This is kinda harsh, Michael. I think it suffices to say that @colewd is not a biologist so he has not understood the papers.
Moreover, he has built his beliefs about rarity of functionality in sequence space on Axe’s wholly unjustified generalization of a highly constrained 1999 research result. We have cited dozens of papers since 1999 that prove Axe to be off by 63 orders of magnitude. That is a fairly large error by Axe, no? But once Bill got the idea lodged deeply into his belief system, it became an important part of his identity. I’m not sure 1000 more citations will dislodge Axe’s fundamental error from Bill’s belief system, given its role.
We should try to be nice to Bill. It might be the best way to help him. And it is commended by our Lord Himself.
How often have you tried to support your claims with real biological experiments, if I may be so bold as to ask?
You do realize, do you not, that it has already been tested quite extensively? Or did you not read the LUCA article I cited, either?
You realize that you have presented zero basis in the literature for this conclusion.
You also realize that you are a non-biologist who does not have the time to read articles served to you on a platter.
That’s fine; you are free to spend your hours as God guides you. However…
However…
If you have no expertise, and you do not have the time to read the literature written by experts, maybe you should not make radical conclusions about the alleged lack of empirical support for what biologists claim.
Is it too much to ask that you, in your admitted lack of expertise and your admitted (totally understandable) inability to read the literature in depth, abstain from making radical conclusions about that very same literature?
Why not write something like this…
“I wonder whether the hypothesized bridge to the eukaryotic cell and multicellularity has empirical support. Could someone point me to a good review article or two?”
…instead of what you actually wrote, which is basically how you start a fight with biologists who care passionately about their field and have invested decades of effort in understanding and even producing that literature–a literature that you have read very, very sparsely, at best, and do not have time to read in sufficient detail.
When you openly confess that you do not have time to read the relevant literature in sufficient depth, but you make conclusory statements about that literature anyway, how do you think that comes across to your readers?
Then he should indicate so, instead of pretending to have understood those papers and then going on to misrepresent them in some instances.
More importantly, I have shown him clear and easy-to-understand examples of new genes coming into existence via some of the mechanisms we keep telling him about. He even acknowledges at times that some novel gene really appeared after showing him a study demonstrating so. Thus, to come here and pretend we don’t have empirically tested models for novel gene evolution is outright falsehood.
Include his appalling understanding of key concepts needed to make the kind of arguments he throws on this forum. For example, he keeps mentioning the Howe diagram as evidence of design, but he doesn’t know the principle guiding its creation and when asked to identify design in Howe-type diagrams where the identities of the analyzed organisms are hidden, he can’t, illustrating the lack of substance in his position. He just keeps throwing one assertion after the other.
Are any of the models tested under real biological conditions? If not how do you know the assumptions are reliable? When they don’t detail the problem of finding new gene function through sequential change then I know they are not real models of biology. Fitness and function are not the same thing. Fitness can improve by losing function at least temporarily.
The Lenski paper is testing under real biological conditions. I think the legitimate and interesting argument is if the fitness of the population approaches steady state or declines. Is the DNA repair mechanism strong enough to avoid decline in fitness. If so @Rumraket will be correct at least in the case of bacteria.
A clear function appeared through promoter gene duplication after many generations and that is the ability to consume citrate in aerobic conditions. That mutation was quickly fixed in the population.
Absolutely. The biology models are generated and tested with empirical data in a manner similar to the models and tests of quantum physics models.
By the way, it is a category error to compare biology models with cosmological models. Relativity-based cosmological models are deterministic, not stochastic, and therefore an irrelevant comparison to evolution. Quantum models, by contrast, have similar underpinnings to those of evolution.
How can you possibly make this bold, categorical claim when you have confessed that you have read only a tiny fraction of the literature recommended to you?
Seriously, did you not read my last comment at all?
If you did, you certainly did not take it to heart!
I do not understand how two human beings can have a productive conversation when one of them openly confesses to not reading the literature recommended by the other, but goes ahead and makes bold conclusions as if he is an expert in that very literature.
You will note that I was describing an open interaction between two individuals, and did not attribute any dark motivations to either of those two individuals.
I am saying nothing about Bill that he would not agree with. He does not claim to be a biologist, and he has openly stated how many of the recently recommended articles he has read.
Fair enough Chris. Can you please point me to the papers that have an explanation which incorporates a search for new function through the sequence.
Your point about quantum physics is interesting and I need to think about it. A model that is tested against itself has not tested its assumptions against what it is modeling.
I know string theory has mathematical models that are not tested against real world experiments. These are simply untested hypotheses in physics.
You have built a case against Raoult by drawing on the abundant anti-Raoult literature that is so easy to find in these times when any speech that is even slightly at odds with the new sanitary order is immediately vilified by its many soldiers. As for me, I take all this stuff with a grain of salt until I have heard the defense.
