In addition, neutral variants that are physically linked to alleles that are under positive selection can reach fixation due to “hitchhiking” with the beneficial mutation. There are many, many examples of this happening from experimental evolution results.
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What evidence is that? Please show us the evidence that the vast majority of mutations that happened independently in the human and chimpanzee lineages were deleterious compared to the ancestral state.
You haven’t studied cancer, at all. You are incapable of reading scientific papers.
I’m getting tired of seeing you engage in this pathetic, and essentially dishonest blustering. You are constantly pretending to know things you don’t even half-way understand. Nobody here ever argues or discusses with you, they are teaching you, and you are just stubbornly refusing to get anything because it comes packaged with entailed refutations of your absurd religious beliefs.
You ignore most of what people say to you, you almost never answer questions directly, and you just write semi-coherent technobabble back in response with technical sounding phrases you have memorized and you have somehow convinced yourself are relevant for reasons you couldn’t articulate even if someone offered to pay you to.
It’s always the same stupid shit you say in response to basically any topic, about “DNA repair”, “wnt signaling pathway in embryo development”, “apoptosis”, “Sal’s flower”, “Guccio/Mung what do you think?”, “eukaryotes/prpf8/spliceosome looks like a separate origin event”, “respectfully I disagree”, “explain it to me(aka please explain it to me so I can understand it too)”. What have I left out?
Now Behe has written a new book, and you’ve learned two new phrases to brainlessly regurgitate endlessly: “above the genus level”, and “fly before traveling to Mars”.
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You read him incorrectly.
You are a software engineer. Why not go run a simulation and see for yourself?
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I understand the frustration. Can’t we be civil?
Am not a software engineer. I think I have mentioned this before.
I just don’t understand that behavior. I dare say, there is no topic on which I would allow myself to behave or argue in the way Bill does. Somehow I just feel too much shame about the prospect of being wrong, looking stupid, and it being apparent to everyone.
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Well a Chemist just checked it for himself. Why not give it a shot?
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You do argue in a very manipulative way Rum. Your own self awareness is not your best asset.
I have simply brought up problems with this transition and don’t have a conclusion yet. Why are the evolutionists not admitting to issues. Is it because they claimed all these transitions are facts and are having trouble back tracking?
You deeply believe in the evolutionary ideology and are emotionally attached to it. I am now very skeptical as every issue your side asks the evolutionary skeptics to prove a negative or they just white wash the evidence.
The evidence is that a 50% difference in exon ordering random genetic change and drift or selection is not supported as a mechanism with 7000 papers in pub med showing cancer with faulty splicing steps. Is this definitive? No? It is however a very serious issue that among other things puts the hypothesis in doubt.
Reading through that paper, I am not seeing the results you are claiming. For example:
"The relative proportions of orthologous exons detected to undergo AS in each sample were determined. "
They are looking at the relative proportion of a splice variant. On top of that, they are looking at a very limited set of exons (around 1500).
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What is “a 50% difference in exon ordering”?
Explain what that is.
So you are saying that their chart showing 50% difference may not be accurate. I accept that possibility but even if the actual difference was 30% that would still be problematic to explain with drift and selection as up to 100k splice variants are possible.
This is pretty straight forward. One iso form may contain 3 exons the other may contain 3 exons but not the same 3.
These numbers are probably going to be wrong, but let’s look at some back of the envelope numbers.
Each human is born with 50 mutations, at the low end. For 10,000 people, that’s 500,000 mutations. If 0.01% reach fixation from that generation, then that is 50 mutations per generation that reach fixation, which sounds right since I remember reading the rate of fixation is equal to the mutation rate. Human generation time is 25 years, so there are 240,000 generations during that time period. 50 mutations per generation for 240,000 generations is 12 million mutations. The chimp lineage will also be going through that same process, so if conditions are the same on their side then they will also fix 12 million mutations for a total of 24 million between human and chimp. The real number is 35 million for substitution mutations. If generation times, mutation rates, and population dynamics were a little different it isn’t difficult to see how you could get 35 million neutral mutations to fix between the two lineages. And all of this is assuming all differences are neutral.
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Good. Now explain how this is at all evidence against common descent of humans and chimp.
Edit: Wait, this makes zero sense. You’re going to have to clarify this. You’re saying there’s a protein coding gene in humans with 3 exons, and a similar gene in chimps(?) also with 3 exons, but those 3 exons in chimp are “not the same” as in human? What do you mean by that? If they’re “not the same”, then what are they? How are the genes then similar?
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Let’s say there is isoform A and isoform B. In humans, 5% of transcripts are isoform A and 1% are isoform B. In chimps, 1% of transcripts are isoform A and 10% are isoform B. The AS profile for chimps and humans is different for this gene, but they are producing the same isoforms.
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I am saying that the 50% difference may not be what you think it is, and it wasn’t measured across the entire genome.
Why don’t you share why you think this evidence is not problematic. How can up to 50K splicing variants can get fixed in the population. T is now trying to explain how 32 million mutations can get fixed in the population most by drift.
He is using the claim that the mutation rate equals the fixation rate yet fixation rates are population dependent. This needs to be reconciled.
You’re going to have to clarify what you wrote in your previous post, it doesn’t make sense.
You’re saying there’s a protein coding gene in humans with 3 exons, and a similar gene in chimps(?) also with 3 exons, but those 3 exons in chimp are “not the same” as in human? What do you mean by that? If they’re “not the same”, then what are they? How are the genes then similar?
Quite easily. The process is sloppy, there’s little metabolic cost associated with nonfunctional splice variants, and as such it is excellent evidence contradicting intelligent design.
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