Intelligent Design

Two Wrongs Don’t Make a Right

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An article in Ecology letters, entitled: “Eco-evolutionary Dynamics in Response to Selection on Life-history,” deals with research conducted on “soil mites that were collected from the wild and then raised in 18 glass tubes.” The researchers
found significant genetically transmitted changes in laboratory populations of soil mites in just 15 generations, leading to a doubling of the age at which the mites reached adulthood and large changes in population size.

At Phys.Org, they write:

Although previous research has implied a link between short-term changes in animal species’ physical characteristics and evolution, the Leeds-led study is the first to prove a causal relationship between rapid genetic evolution and animal population dynamics in a controlled experimental setting.

Further, lead author Tom Cameron tells us:

“We saw significant evolutionary changes relatively quickly. The age of maturity of the mites in the tubes doubled over about 15 generations, because they were competing in a different way than they would in the wild. Removing the adults caused them to remain as juveniles even longer because the genetics were responding to the high chance that they were going to die as soon as they matured. When they did eventually mature, they were so enormous they could lay all of their eggs very quickly.”

Co-author Tim Benton states:

“This demonstrates that short-term ecological change and evolution are completely intertwined and cannot reasonably be considered separate.

There are two things to note:
(1) Darwin insisted on gradual change. This is not “gradual” change, but “rapid” change. You might remember those lizards on the Adriatic Islands that developed cecal valves in probably 20 generations or less.
(2) The vacuousness of the phrase “evolutionary change.” The term that should be used is “adaptive change,” for that is EXACTLY what is happening. The organisms doesn’t change in a way that has any evolutionary importance; it just simply changes.
(3) This “rapid” change indicates that “gene frequencies” cannot be changing, simply because the changes are occurring too rapidly. So, the likely instrument of these “rapid” changes is a change in gene expression, and hence, the turning on, and the turning off of gene promoters, which can easily happen via RNA–and, it can happen in a way that is inherited a la “Lamarkian” notions–not Darwinian.

None of what is being reported is consistent with either Darwinian, or neo-Darwinian, mechanisms. This is just a plain fact. You see, two “wrongs”—being wrong in the Darwinian and neo-Darwinian sense—does not make a “right.”

But “true believers” never let facts get in the way. However, there are so many of these inconvenient facts that day-by-day are collecting that it is but a matter of time before the whole Darwinian artifice comes tumbling down.

81 Replies to “Two Wrongs Don’t Make a Right

  1. 1
    Chance Ratcliff says:

    “However, there are so many of these inconvenient facts that day-by-day are collecting that it is but a matter of time before the whole Darwinian artifice comes tumbling down.”

    I wonder what will replace it. From Darwin’s God:

    “Evolution may make no sense, but it will always be true. It must be, for god would never make this world. So evolution will flit from nonsensical idea to nonsensical idea in its never ending attempt to make sense. Who knows what the theory of origins will be in the future, but it will be called evolution. And it will be true. ” — What Will be the 21st Century’s Theory of Origins?

    I think phenotypic plasticity may well mean death for neo-Darwinism, and perhaps Darwinism in general, but it won’t go quietly, and power-word “evolution” will likely be retained for whatever theory goes in under the hood. There’s too much invested in, change means evolution means natural means all-by-itself.

    This is already hinted at with regard to James Shapiro, who is pushing for the conception of natural genetic engineering to be the mechanism of evolution, but also the result:

    “In elaborating on these generic DNA operations, the vast majority of free-living prokaryotes and eukaryotes have evolved biochemical systems that permit them to mobilize and restructure their genomes in more specialized ways. Essential to any contemporary account of evolution is the inclusion of these well-documented genomic mobilization and restructuring (natural genetic engineering) operators.” — James Shapiro, Evolution: A View from the 21st Century, Kindle location 1121

    In the introduction he writes,

    “But the capacity to change is itself adaptive. Over time, conditions inevitably change, and the organisms that can best acquire novel inherited functions have the greatest potential to survive.” — ibid, Kindle location 311

    So regardless of whether RM+NS survives the next few decades, evolution may not go quietly. Even so, I’m enjoying watching RM+NS crumble to dust.

  2. 2
    Chance Ratcliff says:

    Worth watching:

    Non-Random and Targeted Mutations

    Phenotypic plasticity

    Biological research is revealing the non-random nature of, well, practically everything biological.

  3. 3
    JLAfan2001 says:

    Wouldn’t the appearance of the cecal valves mean that there was a new novel function or body plan introduced? Wouldn’t that mean that there is new genetic information in the DNA to introduce those plans that wasn’t there before? Wouldn’t that refute the claim that we have never seen any new body plans or genetic information introduced in an organism along the lines that BA77 seems to cite?

  4. 4
    Chance Ratcliff says:

    JLAFan2001,

    “Wouldn’t the appearance of the cecal valves mean that there was a new novel function or body plan introduced?”

    I think the question to ask is, introduced how? Just because seemingly new features emerged does not imply that Darwinian evolution occurred. Darwinian evolution calls for gradualism — slight, successive changes accumulating over time, moving an organism from a state of being less-fit to more-fit with regard to environmental pressures. It requires the changes to be entirely random with respect to outcome, and filtered gradually by natural selection. There’s nothing about this so-called Rapid Evolution that appears Darwinian. Why not just call it “Spontaneous Evolution” or “Non-Darwinian Evolution”?

    If a lizard can increase its head size, jaw strength, behavior, and gut configuration without the changes being gradual or selective, then there is no Darwinian evolution happening there.

    “Wouldn’t that mean that there is new genetic information in the DNA to introduce those plans that wasn’t there before?”

    No, I don’t think so. This relation is not the same as genotype determining morphology, with changes in genotype brought on by random mutations expressing a different morphology. This appears to be a case of a pre-existing developmental program mapping environmental factors to the expression of morphological features. In other words, the genetic material is already present, and how it expresses itself is determined by environmental triggers; in the case of the podarcis sicula lizards, the trigger appears to be diet.

    “Wouldn’t that refute the claim that we have never seen any new body plans or genetic information introduced in an organism along the lines that BA77 seems to cite?”

    It shows that the introduction of a “novel” feature was part of the organism’s existing developmental program and genomic makeup. The lizards of Pod Mrcaru are not an example of Darwinian evolution, they appear to be expressions of phenotypic plasticity, which is a very non-random mechanism of change that is goal directed.

  5. 5
    bornagain77 says:

    JLAfan2001 you ask:

    Wouldn’t that mean that there is new genetic information in the DNA to introduce those plans that wasn’t there before?

    Does rapid, and repeatable, cyclical variation mean ‘new genetic information’ to you? Or does it mean ‘front loaded’ variation to you? Did you even watch lifepsy’s video?

    Phenotypic Plasticity – Lizard Cecal Valve – Cyclical Variation – video
    http://www.youtube.com/watch?f.....nTA#t=583s

    Anatomical and Physiological Changes Associated with a Recent Dietary Shift in the Lizard Podarcis sicula – 2010
    Excerpt of Discussion: Many comparative studies have tacitly assumed that the distinctive features of plant-eating lizards (large body size, skull dimensions, special dentition, gut morphology) are a product of genetic adaptation to the special demands of a plant-based diet (e.g., Van Damme 1999; Cooper and Vitt 2002; Espinoza et al. 2004; Herrel et al. 2008). Our results suggest that in P. sicula, at least some of the changes associated with a dietary shift toward a higher proportion of plant material may be plastic. Specimens from the Pod Mrc?aru population, which in nature eat substantial amounts of plant material (Herrel et al. 2008), exhibited a reduction in digestive tract length and a total loss of cecal valves after having been fed an exclusively arthropod diet for 15 wk. Although parts of their gastroinstestinal systems were still better developed than those of specimens feeding mainly on arthropods in the wild, it seems likely that a prolonged exposure to an animal-based diet would have erased even those differences. These observations call for a more flexible view of the digestive system in lizards. Plasticity of gastrointestinal morphology and function has long been described in birds (Savory and Gentle 1976a, 1976b; Karasov 1996; reviews in Starck 1999; McWilliams and Karasov 2001) and mammals (e.g., Sibly et al. 1990; Lee and Houston 1993; Munn et al. 2006). Gut morphology and performance in these animals vary seasonally in concert with changes in internal demand (e.g., reproduction, migration, hibernation) or environmental conditions (food availability, nutrient composition). In reptiles, there is evidence that digestive function may change in response to dietary demands on ontogenetic, seasonal, and instantaneous timescales. Many reptiles shift toward a more herbivorous diet as they age (Kennett and Tory 1996; Bjorndal 1997b ; Rocha 1998; Spencer et al. 1998; Durtsche 2000; Fialho et al. 2000; Bouchard and Bjorndal 2006; but see Cooper and Vitt 2002 on the generality of this phenomenon). At least in some of the species studied, this ontogenetic dietary shift is accompanied by changes in digestive efficiency (Durtsche 2004; Bouchard and Bjorndal 2006). Reptiles living in a seasonal environment have been described as regulating their digestive apparatus according to activity or prey availability (Latif et al. 1967; Tracy and Diamond 2005; Naya et al. 2008; Iglesias et al. 2009). And in snakes and other reptiles with irregular feeding patterns, eating is followed by an immediate up-regulation of digestive functions, resulting in an increased mass of the small intestine and intensified enzyme activity and brush-border transport rates (Secor and Diamond 1995, 2000; Secor and Phillips 1997; Jackson and Perry 2000; Starck and Beese 2002; Ott and Secor 2007). All of these observations suggest that many lineages of vertebrates, including lizards, exhibit considerable phenotypic plasticity in the morphology and physiology of their digestive system. In these lineages, dietary shifts from carnivory to omnivory (as observed in many lizard families; Cooper and Vitt 2002) may constitute less of an evolutionary challenge than previously thought. It has been argued that the transition to exclusive herbivory (typically folivory) would require more substantial adaptations (Cooper and Vitt 2002). However, with the potential exception of the need for specialized dentition for cutting or reducing leaves, most of the changes deemed necessary in this context (elongation of the intestines, development of valves, prolonging retention time, acquisition of commensals, increasing digestive efficiency) have been shown to occur in a short to very short time span in this study and many of the studies cited above.
    http://webhost.ua.ac.be/funmor.....20Zool.pdf

  6. 6
    Chance Ratcliff says:

    This is interesting, developmental plasticity as part of ontogenesis. This is from an article by James Bahram at thebestschools.org:

    “What is developmental plasticity? It is the property that all living things possess of being able to compensate during ontogenetic development for variations in either internal or external conditions. Note that “compensation” is a teleological concept. It implies that there is a particular end- or goal-state that one is trying to attain by means of the compensatory maneuvers.” — Seeing Past Darwin III: Mary Jane West-Eberhard

    He goes on to cite a rather fascinating experiment:

    “Everhard Johannes Slijper (1907–1968) was a Dutch zoologist who during World War II published a report on a goat that had been born without forelegs.(4) He had reared the animal to the age of one year, then sacrificed it in order to study its anatomy.

    With human help, the goat had learned to hop about on its hind legs. Slijper demonstrated that this ability was supported by a whole suite of coordinated changes in the animal’s skeleton and musculature. In fact, upon dissection the animal’s body was found to resemble that of a kangaroo more closely than that of a normal goat.

    As West-Eberhard explains:

    . . . the point is to dramatize how a change in one aspect of the phenotype—in this case the front legs—can lead to correlated changes that show a degree of complexity and functional integration that we usually assume to require generations of natural selection and genetic change at many loci.(5)

    The example of Slijper’s goat is useful because it helps us to represent to ourselves the abstract notions of “developmental plasticity” and “phenotypic accommodation” in a more vivid way. In cases like Slijper’s goat and Faith the Dog, we can see the power of these phenomena in action. But they are equally active in less extreme cases, as well. In fact, whenever any change whatsoever is introduced at the genetic level, some goal-directed compensation must take place in order for a viable adult form to be attained.”

    The article is here:

    Seeing Past Darwin III: Mary Jane West-Eberhard

    A subsequent related article is here:

    Seeing Past Darwin IV: Some Experiments

    Mary Jane West-Eberhard’s book:

    Developmental Plasticity and Evolution.

  7. 7
    Chance Ratcliff says:

    Correction in #6: James *Barham*

  8. 8
    Box says:

    Thanks PaV & Chance Ratciff for the valuable information.

    There is an article about phenotypic plasticity at evolutionnews.org, based on the work of Mary Jane West-Eberhard.
    In her treatise Developmental plasticity and the origin of species differences she writes about Slijper’s goat:

    Slijper’s two-legged goat was born with a congenital defect of the front legs so that it could not walk on all fours, and so it learned to walk and run by using its hind legs alone. Then, when it died an accidental death, Slijper dissected it and documented remarkable changes in muscle and bone, including striking changes in the bones of the hind legs; the leg muscles, including a greatly thickened and elongated gluteal tongue and an innovative arrangement of small tendons, a modified shape of the thoracic skeleton, and extensive modifications of the pelvis.

