Of course. Complexity. The experiments you’re talking about are showing local fitness optimization to a very specific laboratory environment. The fact that you see diminishing returns proves that this is not the kind of information-adding, complexity-increasing beneficial mutation you would absolutely need in order to enable large-scale macroevolution. It’s just jettisoning components you don’t need for the laboratory environment.
You cannot appeal to a “fitness optimum” in these experiments. It’s more like a limit on improvement through random mutation. Remember, we’re supposed to believe that single-celled organisms became multicellular. So to claim that LLTEE is showing us a “fitness optimum”, and thus this explains why they aren’t changing any further, just won’t cut it. Why aren’t they spontaneously becoming multicellular?
You’re straining at a gnat while swallowing a camel. Become a skeptic like me and ask for real proof of evolution before you swallow it whole.
So now you move away from the concept of fitness because GE isn’t occurring, redefine the problem to be solved to be some nebulous concept you can’t quantify (“information-adding, complexity-increasing, beneficial mutations”), that you can’t measure and record into a DFE, and don’t know how to model or put into an equation that can be tested.
Kondrashov’s paradox and Kimura’s curve discarded and into the bin. It’s all about something else then. Not fitness.
Just curious: Why would mutations in single genes also show diminishing returns epistasis? Like, in an enzyme. Selection can push the activity up to a point, and then improve it no further. Is the enzyme losing information to get there, as activity rises? Or is the organism losing information to improve the enzyme?
… which is what we expect to find when we reach a fitness optimum.
The environment. They’re not being selected to solve a problem that multicellularity represents a solution to. For that you should see what happens in the MuLTEE: https://ratclifflab.biosci.gatech.edu/
Sadly to become like you I’d have to deny the laws of physics. I find that to be a greater strain.
Since this is not something I’ve ever heard of, and in the interest of cutting to the chase, I asked Claude whether this experiment has actually demonstrated the spontaneous development of multicellularity out of unicellularity. Here is the response I got:
“So to directly answer your question: the MuLTEE is valuable science, but it doesn’t demonstrate the spontaneous emergence of multicellularity from unicellular life. It demonstrates that once a primitive multicellular form exists (even an engineered one), evolution can elaborate on it rapidly and in interesting ways. The truly hard origin question — why would a free-living single cell ever “choose” to stay attached to its neighbors in the first place — remains open.”
Does that sound about right to you?
Big words, very low on content though. Please let me know if you ever come across a published DFE for any LME that shows anything other than eventual extinction due to mutation load.
Hey, you’re back again! As usual, just showing up to lob a quick ad hominem.
Paul I think you skipped something in your response. Got nothing to say about how you redefined the question, or why even single genes show diminishing returns epistasis as their functions improve?
Sorry my man, but you have this very much backwards. You are the one that started appealing to engineering principles here, not me. Remember? You asked if fish could become infinitely thin. Is that a question about fitness? Indirectly it is, but this gets into a whole new debate about the word “fitness”. I think I’ll stop here for now, since getting into all that is not necessary to show Kondrashov’s paradox. If you want to actually solve it, you won’t get there by asking empty questions or blowing smoke. You would need to actually demonstrate the existence of parameters that can escape the paradox in LMEs, which nobody has done.
And I did this in response to your denial that the same principles apply to both larger and smaller organisms. You’ve basically had four different types of responses now that all fail to argue why the DFE for large multicellular eukaryotes shouldn’t also show diminishing returns epistasis.
First you tried pull the “I need to see a DFE for LMEs” line.
When that did’t work you pretended not to have understood we were discussing the non-fixed DFE as consequence of the fitness landscape and cited irrelevant papers.
Then you pulled the “do you really believe that?” gambit.
And finally when that didn’t work either, you took the “but it’s not about fitness at all” response.
Now that this also failed, you just go back to the beginning and demand to see (1) a DFE for LMEs because the ones from smaller or simpler organisms don’t show GE.
My explaining WHY the DFE changes with fitness regardless of organismal complexity (by logically analyzing the consequences of all organisms obeying the laws of physics) isn’t an excuse for you to start discarding fitness and start talking about information-complexity-evolution-as-progress blather. And you repeating yourself isn’t explaining why the DFE for LMEs wouldn’t also change.
Why do the single enzymes show diminishing returns epistasis Paul? Fitness is ultimately a consequence of physics, regardless of how big or complex organisms are.
A complete mischaracterization. I absolutely never said anything of the kind. The record is here.
