In the News: Experts debunk evolution

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Jason Spaceman

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Jul 18, 2006, 1:53:42 AM7/18/06
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From the article:
--------------------------------------------------------------------
7/14/2006 5:28:17 PM
Daily Journal

BY CHARITY GORDON

Daily Journal

STARKVILLE - "In the beginning God created the heavens and the earth,"
and 6,000 years later, according to a society at Mississippi State
University, scientists will gather to prove it.

The Society for the Advancement of Creation Science, whose purpose is
"to strengthen people's faith in the Creator and his Word," will hold
its first lecture series July 17-20 at Dorman Hall Auditorium on MSU's
campus. Worship starts at 6:30 each evening, and the lectures will
begin at 7:30 p.m. The event is open to the public.

Dr. John Sanford, who will present the July 17 lecture, is the primary
inventor of the gene gun process. His research has been used to
engineer most of the world's transgenic crops.

"My talk will be for non-specialists," Sanford said. "I will show that
evolutionary theory - mutation plus natural selection equals evolution
- can be conclusively shown to be false."
---------------------------------------------------------------------------

Read it at
http://www.djournal.com/pages/story.asp?ID=224002&pub=1&div=Lifestyles

J. Spaceman

Iain

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Jul 18, 2006, 9:06:23 AM7/18/06
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>Re: In the News: Experts debunk evolution

Ah well, never mind.

~Iain

Tiny Bulcher

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Jul 18, 2006, 9:15:37 AM7/18/06
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Jason Spaceman wrote:
> From the article:

> The Society for the Advancement of Creation Science, whose purpose is
> "to strengthen people's faith in the Creator and his Word,"

> Worship starts at 6:30 each evening,

Yeah, this has got absolutely nothing to do with religion. Pure
science.

--
Tiny

Kermit

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Jul 18, 2006, 11:37:21 AM7/18/06
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***************************************************************
A review of Sanford's book at
http://www.amazon.com/gp/product/1599190028/102-1025579-2822519?v=glance&n=283155
"This work is very typical of someone who wants to believe something --
in this case, that evolution could not possibly be the result of "blind
forces" -- and in order to support his belief, is both willing and able
to ignore contrary evidence sitting in front of his nose.

Unlike what both he and "the professor" says, the central premise of
the book (that mutations lead only to degeneration, never to
gain-of-function or "progress", unless some outside force intervenes to
guide things) is actually easily refuted, by anyone who knows what they
are talking about. The easiest path for gain-of-function mutations is
gene duplication; a gene, or part of a gene, is accidentally copied
more than once during sex cell formation. In the resulting organism, as
long as one gene retains its original function, any duplicate copies
can collect mutations -- and many of these mutations will indeed, by
blind chance, lead to novel proteins, with novel functions, and new
results for the organism. Such mutations have been well-documented in
literally hundreds, if not thousands, of papers.

Ironically, Sanford (actually a "Courtesy Associate Professor" at
Cornell's Horticultural Sciences department) ought to be especially
well acquainted with this process, since plants often end up with a
duplicate copy of significant portions of their entire genome to play
with (known as "polyploidy") and gain-of-function mutations from this
are also quite well known. Polyploidy is in fact one of the most common
methods of speciation in plants. And far from polyploidy only weakening
the organism, polyploidy has led to an increase of vigor, increased
pest resistance, increased resistance to environmental stresses, and
enhanced reproductive success in a number of well-documented cases in
plants from grasses to citrus. The fact that such gains can and do
*also* happen as the result of deliberate cultivation and breeding,
does not in any way diminish or negate the fact that they happen "by
accident" in the wild as well.

Despite this, Sanford argues that in nature, mutations only lead to
loss of fitness overall. In support of this thesis, he cherry-picks
data (taking the bits that he likes and ignoring the existence of the
rest, not a valid way of doing science), subtly distorts the
interpretation of real papers, and makes coherent and "logical"
arguments in ways that are appealing to a lay audience and whose
technical problems can only be spotted by people familiar with the
primary literature that he draws from. This is extraordinarily and
subtly deceptive.

I can only see this as the human ability to believe something based on
its emotional appeal regardless of the physical evidence available, a
fallacy that is all too common. What I don't know is whether he is
conscious of what he is doing here, and does so because he believes
that advancing the idea of an "intelligence" behind evolutionary
development is worth a bit of misrepresentation of data; or whether he
genuinely misses the evidence against him because it is not important
to him.

Either way, despite his work at Cornell this work is NOT a good
representation of the science of genetics, nor is it taken at all
seriously by others in the field. It is only a good representation of
the way Sanford thinks. That may not be a good thing to guide one's own
understanding by. If he can only support a thesis by deliberately
ignoring available information, then there is something wrong with that
thesis."
******************************************************************************************
>
>
> J. Spaceman
Kermit

Windy

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Jul 18, 2006, 11:51:13 AM7/18/06
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Jason Spaceman wrote:
> Dr. John Sanford, who will present the July 17 lecture, is the primary
> inventor of the gene gun process. His research has been used to
> engineer most of the world's transgenic crops.

He may have invented the gun, but the bullets come from evolution.

-- w.

Seanpit

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Jul 18, 2006, 11:56:50 AM7/18/06
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Not beyond very low levels of functional complexity . . .

Sean Pitman
www.DetectingDesign.com

Kermit

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Jul 18, 2006, 1:46:31 PM7/18/06
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Sure, for any single mutation. But these duplicated strings can
accumulate numerous mutations without handicapping the organism.

1. The benefits can accumulate.
2. The benefits can have duplicate functions - for example. feathers
can start off as insulation, then add functions of sexual display,
expanding visible size to discourage predators, and aid in flying (and
any chicken will tell you that half a wing is very useful).
3. A structure can drop intermediate uses if a later, additional usage
becomes more important. E.g. feathers which start as mere insulation
may adapt a stiff spine and ability to spread as a sexual display, then
be co-opted for flying, which becomes more important than display, and
those spreadable, stiff feathers now adapt for better flight. Looking
back, it might be difficult to imagine how fluffly down became stiff
flying feathers - if one arbitrarily dismisses additional uses, denies
dropping of functions, insists that the end product was the goal, etc.

>
> Sean Pitman
> www.DetectingDesign.com
>
<snip>
> > ******************************************************************************************
> > >
> > >
> > > J. Spaceman
> > Kermit
Kermit

Kermit

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Jul 18, 2006, 1:46:53 PM7/18/06
to

Sure, for any single mutation. But these duplicated strings can


accumulate numerous mutations without handicapping the organism.

1. The benefits can accumulate.
2. The benefits can have duplicate functions - for example. feathers
can start off as insulation, then add functions of sexual display,
expanding visible size to discourage predators, and aid in flying (and
any chicken will tell you that half a wing is very useful).
3. A structure can drop intermediate uses if a later, additional usage
becomes more important. E.g. feathers which start as mere insulation
may adapt a stiff spine and ability to spread as a sexual display, then
be co-opted for flying, which becomes more important than display, and
those spreadable, stiff feathers now adapt for better flight. Looking

back, it might be difficult to imagine how fluffy down became stiff

Seanpit

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Jul 18, 2006, 2:55:52 PM7/18/06
to

Kermit wrote:

> > > Unlike what both he and "the professor" says, the central premise of
> > > the book (that mutations lead only to degeneration, never to
> > > gain-of-function or "progress", unless some outside force intervenes to
> > > guide things) is actually easily refuted, by anyone who knows what they
> > > are talking about. The easiest path for gain-of-function mutations is
> > > gene duplication; a gene, or part of a gene, is accidentally copied
> > > more than once during sex cell formation. In the resulting organism, as
> > > long as one gene retains its original function, any duplicate copies
> > > can collect mutations -- and many of these mutations will indeed, by
> > > blind chance, lead to novel proteins, with novel functions, and new
> > > results for the organism. Such mutations have been well-documented in
> > > literally hundreds, if not thousands, of papers.
> >
>
> > Not beyond very low levels of functional complexity . . .
>
> Sure, for any single mutation. But these duplicated strings can
> accumulate numerous mutations without handicapping the organism.

Being able to accommodate a mutation without handicapping the organism
is a far different thing from gaining a novel beneficial function.
When it comes to higher levels of functional complexity, it just
doesn't happen regardless of the type or number of mutations that
occur. No function that requires a minimum of more than 3 to 4 fairly
specified Kb of genetic real estate ever evolves in reality - there is
not one example.

> 1. The benefits can accumulate.

The benefits cannot accumulate if they aren't found - and they are
never found by random mutations of any kind, combined with natural
selection, beyond very low levels of functional complexity.

> 2. The benefits can have duplicate functions - for example. feathers
> can start off as insulation, then add functions of sexual display,
> expanding visible size to discourage predators, and aid in flying (and
> any chicken will tell you that half a wing is very useful).

