“Monkey Claims Copyright on Hamlet: Film at 11.”

DaveScot,

Length doesn’t equal complexity. For instance, there’s an amoeba that has 200 times more DNA than humans. It could be just a lot of meaningless repeats or it could be a library of all the basic genetic information required to create all the different phyla.

I think you are making too much of my side note. I know that some amoebas have more DNA than humans and I also know that length does not equal complexity. BUT: 1.) tandem repeats are often REQUIRED for a functional protein (and changes in number of repeats can be detrimental); 2.) although complex specified information in dystrophin is as of yet unknown (to me at least), we do know that there are large portions which are very specific to their current function. Bottom line: search space in genes > search space in Hamlet.

We really don’t know what makes proteins fold the way they do.

We may not know everything about folding, but we do know plenty about it -- enough to know there are sometimes very specific sequences needed in order to fold properly.

“I’m sure it would vary greatly depending on the protein in question.” Unpredictably variable?

Unpredictable based on what? The number of amino acids involved in binding sites varies from protein to protein. Perhaps I am missing your point here... Qualiatative

Qualiatative Length doesn't equal complexity. For instance, there's an amoeba that has 200 times more DNA than humans. It could be just a lot of meaningless repeats or it could be a library of all the basic genetic information required to create all the different phyla. We really don't know what makes proteins fold the way they do. It's quite possible they can endure quite a bit of random amino acid substitutions and still fold in the same manner. "I’m sure it would vary greatly depending on the protein in question." Unpredictably variable? DaveScot

DaveScot,

I can’t say I necessarily agree on the specificity.

I wasn’t using dystrophin as a case of great specificity (although it does have its share of it). The point to be made over dystrophin is its extremely long sequence. It makes Hamlet look short and simplistic.

It might be those 1000 mutations effect binding sites and a zillion other possible mutations don’t effect binding sites….and that doesn’t address the interdependency issue of complimentary binding sites in other enzymes.

You are right about binding sites being very important for proteins to function and therefore more prone to deleterious effects when the sequences coding them are mutated. But remember, there are non-binding sites that are incredibly important for the protein’s function as well (i.e. imperative protein folding and cysteines needed for disulfide bonds).

Has anyone done any studies that establish any kind of rule of thumb as to ratio of amino acid substitutions that do and do not effect binding sites? It could be the ratio varies so much between enzymes there’s no general rule of thumb

I’m sure it would vary greatly depending on the protein in question. Qualiatative

By gosh it is! 6.4711871009905565625207778257989e+4813 I stand corrected. I can't say I necessarily agree on the specificity. It might be those 1000 mutations effect binding sites and a zillion other possible mutations don't effect binding sites. Of course even a zillion is a small number compared to 6.4711871009905565625207778257989e+4813 ;-) and that doesn't address the interdependency issue of complimentary binding sites in other enzymes. Has anyone done any studies that establish any kind of rule of thumb as to ratio of amino acid substitutions that do and do not effect binding sites? It could be the ratio varies so much between enzymes there's no general rule of thumb... then again, mabye not. As often as evolutionists bring up the unknowns about protein search spaces and potentially large number of equivalents for any given protein you'd think someone would have characterized it better by now. DaveScot

DaveScot, 20^3700 = 6.5 * 10^4813 So, it would be on the order of 4813. :) Also, there are over 1,000 known mutations that cause noticeable abnormalities. At the very least, we know the current gene product is rather specific. But I agree with your comments. Qualiatative

Qualiatative "encodes a protein with ~3700 amino acids. An exhaustive search among the amino acid constituents would be on the order of 10^4813" I believe the correct number would be 20^3700. The question is indeed begged how many permutations would function with equivalent efficacy. That said you are certainly right that this is just one enzyme amongst a rather large number of interdependent enzymes. It's utterly absurd to postulate that these enzymes came into existence via the mechanism of randomly generated solutions in search of problems to solve. DaveScot

Natural selection isn't available to get the fist life forms going. So I think we're back to monkeys. avocationist

