Basic understanding. Maybe you should spend your time acquiring it instead of arrogantly pretending to have a deeper understanding than experts.
TBH, I don’t know if Kimura was the one to come up with the concept. However, you are correct in that it is the neutral mutation rate that is equal to the mutation rate. Obviously, beneficial mutations will be fixed more rapidly, and deleterious one’s less so. I should have been more specific.
Since, to a first approximation, all mutations are neutral, or nearly so, that does not matter.
What data do you have on fixation? I agree there are polymorphisms in the population.
The argument has been about genes not being neutral. So despite your diversion it appears we agree.
They are also much longer sequences. A functionally more complex protein can also have more substitutability. There are over 1000 orders of magnitude more possible arrangements of Myh than alpha actin,
This is what Lenski claimed and I will try to find you the paper and the quote. Why bacteria do not die is selection works like a filter. Those that have a killer mutation get purged from the population as they stop replicating.
For genes we know this is not true. 50% of AA substitutions are deleterious.
Knowledge and understanding.
Specifically the knowledge that Neutral Theory postdates the formulae for fixation probabilities and rates, the knowledge of what Neutral Theory is, and the understanding that either can exist without the other.
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Why, yes, Bill. That is absolutely true.
Now: What implications does this have for the creationist idea of “Genetic Entropy”?
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Good question.
Likely limited in many protein coding genes. The rest of the genome may be vulnerable. A functional sequence will break down when randomly changed unless there is something to stop it from becoming fixed in the population as you have identified.
This is one on the interesting aspects of neutral theory as it has no mechanism to move toward a new function.
You just identified what that “something” is. You’ve already forgotten?
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You reckon something like a significantly shorter life expectancy wouldn’t suffice to impact the spread of a gene that produces it? I asked this before, but it seems you don’t quite seem to connect deleteriousness with bad-for-fitness-ness. As if there is anything else it could possibly mean.
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I understand purifying selection and also know it is not necessarily helpful to evolutionary theory as it limits variation.
Do you remember the conversation we had about neutral theory 7 years ago when you pitched the idea (on the sandwalk blog) that humans and chimps share a common ancestor. Your argument was the same as you argued above that we could explain the differences based on neutral mutations. We have a lot more data about this transition now.
Here is what I promised from the Lenski paper
https://www.nature.com/articles/ismej201769#citeas
Clones sampled at generation 50 000 from populations that were not hypermutable averaged ~75 mutations in their genomes, in contrast to the billion-plus mutation events that occurred in each population. Those 75 or so mutations also pale in comparison with the differences between E. coli and Salmonella (Ochman et al., 1999), or between two E. coli isolates from nature (Dixit et al., 2015). However, it is not surprising because the time scale of the LTEE, while long for an experiment, is a drop in the bucket of evolutionary time.
Clearly you don’t. If you did, you would not keep making arguments for GE that assume that purifying selection does not occur.
I can’t really take credit for that idea.
Yes, and that is correct. Of course, many of those mutations would have been beneficial, so the “problem” of accounting for the number is even easier.
Sandwalk: What’s the Difference Between a Human and Chimpanzee?
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Then why were you just denying that they exist?
Bill, if you are unable to distinguish between genes and alleles, it’s hopeless. The adjective “neutral” does not apply to genes.
Since you snipped this, my prediction appears to be correct.
Which according to @gpuccio, means they have more functional information.
You’re completely missing the point. Your arrogance is blinding you.
That’s utterly irrelevant. I’ll ask you again to use ID to explain the polymorphism of human MYH7, the protein whose complex function is making your heart beat as you read this.
You’ll avoid doing so.
That’s irrelevant, because the vast majority of mutations do not change amino-acid residues. We know that your claim is false.
Bill, have you considered thinking long and hard BEFORE you write?
You do? Could’ve fooled me, I’ll say!
Ah, there it is. It “limits variation” by, you know, eliminating grossly unfit variants. Speaking of unknown mechanisms, can you name (let alone explain) one that would make selection limit non-detrimental variation? If you can answer this question, this will be another definitive proof on a mounting stack of such, that you have no understanding of the subject whatsoever, and I’ll explain once it happens.
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Two requests. First, try much hard to make coherent statements. For example in:
What is “this”? Who are “we”? What do you mean by “hanging on to”?
Second, please stop with the sea-lioning. Challenged on one point, you ignore that and raise five more.
No they aren’t. The models say nothing about the nature of the functions. They’re just about a single, pre-specified function. And we have departed far from the original claims.
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If they’re deleterious, they don’t matter. Because they are selected against. You can’t make a valid point to save your life.
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In multicellular eukaryotes. Bill has again mysteriously forgotten the relevance of genome size, fraction of genome devoted to non-coding DNA (and how much of this is junk), and the relevance of population size.
There is no “Behe Lynch” models. Lynch has a model, and Behe & Snoke has a model. Behe outright admits his doesn’t correctly model evolution in his paper. And neither model shows “functions that are mission critical to living organisms.” You’re blathering again.
Everything you say is both stupid and wrong.
So if 70 mutations fixed in 25 years, that would mean E coli could diverge by 108 years / 25 years × 70mutations = 280 million mutations, in 100 million years. Now of course, it couldn’t, since the E coli genome size is a mere 4.5 million basepairs. There’s more to it also, since in the LTEE a phenomenon like clonal interference is reducing the rate of fixation of mutations, as there’s so many beneficial mutations occurring that some on their way to fixation are suddenly outcompeted by newer beneficial mutations with even stronger effects. But that’s enough of that, you’re probably confused already.
Suffice it to say: Congratulations Bill!; you’ve discovered that bacteria with their small genomes consisting almost entirely of protein coding genes(80% or more), extremely low mutation rates, and vast population sizes, are different from large multicellular eukaryotes with their huge swollen genomes with almost no coding DNA (usually in single digit percentages), mostly junk DNA, and small effective population sizes.
Revealing that you’re a total ignoramus and you can’t do math.
No, it doesn’t. There’s no math that supports that claim.
That would mean the other half is neutral or beneficial. So in fact the average protein coding gene can diverge at about half the rate of mutation. That’s a lot.
And in any case, when it comes to the overall genomic divergence of species, protein coding genes are ~3% of the genome or even less in many large multicellular eukaryotes.
Once again you reveal that you are an ignoramus. And you can’t do any math.
No there isn’t you idiot. From what waste-expelling orifice of yours did you extract that absurd number? The entire sequence space of the protein doesn’t cover 1000 orders of magnitude you giga-clown. The entire sequence space for a 500 aa protein is ~10650 (That’s 650 orders of magnitude then) Can you do any math? Like, at all?
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Que the crying about labeling. “Bla bla you insult me because you have nothing bla bla bla not because I’m genuinely thick as molasses by choice bla bla bla.”
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The functions are disulfide bonds in the case of Behe and Lynch models and ligand binding in the case of the Behe models. These are real biological functions and are very simple examples of biological function.
Your any function will do hypothesis has no bearing with reality and will not fly with competent people. It is simply a false simplification to try and salvage a theory and model that no longer fits the data.
Maybe you should consider withdrawing that accusation of incompetence, since it is unjustified.
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John being mistaken on a single claim does not mean he is incompetent. He is very competent because he knows that this issue (biology requiring specific type of functions) is very problematic for the UCD hypothesis.