Sure, I can try.
When you blast the human sequence of astrotactin 2 (accession number in Uniprot is O75129) against pre-vertebrates such as cephalochordates, you get a moderate bitscore of 366. But when you blast it against cartilagenous fishes, you get a much, much higher bitscore of 1853. So, as far as astrotactin 2 is concerned, the transition to vertebrates is associated with a big information jump of 1487.
But @Joe_Felsenstein has disputed the significance of this jump (see here Kitzmiller, the Universe, and Everything - #422 by Joe_Felsenstein) and has suggested that this could be shown by performing the following analysis: Can’t you just flip branches left-to-right at one fork on the phylogeny, so that the sarcopterygians, including the tetrapods, are on the left and the actinopterygians, including the teleosts, are on the right? It’s still the same evolutionary tree. But now measure how similar the sequences of each group are to a fish sequence, say one in a minnow. We will find that “FI” measured that way will be low in starfish, tunicates, lampreys, lungfish, amphibians, lizards, birds, and mammals. But it will jump up in the teleosts, with tuna, salmon, etc showing high “FI” when FI is measured that way. Do we need some special explanation for that jump?
So I have done precisely what Joe proposed, ie., I have blasted the Astrotactin 2 protein of Carassius Auratus (CA), a fish belonging to the same family (Cyprinidea) than the winnow, against the different animals Joe referred to. And it happens that the data don’t match Joe’s expectation but confirm the reality of the impressive information jump that occurred at the dawn of vertebrates.
As for the database, I’ve selected in the search set the “non-redondant protein sequences (nr)” database.
Hope it helps. Don’t hesitate to ask for additional details if needed.
I am trying to point out that genes arising from natural causes is rarely observed and there is good reason for this.
Especially genes with new functions and unique sequences. Genes live in almost infinite sequence space so finding function is not trivial especially complex function like we find in our cells. Many genes interact with other genes and this is also a challenge for new genes arriving by random genetic processes.
Well, again, it matters what you mean by “rarely.” There’s no reason to think that there hasn’t been enough time to account for all of the genes in living things.
Except, of course, that ID advocates tend to overstate the improbability. We see novel genes arising de novo from non coding sequence. Either that means that the improbability of it isn’t as great as the ID advocates would like, or it means that the Designer is getting into the mix all the time and should be detectable.
Why is it that ID attempts to do the math on this always are so spectacularly wrong? Doug Axe’s numbers are so bad that even Behe won’t cite them. Why is it that this “combinatorial inflation” problem obsesses ID proponents and nobody else? Why is it that every blasted time I open another ID book, there’s another wildly inaccurate description of the 1966 Wistar Institute conference, treating that long-forgotten schooling of mathematicians by biologists as though it represented a watershed in evolutionary thinking?
Here’s the thing. When your math doesn’t represent what happens in reality, your math is wrong. Reality is the test of the accuracy of the math, not the other way around. There is the old tale, probably not actually true, that engineers studying the flight of bees did the math and came to a straightforward conclusion: bees cannot fly. When something like that happens, are the mathematics wrong, or are the bees wrong? If you do not commit to trying to understand why your model of reality matches reality so poorly, you are doomed to spend the rest of your life railing at the bees.
That’s what I want to know what specifically you do. So you find the human version of astroactin 2 on uniprot, you copy the amino acid sequence (or what?), and “blast”(NCBI) it against what specifically and where?
There are many species of minnow for example, so which one are you using? “Starfishes” is what exactly?
Psst…hey Bill…does rarely = never?
Gee, if only there was some process whereby better combinations would be fixed in a population while worse combinations would be weeded out. Maybe we could call it something like “natural selection”. 
There is every reason that there is not enough time. People argue that there is not enough time for 1 to arise from scratch. This is the single issue that initiated my interest in evolution.
You need to read these papers carefully as they are speculative.
They are not wrong but they are misstated sometimes. For instance some stated Axe’s numbers were a general solution but they were not. Behe’s approach is different then Axe’s but both methods surface red flags.
