Sure but to be fair I think the people fanboying SFT and you are worse.
Why would body size matter? Like, if you’ve got a larger cross section the laws of physics stop applying to you? In all species tested so far (which are usually microbes because they’re much easier to do such experiments on) it has been true. There is no good reason to think it isn’t true for organisms with larger bodies.
Actually, there is very good reason. The organisms with larger bodies happen to differ from microbes in all the most important ways that affect GE. Mutation rates, population sizes, genome sizes (and complexity). And if you would read Kondrashov’s 1995 paper, he admitted this himself. His paradox only applies to large multicellular eukaryotes.
So can Paul please clarify two things for everyone?
Is he defining GE as Kondrashov’s paradox or not? If not, how is he defining GE?
Does he agree or disagree that selection can operate on mutations with fitness effects below the drift barrier?
Clear, specific answers to each of those questions would go a long way I think, because reading through this, I don’t think the answer to either question is clear, and that leads to some degree to people talking past each other.
So microbes haven’t gone extinct via GE because they have smaller per-generation mutation rates, larger population sizes and smaller genomes sizes.
Mice haven’t gone extinct via GE because they have smaller per-generation mutation rates, larger population sizes and similar genomes sizes.
Elephants haven’t gone extinct via GE because they have similar per-generation mutation rates, smaller population sizes and similar genomes sizes.
Giant tortoises haven’t gone extinct via GE because they have larger per-generation mutation rates, smaller population sizes and similar genome size.
Ferns haven’t gone extinct because they have smaller per-generation mutation rates, larger population sizes and larger genome size.
Maybe if the GE proponents would decide which creatures would be most at risk of GE we could see whether it is happening. (That’s probably why they don’t).
Why do population sizes matter anyway? There’s no selection against the growing collection of microdetrimental mutations, so a larger population couldn’t provide any buffer against them. It’s just an ad hoc excuse.
None of which affects the reality that the shape of the DFE changes with organismal fitness. You are merely giving reasons why the strength of selection would be comparatively weaker in larger organisms, not a reason why larger organisms should have a fixed DFE.
Again, if you want to argue a different DFE that doesn’t show fitness decline, you need to cite it.
Stop, you’re just embarassing yourself. Have you watched the debate? Have you read Sanford’s book? If the answer to both of these is no, then why are you bothering to comment?
I already clarified this in the debate. Kondrashov’s paradox is at the heart of GE, but Sanford did add clarifications and additions to the concept; it’s not as if they are 1:1 identical. Think of it as a Venn Diagram where GE is a larger circle that totally encompasses Kondrashov’s Paradox and then some. But for the sake of the debate, I kept it to Kondrashov’s Paradox only since that is entirely defensible and still unsolved.
This is basic population genetics and is not controversial. Yes, it operates in a technical sense, but in a practical sense it does not matter because it is overwhelmed by drift for mutations of that size.
Since this point has been endlessly muddied, I will quote this one again:
“As such, the definition of neutrality is operational rather than functional; it depends on whether natural selection is effective on the mutation in the population … not solely on the effect of the mutation on fitness.”
- Dr. Adam Eyre-Walker, PhD Molecular Evolution
- Dr. Peter Keightley, PhD Genetics
Eyre-Walker, A., and Keightley P.D., The distribution of fitness effects of new mutations, Nat. Rev. Genet. 8(8):610–8, 2007. The distribution of fitness effects of new mutations | Nature Reviews Genetics
So yes, natural selection is technically there, acting on the mutation, at least in theory, but drift dominates. That’s why it’s called “effectively neutral”. This is why Lynch says that neutral mutations have a probability of fixation equal to their frequency (1/(2N)). It’s technically slightly off from that, but it doesn’t matter in the end.
I can but you reject those with the baseless and ad-hoc excuse that they’re from small/simple organisms. You have no mechanism that explains why it would be different for large organisms. You repeat a sentence that does no actual explanation.
The mechanism that explains why the DFE is different for LMEs is simply this: genomic complexity. Or to use Sanford’s term, it’s the Princess and the Nucleotide Paradox. Here are some citations for you. For context, when they say “robustness” they mean the ability to absorb mutations without any noticible impact on the phenotype. In essence this means a much more leptokurtic DFE.