    West-Eberhard’s definition of phenotypic plasticity from her book Developmental Plasticity and Evolution (Oxford UP, 2003):

    Phenotypic plasticity enables organisms to develop functional phenotypes despite variation and environmental change via phenotypic accommodation — adaptive mutual adjustment among variable parts during development without genetic change.

  9. 9
    Collin says:

    Tell me about those cecal valves that appeared in those lizards.

  10. 10
    Box says:

    What is in need of explanation, in the case of Slijper’s goat, is ’the expression of a whole suite of correlated and adaptive changes in behavior, muscle, and bone.’
    Slijper’s goat developed into a ‘new’ coherent animal that in some respects looks more like a kangaroo than a goat. How do we explain this ‘suite of correlated and adaptive changes’? How can the kangaroo-like development be explained considering the goat’s hereditary makeup?
    IMO the only explanation, since the parts cannot account for this, is that the organism – at the level of the whole – is doing the reorganization.

  11. 11
    Chance Ratcliff says:

    Box @8, thanks for the link to West-Eberhard’s treatise. Have you read her book? If so, do you recommend it?

  12. 12
    Chance Ratcliff says:

    Collin @9, see lifepsy’s video here: Phenotypic Plasticity.

  13. 13
    bornagain77 says:

    Collin also see:

    Lizard Plasticity – March 2013
    http://biota-curve.blogspot.co.....icity.html

  14. 14
    JLAfan2001 says:

    This is kinda funny, BA77.

    I’ve seen you ask for evidence of new genetic material or new body plans arising in organisms many times here. When you finally get the evidence, you say “So what, it was already built into the genes so this doesn’t count.”

    No body plans or information: ID
    New body plans and information: ID

    Congratulations, guys. Intelligent Design is well on it’s way to replacing the Neo-Darwinian dogma of unfalsifiable science.

  15. 15
    Chance Ratcliff says:

    JLAFan2001 @14, Don’t you find it amusing that labeling non-Darwinian evolution “Rapid Evolution” baically translates into “rapid gradual change”? Can you not see the irony there? 🙂

  16. 16
    JLAfan2001 says:

    I think Darwin got it right terms of change in a species or adaptation to an environment. He may have got the timing wrong but that it still up for debate. I don’t think that modern biologists have thrown the theory out just yet. Just imagine if that lizard went through hundreds of adaptations in hundreds of environments in hundreds of years. Would it be a lizard then or something else? That’s Darwin’s theory more or less.

  17. 17
    Box says:

    Chance Ratcliff (11), no I haven’t read her book. I am an amateur but I believe that West-Eberhard is on the wrong track. She believes that phenotypical change somehow precedes (and induces) genetic change.

    Here, I argue that the origin of species differences, and of novel phenotypes in general, involves the reorganization of ancestral phenotypes (developmental recombination) followed by the genetic accommodation of change.

    She doesn’t present a mechanism for this – as far as I know – and I cannot imagine that there is a mechanism which translates changes in morphology into DNA code. So although I enjoy the examples of plasticity she has presented I’m personally not that curious about her book.

  18. 18
    Chance Ratcliff says:

    “…If it could be demonstrated that any complex organ existed, which could not possibly have been formed by numerous, successive, slight modifications, my theory would absolutely break down.” – Charles Darwin, Origin of Species, Chapter 6

  19. 19
    Chance Ratcliff says:

    Box, thanks. It might be worth it if the documented examples are abundant.

  20. 20
    butifnot says:

    JLAfan2001, those lizards did not generate a new body plan, de novo, in a few generations. All observed evidence shows that change can not be continued indefinately – organisms steadfastly remain what they are.

  21. 21
    butifnot says:

    More design, more complexity, more contingency – its amazing that the physical bodies of the lizards can change when needed!

    “…exhibited a reduction in digestive tract length and a total loss of cecal valves after having been fed an exclusively arthropod diet for 15 wk.

  22. 22
    mahuna says:

    Going back to the mites. Did the researchers attempt, and fail, to crossbreed the isolated mites with fresh wild ones to confirm that the lab mites had become a new species? Humans have been breeding odd varieties of dogs for thousands of years. But there’s still only 1 species of dog: they have NOT evolved.

    If the mites haven’t mutated into a new species then they’re just Great Dane mites. Nothing unusual about that.

  23. 23
    JLAfan2001 says:

    Chance Ratliff

    “…If it could be demonstrated that any complex organ existed, which could not possibly have been formed by numerous, successive, slight modifications, my theory would absolutely break down.” – Charles Darwin, Origin of Species, Chapter 6

    Butifnot

    “JLAfan2001, those lizards did not generate a new body plan, de novo, in a few generations. All observed evidence shows that change can not be continued indefinately – organisms steadfastly remain what they are.”

    Do you see the contradiction here, guys? Either there was a gradual change over time (which means Darwin was right) or the body plans appeared de novo. Which was it? IMO, I would bet that if you looked at the first 29 generations, you would indeed see slight changes or time. I seriously doubt that they were just the same until “poof” new skulls and guts in the 30th generation.

  24. 24
    Box says:

    JLAfan2001 #21 do read Bornagain77’s post #5:

    Many comparative studies have tacitly assumed that the distinctive features of plant-eating lizards (large body size, skull dimensions, special dentition, gut morphology) are a product of genetic adaptation to the special demands of a plant-based diet (e.g., Van Damme 1999; Cooper and Vitt 2002; Espinoza et al. 2004; Herrel et al. 2008). Our results suggest that in P. sicula, at least some of the changes associated with a dietary shift toward a higher proportion of plant material may be plastic. Specimens from the Pod Mrc?aru population, which in nature eat substantial amounts of plant material (Herrel et al. 2008), exhibited a reduction in digestive tract length and a total loss of cecal valves after having been fed an exclusively arthropod diet for 15 wk. Although parts of their gastroinstestinal systems were still better developed than those of specimens feeding mainly on arthropods in the wild, it seems likely that a prolonged exposure to an animal-based diet would have erased even those differences. These observations call for a more flexible view of the digestive system in lizards.

  25. 25
    Chance Ratcliff says:

    JLAFan2001 @23, why label gradual evolution, “Rapid Evolution”? Which is it, rapid, or gradual?

    Did the cecal valve evolve by slight successive modifications, each conferring a selectable advantage? Nope. Were the novelties the result of random mutations which were irrespective of outcome? Nuh uh.

    So here we have rapid appearance of traits that weren’t selected in stages, and weren’t random but rather a pre-programmed goal-directed response to an environmental trigger; but it’s still Darwinian, yes? 😉

  26. 26
    bornagain77 says:

    OT: here’s a neat picture – 550 million year old fossil fish – “Most major animal groups appear suddenly in the fossil record 550 million years ago, but vertebrates have been absent from this ‘Big Bang’ of life. Two fish-like animals from Early Cambrian rocks now fill this gap.”
    “Lower Cambrian Vertebrates from South China” – Nov. 1999
    http://www.evolutionnews.org/cambrianfish.jpg

    Three (or Four) Reasons Everyone Should Read Darwin’s Doubt – Casey Luskin – April 9, 2013
    http://www.evolutionnews.org/2.....71001.html

  27. 27
    Chance Ratcliff says:

    From Bornagain’s quote at #5,

    “These observations call for a more flexible view of the digestive system in lizards.”

    Perhaps a more flexible view of evolution would be convenient as well. If we consider that evolution can be rapid or gradual, selective or neutral, vertical or horizontal, genetic or epigenetic, plastic or adaptive, and either random or goal-directed, then we achieve a robust definition of evolution that should accommodate any observation for some time to come. 😛

  28. 28
    butifnot says:

    Wholesale ‘changes’ within dozens of generations, some of which can be lost in weeks(!) are not ‘evolutionary changes’ by definition. This type of environment instigated response is a preexisting, contingent, response ‘protocol’, coded and present somewhere.

  29. 29
    bb says:

    JLAfan2001,

    This is an analogy of what happened to the lizard
    http://www.youtube.com/watch?v=TVwhrJirgp0

    Designed or random?

  30. 30
    Aspire to Solomon says:

    Hey BA77, hope all is well. This question is directly primarily at BA77, but of course anyone is welcome to answer.

    I’ve been reading a lot of your post on adaptive mutations and epigenetics.
    Here is what I don’t understand.

    You claim that these things undermine genetic determinism because it demonstrates that it is environmental conditions and choices therein, as opposed to genes, that ultimately cause our bodies, as well as all life on earth, to change.

    But doesn’t that contradict genetic entropy? If I am not mistaken, the core concept of GE is that we are on a unavoidable path to self destruction, INDEPENDENTLY of our environmental conditions and choices, because of inherent flaws within our genes themselves (and those flaws, apparently, are not only irreversible, but determine our ability to survive, which apparently, isn’t going to be very long). We don’t simply die as individuals; the species as a whole, the genome itself, has a death clock independent of the environment. Is not inevitable extinction as a unavoidable consequence, simply on the basis of genes, not a admission that genes are destiny? Because if we had the ability to adapt to the environment, wouldn’t the body, given the right environmental conditions, be able to reverse the transcription errors? If genes do not determine our fate, then why would genetic decay even matter? I hope these questions make sense. By the way these are separate questions, and I would appreciate it if you responded to these questions individually.

    Thanks!

    Also, anyone is welcome to take a stab at what I’m saying 🙂

  31. 31
    Aspire to Solomon says:

    I don’t see how you can believe that our bodies make directed actions to avoid death, but at the same time, also refrain from making life sustaining actions entirely within it’s control, even if placed under the best conditions for doing so. I don’t understand why the genome could not stay in a state of stasis, given the right environmental conditions.

  32. 32
    bornagain77 says:

    as to: “But doesn’t that contradict genetic entropy?”

    And how does having a extremely sophisticated, ‘front loaded’, environmental response mechanism in place counter the relentless accumulation of slightly detrimental mutations? Sure extremely sophisticated DNA repair mechanisms are in place, but this does not negate the fact that there is now overwhelming evidence giving us very good reason to believe that information in life is slowly ‘corroding’.

    as to: “Is not inevitable extinction as a unavoidable consequence, simply on the basis of genes, not a admission that genes are destiny?”

    No. Genes are not ‘destiny’ for the simple fact that the entirety of body plan information is not reducible to the information in DNA. As you have brought this up before, this seems to be a sticking point for you. If you don’t mind, might I suggest, to help you past this sticking point, that you pre-order Stephen Meyer’s new book “Darwin’s Doubt’,,, due out in early June,,,
    http://darwinsdoubt.com/
    ,, In which I am sure Dr. Meyer will, among other things, clearly articulate why the molecular (genetic) reductionism model of neo-Darwinism is woefully inadequate to explain body plans from DNA alone:

    Three (or Four) Reasons Everyone Should Read Darwin’s Doubt
    Casey Luskin – April 9, 2013
    http://www.evolutionnews.org/2.....71001.html

  33. 33
    Aspire to Solomon says:

    It just doesn’t seem reasonable to me, given how enormously underestimated our ability to adapt is, that the species could not, under the right environmental conditions over an extended period of time, intelligently adapt (NOT evolve, bear in mind) in such a fashion as to avoid this fate by creating and selecting what genetic information is needed at any given time.

  34. 34
    Aspire to Solomon says:

    Thanks BA77 for your prompt courteous reply. I will look over what you have sent me. In the meantime, anyone else is welcome to jump in!

  35. 35
    Aspire to Solomon says:

    BA77, I would appreciate your thoughts on the postulation I made earlier of what seems like a reasonable alternative to me, regarding theoretical genome stability.

    “No. Genes are not ‘destiny’ for the simple fact that the entirety of body plan information is not reducible to the information in DNA. As you have brought this up before, this seems to be a sticking point for you.”

    It very much is a sticking point for me, and I appreciate that you noticed. I’m gonna put this next sentence in asterix, because it really cuts to the heart of what I take issue with, and my number one objection to GE. In fact, I insist that you address this very specific point: **if body plan information is not reducible to information that is in DNA, then why is DNA degradation alone, in itself, capable of destroying our body plans, and further more, inherently inclined to do so? If it doesn’t make the plans, it sure does seem to have an awful lot of control over them.**

  36. 36
    Aspire to Solomon says:

    there are some other lesser points you’ve made that I’d like to address too.

    “And how does having a extremely sophisticated, ‘front loaded’, environmental response mechanism in place counter the relentless accumulation of slightly detrimental mutations?”

