Re: Lack of evolution in computers and living things

On Jun 17, 3:00 pm, carlip-nos...@xxxxxxxxxxxxxxxxxxx wrote:
Seanpit <sean...@xxxxxxxxx> wrote:

[...]

The reason for this is due to the non-beneficial gap problem that
develops in a linear manner as one moves up the ladder of functional
complexity. Getting from one steppingstone to the next becomes harder
and harder because of a linear increase in the average distance
between potentially beneficial steppingstones at higher and higher
levels of functional complexity. This linear increase in the absolute
distance between steppingstones translates into an *exponential*
increase in the average number of mutational events of any kind needed
to cross the gap from a particular steppingstone function to the next
closest potentially beneficial steppingstone system in sequence
space.

Again with the "exponential"...

An uranium nucleus is exponentially unlikely to decay. Yet uranium
nuclei decay all the time. For your statement to mean anything,
you can't just say "exponential" -- you have to give give us the
time constant. Otherwise, this is just a stale rhetorical device.

Please do so, and tell us (in detail, or with references) how it was
measured.

What is the sequence space size for a 10aa protein? 20^10 - right?
What is the sequence space size for an 11aa protein? 20^11 - right?
etc . . .

So, it is clear that with each increase in the size requirement for a
protein-based system, the minimum sequence space size that it occupies
increases 20 fold. That's an absolute number. There's no argument at
this point. The question is, what is the increase in the absolute
number of potentially beneficial sequences that exists in the
potential of sequence space with each 20 fold increase in sequence
space size?

It is a fact that the vast majority of potential sequences in sequence
space would not be beneficial to a given organism in a given
environment. The number of potentially beneficial sequences
constitutes a tiny fraction of the total number of sequences in
sequence space. This tiny ratio of potentially beneficial vs. non-
beneficial only gets smaller with each step up the ladder since the
number of potentially beneficial sequences grows many fold less
rapidly than the total size sequence space grows (i.e., 20 fold with
each increase in the protein size). This exponential decrease in the
ratio of potentially beneficial vs. non-beneficial results in a linear
increase in the average distance between potentially beneficial
islands of sequences in sequence space.

Sure, there is a clustering effect that is known to exist in sequence
space where potentially beneficial sequences are clustered into
islands and groups of islands. However, this clustering effect becomes
less and less prominent at higher and higher levels of size and
specificity requirements - - to the point where the islands become
very remotely isolated well before the 1000aa threshold is reached.
The isolation of islands occurs in a linear manner with each 20 fold
increase in sequence space size. This linear increase in the minimum
distance between one potentially beneficial island at the next closest
island translates into an exponential increase in the number of random
mutations needed to bridge this gap.

For a visual illustration of this see the following:

http://www.pnas.org/content/vol103/issue38/images/large/zpq0370634700004.jpeg

This illustration is a projection of hyperdimensional sequence space
onto just three dimensions. It involves only small protein-based
systems of less than 370aa. Notice, however, that even at these low
levels of functional complexity that there is a clear increase in the
average distance between useful sequences that is linearly related to
the size of the system. Again, this linear increase in the distance
between potentially beneficial sequences results in an exponential
increase in the number of random mutations needed to cross the gap
between one and the next.

Your conclusion is? . . .

Steve Carlip

Sean Pitman
www.DetectingDesign.com

.

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