The Third Way?

Over at the “IDM collapse” thread I rather churlishly rejected CharlieM’s invitation to read an extensive piece by Stephen L. Talbott. Discovering he is a fan of Velikovsky did little to encourage me (that is, I fully realise, an argument from authority, but life is short and authors many. One needs a filter). What did catch my eye, however, is the fact that he is a contributor to Third Way of Evolution. This, on their front page, is what one might term their ‘manifesto’.

The vast majority of people believe that there are only two alternative ways to explain the origins of biological diversity. One way is Creationism that depends upon intervention by a divine Creator. That is clearly unscientific because it brings an arbitrary supernatural force into the evolution process. The commonly accepted alternative is Neo-Darwinism, which is clearly naturalistic science but ignores much contemporary molecular evidence and invokes a set of unsupported assumptions about the accidental nature of hereditary variation. Neo-Darwinism ignores important rapid evolutionary processes such as symbiogenesis, horizontal DNA transfer, action of mobile DNA and epigenetic modifications. Moreover, some Neo-Darwinists have elevated Natural Selection into a unique creative force that solves all the difficult evolutionary problems without a real empirical basis. Many scientists today see the need for a deeper and more complete exploration of all aspects of the evolutionary process.

That puzzles me. We need a root-and-branch rethink because of the widely-accepted phenomena of endosymbiosis, HGT, transposons and epigenetics? I honestly don’t get it. These are refinements easily, and already, accommodated. Neo-Darwinists do not ‘ignore’ these phenomena, nor consider them unimportant. They may fall outside a strict framework of genetic gradualism by ‘micromutation’, but are hardly keeping anyone awake nights.

Perhaps, on reflection, I should punt them my musings on the Evolution of Sex. It is non-Darwinian in the sense they appear to mean, so it should be right up their street!

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378 thoughts on “The Third Way?

  1. Joe Felsenstein:

    CharlieM: his involves stochastic movement towards a purposeful end.

    OK. So the implication is that nothing is “accidental”.

    No. Accidents, chance events, are recognised features of life. Living systems are always in dynamic balance between constructive and destructive forces. A goose may be killed by a fox because it happened to be at the wrong place at the wrong time. This chance event is fatal to the individual but does little or no harm to the higher level, the species.

    There are uncalculable Brownian movements going on in the fluid of our brain ventricles and thankfully these don’t need to be tracked and controlled. One of the many things that does need to be precisely controlled is the cerebrospinal fluid pressure. If there is control at this higher level then the Brownian motion will look after itself.

    Let’s see. Suppose there is a molecule in the cell, perhaps a free radical, that can bring about a mutation if it interacts with DNA. Which site it interacts with depends on where the molecule wanders, owing to Brownian motion.

    How can we model this? Either we could know the initial conditions in the cell and model the positions of all the molecules, including the water molecules, and calculate which base gets to mutate. Good luck with that!

    Or we can say that the bases that change are chosen randomly. That is the basic model of molecular evolution. In that case I suppose that CharlieM would say that we are modeling mutation as being “accidental” and that this is all wrong.

    Why would we need to model every individual point mutation? It is obvious that genomes are constantly being altered by chance encounters with external influences and the vast majority of the time it can cope with this disruption. In fact we know that viruses and bacteria make use of mutations in order to become resistant to destructive forces. As in the case of the goose, individuals are expendable if the species is to survive.

    We know that genomes change accidentally, but we also know that genomes change through active reorganisation. So why when looking at the extant genomes of the various species, assume that they arrived by accident? Why is the default position that these genomes differentiated due solely to a history of accidental changes? When studying evolution all I seem to read about are tinkerings and stumblings, evolution cobbling things together into all sorts of kludges. All I can say is that all this tinkering has produced some exquisite results.

    Evolution is seen as a process by which genes are added to an original limited basic set. Perhaps in the beginning all life had access to a comprehensive set of genetic elements but as the various forms settled into their niches they lost the elements that they did not use. Instead of genes determining behaviour it is more like a case of behaviour determining genes.

    Our genomes consist a measly few billion base pairs but the marbled lungfish has 130 billion base pairs, and many plants also have massive amounts.Why the difference?

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  2. Allan Miller:

    CharlieM:There are stochastic changes to the genome and there are error correcting processes. Some ‘errors’ are not corrected. Is this by accident or design? How would we know?