You don't seem to understand that even with the potential of duplicate
functions, it is exponentially harder and harder to find additional
functions at higher and higher levels of complexity. Beyond low
levels, it just doesn't happen - ever.

> 3. A structure can drop intermediate uses if a later, additional usage
> becomes more important.

That's true, if it ever found the additional usage to begin with. It
doesn't beyond very low levels of functional complexity - ever.

> E.g. feathers which start as mere insulation
> may adapt a stiff spine and ability to spread as a sexual display, then
> be co-opted for flying, which becomes more important than display, and
> those spreadable, stiff feathers now adapt for better flight. Looking
> back, it might be difficult to imagine how fluffly down became stiff
> flying feathers - if one arbitrarily dismisses additional uses, denies
> dropping of functions, insists that the end product was the goal, etc.

Very nice story telling - has nothing to do with reality. The cold hard
truth of the matter is that evolution just doesn't come up with any
novel functions beyond very low levels of functional complexity. It
just becomes exponentially harder and harder to find novel functions at
higher and higher levels. That is why evolutionary potential never gets
beyond the lowest rungs of the ladder this side of trillions upon
trillions of years of average time.

> Kermit

Sean Pitman
www.DetectingDesign.com

Richard Forrest

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Jul 18, 2006, 3:07:34 PM7/18/06
to

Seanpit wrote:
> Kermit wrote:
>
> > > > Unlike what both he and "the professor" says, the central premise of
> > > > the book (that mutations lead only to degeneration, never to
> > > > gain-of-function or "progress", unless some outside force intervenes to
> > > > guide things) is actually easily refuted, by anyone who knows what they
> > > > are talking about. The easiest path for gain-of-function mutations is
> > > > gene duplication; a gene, or part of a gene, is accidentally copied
> > > > more than once during sex cell formation. In the resulting organism, as
> > > > long as one gene retains its original function, any duplicate copies
> > > > can collect mutations -- and many of these mutations will indeed, by
> > > > blind chance, lead to novel proteins, with novel functions, and new
> > > > results for the organism. Such mutations have been well-documented in
> > > > literally hundreds, if not thousands, of papers.
> > >
> >
> > > Not beyond very low levels of functional complexity . . .
> >
> > Sure, for any single mutation. But these duplicated strings can
> > accumulate numerous mutations without handicapping the organism.
>
> Being able to accommodate a mutation without handicapping the organism
> is a far different thing from gaining a novel beneficial function.
> When it comes to higher levels of functional complexity, it just
> doesn't happen regardless of the type or number of mutations that
> occur.

And you base this assertion on what, exactly?

> No function that requires a minimum of more than 3 to 4 fairly
> specified Kb of genetic real estate ever evolves in reality - there is
> not one example.

And you know this because of your exhaustive knowledge of genetics, I
presume?

>
> > 1. The benefits can accumulate.
>
> The benefits cannot accumulate if they aren't found - and they are
> never found by random mutations of any kind, combined with natural
> selection, beyond very low levels of functional complexity.

Perhaps it would help us if you could provide us with a measure of
functional complexity?

What units do you use to measure "functional complexity"?
What level of "functional complexity" is "very low"?
What level of "functional complexity" is too high to be achieved by
natural selection, and on what basis have you determined this metric?

>
> > 2. The benefits can have duplicate functions - for example. feathers
> > can start off as insulation, then add functions of sexual display,
> > expanding visible size to discourage predators, and aid in flying (and
> > any chicken will tell you that half a wing is very useful).
>
> You don't seem to understand that even with the potential of duplicate
> functions, it is exponentially harder and harder to find additional
> functions at higher and higher levels of complexity.


What units do you use to measure "functional complexity"?
What level of "functional complexity" is too high to be achieved by
natural selection, and on what basis have you determined this metric?

> Beyond low
> levels, it just doesn't happen - ever.

And you base this assertion on .....?

>
> > 3. A structure can drop intermediate uses if a later, additional usage
> > becomes more important.
>
> That's true, if it ever found the additional usage to begin with. It
> doesn't beyond very low levels of functional complexity - ever.
>

And you base this assertion on ......?

> > E.g. feathers which start as mere insulation
> > may adapt a stiff spine and ability to spread as a sexual display, then
> > be co-opted for flying, which becomes more important than display, and
> > those spreadable, stiff feathers now adapt for better flight. Looking
> > back, it might be difficult to imagine how fluffly down became stiff
> > flying feathers - if one arbitrarily dismisses additional uses, denies
> > dropping of functions, insists that the end product was the goal, etc.
>
> Very nice story telling - has nothing to do with reality.

So how do you explain the fact that feathers are found in dinosaurs as
predicted by evolutionary theory, and that in some instances the type
of feather is the less developed form predicted by evolutionary theory.

Perhaps you can provide some alternative explanation which makes
predictions which ca be tested against the evidence?

> The cold hard
> truth of the matter is that evolution just doesn't come up with any
> novel functions beyond very low levels of functional complexity.

And we should believe this assertion because.........?

> It
> just becomes exponentially harder and harder to find novel functions at
> higher and higher levels.

And we should believe this assetion because.......?

> That is why evolutionary potential never gets
> beyond the lowest rungs of the ladder this side of trillions upon
> trillions of years of average time.

The idea of evolution as a ladder is very old, and has been completely
discarded by biologists for a long time.

By the way, what mathematical model of evolution have you used, and on
what basis have you calculated all the probabilities which lead you to
the conclusion that it would take "trillions upon trillions of years of
average time" to get beyond the "lowest rungs of the ladder"?

What is the difference between "average time" and ordinary time, by the
way?

Or is this another new Pitman invention?

RF

>
> > Kermit
>
> Sean Pitman
> www.DetectingDesign.com

Andrew Arensburger

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Jul 18, 2006, 4:34:53 PM7/18/06
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Kermit <unrestra...@hotmail.com> wrote:
> 2. The benefits can have duplicate functions - for example. feathers
> can start off as insulation, then add functions of sexual display,
> expanding visible size to discourage predators, and aid in flying (and
> any chicken will tell you that half a wing is very useful).

In other words, don't ask "what is this structure for?", but
rather "what can you do with this structure?"

--
Andrew Arensburger, Systems guy University of Maryland
arensb.no-...@umd.edu Office of Information Technology
"So... yeah." -- Eddie Izzard

Marc

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Jul 18, 2006, 8:07:38 PM7/18/06
to

Seanpit wrote:
> Kermit wrote:
>
> > > > Unlike what both he and "the professor" says, the central premise of
> > > > the book (that mutations lead only to degeneration, never to
> > > > gain-of-function or "progress", unless some outside force intervenes to
> > > > guide things) is actually easily refuted, by anyone who knows what they
> > > > are talking about. The easiest path for gain-of-function mutations is
> > > > gene duplication; a gene, or part of a gene, is accidentally copied
> > > > more than once during sex cell formation. In the resulting organism, as
> > > > long as one gene retains its original function, any duplicate copies
> > > > can collect mutations -- and many of these mutations will indeed, by
> > > > blind chance, lead to novel proteins, with novel functions, and new
> > > > results for the organism. Such mutations have been well-documented in
> > > > literally hundreds, if not thousands, of papers.
> > >
> >
> > > Not beyond very low levels of functional complexity . . .
> >
> > Sure, for any single mutation. But these duplicated strings can
> > accumulate numerous mutations without handicapping the organism.
>
> Being able to accommodate a mutation without handicapping the organism
> is a far different thing from gaining a novel beneficial function.
> When it comes to higher levels of functional complexity, it just
> doesn't happen regardless of the type or number of mutations that
> occur. No function that requires a minimum of more than 3 to 4 fairly
> specified Kb of genetic real estate ever evolves in reality - there is
> not one example.

Perhaps you should read more of the available literature.

See this paper by Liu et al. regarding exon shuffling:
"Significant expansion of exon-bordering protein domains during animal
proteome evolution" Nucleic Acids Res. 2005 Jan 7;33(1):95-105.
PMID: 15640447
http://www.pubmedcentral.gov/articlerender.fcgi?tool=pubmed&pubmedid=15640447
http://nar.oxfordjournals.org/cgi/content/full/33/1/95

Or this paper by Zhang, Dean, Brunet and Long:
"Evolving protein functional diversity in new genes of Drosophila"
Proc Natl Acad Sci U S A. 2004 Nov 16;101(46):16246-50.
PMID: 15534206
http://www.pubmedcentral.gov/articlerender.fcgi?tool=pubmed&pubmedid=15534206
http://www.pnas.org/cgi/content/full/101/46/16246

But, because there *is* a degree of controversy about some aspects
of evolution, you should also read this paper by Conant and Wagner:
"The rarity of gene shuffling in conserved genes"
Genome Biol. 2005;6(6):R50. PMID: 15960802
http://genomebiology.com/2005/6/6/R50
http://www.pubmedcentral.gov/articlerender.fcgi?tool=pubmed&pubmedid=15960802

There are some other papers strongly in support of exon shuffling
especially when you get into mammalian evolution (due to the
degree to which retroviral elements have become embedded in
the genomes - see for example the thread from a couple of weeks
ago about nashtOn's teddy bear - actually about Koala genomes
being under invasion by a retrovirus). I'll cite some more a bit
later when I'm at my office, but these ones are freely available.

