I think he probably understood that Lynch got different numbers. But he thinks those numbers still showed that “new” genes (although that is not what the papers were actually addressing) could not evolve in realistic time frames (without God’s help).
But, like I said, we can see if Bill confirms.
Well, strictly speaking, even trying at all is trying harder than necessary to convince them. People like that are not so much “convinced” of things as they are committed to them. The idea that they get “convinced” suggests what is almost certainly false: that there is any possibility of their believing otherwise.
On bacteria. You were trying to defend the hypothesis that ~3000 human genes are missing in mice, neither of which are bacteria. Focus, man!
Models aren’t evidence.
Come on, Bill! Let’s go from 100 to just 20. Name 20 genes that you think are present in humans but not in mice.
Do you realize how perfectly every word you write supports the hypothesis that you’ve never even looked at any evidence with any relevance to your positions expressed here?
Hi John
My claim is we will have difficulty reconciling 1 new functional protein coding gene with diverged sequences using experimental evidence and/or a realistic model. This should be easy to falsify if you believe in common descent by known evolutionary mechanisms.
A protein to look at which is common to both humans and mice is notch 2 which has different sequences by over 100 amino acids.
You do realize that it is precisely our acquired intuition for recognizing human design that informs us clearly that nothing, zero, found in nature beyond possibly the fundamental laws of nature itself, is designed.
Let us imagine that you are in charge of a 4-person space mission to Mars. You enter a crater and there are just rocks and dirt like any other terrain on Mars. No design. The only visibly designed thing is the ship. That is how it is everywhere you look.
Hi Bill,
Why don’t you start by naming 20 of them?
So you are unable to name even a single new gene, correct, because you haven’t bothered to look at the relevant evidence?
What’s the problem with 100 of ~2500 residues differing, exactly?
How did the change happen given known evolutionary mechanisms and become fixed in the human population?
First easy step is a common functional protein that has different sequences.
The challenge is that amino acids substitutions are not neutral and more than 60% of the time deleterious.
Notch 2 is a critical gene but can unlike notch 1 can survive a gene knock out. Notch 1 has more than 200 AA differences in humans.
Very easily. You do realize that we’re talking a lot of time since the last common ancestor, and that we’re not talking about the mouse one evolving into the human one, right? That changes happened in separate lineages? I suspect that you have no idea.
Are any of the differences functionally significant?
That’s a predictable evasion of evidence, as you have cited a specific case here. How would you classify each of the specific differences that are in right front of you–you know, in that evidence you’re not bothering to examine? All the answers are right there.
Whether single-residue substitutions are neutral or not is extremely dependent on structure. There’s no flat rate one can apply.
So is Notch2 a small, globular enzyme, or is it a transmembrane receptor with multiple domains, separated by “hinge” regions that are almost completely unconstrained? This is Wikipedia-level stuff about which you are obviously clueless.
Look at the evidence itself, Bill. In detail. Stop constructing silly rhetorical arguments.
And when are you going to list some different genes? These are orthologous.
What about ATP synthase that operates like an hydroelectric turbine or the gears found in grasshopper ?
Mutations.
Having its carriers outperform – slightly or severely – their cousins who shared ancestral variants.
That’s just a memory-friendly crude approximation of something that’s somewhat factual. It’s not a challenge. Not everybody is allergic to facts, Bill.
If an organism can survive without it, then critical for survival isn’t what you mean. So what else do you mean by “critical” then?
Here is notch 2 function.
https://grok.com/share/bGVnYWN5_420922ae-13b0-45dc-818e-2a7e460982ae
You need to apply something or you will overestimate feasibility. Here is an AI search for deleterious mutation rate of notch 1 and 2.
https://grok.com/share/bGVnYWN5_88e30ac1-ef7c-4455-aa60-10565c1a9bf7
Evasion of evidence noted. The question was about how structure relates to function or lack thereof, something I’ve studied for decades. Neither you nor Behe have. Why not learn something, Bill?
You need to apply specifics to specific cases. You are refusing to examine the specific evidence you chose so that you can pretend that a general structural rule applies universally.
You have a specific case–what are you afraid of?
How would you classify each of the specific differences that are right in front of you–you know, in that evidence you’re not bothering to examine?
Do you need some hints, or are you going to keep pretending that you understand this?
That’s the most parsimonious explanation. What explanation do you have, if any?
Yes, and then you cited a very bad paper that’s been debunked many, many times.
No problem: I falsify it by pointing to the nested hierarchy that the distribution of presence and absence of genes produces, which is the same as the hierarchy from other data. And I can also point to the phenomenon of paralogy, for which you have no explanation, and pseudogenes, likewise. These are evidence of gene gain and loss, respectively.
I will make a further prediction for what will happen to those 2956 genes if you expand the mammal taxon sample: they will be optimized as appearing on various branches of the tree leading from the common human/mouse ancestor to modern humans, and I further predict that the length of the branch will be roughly correlated with the number of genes appearing on it. Would separate creation make such a prediction?
Judging from his posts above, he’s graduated to claiming that MechaHitler, previously known as Grok, understands it. Who needs to pretend to sound like he understands anything, when a racial-purity-crazed cognition-free text generator is available to do all the pretending for him?
They don’t “look designed”, no. They look natural and organic, like something that grows, not artificial and manufactured.
Designed gears:
Natural gears:
Particularly in context they look almost nothing alike, and the organic is so clearly different from the artificial and manufactured. The only commonality is that both involve a row of matching-spaced teeth. Why that should carry a design inference is beyond me, especially when we know they are present in a growing and evolving organism.
Wrong. You obviously don’t know how people like M. Behe or G. Bechly became ID proponents.
Bechly married into it, then committed murder-suicide*(to escape it?). Behe was always just a fundamentalist conservative catholic.
*Isn’t being religious supposed to protect against poor mental health? Isn’t this the main selling point among conservatives these days?
I hypothesize that both became ID proponents because it was so much easier than doing science. All of their behavior is predicted by that hypothesis.
But neither of us can really know what other people are thinking, can we?
Had I been referring, even obliquely, to them, I suppose that this claim of yours might be relevant. Since it isn’t relevant to what I said, and instead is just out of the blue, why are you raising it?
