Uncommon Descent Serving The Intelligent Design Community

Free Online Course: Introduction to Genetics and Evolution

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Critics of modern evolutionary theory have an intellectual responsibility to strive to understand the paradigm that they are critiquing, preferably to a level where they can clearly articulate the key propositions of evolutionary theory and offer a standard defense of them.

Richard Hoppe, at the Panda’s Thumb blog, drew my attention to a free online course on the subject of genetics and evolution. You can, as I have done, sign up for (and read about) the course at this link.

The course description states,

“Introduction to Genetics and Evolution gives interested people a very basic overview of the principles behind these very fundamental areas of biology.  We often hear about new “genome sequences,” commercial kits that can tell you about your ancestry (including pre-human) from your DNA or disease predispositions, debates about the truth of evolution, and why animals behave the way they do.  This course provides the basic biology you need to understand all of these issues better and tries to clarify some misconceptions.  No prior coursework is assumed.”

Topics that will be covered in this course include:

  • Evidence for evolution
  • Introduction to basic genetics
  • Recombination and genetic mapping simple traits
  • Complications to genetic mapping
  • Genes vs. environment
  • Basic population genetics and Hardy-Weinberg
  • Gene flow, differentiation, inbreeding
  • Natural selection and genetic drift
  • Molecular evolution
  • Evolutionary applications and misapplications
  • Adaptive behaviors and species formation

Dr. Mohamed Noor, who obtained his PhD, I am told, under Jerry Coyne, will be the instructor of the course:

“Dr. Mohamed Noor is the Earl D. McLean Professor and Associate Chair of Biology at Duke University.  His expertise is in molecular evolution, and a large part of his research has been devoted to trying to understand the genetic changes that ultimately lead to the formation of new species. More recently, his research team has used fruit fly species to understand the causes and evolutionary consequences of variation in rates of genetic recombination/ exchange.

Dr. Noor has received several awards for research, teaching, and mentoring, and has been active in the scientific community, including serving as president of the American Genetic Association, chair of the NIH study section in Genetic Variation and Evolution, and editor of the journal Evolution.”

The course lasts 10 weeks and begins on October 10th. The description page also notes that “The class will consist of watching multiple lecture mini-videos which are roughly 10-15 minutes in length.  These contain 1-3 integrated quiz questions per video.  There will also be 3 test assessments, including a non-cumulative final exam.”

I particularly recommend that those among us who don’t have a strong biology background take this course. It is very important that we ID proponents make sure we have a robust grasp of what evolutionary theory is saying and why it says it, so that no one can say we haven’t given it a fair hearing. Go here to register!

