Uncommon Descent Serving The Intelligent Design Community

Darwinism has already been quietly abandoned, and people are mainly afraid of the bereft trolls?

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Here’s an interesting perspective from Paul Benedict (War of Words, July 2, 2011):

Stephen C. Meyer, expounding Intelligent Design in his book Signature in the Cell, makes a point he does not seem to appreciate: for decades microbiologists have been abandoning Darwinism. Breakthrough technologies have shown that life at the cellular level is complex beyond anything Darwin or any 19th century biologist could have predicted. From the variety of cellular functions to the complex information transmitted in the gene, many outstanding scientists recognize that the math just doesn’t work. Intelligent Design represents only one concession to the statistical impossibility that chance caused the life of simple cells. Interrupting the following parade of microbiologists who, like Meyers, recognize that random chance alone cannot have produced the simplest cellular life, are conclusions flowing from this scientific consensus. 

Christian de Duve, for example, a Nobel Prize winner, and in no way an advocate of Intelligent Design, has abandoned random chance as the agent of upwards evolution or the ascent of man. He envisions primordial planet earth as a chemical reaction waiting to happen. Recognizing that the odds of random chance being impossibly against the formation of a single cell, let alone man, he has ceaselessly been searching for the string of chemical reactions that, once started, must have inevitably and, without chance, led to mankind. So far… no luck.

Ilya Prigogine, won his 1977 Nobel Prize for his theory that biological life self-assembled from inorganic non-life through the non-equilibrium thermodynamic processes. Again, random chance was abandoned, this time for the notion of an outside force arising in a thermodynamic process that, somehow, energized evolution. Such a force has never been identified.

Manfred Eigen, won the Nobel Prize in 1967 for his work measuring extremely fast chemical reactions brought about by energy pulses. Though proud to use the term evolution, his models of the origin of life are not based on chance but on self-organizing chemical reactions that cycle to higher and higher levels. He is also the author of Eigen’s Paradox that explains a critical problem in positing cycles of RNA that lead to DNA.

Lynn Margulis believes parasites aided random chance in the evolution of the cell.

Freeman Dyson, feeling random chance and self-organizing molecular scenarios are insufficient seems to believe in a combination of Eigens self-organizing RNA cycles andLynn Margulis sense that cellular evolution was the result of parasites.

Michael Polanyi, whose interest in science often impacted his philosophic notions, rejected chance as the origin of life in Lifes Irreducible Structure.

Bernd-Olaf Kuppers, like Michael Polanyi, supports his notions that the whole (the living cell) is greater than the sum of its parts (chemical reactions) with evidence that random chance cannot result in the irreducible complexity of a living organism (60) nor explain the information it transmits.

Bernd-Olaf Kuppers, using methodology like that of noted Darwinian apologist Richard Dawkins, also modeled mathematical algorithms that guide randomly generated computer simulations of origin of life scenarios. Kuppers calls his theory of self-organization the molecular-Darwinistic approach. It is hard to tell what Kuppers means by statements like, inanimate matter organized itself of its own accord into animate systems (82). More.

A libertarian, he ends with a Cry, Fredom: “Tradition dies hard in every generation. Ignorance is not a lack of information; it is willfully ignoring knowledge. Centralized bureaucratic power breeds fear even in professionals, but tenured teachers can do better. It’s time to tell the kids: it is statistically impossible that Darwin’s explanation of the origin of life is correct.”

Comments
You missed a bit, Clive. This is oscillating evolution so that means the turtle will evolve back into a finch again if you fund the Grants for long enough!Chris Doyle
July 10, 2011
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You missed a bit, Clive. This is oscillating evolution so that means the turtle will evolve back into a finch again if you fund the Grants for long enough!Chris Doyle
July 10, 2011
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My money is on the finch beak growing so large that the whole bird turns into a sea turtle. ;)Clive Hayden
July 10, 2011
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You are making the claim that a mechanism that we observe occuring at directly observable time scales, cannot occur over non-directly observable time scales, even though predictions made from that extrapolation are supported by palaentological and genetic evidence, than you need to support the claim.
Finch beaks? You observed a change in the mean size of beaks in a population of finches over time? What are the predictions supported by extrapolations from changes in that finch beak size? And from this you extrapolate that beaks can turn into something else? Are you daft!?
Newton, famously, stated that a moving body would keep moving until something stopped it. We have shown a moving body. You have claimed it must stop after a certain distance. Therefore, you must show what would stop it,
Death. Death would stop it. Your "moving body" is a finch beak. You claim that a finch beak can grow as small or as large as whatever. You don't say which. And then you say it is up to me to show that a finch beak cannot grow that large or that small. You're insane.Mung
July 10, 2011
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Ah. You're back! Beak size changed. This was caused by differential reproductive success? You don't know. There's a gene that determines beak size, and this gene increased in the population? No no no. G-d. I'm an idiot. There must be many genes for beak size. We're talking about a 'mean' here. The genes for larger beak sizes must have been preferentially selected. The genes for the larger beak sizes must have increased in frequency in the population. And the evidence is? There was a larger proportion of larger beaks in the population than smaller beaks. I'm not impressed. Neither should anyone else be. We really don't know whether this was evolution or natural selection in action or not. It's speculation posing as science.Mung
July 10, 2011
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Mung:
Elizabeth Liddle:
Why couldn’t natural selection achieve this in millions of years? I’m sorry, but it’s not up to us to answer question of the nature, “why could natural selection not do this or that.” As has been pointed out to you, this is a standard ploy engaged in by Darwinists tracing back to Charles Darwin himself. It is up to you to show that it can, and in fact did.
Well, no, it isn't. You are making the claim that a mechanism that we observe occuring at directly observable time scales, cannot occur over non-directly observable time scales, even though predictions made from that extrapolation are supported by palaentological and genetic evidence, than you need to support the claim. Newton, famously, stated that a moving body would keep moving until something stopped it. We have shown a moving body. You have claimed it must stop after a certain distance. Therefore, you must show what would stop it,
because it is your claim.
Where is the "friction" that would necessarily stop a population continuously adapting to a changing environment? Where is the "friction" that would necessarily stop two diverging sub-populations from continuing to adapt to different environmental conditions independently, indefinitely? Of course we know that a very large proportion of all populations end in extinction. But we also know that a minority continue (at least we do if we accept common descent). What barrier are you proposing that would necessarily stop this happening?