    Interesting. Sounds like a very deistic, newtonian designer to me. I’m sure Einstein, Benjamin Franklin and Darwin would be pleased at such an idea. 😉

    But to answer your question, and again, this is also a big point that I have that I would like if you addressed specifically. it is **if it isn’t countering the relentless accumulation of slightly detrimental mutations, it’s by definition not a environmental response mechanism. that’s why the mutations occur. Because there is no response, and thus, mutations develop, like weeds in a garden.**

    I am also under the impression that front loading is still very much an open question as far as scientific data is concerned. That aside, are you seriously suggesting that the intelligent designer designs the ancestors of his creation according to a different specification than their progeny? Do you believe he even directly intervenes in life creation at all, or is the just the first ones who receive such special divine attention? the others, well, he just let’s them fall apart.

    Sure extremely sophisticated DNA repair mechanisms are in place, but this does not negate the fact that there is now overwhelming evidence giving us very good reason to believe that information in life is slowly ‘corroding’.”

    Well I guess that’s going to depend on what information is, isn’t it! 🙂 How do you know what information is, let alone that it is corroding? And who said creation was front loaded? You seem to be suggesting that we we made to different specifications that our originators, and I’m not sure on what basis we should believe that to be so. You seem to suggest that information is a passive, material entity, a one time flash in a pan, and I’m simply not sure that’s true.

  37. 37
    Aspire to Solomon says:

    sorry the last paragraph needed some editing

  38. 38
    Aspire to Solomon says:

    On a different note bornagain, as one Christian to another, you seem to be suggesting that God does not create every individual with the same time and dedication that he created the first ones, adam and eve. Adam and Eve get a robust gene pool. Their children and grand children; not so much. Not that this necessarily matters, but this strikes me as rather offensive, it seems like a direct attack on value of my own existence, one I’m used to encountering from Darwinist, not Christians

  39. 39
    Aspire to Solomon says:

    BA77 I know this is alot of information, but it is very important to me, I have a lot on my mind haha, and the time you take addressing these points is something I very much appreciate.

  40. 40
    NickMatzke_UD says:

    This “rapid” change indicates that “gene frequencies” cannot be changing, simply because the changes are occurring too rapidly.

    So…you’re saying that gene frequencies cannot change in 15 generations? Do you have any idea what you are talking about?

  41. 41
    Joe says:

    Gene frequencies can change in one generation.

  42. 42
    bornagain77 says:

    ATS, it seems you are heavily indebted to a particular interpretation of Theology for your beliefs and hardly at all indebted to what the evidence actually says. For instance, when I claim that the ‘information’ in DNA is ‘corroding’, and you object on Theological grounds, I can cite actual evidence to support my position,,,

    Inside the Human Genome: A Case for Non-Intelligent Design – Pg. 57 By John C. Avise
    Excerpt: “Another compilation of gene lesions responsible for inherited diseases is the web-based Human Gene Mutation Database (HGMD). Recent versions of HGMD describe more than 75,000 different disease causing mutations identified to date in Homo-sapiens.”

    I went to the mutation database website cited by John Avise and found:

    HGMD®: Now celebrating our 100,000 mutation milestone!
    http://www.hgmd.org/

    That 100,000 figure is even higher now!

    Or I can cite,,,

    “Our Missing Genes” – The Scientist – February 18, 2012
    Excerpt: On average, a person will have about 20 genes that are completely “lost”—meaning that both alleles have inactivating mutations.
    http://www.uncommondescent.com.....s-disease/

    Human Genome in Meltdown – January 11, 2013
    Excerpt: According to a study published Jan. 10 in Nature by geneticists from 4 universities including Harvard, “Analysis of 6,515 exomes reveals the recent origin of most human protein-coding variants.”,,,:
    “We estimate that approximately 73% of all protein-coding SNVs [single-nucleotide variants] and approximately 86% of SNVs predicted to be deleterious arose in the past 5,000 -10,000 years. The average age of deleterious SNVs varied significantly across molecular pathways, and disease genes contained a significantly higher proportion of recently arisen deleterious SNVs than other genes.”,,,
    As for advantageous mutations, they provided NO examples,,,
    http://crev.info/2013/01/human-genome-in-meltdown/

    Or I can cite,,,

    New analysis provides fuller picture of human expansion from Africa – October 22, 2012
    Excerpt: A new, comprehensive review of humans’ anthropological and genetic records gives the most up-to-date story of the “Out of Africa” expansion that occurred about 45,000 to 60,000 years ago.
    This expansion, detailed by three Stanford geneticists, had a dramatic effect on human genetic diversity, which persists in present-day populations. As a small group of modern humans migrated out of Africa into Eurasia and the Americas, their genetic diversity was substantially reduced.
    http://phys.org/news/2012-10-a.....nsion.html

    “…but Natural Selection reduces genetic information and we know this from all the Genetic Population studies that we have…”
    Maciej Marian Giertych – Population Geneticist – member of the European Parliament – EXPELLED
    http://www.metacafe.com/watch/4036840

    As far as being firmly grounded Theologically, I can quote,,

    Romans 8:18-21
    I consider that our present sufferings are not worth comparing with the glory that will be revealed in us. The creation waits in eager expectation for the sons of God to be revealed. For the creation was subjected to frustration, not by its own choice, but by the will of the one who subjected it, in hope that the creation itself will be liberated from its bondage to decay and brought into the glorious freedom of the children of God.

    etc..
    ATS, and though I have not cited nor discussed any of the specific evidence for God sustaining the universe, nor any any of the specific evidence of God creating life in it, it seems that you are bucking against the entire ‘fallen world’ concept in that God ‘allows’ a certain amount of ‘evil’ to happen by his permissive will so that a greater good, which He has in mind, can be accomplished. Thus IMO, as far as I can tell, I’m on firmer ground than you currently are both scientifically and Theologically.

  43. 43
    PaV says:

    Nick Matzke:

    So…you’re saying that gene frequencies cannot change in 15 generations? Do you have any idea what you are talking about?

    Yes, Nick, I think I do.

    If you look at the paper, you’ll see that within 5 generations needed changes already appeared to ‘save’ the population from ‘extinction.’ From what I can see from the paper, the populations numbered about 600 maximally.

    Now 5 x 600 = 3,000 replications.

    What, exactly, Nick, can possibly happen, from a statistical point of view, to gene frequencies with this number of genome replications? Any answers?

  44. 44
    Phinehas says:

    Slijper dissected [the goat] and documented remarkable changes in muscle and bone, including striking changes in the bones of the hind legs; the leg muscles, including a greatly thickened and elongated gluteal tongue and an innovative arrangement of small tendons, a modified shape of the thoracic skeleton, and extensive modifications of the pelvis.

    Imagine the headlines if a similar goat were found in fossil form:

    “New transitional fossil found! Goat ancestral to Kangaroo!”

  45. 45
    butifnot says:

    On a different note bornagain, as one Christian to another, you seem to be suggesting that God does not create every individual with the same time and dedication that he created the first ones, adam and eve. Adam and Eve get a robust gene pool. Their children and grand children; not so much. Not that this necessarily matters, but this strikes me as rather offensive, it seems like a direct attack on value of my own existence, one I’m used to encountering from Darwinist, not Christians

    The fall ATS. Physical decay and physical death awaits us all and the whole universe. Dust to dust, and our value is not in our physical bodies, which will be remade/restored anyways. And our genome seems adequate for the time-span thus far. You have a familiar writing style?

  46. 46
    Aspire to Solomon says:

    Bornagain77, did you read through my post, or just glance over them? Do you think this is some sort of game, some sort of contest? I came here with questions, expecting answers. You seem more interested in kicking sand in my face. I was very careful to keep my scientific and theological objections separate, but you seem to think that my scientific skepticism is nothing more than a thinly veiled theological attack (very common attitude amongst Darwinist, as I’m sure your aware)….to which, you simply added your own theological interpretation, which said nothing about the truth status of my own. At any rate, some epistemological humility would do you some good. I have tried to be as cordial as possible, but have been reluctant to ask you more questions because the things that I am particularly concerned about, you cavalierly dismiss as unimportant, ignore, or don’t address explicitly. I came here asking questions to expand my understanding from those who I believed had much to offer, such as yourself, not to have my questions and concerns mocked and ridiculed. Further more, you didn’t even answer my questions! There were two questions that I made especially clear that I wanted answers to, you ignored both of them. It’s a good thing I was already a Christian when I talked to you, because your ambassador skills are lacking.

  47. 47
    Aspire to Solomon says:

    butifnot;

    The fall ATS. Physical decay and physical death awaits us all and the whole universe. Dust to dust, and our value is not in our physical bodies, which will be remade/restored anyways. And our genome seems adequate for the time-span thus far. You have a familiar writing style?

    Not sure what you mean in regards to my writing style haha. Yes, I am familiar with “the fall” concept. I am not doubting that a fall exist. The amount of clearly visible death and destruction in the world makes that quite clear. I am doubting that the fall means everything that BA77, or probably others, say it means, in terms of the reasons why it happens, and what that means for life on earth. If the physical world contains no value, that why did God create it, and why does he hold us to such high standards in how we conduct ourselves in it? Also, I’m not sure what you mean by “adequate”. Adequate by what standard? Also, remade/restored to what?

  48. 48
    bornagain77 says:

    ATS, I did not ‘kick sand in your face’. I merely pointed out the lack of rigor for any evidential basis to your preferred theological position.,, i.e. You ‘want’ to believe that the information in DNA is not corroding. I showed you from empirical evidence why we have very strong reason to believe what you prefer to believe, theologically, is not so empirically.,,, Being wrong is not pleasant, but please do not take me correcting you on this foundational point as to me being a bully towards you. Not that I have not lost patience before and been short towards people, but that simply is not the case in this instance.

  49. 49
    Aspire to Solomon says:

    And to suggest that that the life on earth that God made is, in essence, worthless, makes our choices in life of no consequence to neither God nor man, does it not? And if our choices don’t matter, and our bodies don’t matter, it’s hard to say that we matter at all, isn’t it?

  50. 50
    Aspire to Solomon says:

    thanks BA77, I appreciate your reply

  51. 51
    bornagain77 says:

    Psalm 82:7
    “I said, ‘You are “gods”; you are all sons of the Most High.’ But you will die like mere mortals; you will fall like every other ruler.”

  52. 52
    Aspire to Solomon says:

    Your right, I don’t have any empirical information to support my theological position; just intuition and the rules of logic, which in the absence of knowledge, is about as good as it gets.

  53. 53
    Aspire to Solomon says:

    That’s an interesting quote, but I’m not sure what it means.

  54. 54
    Box says:

    Phinehas #44: Imagine the headlines if a similar goat were found in fossil form:
    “New transitional fossil found! Goat ancestral to Kangaroo!”

    Phinehas, you raise a very important question. Given Slijper’s goat – and many other cases of plasticity – what can we infer with certainty from paleontological evidence?

  55. 55
    Aspire to Solomon says:

    I also think it’s a bit of a stretch to say that Genetic Entropy = the fall. Are you saying that if the fall never happened, GE wouldn’t happen? In that case, in such a place, how would things on earth be different, and why?

  56. 56
    bb says:

    ATS @49:

    And to suggest that that the life on earth that God made is, in essence, worthless, makes our choices in life of no consequence to neither God nor man, does it not? And if our choices don’t matter, and our bodies don’t matter, it’s hard to say that we matter at all, isn’t it?

    No. That life on this earth is short and fragile makes our choices more important. That our life in eternity depends on those choices makes them of utmost importance. That life on this earth is so short compared to eternity makes our brief pain of almost no relevance. Only our response to that suffering matters.

    For we know that the whole creation has been groaning together in the pains of childbirth until now.

    Romans 8:22 ESV

  57. 57
    Aspire to Solomon says:

    That life on this earth is short and fragile makes our choices more important.

    More important to whom, on what basis?

    That our life in eternity depends on those choices makes them of utmost importance.

    Do they really depend on those choices? If goodness is not that which promotes life, I’m not sure what is. If in your fallen world concept you deny man his goodness, then how can he be held responsible for anything?

    That life on this earth is so short compared to eternity makes our brief pain of almost no relevance.

    Of almost no relevance to whom? Someone whose lived in a third world country for an extensive part of their life may find it to be highly relevant.

    Only our response to that suffering matters.

    If the suffering does not matter, then why would the response matter?

  58. 58
    bornagain77 says:

    AtS: I have to say it is rather strange finding a professed Christian arguing against the “fallen world concept”. But then again I didn’t really learn that Christ was real until he he reached me in a moment of brokenness. Thus I have no illusions that man in his own goodness can merit eternal life. i.e. Grace!

  59. 59
    bb says:

    ATS @57
    “More important to whom, on what basis?” –
    To God, who created us to fellowship with Him. To us who can spend eternity in heaven or hell by choice. One would think that’s pretty important.

    “If in your fallen world concept you deny man his goodness, then how can he be held responsible for anything?” –
    “No one is good except God alone.” Mark 10:18 ESV The choice to follow or reject Christ with its consequences of redemption or damnation is before us. We will be held responsible for that choice.