Comments
I think the light moths tasted better. I think that's why the birds ate them. And any self-respecting bird population would have evolved better eyesight so they could see the dark moths better. That way they could eat more and live longer and leave more offspring.Mung
October 21, 2012
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Mung posted this:
So they were choosing to eat light moths rather than dark moths?
You are getting close, but are still fixated with the teleological thing. The birds selectively eat the light-coloured variant on dark-coloured trees because they are easier to see. The melanised moths enjoy a reproductive advantage as a result. Once the industrially induced darkening of the trees is reversed, the selective pressure of predation moves to the variant that is more obvious.timothya
October 20, 2012
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timothya:
In the early, smoggy phase the lichens die off revealing the light coloured moth variant.
Well, surely the lichens evolved too then.
No design required. Just natural selection doing what it does.
Natural selection does not do anything. You evidently understand how natural selection actually works. Saying natural selection works implies a force of some kind. Natural selection does not "work," it is not a "force." It's not a cause, it's an effect. Oh, look, more dark moths! If that's what you guys mean when you say evolution is true, grats to you. If you went around killing light colored moths I'd call that selection.
Predators selectively pick them off...
So they were choosing to eat light moths rather than dark moths?Mung
October 18, 2012
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Mung posted this:
It doesn’t take a genius to figure out if you have a population of light and dark colored moths and you kill off more light colored moths that the relative numbers of dark colored moths will increase, and vice versa
The only mistake you make is in the use of ther term "you" (there is no conscious "you" involved). In the case of the peppered moth, the "killing off" was done by the blind, impersonal pressure of the environment that the moths lived in. In the early, smoggy phase the lichens die off revealing the light coloured moth variant. Predators selectively pick them off, so the population moves inexorably towards an average dark colour. After the Clean Air Act, and the concomitant reduction in industrial pollution, the light coloured lichens return. The predator species find the dark variant easier to locate, and the selective pressure of the environment changes the moth colour allele in lockstep. No design required. Just natural selection doing what it does. Little steps, my friends, little steps. You evidently understand how natural selection actually works. Now ask the next question . . . (Meanwhile avoiding the pitfall of claiming more than you know)timothya
October 18, 2012
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timothya, It doesn't take a genius to figure out if you have a population of light and dark colored moths and you kill off more light colored moths that the relative numbers of dark colored moths will increase, and vice versa. If that's what you guys mean when you say evolution is true, grats to you.Mung
October 17, 2012
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Eric Anderson posted this:
I was frankly astounded — 20 years after Philip Johnson’s disection of the peppered moth story the example of evolution in action that was used by the good professor was, you guessed it, the peppered moth story.
Could you (for my benefit, if not for anyone else) explain your astonishment by providing a brief summary of the salient features of Johnson's rebuttal, and why you think those features remain valid today? A few dot points covering the headland arguments would help me. I have read The Wedge of Truth and I am assuming that the book contains the dissection to which you refer. I am seeking to understand whether and why you think Johnson's arguments still stand.timothya
October 17, 2012
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Ah, PaV, you're just too skeptical. Don't you know that any change over time from generation to generation is 'evolution' in action? Why, just today in our very first day of class we were reminded of this by the good professor. I was frankly astounded -- 20 years after Philip Johnson's disection of the peppered moth story the example of evolution in action that was used by the good professor was, you guessed it, the peppered moth story. BTW, he seems to be a very likeable guy and I think this will be an interesting course if we can manage to survive the scheduled indoctrination of the first week (evolution is a mathematical certainty; only dupes dispute it; there is no debate in the scientific community; etc.). I hope the thought police don't track me down . . . :)Eric Anderson
October 10, 2012
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Genomicus:
However, when I say “species,” I typically mean a population of organisms capable of producing fertile offspring.
