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Survival of the Fittest?

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Here’s a news article about 400,000 antelopes dying off in a short period of time. Looks like it’s due to some sort of bacterial attack, though they’re not fully sure what caused this massive die-off.

There’s lots of questions that come to mind. Here’s one or two:
(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?

(2) In the annals of NS, no one has likely ever seen anything like this. The selection factor is 0.5 (half the population has died off). What other small, gradual change could be this destructive? And it seems it all has to do with bacteria. So, are the “fittest” the ones with the best “immune systems”? If that’s the case, with this kind of selection factor at work, you’d expect that the survivors, the ‘fittest’, would have incredibly good immune systems. Yet, something like this huge die-off happened not too long ago (1988). So, if something this lethal leads to hardly any change, then what great change is NS going to bring about when the selection pressure is far, far less.

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)

Comments
Seversky- Luck is the antithesis of science.Virgil Cain
September 6, 2015
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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
September 6, 2015
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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
September 6, 2015
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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
September 6, 2015
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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
September 6, 2015
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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
September 6, 2015
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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
September 6, 2015
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Bob O'H:
Hiw does that paper contradict what Nick wrote?
If it was designed then natural selection didn't do it.Virgil Cain
September 6, 2015
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Seversky:
That’s right. It’s the luck of the draw.
Then it ain't science. Thank you for admitting that.Virgil Cain
September 6, 2015
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Mung @ 3 - Hiw does that paper contradict what Nick wrote?Bob O'H
September 6, 2015
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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
September 6, 2015
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"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
September 5, 2015
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"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
September 5, 2015
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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
September 5, 2015
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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
September 5, 2015
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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
September 5, 2015
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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
September 5, 2015
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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
September 5, 2015
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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
September 5, 2015
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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
September 5, 2015
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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
September 4, 2015
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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://uncommondescent.com/irreducible-complexity/andre-asks-an-excellent-question-regarding-dna-as-a-part-of-an-in-cell-irreducibly-complex-communication-system/#comment-453291
bornagain77
September 4, 2015
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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
September 4, 2015
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