Re: Theory of the "Possible" = ToE

On Dec 1, 11:38 am, Seanpit <sean...@xxxxxxxxx> wrote:
On Dec 1, 8:54 am, Kermit <unrestrained_h...@xxxxxxxxxxx> wrote:

< snip >

All I have to do is show that there is a
different mechanism (one involving multiple intermediate gaps being
crossed) that could, in principle, produce the result.

This is a just-so story that could always be proposed without any need
for odds analysis at all.  Is it possible? - absolutely!  But, is such
a story likely?  That's the real question here.  You have no idea..  It
is very easy to simply dream up such stories.  It is quite another
thing to back them up with real science.

So, please establish how you determined the closest leap to this
hypothetical 1000aa gene.

How would you determine the most likely distance to the closest
potential target in sequence space?  You have to have at least some
statisitical idea or else all you really have are just-so stories
about what is possible without any consideration of what is likely.

We can see mutations happen. We know the mechanisms for most, if not
all of them.

*You're the one who tap-dances around the likelihood of small gaps;
nobody but *you suggests that a 1000aa gene must be made from scratch.

*You are the one who keeps insisting that a 1000aa sequence is so
improbable that it should be treated as impossible. Well, where do you
get that idea? You know that it has nothing to do with the apparent
processes of evolution.

That's not science.  That's pure fantasy.

Actually, it's observation and a proposed testable explanation.
When I google
evolution mathematics mutation
I get over 400,000 hits. Feel free to browse thru them; perhaps yuo'll
learn what you claim you want to know. I mean no offense, but I
suspect you don't really want the answer, or you'd be researching the
math of it, rather than asking random geeks like me on the internet.


I mean, wouldn't it be different for each
particular gene?

We are talking about the most likely distance to any potential target
in sequence space (at various levels of functional complexity)
starting from any given genome or gene pool of DNA sequence options.

Wait - you want the exact probability, but not for any specified gene?
How does that work?


Please pick one and show how you determined:
1. The closest leap to the 100+aa gene of your choosing, and how many
other precursors there might be within an acceptable range.
2. All possible pathways from that precursor to the existing end
result.
3. All possible useful mutations that could arise from that precursor.
Because of course NS is not teleological.

It is a likely ratio and distribution of potential targets vs. non-
targets in sequence space at various levels of functional complexity
(i.e., different size and specificity minimums).  Knowing this ratio,
the odds of a potential target being within a given distance are
determined by using a Poisson distribution calculation:

You don't know that ratio, however. You're kidding yourself if you
think you do. Pick a large gene, and tell me what the precursor was,
and how many pathways there might have been to all fo the possible
benficial results from, say, no more than three mutations (Lenski's
work show benefits from two mutations, separated over many thousands
of generations).

How could you possibly know all the potential results from a series of
three-or-less mutations from any given gene? And how could you tell
which of them might be beneficial (not to mention the potential
*environments, some which may favor a specific mutation, but not the
other environments?)

Tell me again why *I am obligated to give you hard numbers (snap to
it!) but you are not, except for a simple-minded and irrelevant piece
of work?


http://www.detectingdesign.com/flagellum.html#Calculation

If you have better estimate of such odds, please do let me know.  If
so, it will be a first from an evolutionist when it comes to
scientifically supporting the mechanism of the ToE.

Eh?
http://portal.acm.org/citation.cfm?id=565201
Abstract: "We introduce a model of DNA sequence evolution which can
account for biases in mutation rates that depend on the identity of
the neighboring bases. An analytic solution for this class of models
is developed by adopting well-known methods of nonlinear dynamics.
Results are presented for the CpG-methylation-deamination process
which dominates point substitutions in vertebrates. The dinucleotide
frequencies generated by the model (using empirically obtained
mutation rates) match the overall pattern observed in non-coding DNA.
A web-based tool has been constructed to compute single- and
dinucleotide frequencies for arbitrary neighbor-dependent mutation
rates. Also provided is the backward procedure to infer the mutation
rates using maximum likelihood analysis given the observed single- and
dinucleotide frequencies. Reasonable estimates of the mutation rates
can be obtained very efficiently, using generic non-coding DNA
sequences as input, after masking out long homonucleotide
subsequences. Our method is much more convenient and versatile to use
than the traditional method of deducing mutation rates by counting
mutation events in carefully chosen sequences. More generally, our
approach provides a more realistic but still tractable description of
non-coding genomic DNA, and may be used as a null model for various
sequence analysis applications."

