If this the Mendel’s Accountant stuff then it was refuted a long time ago. Sanford’s work predicted that species with short generations times, like rabbits and mice, should have gone extinct after just a few centuries.
I suggest you don’t sweep this under the rug
It doesn’t address the topic anyway, so it is a red herring.
If you have a functional sequence that with random changes moves almost certainly to non function possibly but rarely with temporary selectable steps then again proceeds to move to non function then the current description of evolutionary mechanisms is broken.
I think their position is important to understand especially as it appears to be backed by empirical data.
That’s just made up. About 25% of the changes aren’t even going to change the amino acid sequence.
See the differences between the chimp and human genomes.
Sure and changing the other two nucleotides will as long as the animal can take the change avoiding purifying selection. This is true for 2% of the genome. The other sequences may affect regulation directly where every change is significant.
I was making a lame joke while being sarcastic. I had forgotten if it was here or on a separate thread where Bill Cole (I think it was) said he was a cancer researcher while making an argument where he sounded somewhat like Greg. I’m not suggesting that the two posters are the same person. It was just a bad joke where I was noticing that they were making a similar kind of argument against the science academy and claiming to have a better grasp than the scientists.
That kind of joke doesn’t work so well in a written discussion where facial expressions don’t clarify the sarcasm. I was in a weird mood that day.
Can you expand on this?
And this is exactly the God-Guided evolution ive been explaining to ID folks for the last year!
What lesson do you draw from those two papers? I find that the mechanisms that give rise to these orphan genes are explained in the papers, for the most part. Is it intended to be an argument against common descent? In favor of intelligent design? So far I don’t see it. I will also note that both papers show quite sparse taxonomic sampling, and denser sampling might illuminate the evolution of the various sequences.
40% of the amino acids are different between human and C. elegans cytochrome c, and both species seem to get along just fine with those proteins.
You may be right. Sampling may reduce the number of orphans. Or it may not. Or some of the mechanisms proposed might work. That should be determined by testing though.
The reason for the two papers was because you asked what taxa had orphans.
I asked that because I’m trying to understand what purpose you have in bringing up orphan genes. What is your purpose?
This is thought to be an argument against CD for some unexplained reason. I’m not sure what the logic is, as it seems like a nonsequitur to me. It could be the beginnings of an argument for ID, but not against CD unless one misunderstands the evidence for CD.
Cytochrome c is a multifunctional protein in mammals and mission critical to forehead development in mice. Not sure this is true in C. elegans.
I have written a piece about orphans that should explain the logic, but it hasn’t been posted yet. You’ll have to wait.
Well you could post it now at the preprint server for biology - BioRxiv
I don’t think I have that privilege. And it’s a simple blog post, not a scientific paper.
I pretty sure you have that privilege. And short letters are allowed. Here are the guidelines for preprint publication.