe they’re the “weakest.” Maybe they were so weak that they couldn’t forage with the rest of the herds, and so stayed behind and didn’t get infected. So, how do we define “fitness” here?

Are you suggesting that question, based on a misconception, really isn't relevant to the OP? You went on to write:

Again, the “survival of the fittest” doesn’t befall the “strongest,” “fastest”, “most aggressive”, most “anything,” but, apparently to almost any member of the population. If 400,000 out of 800,000 antelopes die, and they’re none for the better, then what does NS do anyway? Have we wildly exaggerated what it is able to do? (Read The Edge of Evolution to find out more)

Again, I wrote:.....

So what has been achieved during this period? [Evolution] has not optimized the functional adaptation of a variant gene to its environment, but the relative ability to propagate itself though the population. From the point of view of the species and it’s individual members, the effect of evolution was a disaster. However, evolution does not care in this sense. It merely favors the genes that spread best though the population.

Pav:

But again: the title of the OP is “survival of the fittest.” This is not about neutral drift, but about the problems inherent with defining “fitness,” and with the role of “selection.”

Again, it seems as if your strategy to deny evolution is true is to only accept misconceptions of it. Popperian

DNA-Jock: Sorry, it's not goofy. It's looking at things in a very specific way, through the prism of huge die-offs every thirty years. If the population cannot produce a "particular" allele in a limited amount of time, die-offs exacerbate the process of any significant genetic change. But again: the title of the OP is "survival of the fittest." This is not about neutral drift, but about the problems inherent with defining "fitness," and with the role of "selection." PaV

PaV:

This “adapting” to pathogens makes the antelope population incapable of almost nothing else.

I agree. Although I suspect that isn’t what you meant. Things work better if you take the time to write carefully. I did take the time to read carefully what you wrote @38.

Just imagine that some member of the population is working towards some adaptive trait. It has, let us say, one of two needed a.a. bases in the right location. There it is in the population, waiting for the next a.a. to come along by chance, and, lo and behold, it’s GONE. Poof! Undone by some virus. The “chance” of this potential favorable mutation to remain in the population is 1 in 2, or 0.5. This same ‘halving’ occurred 30 years before. Let’s say this happens, on average, every 33 years, or 3 times a century. Well, in a thousand years, this means it would have occurred 30 times. Thus, the ability of ANY favorable allele (whatever that means) to survive is 1 in 2^30, or, 1 in 10^9, and, for a 2,000 year period, it would be 1 in 10^18.

Your math is correct (for a specific allele – not “ANY favorable allele” – perhaps you meant to write “any PARTICULAR favorable allele”) if and only if this specific allele magically remains at one copy in the population prior to every one of the 60 culls. As in: “Errr, only if it hasn’t replicated.” Waaay beyond goofy. [sound of weeping bears] DNA_Jock

DNA-Jock: Like I said, Only if it hasn’t replicated.

Just imagine that some member of the population is working towards some adaptive trait. It has, let us say, one of two needed a.a. bases in the right location. There it is in the population, waiting for the next a.a. to come along by chance, and, lo and behold, it’s GONE. Poof! Undone by some virus.

I was stating the fact that the animal was the "only" one in the population with the needed a.a., awaiting the second. Then it dies suddenly. The a.a. is gone, needing to show up once again in the population. Things work easier if you take the time to read carefully. Again, if you read carefully, I said this die-off occurred before in 1988. That's 27 years. I used 33 years to make the math more straightforward. So, we have an effective population of at most 400,000, or, 4 x 10^5. This 'die-off' occurs with a frequency of 30 years, let's say. And let's say there's 200 new mutations per new offspring. Crunching the numbers: 4 x 10^5 x 30 generations x 200 mutations per generation= 24 x 10^8, or, 2.4 x 10^9 mutations. The genome size for mammals is 3.2 x 10^9 nucleotides. To get an a.a. to change requires more than 1 nucleotide base to change. Let's say it needs, on average, 1.5 nucleotide changes. Then, this means the odds of getting the "first" a.a. to change is 2.4/(3.2 x 1.5)= 0.5. So, when I said that there was an animal now with the 'first' a.a. in place, that's a concession. And, important for the antelope population. But, it also means that statistically, on average, 30 years is not enough for the "first" mutation to arise, let alone the second one. So much for neutral drift. How can anything happen at all? And what about elephant populations that are much, much smaller, and which mate only infrequently? What then? You see my point now, right? This "adapting" to pathogens makes the antelope population incapable of almost nothing else. So much for neo-Darwinian evolution. PaV

PaV math:

Half the population died off. The chance that the animal died off without passing on the allele, or of the animal to whom the allele is passed off to, are both 1 in 2.