    How indeed? How could we prove that any accident were not ordained, that our very lives are not playthings of the gods?

    Genomic manipulation controls how mutations are dealt with.

    Do you have any idea how? DNA polymerase has its own error-correcting capacity, but it is never going to get to 100%. There are strand-mismatch processes that catch a few that get through the first filter. But some fraction of errors remains, that it pleases you to call ‘non-accidental’, even though the vast majority have no effect. These errors occur whenever a cell replicates, not merely a germ cell. Hence cancer.

    Life progresses by being dynamically balanced. ‘Errors’ and stochasticity at lower levels can be used to the advantage of higher levels. One hundred percent perfection leads to stagnation. Cancer is an imbalance which creates substance while destroying form.

    Cancer is the result of ‘errors’ within the cell. Does this mean that it can have no causes attributed to the lifestyle and environment of the organism as a whole? Should we confine our search for the cause of cancer to the genome?

    What you call ‘genomic manipulation’ is error prevention. There is no known process of error creation.

    If by ‘error’ you mean disruptive influence then apoptosis is an ‘error’ from the point of view of the genome.

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  3. CharlieM: Evolution is seen as a process by which genes are added to an original limited basic set. Perhaps in the beginning all life had access to a comprehensive set of genetic elements but as the various forms settled into their niches they lost the elements that they did not use. Instead of genes determining behaviour it is more like a case of behaviour determining genes.

    That’s how “evolution is seen” (by some see-er)? I didn’t know that. Thanks for correcting my thought. Live and learn.

    (Oh, and thanks to Alan Fox for providing the text of the execrable Susan Mazur’s execrable question to Eugene Koonin. I should have provided that when I quoted Koonin. Apparently the execrable Mazur is most upset with the label “selection” and poses as someone who is trying to get evolutionary biology to be more of a hard science.)

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  4. CharlieM:
    Life progresses by being dynamically balanced. ‘Errors’ and stochasticity at lower levels can be used to the advantage of higher levels.

    Well, some mutations do indeed prove to be beneficial. Do you regard this as a sensational discovery, previously unnoticed? Do you think the existence of this fraction needs an extra explanation, beyond ‘chance’? Why, and how does it work?

    One hundred percent perfection leads to stagnation.

    It’s also unachievable. Because error correction systems are ‘tuned’ by sequence changes, a hypothetical ‘perfect’ system could not be reached from an imperfect one, because the closer it got, the less further variation was possible. It would freeze short of the target. If it started at the hypothetical target, random variation would push it off, since there is no strong penalty for near-perfection. The state we have is a trade-off, integrating costs, benefits and random factors.

    Cancer is an imbalance which creates substance while destroying form.

    Triffic. It also results from imperfect error correction.

    Cancer is the result of ‘errors’ within the cell. Does this mean that it can have no causes attributed to the lifestyle and environment of the organism as a whole?

    Many of those environmental factors are problems because they are mutagenic. They reduce the fidelity of the system, permitting more through the filter.

    Should we confine our search for the cause of cancer to the genome?

    You can look where you like. If your search is in a Mystical Realm, you could be wasting your time, but have at it.

    If by ‘error’ you mean disruptive influence then apoptosis is an ‘error’ from the point of view of the genome.

    Well, I don’t mean disruptive influence, but in any case apoptosis is not a problem from ‘the genome’s perspective. It has many copies in an individual – and the cell lineages in which apoptosis occurs do not in any case contribite to the next generation.

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  5. CharlieM: We know that genomes change accidentally, but we also know that genomes change through active reorganisation.

    Do we? Do you have an example?

    Perhaps in the beginning all life had access to a comprehensive set of genetic elements but as the various forms settled into their niches they lost the elements that they did not use. Instead of genes determining behaviour it is more like a case of behaviour determining genes.

    There is absolutely no evidence for this ‘front-loading’, and plenty of reason to suppose it untrue. You seem to be supporting viewpoints for no better reason that they are non-mainstream.

    Our genomes consist a measly few billion base pairs but the marbled lungfish has 130 billion base pairs, and many plants also have massive amounts.Why the difference?

    Significantly greater amounts of ‘junk DNA’ in the latter, perhaps. No doubt, in your Panglossian world, there’s no such thing.