Elizabeth Liddle
July 8, 2011
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Mung:
So the effect that was observed was a change in beak size? Did the beaks gradually get larger?
Mean beak size increased in the population following an increase in mean seed size.
Or was the effect that was observed an increase in the number of finches with a specific beak size and a reduction in the number of finches in the same interbreeding population with an even larger beak?
The distribution of beak size was continuous.
Or was the effect that was observed an increase in the number of finches with a specific beak size and a reduction in the number of finches in the same interbreeding population with a smaller beak?
As I said, the distribution was continuous (no "specific beak sizes") and the mean changed. Still trying to figure out the precise effect that was observed.
But whatever it was that was observed, the Grants also observed changes in seed size. And they believe the change in beak size was significantly correlated to the change in seed size.
Well, it wasn't a credo, it was a finding. And they said that therefore one caused the other, and then claimed they had shown natural selection in action? Greater prevalence in larger seeds doesn't "cause" beaks to become larger - what causes beaks to be larger is probably alleles of genes that govern beak development (i.e. the expression of other genes during development). What "caused" the differential reproduction by beak size (more chicks from larger-beaked parents, fewer chicks from smaller-beaked parents) was deaths due to shortage of small seeds. And this, in turn, altered mean beak size in the population. It's a fascinating book, and I am doing this from recall, but the amazing thing about the Grants work was that they literally knew every finch on the island, its parentage, who it mated with, how many chicks each pair managed to raise, and, of course, what all the beak sizes were.
By which they meant differential reproduction?
Yes. Do read the book. It's a very well written account of an amazing piece of longitudinal research.Elizabeth Liddle
July 8, 2011
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Elizabeth Liddle:
Yes. Cloning happens as a result of mitosis. Sexual reproduction involves a different process, called meiosis, which is NOT “cloning”. The reason that “cloning” exists as a word is because it is different to sexual reproduction.
Is that supposed to be an argument? Cloning is not the same as sexual reproduction? OK. Meiosis is not cloning. OK Mitosis is cloning? You're a little vague on that, since you say cloning happens as a result of mitosis. And your argument is that sexual reproduction does not involve mitosis? Therefore sexual reproduction does not have fidelity? Because only cloning has fidelity? So there's no fidelity involved in meiosis? It's just helter skelter copy and paste?
ELIZABETH: But it’s a bit silly when talking about sexual reproduction, because we don’t have fidelity anyway – each child genome is unique. ELIZABETH: “I say that in the case of sexual reproduction (as opposed to cloning) fidelity isn’t relevant anyway…”
Mung
July 4, 2011
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But natural selection (as I am using the term) doesn’t “explain everything”. The reason these examples are clear evidence of natural selection (as Darwin defined it) is that in both the Grants’ work and Endler’s work, the population shifts (i.e. mean measures of some phenotypic feature, reflecting, almost certainly, a change in allele frequency) was directly correlated with environmental change. That’s what natural selection is – it’s differential reproduction attributable to heritable variance in the ability to survive and breed. If it were not correlated with environmental chance it could be mere “drift” – stochastic fluctuations in allele frequencies between generations.
Fourthly: in neither of these examples were the phenotypic changes related to genetics, so we don’t know whether brand new alleles, or a simply redistribution of existing alleles, was responsible for the phenotypic chances.
So the effect that was observed was a change in beak size? Did the beaks gradually get larger? Or was the effect that was observed an increase in the number of finches with a specific beak size and a reduction in the number of finches in the same interbreeding population with an even larger beak? Or was the effect that was observed an increase in the number of finches with a specific beak size and a reduction in the number of finches in the same interbreeding population with a smaller beak? Still trying to figure out the precise effect that was observed. But whatever it was that was observed, the Grants also observed changes in seed size. And they believe the change in beak size was significantly correlated to the change in seed size. And they said that therefore one caused the other, and then claimed they had shown natural selection in action? By which they meant differential reproduction?Mung
July 4, 2011
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Elizabeth Liddle:
Why couldn’t natural selection achieve this in millions of years?
I'm sorry, but it's not up to us to answer question of the nature, "why could natural selection not do this or that." As has been pointed out to you, this is a standard ploy engaged in by Darwinists tracing back to Charles Darwin himself. It is up to you to show that it can, and in fact did.Mung
July 4, 2011
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Chris:
Clearly, I disagree that “trivial population shifts” are Selection. You can only advance this claim if you redefine Natural Selection to mean “that which occurs whenever things are born and whenever things die”. It wasn’t Darwin who said “A theory that explains everything, explains nothing” and he certainly didn’t have such an all-encompassing definition of Natural Selection in mind either.
But natural selection (as I am using the term) doesn't "explain everything". The reason these examples are clear evidence of natural selection (as Darwin defined it) is that in both the Grants' work and Endler's work, the population shifts (i.e. mean measures of some phenotypic feature, reflecting, almost certainly, a change in allele frequency) was directly correlated with environmental change. That's what natural selection is - it's differential reproduction attributable to heritable variance in the ability to survive and breed. If it were not correlated with environmental chance it could be mere "drift" - stochastic fluctuations in allele frequencies between generations. Yes, it's on a very small scale, and yes, its possible (but not certain) that no new alleles were involved, but it is most certainly "natural selection" by any definition of the term! Certainly by Darwin's. It has a very specific meaning, and it applies here.
However, I think we both agree (though qualification may be required) with the distinction between: 1. “Selection of pre-existing genetic variation” (which is what people often have in mind when they think of ‘micro-evolution’, I prefer the term ‘sub-specific variety’) and, 2. “Selection on new alleles” (this is more like ‘macro-evolution’, I prefer the term ‘evolution’)
Well, I would dispute this. There is no evidence to think that whether or not an allele is recent or long-standing makes any difference to the process allele frequencies change, except that new alleles start from a number disadvantage. You are right of course, that the greater the phenotypic distance, as it were, travelled by a population, the more sure we must be that at least some new alleles have come on board since the start of the journey, but to assign new alleles to one effect ("macro evolution") and long-standing alleles to a different one (micro-evolution) is not carving nature at its joints! In fact, I don't think nature carves that way at all. Yes, we can distinguish between new alleles and new advantages for old alleles, and we can also distinguish between longitudinal adaptation and speciation, and we can also distinguish between oscillatory adaptation from generation to generation and net adaptation to long term environmental changes, but those divisions don't map on to each other one-to-one. Both new and old alleles can contribute to all three; long term adaptation to long term changes in the environment can happen without speciation; speciation can occur without marked phenotypic changes.
