It's quite possible that a good part of the code evolved with reversible interactions between "coding" nucleic acid, tRNA, and amino acids, with the t-RNA acting as a ribozyme to promote peptide bond formation.

The idea of t-RNA acting as a ribozyme has been repeatedly put forward, but mainly for self-aminoacylation.

Howver, even under the RNA World hypothesis, I don't think that such affinity was neither particularly "simple" nor ,more importantly, "at any step". At some turning point the proteins synthesized under control of the just-starting-to-evolve code began replacing ribozymes. Among these first "imperfect" proteins, there were aminoacyl-tRNA synthetases that played the crucial role in the final shaping of the genetic code. The operational code represented at first by anticodon/codon-like pairs in the acceptor stem of tRNAs began to coevolve with these synthetases and sorta ceased to "coincide" with the anticodons.

It's hard to know when these synthetases came into the picture relative to the development of the genetic code. It's quite possible that a good part of the code evolved with reversible interactions between "coding" nucleic acid, tRNA, and amino acids, with the t-RNA acting as a ribozyme to promote peptide bond formation. The next step might be formation of activated amino acids to make peptide bond formation more favorable, with covalent linkage of the amino acids to the tRNA being an even later elaboration.

The "chemical determinists" have on their side explicit experimental data that supports the hypothesis that the codon/anticodon-amino acid correspondence has a chemical basis.

Actually, the amino acids don't have a direct correspondence to nucleotide triplets on their own, but to larger binding structures that contain the triplets.

–Sorry for the sporadic shot gun posting, i'm on vacation.

Ah, but the relevant question is not how it works now, after millions of years of optimization by rapidly-evolving microorganisms, but how it might have worked in its primitive protolife form, which probably bore only slight resemblance to the modern form.

Howver, even under the RNA World hypothesis, I don't think that such affinity was neither particularly "simple" nor ,more importantly, "at any step". At some turning point the proteins synthesized under control of the just-starting-to-evolve code began replacing ribozymes. Among these first "imperfect" proteins, there were aminoacyl-tRNA synthetases that played the crucial role in the final shaping of the genetic code. The operational code represented at first by anticodon/codon-like pairs in the acceptor stem of tRNAs began to coevolve with these synthetases and sorta ceased to "coincide" with the anticodons.

Wrong again. The parts of myosin that do the walking are called the necks and heads, not legs.

Thats laughably irrelevant. What they use to walk can be viewed as legs (lever arm, head, etc). And they use a "pair" of these "legs" to "walk". Why did you say "wrong again", what did I get wrong before?

Smokey:

Are you getting the picture yet?

Yeah the picture is your just arguing for the sake of arguing, like most obsessed ID critics.

Smokey:

That's not what you wrote. You claimed that "the work itself simulates walking," when it does nothing of the sort. The work itself is a conformational change.

Your claim that "it does nothing of the sort" is simply not true. Actually, without the work itself there would be no walking, even under the brownian rachet model.

Smokey:

Funny, I always thought that the designers of the machines were doing the exploiting.

Yeh, and how do you think they do that?

Smokey:

How? Brownian motion doesn't blow other proteins away.

Myosin sticks to the actin filament so that it won't get blown away. How other machines do it is irrelevant to our discussion.

Smokey:

That's a good explanatory analogy, but you just made my point yet again, because ratchets aren't motors.

This particular logic is very much like a ratchet, but myosin itself is a motor.
Smokey:

What, exactly? Are you trying to claim that the cores of myosins, kinesins, and G proteins don't have the same structure?

But I thought you said the brownian ratchet model was the thing that helped you see that they have a common ancestor, not the similarity. Are you one of those guys that "forgets" what they said in their last post? If you want to say that the function that the G proteins do lead up to the myosin walking mechanism then please as a consequence of brownian motion itself, fully spell it out. Simply asserting it makes you as bad as your imaginary IDists in that you don't like tests. And there's that mysterious reference to a past occurance, how on earth did I make your point before? My point all along is that myosin is in fact a motor.

Smokey:

Nope, what they say is irrelevant. What matters are the data.

Both actually. I'd trust an interpretation of the data comming from the guy who actually worked on this stuff then a guy with a pseudonym who makes up stuff from thin air.

Smokey:

Then why does no one call G proteins motors, despite the fact that they harness the energy from hydrolysis of a nucleoside triphosphate to cause a conformational change by the same mechanism seen in myosins and kinesins?