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  6. Allan Miller: Well, some mutations do indeed prove to be beneficial.

    Can you name one? Thanks.

    Allan Miller: I brought it up as a subject for discussion.

    You can only bring up something to be the subject for discussion. This aside, it’s still strange you do that just to say “nothing to see”. I for one got some humor books recommendations out of this. Which is probably not your intent. Others might take them seriously which is not what you want I guess.

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  7. Nonlin.org:
    Can you name one? Thanks.

    CCR5-delta32. You’re welcome.

    You can only bring up something to be the subject for discussion. This aside, it’s still strange you do that just to say “nothing to see”. I for one got some humor books recommendations out of this. Which is probably not your intent. Others might take them seriously which is not what you want I guess.

    So do you actually have something to say, serious or otherwise?

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  8. Mung: Do you agree that clades have propensities to evolve specific traits?

    Insofar as your question makes sense, no.

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  9. Mung: “Ordained accident” seems to me to be an oxymoron.

    Meaning: “That which is perceived as an accident by someone not in possession of all relevant parameters (that’s us) was, in fact, ordained”.

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  10. Joe Felsenstein:

    CharlieM: Evolution is seen as a process by which genes are added to an original limited basic set. Perhaps in the beginning all life had access to a comprehensive set of genetic elements but as the various forms settled into their niches they lost the elements that they did not use. Instead of genes determining behaviour it is more like a case of behaviour determining genes.

    That’s how “evolution is seen” (by some see-er)? I didn’t know that. Thanks for correcting my thought. Live and learn.

    Well seen in the mind’s eye. You can take it that I meant, ‘understood to be’, but I’m sure you knew that.

    Do you understand (I almost wrote, ‘see’ 🙂 ) the process of evolution to be different from that in which genes have been added to an original basic set?

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  11. Allan Miller:

    CharlieM:
    Life progresses by being dynamically balanced. ‘Errors’ and stochasticity at lower levels can be used to the advantage of higher levels.

    Well, some mutations do indeed prove to be beneficial. Do you regard this as a sensational discovery, previously unnoticed? Do you think the existence of this fraction needs an extra explanation, beyond ‘chance’? Why, and how does it work?

    No, I’m happy to accept that chance mutations work as advertised. They provide a limited plasticity but in my opinion they are not the main drivers of macro evolution.

    One hundred percent perfection leads to stagnation.

    It’s also unachievable. Because error correction systems are ‘tuned’ by sequence changes, a hypothetical ‘perfect’ system could not be reached from an imperfect one, because the closer it got, the less further variation was possible. It would freeze short of the target. If it started at the hypothetical target, random variation would push it off, since there is no strong penalty for near-perfection. The state we have is a trade-off, integrating costs, benefits and random factors.

    Yes, we are saying basically the same thing. Only where you talk of trade-offs I speak about maintaining balance and harmony.

    Cancer is an imbalance which creates substance while destroying form.

    Triffic. It also results from imperfect error correction.

    So there is a situation where there is a faulty genome. But this benefits the cell because it is able to reproduce without hindrance. But it is detrimental to the organ because it loses the ability to function harmoniously and so it can be detrimental to the organism as a whole.

    This is similar to life as a whole. Any person who thinks that life can evolve by means of accidental mutations controlling form below should realise that this is like thinking that cancer will lead to the advancement of life. If the parts benefit without regard to the whole then their success will lead eventually to their own demise. Just as in individual organisms, life need systematic harmony of the whole otherwise is cannot be sustained.

    Cancer is the result of ‘errors’ within the cell. Does this mean that it can have no causes attributed to the lifestyle and environment of the organism as a whole?

    Many of those environmental factors are problems because they are mutagenic. They reduce the fidelity of the system, permitting more through the filter.

    Agreed. External disruptive influences.

    Should we confine our search for the cause of cancer to the genome?

    You can look where you like. If your search is in a Mystical Realm, you could be wasting your time, but have at it.

    I’m looking at life and the processes within life itself. A mystical realm separate from life is something that is in your imagination, not mine.

    If by ‘error’ you mean disruptive influence then apoptosis is an ‘error’ from the point of view of the genome.

    Well, I don’t mean disruptive influence, but in any case apoptosis is not a problem from ‘the genome’s perspective. It has many copies in an individual – and the cell lineages in which apoptosis occurs do not in any case contribite to the next generation.

