From: Josh Bembenek (jbembe@hotmail.com)
Date: Sat Aug 10 2002 - 16:24:54 EDT
{Josh}
> This is
> a tall order, hence the reason chapter 6 of Dawkins book speaks a lot
about
> luck and probabilities and miracles. (Chance happening of a
> self-replicating molecule that also has the capability to synthesize RNA
> sequences or a protein seems to be miraculous to me!) Regardless if the
> methinksitsaweasel analogy is goal oriented, the origin of life IS goal
> oriented.
{Lindsay}
No. You are confusing the goals of the observer - you - with the goals of
the participants - molecules. Molecules have no goal. Until Behe finds
something that can be dignified as evidence, there is no reason to beleive
that molecules were given a goal.
{Note} Semantics again! The fact is, that for things to develop de novo
without a creator by blind chance and miracle-like chance events,
requirements/goals/aims exist for the system and must occur before the
scenario is even possible. Regardless if they were initially GIVEN a goal
to complete, they must have COMPLETED that goal for life to have been
derived by purely materialistic naturalistic means. Therefore, they must
complete this goal regardless if anyone or anything gave them this goal-- it
is a requirement for the formation of life from blind chance. This argument
over semantics highlights the absence of evidence in this area to me (but
absence of evidence is not evidence of absence.....)
{Josh}
> It could not have gotten going even within Dawkins' explanation
> without first achieving the Goal of a self-replicating molecule. The
second
> goal involved in Dawkins' explanations is what I will call the Goal of
> Biological Functionality. My doubt and much of our previous discussion
is
> centered on this Goal of Functionality, so to get back to it......
{previous Lindsay comment}
> "There's also the issue that there can be multiple desirable outcomes.
The
> "adaptive landscape" can have multiple peaks. Just because one peak
(optima)
> was reached does not imply it's the only one."
{Josh response}
> ---Can you provide links to sources that give the evidence to support
this
> claim? From my understanding of structural biology, it seems highly
> improbable that multiple different (non-identical) protein sequences
could
> fold the same way and perform exactly the same function.
{Lindsay}
I didn't say they did.
{Josh}
> Thinking about hemoglobin, the probability for getting hemoglobin from
randomly assembling amino acids is, as Dawkins says, one chance in "1 with
190 noughts" after it > (without cumulative selection- with it, its pretty
much guaranteed as he argues it). Even given that there are multiple optima
in the protein sequence landscape within, for example, the globin fold
family for the binding and delivery of oxygen, say 1,000 (which seems
extremely generous to me,) you still arrive at 1 with 187 noughts after it
for obtaining a globin.
{Lindsay}
We've already talked about sequence dissimilarity. That means that there
are least 10^30 globins. Depending on definitions, possibly far far more.
Suggesting that there are 10^3 mostly says to me that you aren't paying
attention to your own statements. And the relative probability of
different sequences are not identical. Chemistry has consequences.
{Note} Unsupported claims revealing his bias and presuppositions.
Basically I see his numbers as unsupported claims that were not derived from
evidence provided in a peer-reviewed scientific journal. They are whimsical
speculations until they are published, by his own criteria established in
his criticism of Behe.
{Josh}
> Multiple outcomes seem to be a drop in the bucket if they do exist for
> minimizing the extraordinarily improbable odds. Additionally, each
> different protein fold requires a fundamental sequence structure that,
when
> absent, prevents the molecule from adopting that particular fold.
> Therefore, another interpretation of your statement is to hypothesize
that
> there are multiple protein folds (and thus novel families of protein
> sequences) within the sequence landscape that are capable of performing
> identical functions. If this is what you are intending to say, what
> evidence supports this idea?
{Lindsay}
No. There are only 20,000 possible domain folds, or perhaps 4,000, of
which 1865 have been found in the human genome. (See Nature 9nov00 p.13,
15feb01 p.847, 22mar01 p.417) Of course, some sequences don't fold, but
there's evidence about what fraction of random sequences have function:
see Nature 5apr01 p.715. Specifically, 1:10^11 sequences have the function
that that researcher searched for (which was binding to ATP). Given that
there are 10^13 Orbulina alive in the oceans, today, 10^11 is not a big
number. It's a small number.
{Note} This is an interesting observation, which I am still interested in
investigating. I haven't looked all this up yet. I have to correlate the
observations and interpretations he gives with those I make from the
protein-folding chapter later on.
{Lindsay}
When Creationists play these lots-of-zeroes games, I am mostly impressed
by how divorced their arguments are from (a) realistic scenarios and (b)
evidence.
{Lindsay}
> "In Flavobacter, a deletion mutation in junk DNA produces a functional
mylon
> digesting enzyme. The frame shift re-aligns functional groups. So,
> functional molecules have spontaneously come into existence, right in
front
> of our microscopes (as it were)."
{Josh}
> ---I would be interested in viewing this reference. The question I have
for
> this example is, what exactly is "Junk DNA?" How can we be sure that it
was simply junk and not functional in some way?
{Lindsay}
That's a large subject, and moving fast. I suggest a course.
{Josh}
> Is it possible that this was
> previously a gene that had been out of use due to mutation, and then with
> the appropriate frame-shift it is back in service? Even if we assume
that
> this was simply random junk sequence that never previously had any
function,
> it doesn't seem that we are getting far. Thinking about the possible
number
> of different sequences for a given molecule, "1 out of 1 with 190 noughts
> after it," frame shifting only increases our chances for any given
sequence
> by three.... three reading frames, three different possible proteins.
1/1
> with 190 noughts multiplied by three still doesn't appear to get us very
> far.
{Lindsay response in reference to what hemoglobin did before it was able to
bind oxygen}
> "It was doing something else. Not necessarily well, but well enough to be
> useful."
{Josh}
> ---Again, how do you support this conclusion? Any reference to published
> materials would be great.
{Lindsay}
I gave you some.
{Note} He doesn't fully understand the exact scope of this question I am
asking. His previous references do not address my main issue addressed
later.
{Josh}
> This is the essence of my problem. Why should
> hemoglobin evolve into a molecule that carries oxygen, when it started
out
> evolving into a role entirely different? What was this previous function
it
> had
{Lindsay}
I named it.
{Josh}
> and how can we ever observe it or more importantly, how can we ever
> prove/disprove your assertion?
{Lindsay}
By evidence like the evidence in the article?
You're going to have to learn some chemistry if you don't know the
relationships between different binding activities.
{Note} Again, my question is not exactly clear to him here. He never
actually provided anything which directly supports his statements. The
functions he named for the precursor hemoglobin molecule and the references
he gave do not address my question. Additionally, it is thought that the
molecules that he quotes as being precursors to hemoglobin are actually
modified derivatives of hemoglobin. In other words, in one of the reviews
he cited, hemoglobin comes first in evolution, then comes the molecules he
named (electron transport pathway proteins.) Finally, I believe he must
have made his remark about my knowledge of chemistry a little prematurely,
before he read the rest of my comments.
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