Before we start trying to determine “at what rate potentially useful novelty arises”, I would like to know, what grounds do we have to believe that any useful novelty arises?
Fair enough! A fair bit, I would say - were you able to read that review article? I don't know whether it is open access or not.
And, even if we have grounds to believe in useful novelty, I would then like to know, what grounds do we have to believe that any *macro-evolutionarily significant* novelty arises (ie. that required to produce a human out of a single-celled common ancestor)?
Well no-one thinks you can get a human being out of a single-celled ancestor with a single new allele for an existing gene! (As I am sure you are aware.) But yes, it's an important question. Gotta run LizzieElizabeth Liddle
July 4, 2011
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Hi Lizzie, Clearly, I disagree that “trivial population shifts” are Natural Selection. You can only advance this claim if you redefine Natural Selection to mean “that which occurs whenever things are born and whenever things die”. It wasn’t Darwin who said “A theory that explains everything, explains nothing” and he certainly didn’t have such an all-encompassing definition of Natural Selection in mind either. However, I think we both agree (though qualification may be required) with the distinction between: 1. “Selection of pre-existing genetic variation” (which is what people often have in mind when they think of ‘micro-evolution’, I prefer the term ‘sub-specific variety’) and, 2. “Selection on new alleles” (this is more like ‘macro-evolution’, I prefer the term ‘evolution’) Before we start trying to determine “at what rate potentially useful novelty arises”, I would like to know, what grounds do we have to believe that any useful novelty arises? And, even if we have grounds to believe in useful novelty, I would then like to know, what grounds do we have to believe that any *macro-evolutionarily significant* novelty arises (ie. that required to produce a human out of a single-celled common ancestor)? I’m afraid I still can’t see how anyone can get excited over 2 millimetres! Especially when artificial selection yields much more exciting (albeit macro-evolutionarily insignificant) results. To describe an (on average) 2mm oscillation as an “effect of adaptation” is seriously overplaying the evidence. I can understand why the Grants have overplayed the evidence. After all, they were hoping to see a continuing expansion of the beaks beyond 2mm. They had to pretend that they weren’t disappointed when the beaks returned to their original average size again. Darwin certainly did not predict that the effects of adaptation could be undone as though they never happened in the first place! Why can we rule out “brand new alleles” in peppered moths? Because, dark peppered moths have been around for as long as light peppered moths as far we can tell. And “describing the light peppered moth as Biston Betularia and the dark peppered moth as Biston Carbonaria is entirely misleading. The latter is no more a mutant than any other dark coloured creature is. They are both Biston Betularia and, as far as we can tell, always have been.” Why can we rule out “brand new alleles” in 2mm finch beak oscilliation? Well, why would you rule them in? Variations in the size of any body part, in any creature, are perfectly accounted for with-in the pre-existing gene pool wouldn’t you agree? Given that we’re talking about a tiny, insignificant oscillation in this case there is absolutely no need to look for a “brand new allele” (unless there is a desire to overplay the evidence). Yes, you’re quite right, talk of “brand new alleles” is clumsy in the case of E-coli in Lenski’s LTEE. Prokaryotic gene pools are certainly more flexible and nebulous than eukaryotic gene pools. I consider things like plasmids and bacteriophages to be components of the prokaryotic gene pool. I would even argue that just the *potential* of point mutations in prokaryotes is something that we should consider as being a part of a prokaryotic gene pool too. So, when Lenski’s E-coli ‘rediscovered’ the means to bring citrate through its membrane in the presence of oxygen, this was an adaptation that may have been caused by a ‘mutation’ (ie. a point mutation resulting in an over-expressed protein) but one that we can still consider a part of the pre-existing E-coli gene pool. I appreciate that, at first glance, you might consider this move a bit cheeky on my part! However, all too often, I believe people dwell on so-called evolutionary adaptation in bacteria without dwelling on the very obvious, and to my mind, more significant, limits to adaptation in bacteria. The ‘wider’ gene pool I propose for bacteria explains these observations. Particularly when set against the backdrop of a message I posted to Ellazimm (gone, but not forgotten!) back on the ‘Forrest part 1’ thread: https://uncommondescent.com/intelligent-design/at-some-point-the-obvious-becomes-transparently-obvious-or-recognizing-the-forrest-with-alls-its-barbs-through-the-trees/#comment-383560 You ask me why natural selection couldn’t create Chihuahuas and Great Danes in millions of years. I answer: because it didn’t. It needs, dare I say, the Intelligent Design of Artificial Selection to create such dramatic variation in dogs. We know what we’re doing, we can be picky and creative. Nature (especially defined as “things being born and things dying”) doesn’t. It is blind and stupid. This is a fundamental difference between Artificial Selection and Natural Selection – and the emphasis is on how the selection is achieved, not what the selection is acting on. Another way to illustrate it is this. Nature – through erosion, etc - can make peculiar shapes out of rock. But it could never build anything as amazing as Stonehenge. I do not deny that sub-specific variety occurs in nature and that this allows a limited degree of adaptation to particular habitats. Indeed, I would argue that part of the design of gene pools is to give creatures added flexibility should they ever need it. But, there is no evidence whatsoever to suggest that Natural Selection is anywhere near as powerful as Artificial Selection. The fact that it required the input of our Intelligent Design before this planet ever saw variety in things like dogs is compelling evidence that Natural Selection isn’t capable of achieving anything macro-evolutionarily significant.Chris Doyle
July 4, 2011
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No problem Chris! I didn't mean to suggest you were! It was "whoa! hang on a bit, I haven't got there yet!", not "whoa! I can't cope!" But you say we should distinguish between:
1. Trivial population shifts: the kind that occurs within a pre-existing, limited gene pool and, 2. Natural selection: the kind that is responsible for the variety we see between, say, a shrew-like common ancestor of mammals and humans.
Well, maybe, but the important distinction is not, I would argue, between natural selection (2) and something too trivial to be natural selection (1). Both are natural selection. Where I think you are making a valid distinction (or what would be, IMO a more valid distinction!) is between selection of pre-existing genetic variation and selection on new alleles. And I think you are claiming that the former is responsible for (1) and is "trivial" as it can do no more than oscillate between limits imposed by existing allelic variation in the population, and that only the latter could be responsible for (2) and would be too slow. Is that fair enough? And yes, I agree, that for significant net change to occur that moves a population, for example, from shrew-like things to humans, you do need to have brand new alleles! And, indeed, new genes. So, how do we find out at what rate potentially useful (i.e. selectable) novelty arises? There's an interesting fairly recent review paper here, btw, if you can access it, on exactly that subject: http://www.sciencedirect.com/science/article/pii/S0169534707002868
Once again, to cite evidence for the former as having any relevance to the latter is, also IMHO, plainly wrong. To get excited about oscillating finch beaks (less than 2mm oscillation all in) really goes to show how desperate evolutionists have become in the search for any kind of supportive evidence! Leave behind the a priori commitment to evolution and what do you really have here? Confirmation of something we already know: that we’re not all clones and that sub-specific variation is limited and works within the confines of a norm that species tend to return to.