    I am talking about the generation of cells within an individual. You say that the genome has many copies of itself but that’s not the way I would put it. I would say the population of cells all share the same genes.

    ***analogy alert***

    The cells are an army and the genes are part of its equipment to be used as required.

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  12. CharlieM:
    No, I’m happy to accept that chance mutations work as advertised. They provide a limited plasticity but in my opinion they are not the main drivers of macro evolution.

    Yet when we look at differences between taxa, we see the same kinds of difference as are thrown up generationally – point mutation, insertion, deletion, duplication, inversion, transposition. Just more of ’em, as would be expected given time.

    How do your ‘main driver’ changes get into the genomes of an entire species? Why do we even need to hypothesise them?

    Yes, we are saying basically the same thing. Only where you talk of trade-offs I speak about maintaining balance and harmony.

    In which case, we are not talking about the same thing. Error correction cannot reach perfection because progress towards it snuffs out the very mechanism of change. That’s not ‘balance’, unless running out of oxygen is. And, there are diminishing returns in terms of benefit – beyond a certain fidelity, there’s less reward for improvement, and mounting costs start to outweigh the benefits. Again, that’s hitting constraint, not harmony. Not everything is exquisitely poised. Some things just have useful side-effects.

    This is similar to life as a whole. Any person who thinks that life can evolve by means of accidental mutations controlling form below should realise that this is like thinking that cancer will lead to the advancement of life.

    Well, it isn’t anything like that, but above you agreed that small mutations ‘work as advertised’, including benefit. That is ‘accidental mutations advancing life’, to me. So you need to be a bit clearer about what you have decided ‘advancement’ looks like, if it sits beyond that provided by the beneficial fraction of random mutations. Preferably with an example.

    I’m looking at life and the processes within life itself. A mystical realm separate from life is something that is in your imagination, not mine.

    You have a completely opaque mechanism that somehow changes genomes according to need. That sounds close to mysticism to me. Somehow, it samples the outside world and the future and figures what protein folds would do the trick. Then achieves them by mechanisms that are deemed insufficient to account for that amount of change.

    I am talking about the generation of cells within an individual. You say that the genome has many copies of itself but that’s not the way I would put it. I would say the population of cells all share the same genes.

    All copied from the original in the zygote. Mechanistically. No single copy has ‘interests’ above any other. Producing a zygote, then a body, then two successful gametes is exactly the same, from the genome’s perspective, as skipping the ‘body’ part entirely. The odd sacrifice to apoptosis doesn’t change that – most cells aren’t germ cells; their loss is trivial.

    ***analogy alert***

    The cells are an army and the genes are part of its equipment to be used as required.

    Bad analogy.

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  13. Allan Miller:

    CharlieM: We know that genomes change accidentally, but we also know that genomes change through active reorganisation.

    Do we? Do you have an example?

    Recombination.

    Perhaps in the beginning all life had access to a comprehensive set of genetic elements but as the various forms settled into their niches they lost the elements that they did not use. Instead of genes determining behaviour it is more like a case of behaviour determining genes.

    There is absolutely no evidence for this ‘front-loading’, and plenty of reason to suppose it untrue. You seem to be supporting viewpoints for no better reason that they are non-mainstream.

    Not front loading. Top pruning through the archetype.

    Our genomes consist a measly few billion base pairs but the marbled lungfish has 130 billion base pairs, and many plants also have massive amounts.Why the difference?

    Significantly greater amounts of ‘junk DNA’ in the latter, perhaps. No doubt, in your Panglossian world, there’s no such thing.

    I am reluctant to call something junk just because I see no reason for its existence.

    It’s interesting that polyploidy is more common in organisms which also show high powers of regeneration. The whole reflected in the parts.

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  14. CharlieM: Me: Do we [know that genomes change through active manipulation]? Do you have an example?

    Charlie: Recombination.

    The changes this causes are just as ‘accidental’ as mutations, as far as anyone has been able to ascertain. The prime function of crossover is to stabilise bivalents during meiosis. It so happens that there are two ways of resolving a crossover; one gives recombinant products, the other does not. They each happen 50% of the time. This feature is shared with the homologous repair system from which it (genetically) derives. There is no evidence that the process is ‘trying’ to generate variation, in either case. The snipping process has no access to upstream or downstream genes.