In the absence of purifying selection, yes. I don’t think anyone would dispute that. But that is not the full extend of the claim of GE, nor is that inconsistent with evolution or the 4-billion year history of life.
GE is the idea that fitness will always be in net decline until eventual extinction even despite purifying selection, at basically any realistic numbers of population size and mutation rate. This does not seem to be occurring in reality, however, and life is ~4 billion years old. This seems to make the concept of GE inconsistent with observational reality.
First of all there is nothing in Sanford’s models that implies fitness should be increasing or be stable for a while, and then eventually start declining. He has a number of purely verbal rationalizations(excuses) that he brings up in response to evidence that GE does not seem to be occurring, and that instead fitness is increasing, but he can’t seem to ever model this phenomenon. He just makes up excuses like the one Gilbert mentioned earlier about “isolated anomalies” causing fitness increase. But these “isolated anomalies” are in reality neither isolated nor anomalous, and they figure nowhere in Sanford’s actual models of GE. In ALL his attempts to model GE, we see a consistent and stable fitness decline until extinction.
So if you really think his excuses are good, we’re going to need to see models of them. We need predictions that tell us when we should run out of “isolated anomalies” and fitness should suddenly turn around and start declining? Otherwise Sanford’s response here just seems like a rationalization carefully crafted to indefinitely avoid admitting falsification. If we are never told exactly when fitness should start to decline, and we are only ever fed this verbal line about “isolated anomalies”, then we are not dealing with a proper scientific hypothesis that can be tested.
Yes but again, there being such a thing as a too high mutation rate is already part of mainstream evolutionary theory. You cannot invoke that as evidence in favor of Genetic Entropy, which is supposed to be a fundamental problem with all of evolution, not just hypermutator bacterial phenotypes.
You can’t just focus on the hypermutator lines and ignore the rest of the experiment. Also, incidentally, the hypermutator lines are evolving ~30-fold lower mutation rates over time, so it seems like selection has so far been able to at least partially counteract the increased mutational load that initially came with the ~100-fold increase(compared to the ancestor) in mutation rate.
Certainly it will be interesting to see what happens to the hypermutator lines in the future, but you have to be mindful that GE is not just a concept that is supposed to narrowly affect only hypermutating bacteria, but again is being invoked as an argument against the long-term existence and evolution of basically all life on Earth. And life is 4 billion years old, so how can that be if GE is true?
Thanks I appreciate that answer, and I agree it really is a test of the concept of GE. It’s just that Sanford’s models of GE can’t reproduce what happens in that experiment. He has excuses for why that is, but his excuses are not formally part of his model. They are just and only that, excuses that can’t be tested.
I think this is a very interesting discussion and I don’t have an opinion of the validity of his explanation. Under his model the world is young so your explanation of an old earth does not fit his model. I agree the young earth model is challenging but also think the current data showing that fitness will continually improve at a declining rate in bacteria needs more empirical support.
There is something going on here we don’t understand. The hyper mutation data will be an important factor in better understanding this.
Hey I must say I am positively surprised by this part of your answer. For once we have some of that common ground.
The good news, in that respect, is that the experiment goes on. I suppose that just leaves open the question of how much longer it has to continue before you find yourself persuaded. That is of course entirely up to your own to find out.
Here at least I think we find some disagreement. I think mainstream evolutionary theory has a pretty good explanation for the phenomenon of mutational load, and it has been recognized for a long time that there can be a relationship between population size, mutation rate, and genome size in which the long-term consequences of mutation accumulation can be very negative for population fitness. When population sizes become too small, genomes and/or mutation rates too big, the efficacy of natural selection diminishes, and thus mutations with very small negative fitness effects can accumulate. Again, this is fully consistent with population genetics and mainstream evolutionary biology. That such a phenomenon is known and anticipated to occur even under mainstream evolutionary theory should not be misconstrued to supported Genetic Entropy.
That is not at all clear. I’d like you to try to do the actual math here, using what you think is the real values for Sanford’s curve.
What is the selection coefficients of the mutations conferring malaria resistance, and how frequent should those be according to Sanford’s views of the size of the exponential decline in the frequency of beneficial mutations?
What is the proportion of beneficial mutations that have those selection coefficients?
In order for this GE stuff to be a proper falsifiable scientific theory, we’re going to need to see the actual numbers and how they correspond to reality. Not these vapid excuses that only ever take the form of verbal responses.
I am not a population geneticist so I couldn’t tell you what is predicted long-term about the hypermutator lineages given their current values for mutation rate, dynamics of population structure, and so on, in the LTEE.
Ahh but that’s what he means by “turning down”. A turn-around from fitness increase into fitness decline, not just a reduction in the rate of improvement.
OK. I meant the rate of fitness improvement will fall. If Bill is still arguing for “genetic entropy” à la Sandford, then he’s wrong and demonstrably so.