Well, you may have already known it, but it was pretty exciting to me to see it confirmed! However, I agree that it makes sense, and it doesn't demonstrate that allelic novelty was involved. However I would certainly disagree that "it shows how desperate evolutionists have become"! What was pretty exciting was that whereas previously, Darwin had suggested that effects of adaptation would only be observed over millions of years, and therefore be unobservable within the life time of any living scientist (by many orders of magnitude!) here was evidence that his theory actually worked, observable from generation to generation! But as I keep saying, Darwin's theory did not address the origins of heritable variety, merely the selection of it. So to that extent, yes, I guess the Grants's work wasn't that big a deal.
We can rule out “brand new alleles” in the case of peppered moths and finches for the reasons already provided in my original post.
Sorry, I missed that - why can we rule out "brand new alleles" in those examples? I mean, you may be correct, but can you explain why?
We can also rule out “brand new alleles” in the case of Lenski’s E-coli experiments. E. coli has several pre-existing enzymes that use and digest citrate, especially in the absence of oxygen. The only problem E. coli normally has is bringing citrate through its membrane in the presence of oxygen. Nonetheless, E. coli (outside of the LTEE) has been identified which can do just this thanks to an over-expressed protein. There are also plasmids which perform the same function on its behalf.
I'm not actually sure that "allele" is a term applicable to bacterial genetics, though I may be wrong. But there's no mix'n'matching so the scenario is different - evolution is not so much a question of changes in "allele frequency" as "genotype frequency". So let's drop the term for this example, and just use "mutation". Are you saying that the adaptation was not caused by a mutation? What else could it have been?
And the take home point about Chihuahuas and Great Danes is this: Natural Selection couldn’t manage that kind of variation in millions of years. It required the vastly more powerful variation of Artificial Selection. Without our intervention, there would still be no such thing as Chihuahuas and Great Danes. So, if evolution cannot achieve significant sub-specific variation in dogs, then what chance does it have of turning a single-celled common ancestor into a human being? None whatsoever.
Why couldn't natural selection achieve this in millions of years? Artificial selection works on just the same amount of allelic variation (either standing or new) as natural selection does, so there's no difference at that end. Now, instead of breeders, strand your original dogs on different islands, each with different habitats. Why shouldn't each island population adapt to its unique environment just as chihuahuas adapted to the unique environment posed by the whims of chihuahua breeders? You have already conceded that the natural variation on which either form of selection acts is the same in both cases, right? (I'm slightly puzzled here, because you seem to have reversed your argument in mid flow!) Gotta do something else - will check in later! Cheers LizzieElizabeth Liddle
July 4, 2011
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Forgive me Lizzie, I didn’t mean to come across as jumping all over you. I just wanted to wave a rather large flag about moths and finches! I think we have to make a distinction between: 1. Trivial population shifts: the kind that occurs within a pre-existing, limited gene pool and, 2. Natural selection: the kind that is responsible for the variety we see between, say, a shrew-like common ancestor of mammals and humans. To cite evidence for the former as having any relevance to the latter is, IMHO, plainly wrong. Likewise, we have to make a distinction between: 1. Adaptation within a single population: the kind that occurs within a pre-existing, limited gene pool and, 2. Random mutation: the kind that is responsible for the variety we see between, say, a shrew-like common ancestor of mammals and humans. Once again, to cite evidence for the former as having any relevance to the latter is, also IMHO, plainly wrong. To get excited about oscillating finch beaks (less than 2mm oscillation all in) really goes to show how desperate evolutionists have become in the search for any kind of supportive evidence! Leave behind the a priori commitment to evolution and what do you really have here? Confirmation of something we already know: that we’re not all clones and that sub-specific variation is limited and works within the confines of a norm that species tend to return to. We can rule out “brand new alleles” in the case of peppered moths and finches for the reasons already provided in my original post. We can also rule out “brand new alleles” in the case of Lenski’s E-coli experiments. E. coli has several pre-existing enzymes that use and digest citrate, especially in the absence of oxygen. The only problem E. coli normally has is bringing citrate through its membrane in the presence of oxygen. Nonetheless, E. coli (outside of the LTEE) has been identified which can do just this thanks to an over-expressed protein. There are also plasmids which perform the same function on its behalf. And the take home point about Chihuahuas and Great Danes is this: Natural Selection couldn’t manage that kind of variation in millions of years. It required the vastly more powerful variation of Artificial Selection. Without our intervention, there would still be no such thing as Chihuahuas and Great Danes. So, if evolution cannot achieve significant sub-specific variation in dogs, then what chance does it have of turning a single-celled common ancestor into a human being? None whatsoever.Chris Doyle
July 4, 2011
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PS: re dogs - can chihuahuas breed with Great Danes? If not, are they still the same sub-species? And a further point: a "subspecies" division isn't really different from a "species" division, except in terms of how long its been since the populations interbred. We are running out of names (like "genus" and "species" and "class" etc) because there's no reason to suppose the nesting will ever end. Yes, dogs will always be dogs, but, over time, "dog" may cover the same amount of variety that "mammal" does now". Therefore, I'd say that domestic dogs are, in fact, speciating. We can call it a sub-sub-species if you like, but that's not really necessary, except for taxonomic convenience. "Speci..." words work better as verbs than nouns!Elizabeth Liddle
July 4, 2011
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Whoa there Chris! First of all, I did not bring up the peppered moths, because I know that work has a peppered history! Second of all: my point was not that natural selection is responsible for all variety we see (although I think it is) but was a response to Mung's request for information about how the effects of natural selection can be observed and measured. And this is exactly what the Grants' work (and Endler's) did - phenotypic changes were either correlated with environmental changes (Grants) or we seen to result from experimentally manipulated environmental factors (Endler). Thirdly: I was not talking about speciation, but about adaptation. Yes, in both cases this as adaptation within a single population Fourthly: in neither of these examples were the phenotypic changes related to genetics, so we don't know whether brand new alleles, or a simply redistribution of existing alleles, was responsible for the phenotypic chances. However, we know that brand new alleles do arise (so we can't rule that out) and we also know, from fruitfly experiments, that adaptation can result from brand new alleles. We also know this from Lenski's E coli experiments, but bacteria are non-sexually reproducing, we have to be careful about generalising. For one thing, bacteria don't actually speciate in the sense that sexually reproducing species do. As for the oscillations in beak sizes observed by the Grants - yes that was one of their most exciting observations IMO - the observation that adaptation can oscillate from generation to generation, and does not require accumulations of changes over time before measurable phenotypic effects of adaptation are seen. And the interesting thing of course is that oscillation in response to oscillating environmental conditions implies a lively dynamic system that is potentially responsive to longer term changes. The Grants found that the oscillations were correlated with seed-size distributions which in turn were correlated with El Nino events, which, though unpredictable, nonetheless have a predictable frequency. Change that frequency and you'd expect to see lower frequency changes in finch beak sizes, would you not? However, I take it that your main source of skepticism is whether any of the phenotypic changes were due to new alleles, or just a redistribution of old ones. I don't know the answer to that, in the case of the finches. But I agree it's an important question when it comes to extrapolating from oscillatory adaptation to steady movement in a single direction (from land based mammals to marine, for example). Which is why work on how new alleles arise is so interesting.Elizabeth Liddle