    “Of almost no relevance to whom? Someone whose lived in a third world country for an extensive part of their life may find it to be highly relevant.” – The key words in my comment were “compared to eternity”. Suffering is important in that it elicits a response. The response, in the end, is more important than the suffering itself because it has eternal consequence. Suffering in this life is like a phlebotomy when compared to eternity.

    I agree with ba. I’m not convinced that you’re a Christian. If not, would you like to become one? God’s grace is there if you confess your sin and ask His forgiveness. Any suffering you may be going through may very well continue until the end of your life. But that’s training and a constant reminder of our need for Him. It keeps us humble.

  60. 60
    bb says:

    Moderator: My last comments were completely off topic and I apologize. Regardless I believe AtS’ questions, whether honest or not, are important.

  61. 61
    wd400 says:

    What, exactly, Nick, can possibly happen, from a statistical point of view, to gene frequencies with this number of genome replications? Any answers?

    Why don’t you find out for yourself?

    As an example, if you start with a single locus with two alleles with frequencies 0.1 and 0.9 respectively (such that the propotion of individuals with a at least one copy of the rare variant = 0.19).

    Now, imagine the environment changes that the rare allele is ~5 times more likely to survive than common one. Run the simulations an you’ll see in only 5 generations the frequency of the rare allele reaches ~0.85. 98% of the population have at least one copy of the newly benifical allele.

    Now step back and look at the genome as a whole. If 5 genes were subject to the same dynamics then before selection it’s unlijely any individuals in the population would have at least one of the rare alleles at each locus (probability for each individual ~ 2e-4. After selection more than half would, and as a result your population would have changed considerably.

    Perhaps thinking through these things before you lean on the scorn button would be a good idea?

  62. 62
    bornagain77 says:

    wd400, I appreciate you stopping by so as to straighten us out on population genetics. If you don’t mind I have a few questions. How come the numbers don’t work out here?

    More from Ann Gauger on why humans didn’t happen the way Darwin said – July 2012
    Excerpt: Each of these new features probably required multiple mutations. Getting a feature that requires six neutral mutations is the limit of what bacteria can produce. For primates (e.g., monkeys, apes and humans) the limit is much more severe. Because of much smaller effective population sizes (an estimated ten thousand for humans instead of a billion for bacteria) and longer generation times (fifteen to twenty years per generation for humans vs. a thousand generations per year for bacteria), it would take a very long time for even a single beneficial mutation to appear and become fixed in a human population.
    You don’t have to take my word for it. In 2007, Durrett and Schmidt estimated in the journal Genetics that for a single mutation to occur in a nucleotide-binding site and be fixed in a primate lineage would require a waiting time of six million years. The same authors later estimated it would take 216 million years for the binding site to acquire two mutations, if the first mutation was neutral in its effect.
    Facing Facts
    But six million years is the entire time allotted for the transition from our last common ancestor with chimps to us according to the standard evolutionary timescale. Two hundred and sixteen million years takes us back to the Triassic, when the very first mammals appeared. One or two mutations simply aren’t sufficient to produce the necessary changes— sixteen anatomical features—in the time available. At most, a new binding site might affect the regulation of one or two genes.
    http://www.uncommondescent.com.....rwin-said/

    As well wd400, why is negative epistasis not seen as a falsification of neo-Darwinism using the equations of population genetics?

    Mutations : when benefits level off – June 2011 – (Lenski’s e-coli after 50,000 generations which is approx. equivalent to 1 million years of human evolution)
    Excerpt: After having identified the first five beneficial mutations combined successively and spontaneously in the bacterial population, the scientists generated, from the ancestral bacterial strain, 32 mutant strains exhibiting all of the possible combinations of each of these five mutations. They then noted that the benefit linked to the simultaneous presence of five mutations was less than the sum of the individual benefits conferred by each mutation individually.
    http://www2.cnrs.fr/en/1867.htm?theme1=7

    Epistasis between Beneficial Mutations – July 2011
    Excerpt: We found that epistatic interactions between beneficial mutations were all antagonistic—the effects of the double mutations were less than the sums of the effects of their component single mutations. We found a number of cases of decompensatory interactions, an extreme form of antagonistic epistasis in which the second mutation is actually deleterious in the presence of the first. In the vast majority of cases, recombination uniting two beneficial mutations into the same genome would not be favored by selection, as the recombinant could not outcompete its constituent single mutations.
    http://www.uncommondescent.com.....ach-other/

    Response from Ralph Seelke to David Hillis Regarding Testimony on Bacterial Evolution Before Texas State Board of Education, January 21, 2009
    Excerpt: He has done excellent work showing the capabilities of evolution when it can take one step at a time. I have used a different approach to show the difficulties that evolution encounters when it must take two steps at a time. So while similar, our work has important differences, and Dr. Bull’s research has not contradicted or refuted my own.
    http://www.discovery.org/a/9951

    wd400, Why doesn’t empirical evidence count against the equations of population genetics as empirical evidence counts against other mathematical models in other branches of science?

    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’ (1 quadrillion 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

    Experimental Evolution in Fruit Flies (35 years of trying to force fruit flies to evolve in the laboratory fails, spectacularly) – October 2010
    Excerpt: “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 research really upends the dominant paradigm about how species evolve,” said ecology and evolutionary biology professor Anthony Long, the primary investigator.
    http://www.arn.org/blogs/index.....ruit_flies
    http://eebweb.arizona.edu/nach.....l_2010.pdf

    “On the other hand, I disagree that Darwin’s theory is as `solid as any explanation in science.; Disagree? I regard the claim as preposterous. Quantum electrodynamics is accurate to thirteen or so decimal places; so, too, general relativity. A leaf trembling in the wrong way would suffice to shatter either theory. What can Darwinian theory offer in comparison?”
    (Berlinski, D., “A Scientific Scandal?: David Berlinski & Critics,” Commentary, July 8, 2003)

    wd400, Why are most mutations hypothesized to be neutral even though the vast majority are now found to be slightly detrimental?

    Unexpectedly small effects of mutations in bacteria bring new perspectives – November 2010
    Excerpt:,,, using extremely sensitive growth measurements, doctoral candidate Peter Lind showed that most mutations reduced the rate of growth of bacteria by only 0.500 percent. No mutations completely disabled the function of the proteins, and very few had no impact at all. Even more surprising was the fact that mutations that do not change the protein sequence had negative effects similar to those of mutations that led to substitution of amino acids. A possible explanation is that most mutations may have their negative effect by altering mRNA structure, not proteins, as is commonly assumed.
    http://www.physorg.com/news/20.....teria.html

    wd400, why are the population equations of the ‘modern synthesis considered useless for the level of complexity we are dealing with?

    The Fate of Darwinism: Evolution After the Modern Synthesis – David J. Depew and Bruce H. Weber – 2011
    Excerpt: We trace the history of the Modern Evolutionary Synthesis, and of genetic Darwinism generally, with a view to showing why, even in its current versions, it can no longer serve as a general framework for evolutionary theory. The main reason is empirical. Genetical Darwinism cannot accommodate the role of development (and of genes in development) in many evolutionary processes.,,,
    http://www.springerlink.com/co.....03g3t7002/

  63. 63
    bornagain77 says:

    wd400, why is the fact that the vast majority of mutations are now shown to be ‘non-random and targeted’ not count against neo-Darwinism in the equations of population genetics?

    Non-Random and Targeted Mutations (Epigentics to the level of DNA) – video
    http://www.youtube.com/watch?v=qTChu5vX1VI

    wd400, why are ‘fatal flaws’ from population genetics ignored by Darwinists?

    Using Numerical Simulation to Test the Validity of Neo-Darwinian Theory – 2008
    Abstract: Evolutionary genetic theory has a series of apparent “fatal flaws” which are well known to population geneticists, but which have not been effectively communicated to other scientists or the public. These fatal flaws have been recognized by leaders in the field for many decades—based upon logic and mathematical formulations. However population geneticists have generally been very reluctant to openly acknowledge these theoretical problems, and a cloud of confusion has come to surround each issue.
    Numerical simulation provides a definitive tool for empirically testing the reality of these fatal flaws and can resolve the confusion. The program Mendel’s Accountant (Mendel) was developed for this purpose, and it is the first biologically-realistic forward-time population genetics numerical simulation program. This new program is a powerful research and teaching tool. When any reasonable set of biological parameters are used, Mendel provides overwhelming empirical evidence that all of the “fatal flaws” inherent in evolutionary genetic theory are real. This leaves evolutionary genetic theory effectively falsified—with a degree of certainty which should satisfy any reasonable and open-minded person.
    http://www.icr.org/i/pdf/techn.....Theory.pdf

    Mutations expressed early in embryonic development are the least likely to be tolerated by organisms – Paul Nelson – video
    http://www.metacafe.com/watch/5548184/

    Understanding Ontogenetic Depth, Part II: Natural Selection Is a Harsh Mistress – Paul Nelson – April 7, 2011
    Excerpt: The problem may be summarized as follows:
    — There are striking differences in the early (embryonic) development in animals, even within classes and orders.
    — Assuming that these animals are descended from a common ancestor, these divergences suggest that early development evolves relatively easily.
    — Evolution by natural selection requires heritable variation.
    — But heritable variations in early development, in major features such as cleavage patterns, are not observed.

    wd400, If you can help me out with these questions and more like these, there is a job opening for you at Oxford!

    Oxford University Admits Darwinism’s Shaky Math Foundation – May 2011
    Excerpt: However, mathematical population geneticists mainly deny that natural selection leads to optimization of any useful kind. This fifty-year old schism is intellectually damaging in itself, and has prevented improvements in our concept of what fitness is. – On a 2011 Job Description for a Mathematician, at Oxford, to ‘fix’ the persistent mathematical problems with neo-Darwinism within two years.

    Music and verse:

    Love the Lord w/ Lincoln Brewster
    http://www.youtube.com/watch?v=CV7qTD_X0Rk

    Luke 10:27
    He answered, “‘Love the Lord your God with all your heart and with all your soul and with all your strength and with all your mind’; and, ‘Love your neighbor as yourself.'”

  64. 64
    Box says:

    PaV #43: What, exactly, Nick, can possibly happen, from a statistical point of view, to gene frequencies with this number of genome replications? Any answers?

    What exactly is the importance of this question, given the fact that changes in the genome are just part of a much bigger picture? What use are potentially beneficial DNA mutations without an appurtenant epigenome to guide them? Why zero in on DNA mutations and leave out numerous co-adaptations?

  65. 65
    PaV says:

    wd400:

    As an example, if you start with a single locus with two alleles with frequencies 0.1 and 0.9 respectively (such that the proportion of individuals with a at least one copy of the rare variant = 0.19).

    Now, imagine the environment changes that the rare allele is ~5 times more likely to survive than common one. Run the simulations an you’ll see in only 5 generations the frequency of the rare allele reaches ~0.85. 98% of the population have at least one copy of the newly beneficial allele.

    All of what you write is based, not on Darwinism, but Mendelian genetics.

    For example, you can use these very same numbers in a study about artificial selection. IOW, if Mendel’s genetics had first been seized upon, rather than Darwinism, then they would apply to inbred populations. One then could extend this to the Darwinian idea of NS; but it would be an extension. Darwinism is not required for the numbers you propose.

    But now let me explicit about what I mean when I speak of “gene frequencies”. First, I’m not talking about “allele” frequencies. The whole language of “loci” and “alleles” comes from Mendelian genetics and predates molecular biology. We now live in an age of WGA (whole genome analysis). It’s a brave, new world.

    What I am talking about is genetic innovation: i.e., a “new” genetic solution to an environmental change.

    So, when I say that the “gene frequencies” don’t change, I mean that no “new” genes have been developed. I am sure you would agree with me.

    You, however, might object, taking the position that since the “alleles” changed, this is tantamount to a change in “gene” frequencies.

    To this somewhat expected objection I submit the following analysis:

    Let’s suppose we begin with an organism which has, at “locus” L1, the following “alleles” in its population: A1,A2,A3….A_n. These have “frequencies” P1,P2,P3….P_n, respectively. “Selection” is presumed to be occuring at this locus.

    Your population genetics analysis tells us that, due to “selection” one (or possibly several) of these “alleles” will be favored. Thus, due to selection, with each passing generation, the population now contains the following “alleles”: A1,A2,A3…..A_n-1, A1,A2,A3…..A_n-2, and so forth, until, at last, A1,A2,A3……A_n-m. Correspondingly, for the last configuration of locus L1, the “new” “gene frequencies” are: P1,P2,P3,……P_n-m. All of these “frequencies” will have been found to be changed from those of the original population.

    And this is called:……………EVOLUTION!

    But why is this so? We know that if the “new” environmental pressures that brought about this change remain the same, then these frequencies will stay roughly the same. But, more than that, according to the Hardy-Weinberg Law, the actual numbers of alleles in the population (assuming the population size inbreeds and remains roughly the same size) will not fluctuate. This is STASIS, not EVOLUTION.