Now it is your turn... back your arguments up with the literature.


(signed) marc


..

Frank J

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Jul 18, 2006, 8:49:12 PM7/18/06
to

Not so fast.

This is the "creationism" that ID claims not to be when it claims not
to be religious. Well, here's another chance for ID to back up its
claims by telling the world in no uncertain terms, what it's leaders
seem to know - that YEC is nonsense.

Don't hold your breath, though.
>
> --
> Tiny

Greg S

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Jul 18, 2006, 9:31:33 PM7/18/06
to

Sanford's book was on a list I saw an ID proponent provide for
'anti-evolutionary, non-theist perspectives'. His was the only name I
didn't recognise (Behe- check, Dembski- check). I was a little
disappointed to learn that Sanford became an evangelical after he
became an academic. I guess this guy had a different idea of 'nontheist
perspective' than I do. Sanford also lists his research interests as
something like 'exploring the limits of mutation + selection'. If he's
telling the churches that he's proved it's false I wonder why is he
still doing research?

Marc

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Jul 18, 2006, 10:01:27 PM7/18/06
to

Seanpit wrote:
> Kermit wrote:

........ snip

> > Unlike what both he and "the professor" says, the central premise of
> > the book (that mutations lead only to degeneration, never to
> > gain-of-function or "progress", unless some outside force intervenes to
> > guide things) is actually easily refuted, by anyone who knows what they
> > are talking about. The easiest path for gain-of-function mutations is
> > gene duplication; a gene, or part of a gene, is accidentally copied
> > more than once during sex cell formation. In the resulting organism, as
> > long as one gene retains its original function, any duplicate copies
> > can collect mutations -- and many of these mutations will indeed, by
> > blind chance, lead to novel proteins, with novel functions, and new
> > results for the organism. Such mutations have been well-documented in
> > literally hundreds, if not thousands, of papers.
>
> Not beyond very low levels of functional complexity . . .

........ snip

Beside the papers I've cited for you elsewhere in this thread, and
there are a *lot* more such papers in the literature (if you would
read more of the literature you would know this), there are some
very good review articles in the Annual Review series which you
need to get your hands on before you make more such ignorant
comments as the one above. Unfortunately the Annual Review
series are not freely available like the other papers I cited for you,
so you might need to visit a library or ask someone to forward
a copy to you, but you really should read the review from the
2005 Annual Review of Biochemistry by Orengo and Thornton

"Protein families and their evolution - a structural perspective"
Annu Rev Biochem. 2005;74:867-900. PMID: 15954844
http://arjournals.annualreviews.org/doi/abs/10.1146/annurev.biochem.74.082803.133029

There is a section in their review you should focus on, "How do
changes in domains and domain partnerships give rise to new
protein functions and biological processes?" not to mention
the section that follows: "How does the evolution of protein
families influence the complexity and evolution of organisms?"

If you have trouble getting your hands on this paper and are
willing to read it, then you can ask within this group for help
in getting a copy sent to you. You might consider browsing
the PLoS (Public Library of Science) web site as well, since
some recent papers there would provide the evidence you
feel is lacking, and those papers are freely available.

(signed) marc

.

John Harshman

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Jul 18, 2006, 10:23:08 PM7/18/06
to
Marc wrote:

There's another important paper in a recent issue of Evolution: S. R.
Proulx and P. C. Phillips. 2006. Allelic divergence precedes and
promotes gene duplication. Evolution 60:881-892.

The take-home message is that, based on simulations, divergent functions
are most likely to originate as allelic variation at a single locus,
with gene duplication offering the advantage of permanent
heterozygosity, so to speak.

Robert Maas, see http://tinyurl.com/uh3t

unread,
Jul 18, 2006, 11:57:26 PM7/18/06
to
> > any chicken will tell you that half a wing is very useful).
> In other words, don't ask "what is this structure for?", but
> rather "what can you do with this structure?"

Indeed, since nobody designed the structure, it just happened as a
result of a mutation, the first question is meaningless, the structure
isn't *for" anything.

The second question is much more useful. If the critter can use the
structure to survive better than its non-mutated brothers, then the
mutation is likely to persist, and the non-mutated genome is likely to
disappear.

As for chickens: They are too heavy to fly, so a full pair of wings
probably just gets in the way without providing any value, hence the
advantage of mutations to reduce them to half-wings. As for the value
in getting too heavy to fly in the first place, I'll leave that to
somebody else's speculation.

rupert....@gmail.com

unread,
Jul 19, 2006, 12:13:21 AM7/19/06
to

Seanpit wrote:
> Kermit wrote:
>
> > > > Unlike what both he and "the professor" says, the central premise of
> > > > the book (that mutations lead only to degeneration, never to
> > > > gain-of-function or "progress", unless some outside force intervenes to
> > > > guide things) is actually easily refuted, by anyone who knows what they
> > > > are talking about. The easiest path for gain-of-function mutations is
> > > > gene duplication; a gene, or part of a gene, is accidentally copied
> > > > more than once during sex cell formation. In the resulting organism, as
> > > > long as one gene retains its original function, any duplicate copies
> > > > can collect mutations -- and many of these mutations will indeed, by
> > > > blind chance, lead to novel proteins, with novel functions, and new
> > > > results for the organism. Such mutations have been well-documented in
> > > > literally hundreds, if not thousands, of papers.
> > >
> >
> > > Not beyond very low levels of functional complexity . . .
> >
> > Sure, for any single mutation. But these duplicated strings can
> > accumulate numerous mutations without handicapping the organism.
>
> Being able to accommodate a mutation without handicapping the organism
> is a far different thing from gaining a novel beneficial function.
> When it comes to higher levels of functional complexity, it just
> doesn't happen regardless of the type or number of mutations that
> occur. No function that requires a minimum of more than 3 to 4 fairly
> specified Kb of genetic real estate ever evolves in reality - there is
> not one example.

Presumably you concede that functions that require less than "3Kb of
genetic real estate" evolve? (if that's not what you mean then forgive
me but I don't understand what you just said)

Then what is the barrier? I would suggest that you have picked a number
that matches current observations, but you lack a theory that explains
why that number has the value it does. If ID theory predicts a value
for the maximum number of specified base pair mutations that can
happen, please cite it, or better yet give us a short explanation.

How did you come up with the trillions of years figure? Did you know
that some creationists believe that the universe is over one hundred
trillion years old?

>
> > Kermit
>
> Sean Pitman
> www.DetectingDesign.com

Marc

unread,
Jul 19, 2006, 2:11:53 AM7/19/06
to


Thanks for that. What I've read so far is quite interesting, but
I doubt Sean will either be interested or could understand it
even though it does provide a new role for sex.

I do enjoy the ease of access to such articles that the internet
provides (with appropriate library access). It's been ages since
I've actually gone to the library to photocopy something (apart
from a 1981 nature article to sort a quote-mine out for another
thread here).

(signed) marc

.

Von R. Smith

unread,
Jul 19, 2006, 10:45:04 AM7/19/06
to

Seanpit wrote:
> Kermit wrote:
>
> > > > Unlike what both he and "the professor" says, the central premise of
> > > > the book (that mutations lead only to degeneration, never to
> > > > gain-of-function or "progress", unless some outside force intervenes to
> > > > guide things) is actually easily refuted, by anyone who knows what they
> > > > are talking about. The easiest path for gain-of-function mutations is
> > > > gene duplication; a gene, or part of a gene, is accidentally copied
> > > > more than once during sex cell formation. In the resulting organism, as
> > > > long as one gene retains its original function, any duplicate copies
> > > > can collect mutations -- and many of these mutations will indeed, by
> > > > blind chance, lead to novel proteins, with novel functions, and new
> > > > results for the organism. Such mutations have been well-documented in
> > > > literally hundreds, if not thousands, of papers.
> > >
> >
> > > Not beyond very low levels of functional complexity . . .
> >
> > Sure, for any single mutation. But these duplicated strings can
> > accumulate numerous mutations without handicapping the organism.
>
> Being able to accommodate a mutation without handicapping the organism
> is a far different thing from gaining a novel beneficial function.
> When it comes to higher levels of functional complexity, it just
> doesn't happen regardless of the type or number of mutations that
> occur. No function that requires a minimum of more than 3 to 4 fairly
> specified Kb of genetic real estate ever evolves in reality - there is
> not one example.


How many base pairs of sequences coding for the 2,4-DNT pathway are
fairly specified, Sean? How did you arrive at that figure, and how
could somebody else verify it? I'm still waiting for an answer.