    Not front loading. Top pruning through the archetype.

    Call it what you like, it’s a dead bacterioarchaeogiraffodandelionagaricbrontosauroduck.

    Me: Significantly greater amounts of ‘junk DNA’ in the latter, perhaps. No doubt, in your Panglossian world, there’s no such thing.

    Charlie: I am reluctant to call something junk just because I see no reason for its existence.

    Yeah, called it. Well, you asked the question, that’s the answer. The more formal, less triggering, definition of ‘junk’ is ‘cannot suffer a deleterious mutation’.

    Feel free to hypothesise a function. What do you think is the solution to the c-value paradox?

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  15. Allan Miller: Error correction cannot reach perfection because progress towards it snuffs out the very mechanism of change. That’s not ‘balance’, unless running out of oxygen is. And, there are diminishing returns in terms of benefit – beyond a certain fidelity, there’s less reward for improvement, and mounting costs start to outweigh the benefits.

    But organisms don’t “know” that further improvement is possible. They don’t keep stuff around because it may prove useful in the future. So there most be some other reason than the one you are proposing.

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  16. Allan Miller: Yet when we look at differences between taxa, we see the same kinds of difference as are thrown up generationally – point mutation, insertion, deletion, duplication, inversion, transposition. Just more of ’em, as would be expected given time.

    So some taxa have been evolving longer than others? Smacks of Creationism if you ask me.

    If all extant life descends from a universal common ancestor then all extant life has been evolving for the same amount of time. So if there are differences between modern taxa it must be due to some other reason than the amount of time, since that is the same for extant all taxa.

    Ye another example of the incoherence of MET. (Assuming you’re giving an accurate portrayal of it.)

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  17. Mung: Did you even read the abstract then?

    I already said I’m not following closely. RL has precedence.

    I was answering this question:

    Do you agree that clades have propensities to evolve specific traits?

    And I meant that clades don’t have propensities at all. Now if there’s context, you’ll have to provide it. What abstract?

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  18. Alan Fox,

    Then you’re saying “aerobic citrate utilization (Cit+)” is an absolute beneficial mutation. If so, how come all e Coli don’t have that super duper mutation by now? Or are you saying this happened for the first time ever in Lenski’s tube? Now that would be a miracle. Is that what you’re saying? If not, how come it’s not universal by now as Darwin taught you? Just curious.

    Allan Miller: CCR5-delta32. You’re welcome.

    The same question applies to you. If absolutely beneficial, how come this mutation is not universal by now as Darwin taught you?

    In addition, your wikipedia buddies kind of disagree with you:
    “CCR5 Δ32 can be beneficial to the host in some infections (e.g., HIV-1, possibly smallpox), but detrimental in others (e.g., tick-borne encephalitis, West Nile virus). Whether CCR5 function is helpful or harmful in the context of a given infection depends on a complex interplay between the immune system and the pathogen.

    In general, research suggests that the CCR5 Δ32 mutation may play a deleterious role in post-infection inflammatory processes, which can injure tissue and create further pathology.[67] The best evidence for this proposed antagonistic pleiotropy is found in flavivirus infections.”
    What about that?

    And read their origin story for this mutation. Wouldn’t you say they speculate a lot? I mean they got a lot of models for its origin, but obviously nothing we can double check: https://en.wikipedia.org/wiki/CCR5

    Allan Miller: So do you actually have something to say, serious or otherwise?

    I did, but let me say again: thank you for the entertainment.

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  19. Nonlin.org: Then you’re saying “aerobic citrate utilization (Cit+)” is an absolute beneficial mutation.

    He’s not saying that at all. He didn’t even read the abstract. What are the odds then that he read the paper?

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  20. Mung: He didn’t even read the abstract

    I had no idea what you were referring to. You give no clue.

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  21. Nonlin.org: Then you’re saying “aerobic citrate utilization (Cit+)” is an absolute beneficial mutation

    Of course! In the niche created by Lenski.

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  22. Nonlin.org: The same question applies to you. If absolutely beneficial, how come this mutation is not universal by now as Darwin taught you?

    Bait and switch , your asked for a beneficial mutation. Not absolutely beneficial one.

