I gave you some credit but the rest of your argument shows you do not understand the argument. It is very basic issue with molecular biology that gene mutation is often problematic to species. Arguing this point is like the 2+2= 5 discussion.
Would you support a paper that the design argument is badly needed to keep evolutionary biology honest?
Showing at least 10 well referenced papers that make a conclusion based on the assumption of common descent by reproduction alone.
Wow, so this is the go-to rationalization for keeping up the ID tent despite it’s last 25 years of utter failure in producing any meaningful research.
There isn’t any coherent question posed by any IDcreationist that has not already been posed by evolutionary biologists reviewing each other’s work. Often times as much as a century before the IDcreationist dreamt it up.
How else does common descent happen besides reproduction Bill? Are you back to your disembodied mind using magic to POOF new species into existence?
How many scientific papers will it take to keep Intelligent Design proponents honest Bill?
I have a suggestion: @Mercer has asked @colewd a specific and straightforward question that seems to me to cut to the heart of his claim. But it would appear Bill is being distracted by other comments and questions.
I think it would be most productive if we just gave Bill time to answer the question, and leave the discussion between him and @Mercer.
Like I said, just a suggestion.
How is this remotely any evidence against evolution? Every time you cite papers it looks exactly like what Mercer and others here have identified as cargo cult science; you make claims the papers don’t support, you don’t demonstrate any understanding of the paper, you frequently don’t appear to have read more than the abstract, and you co-opt the scientific language of the paper for your own non-scientific conclusions.
I don’t believe “the design argument is badly needed to keep evolutionary biology honest”. In fact it is very much like the other way around; evolutionary biologists help keep IDers honest. However, I would love to see you get such a paper published.
Nevertheless, this does not answer my repeatedly asked questions. How many papers in Pubmed belong to you or Gil providing evidence for the hypothesis under question? Why don’t either of you do actual science and get published? What’s stopping you? Why are you wasting time on a forum when you could reach the scientific world with your evidence?
I tried Jonathan. Happy New Year.
Quote me doing so or issue a retraction/apology, Bill.
We know Bill. You tried making your usual lame excuses, ignoring scientific evidence, and bluffing about papers you never read. It didn’t work just like it doesn’t work every time you do it.
You said it yourself, Bill. Cardiac function.
Bill, please try to focus on cardiac muscle.
Besides, you’re completely wrong. The beta-cardiac myosin heavy chain (gene name MYH7) is also the predominant myosin in slow-twitch skeletal muscle.
So right there, you’ve falsified your own design hypothesis because its mechanistic prediction doesn’t match reality.
How can that be when the identical one predominates in both cardiac and slow-twitch skeletal muscle, Bill?
Progress!
Precisely how many different, functional, human sequences did you align to obtain that score?
Why don’t you try to get yourself published?
It is also a basic issue that deleterious mutations are selected against through natural selection. It is also a basic issue that this naturally causes sequence conservation, which you seem to deny.
What is it about sequence conservation in actins and myosin heavy chains that you think evolutionary mechanisms are incapable of producing?
In that spirit, there’s a simple question Bill has left unanswered:
Maybe you missed it, Bill…
The answer is I obtained the standard human sequence from Uniprot.
The consensus sequence is not the only functional one.
I agree.
You agree that @gpuccio’s “FI” hypothesis has been falsified?
If not, can you explain how you think that you are calculating sequence conservation without considering all of the known functional sequences?
John, you are nit picking. A few more functional sequences added does not affect the math enough to change the conclusion. If there were a variation per every human on the planet it would not affect the math in any noticeable way.
Oh, Bill…you are so dependably arrogant.
Once again, your ID hypothesis has made an objectively false empirical prediction. The fact that you misrepresented its prediction as fact does not detract from it’s scientific utility. After such a failed prediction, a scientist would modestly abandon or modify her/his hypothesis. You, otoh, will do nothing of the sort.
The whole point of my bringing this up is that there are not “a few.”
It’s anything but nitpicking. It falsifies gpuccio’s hypothesis too.
I calculated around 8500 bits. This was based on 54 differences in amino acid positions out of 1935. If you want to falsify the hypothesis show that including the human variation will change the claim. I predict the human variation data will add nothing appreciable to the calculation.