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Darwin proven wrong, again! Experimental Evolution Reveals Resistance to Change

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Natural Selection is daily and hourly scrutinising, throughout the world, the slightest variations; rejecting those that are bad, preserving and adding up all that are good.

C.DARWIN sixth edition Origin of Species — Ch#4 Natural Selection

NOT! Newly appearing good traits in a single individual will rarely get infused (or “fixed” ) into a population. To understand theoretically why this is false, visit: Gambler’s Ruin is Darwin’s Ruin.

And now we have some poignant experimental confirmation of my theoretical prediction! In a paper published by the prestigious scientific journal Nature September 30,2010 we read:

Our work provides a new perspective on the genetic basis of adaptation. Despite decades of sustained selection in relatively small, sexually reproducing laboratory populations, selection did not lead to the fixation of newly arising unconditionally advantageous alleles. This is notable because in wild populations we expect the strength of natural selection to be less intense and the environment unlikely to remain constant for ~600 generations.”

Consequently, the probability of fixation in wild populations should be even lower than its likelihood in these experiments. This suggests that selection does not readily expunge genetic variation in sexual populations, a finding which in turn should motivate efforts to discover why this is seemingly the case.”

Notes:
See: Experimental Evolution Reveals Resistance to Change

HT: Joseph

Comments
Once again PaV is correct- natural selection is not a magical ratchet and that is what it is supposed to be- or least that has been what it has been portrayed as.Joseph
October 4, 2010
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PaV: I agree. I have tried somnetimes to express the concept that NS, if and when it does something, is not so much the environment selecting living beings, but rather living beings self-selecting themselves, taking into account the environment as part of the scenario. I believe that too much emphasis has been given to reproductive advantage and to environmental pressures, including competition, predators and so on. I am not saying those things have no importance, but they are not the only factors implied. Many new functions and structures in life history are not necessarily related to survival only. Survival is certainly important, but it is often a condition which allows new functions to express themselves, and not necessarily the cause for them. A search for diversity, for trying out various possibilities, for exploring new manifestations of life, for expressing new and mor complex functions, is IMO a much better explanation of natural history tham a mere search for survival. I have often argued that, at present, archea and bacteria are still the best reproductors on the planet. And probably the most successful living beings, in terms of number and diffusion. So, why all the complicated rest, if the only driving force is reproductive advantage?gpuccio
October 4, 2010
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About a year and a half ago, there was a study published that analyzed a bacterial population being selected for on the basis of differing nutrients in the culture. IIRC, upon genome wide examination, they came to the conclusion that the population, i.e., any particular bacterial culture, never completely "fixes". This study buttresses the finding of that study. The implication clearly seems to be that gene frequencies are not just about purely stochastic processes; rather, gene frequencies are guided by genomic structures that are 'utilizing' stochastic processes. This calls NS completely into question. I have taken the position for a long time that NS is not what it is supposed to be. What is at work in nature is not NS, but living cells that are built to use stochastic processes to help them adapt. To see NS as fundamental is to mistake an effect for a cause. As Sal noted above, Kimura basically said back in the early seventies that NS, as it is scientifically thought of, doesn't really exist. Here's more dispositive proof of the Darwinian myth.PaV
October 4, 2010
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Haldane, J. B. S., 1957. "The cost of natural selection" Journal of Genetics 55: 511-524 Even the theory of evolution can't escape inflation. What was 300 generations in 1957 is now more than 600! I bet global warming has something to do with it too.Joseph
October 2, 2010
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Flash back to 1957 and biologist JBS Haldane 1 new gene becomes fixed about every 300 generations. He did state his conclusions may require drastic revision and he was right. He was off by at least a factor of 2. Just sayin'...Joseph
October 2, 2010
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To put it in terms of human evolution: Taking at face value the repeated claim that the DNA of chimps and humans is 99% similar, that means that there are about 40 million base pair differences that arose and became virtually universal within the species during the ~350,000 generations since the time of the most recent common ancestors. I suppose that the Darwinists will set forth the notion that changes become established in a species during periods of intense bottle-necking, when new changes have much less competition, and will also go on to modify the theory so that such bottle-necking becomes a primary feature.EvilSnack
October 2, 2010
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scordova: Great post. NS has certainly been vastly overrated on the basis of models of microevolutionary selection in bacteria under completely artificial conditions, like antibiotic resistance. It is really interesting to try to imagine what NS can really do in small-population, slow replicating beings like us. If we are patient enough, maybe we will witness the expansion and fixation of Apo A1 Milan, so dear to darwinian propaganda, in the whole world population! Living in Italy, I will keep my eyes well open for the first signs of that, and let you know :) (With my blood lipid values, I am certainly cut off from the species of the future...)gpuccio
October 2, 2010
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Lest we forget, this experiment vindicates a claim by David Berlinski that was widely criticized by the Darwinists in 2005: The Strength of Natural Selection in the Wild
