Cannibalistic tadpoles and matricidal worms dispute evolution

  1. A recent study identifies phenotypic plasticity as the ability of tadpoles to change how they look and act, and how their tissues function, in response to their environment. If the pond also contains fairy shrimp, some tadpoles turn into aggressive carnivores and sometimes, the carnivorous tadpole stage becomes entrenched – without the need for a dietary trigger. This plasticity has also been confirmed in lizards, roundworms, and yeast. When yeast is exposed to the herbicide paraquat, the yeast copes by eliminating some or all of the DNA in their mitochondria, the cells’energy-producing organelles.
  1. Some consider this a classic example of “plasticity-first evolution”. On the surface, the findings vindicate Lamarck. The plasticity those changeable tadpoles display is built into their genetic code. And when an “acquired” trait does become “permanent”, it is because of mutations that “fixed” the plastic trait – a process biologists call genetic assimilation.
  2. Since plasticity is a built-in trait of so many organisms, it has obviously been mistaken for “evolution”. “Permanent” claim is meaningless given all organisms populations are ever-changing. The main questions are “what are the limits of plasticity?” and “what happens over the very long time?” The evidence to date is very clear:
    a. Plasticity is a built-in widespread if not universal characteristic of organisms
    b. It is limited in scope to a few traits like color, behavior, and metabolism
    c. Plasticity is reversible rather than cumulative
    d. It is not divergent as toads, lizards, roundworms, yeast, etc. never turn into not-toads, not-lizards, and so on.
  3. This is a repackaging of the same stories sold as proof of “evolution”. Darwin’s finches, the peppered moth, antibiotic resistant bacteria and, why not, the tanning humans. Too bad all these not only do not diverge into new organisms, but they all have been shown to revert eventually when the stimulus is removed. Finches change back their beaks depending on environment and never turn into non-finches, the black moths reversed to white and never to not-moths, antibiotic resistance disappears from the population when we reduce the use of antibiotics (see NIH recommendation), and neither light-skinned Nordics, nor dark-skinned Mediterraneans turn into not-humans under any circumstance.

https://www.sciencemag.org/news/2018/11/cannibalistic-tadpoles-and-matricidal-worms-point-powerful-new-helper-evolution

http://science.sciencemag.org/content/362/6418/988

https://www.nih.gov/news-events/nih-research-matters/reducing-antibiotic-prescriptions

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267 thoughts on “Cannibalistic tadpoles and matricidal worms dispute evolution

  1. Alan Fox: Yes, I did. An enjoyable article well aimed, clear and not condescending to a lay audience.

    When did I disappoint you? Feel free to go back and read all my OPs. They’re still standing and waiting for either valid refutations or acceptance (aka deconversion from Darwinism)

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  2. Nonlin.org: Where is that distinction?

    Where is that distinction? You don’t know the difference between a heritable and a non-heritable change?

    You need to bone up on the material, chum.

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  3. Nonlin.org: You have some serious reading comprehension issues.

    You say: “they all have been shown to revert eventually when the stimulus is removed.”, as if this were some grand revelation. Yes, of course adaptation needs retention of the adaptive pressure to ensure retention of the adaptation. This is discussed in Darwin. When a selective or adaptive pressure is removed, the adaptation can be and usually is lost. You wish to turn that into a universal – Nonlin’s Law –

    All adaptive pressures are eventually removed.

    If your Law fails to hold universally, then it is not the blocker to evolution you suppose. It would need to be the case that, eventually, predators will have no need of teeth, or prey of camouflage. Eventually, lungs must become superfluous for terrestrial organisms. Eventually, organisms with legs will ‘regress to the mean’, which is presumably a state of not-having-legs, the average organism being legless.

    Why would you suppose that all adaptations must eventually become unnecessary, just because – in certain circumstances – that happens?

