Utter piffle. That isn’t phenotypic plasticity. Stop using terms you don’t understand.
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I was simply pointing out Ron’s “asking Gil to prove a negative” looks pretty weak after 250 comments of which one guy (Gil) is arguing the contrary position.
Do you really think trying to argue an equivalence between living organisms and non living matter is persuasive?
It appears Gil already answered my question. I see you really did not engage in the analogy discussion.
As expected, @Giltil chose not to clarify his views, but to prattle ineffectually about artificial selection.
He’s not so much a stealth creationist as a creationist who thinks not looking renders him invisible.
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I’ve already formulated an hypothesis on this forum and it is this: : Maybe in the history of life, some special organisms related to each other have played the same role than stem cells play in the development of individual organisms, giving rise abruptly to many different more differentiated organisms. I guess this places me in the saltationist category.
Thanks. What would make these organisms “special”? Can you point to any of these “special” organisms?
And Gilbert got it, he correctly identified that my analogy made the texas sharpshooter fallacy and never provided a rebuttal to the fact that the waiting time-argument does the same, he just changed the subject.
Case closed.
All the cells in your body, aside from somatic mutation and immunity, carry the same DNA as the fertilized egg. Species, however, have distinct DNA, and there is no plausible natural mechanism for such alteration outside of conventional biology. Biotech angels cannot be ruled out of course, but they could not just prep stem animals and leave these to abruptly differentiate later on; so they would have to continuously engineer the gene pool, which would look a lot like regular evolution, except perhaps neater.
Behe & Snoke 2004 basically admit their Texas Sharpshooter and that there could have been other possibilities:
Such numbers seem prohibitive. However, we must be cautious in interpreting the calculations. On the one hand, as discussed previously, these values can actually be considered underestimates because they neglect the time it would take a duplicated gene initially to spread in a population. On the other hand, because the simulation looks for the production of a particular MR feature in a particular gene, the values will be overestimates of the time necessary to produce some MR feature in some duplicated gene. In other words, the simulation takes a prospective stance, asking for a certain feature to be produced, but we look at modern proteins retrospectively. Although we see a particular disulfide bond or binding site in a particular protein, there may have been several sites in the protein that could have evolved into disulfide bonds or binding sites, or other proteins may have fulfilled the same role. For example, Matthews’ group engineered several nonnative disulfide bonds into lysozyme that permit function (Matsumura et al. 1989). *We see the modern product but not the historical possibilities.
So they are well aware of the shortcomings of their own paper and reasoning, and yet their fans just can’t fathom it.
QED.
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So, if any cell has the potential to be a stem cell, then by this analogy pretty much any organism can be one of these “special” organisms that can give rise to new species (or whatever we are talking about here).
This just to remind us that most life is not like mammals. Such as when it comes to stem cells.
So, @Giltil, there is a chance that you are a run-of-the-mill evolutionist after all.
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To reiterate and expand on my previous request, in case you missed it:
How would this “give rise abruptly to many different more differentiated organisms” work? Do you have any idea what could be entailed or how to recognize it?
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Against stupidity, the gods themselves contend in vain.
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Stop wasting your time rebutting Bill. Everything worth saying on this topic already has been fifty million times. It’s like arguing with a chat-bot.
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By appealing to the Texas sharpshooter fallacy, you are assuming that there always exist a multitude of evolutionary pathways to deal with a given problem. But what are the evidence that this is true? In fact, it seems that the available evidence we have suggest the opposite, ie that very few solutions exist.
True enough. Remine however was extrapolating from a rate of substitution of 1 per 300 generations, which Haldane posited as the average tolerable maximum. Here’s the original paper:
The fact that similar niches have been occupied several times by organisms from vastly distinct lineages should be some indication that there is more than one solution to the problem adapting for those respective niches. This happens so often, it has its own name: Convergent evolution. And this is to say nothing of problems much smaller than occupying niches. There are, among currently living animals alone, several rather distinct solutions to swimming, flight, and terrestrial locomotion, just to name a handful of the ones most obvious even to lay folk like you and I.
Now, sure, there is a handful viable solutions for each case, and a handful more if we add the fossil record. After all, any solution has to compete with others available at the time, and if some are inherently better, or get more efficient faster, they will win out, even if many, many other solutions might exist in principle, somewhere far in the depths of unexplored sequence space. The idea that there can only be a handful, in my opinion, is not a default stance on the subject. Even if the number of viable solution is vanishingly small compared to the number of all possibilities, one might argue (and has, in other threads) that merely counting up the numbers this way or the other may ultimately not be a reasonable measure when it comes to genetics.
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Zoology. The existence of multiple things that evolution has produced to address almost every problem it has solved, from flight to venom to arctic survival to stealth to seed scattering to burrowing to oxygen transport to pest repulsion to …
What evidence is that, exactly?
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There are certainly many pathways for most such problems, but further than that, it’s not just the solutions but the problems themselves that are chosen a posteriori. Consider whales. Not only are there many ways in which an artiodactyl could have become aquatic, there are many sorts of aquatic tetrapods, and many sorts of lifestyles adopted by various other tetrapods. What available evidence are you looking at here?
No, just that YOU don’t know that there were not in fact many when X evolved. It is you who is making an unwarranted extrapolation by doing after-the-fact probability calculations.
Everything isn’t chloroquine resistance. You understand that, right? Chloroquine resistance in plasmodium falciparum =/= all other adaptations.
I don’t claim to know how many that were at any given time, but since we have experimental evidence that there can be, and because the fossil record only makes sense as a product of evolution, the burden of proof is on doubters to show that there is a problem. You don’t show that by appealing to chloroquine resistance in plasmodium falciparum.
If you think you can show there is a problem by appealing to chloroquine resistance in plasmodium falciparum, I can show there is not a problem by appealing to the hundreds of possible pathways through which the estrogen, progestagen, androgen, mineralcorticoid, and glucocorticoid receptors diverged from their common ancestor. And the cool thing is my appeal will actually be more directly relevant to the morphological evolution of mammals and other animals, since their various forms of morphological development is in part controlled by hormonal expression.
Very few solution exists for what? For what, specifically? All adaptations are not the same. Can you give at least some hint that this is a concept you are able to come to terms with eventually?
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