Where did they ever claim that “genetic changes are improbable”? They are aware that genetic changes are very common.
You’re engaging in caricature. Dembski’s discussion is very detailed and nuanced. I have the impression you are aware of it only through summaries of it by its opponents.
I didn’t say one could; however, it is quite obvious that there are overall patterns of events that are wildly unlikely to have come about by chance. For example, the computer you type these messages on – that is wildly unlikely to have come about by chance. You and everyone else agrees that such a thing requires a mind, and that no amount of blind searching through probability space would produce a working computer. Would anyone waste his time trying to calculate the exact probability that a computer could arise by such a blind search? Do I need to actually do the computation before drawing the conclusion that computers did not arise in that way?
I don’t think Behe argues that all the paths are equally narrow. In fact, he thinks the paths to many evolutionary changes are quite wide, and he freely grants that Darwinian mechanisms can accomplish many evolutionary changes. But he doesn’t think they can accomplish as much as you think they can. And again, I am not going to argue here that Behe is right and you are wrong, no matter how many times you try to induce me to do so. I am going to stick to my plan, and merely insist that you characterize the arguments of Behe, Dembski, and other ID proponents accurately. If you characterize them accurately, and then indicate that you think their conclusions are wrong, you won’t get any argument from me. (Not because I would agree with you, but because I know that if Behe etc. could not convince you, there is no hope that I could, and it would be a waste of energy on my part.)
Actually, Behe, and @Agauger, both argued exactly this when they criticized the work by Nasvall et al. here. Of course, this was their approach to denying the obvious, that their ideas about the inaccessibility of evolutionary change to unguided processes are completely refuted.
Many in the ID camp absolutely quiver with excitement when they refer to the old work by Cairns and coworkers. IIRC, Spetner even wrote a book that claimed, in essence, that particular mutations are in fact guided by design. Maybe you’ve read it, @Eddie.
Fact is, a core tenet of ID theory is that design guides, creates specific mutations that are required for the unfolding of life as we know it.
I don’t think so. What you call “specification”, Dembski calls “fabrication”. He deals with the distinction on pp. 13-15 of The Design Inference, with specific reference to archers and bull’s eyes, and develops it at length on pp. 137 ff. If appears you have not read his discussion, and have imputed to him a view he explicitly rejects, i.e., that specification and fabrication are the same thing.
The distinction is clear. Dembski is using ‘specification’ to refer to generating information that improbably matches an existing template, and ‘fabrication’ to merely generating information and then saying it’s improbable.
Unfortunately for Dembski et al., they have no existing template for genetic information. Their discussion of ‘specification’ is a smokescreen to hide the fact that they don’t actually have a specification.
You should have written: They concede that improbable events happen all the time, and that mere improbability is not sufficient to establish design. That’s where the notion of specification comes in and they abandon genetic information completely and instead blather on about Mount Rushmore.
You could try to refute this by showing us where Dembski et al. obtained the independent specification for genetic information their argument requires - but that would require discussing evidence and you only deal in credentials and opinions.
It’s implicit in Doug Axe’s 2004 paper and in Ann Gauger’s attempt here to discount the fact that beta-lactamase activity is easy to find in an unimmunized immunoglobulin library.
It’s also implicit in their misuse of the term “fold,” as the beta-lactamase abzymes are, as their derivation makes obvious, one of the many examples of the immunoglobulin fold.
@Eddie (and @Giltil) are correct. I won’t answer for @T_aquaticus, but just note that, in my estimation, the entire ID community (including Dembski, in his later books) has jettisoned the distinction noted by @Eddie, to the point that every mention of “complex specified information” we see in the ID literature is actually a reference to “complex fabricated information”. To a person, ID proponents paint targets around arrows after the fact, ignoring the bajillions of targets already on the wall, and that the arrow has not landed squarely in any particular bullseye.
Malaria was a particularly blatant example of this–Behe misrepresented the actual data to make the targets appear to be few in number.
Another is @gpuccio’s “functional information,” in which he claimed that conservation between species is a proxy for information (it isn’t); his measurement of the false proxy was further removed from reality because it only assessed conservation between species based on reference sequences and failed to assess conservation within species–again, misrepresenting the actual data.
That’s why I keep asking for your ID explanation of the enormous polymorphism (so many targets that work) of the extraordinarily complex human cardiac beta-myosin heavy chain gene MYH7, and it’s why you are incapable of addressing my question.
Put in simple mathematical terms, they are claiming that the ratio of targets to sequence space is tiny, but they are (IMO deliberately) ignoring the vast numbers of obvious targets that exist.
To understand and/or address that, Bill, you’d actually have to make an effort to examine the evidence for yourself. MYH7 is a fine example for showing the folly of all of these.
What is needed for the LUCA hypothesis to be viable is for the target space to almost equal sequence space across all biology. Is this a realistic assumption given current observations?
If in a 30000 plus amino acid structure like the spliceosome there are not more than 10^28850 solutions to splicing introns its formation by random processes is very difficult to model.
This problem is easily explained by mutation. ID again is a method for detecting design in nature.
Including two numbers in an unsupported assertion is not math.
Please show your math.
It’s not a problem, Bill. It’s an observation. Why is there so much polymorphism?
HINT: you’d need to learn just how much polymorphism there is. Have you bothered?
There’s no hypothesis and no method, just a lot of rhetoric that pretends most of the data don’t exist and going further, deliberately misrepresenting inconvenient data.
The math I showed explains the issue. Have you done a feasibility study on the evolvability of the spliceosome beyond vague generalizations like gene duplication and mutation?
Is there so much? How many multiple mutation in individuals are there?