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  4. Nonlin.org: What “difference between plastic and genetic changes”?

    and

    Nonlin.org: Now you’re getting somewhere. What if “speciation” is nothing more than plasticity “in disguise”?

    I humbly present to you: the common garden experiment.

    money quote:

    The rationale behind this protocol is to control for the effects of phenotypic plasticity and, to a certain extent, genotype-by-environment interactions by growing individuals from different populations in a common environment, and by using the quantitative genetics toolbox […] to study the genetic bases of complex traits (for example, life history, morphological and physiological traits).

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  5. Allan Miller: Yes, of course adaptation needs retention of the adaptive pressure to ensure retention of the adaptation. This is discussed in Darwin. When a selective or adaptive pressure is removed, the adaptation can be and usually is lost.

    Hardy and Weinberg say no, unless there is some cost associated with the adaptation.

    ETA: or mutation pressure (which is what you mean, I guess).

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  6. Corneel: Hardy and Weinberg say no, unless there is some cost associated with the adaptation.

    ETA: or mutation pressure (which is what you mean, I guess).

    Hardy-Weinberg never applies in real populations! Regardless, I don’t see why it needs to be costly to maintain. What would maintain sight in darkness, even if it cost nothing? Assuming mutation of course, as you say, but I don’t know why we wouldn’t.

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  7. Allan Miller: Hardy-Weinberg never applies in real populations! Regardless, I don’t see why it needs to be costly to maintain. What would maintain sight in darkness, even if it cost nothing? Assuming mutation of course, as you say, but I don’t know why we wouldn’t.

    Nonlin brought up industrial melanism and antibiotic resistance in bacteria as examples of the reversal of adaptations. These are simple adaptations, and their reversal owes to a reversal of the selection pressure, not their removal.

    In the case of complex adaptations, such as eyes, removal of the adaptive pressure will of course result in regressive evolution, because there are numerous mutational targets.

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  8. Corneel: Nonlin brought up industrial melanism and antibiotic resistance in bacteria as examples of the reversal of adaptations. These are simple adaptations, and their reversal owes to a reversal of the selection pressure, not their removal.

    The first yes, the second I’m not so sure. If antibiotics are removed, it is not a given that the resistance gene becomes burdensome and eliminated by negative selection rather than drift. But of course, it depends how far it has got. Once fixed, a now-neutral allele has tenure, and non-resistant alleles will tend to be the ones eliminated. But they keep on coming. Neutral alleles can’t stay fixed indefinitely.

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  9. Alan Fox: Broken GULO gene?

    Yup. Even in a single gene there are multiple targets for disablement, and many more ways of being wrong than right.

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  10. IIRC, exon 5 of GULOP is actually missing. Even if a lucky reversal of the original deactivating frameshift mutation occurred it could probably not yield a functional GULO enzyme with a missing exon. After the frameshift happen over 60 million years ago, additional mutations have accumulated in the locus.

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  11. Allan Miller: The first yes, the second I’m not so sure. If antibiotics are removed, it is not a given that the resistance gene becomes burdensome and eliminated by negative selection rather than drift.

    Wasn’t quite sure myself, so did some digging in pubmed and found that:

    Most antibiotic resistance mechanisms are associated with a fitness cost that is typically observed as a reduced bacterial growth rate.

    So yes, when they first arise resistance alleles tend to be costly in the absence of the antibiotic. With time the fitness costs will be reduced by compensatory mutations and allelic replacement by cost-free mutations.

    I think it is important to emphasize that genetic adaptations can be maintained outside the environment in which they are beneficial, and do not necessarily revert. That may help our good friend Nonlin distinguish them from plastic responses, which are dependent on environmental triggers.

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  12. Corneel,

    I think it is important to emphasize that genetic adaptations can be maintained outside the environment in which they are beneficial, and do not necessarily revert. That may help our good friend Nonlin distinguish them from plastic responses, which are dependent on environmental triggers.

