Re: The Relationship of Gaps to Thresholds

On Dec 6, 9:24 am, hersheyh <hershe...@xxxxxxxxx> wrote:
On Dec 5, 2:07 pm, Seanpit <seanpitnos...@xxxxxxxxxxxxxxxxxxxxxxxxxxx>
wrote:





On Dec 5, 7:23 am, hersheyh <hershe...@xxxxxxxxx> wrote:

The particular
question at hand in this particular thread concerns the proposed
evolutionary mechanism of random mutation and function-based
selection.

No. It is whether evolution works by a mechanism involving a
completely random walk

Your own proposed mechanism does indeed involve completely random
walks and/or random selections until a beneficial target is actually
realized.

in total sequence space

Random mutations can in fact traverse all of sequence space in a
single bound - from side to the other.

from some unspecified starting point

This is another one of your common lies. The starting point is
clearly specified. As you know, the starting point(s) constitute
anything that exists in the gene pool in question.

That is NOT what your math says. There is, of course, the very real
possibility that you do not have a clue as to what your math says and
so you think you can say "the starting point(s) constitute anything
that exists in the gene pool in question." But you math gives a gap
size (or average gap size) that says something else. So you have to
either give up on the math or on the claim that "the starting point(s)
constitute anything that exists in the gene pool in question."

See, you don't respond to these corrections. You just keep repeating
this same old misrepresentation no matter how many times I correct
you?

When someone who holds as many self-contradictory postions as you do,
it would be impossible not to have to choose either the math or your
verbiage. After all, you are the one that claims that what Yockey
really meant by his ratio is NOT cytochrome c sequences to total
sequence space, but beneficial to non-beneficial sequences.





that is somehow related to the size of the end result

The minimum structural threshold requirements of a target sequence do
indeed have a lot to do with how likely it is that it is remotely
"close" to anything that already exists in the gene pool.

to reach a teleologically determined end point.

Yet another deliberate strawman lie. As you very well know, the end
point or "target" is not teleological since any target with a given
minimum threshold requirement will do - and there are a great many
potentially beneficial targets for every threshold level as one
consider higher and higher rungs of this ladder of functional
complexity.

Again, no response to yet another correction of this same deliberate
misrepresentation? Where do you get off?

Again, that is NOT what your math says; it is only what your verbiage
says.





The math of the model
betrays its nature as nothing but a slight modification of the "747 in
a tornado" strawman argument that assumes proteins are assembled aa by
aa completely at random.

Your own theory suggests that each steppingstone in the pathway is
indeed discovered completely by random chance. The problem is that
these steppingstones do not stay close together at higher and higher
levels of minimum structural threshold requirements. The minimum
distance between the steppingstones that exist and those that might
exist grows with each additional threshold requirement until the odds
of finding another steppingstone at the next higher level drop to
essentially the same odds as a tornado producing a 747. These
extremely remote odds are reached before the threshold level of 1000aa
is reached.

The minor modification is the assumption
that only about a third of the aa's in a protein (see Sean's
calculation for a protein of 1000 aa's in his appendix) are assumed to
be absolutely fixed and generated by completely random assembly from,
effectively, scratch. That is what his 20^308 means.

You forget that not all residues need to be absolutely specified for
1e-400 to a reasonable estimate of the gap distance for a 1000aa
threshold. For example, Yockey calculated 1e-40 as the ratio for
100aa cytochrome c. This ratio is equivalent to 20^31. By your
logic, this would indicate that 31 of 100aa in CytoC are required to
be perfectly fixed to realize this function (i.e. 30%). That's not
true. Only a handful of residues are required to be absolutely
fixed. However, the reason why Yockey's ratio makes sense is because
most of the residue positions are limited to just a few different
amino acid options out of 20. Also, changing multiple positions at
the same time is even more limited.

Did you even understand this correction? If so, why not acknowledge
it?

