Answers Journal on Taxonomically Restricted Genes

@agauger was beginning to look at this as well when she was at PS last. It is rather interesting that ID community was so excited about orphan genes when they first discovered them, but I think it is going to turn into an own goal. They have stated over and over that mutations can’t produce new information (i.e. new genes) in the genome, but orphan genes are perfect example of just that. There are human orphan genes that are just a few mutations different than the orthologous chimp sequence, so we can even point to the mutations that give rise to new information. It would seem that there are plenty of places in essentially random non-coding DNA that are just a few mutations away from gaining function, something that would seem to run counter to ID claims.

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Thanks for the reply, Art.

From a mathematical pov scaling on protein length makes perfect sense if you are looking at the probability that the protein somehow contains something. But here its being used for the probability that the protein doesn’t contain something. It’s backward.

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On the scale that the ID community is using, I don’t think this point is that important. If we change the probability to 10^77 for every 150 amino acids in a protein, then a pool of 1,500 amino acid proteins only changes the probability by one order of magnitude to 10^76. The real issue is the flaws in calculating the initial 10^77 probability.

The most amusing thing about this ID argument is that it leads to the conclusion that there are no functional proteins in the human genome since none of them have beta-lactamase activity, excluding perhaps a handful of antibodies that may have lactamase activity.

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Before rehashing the math it seems the fact that many of the fact citations are wrong is the right starting point.

I reached out to Change Tan. She is out of town, but might join the conversation in a week or so. If she does join us, please treat her with respect.

Aha! We have less than 10^77 protein encoding genes. Much less. If humans weren’t designed, we wouldn’t expect to have a single functional protein.

It’s not even that. It’s the probability that a polypeptide picked at random from the total space of all possible sequences 153 amino acids long will adopt the ß-lactamase fold and function as a lactamase. But that number has very little to do with the probability of finding a lactamase in the same space.
The question is what the probability is of finding some adaptive function, not the probability of finding the particular protein we recognize as ß-lactamase(which could just have been one among many different possible adaptive functions evolution could have alighted upon).

Evolution never searched for that particular protein, it doesn’t have goals, and thinking it would have to for that protein to evolve amounts to the texas sharpshooter fallacy. Evolution works by finding something that works by increasing fitness, whatever it is. That means any imaginable possible molecular solution is on the table. ß-lactamase is just one among an incredible number of potentially adaptive polypeptides that evolution alighted upon.

What’s going on at the node circled in green? Which line takes precedent if the options are at odds with one another? If the non-coding DNA is highly similar, but there are “many other members of the pathways in which the unique essential genes function included”, does that mean the organisms can share a common ancestor or they can’t?

The flow chart suggests that they can share a common ancestor according to this “TREG” criteria, but they would argue that other lines of evidence preclude us from actually sharing a common ancestor.

E.g. the babble.

Yes, but that raises the question that must be answered:

Why did God create us in a way that it looks like we share common ancestry with the great apes?

Tan has given us criteria by which God could have made it really clear that we do not descend from apes. He did not make it clear. Why not?

He wanted to thwart Walter ReMine’s thesis, proactively?

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  1. Targeted mutagenesis experiments show that functional arrangements of amino acids are extremely rare; one in 1077 for a typical protein domain with 153 amino acids.

That’s a lot of false claims packed into a single sentence. The author is cherry-picking one experiment and misrepresenting it as multiple experiments. The reality is that multiple searches for function (the direction in which evolution does it) in random sequences find that specific enzymatic functions are routinely obtained from only 10^8 sequences.

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Good point, it was one experiment. And it didn’t actually show that, it was extrapolated from the results. A more honest sentences would have said:

    1. One targeted mutagenesis experiment was extrapolated to indicate that arrangements of 153 amino acids adopting a specific fold and carrying out a specific biochemical function could be extremely rare; one in 10^77.
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Which has then been overturned by abzyme research, and is irrelevant to the primary argument being made here any ways.

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There, fixed it (caps added by me). :grin:

Conversation has been fun! @Paul_Nelson requested that I put this on hold till Change and he get back back from Asia, where they are both under a heavy teaching load. Early July, I will reopen this topic.

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This topic was automatically opened after 10 days.

OK, now what?

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@pnelson can you join us with Change now?