An appropriate, responsive answer will include a number relevant to the
2,4-DNT pathway, as well as a justification of that number. It will
not include trying to change the subject to how much more complex the
flagellum is than enzyme cascades.

sea...@gmail.com

unread,
Jul 19, 2006, 5:29:38 PM7/19/06
to

Perhaps you could show me a paper where a real-time example of
evolution is actually taking place beyond very low levels of functional
complexity? The papers you've listed here do not present experimental
evidence of real evolution in action. Rather, they are nothing more
than "just-so stories" about how the scientists think evolution
happened in the past. There are no papers dealing with real time
evolution, happening right now, that goes beyond very low levels of
functional complexity. This sort of evolution just doesn't happen.
Sequence comparisons and homologies can be equally explained by common
design. Evolution is not the only option to explain homologies or
nested hierarchies.

sea...@gmail.com

unread,
Jul 19, 2006, 5:35:30 PM7/19/06
to
Von R. Smith wrote:

> How many base pairs of sequences coding for the 2,4-DNT pathway are
> fairly specified, Sean? How did you arrive at that figure, and how
> could somebody else verify it? I'm still waiting for an answer.

Again, Von, enzymatic cascades are not highly specified, relatively
speaking, because they do not require 3D orientation in order to work
and enzymatic functions, in general, need not be very specific at each
step along the way in order to work to a useful degree. Compare this
with functions like pinocytosis or flagellar motility where a specific
3D orientation to all the parts is required and they all work together
at the same time. Such a system of function requires a much greater
degree of minimum size and specificity.

> An appropriate, responsive answer will include a number relevant to the
> 2,4-DNT pathway, as well as a justification of that number. It will
> not include trying to change the subject to how much more complex the
> flagellum is than enzyme cascades.

That's because you don't seem to grasp the concept that cascading
functions are much different than functions like flagellar motility.
This difference is very important to understanding the problem with
evolving high-level functions like flagellar motility.

Sean Pitman
www.DetectingDesign.com

Seanpit

unread,
Jul 19, 2006, 5:52:31 PM7/19/06
to

Yes, functions that require a fair degree of specificity, but
significantly less than 3kb of genetic real estate, can evolve via
random mutation and natural selection.

> Then what is the barrier? I would suggest that you have picked a number
> that matches current observations, but you lack a theory that explains
> why that number has the value it does. If ID theory predicts a value
> for the maximum number of specified base pair mutations that can
> happen, please cite it, or better yet give us a short explanation.

If you care to visit my website (www.DetectingDesign.com) I discuss the
reason for the limitation at this level in detail.

In short, each additional minimum size and/or specificity requirement
that a functional system has puts it into a category with relatively
few other sequences at that size (within the entire sequence space of
potential genetic sequences) that would also be beneficial within the
given gene pool. For example, how many potential 3-letter sequences
are there in the English language system? The answer is 17,576. But,
how many meaningful (do worry about "beneficial" for now) 3-letter
sequences are there? About 930 or so. This produces a ratio of
meaningful vs. non-meaningful of about 1 in 18. Now, what do you think
happens to this ratio when we move up to the 7-character level? The
ratio drops dramatically to about 1 in 250,000 - and we aren't even
talking "beneficial" yet.

With each step up the ladder of minimum size and/or specificity
requirements, this ratio drops off exponentially. What does this
dramatic drop in ratio do to the ability of random mutations, of any
kind, to find a new sequence with a novel as well as beneficial
function attacked to it? - from the perspective of a particular gene
pool? Well, it increases the average time involved to achieve success.
At higher and higher levels, this time to success starts to increase
exponentially as well.

Very quickly, trillions upon trillions of years are needed to achieve
success and evolutionary progress simply stalls out on the lowest rungs
of the ladder.

It doesn't matter what creationists believe. It matters what you
believe. How old do you think the Earth or the entire universe is? Do
you think that there is enough time for evolution to have happened if
relatively simple functions that require only 3 or 4 ka bp of genetic
real estate would take many trillions of years to evolve?

> > > Kermit

Sean Pitman
www.DetectingDesign.com

Seanpit

unread,
Jul 19, 2006, 5:57:45 PM7/19/06
to

Marc wrote:
> Seanpit wrote:
> > Kermit wrote:
>
> ........ snip
>
> > > Unlike what both he and "the professor" says, the central premise of
> > > the book (that mutations lead only to degeneration, never to
> > > gain-of-function or "progress", unless some outside force intervenes to
> > > guide things) is actually easily refuted, by anyone who knows what they
> > > are talking about. The easiest path for gain-of-function mutations is
> > > gene duplication; a gene, or part of a gene, is accidentally copied
> > > more than once during sex cell formation. In the resulting organism, as
> > > long as one gene retains its original function, any duplicate copies
> > > can collect mutations -- and many of these mutations will indeed, by
> > > blind chance, lead to novel proteins, with novel functions, and new
> > > results for the organism. Such mutations have been well-documented in
> > > literally hundreds, if not thousands, of papers.
> >
> > Not beyond very low levels of functional complexity . . .
>
> ........ snip
>
> Beside the papers I've cited for you elsewhere in this thread, and
> there are a *lot* more such papers in the literature (if you would
> read more of the literature you would know this), there are some
> very good review articles in the Annual Review series which you
> need to get your hands on before you make more such ignorant
> comments as the one above.

You need to know what the challenge is before you go off and list a
bunch of referneces that have nothing to do with my challenge. I'm not
asking for a list of reference detailing how evolution is thought to
have happened. I'm asking for references detailing real experimental
demonstration of evolution in real time. For example, Berry Hall
demonstrated evolution of the lactase function in real time using E.
coli bacteria. The only problem is, the lactase function requires a
fairly specified minimum size of no more than about 400aa (~1,200bp).
Do you have any such experiment that goes beyond this level of
functional complexity? All I need is one paper at a time. Give me
your best example, with a relevant quote from the referenced paper, and
we'll work with that first - ok?

Marc

unread,
Jul 19, 2006, 6:14:10 PM7/19/06
to

snex

unread,
Jul 19, 2006, 6:13:27 PM7/19/06
to

do you have the number of fairly specified base pairs for the 2,4-DNT
pathway or do you not? do you have a methodology that can yield such a
number or do you not?

Marc

unread,
Jul 19, 2006, 6:13:11 PM7/19/06
to


What is wrong with understanding evolution in general?
Since you don't, this sort of paper is important for you to read.

However, a recent issue of Nature had an article showing evolution
in action. In this case, it is an invasion of the koala genome by a
retrovirus, with implications for cancer, gene shuffling and so on.
http://www.nature.com/nature/journal/v442/n7098/abs/nature04841.html

Do *not* say that this is unrelated to us or to other species, since
this shows what was going on those hundreds of times that such
viral invasions occurred in ourselves and in other species, and if
you knew anything about biology, genetics and evolution you
would know that this has important repercussions. (But if you
knew the science-stuff, you wouldn't need this "show me it
happening in front of my eyes" type proof, would you?)

(signed) marc

..

Kermit

unread,
Jul 19, 2006, 6:51:57 PM7/19/06
to

Seanpit wrote:
> rupert....@gmail.com wrote:

<snip>


>
> In short, each additional minimum size and/or specificity requirement
> that a functional system has puts it into a category with relatively
> few other sequences at that size (within the entire sequence space of
> potential genetic sequences) that would also be beneficial within the
> given gene pool. For example, how many potential 3-letter sequences
> are there in the English language system? The answer is 17,576. But,
> how many meaningful (do worry about "beneficial" for now) 3-letter
> sequences are there? About 930 or so. This produces a ratio of
> meaningful vs. non-meaningful of about 1 in 18. Now, what do you think
> happens to this ratio when we move up to the 7-character level? The
> ratio drops dramatically to about 1 in 250,000 - and we aren't even
> talking "beneficial" yet.

Ooh! Word games; good. I don't know much about genetics - I haven't
trained in it.

How about if we assemble randomly chosen 4-letter words with randomly
chosen 3-letter prefixes? What's the ration then? What if we just add
"S" to the end of the entries in your seven-letter word list - will we
get many real words?

You seem to talking about assembling these long strings of genetic code
from scratch; but surely you're not. That would be silly.

>
> With each step up the ladder of minimum size and/or specificity
> requirements, this ratio drops off exponentially.

I never really have understood this claim of yours. If we're modifying
what came before, why is the modification necessarily so complicated? A
single point mutaion is a single change, not all of the thousand of
base pairs that may be associated with it.

> What does this
> dramatic drop in ratio do to the ability of random mutations, of any
> kind, to find a new sequence with a novel as well as beneficial
> function attacked to it? - from the perspective of a particular gene
> pool?

How novel do you think average cnages are from generation to
generation?