July 4, 2011
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Morning Lizzie, I don’t want to steal Mung’s thunder but I’ve noticed your comments about finches and moths and would like to make the following observations. Both varieties of the peppered moth existed before the industrial revolution. Bernard Kettlewell's observations were faked and his population counts were flawed. The truth is, peppered moths don't rest on tree trunks (polluted or otherwise). In the words of Jerry Coyne: "From time to time, evolutionists re-examine a classic experimental study and find, to their horror, that it is flawed or downright wrong. …Until now, however, the prize horse in our stable of examples has been the evolution of 'industrial melanism' in the peppered moth, Biston betularia, presented by most teachers and textbooks as the paradigm of natural selection and evolution occurring within a human lifetime. The re-examination of this tale is the centrepiece of Michael Majerus's book, Melanism: Evolution in Action. Depressingly, Majerus shows that this classic example is in bad shape, and, while not yet ready for the glue factory, needs serious attention…." "Majerus concludes, reasonably, that all we can deduce from this story is that it is a case of rapid evolution, probably involving pollution and bird predation. I would, however, replace "probably" with "perhaps". B. betularia shows the footprint of natural selection, but we have not yet seen the feet. Majerus finds some solace in his analysis, claiming that the true story is likely to be more complex and therefore more interesting, but one senses that he is *MAKING A VIRTUE OF NECESSITY*. My own reaction resembles the dismay attending my discovery, at the age of six, that it was my father and not Santa who brought the presents on Christmas Eve." (my emphasis) In the words of Ken Miller: "Since (Kettlewell’s) work it has become clear that birds see ultraviolet much better than we do, and therefore what seems well-camouflaged to the human eye may not be to a bird. In addition, neither Kettlewell nor those who checked his work were able to compensate for the degree to which migration of moths from surrounding areas might have affected the actual numbers of light and dark moths he counted in various regions of the countryside." So, when Kettlewell was heating moths up on the bonnet of his car and pinning them to trees hoping to see birds coming along to eat them, it wasn't just contrived but also pointless: birds may be able to see through the camouflage... assuming birds are even a major predator of peppered moths in the first place. The release and count method that Kettlewell used to measure the populations of the light and dark varieties didn't measure the actual ratio of light to dark moths, in fact it distorted it and like Miller says, didn't allow for migration. So we don't even know if there was a population shift in the first place, let alone natural selection. Perhaps the most important fact about peppered moths is that both the light moths and the dark moths belong to the same sub-species. They interbreed with each other and so there is a spectrum of colour within the peppered moth gene pool. Nature is full of creatures that belong to the same sub-species and yet vary in colour: humans are a prime example. Describing the light peppered moth as Biston Betularia and the dark peppered moth as Biston Carbonaria is entirely misleading. The latter is no more a mutant than any other dark coloured creature is. They are both Biston Betularia and, as far as we can tell, always have been. At best, peppered moths demonstrate sub-specific variation and therefore tell us nothing about evolution. As for finches, the Grants' observations were as follows: 1. In 1977, it was observed that the average beak size and depth in one variety of finch - Geospiza fortis - grew by less than 2 millimetres 2. In 2003, it was observed that the average beak size and depth in the same variety of finch - Geospiza fortis - declined by less than 2 millimetres So, that is also merely sub-specific variety, and not very impressive at that considering that the finches ended up back where they started again. All 14 of the so-called different species can breed with each other. It is therefore doubtful that they are different species: after all the only difference between them all is the shape and size of their beaks (less than 4 inches variation amongst them all). This is much less variation than found in the common dog which doesn't just belong to the same species, but the same sub-species: Canis lupus familiaris. Again, they tell us nothing about evolution.Chris Doyle
July 4, 2011
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OK, sorry, Mung - I find it difficult to strike a balance between assuming people are familiar with certain evidence, and appearing to assume that people are ignorant! Re the finch beaks: I'm referring to Peter and Rosemary Grant's work on finches in the Galapagos, as documented in Jonathan Weiner's book, The Beak of the Finch http://en.wikipedia.org/wiki/The_Beak_of_the_Finch They worked on the island of Daphne Major for many years, constructing a complete family tree of every finch on the island (IIRC), measuring beak sizes, and also the distribution of seed sizes, each year (El Nino years tended to result in a different distribution from non El Nino years), and noting the corresponding changes in beak size distributions following a change in seed size distributions. Weiner also talks about other comparable field studies, including Endler's work on guppies. I'm trying to find a primary source for Endler's experiments, but in the mean time, there's a good Cliff Notes version here: http://evolution.berkeley.edu/evosite/evo101/IVB1bInthelab.shtml AFAIK it was the first time that natural selection had been directly observed in a true experiment (i.e. where a variable is manipulated by the experiment, enabling the direction of causality to be inferred). As for your moth question (and the question is germane to the other examples too): No, natural selection doesn't "cause" new successful alleles to appear. But if an environment strongly favours an existing allele, (dark moths, for example, or spotted guppies, or large beaks), whether new or old , then those alleles will increase in prevalence, so that if a second allele arises (for example, one that makes a dark moth still darker, a spotty guppy spottier and a large beak larger),or already exists there will be a high probability that that allele will be inherited by some individual that already bears the first, and those individuals will be at even greater advantage in the offspring stakes. Essentially, a change in the environment tends to concentrate alleles that together produce a trait that is advantageous in that environment, and that both existing and any new allele be subject to that process.Elizabeth Liddle
July 4, 2011
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Ilion @ #58 If that was directed at me, can you tell me what question you are referring to? I am more than willing to attempt to answer questions, but I am more than capable of missing or forgetting them. A reminder or link would be appreciated, thanks. LizzieElizabeth Liddle
July 4, 2011
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Mung:
Elizabeth, do you honestly think that “cloning” plays no part in sexual reproduction?