    And the thought experiment you’re carrying out simply amounts to applying the Hardy-Weinberg Law with a “changed” number of alleles. This is like applying the laws of motion to a dynamical system that remains the same, but just simply starts out with different initial conditions. The “laws of motion” don’t change; only the initial conditions.

    Applied to a population, this means that the Hardy-Weinberg Law—which results in “stasis”—is at work in a population until such time as environmental stress takes place. Under this stress, “ALLELES” are LOST!! Then, with a different array of “alleles” present, the Hardy-Weinberg Law is in effect once again. And “stasis” returns once again.

    What all of this demonstrates is that, with time, “alleles” are “lost”, genetic variance decreases, and the ability of this particular “locus” to help the organism survive a new challenge is diminished. (With time, fresh mutations may restore, once again, the “alleles” that were “lost.” But, given the size of the population, and other factors, this may take a considerable amount of time).

    So, based on what I’ve just described, what would we expect to see over long stretches of time: species appear, remain the same(the Hardy-Weinberg Law), and eventually die out (genetic entropy: i.e., they run out of “alleles” as they face “new” environment after “new” environment, and not enough time in-between to ‘restore’ the “alleles”.) This is exactly what the Fossil Record portrays. Consult Stephen J. Gould on this.

    So, why on earth would you call this: “EVOLUTION”! I don’t get it. Why not call it what it is: ADAPTATION.

    This “stasis” found in the Fossil Record suggests that the ability of an organism to ‘mutate’, with its concomitant ‘harm’ (most mutations are harmful—this has been demonstrated experimentally over and over) is ‘balanced out’ by NS, which simply eliminates what is harmful. And, that phenotypic and genotypic change can, and does, occur with ‘changing environments’, with the ‘changing environment’ simply ‘changing’ the ‘definition’ of what is ‘harmful.’ And the whole while, the organism remains roughly the same.

    And there you have it: NS is a force in nature that weeds out what is harmful in an organism. And, no more!

    Yet, what is left completely unexplained here, is this: How did the species ‘appear’ in the first place given that NS simply eliminates “new” (that is, ‘harmful’) “alleles.”

    Where do the new “genes” come from? In strict analogy to classical dynamics, NS is a “conservative force.” It’s not an innovator or generator of anything. So what “force” is supplying these “new alleles”?

    Going back to what I wrote above, if, let us say, “allele” A_n-r, with r less than m, is removed from the population as a consequence of the “genetic load” experienced by the population under the new environmental stress, then it represents a “loss” of an “allele” with one, maybe two, particular amino acids located at very particular spots along the length of the “allele.” If the “new” environment stays the same for a long stretch of time, then this “new” allele, A_n-r, is ‘harmful’ (that is, organisms with this “allele” died in the “new” environment, so, if they occur again, they will likely die once again since the environment is still the same.

    The population of the mites in this study was around 600. If A_n-r is to be restored—and using the easier case of just one a.a. substitution—then, given a mutation rate of, let’s say, 10^-8, this means that to “restore” this “allele” the mite population would have to undergo 10^8/600 rounds of replication (generations). Or, 166,000 generations. And, if the environment hasn’t changed, it will likely die, and the process has to begin again.

    If you counter with saying that in a larger population this needed ‘mutation’ would occur more rapidly, given that the environment has not changed back to its former mode, it’s likely NS would remove it, or, at best, it would be subject to neutral drift, and a fixation expectation of 1/4N, which likely renders another large number.

    Noting these constraints, another question arises: how can you ‘construct’ an entirely “new allele” based on Mendelian genetics? And WGA tells us that, yes, indeed, there are de novo “genes” that differentiate major groups of species. So, how is this done? What is the mechanism?

    Two final remarks that put this last question into perspective:

    (1) Michael Behe uses the example of the malarial parasite to demonstrate (again using WGA) that it takes 10^20 replications of the malarial parasite population to come up with a 2 a.a. change in its genome in the face of eminent death due to chloroquine. Now, if, using the above example, the malarial parasite had these “alleles” already in place, then why did it take so long for this population to develop resistance to chloroquine: IOW, this demonstrates that we just can’t assume that organisms have all their needed “alleles” already in place; and, that it takes a huge amount of replications [which is equivalent to time (yrs)] to ‘find’ these “new alleles”.

    (2) Environmental pressures leads to a “loss” of information (in this case, “alleles”), rather than to any “gain.” This is consistent with Behe’s “Rule” for ‘adaptation’.

  66. 66
    wd400 says:

    All of what you write is based, not on Darwinism, but Mendelian genetics.

    Lol. Do you see the bit about selection? Mendel didn’t have anything to say about that, nor did Messrs Hardy and Weinberg.

    The rest of if seems to be a rant about evolution not fitting your own misunderstandings of genetics and evolutionary biology.

  67. 67
    Joe says:

    Natural selection is not a magical ratchet and whatever is good enough gets to add to the population.

  68. 68
    PaV says:

    wd400:
    Mendel didn’t have anything to say about that, nor did Messrs Hardy and Weinberg.

    Really? Do you want to stand by this comment?

    Tell me, wd400, the notion of “alleles”, does that come from Mendel or from Darwin? Tell me, wd400, your calculations of what happens in 5 generations, is that based on Darwin’s notion of gemmules, or is it based on Mendel’s Law of Segregation?

    And isn’t the Hardy-Weinberg Equilibrium based directly on this Law of Segregation while having nothing at all to do with NS, or anything else Darwinian? *** [see below]

    Would you like to answer these questions? Is it OK if I laugh a little bit in the meantime?

    wd400:
    The rest of it seems to be a rant about evolution not fitting your own misunderstandings of genetics and evolutionary biology.

    “A rant about evolution not fitting [my] own misunderstandings of genetics …”

    Really?

    Please enlighten me (and any others who happen to take a look-see here at UD):

    I wrote this:

    To this somewhat expected objection I submit the following analysis:

    Let’s suppose we begin with an organism which has, at “locus” L1, the following “alleles” in its population: A1,A2,A3….A_n. These have “frequencies” P1,P2,P3….P_n, respectively. “Selection” is presumed to be occuring at this locus.

    Your population genetics analysis tells us that, due to “selection” one (or possibly several) of these “alleles” will be favored. Thus, due to selection, with each passing generation, the population now contains the following “alleles”: A1,A2,A3…..A_n-1, A1,A2,A3…..A_n-2, and so forth, until, at last, A1,A2,A3……A_n-m. Correspondingly, for the last configuration of locus L1, the “new” “gene frequencies” are: P1,P2,P3,……P_n-m. All of these “frequencies” will have been found to be changed from those of the original population.

    Now, please tell me where I have gone wrong in summarizing your understanding of what actually takes place as NS works on a population faced with a new, challenging environment. How have I misstated your analysis (other than what the actual dimunition of “alleles” looked like from one generation to another—a matter of little consequence here)?

    Let’s remember that Kimura invented the Neutral Theory to deal with the unanticipated high level of protein polymorphisms found in the early 60’s via gel electrophoresis, so I’m purposely not dealing with a ‘two-allele per locus’ model. (Yet, even with the ‘two-allele’ model, either (1) the ‘rare’ allele becomes very rare, but still present, or (2) it is eliminated from the population entirely, in which case, we have a “loss” of an allele, the very same point I was making. Either way, it’s either stasis, or ‘loss’, and nothing new!)
    _____________________ . . . . . . ________

    *** [In 1908 G.H. Hardy, a mathematician, found that in order for “a 3:1 phenotypic ratio to occur, the frequency of the dominant and recessive alleles each had to be 0.5, as they are a monohybrid cross between AA and aa parents”, thus both alleles equal 1. The reason that he noticed this is due to Yule not observing that phenotypic frequencies are a direct function of the allele frequency. Also in 1908 Wilhelm Weinberg, a German physician, did ground breaking work using Mendel’s principles. Shockingly enough, he was the first person to take Mendel’s genetic principles and apply them to the human population. His work in addition to Hardy’s basically related the frequency of genotypes to the frequency of alleles in populations. These two insights are known the Hardy-Weinberg Principle.

    Two conclusions come from this:

    The allele frequencies in a population will not change, generation after generation.

    If allele frequencies in a population are given by p and q the genetic frequencies will be given by p², 2pq, and q².

    -Basically this means p=A1(allele 1) and q=A2 (allele 2): they are both part of a larger statistical equation. Hardy and Weinberg used the p and q equations to find the genetic frequencies and the allelic frequency which is steady at all values between 0 and 1, as long as p+q=1.

    -(Jenkins, Simmions, & Snustad, 722) and (Freeman & Herron, 126-127).

    The Hardy-Weinberg principles will only hold true if all the assumptions of Mendel’s law of segregation are not violated.

    In general they proved that, all things being equal (ceteris paribus), in the limits of those assumptions evolution does not happen. Yes, they proved that evolution does not happen. From the Univ of Dayton website on the Evolutionary Synthesis]

  69. 69
    wd400 says:

    Tell me, wd400, the notion of “alleles”, does that come from Mendel or from Darwin?

    Bateson, actually.

    Tell me, wd400, your calculations of what happens in 5 generations, is that based on Darwin’s notion of gemmules, or is it based on Mendel’s Law of Segregation?

    It’s based population genetics, specifically selection (Darwinian) and segregation (following Hardy and Weinberg’s idea, which Mendel had no clue about, and most Mendelians failed to grasp).

    You have, indeed, reworded more or less what I wrote. As I said, if you start off with a population where it’s unlikely any individuals have at least one “beneficial” allele at each locus and end up with on in which most individuals do, then evolution has surely happened (even if you don’t want that to be called evolution, for reasons that remain your own).

    I’m not sure what your point about HWE is? Yes, if the assumptions of HWE held (and populations were infinte!) then no changes in gene frequency would be possible. They don’t. So?

  70. 70
    bornagain77 says:

    wd400 you claim:

    ,,, if you start off with a population where it’s unlikely any individuals have at least one “beneficial” allele at each locus and end up with on in which most individuals do, then evolution has surely happened,,,

    Do you mean that the neo-Darwinian version of atheistic evolution has surely happened? And that this provides scientific proof that microbes can turn into whales, elephants, and men? Surely even you know that this is far, far, cry from that level of scientific proof?!? If you are claiming this as proof for ‘naturalistic/atheistic’ evolution, then it is well to remind that even what are presupposed to be the purely random processes of the universe are now found to be dependent on a ‘non-local’, beyond space and time, cause in order to derive their most minute movement and even their ‘being’:

    i.e. Quantum Mechanics has now been extended to falsify local realism (reductive materialism) without even using quantum entanglement to do it:

    ‘Quantum Magic’ Without Any ‘Spooky Action at a Distance’ – June 2011
    Excerpt: A team of researchers led by Anton Zeilinger at the University of Vienna and the Institute for Quantum Optics and Quantum Information of the Austrian Academy of Sciences used a system which does not allow for entanglement, and still found results which cannot be interpreted classically.
    http://www.sciencedaily.com/re.....111942.htm

    Falsification of Local Realism without using Quantum Entanglement – (Where is the photon?) – Anton Zeilinger – video
    http://vimeo.com/34168474

    i.e. Photons, on which everything in the universe is dependent on so as to derive their most minute movements, are found to require a beyond space and time, ‘non-local’, cause to explain their continued existence in space time. It is also very interesting to point out how these recent findings for quantum non-locality for photons, (and even for material particles), dovetails perfectly into some of the oldest philosophical arguments for the existence of God and offers empirical confirmation for those ancient philosophical arguments. The argument from motion is known as Aquinas’ First way. (Of note, St Thomas Aquinas lived from 1225 to 7 March 1274.)

    Aquinas’ First Way – (The First Mover – Unmoved Mover) video
    http://www.youtube.com/watch?v=Qmpw0_w27As

    Aquinas’ First Way
    1) Change in nature is elevation of potency to act.
    2) Potency cannot actualize itself, because it does not exist actually.
    3) Potency must be actualized by another, which is itself in act.
    4) Essentially ordered series of causes (elevations of potency to act) exist in nature.
    5) An essentially ordered series of elevations from potency to act cannot be in infinite regress, because the series must be actualized by something that is itself in act without the need for elevation from potency.
    6) The ground of an essentially ordered series of elevations from potency to act must be pure act with respect to the casual series.
    7) This Pure Act– Prime Mover– is what we call God.
    http://egnorance.blogspot.com/.....t-way.html

    or put more simply:

    “The ‘First Mover’ is necessary for change occurring at each moment.”
    Michael Egnor – Aquinas’ First Way
    http://www.evolutionnews.org/2.....first.html

    Not only is motion dependent on “Prime Act’, i.e. a ‘first mover’, but quantum non locality also provides empirical confirmation for the philosophical argument from ‘being’, from ‘existence’ itself!