    A course in genetics might help too …

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  13. Corneel: We ARE the genetics course

    Haha! Most students tend not to take the attitude “prove me wrong, Darwinistas!”. It’s a bit of a barrier to pedagogy. 😀

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  14. Corneel: Hardy and Weinberg say no, unless there is some cost associated with the adaptation.

    There is always a cost.

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  15. Corneel: In the case of complex adaptations, such as eyes, removal of the adaptive pressure will of course result in regressive evolution, because there are numerous mutational targets.

    Evolution as progress and regress. I love it.

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  16. Mung: Evolution as progress and regress. I love it.

    This is actually one of the things people fail to get about it. Because allele frequencies must add up to 100%, it is inevitable that moving towards fixation of one allele means a move towards extinction for another. Regress is progress, to be Orwellian.

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  17. Nonlin.org: Total nonsense.

    What does this even mean: “Mutations that change phenotypic plasticity”?

    What about: “DNA sequences that result in phenotypic plasticity”?

    I already explained it. Phenotypic plasticity is due to the interaction of proteins with the environment. Change the amino acid sequence of the proteins and you an change how the organism reacts to the environment. Mutations that change the other protein interactions and DNA interactions further down the chain can also change phenotypic plasticity.

    Look up the lac operon. This is the classic example of phenotypic plasticity. There are two binding sites upstream of a group of lactase enzymes. When there is glucose present the cell doesn’t produce cAMP which prevents RNA transcriptase from binding to the promoter. When there is no lactose the lac inhibitor (a protein) is bound to a site near the lac promoter and prevents RNA polymerase from binding to the promoter. When there is lactose present it’s metabolites interact with the lac inhibitor and cause it to fall off of the DNA binding region. When glucose runs low cAMP builds up and allows RNA transcriptase to bind and transcribe the lac genes. From start to finish this entire process of phenotypic plasticity requires specific DNA sequences for the cAMP binding region, RNA transcriptase binding region, and the ability of the lac inhibitor protein to bind lactose metabolites and bind a specific region of DNA. It is all dependent on DNA sequence from start to finish, and all of it is accessible to evolutionary mechanisms.

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  18. Allan Miller: Where is that distinction? You don’t know the difference between a heritable and a non-heritable change?

    Your comment makes no sense given the thread history:

    Nonlin.org: How so? Are you saying “Darwin’s finches, the peppered moth, antibiotic resistant bacteria and, why not, the tanning humans” are not examples of plasticity similar to those quoted by Sciencemag? Explain.

    Allan Miller: It would depend on whether or not the change was heritable – ie, the distinction is between adaptation by an individual (e.g. tanning) and a population.

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  19. Allan Miller: You say: “they all have been shown to revert eventually when the stimulus is removed.”, as if this were some grand revelation. Yes, of course adaptation needs retention of the adaptive pressure to ensure retention of the adaptation. This is discussed in Darwin.

    It is a ‘grand revelation’! If everything goes back to what it was, there is no “evolution”. Remember “divergence of character” nonsense? The one nobody has ever seen? “Random mutations” are supposed to take you elsewhere (anywhere), not back! Why always back and never elsewhere?

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  20. Corneel: I humbly present to you: the common garden experiment.

    money quote:

    Unimpressive. You need to demonstrate your claim, not just cite some keywords from a random paper.

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  21. Corneel: I think it is important to emphasize that genetic adaptations can be maintained outside the environment in which they are beneficial, and do not necessarily revert. That may help our good friend Nonlin distinguish them from plastic responses, which are dependent on environmental triggers.

    I explained several times that there’s no such thing as “beneficial mutation”. All mutations have trade offs. When you say “do not necessarily revert”, do you have an example to share or is this another one of those “take my word for it”? Please don’t claim some unverifiable 60 mil yrs nonsense.

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  22. Rumraket: After the frameshift happen over 60 million years ago, additional mutations have accumulated in the locus.

