Of course. As I said elsewhere, I’m focusing on the vast majority of mutations that are relevant to GE.
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You’re free to admit that “noncoding = junk” is objectively false, but you won’t. Why?
Is this misrepresentation in error or is it deliberate?
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If only you could get the GE proponents to focus on the mutations that are relevant to GE…
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We can move past this, yes. I apologize for not properly representing the views there. It’s not important for the sake of this discussion to make that point into a debate. I’m was just trying to figure out how it’s supposed to be relevant to GE. I’m not entirely sure that Dr Felsenstein and Dr Schaffner are giving the same answer though.
Great! How about continuing the discussion and correcting the misrepresentations? Let’s start with your #2.
You were asked to describe the objections to GE. You failed to describe them accurately.
There’s no real discussion without trying to understand what others are saying.
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No one in this thread used those terms to describe you. People merely pointed out how often you misrepresent what others have said and how little of the science under discussion you actually seem to understand. It’s possible you don’t grasp how you come across. Those things are fixable if you wanted to fix them.
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It gets more complicated, and starts getting closer to where actual science is done. Mutational bias tends to produce GC->AT, while GC-biased gene conversion pushes in the other direction. Active transposons add new junk sequence with its own GC content, and deletions gradually remove existing junk. There’s no reason to think all of the active processes together create any overall direction, nor any reason to think even a considerable change in junk sequence composition would have more than a negligible effect on fitness.
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Adding a grain of sand to the trunk of your car does slightly change its fuel efficiency, but does it really matter?
In the case of junk DNA, we are adding and removing grains of sand at about the same rate, and it would be a very, very small amount of sand at any one time. The energy needed to make new copies of DNA is a very tiny fraction of the body’s overall energy usage. In fact, I would suspect transcription to be much, much more costly than replication. I wouldn’t expect any noticeable reduction in fitness if junk DNA doubled in the human genome. Of course, the size of primate genomes are all pretty much the same, so that really isn’t an issue.
I just don’t see how accumulation of mutations in junk DNA can add up to the effects Sanford is talking about.
This hardly seems to need pointing out, but yes. It really matters. If you keep adding grains long enough, you get a whole pile of sand. So the important point isn’t the size of the grains, it’s whether they’re accumulating at all. So far the only person who has given a response that even attempts to suggest there’s no accumulation would be @glipsnort. Besides him, everybody else has just been obfuscating and/or getting confused.
Look! Everyone is marching out of step except for @PDPrice! “Obfuscating” is an insult, which you have been instructed to avoid. “Getting confused” isn’t an insult, but it’s wrong; you’re the one who’s confused here.
And what if instead of 1 base insertion, you had insertion of 10^9 bases? Wouldn’t it be an energy cost that matter?
Exactly ! To see this, let’s take 2 human genomes A and B, with genome A harboring 90% junk DNA and genome B completely devoid of junk DNA. The sizes of genome A and B would be 3x10^9bp and 3x10^8bp, respectively. Given that genome A is 10 times bigger than genome B, it will accumulate 10 times more mutations than genome B. But the number of mutations that will land within the non junk fraction of genome A will be the same than the number of mutations accumulated by genome B. IOW, assuming GE is true, both genomes will degrade at the same rate.
Wrong. The mutations GE refers to are those which have effects so small as to be non-selectable. It is far from obvious that such small effects will be universally deleterious or beneficial.
Wronger.
The genetic context of a mutation is the nature of the surrounding genome, which is not fixed because mutations are happening there too. And yes, mutations can move around after they’ve happened. That’s what insertion mutations do - they take sections of DNA, which might include a new mutation, and move it to somewhere else in the genome, thus giving it a new genetic context.
So yes, mutations can get moved around after they’ve happened.
Since your kind are so fond of using words to illustrate mutations, I’ll do that here:
Original information: STUMPY
Mutation reducing information: STRMPY
Second mutation increasing information again: STRIPY
Positive changes can indeed compensate for negative changes.
Of course you’ll argue that the original information is still missing, but that’s because, as your statements here show, you don’t know enough about evolution or genetics to know how wrong you are.
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They do have an impact. But the reason why they have an impact has clearly not been remembered or understood.
Performing a rough calculation based on this paper, an extra billion bases being added to the genome somehow would use up about an extra 0.05% of a eukaryotic cell’s energy budget. Let’s say that reduces fitness by 0.05%, so it would be noticeable by selection.
https://www.pnas.org/content/pnas/early/2015/10/29/1514974112.full.pdf
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Yes…
Yes!
YES!!!
Noooooo…
Yes…
Yes
Two steps forward, two steps back. Changes in PDPrice’s level of understanding is a better analogy for the effect of mutations than anything else presented so far.
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This is interesting… Thanks for the link.
It’s also worth mentioning that (IIRC) Graur was an enthusiastic reviewer for that paper, so it’s a good example of promoting ideas even if they conflict with your previous publications. Accepting correction is a good thing.
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Apparently it needs to be stated that no-one here has actually advanced an argument that junk-DNA protects against deleterious mutations. The mutation rate is calculated pr. nucleotide pr. generation, so genome-size is irrelevant to mutational load as having more junk-DNA doesn’t alter the probability that a deleterious mutation will occur in something functional. Increased genome size is actually known to be weakly deleterious. That extra DNA has to be replicated, and maintenance processes can’t distinguish between functional and nonfunctional DNA, so will also have a slight metabolic cost there.
Rather, the argument is that the weakly deleterious mutations that occur in junk-DNA, that is to say those weakly deleterious mutations that are supposed to be relevant to the concept of GE, are so weak that their effects are practically neglible, and that when and if strongly deleterious mutations occur in junk-DNA, they are so strong that they are visible to selection(for example by creating spurious sites of transcription). And it’s important to understand that since junk-DNA consists of large stretches of nonfunctional DNA, having many slightly deleterious mutations accumulate in it is not a problem in the same way it would be to a functional gene. You can’t just delete a critical functional gene. But you can delete a nonfunctional piece of DNA and therefore get rid of a large chunk of deleterious mutations simultaneously.
Having an understanding of the biochemistry of gene regulation and replication actually helps understand why and when mutations in junk-DNA (be they substitutions, or insertions/deletions) have selective effects that are or aren’t visible to selection.
This is remarkable and deserves a bit more exploration. Do you have any evidence to back up the idea that GC-biased gene conversion exactly counterbalances the effect of biased mutations, such that there isn’t even a slight overall direction to it all? Doesn’t this seem implausible, granted that these are completely independent processes in nature? If these two phenomena exactly counterbalanced each other, we would call this fine tuning.