Is this Hardy-Weinberg?

Yes.

When would there ever be an absence of selective pressures? What does the environment have to do with it, is the environment the only source of selective pressure?

The HWE applies to individual non-linked genes and the stasis of their frequencies, as well as for the stasis of large arrays of genetic elements or entire gene pools. For the case of us, H. sapiens, we're in a static equilibrium, with little or no natural selection - even frequencies of hereditary diseases are stable from one generation to the next in people.

For selective pressures, yes, the environment(s) in which a species exists provides selective pressures: forms of selection can include both survival (health, predatory evasion, finding food, etc.) and reproductive success (appeal to the opposite sex, parenting skills, etc.). Selection can be stabilizing, directional, or disruptive of individual traits of an organism. More info is available here.

Other evolutionists seem to think that genetic drift is a major component of evolution. Doesn't the effect of drift depend on the population size or effective population size?

Yes, genetic drift (e.g. the bottleneck and founder effects) depends to a large extent on population size. The smaller the population, the less negligible genetic drift becomes. Think of it like flipping a coin 10 times versus 1000 - the fewer the times you flip the coin, the more likely the number of times it lands on "heads" will deviate greatly from 50%.

…in the absense of selective pressures in a population's environment, the population's gene pool tends to maintain static gene frequencies.

Is this Hardy-Weinberg?

When would there ever be an absence of selective pressures? What does the environment have to do with it, is the environment the only source of selective pressure?

Other evolutionists seem to think that genetic drift is a major component of evolution. Doesn't the effect of drift depend on the population size or effective population size?

Krauze,
MG's response to the universal genetic code is fine for just that subset of data, but completely ignores the other aspects I mentioned, as you note…

Regarding the DNA replication machinery and the cell membrane architecture, yes, there are significant differences, but none of these features are completely alien to each other. This is moot though, since you say you accept common ancestry but your concerns lie with the origin of life.

Personally, I think there's a lot of intriguing guesswork going on out there as to the origin of life, but I think the reality has something to do with the hydrothermal vents and RNA World possibilities that are in vogue these days. In particular, the hydrothermal vents raise the possibility for transition-metal catalysts and thermal cycling (like PCR) to jump-start the first organic chemical replication processes. But that's just speculation of course. The possibility of inorganic bubbles or compartments preceding lipid bilayers seems to add strength to this view, also.

You end your initial response to me (on Thursday) by saying that you only accept common ancestry of eukaryotes though, based on common features throughout these more complex cells, yet maybe you don't accept common ancestry of eukaryotes and prokaryotes, despite their common features.

But common design, you say? Given that ID doesn't specify anything about the "design," this sounds fishy - highly arbitrary and speculative: anything is possible for an omnipotent deity, but making such claims throws falsifiability right out the window.

Mung has some further insights worth looking at:

It really looks to me like organisms are designed to not evolve…

Quite true. Such is the basis for Punctuated Equilibrium - in the absense of selective pressures in a population's environment, the population's gene pool tends to maintain static gene frequencies. Sure, genetic drift may occur in some rare instances, but not to any noteworthy extent. This is the basis for the field of population genetics, of course.

So I think the "buffering" of the genetic code against mutational effects (as well as proof-reading mechanisms) represent an attempt to have an accurate-yet-not-too-accurate replication of genetic material.

My point is that the MG article isn't so broad as "mutational effects" and seems to limit the "buffereing" of the code to "deleterious" mutations alone. Is a correction in order, or does it truly let beneficial mutations pass while blocking deleterious ones? What do MG's cited sources say?

I'm pointing out that MG seems to restrict the effectiveness of the code to deleterious mutations. What is the justification for this?