    Let’s get some use out of that time machine. Go check this.

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  23. T_aquaticus: I already explained it. Phenotypic plasticity is due to the interaction of proteins with the environment. Change the amino acid sequence of the proteins and you an change how the organism reacts to the environment. Mutations that change the other protein interactions and DNA interactions further down the chain can also change phenotypic plasticity.

    You do tell a long and random story. But you’re not addressing my initial comment:

    Did you read the part about Lamarck? How about “a powerful new helper”? Now, why would “evolution” need a “new helper”? Because it can’t stand on its own feet? Now, it would be naive to not read through the lines for the actual meaning of this “new” force of plasticity.

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  24. Since we’re not getting anywhere and you guys are starting to fight like different sects of the same religion (which you are), let’s focus a little bit:
    who among the Darwinistas can tell me where ‘plasticity’ ends and “evolution” begins?

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  25. Allan Miller: Where is that distinction? You don’t know the difference between a heritable and a non-heritable change?

    Are you saying ‘plasticity’ is not heritable? Because the sciencemag article claims otherwise: ‘On the surface, the findings vindicate Lamarck: Acquired traits can be inherited” …and with examples

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  26. Nonlin.org: Are you saying ‘plasticity’ is not heritable? Because the sciencemag article claims otherwise: ‘On the surface, the findings vindicate Lamarck: Acquired traits can be inherited” …and with examples

    I’m saying the state of a plastic character is not inherited. Babies aren’t born with a suntan, but they can tan.

    Examples of true Lamarckian inheritance are not convincing, though Creationists trumpet this from the rooftops, perceiving it to be the ‘death of Darwinism’. Ironically, Darwin was actually quite Lamarckian in his thinking. Mendel put paid to all that. Great-Grandchildren don’t exhibit the acquired characteristics of 14 separate individuals. That would be a mess to sort out.

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  27. Nonlin.org: Unimpressive. You need to demonstrate your claim, not just cite some keywords from a random paper.

    Question: how did the researchers find out which species of spadefoot toad display phenotypic plasticity and which ones don’t? Answer: by raising them under controlled conditions in a common environment. Differences that persist in a common environment cannot be due to plasticity, and are therefore genetic. Differences that occur between environments within genetically uniform lines cannot be due to genetical differences and must be due to environmental causes. TADAA. That’s science baby.

    The common garden experiment is an old trick to distinguish genetical from environmental variation (the latter includes phenotypic plasticity). It is extremely basic genetics and, in contrast to what the author of the science paper is suggesting, already used for decades in research on phenotypic plasticity.

    Genetic population changes count as evolution, phenotypic plasticity does not.

    *puts spoon and bib back in drawer*

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  28. Nonlin.org: All mutations have trade offs. When you say “do not necessarily revert”, do you have an example to share or is this another one of those “take my word for it”?

    I could name a few, but will take the easy option first: Once a mutation fixes (thus the ancestral allele is lost), the population cannot readily revert to the old state, even if an environmental change would make that favorable. This clearly distinguishes it from phenotypic plasticity.

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  29. Nonlin.org: Wait! What has Mendel to do with Darwin?

    *gets spoon and bib again*

    The modern synthesis was the early 20th-century synthesis reconciling Charles Darwin’s theory of evolution and Gregor Mendel’s ideas on heredity in a joint mathematical framework.

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  30. Nonlin.org: It is a ‘grand revelation’! If everything goes back to what it was, there is no “evolution”. Remember “divergence of character” nonsense? The one nobody has ever seen? “Random mutations” are supposed to take you elsewhere (anywhere), not back! Why always back and never elsewhere?

    Are you sure it’s always back? If an allele has been lost from a population, what would revive it? You are trying to make a principle from a couple of instances.

    Eta – written before I saw Corneel make the self-same point.

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  31. Nonlin.org:

    who among the Darwinistas can tell me where ‘plasticity’ ends and “evolution” begins?

