Do you understand the concept of junk DNA and do you understand how you’ve falsely conflated it with noncoding DNA?
Do you understand that the larger saltatory genetic changes in influenza virus are caused by genomic segment reassortment, not mutation?
In precisely the same way you claim that there are no strictly neutral mutations. ‘Equal effect’ in my comment would mean ‘exactly, without any difference whatsoever, precisely the same’, which is impossible for something like that. Also, because an equal percent increase in diameter of a blood vessel has a proportionately larger impact on smaller organisms, all else being equal, because of the square-cube law.
So basically, I actually thought about it before I hit ‘reply’. Give it a try.
Why do you say “I claim”? This is what population geneticists say, including the ones participating here.
But what I don’t understand is how this is supposed to prevent fitness decline from happening.It affects it by implying that if 60 (or 100 or whatever your estimate is) mutations occur in the genome, the number that is imposing a mutational load is correspondingly smaller. You then don't have to explain how we could possibly survive that many deleterious mutations per individual per generation. It does not rule out that fitness decline may be happening, but it affects the quantitative calculations a lot.
That isn’t relevant. Whether or not the difference in circulation is adaptive is relevant is. And that is down to context.
I have to say I keep being surprised by your unwillingness to think for yourself instead of just feigning ignorance. Who is it you think is impressed by your volitional inability to reason?
The point is, if mutations in junk DNA are of sufficiently small magnitude, and given that junk-DNA is already junk, as in nonfunctional, then gain-of-function mutations with larger fitness effects must be much more likely than if the DNA was functional and highly adapted. That means deleterious gain-of-function mutations in junk-DNA are likely to be visible to selection, but the same goes for beneficial gain-of-function mutations, which means they can have magnitudes of selection coefficients large enough to overwhelm the tiny effects of deleterious mutations in junk DNA.
And then there’s the magnitude of mutations in coding regions, which are usually much larger than mutations in junk-DNA, which means that delerious mutations in coding regions are much more likely to be removed by selection(here they generally are visible to selection), and that beneficial mutations in coding regions therefore really can have magnitudes of selection coefficients large enough to compensate for extremely tiny deleterious effects in junk-DNA.
I agree, that’s certainly true. But this looks like the final answer I was looking for. Junk DNA is not really all that relevant to the question of whether GE is happening, only the speed at which it may be happening.
Grammatical symmetry with your comment to me. My statement about them not having ‘equal’ fitness effects is as necessarily true as your statement about mutations not being ‘neutral’.
Just. Wow. That’s even worse than your conflation of junk with noncoding DNA and misrepresentations of influenza virus genetic data.
Speaking of context, Paul, have you considered just maybe learning something about genetics as it is understood and used outside the context of evolutionary biology? There’s a lot of it and learning it may overcome your resistance to learning about the most basic concepts.
Those are meaningless phrases.
The variation in the wolf population is due to differences in DNA sequence. Differences are changes.
Yes, and when you whittle a boat out of a block of wood, each of those pieces you whittled off were just “changes” as well.
A bank account has a savings balance of $1999.
Feb. balance $1998. → mutation with small deleterious effect
Mar. balance $1997. → mutation with small deleterious effect
Apr. balance $1996. → mutation with small deleterious effect
May balance $2996. → mutation with large beneficial effect
Oops! Looks like PDP is wrong again. 
I’m sorry, but it’s impossible to take you seriously when you spout things like that. You are misunderstanding what Joe said. As you misunderstand everything for which understanding would be a disadvantage.
Changes to functionless DNA can easily be deleterious, as they may influence the amount of energy or materials required to replicate them, may introduce spurious function, such as a binding or splice site that interferes with function elsewhere, or increase transcription rate at some energy or materials cost. And a mutation to the mutation would then be advantageous. The point is that most of these mutations are so weakly deleterious or advantageous that they would even in the aggregate make no significant impact on fitness.
The other point is that if the selection coefficient is small enough, the genome cannot contain enough such mutations to have a significant impact on fitness. There is a limit to how much fitness decrease can happen, regardless of the time allowed. And this limit is probably small.
Then why don’t we see any of this “pre-loaded genetic diversity” in the sequenced genomes of any extinct ice age species? You’re making up stuff again PD. That’s not allowed in science.
Dude, please just think for a moment.
He may be confused because the more common term is “genetic background”. But probably not.
I suck at genetics and even that made me cringe.
The aggregate? Mutations are ongoing … forever!
This makes no sense at all. Please retract. The genome does not “contain” mutations. Mutations keep happening every generation, forever. If their aggregate effect is downhill, your population is going to extinction.
It might be helpful to consider genetic distance between two sequences, in a simple model in which mutations are randomly distributed and each possible mutation at each site is equally likely. Now suppose we assay genetic distance, just by counting the percentage of sites differing between the sequences. Clearly, two sequences that start out with 0% difference will increase in distance for a while, even linearly for a while. But will that difference increase linearly forever? Or will it reach a limit? If so, what do you suppose the limit of percent difference will be?
The case with junk DNA mutation is similar, if a bit more complex.
No, you just don’t understand it. Do you know what multiple hits are?
So, you think the bacteria colonies that grew up in the most toxic region of the agar (in the Harvard Medical School experiment) ALWAYS had the ability to survive toxic antibiotics? So why did it require a noticeable pause every time populations were confronted with a new level of toxicity? Why didn’t the bacteria colonies simply spread into the newer more toxic areas without even the slightest pause?
There is a genetic difference between the starting bacteria populations and the ones that made it to the most toxic regions.