Can you move past speculation independent of common descent?
Being able to say there is enough time requires the events to happen inside that time. What needs to be established is there is enough time.
-To search for new gene/protein functions and have those function fixed
-Lose genes and have their loss become fixed in the population
Why can’t we explain the pattern as the product of different trees? Sal’s flower appears to support the different tree hypothesis.
From what we are observing separate kinds have different incompatible genetic structures. Incomparable genetic structures are evidence for separate creation.
There is no evidence that there isn’t enough time, and without such evidence there is no basis for even suspecting there isn’t enough.
Both are routinely observed in both wild and laboratory populations.
Because the data is most consistent with a single tree.
No, it does not.
You haven’t defined where one kind stops and another begins, and “incompable genetic structures” is word salad. What does that even mean? Is one organism’s “genetic structures”(what is that?) “compatible” with another organisms? Are they required to be? In what way?
You’re blathering again Bill.
First of all, why should separate creation entail that different “genetic structures”(what is that btw?) can’t be compared?
And we seem to be able to do that just fine, compare organisms. Physiologically, anatomically, developmentally, and genetically. Unsurprisingly these all conform to the nested hierarchy, expected on common descent, yet not expected on separate creation.
No idea what you mean by that. This is not speculation at all.
Nobody is searching. It just happens. Fixation by selection is quite fast. Genes are commonly lost by drift; that’s slower than selection but remember that lots of genes are drifting at any one time, and all we need is for some of them to be lost. Let’s remember that there are hundreds of millions of years to work with here. If you think that’s too short, you are probably imagining some version of the Texas sharpshooter fallacy.
No, Sal’s flower supports the standard tree. Not sure why you can’t see that. What are you talking about that supports different trees?
Circular reasoning. Before you can observe what separate kinds have you have to first establish what the kinds are, and currently you’re trying to find evidence for that. Not sure what you mean by “incompatible” or “incomparable”, but they clearly aren’t the same thing.
Gpuccio really doesn’t get it. When you point to an extant protein and proclaim, “the odds of that specific protein evolving is way too improbably, so it couldn’t have evolved” you are committing the Texas Sharpshooter fallacy. You are drawing the bulls eye around the protein that already evolved.
The way to avoid the fallacy is to find all of the possible functions that could evolve in a genome at any one point in history.
Not against misrepresentations and logical fallacies as @T_aquaticus has demonstrated above. If the discussion is factual I think @gpuccio analysis is quite straight forward.
You need to get that chip off your shoulder right now. I agree with @T_aquaticus; @gpuccio is indulging in Texas sharphooter big time. Another problem is that his definition of “human conserved functional information” makes no sense and is certainly not a guide to pre-specified information. I think you call the analysis “straight forward” because it comes out the way you like and for no other reason. Now that’s a pre-specified result.
True, he doesn’t make that exact claim. What he claims is that 1) you can determine the size of an island in sequence space by looking at the protein variation we observe and 2) evolution must be a random shot into sequence space. Put together, they translate to @T_aquaticus’s statement. And I still don’t know how he defines “human conserved functional information”. Do you?
Which is ridiculous if you look at the scientific literature.
A paper that found that 8000 mutants of DNA polymerase MOTIF A ALONE (that is, only the 13 amino acid functional site) were functional, most of which had activity similar to the wild type; They found only ONE of the 13 amino acid was required to stay the same.
There would be so many more functional mutants if they mutated other parts of the enzyme.
The enzyme active site, is probably the part that can vary LEAST.
For example, if we extrapolated 8000 functional sequences from varying the core 13 AAs to the rest of 130 AA protein, then there would be 8000^10 functional variants.
There are likely more than 8000^10 (ie, 10^39) 130AA functional variants of DNA polymerase A. And of course, more if you allow the number of AAs vary.
To ID proponents these statements are effectively interchangeable, since you’re all laboring under the delusional axiom that functional islands are so small and far apart they couldn’t possibly be hit by blindly sampling sequences in that space.
Since the functions are nevertheless found (as in, they exist in life and can be shown to be conserved in certain clades on phylogenies) you guys say we must infer that someone must have been “aiming” for them.
By focusing the argument specifically on a protein like ubiquitin and it’s variants (rather than anything that works), you have drawn a target around it, and now argue someone must have been aiming because your “target” was hit. Because with your unsupported axiom that the “targets” are extremely small and rare, they couldn’t have been hit by just blindly shooting into sequence space.
That’s the ID argument in a nutshell, and it’s why it really does commit the Texas Sharpshooter Fallacy. As soon as you pick a concrete example (a known protein sequence including all it’s variants used to extrapolate a rough size of it’s “island”) with some function and then try to extrapolate the prior probability of hitting that “target” in sequence space with blind shots without aiming, you are committing the fallacy. Doing that is what commits the fallacy.
It’s like drawing a particular set of cards from the deck, finding that it’s a useful set of cards in your particular situation, then calculating the odds of that draw after having drawn it, then saying the odds of that draw is so small the deck must have been stacked on purpose to yield that set of cards. This would be analogous to what you are doing with sets of cards (protein sequences).
The issue (as @gpuccio describes) is not the size of the Island. It’s the ratio of the size of the island to the ocean. The Island being relevant function and the ocean being all possible combinations.
The difficulty of understanding this intuitively is that numbers get much larger than things we can imagine like Islands and oceans.
The island can actually be very large relative to other islands yet relative to the ocean it is very small.
And it can be quite large relative to the ocean too. It all depends on the data. @dpuccio makes sure his islands are small by defining them in a restricted way. He’s looking at the surfaced part of an iceberg and telling you that icebergs aren’t all that big.
And for the third time, what is “human conserved functional information”?
How does that translate to “human conserved functional information”? As you describe it, it’s nothing more than a measurement of similarity. And your link doesn’t explain what the term means. It just mentions it. Since you understand all this, please define “human conserved functional information” so I can determine how many bits of it are in a given protein.
Their are reason for DNA the Introns and the Spliceosome. Its to make a wide range of proteins to allow for life diversity. If almost all protein sequences were equally functional this complex machinery would not be necessary.
I am not going into the blast math at this point but to get an idea to translate to bits take a human protein with 100 amino acids and a mouse with the same positions except for 10. The number of bits of human functional information would be 20^90 or about 2^390 or 390 bits.