    Aquinas’ Third way – video
    http://www.youtube.com/watch?v=V030hvnX5a4

    Thus wd400, no matter what motion occurs in the universe, one is forced to appeal to a ‘non-local’, beyond space and time, cause to explain that motion. Of course wd400, you could argue, as Charles Darwin did, that some actions/motions in the universe are so evil (earthquakes, hurricanes, diseases, etc..) that God would never allow those sorts of things to happen in this universe, but that would be a theological argument from theodicy, and would not be a ‘scientific’ argument for the validity of atheism/naturalism. To provide ‘scientific’ proof for atheism/naturalism, you would have to overturn either quantum non-locality for photons, or you would have to show that this ‘non-local’, non-material, beyond space and time, cause for motion and ‘being’ is consistent with atheism. Good luck with that endeavor wd400. Don’t fret, obfuscation is easy for those bent on denying the reality of God.

    supplemental note; ‘true randomness’ does not exist in this universe in that a ‘constant’ is now found for what are perceived to be purely random processes:

    The Austrian physicist Ludwig Boltzmann first linked entropy and probability in 1877. However, the equation as shown, involving a specific constant, was first written down by Max Planck, the father of quantum mechanics in 1900. In his 1918 Nobel Prize lecture, Planck said: “This constant is often referred to as Boltzmann’s constant, although, to my knowledge, Boltzmann himself never introduced it – a peculiar state of affairs, which can be explained by the fact that Boltzmann, as appears from his occasional utterances, never gave thought to the possibility of carrying out an exact measurement of the constant. Nothing can better illustrate the positive and hectic pace of progress which the art of experimenters has made over the past twenty years, than the fact that since that time, not only one, but a great number of methods have been discovered for measuring the mass of a molecule with practically the same accuracy as that attained for a planet.” (of note: Max Planck was/is a Christian Theist)
    http://www.daviddarling.info/e.....ation.html

    Verse and music:

    Revelation 4:11
    “You are worthy, our Lord and God,
    to receive glory and honor and power,
    for you created all things,
    and by your will they were created
    and have their being.”

    Acts 17:28
    For in him we live and move and have our being.’ As some of your own poets have said, ‘We are his offspring.’

    Kari Jobe – Revelation Song – Passion 2013
    http://www.youtube.com/watch?v=3dZMBrGGmeE

  71. 71
    PaV says:

    wd400:

    You have, indeed, reworded more or less what I wrote. As I said, if you start off with a population where it’s unlikely any individuals have at least one “beneficial” allele at each locus and end up with on in which most individuals do, then evolution has surely happened (even if you don’t want that to be called evolution, for reasons that remain your own).

    What I’ve tried to illustrate is that when this supposed process of NS is taking place, we’re simply witnessing the ‘loss’ of ‘alleles’, with no more than a simple substitution of one ‘allele’ for another. with the former ‘allele’ going from ‘beneficial’ to either ‘neutral’ or ‘slightly harmful’, and the latter going from either ‘neutral’ or slightly harmful’ to ‘beneficial’. But nothing “new” has been introduced: we’re just sliding things around.

    That was the reason for the calculation showing that there simply was not enough time for a “new” allele to have come int existence. So, if there is a possible ‘loss’ of alleles (that is, some very ‘rare’ alleles are completely lost to the population), and no “new” alleles forming, then, how can you begin to talk about “evolution”? It’s just, at most, shifting things around (which is a mild form of ‘stasis’).

    Which brings us to this:

    I’m not sure what your point about HWE is? Yes, if the assumptions of HWE held (and populations were infinte!) then no changes in gene frequency would be possible. They don’t. So?

    My point is that the HWE is a form of stasis, and, coupled to the fact that when the environment changes (and NS is assumed at play) “alleles” are either ‘lost’ or, at most ‘shifted around’, nothing new has happened. And, in the “new” environment, the HWE will take over.

    Repeat this process indefinitely, and, with eons of time, most of the “alleles” will have been lost, and genetic variance will be at a minimum, and, with the very next severe environmental change, extinction will take place simply because the “alleles” that used to get shifted to the ‘common’ frequency are no longer available, lost somewhere in the long stretches of time the species has been present.

    This fits the Fossil Record. But it means that “new” species have had to somehow been “front-loaded” because NS simply doesn’t provide for “new” alleles. Genetic drift, given enough time, can restore some alleles that get lost along the way, but, overall, there is a downward trajectory as far as the number of alleles/genetic variance that is present.

    And, given the fact that de novo genes separate major lineages, somehow neo-Darwinism has to account for their origin. And I don’t see any mechanisms being proposed that can overcome the incredible improbabilities of these coming about via random processes.

    Anyways, this is how I see things at present.

  72. 72
    wd400 says:

    This is bizarre.

    HWE tells us how allele frequencies {A1, A2…} fall into genotype frequencies {A1A1, A2A1, A2A2 …} in the absence of any evolutionary force (including drift and mutation!).

    Again, in the little back-of-an-envelope example, the population went started with no individuals with beneficial alleles at all loci, and ended up with half of them being like this. Simply moving existing alleles around can profoundly change populations, and that’s evolution. (In fact, over short periods it’s like that most evolutionary change may come from standing variation, you ought to read a little about “soft sweeps” in the human genome).

    Of course selection removes variation, but mutation (and not , as you say, drift) introduces new alleles in every generation.

    The experiment you are talking about what carried out over a few generations, so it won’t have the answer to questions about how lineages that diverged tens of millions of years ago came to have different genes (loci). The answer, though, is mainly though gene duplication (and gene loss). There is a very rich literature on this topic.

  73. 73
    bornagain77 says:

    wd400, you claim:

    the answer to questions about how lineages that diverged tens of millions of years ago came to have different genes (loci). The answer, though, is mainly though gene duplication (and gene loss). There is a very rich literature on this topic.

    wd400, how come we can never seem to catch evolution in the act of evolving new genes and proteins? In antibiotic resistance, the most popularly known example of ‘evolution’, we find loss of information mutations all the time but never seem to find mutations on their way to building up functional complexity:

    Is antibiotic resistance evidence for Darwinian evolution?
    http://www.youtube.com/watch?v=rYaU4moNEBU

    (Ancient) Cave bacteria resistant to antibiotics – April 2012
    Excerpt: Antibiotic-resistant bacteria cut off from the outside world for more than four million years have been found in a deep cave. The discovery is surprising because drug resistance is widely believed to be the result of too much treatment.,,, “Our study shows that antibiotic resistance is hard-wired into bacteria. It could be billions of years old, but we have only been trying to understand it for the last 70 years,” said Dr Gerry Wright, from McMaster University in Canada, who has analysed the microbes.
    http://www.scotsman.com/news/h.....1-2229183#

    List Of Degraded Molecular Abilities Of Antibiotic Resistant Bacteria:
    http://www.trueorigin.org/bacteria01.asp

    Unexpectedly small effects of mutations in bacteria bring new perspectives – November 2010
    Excerpt: Most mutations in the genes of the Salmonella bacterium have a surprisingly small negative impact on bacterial fitness. And this is the case regardless whether they lead to changes in the bacterial proteins or not.,,, using extremely sensitive growth measurements, doctoral candidate Peter Lind showed that most mutations reduced the rate of growth of bacteria by only 0.500 percent. No mutations completely disabled the function of the proteins, and very few had no impact at all. Even more surprising was the fact that mutations that do not change the protein sequence had negative effects similar to those of mutations that led to substitution of amino acids. A possible explanation is that most mutations may have their negative effect by altering mRNA structure, not proteins, as is commonly assumed.
    http://www.physorg.com/news/20.....teria.html

    Dr. Behe, as I’m sure you have been reminded again and again wd400, searched the experiments going back 4 decades, including Lenski’s infamous LTEE and could find no examples of evolution generating new genes or proteins,,

    “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.co.....evolution/

    Before that, as I’m sure you have been reminded again and again wd400, Dr. Behe examined the adaptations of malaria and HIV, which far outclasses the ‘mutational firepower’ of all higher life on earth for hundreds of millions of years and could find no instances of a gene or protein being generated,,

    “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

    wd400, you claim that ‘lineages that diverged tens of millions of years ago came to have different genes (loci).’ Yet if we look at ancient bacteria from 250 million years ago they are virtually the same at the molecular and morphology level as they are today.

    The Paradox of the “Ancient” (250 Million Year Old) Bacterium Which Contains “Modern” Protein-Coding Genes:
    “Almost without exception, bacteria isolated from ancient material have proven to closely resemble modern bacteria at both morphological and molecular levels.” Heather Maughan*, C. William Birky Jr., Wayne L. Nicholson, William D. Rosenzweig§ and Russell H. Vreeland ;
    http://mbe.oxfordjournals.org/...../19/9/1637

    The can confirm morphology even further back,,,

    AMBER: THE LOOKING GLASS INTO THE PAST:
    Excerpt: These (fossilized bacteria) cells are actually very similar to present day cyanobacteria. This is not only true for an isolated case but many living genera of cyanobacteria can be linked to fossil cyanobacteria. The detail noted in the fossils of this group gives indication of extreme conservation of morphology, more extreme than in other organisms.
    http://bcb705.blogspot.com/200.....st_23.html

    Static evolution: is pond scum the same now as billions of years ago?
    Excerpt: But what intrigues (paleo-biologist) J. William Schopf most is lack of change. Schopf was struck 30 years ago by the apparent similarities between some 1-billion-year-old fossils of blue-green bacteria and their modern microbial counterparts. “They surprisingly looked exactly like modern species,” Schopf recalls. Now, after comparing data from throughout the world, Schopf and others have concluded that modern pond scum differs little from the ancient blue-greens. “This similarity in morphology is widespread among fossils of [varying] times,” says Schopf. As evidence, he cites the 3,000 such fossils found;
    http://www.thefreelibrary.com/.....a014909330

  74. 74
    bornagain77 says:

    wd400 you also claim that ‘The answer, though, is mainly though gene duplication (and gene loss). There is a very rich literature on this topic.’ Yet we find that,,

    Evolution by Gene Duplication Falsified – December 2010
    Excerpt: The various postduplication mechanisms entailing random mutations and recombinations considered were observed to tweak, tinker, copy, cut, divide, and shuffle existing genetic information around, but fell short of generating genuinely distinct and entirely novel functionality. Contrary to Darwin’s view of the plasticity of biological features, successive modification and selection in genes does indeed appear to have real and inherent limits: it can serve to alter the sequence, size, and function of a gene to an extent, but this almost always amounts to a variation on the same theme—,,,
    http://www.creationsafaris.com.....#20110103a

    This is the mother of all ad-hoc explanations:

    Phylogenetic patterns of emergence of new genes support a model of frequent de novo evolution – 21 February 2013
    CONCLUSIONS:
    We suggest that the overall trends of gene emergence are more compatible with a de novo evolution model for orphan genes than a general duplication-divergence model. Hence de novo evolution of genes appears to have occurred continuously throughout evolutionary time and should therefore be considered as a general mechanism for the emergence of new gene functions.
    http://www.biomedcentral.com/1.....7/abstract

    Yup, Orphan genes (comprising 10 to 30% of every new genome sequenced, including humans) can now just ‘poof’ into existence. That whole evolutionary model of functional sequences being selected for in small increments is no good anymore. If you need a new gene you can just call on ‘de novo evolution’ to do your dirty work and once again evolution is protected from falsification:.

    Orphan Genes (And the peer reviewed ‘non-answer’ from Darwinists) – video
    http://www.youtube.com/watch?v=1Zz6vio_LhY

    Moreover wd400, there is experimental evidence against the whole concept of gene duplication being viable at the bacteria level,,

    Experimental Evolution of Gene Duplicates in a Bacterial Plasmid Model
    Excerpt: In a striking contradiction to our model, no such conditions were found. The fitness cost of carrying both plasmids increased dramatically as antibiotic levels were raised, and either the wild-type plasmid was lost or the cells did not grow. This study highlights the importance of the cost of duplicate genes and the quantitative nature of the tradeoff in the evolution of gene duplication through functional divergence.
    http://www.springerlink.com/co.....4014664w8/

    Now wd400, I know you believe in Darwinism with the faith that would make a suicide bomber jealous, but for those of us that find room to doubt that we evolved from pond scum could you please provide us some evidence that Darwinian processes can do what you insist they can do? Perhaps a falsification of this following null hypothesis if that is not too much to ask of you?

    The Law of Physicodynamic Incompleteness – David L. Abel – August 2011
    Summary: “The Law of Physicodynamic Incompleteness” states that inanimate physicodynamics is completely inadequate to generate, or even explain, the mathematical nature of physical interactions (the purely formal laws of physics and chemistry). The Law further states that physicodynamic factors cannot cause formal processes and procedures leading to sophisticated function. Chance and necessity alone cannot steer, program or optimize algorithmic/computational success to provide desired non-trivial utility.
    http://www.scitopics.com/The_L.....eness.html

    You know wd400, with the continued failure of Darwinists to provide evidence for Darwinism to build functional complexity/information, I am really beginning to think that it is completely impossible for material processes to ever generate functional information! In fact (don’t tell anyone), but I’m beginning to think that the first verse of John is actually true!

