I agree that the strongest case for guys like Behe and Gpuccio are the major transitions and innovations and we have common ground here. As far as the “tweeks” required for other less dramatic speciation events I am open. Here is some data that needs resolving. The origin and evolution of the splicing codes that separate vertebrates.
Science 21 December 2012:
Vol. 338 no. 6114 pp. 1587-1593 DOI: 10.1126/science.1230612
Define unsupported assertions 
Any post made by Bill Cole concerning a disembodied mind using magic to POOF biological life. 
I am not saying that you claim that.
Suppose someone else made that claim. Are you required to demonstrate that it was NOT created by alien beings? Or is the burden of proof on the other person?
That does not answer my questions. Please re-read and try again.
“Strongest” as in the mightiest of tadpoles, in my view.
While I have read the paper only once, and quickly, I am completely baffled at the notion that it presents anything that “needs resolving” in order to accept common ancestry of the vertebrates. Novel alternative splices would seem to be just the sort of thing which renders the objections the ID people to evolution of the genome irrelevant, as they do not necessarily destroy any existing function while creating new ones.
And the authors don’t seem to see any intractable problem in any of this. The conclusion:
“Our work offers conclusive evidence that the reassortment of splicing code features can account for the majority of AS differences between vertebrate species. Consistent with this observation, species-classifying exons identified in this study are often found in genes encoding trans-acting regulators but are underrepresented in the nucleic acid binding domains of these proteins. Instead, they are highly enriched in disordered regions, which are known to function in signaling and in mediating PPIs. Because these AS changes affect trans-acting factors involved in gene regulation, they represent an additional mechanistic basis for the remarkable diversification in AS and other transcriptomic changes associated with phenotypic change among vertebrate species.”
Where is the problem?
This is the best I can do at this point with your question. The best evidence for design is the transcription translation mechanism. How this was designed I don’t know. The Designers identity is revealed in scripture.
This all I have.
So your “best evidence” is actually no evidence. And you have no clue about a possible mechanism for the process you imagine.
Yeah, that’s something scientists should be spending their time on.
I asked Tim to define evidence. He has yet to do this. Do you want to give it a shot?
I most definitely see things differently.
I know you do and I respect your opinion. The evidence you brought forward with new corn gene was eye opening to me. Any more evidence of this type of evolution you can bring forward would be appreciated.
You have zero evidence they actually were consciously designed. As always all you have is your religiously inspired personal beliefs.
We know Bill. All you’ve ever offered are your scientifically unsupported personal opinions.
The opening post and link of this thread provides come compelling evidence along these lines. Keep in mind that the protein encoded by T-urf13 is a transmembrane protein. I think the paper by Vakirlis et al. may help to understand just how common (in sequence space) proteins like the T-urf13 gene product really are.
The problem is the evolution of the new splicing codes by random genetic change.
I think that the actual splicing “code” (which I take to mean the RNA sequence preferences that guide the core spliceosome, accessory splicing factors, and RNA-binding regulatory proteins that control some alternative splicing decisions) is the same in all vertebrates. There is no “new splicing code” described in the cited paper, or probably anywhere in the literature. What changes is the occurrence of particular code “elements” (trying to keep in the vernacular here) across the genome. These changes are well within the reach of random genetic changes.
Well it’s of a similar nature to many other papers on de novo genes where comparative genetics are used to infer that (and how) novel protein coding genes emerge de novo from non-coding DNA. For example the paper that was discussed here not too long ago about de novo genes in rice.
And don’t forget this, which fits the same hypothesis with novel genes inserting into the membrane:
https://mbio.asm.org/content/10/3/e00837-19
IMPORTANCE De novo gene origination from nonfunctional DNA sequences was long assumed to be implausible. However, recent studies have shown that large fractions of genomic noncoding DNA are transcribed and translated, potentially generating new genes. Experimental validation of this process so far has been limited to comparative genomics, in vitro selections, or partial randomizations. Here, we describe selection of novel peptides in vivo using fully random synthetic expression libraries. The peptides confer aminoglycoside resistance by inserting into the bacterial membrane and thereby partly reducing membrane potential and decreasing drug uptake. Our results show that beneficial peptides can be selected from random sequence pools in vivo and support the idea that expression of noncoding sequences could spark the origination of new genes.
Evidence of splicing codes is offered in newer papers and attributed to specific transcription factor proteins. Splicing is active in embryo development and its accuracy seems important as changes have implications in human disease. Random changes may incur purifying selection.
I am not firm on this issue however I think skepticism of random change being responsible for these differences is warranted.
Yeah, but that’s not a problem, is it? As Arthur Hunt points out,
So, the same mechanisms which work well for such things as generating binding sites are at work. When a mutation produces a new splice which is fatal, it won’t be preserved. When it’s neutral, it may be preserved. When it’s beneficial, it likely will. How does this pose any problem? Do any actual biologists claim it poses a problem, or is this just your faith in The Designer talking?
James Shapiro agrees this may be an issue along with gene expression differences. This is a subject that is not really discussed frequently in evolutionary circles but is an issue when you say transitions that appear straight forward may not be.
As you saw by my comment I am almost sure there is not enough known here for @Art to make a definitive claim. Will see if he does then we can have a discussion.