Are you saying that God's intervention was necessary to help e. coli
putt around like a motor boat, but natural selection and random
mutation was sufficient to produce us from a chimpier ancestor?

> Well, it increases the average time involved to achieve success.
> At higher and higher levels, this time to success starts to increase
> exponentially as well.

Good thing nature doesn't have to start from scratch each time, then.

We'd have never gotten to escheria coli, I think.

>
> Very quickly, trillions upon trillions of years are needed to achieve
> success and evolutionary progress simply stalls out on the lowest rungs
> of the ladder.

How, exactly, do you climb ladders? I take 'em one rung at a time. I
think you believe that you need to leap from the floor to scale each
succeeding rung. That's really not the easiest way to do it.

I think you don't understand the concept of "adaption". And I think
that you have found a way to baffle with bullshit, but I notice that
the geneticists and mathemticians are not impressed. When you do talk
about something I know a little about, I am *way not impressed.

Explain why 300,000 or so generations between us and the common
ancestor with chimps needed anything other than NS and the variety
available from mutation. Why does the change from me to my daughter
require these humongous numbers of yours? At what point were these
unlikly odds necessary if we work back 7,000,000 years?

>
> > > > Kermit
>
> Sean Pitman
> www.DetectingDesign.com

Kermit

Kermit

unread,
Jul 19, 2006, 7:01:38 PM7/19/06
to

City kid, huh? Many chickens can fly. Not like a sparrow, but roosting
in trees or flying over fences is not uncommon. Some farmers clip the
wings of their chickens to minimize that. Their recent ancestors easily
flew short distances, like a pheasant or guinea hen. They wouldn't be
migrators, but their "half-wings" would give them a serious advantage
when escaping from predators.

Kermit

Seanpit

unread,
Jul 19, 2006, 7:05:26 PM7/19/06
to

A cascading system is no more functionally complex than the most
complex single link in its chain. So, pick the most complex single
enzyme in this cascade and find the shortest possible genetic sequence
that can code for that type of functional enzyme - and you have your
answer.

Sean Pitman
www.DetectingDesign.com

snex

unread,
Jul 19, 2006, 7:11:31 PM7/19/06
to

without the other less complex enzymes, the cascade is not complete.
the cascading system is the system under examination. you still have
neither supplied the number of fairly specified base pairs or any
method to determine that number.

>
> Sean Pitman
> www.DetectingDesign.com

Seanpit

unread,
Jul 19, 2006, 7:35:27 PM7/19/06
to

Kermit wrote:
> Seanpit wrote:
> > rupert....@gmail.com wrote:
>
> <snip>
> >
> > In short, each additional minimum size and/or specificity requirement
> > that a functional system has puts it into a category with relatively
> > few other sequences at that size (within the entire sequence space of
> > potential genetic sequences) that would also be beneficial within the
> > given gene pool. For example, how many potential 3-letter sequences
> > are there in the English language system? The answer is 17,576. But,
> > how many meaningful (do worry about "beneficial" for now) 3-letter
> > sequences are there? About 930 or so. This produces a ratio of
> > meaningful vs. non-meaningful of about 1 in 18. Now, what do you think
> > happens to this ratio when we move up to the 7-character level? The
> > ratio drops dramatically to about 1 in 250,000 - and we aren't even
> > talking "beneficial" yet.
>
> Ooh! Word games; good. I don't know much about genetics - I haven't
> trained in it.

Yet you feel yourself well able to explain genetic evolution to others?

> How about if we assemble randomly chosen 4-letter words with randomly
> chosen 3-letter prefixes? What's the ration then? What if we just add
> "S" to the end of the entries in your seven-letter word list - will we
> get many real words?

If you have a bunch of 4-letter words how would you go about getting
only 3-letter prefixes attached to the right spot on these words?
Random multi-character mutations don't know what is or isn't a prefix
and they don't know that prefixes are supposed to only get stuck onto
the beginning of your 4-letter words. Random mutations may randomly
snip out 1 or 2 or 3 or 4 or . . . characters from one place and insert
them randomly into another place within the genome. But, what are the
odds that the snippet, once inserted, will create a novel beneficial
sequence?

A series of single point mutations is analogous to a random walk
through sequence space while multicharacter mutations are analogous to
random jumps or random selections within sequence space - from a given
beneficial starting point. As it turns out, the odds that a random
walk will hit a novel beneficial sequence within sequence space is
about the same as the odds that random selection will land on a
beneficial sequence in sequence space. So, multicharacter mutations
really don't solve the time gap problem for finding novel beneficial
sequences in a level of sequence space where they are very rare.

> You seem to talking about assembling these long strings of genetic code
> from scratch; but surely you're not. That would be silly.

Not true. You can start at whatever beneficial starting point you want
and use a very large pre-established gene pool of options to begin
with. It won't help beyond very low levels of functional complexity.

> > With each step up the ladder of minimum size and/or specificity
> > requirements, this ratio drops off exponentially.
>
> I never really have understood this claim of yours. If we're modifying
> what came before, why is the modification necessarily so complicated? A
> single point mutaion is a single change, not all of the thousand of
> base pairs that may be associated with it.

Yes, and what are the odds that the single change of a single point
mutation will hit upon a novel beneficial genetic sequence? The answer
is that it depends upon the density of beneficial sequences at a given
level of functional complexity. The less the density, the less the
odds of success. And this is true for both single point mutations as
well as multi-character mutations (insertions, deletions,
translocations etc).

> > What does this
> > dramatic drop in ratio do to the ability of random mutations, of any
> > kind, to find a new sequence with a novel as well as beneficial
> > function attacked to it? - from the perspective of a particular gene
> > pool?
>
> How novel do you think average cnages are from generation to
> generation?

If a novel beneficial function is not found from generation to
generation, then nature cannot select to keep a mutated sequence. It
will either be lost from the gene pool over time, or will, at best,
continue its random walk in a blind search for a novel beneficial
sequence.

> Are you saying that God's intervention was necessary to help e. coli
> putt around like a motor boat, but natural selection and random
> mutation was sufficient to produce us from a chimpier ancestor?

Most certainly a highly intelligent designer was necessary to produce a
functional bacterial flagellar motility system. That's exactly what
I'm saying. As far as humans and chimps go, we simply don't know
enough about the genetics of our functional differences to be able to
tell if there is definitely an uncrossable gap between us. I
personally do not believe humans share a common ancestor with apes, but
I cannot base this belief on genetic evidence at this time.

> > Well, it increases the average time involved to achieve success.
> > At higher and higher levels, this time to success starts to increase
> > exponentially as well.
>
> Good thing nature doesn't have to start from scratch each time, then.

It doesn't matter where nature starts. It cannot evolve novel
functions beyond very low levels of complexity - novel functions that
were not already in the gene pool to begin with.

> We'd have never gotten to escheria coli, I think.

Well, we'd at least never gotten to certain functions that E. coli have
- that's for darn sure.

> > Very quickly, trillions upon trillions of years are needed to achieve
> > success and evolutionary progress simply stalls out on the lowest rungs
> > of the ladder.
>
> How, exactly, do you climb ladders? I take 'em one rung at a time. I
> think you believe that you need to leap from the floor to scale each
> succeeding rung. That's really not the easiest way to do it.

No. Each rung takes exponentially greater amounts of time to achieve
from the rung below. I'm not talking about jumping from the ground
each time. I'm talking about jumping from the rung below each time.
It is like a staircase where each step gets higher and higher than the
last - exponentially higher. Pretty soon, you are simply not able to
take the next step no matter how long you try to jump for it.

Then explain it to me yourself - if you know so much about how it is
supposed to work. You are just trusting that someone else must know
how it works even though you yourself have no clue? Is that it?

> Explain why 300,000 or so generations between us and the common
> ancestor with chimps needed anything other than NS and the variety
> available from mutation.

Again, we don't know nearly as much about the functional differences
between us and chimps as we know about more simple systems like those
that bacteria or single cells use, like systems of flagellar motility
or pinocytosis (cell drinking), or HIV docking, or transcription and
translation, etc. If you talk about a specific function that we humans
actually know a fair bit about, then it is much easier to tell if that
function could or could not have evolved.

> Why does the change from me to my daughter
> require these humongous numbers of yours?

You need to read about Mendelian genetics a bit. The differences
between you and your daughter or you and a son that you might have are
not the result of the evolution of anything new within your gene pool
at all. The potential for these differences was already there -
preprogrammed into the genetics of you and your wife. Mendelian
variation/genetic recombination, allows you and your wife to literally
be able to produce an almost infinite variety of children (trillions
upon trillions of different children). Yet, no new function is involved
that either your or your wife didn't already have. In other words,
mutations are not needed to produce this variety.

> At what point were these
> unlikly odds necessary if we work back 7,000,000 years?