Cytochrome c, as I pointed out, is not an "average" protein. Choosing
such a highly conserved protein is going to produce a biased result.
I will *repeat* my claim. Show me a 1000 aa protein (there aren't
many) that has 30% or more of its aa sites invariant over, say, 200
million years.





Beyond this little confusion, it really doesn't matter what ratio you
use. It is the pattern that is important - the pattern of exponential
decline of beneficial vs. non-beneficial with each increase in the
minimum structural threshold requirement.

The answer, of course, is that evolution does not work by that method.

You are confusing method with the nature of sequence/structure space.
They aren't the same thing.

Can this proposed mechanism actually do the job you
evolutionists claim it did? That's the only question under discussion
here.

And I agree with Sean. Evolution does not work
by the mechanism that Sean's model proposes.
But no one but Sean and creationists thought
it did. That mechanism is nothing but a
creationist strawman.

Again, the mechanism is random mutation and function-based selection.

Yes. That is the mechanism. It is NOT, however, the mechanism you
are proposing.

It most certainly is.

No it isn't.

The mechanism you are proposing is random change ONLY
from some random sequence until some keystone sequence is reached.

That's exactly right. According to your own proposed mechanism, ONLY
random changes of sequences/structures is in play until it happens
upon a beneficial sequence/structure. ONLY at this point does
function-based selection kick in. To argue otherwise is to
mischaracterize the proposed evolutionary mechanism of random mutation
and function-based selection. The "keystone" sequence you mention
represents a beneficial target sequence/structure - by the way.

And your working assumption is that the starting point is always
somewhere close to the maximal *functional* distance away, in that the
starting point is assumed to be *different* at each and every one of
the aa's you consider to be absolutely required for cytochrome c
function. Although you hand wave in the possiblity that the actual
number may be smaller by chance alone (hence the Poisson
distribution), you reject the idea that intermediates can be
functionally useful, at least in your MATH, if not your WORDS. That
is, you assume that the starting point for cytochrome c has absolutely
no function in common with cytochrome c. The starting protein does not
bind heme *at all*. It is as far away from the cytochrome c end
function as you can get in sequence space. Every single aa that is
crucial to cytochrome c function is assumed to be different from the
one required for that function. That is what your gap size
represents: the total number of sites which must be entirely specified
to have cytochrome c function. And then you assume that all the
intermediates between that starting protein can only be reached by
randomness *alone* because they have no selective utility. Selection
only comes into play when every single aa that is crucial to
cytochrome c function has the aa that allows a protein to have cyt c
function. All the other intermediates have NO FUNCTION at all. They
do not have the original function (which, by your math, is unrelated
to cytochrome c) and they don't have any level of cytochrome c
function. They are garbage random sequences. THAT is what the MATH
of your model says.







When that sequence is reached, your proposed mechanism ends.

Where did you get that idea from anything I've ever said? The
mechanism of random mutation and function-based selection never ends
as long as there is life and reproduction.

That's the mechanism. There is no argument here. The nature of
sequence space where the closeness of the closest potential target
doesn't significantly change with increasing structural threshold
requirements - that your notion.

No. My mechanism is that the 'random' part of searches *always*
involves searches that start from pre-existing *functional* sequences

That's right. I've never said otherwise.

But your MATH says that there is almost always a large functionless
gap between any starting ancestral function and the end derived
function. That is because you calculate the probability of a new
function occurring by assuming that the starting point is (at least on
average) a distance that involves a gap (number of aa's that need to
change to a *specific* single aa) that is 30% of the total size. That
assumes that the end product has absolutely no trace or any sequence
that would have functionalities at all relevant to new function. IOW,
you MATH assumes a starting point that has absolutely no pre-existing
sequences relevant to the end activity. That is, if one is talking
about say, evolving cytochrome c ...

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Sean, if you truly believe Hershey is a liar, why bother even
responding to him? Make him admit his lie and apologize before
wasting another key stroke on him. Until then, why not save his lies
and post them as a response every single time he replies to you. As
one of my scientist friends once said with respect to the fraud being
perpetrated in another area of science--you don't debate liars, you
expose them.

.

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