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  23. newton:
    Nonlin.org: The same question applies to you. If absolutely beneficial, how come this mutation is not universal by now as Darwin taught you?

    Bait and switch , your asked for a beneficial mutation. Not absolutely benefical

    There’s no such thing as absolutely beneficial. Did I mention it depends on the niche?

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  24. Nonlin.org:
    The same question applies to you. If absolutely beneficial, how come this mutation is not universal by now as Darwin taught you?

    1. Darwin never ever talked about mutations, let alone about absolutely beneficial ones.

    2. Darwin did talk about differential survival given an environment.

    3. Adaptations are environment-dependent by definition. Evolution is environmentally-dependent by definition.

    4. You have absolutely no idea what you’re trying to defeat. You’re just trying to defeat it because you imagine it to contradict your religious fairy tales.

    5. I’m sure you will not understand this and you’ll never correct your misunderstandings.

    6. Unlike you, I have direct knowledge of what Darwin wrote. I read the Origin, I read The Voyage, you read some creationist straw-men, and some simple wikipedia pages that you managed to misunderstand. Even wikipedia is too advanced for you.

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  25. Alan Fox: I had no idea what you were referring to. You give no clue.

    I provided at least three clues, one rather blatant. First was the mention of clades and propensities, drawn straight from the abstract. Second was the posting of the link to the paper itself. Third was a link back to the post of yours to which I was responding.

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  26. Alan Fox: There’s no such thing as absolutely beneficial. Did I mention it depends on the niche?

    Then this is non-Lin’s or any design theorist’s lucky day. All that is needed is to provide an example as evidence for design.

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  27. Mung: I provided at least three clues, one rather blatant. First was the mention of clades and propensities, drawn straight from the abstract. Second was the posting of the link to the paper itself. Third was a link back to the post of yours to which I was responding.

    Four if you count this post.

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  28. Mung: Evolution by created niche!

    Sure, some claim that humans are doing it to the planet right now.

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  29. Mung: But organisms don’t “know” that further improvement is possible. They don’t keep stuff around because it may prove useful in the future. So there most be some other reason than the one you are proposing.

    What are they ‘keeping around’? I’m not sure I grasp your point. From a position of poor fidelity, there is selective advantage in improving it, and hence disadvantage in making it worse. Improvement reduces the mutational load per round of copying. But once that load has been diminished beyond a certain point, the selective advantage of further improvement starts to diminish. It also takes longer, which may be a cost. In tandem with that, the very mechanism of ‘improvement’ is frozen by improvement itself, leaving 100% unattainable in any case.

    Therefore, for all that there is likely directional selection for improvement in fidelity, it would be an error both to see that as leading inexorably to 100% fidelity, and to see the retention of some mutational ‘headroom’ as a positive design feature. Rather like (to permit myself an analogy) insisting that failing to reach 100% fuel efficiency is indicative of an engineer’s wisdom, rather than constraint.

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  30. Mung: So some taxa have been evolving longer than others? Smacks of Creationism if you ask me.

    Some branches are deeper than others, since their common ancestors lived longer ago.

    If all extant life descends from a universal common ancestor then all extant life has been evolving for the same amount of time. So if there are differences between modern taxa it must be due to some other reason than the amount of time, since that is the same for extant all taxa.

    Some taxa have more recent common ancestors than others. It’s like a branching … well, tree.

    Ye another example of the incoherence of MET. (Assuming you’re giving an accurate portrayal of it.)

    The problem here lies entirely in your comprehension of it.

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  31. Nonlin.org:
    The same question applies to you. If absolutely beneficial, how come this mutation is not universal by now as Darwin taught you?

    Benefit depends entirely on environmental context. And there must be some point at which a beneficial mutation is not possessed by every member of a population, between origin and fixation. You want a fixed beneficial mutation?

    In addition, your wikipedia buddies kind of disagree with you:

    Since I did not say this was universally beneficial, they don’t. The position is more subtle than the cartoon in your head.

    And read their origin story for this mutation. Wouldn’t you say they speculate a lot? I mean they got a lot of models for its origin, but obviously nothing we can double check:

    Inevitably. Just as we can’t check your magic bloke wiggling his fingers.

    I did, but let me say again: thank you for the entertainment.

    So no, then.

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  32. Allan Miller: You want a fixed beneficial mutation?