As Paul Davies points out in The Fifth Miracle, there is a limit, where too high a mutation rate makes it impossible for organisms to replicate all their vital functions without any crippling mutations. Being right at this threshold would present the best compromise between stability and adaptability to new challenges. Where the threshold is placed for each organism depends on the length of its genome. (If you need to faithfully replicate X nucleotides for your offspring to survive, you will need, at the very least, a process that fails less than one out of X times. The longer your genome becomes, the higher fidelity you'll need.) So, we should expect to see mutation rates correlate inversely with genome length. And that is just what we see: Bacteria have shorter genomes than eukaryotes, and they also have higher mutation rates. And viruses, which have even shorter genomes, also have even higher mutation rates.

So I think the "buffering" of the genetic code against mutational effects (as well as proof-reading mechanisms) represent an attempt to have an accurate-yet-not-too-accurate replication of genetic material.

Thanks for the correction. It was a while since I last looked at the paper, and I should have read it again before responding to Daniel.

An ID perspective on that observation is presented here.

Krauze,

I read Mike's essay and would like to ask about some things in it. The word "deleterious" appears a number of times in the essay, but never in any of the quoted text. Is this because the cited papers make no distinction between the type of mutation? How can the genetic code possibly be used to distinguish deleterious mutations from non-deleterious mutations? Do you think there would be a better way to state what it is that the code accomplishes wrt mutations than to say that it weeds out only (implied) deleterious ones?

But if the code functions to reduce mutations without regard to how they might help or harm the organism what does this say about a scenarion in which organisms are designed to evolve?

It really looks to me like organisms are designed to not evolve, unless the driving force of evolution is something other than nucleotide mutations.

The lipids from which the membranes are constructed, however, differ widely between bacteria and eukaryotes, leading Martin and Russel to conclude that the two groups acquired their membranes independently. ("On the origins of cells", 2003, Philosophical Transactions of the Royal Society of London, Biological Sciences 358(1429):59-83)

Actually, that study shows the lipids from which the membranes are constructed differ widely between bacteria and archaebacteria, those lipids probably arose independently. Eukaryotes and eubacteria have the same kind of lipids.

"Ok, back to the molecular and cellular homology argument then: simply put, the universal genetic code (UGC) is the standard centerpiece for arguing that there was a common origin for all life known to have existed on Earth."

An ID perspective on that observation is presented here.

As for the other traits you mention, if similarity of core processes is evidence for universal common descent, does that mean that fundamental dissimilarity of core processes counts as evidence against it?

By any stretch of the word, DNA replication is a core process. Yet the machinery that carries it out in bacteria and eukaryotes is so different that some researchers have suggested that "the modern-type system for double-stranded DNA replication likely evolved independently in the bacterial and archaeal/eukaryotic lineages." (Leipe, Aravind & Koonin, 1999, "Did DNA replication evolve twice independently?", Nucleic Acids Researc 27(17):3389-401)

The presence of a boundary separating inside from outside is characteristic of all independent life, and cell membranes must also be considered a core trait. The lipids from which the membranes are constructed, however, differ widely between bacteria and eukaryotes, leading Martin and Russel to conclude that the two groups acquired their membranes independently. ("On the origins of cells", 2003, Philosophical Transactions of the Royal Society of London, Biological Sciences 358(1429):59-83)

"That's fine. But again, Darwin's theory has been corrected and revised on a few occaisions in the past 150 years, in the details (so you're right there), but at every twist and turn, the roles of Descent With Modification, and Natural Selection have been resoundingly confirmed;"

I'm not questioning "Descent with Modification". I accept common descent in Darwin's agnostic sense, from "one or a few" lifeforms. What we're discussing is universal common descent, which demands the existence of a LUCA. Nor do I question natural selection and its important role in the evolution of life. My ID interests lie with the origin of life.

"not to mention the confirmation that many proteins from E. coli and S. cerevisiae have been shown to be interchangable with their mammalian counterparts, to demonstrate their functional homology and redundancy."

Given that I accept the common ancestry of eukaryotes, I have no problem with mammal-yeast homologies. As for the mammal-E. coli interchangeability, that's just an illustration of the similarity of their genes. This similarity could also be explained by common design, as laid out in Mike's essay, linked to above.

What kind of membrane did this entity possess?

Presumably the same sort that all of its descendants have, a lipid bilayer.