Yes. Cloning happens as a result of mitosis. Sexual reproduction involves a different process, called meiosis, which is NOT "cloning". The reason that "cloning" exists as a word is because it is different to sexual reproduction. And my point was a simple, even trivial one - that using words like "mistake" to describe the products of mitosis and fertilisation is misleadingly pejorative, as one of the beneficial results (for a population) of sexual reproduction is the introduction of novelty. Similarly, the word "fidelity" to describe a replication process that does not involve producing a daughter outpt that is identical to either parent seems, again, a potentially misleading use of the word. That's all. We do not disagree about the process, I'm just saying that I find the use of those words misleading in the context of sexual reproduction. You obviously disagree. That's fine.Elizabeth Liddle
July 4, 2011
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Elizabeth Liddle:
I say that in the case of sexual reproduction (as opposed to cloning) fidelity isn’t relevant anyway, because each child’s genotype is a unique combination of two parental genotypes (actually four grand-parental genotypes), and you respond to that with several quotes about cloning (i.e. cell-division) processes! I was talking about meiosis, and said so, explicitly. Your response is about mitosis.
Elizabeth, do you honestly think that "cloning" plays no part in sexual reproduction? Elizabeth, do you honestly think that "cell division" plays no part in sexual reproduction? Elizabeth, just where do you think the DNA in a gamete cell comes from? Elizabeth, how do you think a zygote is formed? Does it involve the DNA from the two parents?
Sexual reproduction is the creation of a new organism by combining the genetic material of two organisms. The two main processes are: meiosis, involving the halving of the number of chromosomes; and fertilization, involving the fusion of two gametes and the restoration of the original number of chromosomes. During meiosis, the chromosomes of each pair usually cross over to achieve homologous recombination. http://en.wikipedia.org/wiki/Sexual_reproduction
How long will you continue to maintain that fidelity is not relevant to sexual reproduction?Mung
July 3, 2011
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And, if one dusts around enough pepper, perhaps others will sneeze ... and forget the question.Ilion
July 3, 2011
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LIZZIE: "… the effects of natural selection can be observed between one generation and the next." MUNG: "So natural selection is the cause and it’s effects are observed how?"
Natural selection is not the cause of natural selection! And I didn’t say so.
I didn't say you said natural selection was both the cause and the effect. I was pointing out that you had asserted that natural selection was the cause and that it's effects could be observed.
I said “the effects of natural selection can be observed between one generation and the next”.
Indeed. And I wondered how we could observe it's effects?
And they are observed by either correlating, in the wild, phenotypic measures (beak size, for instance, by the Grants, in the Galapagos) with environmental measures (seed size distributions, ditto), or actually manipulating the environment experimentally (e.g. predators and gravel colour as in Ender’s guppie tanks) and measuring the resulting change in some phenotypic measure (spots, in the guppies). But you know this, don’t you?
No, I don't know this. At times my questions are rhetorical. At times they are of a true inquisitive nature as to something I'd like to be informed about. I may seem like i know everything, or that I think I know everything, but I don't. :) Really, I am confused. So we look at finch beak size, and we look at seeds, and we infer that natural selection caused what? A change in beak size? A change in seed size? That can't be right, can it? Are you sure you don't want to talk about moths? ;) Light moths, dark moths. Melanism. Did natural selection cause the dark moths?Mung
July 3, 2011
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ME: "For the record, you are still claiming that there is no fidelity in sexual reproduction, correct? You haven’t retracted your claim?" ELIZABETH: "I didn’t make it! If you thought I did, then I expressed myself badly, and I would certainly like to retract the impression. My point was that fidelity isn’t the gold standard in the way it is in meiosis. The system is actually optimized to ensure optimal variance, not maximal fidelity. Hence my jibbing at talk of “mistakes”." It is clear that the word "mistake" had as it's referent DNA replication."
…genetic variation in populations arises by chance through mutation (it is now known to be caused sometimes by mistakes in DNA replication and via genetic recombination—the crossing over of homologous chromosomes during meiosis).
If we snip that bit our what we have is:
…genetic variation in populations arises by chance through mutation (it is now known to be caused ... via genetic recombination—the crossing over of homologous chromosomes during meiosis).
Genetic recombination is a source of genetic variation. You find THAT objectionable? ME: "For the record, you are still claiming that there is no fidelity in sexual reproduction, correct?" ELIZABETH: "I didn’t make it! ELIZABETH: But it’s a bit silly when talking about sexual reproduction, [keeping in mind, that what was under discussion was mistakes in DNA replication] because we don’t have fidelity anyway – each child genome is unique. We don't have DNA replication fidelity in sexual reproduction? ELIZABETH: "I say that in the case of sexual reproduction (as opposed to cloning) fidelity isn’t relevant anyway..." Fidelity isn't relevant in sexual reproduction? Please. ELIZABETH: "The system is actually optimized to ensure optimal variance, not maximal fidelity. Hence my jibbing at talk of “mistakes”." Do tell. We're talking about mistakes in DNA replication right? So the system is designed to make lots of mistakes so we'll have maximal variation? Wouldn't that tend to result in a lot of dead cells? Optimal Variance? Oh my. Are you a closet ID supporter? I really do apologize about the comment on repeated false claims. If I could have taken it back I would have. But I'm not one of those who once it is said pretends like it wasn't said.Mung
July 3, 2011
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mistakes do happen Well Lizzie, I'm going to put on my lawyer hat now, so feel free to go catch a movie if you find the courtroom drama boring. You were commenting on the description of Darwinism: https://uncommondescent.com/glossary/ You were making reference to the following statement:
...genetic variation in populations arises by chance through mutation (it is now known to be caused sometimes by mistakes in DNA replication and via genetic recombination—the crossing over of homologous chromosomes during meiosis).