    John 1:1
    In the beginning was the Word, and the Word was with God, and the Word was God.

    Music:

    Creed – Bullet
    http://www.youtube.com/watch?v=KtCHFLMRX78

  75. 75
    bornagain77 says:

    semi related:

    Angolan Witch Spider, Giant Spider Found In Texas Is A Hoax… – March 24, 2013
    Excerpt: Most spiders possess what are called “book lungs“, which are completely unrelated to what we normally call lungs, and developed independently. And from fossil evidence, we can determine that these structures have remained more or less unchanged throughout the past 400 million years because of how effective they are. There are downsides/limits to them though, with relation to lungs as we know them. As body size increases in relation to gas molecule size, they become less effective. This means that as animals with these structures get bigger they become less and less effective at “breathing”, which places limits on their maximum size.
    http://planetsave.com/2013/03/.....is-a-hoax/

  76. 76
    Joe says:

    wd400:

    The experiment you are talking about what carried out over a few generations, so it won’t have the answer to questions about how lineages that diverged tens of millions of years ago came to have different genes (loci). The answer, though, is mainly though gene duplication (and gene loss). There is a very rich literature on this topic.

    Different genes? Evolutionism needs to explain new body plans and new body parts. And no one can link new genes to those

  77. 77
    PaV says:

    wd400:

    This is bizarre.

    HWE tells us how allele frequencies {A1, A2…} fall into genotype frequencies {A1A1, A2A1, A2A2 …} in the absence of any evolutionary force (including drift and mutation!).

    I don’t think there’s anything bizarre about it.

    The difference between you and me is that you very likely work at some college or institution, and, therefore, have no motivation or urge to think “outside of the box.” OTOH, I have this luxury. And the curiosity.

    The bottom-line is that I have yet to discover any plausible mechanism for genetic innovation. Mircorevolution—which I consider a misnomer; the word that should be used is simply “adaptation”—is accepted by the vast majority of those holding to the ID view. So, for basically ALL of us here at UD, to talk about “microevolution” is of extremely limited interest. What interests us here is so-called “macroevolution.”

    What I’ve been demonstrating (not just trying to) is that NS is a conservative force, HWE is a conservative principle of genetics, and that the mutation rate in most populations is not large enough to conceivably account for de novo genes. BA77 has a link to a very recent article demonstrating that there are genetic ‘gaps’ between major lineages. Neo-Darwinism has no answer for this, in my estimation. You can try to convince me otherwise, but, so far, you haven’t said anything that I’m not familiar with or that remotely comes close to my changing my view.

    Let’s look at the first part of your reply:

    Yes, HWE says exactly what you say that it it does, presuming random mating. It is a statement of stasis, is it not?

    I don’t see how you can deny this.

    You, of course, will very quickly add: but there’s always mutation and drift.

    Well, let’s take a look first at ‘drift.’

    We’re considering now only ‘drift.’ Mutation is now out of the picture—at least for the time being.

    Well, then, you begin with the HWE since mutation is “off”. This is “stasis.” Then you throw in ‘drift’, meaning that if part of the population gets seperated from the larger population, both the larger and smaller population form a new starting point for HWE. But, again, in the absence of ‘mutation’, we have nothing more here than “stasis.”

    I don’t see how you can deny this either. Maybe you have some objection. Be happy to hear it.

    Now, finally, we couple ‘drift’ with ‘mutation.’ But, as has just been demonstrated, when ‘drift’ takes place, we’re simply dealing again with the HWE, but now with new starting points. IOW, there are NO “new” alleles. Nothing “new” has happened genetically. Maybe something “new” has happened phenotypically; but not genetically (other than different gene frequencies based on the fact that there has been a re-shuffling of the original alleles: BUT, again, no “new” alleles—just different proportions [Again, ‘microevolution’=’adaptation’ isn’t of much interest here]).

    Now, we throw in mutation.

    Let’s assume there are 30,000 genes (loci). And let’s assume that there are two or three ‘major’ alleles (by this, I mean the most dominant alleles in terms of phenotypic expression), and a much larger number of ‘minor’ alleles. These ‘alleles’ will be characterized by different nucleotides and a.a.s along the length of DNA that codes for a particular gene (loci).

    If an average size protein has 200 a.a.s, let’s say that 25%, or 50 of these a.a.s are NOT neutral, and can be considered an ‘allele’. At the very least, if we look at the genome, we find 50 different locations along the length of the protein-coding portion of DNA where different a.a.s are found, and which might have some kind of functional activity (are non-neutral).

    If the population size is, let’s say, 10,000, then, we have 30,000 loci, each having around 50 a.a.’s that have some slight, or major, phenotypic effect for each of these 10,000 organisms comprising the population. That means that there are: 10^4 x 3 x 10^4 x50 chances for a mutation to change an allele.

    This equals 1.5 x 10^10. Thus, with a mutation rate of 10^-8, each generation brings a potential change for 150 alleles. Now there are 3 x 10^4 x 50 alleles in the entire organism, or, 150 x 10^4. Obviously, in 10,000 generations, it is likely that each of these alleles has exprienced a mutation in some organism within the population.

    Is this, then, great news for neo-Darwinian novelty? No. And for two reasons.

    First, most mutations are harmful.
    Second, no “new” alleles have been formed. That is, either the a.a. in the minor alleles are ‘neutral’, and NS doesn’t “see” them, or, if NS does “see” them, then if it is now “harmful”, NS will eventually eliminate it; and if it is ‘beneficial’, we’re almost exactly back to where we started from. Again, no “new” alleles.

    So, while ‘drift’ can lead to phenotypic change and new-looking populations, nothing new has happened genetically. Thus, genetically, we’re dealing with a situation that is almost entirely analogous to “stasis.”

    Please feel free to counter my argument.

    Again, in the little back-of-an-envelope example, the population went started with no individuals with beneficial alleles at all loci, and ended up with half of them being like this. Simply moving existing alleles around can profoundly change populations, and that’s evolution. (In fact, over short periods it’s like that most evolutionary change may come from standing variation, you ought to read a little about “soft sweeps” in the human genome).

    Of course selection removes variation, but mutation (and not , as you say, drift) introduces new alleles in every generation.

    None of this statement is inconsistent with what I wrote above. And the conclusion there was, and still is: you’ve described “adaptation”; you haven’t described genetic innovation, as in de novo genes.

    The experiment you are talking about what carried out over a few generations, so it won’t have the answer to questions about how lineages that diverged tens of millions of years ago came to have different genes (loci). The answer, though, is mainly though gene duplication (and gene loss). There is a very rich literature on this topic.

    As BA77 has pointed out, this whole notion—the life-line of Darwinism—is now under a cloud and is being questioned. (So-called “pseudogenes”, for example, formerly thought to be mere degraded duplicated genes, are now found to be involved in gene regulation.)

    Here again, though, one has to ask: what exactly is “new” when you have “gene duplication”?

    [As to “gene loss”, a mild form of what happens through ‘drift’, obviously this cannot produce de novo genes. They might “look” different, but everything that is NOW there, was there before the change took place. Hence the “change” did not produce anything “new.”]

    What we’re told is that via gene duplication, a sort of ‘spare’ gene is now present in the genome, freed from any functional task, ready to mutate itself any which way.

    When a Cadillac starts rusting, this is ‘phenotypic’ change, but it isn’t an instance of a way forward, but a way back wards. If a gene is left loose to mutate itself any old way, then here’s a question: what is different between taking any stretch of DNA, and then allowing it to mutate itself crazy over time, and having a “duplicated gene” mutate itself crazy over time? I see no real difference.

    Now, you will likely object that we “know” that the ‘duplicated gene’ had function, and we don’t know this about ‘any’ stretch of DNA. I concede this point. However, if this ‘duplicated gene’ had ‘function’ before, then, very likely, there are variants (alleles) of this gene throughout the population. Now, if something ‘other than’ one of these already present ‘alleles’ shows up—produced via mutation—then what should we conclude? I say that either: (1) the mutation is ‘neutral’, or (2) NS eliminates it if it is harmful, or (3) you simply end up with one of the already present alleles.

    Now it may be argued that, under a changed “environment” some “new” allele, probably one that was ‘neutral’ at a particular a.a. location, but which now, with a changed a.a. at that former ‘neutral’ site, is non-neutral and beneficial, can, and does, occur.

    But doesn’t this simply mean that at that gene (loci), we now have 51 alleles, rather than just the 50 we started with?

    Where is the de novo gene in all of this?

    Please feel free to proffer a mechanism. I’d be happy to think about it.

    But I hope that in all of this, you can see that when I start thinking “outside of the box,” I come up with no answers to my questions regarding “macroevolution” based on what population genetics wants to teach me.

  78. 78
    wd400 says:

    Well, then, you begin with the HWE since mutation is “off”. This is “stasis.” Then you throw in ‘drift’, meaning that if part of the population gets seperated from the larger population, both the larger and smaller population form a new starting point for HWE.

    That’s not what drift means. Populations are not infinite, so allele frequencies (and, as we know from HWE genotype frequencies) change in each generation.The effect is more pronounced in small populations, since drift can be thought of as a population being sampled from the infinitely many potential populations made possible by the gene frequencies.

    Now, we throw in mutation. Let’s assume there are 30,000 genes (loci). And let’s assume that there are two or three ‘major’ alleles (by this, I mean the most dominant alleles in terms of phenotypic expression)

    I wouldn’t use the word ‘dominant’ like this while talking abut genetics.

    First, most mutations are harmful.
    Second, no “new” alleles have been formed.

    First, so? Second, yes they have

    That is, either the a.a. in the minor alleles are ‘neutral’, and NS doesn’t “see” them, or, if NS does “see” them, then if it is now “harmful”, NS will eventually eliminate it; and if it is ‘beneficial’, we’re almost exactly back to where we started from. Again, no “new” alleles.

    You missed the bit where you explain why we are “back where we started from” when newly arising alleles are beneficial.


    So, while ‘drift’ can lead to phenotypic change and new-looking populations, nothing new has happened genetically. Thus, genetically, we’re dealing with a situation that is almost entirely analogous to “stasis.”

    No. I can’t see an argumentin here to counter. You’ve just decided beneficial alleles take us back to square one, and decreed that changes in allele frequency aren’t evolution.

    And the conclusion there was, and still is: you’ve described “adaptation”; you haven’t described genetic innovation, as in de novo genes.

    No. Because I’m talking about what happened in 5 generations!

    When a Cadillac starts rusting, this is ‘phenotypic’ change, but it isn’t an instance of a way forward, but a way back wards. If a gene is left loose to mutate itself any old way, then here’s a question: what is different between taking any stretch of DNA, and then allowing it to mutate itself crazy over time, and having a “duplicated gene” mutate itself crazy over time? I see no real difference.

    Life is chemisty. If you have a gene that does Job A very well it probably also does Job B poorly (search for enzyme “moon lighting”). Once you have a gene duplication one of the daughter genes is freed from the contstraint to perform JobA and can explore the surrounding sequence space. There is quite a lot of evidence for these sorts of models. Search “Subfunctionalization”, “neofunctionalization” and “innovation, amplification, divergence” for popular models.

    Where is the de novo gene in all of this?

    Gene duplication means going from one locus to two. Is all this rant based on a misunderstanding of the term?

  79. 79
    PaV says:

    PaV:
    Well, then, you begin with the HWE since mutation is “off”. This is “stasis.” Then you throw in ‘drift’, meaning that if part of the population gets seperated from the larger population, both the larger and smaller population form a new starting point for HWE.

    wd400:

    That’s not what drift means. Populations are not infinite, so allele frequencies (and, as we know from HWE genotype frequencies) change in each generation.The effect is more pronounced in small populations, since drift can be thought of as a population being sampled from the infinitely many potential populations made possible by the gene frequencies.

    You seem to have completely misunderstood what I was saying. I don’t think it is because I didn’t state it well enough. I think it is because you refuse to think outside of the box. You prefer rote answers.

    Yes, ‘drift’ means changing frequencies.** However, remember, that in the hypothetical I was dealing with, the environment was not changing, and an isolated, randomly mating population was assumed. Yet, it should be quite clear that I’m not interested in gene frequencies, which can, and do, change while HWE is present, but in the actual composition of alleles in the overall population—which the HWE informs us ‘move around, but don’t change.’

    The reason I mentioned ‘smaller’ and ‘larger’ populations is because when a population breaks up into ‘smaller’ and ‘larger’ sub-populations, then, and only then [assuming mutation is not at work, which was the assumption] do you have a ‘change’ in the number of alleles. And the number of alleles becomes smaller for both populations. This is the “loss” I talked about in an earlier post.