Mendelian variation is not the same thing as Darwinian-style evolution.
Read up on it a bit. It is very interesting. I personally think that
if Mendelian genetics had become widely known before Darwin came along,
the Theory of Evolution would have had a much harder time getting off
the ground. Why? Because all of Darwin's examples of evolution in
action can all be explained now as nothing more than Mendelian
variation.

> Kermit

Sean Pitman
www.DetectingDesign.com

Seanpit

unread,
Jul 19, 2006, 7:38:08 PM7/19/06
to

A cascade doesn't have to be complete in order for each step in the
cascade to be useful. Beyond this, none of the parts of an enzymatic
cascade require specific 3D orientation with the other parts.

> > Sean Pitman
> > www.DetectingDesign.com

Desertphile

unread,
Jul 19, 2006, 7:44:19 PM7/19/06
to
Jason Spaceman wrote:

> From the article:
> --------------------------------------------------------------------
> 7/14/2006 5:28:17 PM
> Daily Journal
>
> BY CHARITY GORDON
>
> Daily Journal
>
> STARKVILLE - "In the beginning God created the heavens and the earth,"
> and 6,000 years later, according to a society at Mississippi State
> University, scientists will gather to prove it.
>
> The Society for the Advancement of Creation Science, whose purpose is
> "to strengthen people's faith in the Creator and his Word," will hold
> its first lecture series July 17-20 at Dorman Hall Auditorium on MSU's
> campus. Worship starts at 6:30 each evening, and the lectures will
> begin at 7:30 p.m. The event is open to the public.
>
> Dr. John Sanford, who will present the July 17 lecture, is the primary
> inventor of the gene gun process. His research has been used to
> engineer most of the world's transgenic crops.
>
> "My talk will be for non-specialists," Sanford said. "I will show that
> evolutionary theory - mutation plus natural selection equals evolution
> - can be conclusively shown to be false."


If he can do so, I very much hope he does so. Imagine the world-wide
amazement, accolades, and applause he will receive when he shows
evolutionary theory is false.

I brethlessly await the hundreds of front-page headlines regarding this
amazing accomplishment.

Seanpit

unread,
Jul 19, 2006, 7:43:22 PM7/19/06
to

I don't have access to the full article. Please quote the relevant
portion of the article describing the real-time evolution of the novel
function. If the function is nothing more than a virus being able to
gain entrance into a cell via some sort of template matching, then this
is very low-level evolution. It is not the type of evolution that
would explain the creation of a functional system like flagellar
motility.

> (signed) marc

Sean Pitman
www.DetectingDesign.com

snex

unread,
Jul 19, 2006, 7:48:52 PM7/19/06
to

irrelevant.

> Beyond this, none of the parts of an enzymatic
> cascade require specific 3D orientation with the other parts.

then factor this into your equations - you know, the ones you are being
asked for.

>
> > > Sean Pitman
> > > www.DetectingDesign.com

Seanpit

unread,
Jul 19, 2006, 7:50:11 PM7/19/06
to

I understand evolution in general just fine. I am fully aware of how
evolution is supposed to work and have read many of these just so
stories about how various functions are supposed to have evolved. I've
yet to read about a real-time demonstration to back up even one of
these just-so proclamations beyond very low levels of functional
complexity.

> However, a recent issue of Nature had an article showing evolution


> in action. In this case, it is an invasion of the koala genome by a
> retrovirus, with implications for cancer, gene shuffling and so on.
> http://www.nature.com/nature/journal/v442/n7098/abs/nature04841.html

Please quote the relevant portion of this paper detailing the novel
function that evolved in this case. Some novel functions, especially
those that given rise to cancer and the like via viral involvement, are
the result of a deregulation or loss of what was there before. Almost
no cancer arises as the result of the creation of a truly novel
function. Cancer is almost always the result of a loss of regulation
or an imbalance in functional systems that are already there.

> Do *not* say that this is unrelated to us or to other species, since
> this shows what was going on those hundreds of times that such
> viral invasions occurred in ourselves and in other species, and if
> you knew anything about biology, genetics and evolution you
> would know that this has important repercussions. (But if you
> knew the science-stuff, you wouldn't need this "show me it
> happening in front of my eyes" type proof, would you?)

If you can show a novel function evolving in any species or even
computer program that goes beyond very low levels of functional
complexity, I'll become an evolutionist. So far, all I've seen are
thousands upon thousands of these just-so stories you've listed here.

Seanpit

unread,
Jul 19, 2006, 8:14:56 PM7/19/06
to

This point is not at all irrelevant. It is very relevant indeed since
the whole question is about how long it would take to gain the next
beneficial steppingstone along a evolutionary pathway.

> > Beyond this, none of the parts of an enzymatic
> > cascade require specific 3D orientation with the other parts.
>
> then factor this into your equations - you know, the ones you are being
> asked for.

Like I said, cascading systems are no more complex than their most
complex single part.

> > > > Sean Pitman
> > > > www.DetectingDesign.com

snex

unread,
Jul 19, 2006, 8:25:50 PM7/19/06
to

i am not interested in your assertions. provide the numbers and how you
arrived at them or stop maintaining you have the authority to
pontificate on these matters.

>
> > > > > Sean Pitman
> > > > > www.DetectingDesign.com

wf3h

unread,
Jul 19, 2006, 9:41:17 PM7/19/06
to

Seanpit wrote:
>
> I understand evolution in general just fine. I am fully aware of how
> evolution is supposed to work and have read many of these just so
> stories about how various functions are supposed to have evolved. I've
> yet to read about a real-time demonstration to back up even one of
> these just-so proclamations beyond very low levels of functional
> complexity.

as a scientist who is objective, since i'm not an evolutionary
biologist, i find seanpit's argument unconvincing

evolution has been demonstrated in the lab. the long timeframes
necessary for evolution of species can't be demonstrated in the lab
because of the reason already stated: it takes a long time. BUT
evolutionary bio is an EXPERIMENTAL science

christianism/islamism, however, is not. the 'just so stories' of
religion are being played out today across the world in death,
slaughter, genocide and destruction. seanpit's world is a world of
ignorance, betrayal and evil. it is the replacement of logic by faith,
the substitution of reason by ignorance...

> >
> If you can show a novel function evolving in any species

and when you show a god creating ANYTHING besides genocide you be sure
and let me know.

bro...@noguchi.mimcom.net

unread,
Jul 20, 2006, 12:59:14 AM7/20/06
to

He cannot produce any specific numbers bcause he doesn't have a
specific model of anything at all. And if he pulls some number out of
his nether regions he certainly will not be able to justify them.


>
> >
> > > > > > Sean Pitman
> > > > > > www.DetectingDesign.com

Marc

unread,
Jul 20, 2006, 2:28:53 AM7/20/06
to


Not access to *a* cell, you git, it is embedding itself within the
genome.

Much of the Koala population now has this embedded retrovirus as a
new part of their genome but some isolated subpopulations do not yet
have it. When a virus like this is in the genome, it is there in the
sperm
and egg at the point of conception and so the virus is now a part of
every cell - every single cell - of each affected individual. That is
one
of the features of a "retrovirus", that it can become a part of a
genome.

Now that it is a part of the genome it can start to have other effects
such as shifting parts of the genome around (a side effect of which
may be to cause some forms of cancer). Obviously you do not
know much about the HERVs in our genome, do you?

As a service to mankind I will try to e-mail you a copy if I can
figure out where to send it.

(signed) marc

Seanpit

unread,
Jul 20, 2006, 5:10:31 AM7/20/06
to

Marc wrote:

> > > Explain this then....
> > > http://www.nature.com/nature/journal/v442/n7098/abs/nature04841.html
> >
> > I don't have access to the full article. Please quote the relevant
> > portion of the article describing the real-time evolution of the novel
> > function. If the function is nothing more than a virus being able to
> > gain entrance into a cell via some sort of template matching, then this
> > is very low-level evolution. It is not the type of evolution that
> > would explain the creation of a functional system like flagellar
> > motility.
>
> Not access to *a* cell, you git, it is embedding itself within the
> genome.

Great, what novel function is evolved? Please do describe the function
itself that evolved with the introduction of this retrovirus to the
Koala gene pool.

> Much of the Koala population now
> has this embedded retrovirus as a
> new part of their genome but some
> isolated subpopulations do not yet
> have it. When a virus like this is
> in the genome, it is there in the
> sperm and egg at the point of conception
> and so the virus is now a part of
> every cell - every single cell - of
> each affected individual. That is
> one of the features of a "retrovirus",
> that it can become a part of a
> genome.

Yes, but what novel function evolved? Please do describe it. The
simple entrance of outside DNA to a gene pool is not the same thing as
the evolution of something that was not already in the gene pool of
either the virus or the Koala - via random mutation and natural
selection. Bacteria pick up outside DNA all the time and are often
able to incorporate new functions encoded by this outside DNA - such as
enzyme producing plasmids that might produce antibiotic resistance.
This sort of thing is not the evolution of anything new. It is simply
the transfer of something that was preformed elsewhere. I'm talking
specifically about Darwinian-style evolution here were novel functions
that did not exist anywhere before were evolved in a particular gene
pool via random mutations and natural selection. Do you have any
examples of functions evolving via this method beyond very low levels
of functional complexity?