Natural selection disappears as a biological force and reappears as a statistical artifact. The change is not trivial. It is one thing to say that nothing in biology makes sense except in the light of evolution; it is quite another thing to say that nothing in biology makes sense except in the light of various regression correlations between quantitative characteristics. It hardly appears obvious that if natural selection is simply a matter of correlations established between quantitative traits, that Darwin's theory has any content beyond the phenomenological, and in the most obvious sense, is no theory at all. Be that as it may, the real burden of Kingsolver's study lies in the quantitative conclusions it reaches. Two correlations are at issue. The first is linear, and corresponds to what in population genetics is called directional selection; and the second quadratic, and corresponds either to stabilizing or disruptive selection. These are the cornerstones of the modern hill and valley model of much of mathematical population genetics. Kingsolver reported a median absolute value of 0.16 for linear selection, and a median absolute value of 0.10 for quadratic selection. Thus an increase of one standard deviation in, say, beak finch length, could be expected to change fitness by only 16 percent in the case of linear selection, and 10 percent in the case of quadratic selection. These figures are commonly understood to represent a very weak correlation. Thus if a change in the length of a beak's finch by one standard deviation explains 16 percent of the change in the population's fitness, 84 percent of the change is not explained by selection at all. These results, although at odds with those reported by Endler, are not in themselves astounding. It is when sample sizes pass beyond samples of 1000 that results become far more difficult to accommodate, for under these circumstances, Kingsolver reported, both linear and quadratic selection were virtually non-existent. The significance of these results is, of course, not entirely clear. Kingsolver goes no further than observing that "important issues about selection remain unresolved." Considering the fundamental role of both linear and quadratic selection in population genetics and in popular accounts of Darwin's theory, one of those "unresolved" issues may well be whether natural selection exists to any appreciable extent, and if it does, whether it plays any real role in biological change altogether.
And in light of Pagels work published this year, we know "speciation" events are mostly NOT due to selection either, thus obliterating Darwin's main thesis: Origin of Species by Means of Natural Selection And then it also agrees with Nei's interpretation Kimura's work that the majority of molecular evolution is NON-Darwinian, therefore all other evolution is mostly NON-Darwinian. Recall what Dick Dawkins ssaid:
Natural seleciton is the exact opposite of random
Not so, most of the NS time is hardly distinguishable from random. This observation was made by Kimura:
if a mutant gene is selectively neutral the probability is 0.79 that it will be lost from the population …. if the mutant gene has a selective advantage of 1%, the probability of loss during the fist seven generations is 0.78. As compared with the neutral mutant, this probability of extinction [with natural selection] is less by only .01 [compared to extinction by purely random events]. …. Theoretical Aspects of Population Genetics Motoo Kimura and Tomoko Ohta
Kimura and Ohta right, Darwin and Dawkins, wrong. :-)scordova
October 2, 2010
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Just to be clear, they did not say the say "zero novel, advantageous mutations". There were none that were fixed. They did see "several dozen genomic regions that show strong allele frequency differentiation between a pooled sample of five replicate populations selected for accelerated development and pooled controls." And from there results they hypothesized that the vast changes in the genomes that they saw which were linked to the evolution of accelerated development may be due to "‘incomplete’ sweep models, in which mutations have not had enough time to fix, and ‘soft’ sweep models, in which selection acts on pre-existing, common genetic variants." Whether this is true or not will require further study of course.Winston Macchi
October 1, 2010
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I wonder if the Gambler's odds are even more generous than what evolution can depend on. This conclusion from the quoted text is important (the whole study is pretty devastating):
This is notable because in wild populations we expect the strength of natural selection to be less intense and the environment unlikely to remain constant for ~600 generations
The experimental conditions use an environment that "remains constant". In the wild, the environment itself is a random variable. So, there's not just the probability of random mutations in an ideal condition but an additional layer of unpredictibility added. Would it be like predicting Blackjack using a deck of cards that added or deleted any number (or mutated) cards at each draw? In this case, the researchers note that advantageous mutations will not become fixed because "selection coefficients change over time". Thus, a lab setting showed zero novel, advantageous mutations, and the wild will show even fewer. :-)Proponentist
October 1, 2010
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This is great, for it offers related empirical verification to what Dr. Sanford 'predicted" for fixation of a single beneficial mutation: Dr. Sanford calculates it would take 12 million years to “fix” a single base pair mutation into a population. He further calculates that to create a gene with 1000 base pairs, it would take 12 million x 1000 or 12 billion years. This is obviously too slow to support the creation of the human genome containing 3 billion base pairs. http://www.detectingtruth.com/?p=66 as well the study further offers much more weight to what Behe and Sternberg were saying about the constraints for the fixation of two 'coordinated' beneficial mutations: Waiting Longer for Two Mutations - Michael J. Behe Excerpt: Citing malaria literature sources (White 2004) I had noted that the de novo appearance of chloroquine resistance in Plasmodium falciparum was an event of probability of 1 in 10^20. I then wrote that ‘‘for humans to achieve a mutation like this by chance, we would have to wait 100 million times 10 million years’’ (Behe 2007) (because that is the extrapolated time that it would take to produce 10^20 humans). Durrett and Schmidt (2008, p. 1507) retort that my number ‘‘is 5 million times larger than the calculation we have just given’’ using their model (which nonetheless "using their model" gives a prohibitively long waiting time of 216 million years). Their criticism compares apples to oranges. My figure of 10^20 is an empirical statistic from the literature; it is not, as their calculation is, a theoretical estimate from a population genetics model. http://www.discovery.org/a/9461 Whale Evolution Vs. Population Genetics - Richard Sternberg PhD. in Evolutionary Biology - video http://www.metacafe.com/watch/4165203bornagain77
October 1, 2010
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