    Evolution begins when a heritable change occurs in the genome. You know what a genome is, I presume.

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  32. Allan Miller: Examples of true Lamarckian inheritance are not convincing, though Creationists trumpet this from the rooftops, perceiving it to be the ‘death of Darwinism’. Ironically, Darwin was actually quite Lamarckian in his thinking. Mendel put paid to all that. Great-Grandchildren don’t exhibit the acquired characteristics of 14 separate individuals. That would be a mess to sort out.

    Until we find out where knowledge is stored in DNA, you can’t make the claim that great grandchildren don’t inherit the acquired characteristics of great grandparents.

    So far no one knows where this knowledge is stored. Where do beavers learn to build dams? Where do birds learn to fly? Where do babies learn that opening their mouths and moving their throat makes them scream? Which gene is that?

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  33. phoodoo,

    Imagine a baby being born with zero information already stored in its brain. It would be like a computer with all the hardware but no operating system installed. It wouldn’t do much.

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  34. phoodoo: Where do beavers learn to build dams? Where do birds learn to fly? Where do babies learn that opening their mouths and moving their throat makes them scream? Which gene is that?

    And spider’s webs! These are good questions. Further study is required.

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  35. phoodoo,

    I think you missed the point. You have 2 individuals to get experiences from at 1 generation’s remove, 6 at 2, 14 at 3, 30 at 4 and so on. It soon becomes explosive, if these things are to be passed down that many generations. That’s why Mendelian inheritance is so neat – it keeps things manageable by discard. On the other hand, if these ‘Lamarckian’ experiences pass through the genome, which gets discarded?

    You only have 2 ways to pass the info, in genes or ‘somehow else’.

    The desperation of Creationists to find a long term role for Lamarckism is so cute.

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  36. Allan Miller: I think you missed the point. You have 2 individuals to get experiences from at 1 generation’s remove, 6 at 2, 14 at 3, 30 at 4 and so on. It soon becomes explosive, if these things are to be passed down that many generations.

    Huh? Babies get passed down from two people the knowledge that if they move their throats and open their mouths it will produce a scream?

    Do you think spider’s that never met their parents won’t figure out how to make a web?

    I have no idea what you are trying to say here.

    The desperation of evolutionists to deny knowledge that does not exist in an allele is so cute.

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  37. Allan Miller: If no-one can point to the exact genes, it’s not the genes? What is it then?

    Where else, indeed? Still a fascinating question how quite complex innate behaviours are incorporated in the genome.

    ETA, well, it intrigues me, anyway.

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  38. phoodoo: Huh?Babies get passed down from two people the knowledge that if they move their throats and open their mouths it will produce a scream?

    No. I’m talking there about the inheritance of acquired characters, and the exponential/dilution problem if it doesn’t pass via the genome.

    Do you think spider’s that never met their parents won’t figure out how to make a web?

    No. I think that’s genetic.

    The desperation of evolutionists to deny knowledge that does not exist in an allele is so cute.

    The way you parrot phrases that bug you is so cute.

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  39. Alan Fox: Where else, indeed? Still a fascinating question how quite complex innate behaviours are incorporated in the genome.

    ETA, well, it intrigues me, anyway.

    Sure, it’s interesting, but I don’t know why we should just summarily dismiss genetics for behaviours specifically. They can be mutated, hybridised, etc, and nothing I am aware of favours a route bypassing the genome (eta – beyond learning, obvs!). But Creationists – a reaction to The Selfish Gene, I suspect – over-egg non-genetic inheritance to a quite laughable degree.

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  40. Allan Miller: Sure, it’s interesting, but I don’t know why we should just summarily dismiss genetics for behaviours specifically.

    And

    Allan Miller: No. I think that’s genetic.

    You think there is a gene for babies knowing how to cry? You think there is a gene for snakes knowing how to slither? And if that gene is mutated they will try to fly instead?

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