> Now that it is a part of the genome it can start to have other effects


> such as shifting parts of the genome around (a side effect of which
> may be to cause some forms of cancer).

Yes, but do you know of any novel functions that evolve via this
ability to shift parts of the genome around? - functions that were not
already there in the genome? Most of the time, cancer is not the
result of the evolution of a novel function, but arises as a result of
a loss of regulation of pre-existing functions.

> Obviously you do not
> know much about the HERVs in our genome, do you?

I know a bit about human endogenous retroviruses (HERVs). I have yet
to see where viral DNA incorporated into a genome produces novel
functions beyond very low levels of complexity that were not already in
existence. Do you have a real time example showing otherwise?

> As a service to mankind I will try to e-mail you a copy if I can
> figure out where to send it.

First tell me what novel function was described as evolving in this
paper . . .

Seanpit

unread,
Jul 20, 2006, 5:10:25 AM7/20/06
to

Marc wrote:

> > > Explain this then....
> > > http://www.nature.com/nature/journal/v442/n7098/abs/nature04841.html
> >
> > I don't have access to the full article. Please quote the relevant
> > portion of the article describing the real-time evolution of the novel
> > function. If the function is nothing more than a virus being able to
> > gain entrance into a cell via some sort of template matching, then this
> > is very low-level evolution. It is not the type of evolution that
> > would explain the creation of a functional system like flagellar
> > motility.
>
> Not access to *a* cell, you git, it is embedding itself within the
> genome.

Great, what novel function is evolved? Please do describe the function


itself that evolved with the introduction of this retrovirus to the
Koala gene pool.

> Much of the Koala population now


> has this embedded retrovirus as a
> new part of their genome but some
> isolated subpopulations do not yet
> have it. When a virus like this is
> in the genome, it is there in the
> sperm and egg at the point of conception
> and so the virus is now a part of
> every cell - every single cell - of
> each affected individual. That is
> one of the features of a "retrovirus",
> that it can become a part of a
> genome.

Yes, but what novel function evolved? Please do describe it. The


simple entrance of outside DNA to a gene pool is not the same thing as
the evolution of something that was not already in the gene pool of
either the virus or the Koala - via random mutation and natural
selection. Bacteria pick up outside DNA all the time and are often
able to incorporate new functions encoded by this outside DNA - such as
enzyme producing plasmids that might produce antibiotic resistance.
This sort of thing is not the evolution of anything new. It is simply
the transfer of something that was preformed elsewhere. I'm talking
specifically about Darwinian-style evolution here were novel functions
that did not exist anywhere before were evolved in a particular gene
pool via random mutations and natural selection. Do you have any

examples of functions evolving via this method beyond very low levels
of functional complexity?

> Now that it is a part of the genome it can start to have other effects


> such as shifting parts of the genome around (a side effect of which
> may be to cause some forms of cancer).

Yes, but do you know of any novel functions that evolve via this


ability to shift parts of the genome around? - functions that were not
already there in the genome? Most of the time, cancer is not the
result of the evolution of a novel function, but arises as a result of
a loss of regulation of pre-existing functions.

> Obviously you do not


> know much about the HERVs in our genome, do you?

I know a bit about human endogenous retroviruses (HERVs). I have yet


to see where viral DNA incorporated into a genome produces novel
functions beyond very low levels of complexity that were not already in
existence. Do you have a real time example showing otherwise?

> As a service to mankind I will try to e-mail you a copy if I can


> figure out where to send it.

First tell me what novel function was described as evolving in this
paper . . .

> (signed) marc

Sean Pitman
www.DetectingDesign.com

Seanpit

unread,
Jul 20, 2006, 5:25:51 AM7/20/06
to

If you understand the notion that cascading enzymatic systems are no
more complex than their most complex protein part, then you determine
the minimum size and specificity for that protein part that will still
do the job and you have your answer. That's it. If you think
otherwise, please do explain yourself instead of trying to be thick.

> >
> > > > > > Sean Pitman
> > > > > > www.DetectingDesign.com

Seanpit

unread,
Jul 20, 2006, 5:22:56 AM7/20/06
to

wf3h wrote:
> Seanpit wrote:
> >
> > I understand evolution in general just fine. I am fully aware of how
> > evolution is supposed to work and have read many of these just so
> > stories about how various functions are supposed to have evolved. I've
> > yet to read about a real-time demonstration to back up even one of
> > these just-so proclamations beyond very low levels of functional
> > complexity.
>
> as a scientist who is objective, since i'm not an evolutionary
> biologist, i find seanpit's argument unconvincing
> evolution has been demonstrated in the lab.

Not beyond functions that require more than a few hundred fairly
specified amino acid residues working together at the same time (less
than 3 to 4 thousand bp of genetic real estate at minimum).

> the long timeframes
> necessary for evolution of species can't be demonstrated in the lab
> because of the reason already stated: it takes a long time. BUT
> evolutionary bio is an EXPERIMENTAL science

I'm not talking about evolving an entirely new creature, just a new
relatively simple functional biosystem that requires more than a few
thousand bp of genetic real estate. I mean really, not even one of the
proposed steps in the evolution of a system like the flagellum as ever
been demonstrated in the lab - not one step. If such a step were so
simple, it should be quite easy to set up such a demonstration under
real time laboratory conditions. This sort of demonstration has yet to
be done beyond very low levels of functional complexity.

The fact that low-level evolution can be demonstrated does not mean
that these low level examples can be reasonably extrapolated up the
ladder since the ratio of potentially beneficial vs. potentially
non-beneficial decreases exponentially with each step up the ladder.
This is why you don't see anything beyond very low-level evolution
demonstrated in the lab or in real life in real time. There is a gap
problem for evolution that grows exponentially with each increase in a
functions minimum size and/or specificity requirements.

> christianism/islamism, however, is not. the 'just so stories' of
> religion are being played out today across the world in death,
> slaughter, genocide and destruction. seanpit's world is a world of
> ignorance, betrayal and evil. it is the replacement of logic by faith,
> the substitution of reason by ignorance...

Oh give me a break with your sob stories. Religions do not have a
market on evil people who claim to belong to these groups. All groups
have their bad eggs - even atheists and evolutionists have evil people
in the ranks. There are also very brilliant and well-educated people
on both sides of this issue. So, try and come up with an actual
argument that is on topic instead of trying to make blanket
generalizations that simply aren't true or relevant.

> > If you can show a novel function evolving in any species
>
> and when you show a god creating ANYTHING besides genocide you be sure
> and let me know.

Humans can create many things as well as genocide. You would think
that someone smarter than a human could do at least as well . . . What
if that someone made you with free will - and you go off and do
something evil. Who's responsible? Who do you blame? - your Creator
or yourself?

Sean Pitman
www.DetectingDesign.com

Von R. Smith

unread,
Jul 20, 2006, 7:38:06 AM7/20/06
to

sea...@gmail.com wrote:
> Von R. Smith wrote:
>
> > How many base pairs of sequences coding for the 2,4-DNT pathway are
> > fairly specified, Sean? How did you arrive at that figure, and how
> > could somebody else verify it? I'm still waiting for an answer.
>
> Again, Von, enzymatic cascades are not highly specified, relatively
> speaking,


"Relatively speaking" compared to what? To individual proteins? I
should think that, at very least, the number of "fairly specified"
amino acids needed for a cascade would be the sum total of the amino
acids needed for each of the enzymes in that cascade. Also, I'm not
asking you about "highly specified", but about "fairly specified",
which I assume is a slightly less stringent standard. All 400 amino
acids of lacZ are not "highly specified" by any reasonable definition
of the term, but you contend that they are "fairly specified". Same
goes for 10,000 or so aa of all the proteins going into making a
eubacterial flagellum.


> because they do not require 3D orientation in order to work
> and enzymatic functions, in general, need not be very specific at each
> step along the way in order to work to a useful degree. Compare this
> with functions like pinocytosis or flagellar motility where a specific
> 3D orientation to all the parts is required and they all work together
> at the same time. Such a system of function requires a much greater
> degree of minimum size and specificity.


So what is the minimum size and specificity of the sequence coding for
the 2,4-DNT cascade? I just want a number, Sean, along with a
sufficiently-detailed explanation of how you got it that I can verify
that you didn't just make it up.

>
> > An appropriate, responsive answer will include a number relevant to the
> > 2,4-DNT pathway, as well as a justification of that number. It will
> > not include trying to change the subject to how much more complex the
> > flagellum is than enzyme cascades.
>
> That's because you don't seem to grasp the concept that cascading
> functions are much different than functions like flagellar motility.
> This difference is very important to understanding the problem with
> evolving high-level functions like flagellar motility.