Because they don't "move things". They function as molecular switches.

Smokey:

Who would "they" be, and who is the "senior biologist,"

Let me know when you figure it out.

Smokey:

This is why ID proponents produce no new data, Guts. We real scientists are always ready to abandon our analogies. You're stuck with one that you are afraid to test.

I test it above, I can actually measure the degree of similarity with that of human designed linear motors, in fact I've done this against your falsification criteria, which at first was "they don't spin". I tested this and found that many human motors don't spin either. Then it was "they don't walk", and whaddaya know, I found a human made motor that walks , and who knows whats next. Look, this isn't that hard. Get a piece of paper, write a line down the middle. Write A on one side of the line, and B on the other. Write "linear motor" on the A column and "myosin" on the B column. Then study each object and only write down the similarities. Feel free to use crayons if it helps.

You're creating a strawman. Detection and repair mechanisms do eliminate variation possibilites. That was the claim I made.

The spontaneous mutation rate (per bp per generation) can and has been directly measured (not inferred from sequence comparisons). It is on the order of 10^-6 or so. It may be lower in germ line cells, but it is definitely not zero, nor anywhere near zero.

Do the math, Bradford, and you'll find that trrll's claims are pretty reasonable. Repair and proofreading work to reduce an inherent error rate to these numbers, but the simple fact is that the rates of changes that "escape" correction mechanisms is easily enough to provide essentially unlimited variation in reasonably-sized populations of organisms.

Google/Pubmed search term for the day - "Big Blue mouse". Enjoy.

trrll: Also known as "reading." Yes, I am saying what I mean, not necessarily what you would like me to say. A limitation on the mutation rate is not a limit on the number of mutations that can accumulate in an organism, and hence is not an obstacle to evolution.

You're creating a strawman. Detection and repair mechanisms do eliminate variation possibilites. That was the claim I made.

You're parsing words.

Also known as "reading." Yes, I am saying what I mean, not necessarily what you would like me to say. A limitation on the mutation rate is not a limit on the number of mutations that can accumulate in an organism, and hence is not an obstacle to evolution.

Controlling the fidelity of replications entails eliminating genomic changes that would otherwise occur. The limitation is real.

The differences among species are consistent with observed mutation rates after all correction mechanisms.

The accumultation of small mutations can be slightly deleterious ones harmful to the fitness of an organism.

All kinds of mutations will occur. Correction mechanisms cannot in general distinguish between a favorable or unfavorable mutation. Indeed, whether a mutation is beneficial, deleterious, or neutral depends upon its context"”the context of the protein (i.e. what other mutations are present) as well as the context of the organism and the context of the organism's environment. A mutation may be neutral or harmful in one context and beneficial in another.

We could see corrected mutations experimentally. It could be very instructive.

Yes, this can be and has been done experimentally. There are known mutations that disable correction mechanisms, making it possible to see all mutations.

You're parsing words. Controlling the fidelity of replications entails eliminating genomic changes that would otherwise occur. The limitation is real. The accumultation of small mutations can be slightly deleterious ones harmful to the fitness of an organism.

Mutations must not only occur and must not only be beneficial they must avoid detection and neutralizing mechanisms. Omitting consideration of this last reality significantly impacts any objective analysis of outcomes.

We can't very well omit it. We never see the mutations that are corrected by these mechanisms, so they do not enter into our calculations of the mutation rate, which is high enough (even after all correction mechanisms) that virtually every living creature contains some unique mutations.

We could see corrected mutations experimentally. It could be very instructive.

I point out the existence of mechanisms that clearly do eliminate many variation possibilites that would otherwise occur and you now state the obvious namely, some mutations escape the detection and repair process.

I said that there is no limit to variation–i.e. there is no mechanism that measures the amount of variation and sets a maximum. That does not mean that organisms do not have mechanisms to control the fidelity of replication, simply that those mechanisms do not establish a limit to variation. Hence, you cannot appeal to some such imaginary "limit" to argue that large changes cannot occur through accumulation of small mutations.

Mutations must not only occur and must not only be beneficial they must avoid detection and neutralizing mechanisms. Omitting consideration of this last reality significantly impacts any objective analysis of outcomes.

We can't very well omit it. We never see the mutations that are corrected by these mechanisms, so they do not enter into our calculations of the mutation rate, which is high enough (even after all correction mechanisms) that virtually every living creature contains some unique mutations.