That's just one from the first two pages of 40,000 pages of hits. That
was just *mathematical support. They're *all scientific.
Here's a few just on neutral drift, from the Wikipedia article:
# Gillespie, J. H (1991). The Causes of Molecular Evolution. Oxford
University Press, New York. ISBN 0-19-506883-1.
# Graur, D. and Li, W-H (2000). Fundamentals of Molecular Evolution,
2nd edition. Sinauer Associates. ISBN 0-87893-266-6.
# Kimura, M. (1968). "Evolutionary rate at the molecular level".
Nature 217: 624–626. doi:10.1038/217624a0. [1]
# Kimura, M. (1983). The Neutral Theory of Molecular Evolution.
Cambridge University Press, Cambridge. ISBN 0-521-23109-4.
# King, J.L. and Jukes, T.H (1969). "Non-Darwinian Evolution". Science
164: 788–798. doi:10.1126/science.164.3881.788. PMID 5767777. [2]
# Lewontin, R (1974). The Genetic Basis of Evolutionary Change.
Columbia University Press. ISBN 0-231-03392-3.
# Ohta, T (1973). "Slightly deleterious mutant substitutions in
evolution". Nature 246: 96–98. doi:10.1038/246096a0.
# Ohta, T (1992). "The nearly neutral theory of molecular evolution".
Annual Review of Ecology and Systematics 23: 263–286. doi:10.1146/
annurev.es.23.110192.001403.
# Ohta, T. (2002). "Near-neutrality in evolution of genes and gene
regulation". Proceedings of the National Academy of Sciences 99: 16134–
16137. doi:10.1073/pnas.252626899. PMID 12461171. Inaugural Article,
[3]
# Ohta, T. and Gillespie, J.H (1996). "Development of Neutral and
Nearly Neutral Theories". Theoretical Population Biology 49: 128–142.
doi:10.1006/tpbi.1996.0007.
# Sueoka, N. (1962). "On the genetic basis of variation and
heterogeneity of DNA base composition". PNAS USA 48: 582–592. doi:
10.1073/pnas.48.4.582. [4]
# Kimura, M. (1986). "DNA and the Neutral Theory". Philosophical
Transactions of the Royal Society of London. Series B, Biological
Sciences 312 (1154): 343–354. doi:10.1098/rstb.1986.0012.
# Provine W.B. Rise of the null selection hypothesis. In Cain A.J. and
Provine W.B. 1991. Genes and ecology in history. In Berry R.J. et al
(eds) Genes in ecology: the 33rd Symposium of the British Ecological
Society. Blackwell, Oxford, p15-23.
# Leigh E.G. (Jr) (2007). "Neutral theory: a historical perspective.".
Journal of Evolutionary Biology 20: 2075–2091. doi:10.1111/j.
1420-9101.2007.01410.x.

Cut it out with the nonsense "It's not science unless you do the
math." MAth is atool, and not the only one in science. And your math
is hogwash. It doesn't apply, so it's *worse than useless - it's a
lie.




That such a
process is much more probable and much more evidenced than the
mechanism you describe, which no one thinks is how evolution works, is
gravy.

LOL - Again, you use words like "probable" without using any odds
analysis whatsoever - amazing!  What is the actual probability of your
needed gap-filling steppingstones actually existing Howard?  Have any
real numbers to back up your baldly asserted just-so stories?  Any
real science?

I am reasonably able bodied. I walk along, decide to cross the street,
and see a puddle of water about 0.5 meters across. I decide to step
over it. Is it probably? Don't be silly - you can't decide that unless
you determine the exact probability. Perhaps you would be so kind as
to tell us how you would measure and weigh all probabilities in this
scenario, or how you function in the real world if you can't decide
whether or not to cross the street.

Science isn't based on determining "exact" probabilities.  You'd need
all possible information in the universe in order to be truly "exact"
with absolute perfection.

Agreed. And we can probably both agree that the more accurate the
math, the more useful it is, to varying degrees, depending on the
problem and what's being measured. And you would need far more
information than is available, and more computational potential than
is currently available, to calculate what you are asking for. We
don't know how many pathways are available, we can't know under what
circumstances a particular mutation would be advantageous, or how
likely those circumstances are... But we know it happens, and we know
how likely certain kinds of mutations are (seen from a chemical point
of view, not necessarily the phenotype expressed). We also know that
your scenario - 747 assembled by a tornado, also know as the 1000aa
gap - is not how it works.

That doesn't mean it's unlikely. My stepping over a medium sized
puddled may not be calculable precisely, but that doesn't mean it's
unlikely. If you want to claim that a 1000aa gap is especially
improbably, you'll have to do better than a strawman.

 That requirement would remove the need for
science itself.  What you do need, however, is a probability estimate
that carries with it at least some useful level of predictive value
over a random guess.  That's what science is all about - the
establishment of a theory on predictive value that never reaches
perfection and is always subject to potential falsification.

Sure, OK, when it's available. What it doesn't need is prevarication
and a description of a process which everyone in the field agrees
doesn't happen. A precise calculation of something which doesn't
happen is worse than ignorance. And there is plenty of math being done
in evolutionary science. Apparently neither of us are interested in
digging into it, but for rather different reasons.


< snip >

Kermit

Sean Pitmanwww.DetectingDesign.com

Kermit

.

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