Like I said, Only if it hasn't replicated. If the potentially favorable mutation occurred a couple of generations before the cull, then there might be two to four animals with the allele, thanks to drift. Chance that the allele survives the cull is now 75% - 93%. (There might also be zero alleles, making the cull irrelevant for that mutation.) Your math assumes that a potentially beneficial mutation arises once every 33 years, and in that generation there is a 50% cull. It's beyond goofy. Now Josie Bruin is sad too. DNA_Jock

Popperian: The OP was meant to underscore problems with common analyses used in population genetics. If you have a problem with NS, take it up with them. I'm afraid that I am not interested in having the discussion. PaV

DNA-Jock: "Only if it hasn't replicated." Is this supposed to be a thoughtful reply? If it is, you'll have to try harder. Half the population died off. The chance that the animal died off without passing on the allele, or of the animal to whom the allele is passed off to, are both 1 in 2. Please don't obfuscate any further. PaV

PaV @38 writes:

The “chance” of this potential favorable mutation to remain in the population is 1 in 2, or 0.5.

Errr, only if it hasn't replicated. Your math is (hopelessly) wrong. This makes Joe Bruin sad. DNA_Jock

Box Yes I've read it :) poetry I tell you!

Interestingly, even so-called "simple" cells like bacteria have programmed cell death routines subject to control by signals from other cells.

Evolution didit...... yeah whatever....... Andre

Andre, //off-topic:// Have you read this article by Shapiro that (also) deals with PCD? He refers to this research. You probably read it already, I just want to make sure. Box

Roy Because we all know, and so should you that survival of the fittest is a circular argument and it literally goes like this;

Those that are fit survive, and those that survive, are fit.

Surely you know this? Andre

Roy, We are critics of evolutionISM, not mere evolution. And fitness is defined as reproductive success (due to some physical attribute). That means the fittest are the organisms that have the best reproductive success (due to some physical attribute).

Spot on. Why don't you tell PaV? Roy

Seversky I think this has been said to death but for the sake of science lets do this again..... For anything to qualify as a scientific theory the following 3 conditions have to be met, I will also list them in order. 1.) Observation 2.) Repeat 3.) Verify Now let me ask you how exactly does the 3 above apply to luck? For once in your life try and work this out instead of sucking on your dogma lollipop. Andre

Again Nick Matzke comes and pulls one of his signature bluffs! You might not know if evolution is true or not but you can know with certainty that Nick Matzke is an idiot. Here is the conclusion for those to lazy to read; "Owing to the non-exclusivity of the mechanisms of PMS, alongside the likely interference of other selective and neutral forces, we do not believe that it is possible to convincingly elucidate the relative roles of mechanisms of PMS within specific wild populations. A more realistic approach is to attempt to demonstrate whether a particular mechanism of PMS is occurring within a specific system. Doing so will be extremely difficult, not least because appropriate long-term study systems are vital for this. Researchers of contemporary MHC evolution therefore need to carefully consider which mechanisms of PMS can be detected within their study system and which can be ruled out, and interpret their findings accordingly. Technical issues concerning the characterization of expressed MHC variation also need to be carefully considered, as they have not been in much of the MHC literature to date. Nonetheless, with enough appropriate studies, we may be able to determine how often different mechanisms of PMS occur, as well as the different spatial and temporal scales at which they prevail. The accumulation of such knowledge across systems will allow us to evaluate the general importance of the different PMS mechanisms across vertebrates as a whole. Advancements in our understanding of what maintains MHC diversity will also feed into our general understanding of host–pathogen coevolution and the maintenance of genetic diversity." Why does these guys say? In a nutshell? Not what Nick is advocating! Andre

Thanks EugeneS, I was painting with a broad brush- all survivors that reproduce are the fittest by my broad paint strokes! I should have said "fit" instead of "fittest". Thanks again :cool: Virgil Cain

Popperian- no one is arguing against mere evolution. Also science requires metrics. No metrics no science Virgil Cain

Survival of the fittest has no measurable metric. This like the grand theory, it really boils down to a just-so story

The misconception has evolution is the "survival of the fittest" has no metric? Therefore evolution is a just-so story? It's as if your strategy for knowing that evolution is wrong is to refuse to accept anything but misconceptions of it. Popperian

Seversky- Even Dawkins admits science can only allow so much luck. Your position relies on it making it untestable and out of the reach of science. Virgil Cain

Survival of the fittest has no measurable metric. This like the grand theory, it really boils down to a just-so story. Dr JDD

The OP implies that evolution is the "survival of the fittest", then asks questions about how we could tell if something was the fittest, and therefore should survive under evolution. But, as I pointed out, that is a misconception. Again, if we cannot agree on terms to the degree necessary to discuss the issue, in practice, then why would you expected us to make progress? Popperian

Popperian: The "answers" I'm talking about are the ones I posed in the OP. PaV

Since no “answers” are going to be given, then let me point out the problems this hyperselection represents.

We still haven't addressed the misconception that evolution must always advance a population or individual member. Why would you expect progress without addressing that first? Popperian

Since no "answers" are going to be given, then let me point out the problems this hyperselection represents. Just imagine that some member of the population is working towards some adaptive trait. It has, let us say, one of two needed a.a. bases in the right location. There it is in the population, waiting for the next a.a. to come along by chance, and, lo and behold, it's GONE. Poof! Undone by some virus. The "chance" of this potential favorable mutation to remain in the population is 1 in 2, or 0.5. This same 'halving' occurred 30 years before. Let's say this happens, on average, every 33 years, or 3 times a century. Well, in a thousand years, this means it would have occurred 30 times. Thus, the ability of ANY favorable allele (whatever that means) to survive is 1 in 2^30, or, 1 in 10^9, and, for a 2,000 year period, it would be 1 in 10^18. Now, if a population never exceeds one million in number, in two thousand years, they would have produced (assuming annual breeding and two offspring per pairing) 2 x 10^9 offspring. So, how can ANY "beneficial" mutation ever get anywhere? This, I believe, is why we haven't seen too many "answers" given. Our critics prefer to dance around the subject. PaV

Virgil Cain @ 23

Seversky- Luck is the antithesis of science.