I'm currently reading The Beak of the Finch by Jonathan Weiner. We find out that the "Grants," working with the Galapagos finches on the island of Daphnea, could isolate 'seven' different species of ground finches. But, then, surprisingly, out of nowhere, two of the finches produced full-fertile hybrids. And, not only that, but the hybrids are increasing at a much higher rate than the crossed species. So they're "really" fertile. But, wait a second, this is a hybrid from 'two' of the 'species.' Per your definition, this looks like we don't have 'seven' species, but perhaps only 'six'. Or is it even fewer. But, taxonomically, these 'species' are considered separate 'species.' So, when you say that Darwinian processes can bring about new species, how can that be so given we have such a hard problem deciding what does, or does not, constitute a new 'species'? And, should I mention that the untrained eye couldn't tell the difference between any of these supposed 'seven' species, yet, I have no problem at all telling a Poodle from a Dalmatian, which are considered the SAME species. What a mess. In the end, I don't know how we can be justified in saying that RM+NS has brought about new and separate 'species', while freely admitting that, indeed, there are separate 'species.' BTW, Weiner's book is a really good read, full of very interesting information, and gives a great overview of "evolution in action." However, a careful read of it leads one to clearly see that Darwinian mechanisms have nothing at all to do with 'speciation.' It's a great book for disproving Darwinian evolution---contrary to the author's purpose. Genomicus, we'll just have to disagree on all of this.PaV
October 10, 2012
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PaV:
At long last: what constitutes a ‘species’?
That's a good question, but unfortunately there is no truly rigorous definition of what constitutes a species. However, when I say "species," I typically mean a population of organisms capable of producing fertile offspring.Genomicus
October 10, 2012
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Jonathan M, having recently completed your master's in evolutionary biology (congrats BTW), what's your purpose in taking this course?JoeCoder
October 10, 2012
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Genomicus:
No. Allele frequencies of particular genes can differ within a species.
At long last: what constitutes a 'species'?PaV
October 9, 2012
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Genomicus @52: Yeah, OK, I know the graph you are talking about. And I remember thinking when I hit that page that he was giving away the store. After all, he had spent the whole book demonstrating that even in a massive population with huge selection pressure you would only get a small handful of nucleotide substitutions, possibly only 2 or 3. But we have to remember that he was trying to establsh an absolute boundry and wasn't willing to put species outside that boundry. (I'm not sure I would be either, particularly given the rather fluid definition of species in particular circumstances.) Also, Behe doesn't state that all species can result from RM+NS, just that it is possible that some species could. Thus, I think I understand where you are coming from. But rather than saying that Behe thinks RM+NS "is perfectly capable of giving rise to new species" we should say something more along the lines of: "Behe doesn't dispute the possibility of RM+NS producing new species under certain circumstances."Eric Anderson
October 9, 2012
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Genomicus, I would be interested in a statement from Behe that RM+NS can result in new species. That is very different from my understanding of his position.
Well IIRC, if you take a look at one of the figures in The Edge of Evolution,you'll find that Michael Behe suggests that the edge of evolution lies between species and class (with some ambiguity there). Which means that species are within the limits of non-teleological evolutionary processes. I don't have a clear idea of this figure because I read the EoE from a library copy, so I don't have it with me.Genomicus
October 9, 2012
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PaV:
Does this mean their “allele frequencies” are identical?
No. Allele frequencies of particular genes can differ within a species.Genomicus
October 9, 2012
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Genomicus: I hope you reply to my last post. I suspected that we would see things differently when it came to what constitutes a species. We're very close to discovering where we differ, so I hope the conversation can continue.PaV
October 9, 2012
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Jonathan, could I suggest that the Intelligent Design scholars make an effort to produce a video course. Some of us live off these types of courses, but www.thegreatcourses.com for example have no Intelligent Design friendly courses that we know of.Christian-apologetics.org
October 8, 2012
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Genomicus, I would be interested in a statement from Behe that RM+NS can result in new species. That is very different from my understanding of his position.Eric Anderson
October 8, 2012
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Genomicus:
St. Bernard: Canis lupus familiaris. Chihuahua: Canis lupus familiaris.
Does this mean their "allele frequencies" are identical?PaV
October 8, 2012
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PaV:
Are Chihuahuas and St. Bernards different “species”?
It doesn't look like it: St. Bernard: Canis lupus familiaris. Chihuahua: Canis lupus familiaris.Genomicus
October 7, 2012
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Genomicus:
In agreement with Professor Behe, and others, I am suggesting that random mutation coupled to natural selection is perfectly capable of giving rise to new species.
Are Chihuahuas and St. Bernards different "species"?PaV
October 7, 2012
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Hmm he recommends Jerry Coyne? He's not very fair nor open minded. See an expose of him here in one incident: http://jerrycoyne.blogspot.co.uk/2012/10/jerry-coyne-and-open-mindedness.htmlsuyuti
October 7, 2012
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This site is a goldmine. Thanks a lot, im gonna try the epigenetics course too!MaxAug
October 7, 2012
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That is very interesting, Genomicus - especially, 'new to the field.' It is odd though that it should tend (my impression is, 'very pronouncedly), to be the young. I hadn't spotted, 'very young', which seems yet more remarkable. The more so, perhaps, in the light of a remark of the atomic physicist, Oppenheimer, which seems to bear on the subject: 'There are children playing in the streets who could solve some of my top problems in physics, because they have modes of sensory perception that I lost long ago.' That latter point, his explanation, is also interesting in terms of the course of the mundane course of our lives. I believe our brain routinely prioritizes the retention of what we remember and what skills we have learnt, according to our present needs, in terms of the more recent course of our lives. I believe that was why an Australain woman said to me anxiously that, when she thought of the work she had been doing as an accounts manager with an oil company, it kind of scared her, as she couldn't imagine being able to do it now - evidently fearing a pathological (if modest, in the scheme of things) loss of her cognitive powers. But she presumably, feared the loss was due to some medical, demential condition. Also, if you spread out a pack of cards, or an appreciable number of them, on a table - there is a game in which this takes place, a young child will normally, I believe, have a far better memory of the location of the cards. It was certainly the case with a young cousin of mine. But then, are not young children the truest of intellectuals, motivated purely by a desire to learn, to know. The world and its pressures and exigencies has not yet affected their outlook. They want to learn everything, on a far more undiscriminating basis than we.Axel
October 7, 2012
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G:
In agreement with Professor Behe, and others, I am suggesting that random mutation coupled to natural selection is perfectly capable of giving rise to new species.
But taht doesn't mean anything wrt biological complexity.Joe
October 7, 2012
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Damn, I was really hoping this course had evidence of macro evolution, who is arguing about micro? I don't think anybody on the planet denies adaptations....Andre
October 6, 2012
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Axel: I concur. To quote from Thomas Kuhn: "Almost always the men who achieve these fundamental inventions of a new paradigm have been either very young or very new to the field whose paradigm they change."Genomicus
October 6, 2012
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'It’s not at all that you need a PhD to hold a dissenting view, but age, thought and experience count for a lot.' I don't think so, JoeCoder. Max Planck summed it up all too epigrammaticaly: 'Science advances, one funeral at a time.' The teacher - assuming the youngster is correct - rightly feels his status is threatened, doesn't he? Your point is really tangential, indeed, another issue. It all hinges on who is correct. Nobody likes a smart Alec. Sure. But on such an occasion, the truth may dwarf personal feelings. Einstein was apparently a cocky student.Axel
October 6, 2012
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to highlight the monumental problem that Darwinian processes face in generating fundamentally new species (as opposed to a new sub-species of a already existent parent kind): to reiterate:
"The likelihood of developing two binding sites in a protein complex would be the square of the probability of developing one: a double CCC (chloroquine complexity cluster), 10^20 times 10^20, which is 10^40. There have likely been fewer than 10^40 cells in the entire world in the past 4 billion years, so the odds are against a single event of this variety (just 2 binding sites being generated by accident) in the history of life. It is biologically unreasonable." Michael J. Behe PhD. (from page 146 of his book "Edge of Evolution")
And yet, Dr. Behe, on the important Table 7.1 on page 143 of Edge Of Evolution, finds that a typical cell might have some 10,000 protein-binding sites. Whereas a conservative estimate for protein-protein binding sites in a multicellular creature is,,,