Thatn's nice. Unfortunately it does not answer the question. I asked
you for a number, and for a justification of that number. How many
base pairs of the sequences coding for the 2,4-DNT cascade are fairly
specified? How did you arrive at that sequence? How could another
person verify that number?

Marc

unread,
Jul 20, 2006, 8:10:32 AM7/20/06
to

Seanpit wrote:
> Marc wrote:
>
> > > > Explain this then....
> > > > http://www.nature.com/nature/journal/v442/n7098/abs/nature04841.html
> > >
> > > I don't have access to the full article. Please quote the relevant
> > > portion of the article describing the real-time evolution of the novel
> > > function. If the function is nothing more than a virus being able to
> > > gain entrance into a cell via some sort of template matching, then this
> > > is very low-level evolution. It is not the type of evolution that
> > > would explain the creation of a functional system like flagellar
> > > motility.
> >
> > Not access to *a* cell, you git, it is embedding itself within the
> > genome.

... snip

> > As a service to mankind I will try to e-mail you a copy if I can
> > figure out where to send it.
>
> First tell me what novel function was described as evolving in this
> paper . . .

The novel function is called "evolution".

That you insist it must have "function" and you refuse to read
the paper shows your agenda. Why even post here if you don't
want to hear an answer apart from the one you insist on?

(signed) marc

Von R. Smith

unread,
Jul 20, 2006, 8:35:52 AM7/20/06
to

The answer to what? Not to the question of how many of the base-pairs
in the coding sequence are "fairly-specified". Just the other day you
wrote this:

"As I've told you over and over again, specificity is a description of
the minimum sequence order or limitations of character differences
within a sequence that can be sustained without a complete loss of the
function in question."

This is a non-standard usage of the term "specificity", but we'll let
that pass. Now, it is trivial that it takes a longer sequence to code
for the entire 2,4-DNT pathway than it does for any individual step in
that pathway. So unless you think poor dntAbAcAd can do the entire
pathway all by itself, then the pathway must have a greater "minimum
size requirement" than the largest individual gene within it. And
unless you are saying that any random sequence can fill in the rest of
the "size requirement" in order to perform the rest of the steps of the
pathway than there must be at least some "limitations of character
differences" wiithin the rest of the coding sequence.

So now that we have established that the answer to my question cannot
be "the minimum coding sequence for the largest protein in the
pathway", let me ask again: How many of the base pairs in the genetic
sequences encoding the 2,4-DNT pathway are "fairly specified"?

Let me give you some help with the numbers. You have yourself
identified 4 enzymes that are central to and specific to the cascade in
question. Here are the smallest sequences performing their functions
that I could find in the NCBI database:


dntAb ~ 104
dntAc ~ 447
dntAd ~ 194

dntB ~ 548

dntD ~ 314

dntG ~ 281

for a total of 1,888 amino acids.


Note that I have not included dntAa (which can be deleted without
compromising the function in question), dntC (the putative non-specific
reductase), or ORF13 (the role of which is unknown and may or may not
be essential). I even left out dntE, which you dissed for some reason.


On at least three other occasions, when asked to put a number on
"minimum size requirements" for a given function, you have estimated
that requirement using the smallest published sequence known to perform
that function. In the case of 2,4-DNT, that number is about 1,888aa,
which would require roughly 6,000 base pairs to code for it.

Now I'm pretty sure that you don't think that dntAbAcAd could perform
the entire pathway by itself (meaning that it does not single-handedly
account for the "minimum size requirement"), and I know you don't
believe that any random peptide sequence could perform the subsequent
of the steps of the pathway (meaning that dntAbAcAd does not
single-handedly account for your sequence conservation criterion,
either). So by your own stated criteria, the answer to the question is
*not* "pick the most complex single enzyme in this cascade and find the


shortest possible genetic sequence that can code for that type of

functional enzyme".

And now that we've gotten that out of the way, let me ask once more:

How many of the base pairs coding for the 2,4-DNT pathway are "fairly
specified"? How did you arrive at that number, and how could an
independent observer verify that number?

John Harshman

unread,
Jul 20, 2006, 10:56:14 AM7/20/06
to
Marc wrote:

Seldom have I witnessed a more egregious case of people talking past
each other, and I think you are largely at fault. What do you think Sean
is asking for? What point do you think you're making with these
semi-endogenous retroviruses? I have no idea. Please explain.

Andrew Arensburger

unread,
Jul 20, 2006, 12:02:56 PM7/20/06
to
Kermit <unrestra...@hotmail.com> wrote:
> City kid, huh? Many chickens can fly. Not like a sparrow, but roosting
> in trees or flying over fences is not uncommon.

I wonder if anyone's brought up feral chickens on t.o
before...

<Ducks, before he gets goosed>

--
Andrew Arensburger, Systems guy University of Maryland
arensb.no-...@umd.edu Office of Information Technology
/etc/passwd is full -- go away!

snex

unread,
Jul 20, 2006, 12:09:31 PM7/20/06
to

i am not interested in your assertions. provide the NUMBERS and HOW YOU
ARRIVED AT THEM or stop maintaining you have the authority to
pontificate on these matters.

really, what is so hard to understand about my request? would you write
a scientific paper in this manner, or would you supply the methodology
and the numbers right off the bat?

>
> > >
> > > > > > > Sean Pitman
> > > > > > > www.DetectingDesign.com

Seanpit

unread,
Jul 20, 2006, 1:03:36 PM7/20/06
to
Marc wrote:
> Seanpit wrote:
> > Marc wrote:
> >
> > > > > Explain this then....
> > > > > http://www.nature.com/nature/journal/v442/n7098/abs/nature04841.html
> > > >
> > > > I don't have access to the full article. Please quote the relevant
> > > > portion of the article describing the real-time evolution of the novel
> > > > function. If the function is nothing more than a virus being able to
> > > > gain entrance into a cell via some sort of template matching, then this
> > > > is very low-level evolution. It is not the type of evolution that
> > > > would explain the creation of a functional system like flagellar
> > > > motility.
> > >
> > > Not access to *a* cell, you git, it is embedding itself within the
> > > genome.
>
> ... snip
>
> > > As a service to mankind I will try to e-mail you a copy if I can
> > > figure out where to send it.
> >
> > First tell me what novel function was described as evolving in this
> > paper . . .
>
> The novel function is called "evolution".

Evolution is a process not a novel function in and of itself. Evolution
is supposed to produce novel functions in living things over time. I
say that evolution doesn't do this beyond very low levels of functional
complexity. If you are challenging me on this point, what novel
function is described as evolving in this paper of yours?

> That you insist it must have "function" and you refuse to read
> the paper shows your agenda. Why even post here if you don't
> want to hear an answer apart from the one you insist on?

I'm only interested in evolving functions. If the paper doesn't talk
about the real time evolution of a novel function, what is your point
in presenting it to me for review?

I get this all the time. People tell me to read this or that paper.
When I do, it almost always does not say what I was told it said.
Often it isn't even dealing with the topic at hand. The topic here is
the evolution of novel functions in real time. If you have an example
that goes beyond very low levels of functional complexity, I'd like to
see it. Otherwise, though perhaps quite interesting, papers that do
not deal with this topic are, well, off topic.

Ken Denny

unread,
Jul 20, 2006, 1:21:24 PM7/20/06
to
Seanpit wrote:
>
> Evolution is a process not a novel function in and of itself. Evolution
> is supposed to produce novel functions in living things over time. I
> say that evolution doesn't do this beyond very low levels of functional
> complexity. If you are challenging me on this point, what novel
> function is described as evolving in this paper of yours?

So what you are asking for is an example of a process that takes
thousands of years being observed completing in a few decades. Do I
have that right?

snex

unread,
Jul 20, 2006, 1:46:43 PM7/20/06
to

his claim is that it would take trillions of years, not just thousands.

how he thinks the lack of observation of a process hypothesized to take
thousands of years implies that it takes trillions of years is anyone's
guess.

perhaps sean would like to stop whining that no such process has been
observed (since thousand year processes are unobservable by definition)
and show how indirect observations support trillions of years rather
than thousands.

my guess is that he will resort back to flawed english language
analogies that have a far greater ratio of useless sequences to all
sequences than DNA. and even these do not support him, as zachariel's
word mutagenator demonstrates.

lannybudd

unread,
Jul 20, 2006, 3:42:23 PM7/20/06
to

Seanpit wrote:

"I've yet to read about a real-time demonstration to back up even one
of
these just-so proclamations beyond very low levels of functional
complexity."

Stop wasting electrons arguing with this clod. He wants you to cite a
paper where a cat gave birth to a dog. More subtle reasoning need not
apply.

Ken Denny

unread,
Jul 20, 2006, 3:53:38 PM7/20/06