Luck - in the sense of a random, unpredictable event - is part of the process science studies, not the science itself. Although even scientists get lucky sometimes. Seversky

But then again, maybe it's Nick M who was trolling. Mung

Imagine an hypothetical island where a population of birds of a particular species would be maximized if they nested around the beginning of, say, April. The reason why it's optimal will be due to various trade offs, including climate, the appearance of predators, the availability of food supplies, nesting materials, etc. Now imagine the entire population currently has genes that cause them to nest at this optimal time. That is, those genes are well adapted to maximizing the number of birds on the island - which would could be thought of as maximizing the good of the species as a whole. However, let's suppose this cycle is disturbed by the appearance of a mutant gene in a single bird which causes it to nest slightly earlier, such as the end of March. Let's also suppose that when a bird builds a nest, genes in the population also result in suitable cooperation from a mate, which which would result in a pair of birds matting and having access to the best nesting site on the island. This would be an advantage, which would outweigh the slight disadvantage of nesting earlier. In the next generation, there will be more birds with the March nesting gene, which will provide all of them with the best nesting sites. As a result, there will be a smaller percentage of birds with the optimal April-nesting variety, that will find good nesting sites. This is because the good nesting sites will have already been taken. In future generations, the population will continue to shift toward the March-nesting variant, which could cause the April-nesting variants to go extinct. And if the April-nesting gene arises again, it's holder will have no offspring for the same reason. IOW, the idea that genes are optimally adapted to maximize the fitness of the population is not always applicable. The change just described actually reduced the total population since they are no longer nesting at the optimal time, which has harmed the species. Furthermore, it may have increased its risk of extinction, making it less likely to expand to her environments, etc. As such, an optimally adapted species may evolve in a way that makes it less well off. Now imagine another mutation occurs that results in nesting earlier still, in March. the same progress may be repeated, causing the the earlier nesting gene to take over and causing another population drop. This may continue until the disadvantage of getting the optimal nesting site is outweighed by the disadvantage of slightly earlier nesting. This could be quite far from the original optimal state of the species. Another misconception is that evolution is always adaptive. That is, it always results in progress. Or, at least some kind of improvement in function which it acts to optimize. This is what is being referred to here as "survival of the fittest". But, as the above thought experiment illustrates, this is simply not the case, either. Not only has the entire species been harmed but so have individual birds as they have a harsher life than before due to nesting earlier. So what has been achieved during this period? It has not optimized the functional adaptation of a variant gene to its environment, but the relative ability to propagate itself though the population. From the point of view of the species and it's individual members, the effect of evolution was a disaster. However, evolution does not care in this sense. It merely favors the genes that spread best though the population. Popperian

semi OT:

What Sparked the Mammal Explosion? - September 3, 2015 Excerpt: Mammals first appear in the fossil record at about the same time as the earliest dinosaurs (approx. 220 million years ago),,, Mesozoic mammals were long portrayed as tiny, shrew-like creatures, unable to diversify due to severe competition and predation from dinosaurs and other reptiles. However, discoveries in the past two decades have greatly expanded the known diversity of Mesozoic mammals, revealing the existence of specialised gliders, climbers and burrowers, semi-aquatic forms and even badger-sized carnivores that ate small dinosaurs.,, Evidence of extensive ecological differences has been found even between closely-related species, and quantitative analyses of the skulls and skeletons of Mesozoic mammals suggest a diverse range of diets and locomotor modes,,, This period,, also broadly coincides with peaks in morphological disparity (as measured by the average morphological difference between contemporaneous species),, Early mammals, despite living in the shadows of the dinosaurs, were diverse and successful.,, These finds extend the early mammal repertoire to include digging, climbing, gliding, and swimming and show that some non-therian lineages achieved surprisingly large body sizes,,, http://crev.info/2015/09/what-sparked-the-mammal-explosion/

bornagain77

VC: Actually, it is not even about the fittest organism (though I agree, the selfish gene concept is obsolete). It is survival of any organism except absolute no-hopers. The natural selection filter is too coarse for the survival of (only) the fittest. EugeneS

Popperian:

Except, It’s not survival of the fittest organisms. It’s the survival of the genes that play a causal role in being passed on to future generations.