You objected that the term "mistake" is misleading. Also “mistakes” is misleading. It implies that there is a “correct” process and a “mistaken” process. Quibbling, are we? And it implies no such thing. There is a process by which DNA is copied (replicated). The result of that process may be a faithful copy of the original DNA or it may not be a faithful copy. Fidelity - see fide - Latin. http://en.wikipedia.org/wiki/Fidelity But you make my point – by using words like “error-checking” just as that glossary entry uses “mistakes” you are conveying the impression that there is a correct and incorrect process for cell replication. You are truly grasping at straws. The DNA is copied. How faithful is the copy to the original. Let's call that fidelity. Is it somehow less faithful in meiosis than in mitosis? That might be just about OK when talking about cloning species like bacteria, where it might be legitimate to talk about less-than 100% faithful replication as “mistakes”, but even then “non-fidelity” would be better. OK. But non-fidelity implies no fidelity. And that would be false. So mistake is better. Do you have any references from the literature for your claim that "non-fidelity" would be better? Wnat me to list the sources that use "mistake"? You're quibbling.
DNA replication is a truly amazing biological phenomenon. Consider the countless number of times that your cells divide to make you who you are—not just during development, but even now, as a fully mature adult. Then consider that every time a human cell divides and its DNA replicates, it has to copy and transmit the exact same sequence of 3 billion nucleotides to its daughter cells. Finally, consider the fact that in life (literally), nothing is perfect. While most DNA replicates with fairly high fidelity, mistakes do happen, with polymerase enzymes sometimes inserting the wrong nucleotide or too many or too few nucleotides into a sequence. Fortunately, most of these mistakes are fixed through various DNA repair processes. Repair enzymes recognize structural imperfections between improperly paired nucleotides, cutting out the wrong ones and putting the right ones in their place. But some replication errors make it past these mechanisms, thus becoming permanent mutations. These altered nucleotide sequences can then be passed down from one cellular generation to the next, and if they occur in cells that give rise to gametes, they can even be transmitted to subsequent organismal generations. Moreover, when the genes for the DNA repair enzymes themselves become mutated, mistakes begin accumulating at a much higher rate. - http://www.nature.com/scitable/topicpage/dna-replication-and-causes-of-mutation-409
to be continued...Mung
July 3, 2011
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Mung:
Elizabeth Liddle:
I was talking about meiosis, and said so, explicitly. Your response is about mitosis.
I anticipated this response. My response was about both. You just weren’t paying attention.
Apologies.
Please see my last linked:
Meiosis Is a Special Type of Cell Division That Occurs in Sexually Reproducing Organisms
Do you have any evidence whatsoever for you implicit assertion that the same sorts of regulation and control and error checking are not taking place during meiosis?
I made no such assertion implicitly or explicitly. But you make my point - by using words like "error-checking" just as that glossary entry uses "mistakes" you are conveying the impression that there is a correct and incorrect process for cell replication. This is sort of reasonable in the case of mitosis, because, firstly, there is a clear "standard" against which to check fidelity of DNA reproduction, and secondly, because non-fidelity is often harmful, and, to my knowledge, not beneficial to the organism (not counting epigenetic marking, of course). But my point was that that the pejorative overtones of words like "error" and "mistake" are misleading when it comes to the germline because a) there is no single parental model, and b) the whole mix n'match process, which includes opportunities for novelty, may well have evolved because a process that promotes novel alleles benefits a population. What you call "error-checking" may have optimised at a level that ensures that allele-production is optimised for population adaptation. This remains speculative, but it's an exciting area of research.
Do you really expect us to believe that meiosis evolved and all of a sudden all fidelity in passing on the genetic information went out the window? I guess that’s what we’d expect if evolution was true.
No, and I didn't say so.
I meant to edit out the part about false claims, but not because your assertion that there is no fidelity in sexual reproduction wasn’t a false claim, and not because the claim I made about your propensity to make false claims that are easily refuted is itself not true, but rather because it was inflammatory. Unfortunately I hit Submit and it was too late.
No problem :) Thanks for the explanation! Yeah, no edit window is a bit of a bummer.
I apologize for the inflammatory statement. I am trying to do better.
Thanks :)
For the record, you are still claiming that there is no fidelity in sexual reproduction, correct? You haven’t retracted your claim?
I didn't make it! If you thought I did, then I expressed myself badly, and I would certainly like to retract the impression. My point was that fidelity isn't the gold standard in the way it is in meiosis. The system is actually optimized to ensure optimal variance, not maximal fidelity. Hence my jibbing at talk of "mistakes".
Mitosis maintains ploidy level, while meiosis reduces it. Meiosis may be considered a reduction phase followed by a slightly altered mitosis. http://www2.estrellamountain.e.....iosis.html The special behavior of the chromosomes in meiosis I requires some special controls. Nonetheless, passage through the cell cycle in meiosis I (as well as meiosis II, which is essentially a mitotic division) uses many of the same players, http://users.rcn.com/jkimball......ml#Meiosis compare physical differences* between nuclear divisions of MEIOSIS & MITOSIS so the Distinct Differences are: meiosis = 4 progeny cells [1 = 2 = 4]… thus 2 divisions mitosis = 2 daughter cells only… thus 1 cell division Stages of Sexual Cell Division same 3 phases of cell cycle… just as in asexual division Names of stages are same & have analogous functions Meiosis II… is just like mitosis [but without an S phase] http://www.bio.miami.edu/~cmal.....itosis.htm More divisions in Meiosis kind of cool: http://www.cellsalive.com/meiosis.htm Shall we say that you didn’t mean to say that we don’t have fidelity in sexual reproduction, but merely that: daughter cells are not genetically identical ?
Well, I hope what I meant is now clearer. See you later :)Elizabeth Liddle
July 3, 2011
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Driver: "then if you can establish by rational means (and judicious links, no doubt) that the wavefunction cares about conscious observers I will convert to theism." This is a tough one, however, if we take a look at the Copenhagen interpretation vs. multi-worlds, decoherence etc, and we are forced to adhere to a specific interpretation (ignoring for now the possibility that none of these interpretations are true), naturally to strengthen our decision we would look for other possible correlations in another particular arenas. One possible argument for consciousness causing collapse of wave function may be found in neuroscience, with the phenomenon of nuero-plasticity, where it can be argued that mind changes brain. So if we consider the Copenhagen interpretation of QM, further interpreting that consciousness causes collapse, coupled with neuro-plasticity in the sense that mind changes brain, you could loosely argue that consciousness does in some way effect matter. Quantum mind problem: "There exist external observers which cannot be treated within quantum mechanics, namely human (and perhaps animal) minds, which perform measurements on the brain causing wave function collapse." http://en.wikipedia.org/wiki/Quantum_mind%E2%80%93body_problem Is it consciousness and measurement different? This becomes philosophical I guess. "Neurological research indicates that experience can actually change both the brain's physical structure (anatomy) and functional organization (physiology) from top to bottom." http://en.wikipedia.org/wiki/Neuroplasticityjunkdnaforlife
July 3, 2011
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Elizabeth Liddle:
I was talking about meiosis, and said so, explicitly. Your response is about mitosis.