Largest-Ever Map of Plant Protein Interactions - July 2011 Excerpt: The new map of 6,205 protein partnerings represents only about two percent of the full protein- protein "interactome" for Arabidopsis, since the screening test covered only a third of all Arabidopsis proteins, and wasn't sensitive enough to detect many weaker protein interactions. "There will be larger maps after this one," says Ecker. http://www.sciencedaily.com/releases/2011/07/110728144936.htm
So taking into account that they only covered 2%, of the full protein-protein "interactome", then that gives us a number, for different protein-protein interactions, of 310,000. Thus, from my very rough 'back of the envelope' calculations, we find that this is at least 30 times higher than Dr. Behe's estimate of 10,000 different protein-protein binding sites for a typical single cell (Page 143; Edge of Evolution; Behe). Therefore, at least at first glance from my rough calculations, it certainly seems to be a gargantuan step that evolution must somehow make, by purely unguided processes, to go from a single cell to a multi-cellular creature. Moreover, there is, 'surprisingly', found to be 'rather low' conservation of Domain-Domain Interactions occurring in Protein-Protein interactions between different species:
A Top-Down Approach to Infer and Compare Domain-Domain Interactions across Eight Model Organisms Excerpt: Knowledge of specific domain-domain interactions (DDIs) is essential to understand the functional significance of protein interaction networks. Despite the availability of an enormous amount of data on protein-protein interactions (PPIs), very little is known about specific DDIs occurring in them.,,, Our results show that only 23% of these DDIs are conserved in at least two species and only 3.8% in at least 4 species, indicating a rather low conservation across species.,,, http://www.plosone.org/article/info:doi/10.1371/journal.pone.0005096
Thus Genomicus, whatever you may have imagined for the ease of Darwinian processes to give rise to new species,,,
In agreement with Professor Behe, and others, I am suggesting that random mutation coupled to natural selection is perfectly capable of giving rise to new species.
,,, the fact of the matter is that Dr. Behe's work, despite what you may have imagined it to suggest, is completely antagonistic to the belief that RM and NS can do as such! As well, Dr. Behe's empirical research, that had found extreme difficulty for Darwinian processes to create just two binding sites, agrees with the extreme difficulty that is found for scientists trying to purposely design just a single protein-protein binding site:
Viral-Binding Protein Design Makes the Case for Intelligent Design Sick! (as in cool) - Fazale Rana - June 2011 Excerpt: When considering this study, it is remarkable to note how much effort it took to design a protein that binds to a specific location on the hemagglutinin molecule. As biochemists Bryan Der and Brian Kuhlman point out while commenting on this work, the design of these proteins required: "...cutting-edge software developed by ~20 groups worldwide and 100,000 hours of highly parallel computing time. It also involved using a technique known as yeast display to screen candidate proteins and select those with high binding affinities, as well as x-ray crystallography to validate designs.2" If it takes this much work and intellectual input to create a single protein from scratch, is it really reasonable to think that undirected evolutionary processes could accomplish this task routinely? In other words, the researchers from the University of Washington and The Scripps Institute have unwittingly provided empirical evidence that the high-precision interactions required for PPIs requires intelligent agency to arise. Sick! http://www.reasons.org/viral-binding-protein-design-makes-case-intelligent-design-sick-cool Computer-designed proteins programmed to disarm variety of flu viruses - June 1, 2012 Excerpt: The research efforts, akin to docking a space station but on a molecular level, are made possible by computers that can describe the landscapes of forces involved on the submicroscopic scale.,, These maps were used to reprogram the design to achieve a more precise interaction between the inhibitor protein and the virus molecule. It also enabled the scientists, they said, "to leapfrog over bottlenecks" to improve the activity of the binder. http://phys.org/news/2012-06-computer-designed-proteins-variety-flu-viruses.html
Further notes:
Two Domain Protein - video (several binding sites required) http://www.facebook.com/photo.php?v=421708024519477 Why Proteins (Protein Domains) Aren't Easily Recombined - Ann Gauger - May 2012 Excerpt: each particular helix or sheet has a distinct set of side chains sticking out from it, requiring a distinct set of chemical interactions with any nearby protein sequence. Thus, helices and sheets are sequence-dependent structural elements within protein folds. You can’t swap them around like lego bricks. This necessarily means that when you bring new secondary structure elements into contact by some sort of rearrangement, they will be unlikely to form a stable three dimensional fold without significant modification. http://www.biologicinstitute.org/post/22595615671/why-proteins-arent-easily-recombined "Why Proteins Aren't Easily Recombined, Part 2" - Ann Gauger - May 2012 Excerpt: "So we have context-dependent effects on protein function at the level of primary sequence, secondary structure, and tertiary (domain-level) structure. This does not bode well for successful, random recombination of bits of sequence into functional, stable protein folds, or even for domain-level recombinations where significant interaction is required." http://www.biologicinstitute.org/post/23170843182/why-proteins-arent-easily-recombined-part-2