It is survival of the fittest organism. Perhaps the genes allowed the organism to be fit but the selfish gene concept has been shot full of holes. Virgil Cain

Arthur Hunt- What evidence demonstrates Dutch elm disease- and the trees' response- was due to natural selection? Why isn't the response an example of the trees responding as opposed to waiting for an accidental genetic change? Virgil Cain

In the annals of NS, no one has likely ever seen anything like this. This statement seems preposterous. It should at least by qualified to include that this is only to the author's (extremely limited) knowledge. Of course, it seems hard to believe that the author has not heard of things like Dutch elm disease. But one never knows... Arthur Hunt

I'm not sure if you are trolling or just ill-equipped for this discussion Mung but I already answered you question. wd400

Popperian: Except, It’s not survival of the fittest organisms. Whatever. Since when did genes obtain an independent existence? Mung

wd400: Directional selection (selection for or against a given allele) removes genetic diversity. You mean natural selection? wd400: Balancing and directional selection obviously exist (right?) You mean natural selection? Which of those two, balancing selection and directional selection, is not natural selection? Heck, may as well include drift in natural selection. I admit some times my remarks are cryptic, but i don't see this as one of those cases. If "natural selection" produces opposite effects, of what use is it as a scientific concept? Balancing selection is natural selection that maintains diversity. Directional selection is natural selection that does not maintain diversity. Same mechanism: Natural Selection. Opposite effects: genetic diversity/loss of genetic diversity. Nick plays the natural selection as semantics word game. Typical Nick. Mung

Except, It's not survival of the fittest organisms. It's the survival of the genes that play a causal role in being passed on to future generations. Again, knowledge is information that, when embedded in a storage medium, plays a causal role in it being retained. This includes information in books, brains and even the genomes of organisms. Knowledge is knowledge not because of its source but because it solves a problem. Popperian

Roy, We are critics of evolutionISM, not mere evolution. And fitness is defined as reproductive success (due to some physical attribute). That means the fittest are the organisms that have the best reproductive success (due to some physical attribute). Virgil Cain

There’s lots of questions that come to mind. Here’s one or two: (1) How do we define the “fittest”?

The same way it's always defined. Apparently you don't know what that is. Equally apparently, nor do the other evolution critics here. Not even bornagain"Time to call you an organlegger"77. Understand then criticise. Roy

Seversky- Luck is the antithesis of science. Virgil Cain

Directional selection (selection for or against a given allele) removes genetic diversity. I'm afraid this

And if “natural selection” has opposite effects, of what use is it as a scientific concept?

makes about as much sense as the O.P. Balancing and directional selection obiously exist (right?), and each generates different population genetic signals that we can detect (and of course, each can e measured in the wild). So I'm not really sure what you are trying to say. wd400

Bob O'H, If balancing selection "operates to maintain genetic variation in populations," just what sort of election is it that operates to reduce genetic variation in populations? And if "natural selection" has opposite effects, of what use is it as a scientific concept? Nick, as usual, is playing at semantics. Nothing of actual substance as PaV has pointed out. Mung

This is from the conclusion, as is, perhaps, what Mung had in mind:

Owing to the non-exclusivity of the mechanisms of PMS, alongside the likely interference of other selective and neutral forces, we do not believe that it is possible to convincingly elucidate the relative roles of mechanisms of PMS within specific wild populations.

So, research, from this 2010 article in Royal Proceedings, tells us that they can't figure out what the mechanism is. They can't say it's NS as work, or neutral theory, or what. So, research doesn't seem to help; it almost makes things worse, Nick. Those answers? PaV

Virgil Cain @ 15

That’s right. It’s the luck of the draw

Then it ain’t science. Thank you for admitting that.

How is that not science? Seversky

Here's this little snippet from the article Mung linked to:

However, in the majority of cases, the exact causes and mechanisms behind the selection remain unclear. A major reason for this is that while DNA data have been relatively easy to collect, it has proved more difficult to identify gene function and more difficult still to show how variation in function is influenced by selection (Ford 2002). In wild-living organisms, finding suitable candidate genes for studying balancing selection is an especially difficult task, as the genetic basis of traits of interest is usually poorly understood. Genes of the vertebrate major histocompatibility complex (MHC) arguably provide the most promising opportunity for studying how balancing selection operates to maintain genetic variation in populations.

Let's translate: "We have a really big problem because trying to find out how 'balancing selection' works is to complicated. It's like all these genes are working all at once, and we can't single out any one of them. So, it's hard to see how NS is working. We're relying mostly on neutral theory (you know, Kimura's baby that eliminates the need for NS entirely). But, hey, looking at MHC might give us a chance at trying to understand what's going on." So, that seems to be the status of the "research." Still no answers to the questions I posed. PaV

ppolish @ 11

“That’s right. It’s the luck of the draw.” Nope, this isn’t bad luck or blind watchmaker. That’s an easy answer that gives us squat.

It’s an alternative explanation to a designer that has never been reliably detected or identified. What is it supposed to give you?

There is a design defect in this critter. Understand the design and this die off could have been predicted. These deer have been afflicted before

A design defect is only possible where’s there’s design and a designer. Neither has been shown.

Use your brain not your dogma.

Ditto. Seversky

Bob O'H:

Hiw does that paper contradict what Nick wrote?

If it was designed then natural selection didn't do it. Virgil Cain

Seversky:

That’s right. It’s the luck of the draw.