    **[If you look back at my post, I talked about ‘phenotypic change’—that’s the sort of thing that changed “frequencies” can bring about. (In fact you’ve quoted it below) But, again, it’s insignificant ‘microevolution’, better described as ‘adaptation.’]

    PaV:
    First, most mutations are harmful.
    Second, no “new” alleles have been formed.

    wd400:
    First, so? Second, yes they have.

    You say “so?”.

    Alright. But this serves to highlight NS’ true role: eliminate harmful genes. It’s not in the business of developing “new” genes, but of getting rid of bad ones.

    “Yes, they have.”

    How? How have “new” alleles formed? Did you follow the logic of my argument? What I’m saying is that just like electrons in atoms can only enjoy certain energy states, so, too, you can only have “alleles” existing in certain configurations since either the changed a.a. is neutral, or more likely harmful, and so subject to elimination by NS.

    PaV:

    That is, either the a.a. in the minor alleles are ‘neutral’, and NS doesn’t “see” them, or, if NS does “see” them, then if it is now “harmful”, NS will eventually eliminate it; and if it is ‘beneficial’, we’re almost exactly back to where we started from. Again, no “new” alleles.

    wd400:
    You missed the bit where you explain why we are “back where we started from” when newly arising alleles are beneficial.

    I also wrote later on—to clarify: “Now it may be argued that, under a changed “environment” some “new” allele, probably one that was ‘neutral’ at a particular a.a. location, but which now, with a changed a.a. at that former ‘neutral’ site, is non-neutral and beneficial, can, and does, occur.

    But doesn’t this simply mean that at that gene (loci), we now have 51 alleles, rather than just the 50 we started with?”

    Can’t you see that an “allele” that represents a single a.a. change from another of the 50 “alleles” already present is, as I said, but as you wrongly quoted: ” . . . almost exactly back to where we started from.”

    Should we jump up and down and yell, “Alleleuia,” because a single a.a. has changed on a string of 200 a.a.? Is this earth shattering change? Or is it almost an insignificant shift? I think common sense tells you it’s the latter.

    PaV:
    So, while ‘drift’ can lead to phenotypic change and new-looking populations, nothing new has happened genetically. Thus, genetically, we’re dealing with a situation that is almost entirely analogous to “stasis.”

    wd400:
    No. I can’t see an argument in here to counter. You’ve just decided beneficial alleles take us back to square one, and decreed that changes in allele frequency aren’t evolution.

    You’re completely unresponsive here.

    Changing allele frequency has a name for it: animal breeding!! But for you, it’s “evolution.” Tell me that this isn’t exactly what happens when new breeds are come by: the gene frequencies have changed.

    And you call it “evolution” by decree. Wasn’t Sewell Wright a “breeder”? Oh, yes, that’s right; he was.

    He’s the one who’s given us adaptive landscapes and such, work that I admire; though I consider it now mostly wrong and outdated by the findings of modern molecular biology.

    And, again, you’ve simply (1) mis-characterized what I said, and (2) refused to think things through in a fresh way. What can I say? Tenure and prestige are powerful forces.

    PaV: And the conclusion there was, and still is: you’ve described “adaptation”; you haven’t described genetic innovation, as in de novo genes.

    wd400: No. Because I’m talking about what happened in 5 generations!

    I’ll give you a 100 million generations, and you’ll still not have a true de novo gene. Population genetics can’t explain it—though they pretend to.

    I wonder: have you ever read R.A. Fisher’s “The Genetical Theory of Natural Selection”? Are you aware of what his “fundamental theorem of natural selection” was based on? Just wondering.

    wd400:

    Life is chemisty. If you have a gene that does Job A very well it probably also does Job B poorly (search for enzyme “moon lighting”). Once you have a gene duplication one of the daughter genes is freed from the contstraint to perform JobA and can explore the surrounding sequence space. There is quite a lot of evidence for these sorts of models. Search “Subfunctionalization”, “neofunctionalization” and “innovation, amplification, divergence” for popular models.

    ” . . . one of the daughter genes is freed from the constraint to perform Job A and can explore the surrounding sequence space.”

    This is no more than “hand-waving.” If you believe this stuff, that’s your business. I know what it really is: navel-gazing at its finest. (If you re-visit what I wrote, you’ll see that I have addressed this issue of “surrounding sequence space”** and have effectively argued that hardly any of it exists. OTOH, if we have a lot of imagination—as Darwin tells us we must—then I guess you can believe anything you want.)

    [N.B. I have to use this kind of edgy language because it’s impossible to get you to think outside of the box otherwise; although I know full well that even edgy language isn’t enough for that.]

    **[My essential argument up above is that this “sequence searching” will, in all likelihood, lead directly back to one of the 50 (now make it 51) alleles. IOW, the searching must, perforce, reach a limit. But, of course, Darwinists don’t believe in ‘limits.’ After all, organisms are infinitely plastic, aren’t they?]

    wd400:
    “Subfunctionalization”, “neofunctionalization” and “innovation, amplification, divergence” for popular models.

    I say that it’s always a good thing, when you’re in the ‘hand-waving’ business, to come up with new terms to dazzle others with . . . . Good job.

    And you say that they’re “models”? Is this as in “climate change models”?

    PaV:
    Where is the de novo gene in all of this?

    wd400:

    Gene duplication means going from one locus to two. Is all this rant based on a misunderstanding of the term?

    How in the world did you get the impression that I thought gene duplication was anything other than an added locus? Isn’t the language rather self-evident as to what it describes?

    Thus, your response appears to me to be a complete non sequiter.

    And why is what I write a “rant”? Because you’re not ready to think it through, and not ready to change your mind about things? Is that it?

  80. 80
    wd400 says:

    which the HWE informs us ‘move around, but don’t change.’

    Yeah. Amazingly enough if you ignore for the source of new alleles you don’t get new alleles. If there is an insight in this I have failed to grasp it.

    I’m saying is that just like electrons in atoms can only enjoy certain energy states, so, too, you can only have “alleles” existing in certain configurations since either the changed a.a. is neutral, or more likely harmful, and so subject to elimination by NS

    Alleles that are neutral today aren’t necessarily so in the future. Even slightly harmful mutations survive in small populations (search “nearly neutral theory”). It if very likely the accumulation of mildly deleterious mutations changes the fitness landscapes such that complexity can evolve (bacteria are too slick to allow the sort of mess our genomes accumulate). And you still haven’t accounted for newly-arising beneficial alleles.

    But doesn’t this simply mean that at that gene (loci), we now have 51 alleles, rather than just the 50 we started with?”

    50 alleles? Which genes do you think have 50 alleles?

    say that it’s always a good thing, when you’re in the ‘hand-waving’ business, to come up with new terms to dazzle others with . . . . Good job.

    I didn’t give you terms in the hope you’d be impressed. I gave them in the hope you’d read about them and see the evidence for each model. I like thinking “outside the box” on pop. gen. The idea of close-minded academics is one of the most comically wrong cractitures going around. But you have to remember there is a great deal of evidence supporting the population genetics we have. If you say somethng as stupid as “give me a 100 million years and you still won’t get a de novo gene” then I’m afraid you aren’t presenting an informed argument.

    How in the world did you get the impression that I thought gene duplication was anything other than an added locus?

    Welll, you said

    “Wut doesn’t this simply mean that at that gene (loci), we now have 51 alleles, rather than just the 50 we started with? Where is the de novo gene in all of this?”

    The outcome of a gene duplication is no a new allele, it’s a new locus. With one allele.

    I’m happy to think “outside the box” about population genetics, that’s kind of my job. I just think maybe there

  81. 81
    PaV says:

    wd400:

    Yeah. Amazingly enough if you ignore for the source of new alleles you don’t get new alleles. If there is an insight in this I have failed to grasp it.

    Typical Darwinian response: you presume what you have yet to prove. Science is easy that way.

    You should have said this, which would have been more accurate: “Yeah. Amazingly enough if you turn off mutations, no new alleles show up.”

    IOW, stasis is the rule. Now, you have to prove that “mutations” + NS can produce new alleles.

    wd400:

    Alleles that are neutral today aren’t necessarily so in the future. Even slightly harmful mutations survive in small populations (search “nearly neutral theory”). It if very likely the accumulation of mildly deleterious mutations changes the fitness landscapes such that complexity can evolve (bacteria are too slick to allow the sort of mess our genomes accumulate). And you still haven’t accounted for newly-arising beneficial alleles.

    PaV: But doesn’t this simply mean that at that gene (loci), we now have 51 alleles, rather than just the 50 we started with?”

    wd400:

    50 alleles? Which genes do you think have 50 alleles?

    [Pardon the ‘blockquote’, but it was a pretty long quote.]

    ” It is very likely the accumulation of mildly deleterious mutations changes the fitness landscapes such that complexity can evolve.”

    It’s “likely,” but not known, I suppose.

    This, again, is typical Darwinian thought: what is “bad” for now, might be “good” later on. And then we can substitute almost anything we want for “bad” and “good”, resulting in nothing more than equivocation.

    If some alleles were ‘beneficial’, and some were ‘harmful’, and the environment changes, then perhaps some of the ‘harmful’ ones become ‘beneficial’; but, likewise, some of the ‘beneficial’ ones become ‘harmful’. Touche. It’s like a balanced polymorphism.

    Now, I ran the long quote up above for a reason: you ask now (why you didn’t before is beyond me): “Which genes do you think have 50 alleles?”

    Well, maybe most of them. Just because population genetics doesn’t take account of this genetical reality doesn’t mean the reality doesn’t exist.

    Why did Kimura propose his Neutral Theory? Do you remember? It’s because he found so MANY polymorphisms!! Too many for neo-Darwinian theory to be able to account for due to the genetic load associated with maintaining each of these polymorphisms via positive selection. So he left Sewell Wright, and traditional population genetics behind, and proposed his new theory.

    And, of course, a “polymorphism” is just another way of saying “allele”. So, in reality, each locus, when studied throughout a population, very likely has lots of polymorphisms/alleles, unless it’s highly conserved.

    But, of course, if it’s highly conserverd, then that means that NS is very busy weeding out additional polymorphisms/allleles.

    And this exactly proves the point I’ve been making: i.e., any given gene/locus has only so many possible permutations of a.a.s that NS will allow, and once those permutations have been explored, then the organism has no place to go: i.e., “stasis”. And, of course, the fossil record shows, as Stephen J. Gould has written, that species “appear, continue on in the same way, and then disappear.” Yes, that’s right: “stasis.”

    wd400:

    I didn’t give you terms in the hope you’d be impressed. I gave them in the hope you’d read about them and see the evidence for each model.

    You misunderstood me. What I said, I said ‘tongue in cheek.’ What I was saying is that you theorize this way and that, arrive at some conclusion, and give it a name. All of this “looks” like knowledge, when, in fact, it is the invention of names which can then be applied to certain situations in pop. gen. giving the appearance that all of these things are well understood, and conformable to reality.

    If you say somethng as stupid as “give me a 100 million years and you still won’t get a de novo gene” then I’m afraid you aren’t presenting an informed argument.

    I was just reading an article today on the Coelocanth—a living fossil. It’s been around for over 300 million years (generations). It’s still the same. Apparently no de novo gene there, eh.

    wd400:

    The outcome of a gene duplication is no a new allele, it’s a new locus. With one allele.

    Sorry you misunderstood this. What I was saying was not that an added allele now constitutes a de novo gene, but, rather, that very little “new” has happened—and so this is a very long stretch away from what we would expect for a true ‘de novo’ gene.

    Having said this, however, gene duplication—all by itself—simply reproduces an “allele” somewhere else on the genome. I.e., in, and of itself, there is no novelty.

    Let me just conclude with this:

    If—and this is a big ‘if’—every living eukaryotic organism had the very same set of genes, then I would be convinced by this that “changing gene frequencies” can bring about evolution. OK.

    But this isn’t the case. And recent evidence, as BA77 has cited, indicates that there are ample portions of ‘de novo’ genes that separate major lineages. Neo-Darwinism has not yet proposed a mechanism that can feasibly explain the appearance of said ‘de novo’ genes. When you come up with one, then, as Ross Perot said: “I’m all ears.”

    In the meantime, epigenetics, inheritance via RNA, and other such things, are quickly undermining the entire relevance of population genetics, so complex is life.

    And I hope you continue to ‘think outside the box.’ It’s good for science. But maybe more than just ‘thinking outside the box’, I have a very intuitive way of sizing things up—maybe it’s the engineer in me—and, frankly, I don’t see population genetics either now, or in the future, measuring up to the task of explaining cellular and biological complexity.

    After reading the ‘bible’ of population genetics, I just say: “This stuff can’t be believed.” Alas.

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