I anticipated this response. My response was about both. You just weren't paying attention. Please see my last linked:
Meiosis Is a Special Type of Cell Division That Occurs in Sexually Reproducing Organisms
Do you have any evidence whatsoever for you implicit assertion that the same sorts of regulation and control and error checking are not taking place during meiosis? Do you really expect us to believe that meiosis evolved and all of a sudden all fidelity in passing on the genetic information went out the window? I guess that's what we'd expect if evolution was true. I meant to edit out the part about false claims, but not because your assertion that there is no fidelity in sexual reproduction wasn't a false claim, and not because the claim I made about your propensity to make false claims that are easily refuted is itself not true, but rather because it was inflammatory. Unfortunately I hit Submit and it was too late. I apologize for the inflammatory statement. I am trying to do better. For the record, you are still claiming that there is no fidelity in sexual reproduction, correct? You haven't retracted your claim?
Mitosis maintains ploidy level, while meiosis reduces it. Meiosis may be considered a reduction phase followed by a slightly altered mitosis. http://www2.estrellamountain.edu/faculty/farabee/biobk/biobookmeiosis.html
The special behavior of the chromosomes in meiosis I requires some special controls. Nonetheless, passage through the cell cycle in meiosis I (as well as meiosis II, which is essentially a mitotic division) uses many of the same players, http://users.rcn.com/jkimball.ma.ultranet/BiologyPages/C/CellCycle.html#Meiosis
compare physical differences* between nuclear divisions of MEIOSIS & MITOSIS so the Distinct Differences are: meiosis = 4 progeny cells [1 = 2 = 4]... thus 2 divisions mitosis = 2 daughter cells only... thus 1 cell division Stages of Sexual Cell Division same 3 phases of cell cycle... just as in asexual division Names of stages are same & have analogous functions Meiosis II... is just like mitosis [but without an S phase] http://www.bio.miami.edu/~cmallery/150/mitosis/mitosis.htm
More divisions in Meiosis kind of cool: http://www.cellsalive.com/meiosis.htm Shall we say that you didn't mean to say that we don't have fidelity in sexual reproduction, but merely that: daughter cells are not genetically identical ?Mung
July 3, 2011
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Driver, how did I know that you would find smug satisfaction in shallow lies???
ba77, Where have I lied? Point out a lie.Driver
July 3, 2011
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Mung:
For instance we now know that evolution can be quite rapid – yes, it proceeds incrementally, but the effects of natural selection can be observed between one generation and the next.
How is that non-Darwinian?
It isn't! But as a summary of "NDE" which was what we were talking about, and the definition of which, in the UD glossary we were discussing, it's very out of date! Pretty well all modern biology is rooted in Darwin's basic principle. But we now know not only a lot more that Darwin did about how those mechanisms are actually implemented, but a lot more than the people who pulled together the genetic-Darwinian synthesis between 30 and 80 years ago. That's my point.
… the effects of natural selection can be observed between one generation and the next. So natural selection is the cause and it’s effects are observed how?
Natural selection is not the cause of natural selection! And I didn't say so. I said "the effects of natural selection can be observed between one generation and the next". And they are observed by either correlating, in the wild, phenotypic measures (beak size, for instance, by the Grants, in the Galapagos) with environmental measures (seed size distributions, ditto), or actually manipulating the environment experimentally (e.g. predators and gravel colour as in Ender's guppie tanks) and measuring the resulting change in some phenotypic measure (spots, in the guppies). But you know this, don't you?
about evo devo, we know that small genetic changes can result in quite large phenytopic changes.
How is that non-Darwinian?
It isn't. See above, and stop moving the goal posts. We were talking about the "NDE" remember? Since then we know that evolutionary steps may not involve such tiny phenotypic changes as Darwin originally envisaged, another factor in leading is to revise our ideas of just how slowly adaptation occurs.
You think Darwin wasn’t aware of mutant creatures?
I'm not sure what you mean by "mutant creatures" but if you mean grossly deformed creatures I'm sure he was. But grossly deformed creatures are not usually considered as candidates for a useful heritable novelty, and, in fact, many gross deformities are not genetic but developmental. As Darwin didn't know about genetics, he wouldn't have know the difference anyway.
Drift is now known to be responsible for many important changes in allele frequency over time, and adaptation is not explicitly mentioned (though it is implicit in “natural selection).
How is that non-Darwinian?
Again, we were talking about the "neo-Darwinian synthesis" not Darwinian evolution. But drift is a factor that Darwin didn't consider as he was thinking about adaptation to the environment. Drift is non-adaptive, by definition. Although, as it may alters the fitness landscape it is important to Darwinian evolution, and a trait that becomes prevalent simply by drift may end up being selectable in the new fitness landscape. The obvious example is with sexual selection. A long tail may actually be disadvantageous at first, but propagate by drift. Then, precisely becauses it is advantageous, only the fittest long-tailers survive (in addition to the short-tailers). So, if a second trait for sexual attraction to long-tails happens, the offspring of those bearing the second trait will tend to be fitter, as the chances of a long-tailer being extra fit is higher than for a short-tailer. So long tails become beneficial, where they were originally disadvantageous and just happened, nonetheless, to propagate by drift. And that builds in a feedback loop, so tails get longer and longer, and you end up with a peacock.
I’m pretty sure it was pointed out to Darwin early on that not all traits are adaptive. He didn’t seem to have a problem with that. and on it goes…
Well, as I said, I wasn't critiquing Darwin, but your linked UD glossary description of NDE, which may well be accurate, but, if so, NDE is very out of date. What the glossary describes is a poor description of the current state of understanding of evolutionary processes. And I simply don't know whether people critiquing Darwin made the point that not all traits are adaptive. If so, they were correct.Elizabeth Liddle
July 3, 2011
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