“Complexity, in the context of multi-scaled evolving systems, clearly demands evolvability to form such systems and robustness to maintain such systems at every step along the way … growth in complexity cannot inhibit the future evolvability of a system. … How evolving systems actually satisfy these requirements remains a true mystery.” [Emphasis added]
“We show in this article that both robustness and evolvability are enhanced by the superposition of additional levels of organization.”
- Pablo Catalán et al.
Catalán, P., Wagner, A., Manrubia, S., & Cuesta, J. A. (2018). Adding levels of complexity enhances robustness and evolvability in a multilevel genotype–phenotype map. Journal of the Royal Society Interface, 15(138), 20170516. https://doi.org/10.1098/rsif.2017.0516
“Summarizing, it is apparent that robustness and complexity are intimately intertwined and moreover that robustness is a precondition for complexity, at least for multi-scaled systems.”
- Dr. James Whitacre
Whitacre, J. M. (2010). Degeneracy: A link between evolvability, robustness and complexity in biological systems. Journal of Theoretical Biology, 263(1), 143–153.
None of that has to do with the non-fixity of the DFE. That is the effect that when you move away from a fitness peak, more opportunities for compensatory beneficial mutation, and of course direct reversals too, open up. Try again.
This is what I get after zeroing in on your exact question and answering it with peer-reviewed citations? Please!
Unless you can show an actual example of data showing this alleged other, non-fitness-declining DFE, then you’re just handwaving and offering up our typical evolutionary storytelling minus facts.
Paul can a fish become infinitely thin?
No it can’t, now you’re talking about engineering principles. But for any problem there is an essentially infinite array of different possible strategies to tackle and solve it using various engineering solutions. This is why we cannot identify any one “optimum car” that is perfect and cannot be improved upon.
Now you’re just lying about the contents of those papers. Nowhere in any of those articles do they show, nor argue, nor even imply or indicate that the DFE for large multicellular eukaryotes stays constant with organismal fitness.
This is a poor excuse provided simply to distract from the fact that you can’t give a physical reason why the DFE should change with organismal fitness for simpler organisms, but not also do so for more complex organisms.
Nobody is falling for it. Except perhaps your credulous and ill-informed followers in creationist circles. I can’t speak for those.
That’s not what you asked for. You asked for a reason why the DFE would not be the same between microbes and complex organisms.
You are the one making the claim that the DFE can wildly change such that organisms can be rescued from fitness decline by changes in environment. You are the one that would need to back up that claim with solid evidence.
You think they are reading any of this?
Organisms obey the laws of physics. So this outright admits there’s some optimal compromise between the shape and size of a fish that has to swim through the ocean to catch prey.
This is also ironic because I often hear from creationists who insist it’s not possible to improve on God’s designs. And yet here you are basically implying that is always possible.
Cars have to drive down the road, obeying the laws of physics. So do you actually believe there is an “optimum car” that cannot be improved?
After thousands of years of genetic decay, we are not really seeing God’s designs in their full greatness, we are seeing a degraded version of them (which is still great).
No, I am saying that the idea of a “perfect organism” for an environment is just silly nonsense. God doesn’t design things merely for the purpose of survival and reproduction. That’s evolutionary reductionism.
No I didn’t. This was always about the DFE not being fixed. If you misread me then fair enough, but now you know.
We observe fitness go up in experiments with microorganisms. And that the DFE changes “wildly” as a function of organismal fitness.
You think the fact that we have seen fitness go up in some experiments with microbes is a sufficient resolution to Kondrashov’s paradox in LMEs?
Of course there is. In relation to some set of requirements (how many passengers must it carry, how uncomfortable are they allowed to get, how far must it travel before being refueled, etc), the laws of physics imply there’s going to be some hard limit. Bonds between atoms can only become so strong, the material will unavoidably have some weight and density, and so on and so forth.
“Perfect organism” is not my term, but there is an optimal (allowed by physics) solution to any given set of problems. When an organism has to solve multiple problems, the optimum is often the best possible compromise between them given it’s environment.
Yeah I have no reason to believe it would be any different for those. Can you think of any?