Then it ain't science. Thank you for admitting that. Virgil Cain

Mung @ 3 - Hiw does that paper contradict what Nick wrote? Bob O'H

The ironic thing is that thymic selection is such a fine balance it takes great faith to believe such a system can come through RM+NS. The diversity of MHC supports the idea that particular genes (quite a few in the immune system) are purposefully diverse. But evolution has no purpose.... Dr JDD

"Wow, it’s like you’ve never heard of all of the research on natural selection and immune system genes" "All the research" on Natural Selection lol. What does NS have to do with these doomed herds? Survival of the Fittest and Death to the Weaklings. Wow, that is SO scientific. ppolish

"That’s right. It’s the luck of the draw." Nope, this isn't bad luck or blind watchmaker. That's an easy answer that gives us squat. There is a design defect in this critter. Understand the design and this die off could have been predicted. These deer have been afflicted before. Use your brain not your dogma. ppolish

Virgil Cain @ 7

True- faster, slower, middle-of-the pack, fatter, slimmer, longer, shorter, taller- contingent serendipity– whatever it happens to be.

That’s right. It’s the luck of the draw. There’s an awful lot of species not around any more because they never got lucky. The dinosaurs did get lucky. They were around for way longer than we’ve been around but now they’re also long gone. The same could happen to us. There’s no guarantees. Seversky

Nick Matzke:

Wow, it’s like you’ve never heard of all of the research on natural selection and immune system genes.

It is all hearsay and speculation. Natural selection couldn't produce an immune system- it isn't capable. NS can't produce genes. So what, exactly, is this alleged research? Virgil Cain

Nick Matzke: You place your hopes in research. Well, based on your research, answer the questions I pose. Did you notice you answered none of them? PaV

Seversky:

Fitness refers to literally anything that gives an organism a better chance of surviving than its competitors in a given environment.

True- faster, slower, middle-of-the pack, fatter, slimmer, longer, shorter, taller- contingent serendipity- whatever it happens to be. Virgil Cain

Fitness refers to literally anything that gives an organism a better chance of surviving than its competitors in a given environment. It's entirely context-dependent. What might be an advantage in one environment might be detrimental in a different one. Rapidly-reproducing single-celled organisms are clearly immensely successful creatures but that doesn't necessarily mean they are going to be the best in all environmental contexts. Under certain circumstances, there might be advantages to clustering together to form multi-cellular organisms. Isn't that possible? Seversky

as to PaV's suggestion:

(Read The Edge of Evolution to find out more)

here are a few notes in that regards:

“Indeed, the work on malaria and AIDS demonstrates that after all possible unintelligent processes in the cell–both ones we’ve discovered so far and ones we haven’t–at best extremely limited benefit, since no such process was able to do much of anything. It’s critical to notice that no artificial limitations were placed on the kinds of mutations or processes the microorganisms could undergo in nature. Nothing–neither point mutation, deletion, insertion, gene duplication, transposition, genome duplication, self-organization nor any other process yet undiscovered–was of much use.” Michael Behe, The Edge of Evolution, pg. 162 "The immediate, most important implication is that complexes with more than two different binding sites-ones that require three or more proteins-are beyond the edge of evolution, past what is biologically reasonable to expect Darwinian evolution to have accomplished in all of life in all of the billion-year history of the world. The reasoning is straightforward. The odds of getting two independent things right are the multiple of the odds of getting each right by itself. So, other things being equal, the likelihood of developing two binding sites in a protein complex would be the square of the probability for getting one: a double CCC, 10^20 times 10^20, which is 10^40. There have likely been fewer than 10^40 cells in the world in the last 4 billion years, so the odds are against a single event of this variety in the history of life. It is biologically unreasonable." - Michael Behe - The Edge of Evolution - page 146 Diverse mutational pathways converge on saturable chloroquine transport via the malaria parasite’s chloroquine resistance transporter - Robert L. Summers - March 17, 2014 Abstract: Mutations in the chloroquine resistance transporter (PfCRT) are the primary determinant of chloroquine (CQ) resistance in the malaria parasite Plasmodium falciparum. A number of distinct PfCRT haplotypes, containing between 4 and 10 mutations, have given rise to CQ resistance in different parts of the world. Here we present a detailed molecular analysis of the number of mutations (and the order of addition) required to confer CQ transport activity upon the PfCRT as well as a kinetic characterization of diverse forms of PfCRT. We measured the ability of more than 100 variants of PfCRT to transport CQ when expressed at the surface of Xenopus laevis oocytes. Multiple mutational pathways led to saturable CQ transport via PfCRT, but these could be separated into two main lineages. Moreover, the attainment of full activity followed a rigid process in which mutations had to be added in a specific order to avoid reductions in CQ transport activity. A minimum of two mutations sufficed for (low) CQ transport activity, and as few as four conferred full activity. The finding that diverse PfCRT variants are all limited in their capacity to transport CQ suggests that resistance could be overcome by reoptimizing the CQ dosage. http://www.pnas.org/content/early/2014/04/10/1322965111 podcast - Michael Behe: Vindication for 'The Edge of Evolution,' Pt. 2 http://intelligentdesign.podomatic.com/entry/2014-08-06T15_26_19-07_00 "The Edge of Evolution" Strikes Again 8-2-2014 by Paul Giem - video https://www.youtube.com/watch?v=HnO-xa3nBE4 An Open Letter to Kenneth Miller and PZ Myers - Michael Behe July 21, 2014 Dear Professors Miller and Myers, Talk is cheap. Let's see your numbers. In your recent post on and earlier reviews of my book The Edge of Evolution you toss out a lot of words, but no calculations. You downplay FRS Nicholas White's straightforward estimate that -- considering the number of cells per malaria patient (a trillion), times the number of ill people over the years (billions), divided by the number of independent events (fewer than ten) -- the development of chloroquine-resistance in malaria is an event of probability about 1 in 10^20 malaria-cell replications. Okay, if you don't like that, what's your estimate? Let's see your numbers.,,, ,,, If you folks think that direct, parsimonious, rather obvious route to 1 in 10^20 isn't reasonable, go ahead, calculate a different one, then tell us how much it matters, quantitatively. Posit whatever favorable or neutral mutations you want. Just make sure they're consistent with the evidence in the literature (especially the rarity of resistance, the total number of cells available, and the demonstration by Summers et al. that a minimum of two specific mutations in PfCRT is needed for chloroquine transport). Tell us about the effects of other genes, or population structures, if you think they matter much, or let us know if you disagree for some reason with a reported literature result. Or, Ken, tell us how that ARMD phenotype you like to mention affects the math. Just make sure it all works out to around 1 in 10^20, or let us know why not. Everyone is looking forward to seeing your calculations. Please keep the rhetoric to a minimum. With all best wishes (especially to Professor Myers for a speedy recovery), Mike Behe http://www.evolutionnews.org/2014/07/show_me_the_num088041.html Kenneth Miller Resists Chloroquine Resistance - Michael Behe - January 14, 2015 Excerpt: Kenneth R. Miller has posted a (11 page) reply to my challenge to him to give a quantitative account for the extreme rarity of the origin of chloroquine resistance in malaria.,,, The first two and a half pages of the PDF version of Miller's essay consist of stage-setting and throat-clearing. The last six pages are a reprise of his review of The Edge of Evolution and a defense of the evolutionary musings of University of Chicago biologist Joseph Thornton from my skepticism. I'll deal with those later. Miller's only response to my take on the importance of Summers et al. is in the section "Parasites and Drugs." Although the section is less than three pages (including several large figures), as we shall see it includes a number of serious mistakes. Unfortunately, Miller dodges my challenge to provide a quantitative account of the rarity of the origin of chloroquine resistance. I had asked him to "Please keep the rhetoric to a minimum." Alas, to no avail. He cites no relevant numbers, makes no calculations -- just words.,,, Miller's reading of Summers et al. is seriously mistaken. Sadly, a person who can't accurately report the results of a paper makes for an unreliable guide. I urge everyone who has sufficient background to read at least the disputed parts of Summers et al. Determine for yourself which account is correct. http://www.evolutionnews.org/2015/01/kenneth_miller092691.html Kenneth Miller Steps on Darwin's Achilles Heel - Michael Behe - January 17, 2015 Excerpt: Enter Achilles and his heel. It turns out that the odds are much better for atovaquone resistance because only one particular malaria mutation is required for resistance. The odds are astronomical for chloroquine because a minimum of two particular malaria mutations are required for resistance. Just one mutation won't do it. For Darwinism, that is the troublesome significance of Summers et al.: "The findings presented here reveal that the minimum requirement for (low) CQ transport activity ... is two mutations." Darwinism is hounded relentlessly by an unshakeable limitation: if it has to skip even a single tiny step -- that is, if an evolutionary pathway includes a deleterious or even neutral mutation -- then the probability of finding the pathway by random mutation decreases exponentially. If even a few more unselected mutations are needed, the likelihood rapidly fades away.,,, So what should we conclude from all this? Miller grants for purposes of discussion that the likelihood of developing a new protein binding site is 1 in 10^20. Now, suppose that, in order to acquire some new, useful property, not just one but two new protein-binding sites had to develop. In that case the odds would be the multiple of the two separate events -- about 1 in 10^40, which is somewhat more than the number of cells that have existed on earth in the history of life. That seems like a reasonable place to set the likely limit to Darwinism, to draw the edge of evolution. http://www.evolutionnews.org/2015/01/kenneth_miller_1092771.html Michael Behe - Observed (1 in 10^20) Limits of Evolution - video - Lecture delivered in April 2015 at Colorado School of Mines 25:56 minute quote - "This is not an argument anymore that Darwinism cannot make complex functional systems; it is an observation that it does not." https://www.youtube.com/watch?v=9svV8wNUqvA

Of related interest

“The First Rule of Adaptive Evolution”: Break or blunt any functional coded element whose loss would yield a net fitness gain – Michael Behe – December 2010 Excerpt: In its most recent issue The Quarterly Review of Biology has published a review by myself of laboratory evolution experiments of microbes going back four decades.,,, The gist of the paper is that so far the overwhelming number of adaptive (that is, helpful) mutations seen in laboratory evolution experiments are either loss or modification of function. Of course we had already known that the great majority of mutations that have a visible effect on an organism are deleterious. Now, surprisingly, it seems that even the great majority of helpful mutations degrade the genome to a greater or lesser extent.,,, I dub it “The First Rule of Adaptive Evolution”: Break or blunt any functional coded element whose loss would yield a net fitness gain. http://behe.uncommondescent.com/2010/12/the-first-rule-of-adaptive-evolution/ Biological Information - Loss-of-Function Mutations by Paul Giem 2015 - video (Behe - Loss of function mutations are far more likely to fix in a population than gain of function mutations) https://www.youtube.com/watch?v=hzD3hhvepK8&index=20&list=PLHDSWJBW3DNUUhiC9VwPnhl-ymuObyTWJ

bornagain77

Thanks BA77, specifically for referencing to Nesse’s discussion with Dawkins. I’m looking forward to Nick commenting on this.