    Nope, Nonlin wants a context-independently beneficial mutation because Nonlin imagines that Darwin said that evolution consisted on accumulating context-free, non-environmentally-dependent, beneficial mutations.

    I know, I know, that doesn’t make sense, that’s not what Darwin was talking about, but Nonlin’s word carries much more weight than reality.

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  33. Allan Miller: Just as we can’t check your magic bloke wiggling his fingers.

    And it wouldn’t matter if you could, since it’s the wiggling of his toes that matters.

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  34. Allan Miller: Some branches are deeper than others, since their common ancestors lived longer ago.

    So what? What do branch lengths indicate? Time? Difference?

    Assume they indicate time. All branches connect to other branches that connect back to the same trunk and if you measure from trunk to tip the length would be equal and the time would be equal. So all extant taxa have been evolving for the same amount of time.

    So “time” is the wrong answer. Is it so hard to admit it?

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  35. Mung: All branches connect to other branches that connect back to the same trunk and if you measure from trunk to tip the length would be equal and the time would be equal.

    Is that true in everyday trees? If you measure branches , they are the same length from the trunk to the tips?

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  36. Mung: Evolution by created niche!

    Well, it’s how theists can reconcile evolution with God’s creation. If God created the Universe and all its little nooks and crannies and the laws of physics then evolution does the rest. Personally, I have no need of that hypothesis.

    And it intrigues me how theists get from “Creator of the Universe” to the theology. I don’t see the link. “It’s Jesus” seems a bit circular.

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  37. newton: Is that true in everyday trees?

    Why does that matter? Evolutionary trees are not literal trees. Trees develop, they don’t evolve. And if you insist on pressing the analogy, rather than accepting evolutionary trees are metaphorical not analogical, then all of life is pre-programmed in the first cell the way a tree is pre-programmed in the seed from which it grows. That’s a hard pill for today’s evolutionists to swallow.

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  38. Mung: So what? What do branch lengths indicate? Time? Difference?

    Assume they indicate time. All branches connect to other branches that connect back to the same trunk and if you measure from trunk to tip the length would be equal and the time would be equal. So all extant taxa have been evolving for the same amount of time.

    So “time” is the wrong answer. Is it so hard to admit it?

    Not sure what I can ‘admit’ here, since from where I sit your reasoning is fallacious. Perhaps you have a different understanding of the word ‘taxon’.

    The hippopotamus lineage has been evolving for the same time as both the giraffe and the dandelion. But measured from ‘trunk to tip’, would you seriously expect to see the same amount of difference between any two of those three?

    All three taxa trace their lineage back to a single common ancestor (under UCD). But as far as giraffes and hippos are concerned, a lot of the accumulated difference is shared, accumulating in the past history of their common ancestor when compared to dandelions, so they differ from each other less.

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  39. Mung: And if you insist on pressing the analogy, rather than accepting evolutionary trees are metaphorical not analogical, then all of life is pre-programmed in the first cell the way a tree is pre-programmed in the seed from which it grows. That’s a hard pill for today’s evolutionists to swallow.

    It’s a diagram of evolutionary lineages. If we are approximating the situation by assuming that the expected rate of evolutionary change is equal in all lineages, then we have a tree where all tips are at the same height from the root. If we don’t make that assumption but are willing to assume that change is generally faster in some lineages than in others, we have different branch lengths per unit time in different lineages. And everyone (maybe with one exception here) knows that this is simply an analogy in the shape of a diagram, it’s OK, it doesn’t cause trouble.

    If you get away from those two assumptions, then you need some more description of how the rates of change differ in different characters. All of these are in effect statistical models, and their fit to the data can be tested statistically.

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  40. Joe Felsenstein: If we are approximating the situation by assuming that the expected rate of evolutionary change is equal in all lineages, then we have a tree where all tips are at the same height from the root.

    That’s pretty much what I said. The time from LUCA is the same, it’s the rate that maybe be changing, not the time.

    Joe Felsenstein: If we don’t make that assumption but are willing to assume that change is generally faster in some lineages than in others, we have different branch lengths per unit time in different lineages.

    As I said. In this case it’s the difference in rate along some lineages, not the difference in time since LUCA.

    Everyone gets 3.5B to 3.8B years of evolution since LUCA in their history. Unless you’re a creationist. 🙂

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