As I said previously, I don’t have thermometer measurements, or mathematical formulas about this. So I say they are related concepts, not correlated, and I explain why. I say you cannot have a fit organism which is missing important function, and that having a functioning organism is what we mean by a fit one.
The major problem with that is that it treats fitness and function as binary concepts, either fit or not, functional or not. But in biology they’re scalar, greater or lesser fitness, greater or lesser function. Larry Moran’s definition might help you here: a functional DNA sequence is one whose removal would have a negative effect on an organisms fitness. And that’s the connection between function and fitness.
In other words, you have no reason to assert that they are in any way related, yet you say they are anyway.
No, you do not. You just say they are related because having one, you say, correlates with having the other (as if either is a binary attribute like that, and on a whole-organism level at that, and also not), except in a way that is not experimentally detectable and best not be called a correlation at all.
Actually, what Axe meant was that using the wild-type enzyme as the threshold for functionality would result in finding fewer functional sequences, which does make sense. We were discussing thresholds, and somehow switched to discussing whether the wild-type enzyme should have been used. So I got somewhat confused, and you seem to be confusing the two as well.
Well, Axe explains why he picked a disabled enzyme for his study, “The remedy is to use a different starting sequence. Specifically, we need the starting sequence to be of the same quality that we intend to require of mutant sequences in order for them to be accepted. Otherwise the mismatch in quality will skew our results.” So your objection does not address his point.
No, I don’t say that, I said I believe there can indeed be levels of function, and levels of fitness.
No, I’m saying if you’re doing a study on fitness, or measuring for function, you need to pick a threshold, in order to make conclusions.
Correct, I don’t know why you seem to be insisting that only statements that can be verified by measurements, can be true.
This gets back to the question of whether small-scale mutations, like the ones Axe examined, are predominate in evolution. As far as I have seen, the consensus seems to be that they are. So pointing to other types of mutations, such as gene fusion, doesn’t overturn Axe’s results.
He has measurements, right? Not just an analogy.
“Proteins in a family descend from a common ancestor and typically have similar three-dimensional structures, functions, and significant sequence similarity.” (Wikipedia)
So Axe’s paper is all about protein families! All his variants have some sequence similarities.
Is that true, though?
I never said anything of the sort. Though if I must commit to something along these lines, I might suggest that a statement which is not a tautology nor can be verified by measurement may be one whose truthfulness would be impossible to demonstrate to a sincere and rational interlocutor.
Again, Axe picked a threshold that was intentionally favorable to Darwinism. So he’s including a class of variants in his results, not just pointing to specific variants. And he’s being generous in the types of variants he includes.
Well, Bechly refers to body plans, and explains what he means.
So Bechly wouldn’t consider them to be different body plans, they’re still birds.
Evidently not, Bechly being a qualified paleontologist, presumably he knew his subject, and also the fact that people (here!) have proposed counterexamples implies they accept this aspect of Bechly’s challenge.
Right, so the next step would to be to explain why you reject Bechly’s reasoning.
Yes, they’re connected! Glad to agree. And I also have said I agree that there are degrees of function and fitness, but when you set out to study function and fitness, people generally propose a threshold, to get a binary decision. We want to know if an antibiotic is effective enough, to be useful. Yes or no…
You’re not really explaining why, so much as just asserting it. And that’s the issue, this is little more than a blunt assertion on your part with nothing to support it.
Part of the problem with treating this in this fashion is it ignores things like environmental impacts on fitness.
It also suggests things like gain-of-function mutations should increase fitness, which isn’t necessarily the case. Likewise, loss-of-function mutations should decrease fitness, but that also isn’t necessarily the case.
No, he doesn’t. Or rather, his explanations, and there are several, are mutually contradictory and ambiguous. But don’t hide behind a deceased paleontologist. Let’s discuss the criteria here.
You’re saying that all birds have the same body plan? Do you think all mammals have the same body plan too? See how the definition is hard to apply?
Still hiding behind Bechly, I see. And hiding behind the unexpressed and unevidenced beliefs of other posters too. What new body plans emerged in the Jurassic?
What was Bechly’s reasoning?
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Yes, as I said to John Harshman, we pick a threshold when evaluating antibiotics, to decide if it is effective enough to be useful. Yes or no…
Well, you’re not going to know very much of importance, then! Most important principles and beliefs are not established by getting out a thermometer. I don’t say that there’s no evidence for beliefs, though. I believe in Jesus’ resurrection, for instance, based partly on historical evidence, which is pretty good, actually. But it’s not based on measurements.
Well, listen to John Harshman, then, he says they are related. And I’ve tried to explain why I think this, and John Harshman gives reasons for his conclusion, too.
No, they don’t. What makes you think so?
Do you think that a loss-of-function mutation could result in an increase in fitness? Vice-versa, can a gain-of-function mutation result in a loss of fitness?
Not under Larry Moran’s definition. I’m afraid we have dueling definitions of “function”. Your definition appears to be that a sequence has function if it does something, or perhaps does something that affects fitness, whether good or bad.
Except that using the wild-type enzyme as the threshold for functionality does not make sense. We’d expect the wild-type enzyme to be better than barely adequate. And Axe’s only test for functionality is not discriminating enough to be helpful anyway.
Besides the issue is not the establishing of the threshold but the bizarre idea that we must start with a variant on the threshold - and one that is particularly likely to be degraded by mutation at that.
That doesn’t come close to answering my question. If functional proteins are isolated in sequence space why would protein families even exist? Axe’s paper doesn’t look at protein families at all!
I’m not sure how the conclusion follows. Perhaps you can help:
Premise 1: We pick a threshold (for something) when evaluating antibiotics, to decide if it (sic) is effective enough to be useful. Yes or no…
- - - Enter the rest of your argument here - - -
Conclusion: Therefore, if you’re doing a study on fitness, or measuring for function, you need to pick a threshold, in order to make conclusions.
Premise 1: A statement which is not a tautology nor can be verified by measurement may be one whose truthfulness would be impossible to demonstrate to a sincere and rational interlocutor.
- - - Enter the rest of your argument here - - -
Conclusion: Therefore, I am not going to know very much (what ever that is) of importance (who ever decides that).
I should point out, I am perfectly comfortable with your conclusion. I would rather know nothing of import at all, than be convinced of many a thing based on vibes alone. Better, I say, to leave questions unanswered than answers unquestioned. Your conclusion, once again, does not seem to follow from the premise, but if it did, it would be an emotional appeal of the sort that means nothing much to me anyway.
One of the challenges I have with tying fitness to function is how does one account for environmental effects on different phenotypes and fitness in the context of that definition?
Or to put it another way, if fitness is tied to function, then is function also dependent on environment?
One example is the differing levels of melanin production in humans in different populations with respect to different environments (i.e. differing levels of solar radiation). Individuals with increased skin pigmentation may have reduced fitness in regions with lower solar radiation. And vise-versa, individuals with light skin may have reduced fitness in equatorial regions with high solar radiation.
But is the function of the genes on the production of melanin functionally different depending on which region they are in?