Verse and music:
Psalm 104:24 O Lord, how manifold are your works! In wisdom you have made them all. The earth is full of Your possessions Evanescence - The Other Side (Lyric Video) http://www.youtube.com/watch?v=HiIvtRg7-Lc
bornagain77
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as to:
In agreement with Professor Behe, and others, I am suggesting that random mutation coupled to natural selection is perfectly capable of giving rise to new species.
And yet even though Dr. Behe may give far more credence to the supposed (contrived) evidence for common descent than is warranted, the fact is that, whatever views Dr. Behe personally has on common descent, he, in his book Edge of Evolution, adamantly does not hold that the mechanism of 'random mutation coupled to natural selection is perfectly capable of giving rise to new species':
The Edge Of Evolution - Michael Behe - Video Lecture http://www.c-spanvideo.org/program/199326-1 A review of The Edge of Evolution: The Search for the Limits of Darwinism The numbers of Plasmodium and HIV in the last 50 years greatly exceeds the total number of mammals since their supposed evolutionary origin (several hundred million years ago), yet little has been achieved by evolution. This suggests that mammals could have "invented" little in their time frame. Behe: ‘Our experience with HIV gives good reason to think that Darwinism doesn’t do much—even with billions of years and all the cells in that world at its disposal’ (p. 155). http://creation.com/review-michael-behe-edge-of-evolution Michael Behe, The Edge of Evolution, pg. 162 Swine Flu, Viruses, and the Edge of Evolution "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." http://www.evolutionnews.org/2009/05/swine_flu_viruses_and_the_edge.html
In fact, Dr. Behe puts the 'edge of evolution' somewhere between species and class:
Behe comes to the conclusion that the edge of Darwinian evolution for a vertebrate lies somewhere between the level of species and class. That is, evolution cannot explain the categories above this level. Interestingly, creationist biologist Frank Marsh proposed in 1976 that the created kinds (baramins) were often at the level of genus or family, although sometimes at the level of order. (Figure 10.1, p. 218). http://creation.com/images/journal_of_creation/vol22/6472chart-lge.jpg
Dr. Behe states in The Edge of Evolution on page 135:
"Generating a single new cellular protein-protein binding site (in other words, generating a truly beneficial mutational event that would actually explain the generation of the complex molecular machinery we see in life) is of the same order of difficulty or worse than the development of chloroquine resistance in the malarial parasite." "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
Dr. Behe's subsequent work has only further refined what he had originally found to the severe limitation of what random variation and natural selection could accomplish:
Severe Limits to Darwinian Evolution: - Michael Behe - Oct. 2009 Excerpt: The immediate, obvious implication is that the 2009 results render problematic even pretty small changes in structure/function for all proteins — not just the ones he worked on.,,,Thanks to Thornton’s impressive work, we can now see that the limits to Darwinian evolution are more severe than even I had supposed. http://www.evolutionnews.org/2009/10/severe_limits_to_darwinian_evo.html Wheel of Fortune: New Work by Thornton's Group Supports Time-Asymmetric Dollo's Law - Michael Behe - October 5, 2011 Excerpt: Darwinian selection will fit a protein to its current task as tightly as it can. In the process, it makes it extremely difficult to adapt to a new task or revert to an old task by random mutation plus selection. http://www.evolutionnews.org/2011/10/wheel_of_fortune_new_work_by_t051621.html
The following study surveys four decades of experimental work, and solidly backs up the preceding conclusion that there has never been an observed violation of genetic entropy:
“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.(that is a net 'fitness gain' within a 'stressed' environment i.e. remove the stress from the environment and the parent strain is always more 'fit') http://behe.uncommondescent.com/2010/12/the-first-rule-of-adaptive-evolution/
Out of the horse's mouth, Dr. Michael Behe talks about the preceding paper on this podcast:
Michael Behe: Challenging Darwin, One Peer-Reviewed Paper at a Time - December 2010 http://intelligentdesign.podomatic.com/player/web/2010-12-23T11_53_46-08_00
Thus, although Dr. Behe may support some form of common descent, he certainly does not think that Random Variation and Natural Selection are the main driving mechanisms behind common descent.bornagain77
October 6, 2012
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Nevermind. I see now that the workload on the page is listed as 5-6 hours a week.JoeCoder
October 6, 2012
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