Re: Cascading vs. Specified Systems

On Feb 24, 8:22 am, Seanpit <seanpitnos...@naturalselection.
0catch.com> wrote:
On Feb 22, 3:01 pm, hersheyh <hershe...@xxxxxxxxx> wrote:



Of course, you are applying the typical creationist random assembly
notions.

The assembly must be random, by defintion.

No. Mutation is random. But *changing* a protein from a pre-existing
functional sequence to a different functional sequence is NOT random
assembly.

Yes, it is. There is no guiding force until the change is complete.
This change is completed by random mutation alone.

The word "random" is flashed around quite freely by creationists, but
the
mathematical usage of the term is always accompanied by a
characterization
of the function that describes the distribution of the events. In the
case
of pointwise mutations we would consider these to be a Poisson
process.
However, if we consider the duplication and/or modification of an
existing sequence, influenced by natural selection, then this is far
from the kind of
"random assembly" Poisson process that creationists would like it to
be.
This is the sort of thing that makes genetic algorithms useful.

The real question is how "target rich" the environment of genetics
and
are in terms of genetic sequences that do something, and do not
prevent
the organism from reproducing. Indeed, the real question is "How large
is the space of viable mutation targets, where a mutation target is
defined
as any viable organism?"




That's what the term
"random mutation" means. It isn't until the novel target is actually
found via random mutations that natural selection kicks in.

And the size of the gap (if any) needed to go from one functional
state to another that has some functional differences is idiosyncratic
and not mathematically definable. It most certainly is not correlated
with total size.

How do you know this? Do you have any observational or statistical
evidence? Can you demonstrate that your notion of the minimum
possible gap size of one exists anywhere for systems with higher-level
complexity - i.e., systems that require at least 1000aa at minimum and
are NOT based on the loss of some other system or interaction? (Don't
try your antibiotic resistance examples again. Those are about as low
level as you can get since they are based on loss, not gain, of a
system).

So what happens if we cascade a bunch of 1000aa limit changes?

1000aa is irrelevant. Total sequence size is irrelevant *unless* you
are claiming that the starting point is some *random* distance away
from the end point.

The 1000aa threshold is very relevant to your notion that the starting
point is always the minimum possible distance of one. That notion is
completely unsupported by the evidence. The evidence strongly
supports the hypothesis that this minimum possible distance becomes
less and less likely to be the true distance as one moves toward the
1000aa level of functional complexity.



I daresay, but isn't it obvious that the space of viable mutation
targets is
indeed large. If it were not we would have only genetically identical
organisms.
Yet, that is not what we see. Somehow, all of these millions of
species seem
to do just fine, and each of those millions differs genetically from
its fellow
organisms considerably.



No evolutionary model presumes that gap distance
is a function of total size *except* the strawman '747 in a tornado'
model that *you* used in calculating the "gap size" of cytochrome c.

No evolutionary model even considers what happens to the gap distances
at different levels of functional complexity. It isn't even discussed
in literature. There is no "model" at all really for evolutionary
progress beyond very low levels of functional complexity. You have no
real scientific theory to support your proposed mechanism beyond a lot
of hot air, bluster, and fairytale-style story telling.

You have no real scientific ground to criticise the mainstream view
on, either,
apparently.



That you have not even bothered to address what your math for "gap
size" in that example *really* represents (the total number of
effectively invariant aa sites if there were only invariant and fully
free to vary sites) is an example of the bankruptcy of your so-called
idea.

I've told you many times that the gap size does indeed represent the
effective number of invariant aa sites. Sure, in reality the vast
majority of sites are only partially invariant. However, one can use
an overall average to get a good idea as to the overall degree of
flexibility/specificity of system requirements for a particular
system.


I believe that I have told you that if you have a piece of science to
share
then publish it! I think that if you made a pact of honesty, you would
write
the paper, try to get it published. The reviewers comments would be
interesting
to read. Post the whole collection for everybody to see, and be done
with
it. It would be more interesting than the anti-science you currently
have on
your web site.


The total complexity/evolvability of the new system will not be
significantly greater than the largest individual part of the system
that requires a specific arrangement of all of its amino acid residues
- i.e., 1000aa.

Nonsense based on bogus _ad hoc_ assumptions.

This is not an assumption. It is a statistical fact if you care to
actually do a little math. The odds that all the parts of a cascading
system will exist in a particular pool of options is not significantly
less than the odds that the largest most specified single part will
exist in this pool.

You have never shown the math. Basically you are assuming that there
is only one target. This would be like assuming that the current state
of a
person's life were, in some sense, preordained, and you calculate the
odds
of that person having the life they have, given the number of choices
they
had along the way. It would be one of those 2^{number of choices} sort
of thing,
assuming all choices were binary.






For example, the odds of finding three specific 3aa sequences
somewhere in a pool of 3 million character genome, without any
specific relative arrangement between them, are not significantly less
than finding one specific 3aa sequence.

For another example, say that a system requires four different specfic
sequences with sizes as follows: 2aa, 2aa, 3aa, and 5aa. The odds
that all four will exist in a given genome are not much different
thant the odds that the specific 5aa will exist in the genome.

So, for all practical purposes, a cascading system that does not
require a specific 3D orientation of its parts with each other is not
significantly more "complex" or less evolvable than its most complex
single part.

You only invoke 'structure' when it suits you.

How is that? The end structure has always been the requirement for
evolution. As I've noted for you many times before, there is no
function without structure.

What is the most complex single part of a flagellum? Well, if a
"part" is defined as something that requires a specific 3D arrangement
of all its amino acid "characters", the entire system is defined as
one single part. That is why the flagellar system is far more
"complex" than a cascading system of equivalent overall size.

Yet even Behe can clearly see that the flagellar system is composed of
subsystems that have independent functionality. You can't according
to this.

I've pointed this fact out myself. All higher-level systems have
subsystems that could have independent functionality. This doesn't
remove the fact that some types of larger "emergent" system have a
significantly larger minimum structural 3D requirement. This is the
case for the flagellar motility system. It is not the case for
enzymatic cascades where there is no significantly larger structural
requirement that goes very far beyond that of the largest single part
in the cascading system.

A flagellar motility system apparently is a broken secretory system.


Sean Pitmanwww.DetectingDesign.com


-John

.

Relevant Pages

  • Re: "Reasonable Guesses"
    ... When is a target and starting point likely to be close enough together ... for RM/NS to actually work? ... the sequence complexity of proteins with a specific defined function. ...
    (talk.origins)
  • Re: Cascading vs. Specified Systems
    ... Modification of sequence is ... This change is completed by random mutation alone. ... the minimum *possible* gap size ... 1000aa level of functional complexity. ...
    (talk.origins)
  • Re: Crossing a Vast "Neutral Gap" in One Step
    ... >> caused by evolution? ... > of resistance are caused by a mutation that disrupts the ... But the point is that you say you have defined "functional" complexity ... >>>beneficial sequence neighbors is incorrect. ...
    (talk.origins)
  • Re: Pitman numerology
    ... complexity, the odds that *any* target will exist within the common ...  If you know anything about evolution, ... selectable" and thereby qualify as a "target" of NS. ... You just think there are more targets in sequence ...
    (talk.origins)
  • Re: Pitman numerology
    ... nucleotide mutation away from the "target", ... minimum sequence specificity requirement for a target, ... There are several problems I see with your macromutation idea. ...
    (talk.origins)