Evolution explains the differences just as easily as the similarities. We see lineage specific mutations which is what we would expect to see with evolution. There is also the pattern of transversions, transitions, non-CpG, and CpG mutations that we have spoken of before.
When you ask a question whose answer you already know, you are presumably trying to make some kind of point. But what point?
Sorry, John. Can’t help you with your uncomprehension.
If this was the total differences I would agree but this good work needs to be followed up with AA changes and analysis as we know there is redundancy in the genetic code.
For your statement to be true the spliceosome emergence in eukaryotic cells should be as easy to explain as a protein that exists in both prokaryotic and eukaryotic cells.
That’s just crazy wrong. In the case of nested hierarchies derived from sequences, the length of the branch IS the amount of difference!!!
My point is about the cause not the branch length.
Nice try. Your point was:
My point is that your claim is crazy wrong, because it explains the differences equally well. The standard creationist misrepresentation is that these analyses show nothing more than a vague similarity.
This is a false assertion. See my comment on the prokaryotic eukaryotic transition.
May I, as a “lay” observer in this discussion, ask one of @swamidass “ridiculous what-ifs?”
Discussions like this focus (artificially, I’m prone to wonder) on the evolution / development of new variants / kinds as if they arise in an environmental vacuum, by accident and then get selected, and then everything else keeps “accidentally” adapting. It makes me wonder, what’s stable in such a model, in the aggregate?
But what if the goal of a totality of sustained function across an entire ecosystem is somehow being upheld, with changes being slowly implemented or orchestrated, and the seemingly random changes when focused on a single species, as if it is / was living in a vacuum, actually is a means of losing the big picture?
We all seem to searching for physical mechanisms of change as the only sources of novelty, when it’s certainly not impossible for God to “download” new informational content into genetic “codes” in order to accomplish coordinated, planned changes.
That is an understandably upsetting proposal, rather like a silicon chip engineer trying to account for a running computer by insisting that the system must lie dormant in the chip’s physical architecture, when a whole separate regime of organization and input is availabe to transcend their aggregated singular, limited potential.
Only to discover that the chips’ usual function can actually be altered through other coded feedback loops?
Comments? @AJRoberts , @Agauger , @pnelson , and any others not inclined to brush this proposal aside?
I did. It makes no sense.
That doesn’t make much sense. Assuming you know about the PM capabilities of this board, such comments appear to be completely unwarranted.
I don’t see how this applies. AA changes are due to DNA sequence changes, so the same concepts apply.
The splicesome follows the same tree-like distribution as other systems.
The cause is evidenced by shared differences in a lineage. For example, mammals have three middle ear bones while reptiles have a single middle ear bone. This is a difference shared by all mammals, and it follows the expected tree-like pattern. Evolution explains the differences.
Synonymous mutations can happen without a AA change due to the redundancy of the code.
How do you explain the emergence of the genetic code that builds this protein complex by cell division alone. The Lenski experiment did not produce a new functional working enzyme sequence.
The differences are much harder to explain as we know cell division replicates whats there. We don’t know how it creates what does not exist in the mother cell.