Wait 'til PETA hears about all these exploited, over-worked monkeys ... Jack Golan

SteveB, The point is that although humans need not be thrown together all at once, there are still large, specified proteins that require multiresidue participation and do not have an intermediately selectable product. Random mutation is not a tenable hypothesis for this kind of complexity. (I suggest reading the Snokes/Behe paper "Simulating evolution by gene duplication of protein features that require multiple amino acid residues" as well as Spetner's "Not By Chance".) P.S. On a side note, our genes are far more complicated (and, obviously, store much more information) than a mere novel like Hamlet. Consider the dystrophin gene. It is ~2,300,000 base pairs and ultimately encodes a protein with ~3700 amino acids. An exhaustive search among the amino acid constituents would be on the order of 10^4813. (This number disregards the complexities involved in protein manipulations in the secondary, tertiary, and quaternary structures.) I understand that there are other functionally isomorphic combinations of amino acids (although the order of an exhaustive search is still unfathomable); yet still, this gene serves as a reminder of some of the underlying complexities most people take for granted. Qualiatative

If this guy is representative of the trend, the ground that they’ve staked out is really pretty narrow. On the one hand, they reject random chance as a mechanism; on the other, they also reject explicit design. So, what they have left is basically a natural law that somehow expresses preferences, which really does seem like magic--hate to say it, but it does. The comparison of NS to something like thermodynamics (a comparison that the author I cited above made) would be valid if heat got transferred to the pan that I put on the stove UNLESS thermodynamics perceives a "competitive advantage" in not doing so, or UNLESS it could determine that the pan would somehow become less "fit" as a result. Of course, no one would ever claim that thermodynamics actually works this way, and yet that is exactly what we are expected to believe about NS. Am I missing something here? SteveB

SteveB, I think the issue is that the "selection preference" of Darwinism is drawn from the local environment and is not therefore an "independent" specification. The Monkey illustration holds in that it demonstrates the probability of a process arriving at an "independently" specified alignment. Irving

"a decision-making capacity in an impersonal natural law is untenable." You hit on the key issue right there. Attributing a cognitive decision making ability to this magical (yet purely natural) mechanism, is precisely where they lose me. It seems to me that they are ascribing to it capabilities that are completely unwarranted. They are making assumptions about how powerful NS is, despite the fact that such power has never been observed. Bombadill

I suppose many neodarwinist (ND) critics would respond by objecting to the validity of the typing monkeys by disagreeing with its key assumption: that macroevolution works according to random chance. As the monkey author says, "a monkey... will do so in a totally random manner..." A quick Google search produced a number of polemics in which ND advocates claim that ND doesn’t work according to chance; one in particular completely conceded the monkey author’s bottom-line point. He says, "Creationists find it inconceivable that pure chance could produce the order and complexity of life. This is absolutely true. Fortunately, evolution says nothing of the kind. This cannot be emphasized too strongly, so to repeat: EVOLUTION IS NOT CHANCE." (emphasis in the original, http://www.ebonmusings.org/evolution/evonotchance.html) He goes on to explain that evolution is capable of "selection," "preference" and the evaluation of "benefit"--essentially positing an anthropomorphic natural law: one that prefers one option to another and takes the "fitness" of the organism into account when doing so. He continues with the claim that this is analogous to gravity and heat transfer, even blithely remarking at one point, "that’s all there is to it." (Darn if I wasn't so stubborn in my recalcitrance; I could understand that "that's all there is to it too!") Anyway, because of this, it seems to me that the monkey illustration (or the tornado in the junkyard, or the pieces of the watch shaken in a box--all variations on the same theme) is a bit out of date--not that it doesn’t illustrate well the weaknesses of the random chance model, but rather that most evolutionists--like the one cited above--seem to have moved off of that particular indefensible parcel of ground. Thus, it seems that Darwin critics/ID advocates need to be able to demonstrate either that these defenders of Darwin are misrepresenting the theory by claiming that chance isn’t the key mechanism, or that the revision of the theory that attempts to house a decision-making capacity in an impersonal natural law is untenable. SteveB