This problem is real but difficult to parse through as it is hard to estimate functional space. The evidence is very strong that this is a show stopper for current evolutionary mechanistic paradigms.
Right, but since you now know that this is incorrect, because genes can even originate de novo from non-coding sequence, doesn’t that change your views? I understand that the CLAIM is quite compelling. If genes could not originate by any process known to us, we’d have to search for processes unknown to us. But that’s not the situation at all.
And yet, nobody who actually works with genes seems to think that that’s so. Why do you suppose that is?
We’ve seen dozens “arise from scratch” in the last 60 years since we began studying genetics. What makes you think 3.5 billion years is not enough time?
Sure Bill. You don’t understand the science so the science must be wrong. 
Have you ever seen an experiment where a gene comes from a non coding region? If someone has a non speculative paper on this I would be very interested.
“Rarely”? Compared to the frequency at which they magically poof into existence because a disembodied mind thought about them?
I don’t have the cites at hand (and they are buried deep in some Amazon thread, which I will look for, though Amazon threads are non-searchable…), but did read papers where this was documented. As for it happening during an “experiment,” I don’t think so. Why would you want it to happen during an experiment?
Here ya go. Of course, you can define “speculative” anyway you want, so I suspect you will find a way to dismiss this as “speculative.”
https://royalsocietypublishing.org/doi/10.1098/rstb.2014.0332
Then we know its not speculative. Most papers start from the assumption that what is being observed is the result of evolution. If we see a gene in one animal and a similar sequence in a non coding region in another it is assumed that is the result of the gene being generated from a non coding region.
Here ya go. Of course, you can define “speculative” anyway you want, so I suspect you will find a way to dismiss this as “speculative.”
Thanks for quoting this. Here the paper assumes:
Clearly, protein-coding genes must have arisen de novo from non-coding sequence in very early life evolution.
No, that is inferred on the basis of the phylogenetic relationship of at least three species, it can’t be done with only two because with only two species you don’t know whether the non-coding evolved into a gene, or the gene degraded into nonfunctional non-coding DNA.
So that is actually NOT automatically assumed.
But if you have three or more species, you can infer a direction to the change in the same way you can infer that two species are more closely related to a each other than they are to a third. If you have a rooted phylogenetic tree the order of changes can be inferred.
The principle is sort of like in this figure: 
Because you have a root to the tree which defines the oldest node, you can then straightforwardly see whether something is evolving or degrading.
I doubt anyone would assume that. But a more rigorous phylogenetic analysis could demonstrate it. The alternative hypothesis would be that the non-coding region in the one organism is a deteriorated copy of a functioning gene which both organisms received from a common ancestor. But phylogenetics can clear up which of these hypotheses is viable, and other methods of analysis may contribute as well.
EDIT: the preceding message was written prior to my reading Rumraket’s better statement to the same effect, above.
No Bill, evolution through common descent is not an assumption. It is a conclusion based on 160+ years of positive evidence from dozens of independent scientific disciplines.
Why do you keep repeating your false statement despite being correct so many times?
I am interested in data that is independent of evolutionary assumptions.
Bill needs an excuse, any excuse, to hand wave away the scientific evidence. It’s Bill’s version of the “no true Scotsman” fallacy - the “no true non-speculative science paper” fallacy.
For anyone interested in how Bill’s quote mine misrepresents the paper, here is what follows.
However, it is likely that the processes of evolution once life was established were very different from those processes that established life [9]. Consequently, de novo origin was usually considered so improbable as to be impossible for more recent evolution [2,8]. Instead, gene duplication, fusion and fission of genes, exon shuffling and other ‘bricolage’ events were considered to be the only viable sources of novel protein-coding genes—all variations on a genetic theme [9]. Proteins were thought to be made from a small and finite ‘universe of exons’ [10]. François Jacob articulated this best when he said ‘To create is to recombine’ [9]. However, in recent years, there has been a growing appreciation for the role of de novo gene origination.