D.Klinghoffer: Finally he makes a design argument -- not that he intends it as such -- that I for one hadn't heard before:

Nesse: I am amazed, Richard, that what we call metazoans, multi-celled organisms, have actually been able to evolve, and the reason [for amazement] is that bacteria and viruses replicate so quickly -- a few hours sometimes, they can reproduce themselves -- that they can evolve very, very quickly. And we're stuck with twenty years at least between generations. How is it that we resist infection when they can evolve so quickly to find ways around our defenses?

"Amazing" is the right word. He's talking about the origins of multi-celled organisms like us: How did we ever survive, under a Darwinian view, long enough to escape being consumed by creatures that reproduce so much more quickly? [and how do we keep surviving? ; Box]

Nesse: What exactly that transition was between one-celled organisms or few-celled organisms and multi-celled organisms -- the ability of an immune system to protect us from things that evolve so much faster than we do, that want to have us for lunch -- must be very crucial in the origins of life.

"Crucial"! Yes that's the word all right. This leaves Richard Dawkins with a frown on his face, as well it might. Watch the whole thing for yourself. It repays the investment of time. video & article

Box

Always good to see Nick here at UD. It would be even better to see him publish a book on macroevolution. So I googled MHC diversity selection. Looks designed to me! How pathogens drive genetic diversity: MHC, mechanisms and misunderstandings Well there you have it. NickM doesn't even understand his own theory. Mung

NickMatzke_UD, (who has been busted for lying more times than Hillary Clinton), states:

"you seem to have forgotten that the pathogens evolve too."

REALLY Nick??? And you think pathogens evolving too helps your case for neo-Darwinian evolution how exactly? The fact that pathogens 'evolve too' is devastating to a Darwinian scenario! If evolution by natural selection were actually the truth about how all life came to be on Earth then the only ‘life’ that would be around would be extremely small organisms with the highest replication rate, and with the most mutational firepower, since only they, since they greatly outclass multi-cellular organism in terms of ‘reproductive success’, would be fittest to survive in the dog eat dog world where blind pitiless evolution rules and only the fittest are allowed to survive. The logic of this is nicely summed up here:

Richard Dawkins interview with a 'Darwinian' physician goes off track - video Excerpt: "I am amazed, Richard, that what we call metazoans, multi-celled organisms, have actually been able to evolve, and the reason [for amazement] is that bacteria and viruses replicate so quickly -- a few hours sometimes, they can reproduce themselves -- that they can evolve very, very quickly. And we're stuck with twenty years at least between generations. How is it that we resist infection when they can evolve so quickly to find ways around our defenses?" http://www.evolutionnews.org/2012/07/video_to_dawkin062031.html

i.e. Since successful reproduction is all that really matters on a neo-Darwinian view of things, how can anything but successful reproduction be realistically 'selected' for? Any other function besides reproduction, such as sight, hearing, thinking, etc.., would be highly superfluous to the primary criteria of successfully reproducing, and should, on a Darwinian view, be discarded as so much excess baggage since it would, sooner or later, slow down successful reproduction. Humorously, the real world example that Dawkins gave to Dembski, (in Dembski's critique of the 'hidden' teleology within Dawkins' "WEASEL" program), illustrates exactly this point, i.e. the point that natural selection can only 'see' successful reproduction and will 'discard excess baggage':

"Perhaps you should look at the work of Spiegelman and others on evolution of RNA molecules in an RNA replicase environment. They have found that, repeatedly, if you 'seed' such a solution with an RNA molecule, it will converge on a particular size and form of 'optimal' replicator, sometimes called Spiegelman's minivariant." Richard Dawkins http://www.evolutionnews.org/2012/08/conservation_of063671.html

Yet when we look at 'Spiegelman's minivariant' we find:

Spiegelman Monster is the name given to an RNA chain of only 218 nucleotides that is able to be reproduced by an RNA replication enzyme. It is named after its creator, Sol Spiegelman, of the University of Illinois at Urbana-Champaign. Spiegelman introduced RNA from a simple bacteriophage Q? (Q?) into a solution which contained Q?’s RNA replication enzyme, some free nucleotides, and some salts. In this environment, the RNA started to replicate. After a while, Spiegelman took some RNA and moved it to another tube with fresh solution. This process was repeated. Shorter RNA chains were able to replicate faster, so the RNA became shorter and shorter as selection favored speed. After 74 generations, the original strand with 4,500 nucleotide bases ended up as a dwarf genome with only 218 bases. Such a short RNA had been able to replicate very quickly in these unnatural circumstances. In 1997, Eigen and Oehlenschlager showed that the Spiegelman monster eventually becomes even shorter, containing only 48 or 54 nucleotides, which are simply the binding sites for the reproducing enzyme RNA replicase. http://www.revolvy.com/main/index.php?s=Spiegelman%20Monster