This is not an example of “pulling a line”. This is the very basics of what science is supposed to be about: showing real evidence. You can’t do it, so instead you appeal to suggestions and just-so stories.
Okay so we have a contradiction here that you need to address.
So we’re talking about Sanford’s model here.
But then…
Sanford very explicitly rejects this bit of basic population genetics. I can again direct you to his figures annotated with “No Selection Zone”, and the statement that mutations within that zone “are not subject to selection”.
So can you please clearly state whether you agree or disagree with Sanford’s concept of genetic entropy? If yes, we have a contradiction between your understand of selection and his, and that needs to be resolved. If no, you need to present your version of the concept, mathematically, so it can be evaluated indepedent of Sanford’s.
Sanford also frequently argued that microorganisms are not exempt from GE. Saying GE is somehow just Kondrashov’s paradox and doesn’t apply to things that aren’t multicellular eukaryotes is historical revisionism.
I’m happy to accept if GE proponents will concede that the concept of GE has changed since Sanford first defined it, and that the original version was falsified by experiment and they’ve now changed the concept to only apply to multicellular eukaryotes with relatively small effective population sizes.
This is just physics denial. You concede a fish can’t get infinitely thin but you’re afraid to follow the logic where it unavoidably leads. You calling it a “just so story” is just your attempt to distract from this.
Why do even single genes show diminishing returns epistasis Paul?
That’s another thing. we have ancient DNA, human and animal, conventionally dated to prior to the time of the flood, and there is nothing particularly great to be found or indicative of progressive genetic decline or even wider variation. Neanderthal DNA is much more distinct from the range of modern haplogroups.
I would not agree with that dating. It’s definitely going to be post-Flood.
You can’t measure population fitness from looking at ancient DNA. Even if you were able to reliably show the total number of segregating SNPs, that wouldn’t show you the picture you need to show either, since we saw in my simulation that the total segregating load stabilizes at an equilibrium after a while. It’s the population-wide mean deleterious allele frequency (the fixation ratchet as I called it) that would show you about where we are on the path to extinction. But lately humans have been exploding in population size due to the industrial revolution, which means there has been a temporary decrease in this metric until population re-stabilizes (which I think it now has, and is now roughly headed back in the downward direction as our civilizations reach the stage where fertility rates are plummeting).
The answer to your question of why LMEs have not gone extinct is that enough time has not yet elapsed for them to do so. On an evolutionary timescale, they certainly should have long ago.
That works against you. In wild ecologies which are neither specific nor confined to a petri dish, the same variant which is deleteriaous in one environment may thrive in shoulder situation, and this is routine. Island bound organisms which are smaller than their mainland counterparts, mice coloration depending on the their habitat to escape predation, cell membrane protein substitutions which are less efficient but confer immunity. There are tradeoffs to many things, and DFE shifts with environment all the time.
In YEC land, there are only 10 generations from Adam’s pristine DNA to Noah, incestuous with more inbreeding than the Habsburg dysnasty, followed by the population explosion of all time. In the light of ancient DNA variation, this makes no sense, for GE and more broadly.
Apply the same math to mice, accounting for fewer mutations per generation and WAY more generations, and they should be dead. And not like “they’d have gone extinct within the post-flood time frame”. Like “they’d go extinct in a century”.
And before you say “well larger Ne, more efficient selection, blah blah blah less effected by genetic entropy”…you’re SO close! You’re THIS close to understanding why genetic entropy is fake.
Interesting, so your claim is that with accurate parameters in a forward-time simulation, mice should go extinct within a century. Can you show your work?
By the way, I hope the irony is not lost on everyone that this is literally the exact opposite claim compared to the one he made in his coauthored paper.
I’m using creationist math here, not real math, but here are some pretty conservative calculations for you:
During the debate you said, if I recall, humans would be extinct within 20ky. Other creationists have said less, but I think you said 20k, so we’ll go with that.
Mice can have, conservatively 4 generations per year, vs about 20 years per generation for humans. That’s a difference of 80x. Mice can reproduce faster than that, but lets go with 4 generations/year.
But they also have fewer mutations per generation. Not by a lot, but a little. So let’s cut the difference in half and call it 40x.
20k divided by 40 is 500 years for mice to go extinct, and that’s using conservative numbers. If you use more realistic numbers (shorter generation time for mice, longer for human, a smaller difference in mutation rate), and also the lower end of the range creationists say for humans, you get down to a century or two. I and others have done more precise math but I honestly just don’t feel like tracking it down this minute. 500 years gets the point across well enough.