Needless to say, Dawkins real world example of 'Spiegelman's minivariant', i.e. loss of information to gain a reproductive advantage, to support his WEASEL program to Dembski is NOT what Dawkins needed to prove his point. Also of note: Although neo-Darwinists are notorious for telling 'just so stories' about the creative power of natural selection,,,

Natural selection makes humans self-centered and aggressive – except when it makes them altruistic and peaceable. Or natural selection produces virile men who eagerly spread their seed – except when it prefers men who are faithful protectors and providers. When an explanation is so supple that it can explain any behavior, it is difficult to test it experimentally, much less use it as a catalyst for scientific discovery. Darwinian evolution – whatever its other virtues – does not provide a fruitful heuristic in experimental biology. - Philip Skell - Why Do We Invoke Darwin? http://www.discovery.org/a/2816 EVOLUTIONARY JUST-SO STORIES Excerpt: ,,,The term “just-so story” was popularized by Rudyard Kipling’s 1902 book by that title which contained fictional stories for children. Kipling says the camel got his hump as a punishment for refusing to work, the leopard’s spots were painted on him by an Ethiopian, and the kangaroo got its powerful hind legs after being chased all day by a dingo. Kipling’s just-so stories are as scientific as the Darwinian accounts of how the amoeba became a man. Lacking real scientific evidence for their theory, evolutionists have used the just-so story to great effect. Backed by impressive scientific credentials, the Darwinian just-so story has the aura of respectability. Biologist Michael Behe observes: “Some evolutionary biologists--like Richard Dawkins--have fertile imaginations. Given a starting point, they almost always can spin a story to get to any biological structure you wish” (Darwin’s Black Box).,,, http://www.wayoflife.org/database/evolutionary_just_so_stories.html

Despite the neo-Darwinian penchant for weaving imaginary 'just so stories' out of thin air that make it seem like natural selection is a master craftsman that can turn an amoeba into a man, the fact of the matter is that natural selection can't even see one microsecond into the future so as to 'select' for any potential future function (i.e. all natural selection can 'see' is directly what is right in front of it. Namely, all natural selection 'sees' is successful reproduction.):

Natural Selection Can’t Select a Future Function – June 2015 Excerpt: In this short video from the Discovery Institute, Paul Nelson follows the development of a C. elegans worm from one cell to an adult, showing how “even these little worms, a millimeter long, humble little creatures out there in the compost heap…carry the signal of design unmistakably.”… If something’s going to function in natural selection, it’s got to function now, at this particular moment in time—not five minutes from now, half an hour, a week, a thousand years. So a process that lacks foresight in principle cannot build a[n] unfolding trajectory, an unfolding lineage [of intermediate cells], where you need to know the target. That’s the fundamental difficulty for any undirected process of evolution. What natural selection and other undirected natural mechanisms cannot achieve, intelligent agents can. Intelligent agents are able to foresee distant functional goals. Intelligent agents can coordinate and choreograph the assembly of many separately necessary parts to achieve a functional end. http://str.typepad.com/weblog/2015/06/natural-selection-cant-select-a-future-function.html

of supplemental note. Here is a brief look at some of Matzke's history of dishonesty towards ID:

Calling Nick Matzke's literature bluff on molecular machines - DonaldM UD blogger - April 2013 Excerpt: So now, 10 years later in 2006 Matzke and Pallen come along with this review article. The interesting thing about this article is that, despite all the hand waving claims about all these dozens if not hundreds of peer reviewed research studies showing how evolution built a flagellum, Matzke and Pallen didn’t have a single such reference in their bibliography. Nor did they reference any such study in the article. Rather, the article went into great lengths to explain how a researcher might go about conducting a study to show how evolution could have produced the system. Well, if all those articles and studies were already there, why not just point them all out? In shorty, the entire article was a tacit admission that Behe had been right all along. Fast forward to now and Andre’s question directed to Matzke. We’re now some 17 years after Behe’s book came out where he made that famous claim. And, no surprise, there still is not a single peer reviewed research study that provides the Darwinian explanation for a bacterial flagellum (or any of the other irreducibly complex biological systems Behe mentioned in the book). We’re almost 7 years after the Matzke & Pallen article. So where are all these research studies? There’s been ample time for someone to do something in this regard. Matzke will not answer the question because there is no answer he can give…no peer reviewed research study he can reference, other than the usual literature bluffing he’s done in the past. https://uncommondesc.wpengine.com/irreducible-complexity/andre-asks-an-excellent-question-regarding-dna-as-a-part-of-an-in-cell-irreducibly-complex-communication-system/#comment-453291

bornagain77

Wow, it's like you've never heard of all of the research on natural selection and immune system genes. Google MHC diversity selection for starters. Immune system genes typically have some of the strongest statistical signatures of selection, in almost any animal anyone looks at. Also, you seen to have forgotten that the pathogens evolve too. Why should anyone take you seriously if you get step 1 (do your background research) wrong in commenting on science? NickMatzke_UD