Ron Okimoto and the Gap Problem
Seanpit
> > Why not just try and list a single argument that Ron has made
> > regarding an explanation as to why the proposed mechanism of random
> > mutation and function-based selection produces plenty of examples of
> > observable evolution in action where only a few dozen specified
> > residues are required, a few where a few hundred are required, but
> > absolutely none when more than 1000 are required? - not a single
> > example in all of literature. How is this observation explained?
>
> Why the bogus obfuscation? Have I ever made any claims about a few
> dozen whatevers? I think the claim was that you can't even come up
> with an example where three changes were required to get a selectable
> function, and you never could come up with one.
Talk about strawman building and obfuscation - - The 1,000aa
threshold is NOT a measure of any "change" or "gap size". You and
Howard Hershey constantly build this strawman no matter how many times
I've corrected you both on this otherwise elementary concept. Again,
as I've explained many many times before, the 1000aa threshold is a
measure of the absolute number of amino acid residues that have to be
in a specified arrangement before a particular type of function can be
realized - i.e., the minimum structural threshold requirement.
For example, flagellar motility requires a minimum of at least 10,000
residues for the motility part of the function to be realized.
Kenneth Miller's argument that 40 of the 50 or so proteins can be
removed without a complete loss of function (since the TTSS system
remains intact) completely misses the point. The TTSS system does not
have the motility function of the flagellum. This motility function
requires around 10,000 residues at minimum. Without this minimum
structural threshold requirement in place the function of flagellar
motility cannot be realized at all - not even a little bit.
You do understand this fist very basic concept - right? Perhaps not,
but for those who do, it is very easy to demonstrate that no type of
functional system that requires at least 1,000 specifically arranged
amino acid residues evolves in observable time. There is not a single
example in all of literature.
So, the question is, "Why not?" Did you get that question Ron? What
is your answer for this observation? Why do systems with structural
threshold requirements of just a few amino acid residues evolve so
rapidly while those that require a few hundred evolve much less
commonly and those that require over 1,000aa never evolve at all in an
observable way? What is your explanation for this exponential
stalling out effect of evolutionary potential?
> Your own math told
> you that 2 or three were no problem
> and you had to go with 10 or more,
> remember?
This discussion concerned the minimum gap distance. Remember Ron? As
it turns out, the likely minimum gap distance increases in a linear
manner with each increase in the minimum structural threshold
requirements of the system in question. The gap is not the same thing
as the minimum structural threshold requirements. These are different
but related concepts. In other words, the 1000aa threshold is NOT the
gap distance. It is just that this minimum threshold requirement
almost certainly produces a minimum gap distance between what is and
what might be beneficial that is much wider than a few dozen residue
changes.
> Then you made the bogus jump to 1000 when you couldn't even
> justify claims of 10.
You are very confused Ron. This is because you really haven't spent
any time with the arguments at hand and still don't grasp the concept
that the 1000aa structural threshold requirement is not the same thing
as the gap distance.
> I claim that there isn't a single instance of
> where 12 changes were required because we've haven't found any that
> required 12. Demonstrate differently. You never could, now it is
> suddenly my fault that you can't come up with an example of 12 changes
> being required? What kind of bogus argument is that?
The demonstration here is found in the exponential decline of
evolvability with increasing minimum structural threshold requirements
until evolution completely stalls out well shy of the 1000aa
threshold. You haven't presented any counter arguments or
explanations to explain how this very real phenomenon might be the
result of some other cause beside the linear expanding gap problem
I've been proposing for many years now.
> Remember the Hall junk that you used to claim meant something? He
> found that only 1 change was required to change ebg to having beta gal
> activity. Two changes made it even better. He found this in an
> organism with only around 2000 protein genes. Only 2000 chances for a
> sequence to be close enough to the desired activity to get there in 1
> or two mutations. Halls experimental methodology limited the number
> of mutations required because it was a single step selection and at
> best he could expect to select for double mutations. He even repeated
> it with other species of bacteria. I believe your own references
> cited 2 or 3 other bacteria that he could get to evolve beta gal
> activity, but he might not have figured out which genes had been
> altered in them. Like he had in identifying the ebg gene in E. coli.
You continually forget that the minimum structural requirement for
lactase activity is only 400 or so fairly specified amino acid
residues. That's the whole point Ron. The E. coli in Hall's
experiment were successful because the functional system in question
has a relatively low minimum structural threshold requirement - not
even close to the 1,000 level. The same thing is true of the famous
nylonase example that evolutionists love to quote. As it turns out,
nylonase requires less of a structural threshold than the lactase
enzyme - only 280 or so residues.
> Your bogus argument fell apart and you finally did some off the cuff
> calculations using expected evolutionary assumptions like mutation
> selection balance and figured out that jumping short gaps of 2 or 3
> were not as rare as you thought.
I never argued that jumping gaps of only 2 or 3 residues changes would
be hard for a bacterial colony at all. I've always argued that
crossing such small gaps would be very easy in a very short period of
time - far more quickly than Hall's own calculations seemed to
indicate. The problem's come when such small gap distances are not
longer likely to be present - i.e., when structural threshold's start
moving beyond minimum requirements of just a few hundred to over
1,000aa.
> For those that don't know what that
> is it just means that populations that exist for any length of time
> would expect to reach mutation selection balance where the genetic
> variation of a population would reach an equilibrium with new
> mutations equalling the loss of existing mutations from the
> population. Populations have an amazing amount of genetic variation.
> They don't have to rely on multiple simultaneous mutations.
Hall's bacteria actually did have to undergo at least 2 mutations
before the beneficial function of lactase activity could be realized.
Population variation did not come into play because Hall set up the
experiment based on a clonal population where the original genetic
sequence was already known as was identical at the start of the
experiment.
> When Sean
> realized this the gap inflation started. It lept to 10 or 12 but then
> rose quickly to 40 if my memory is correct. Now it is a raving 1000,
> but the key point to note is that Sean doesn't have an example of 3 or
> 4 being required. No science paper that I know of have found such an
> example. Now he is trying to turn something that obviously
> invalidates his 1000 argument into something that I have to worry
> about. My claim was that Sean couldn't come up with an example of 3
> let alone 40 mutations being required. Sean just convieniently
> forgets that.
What Ron forgets, or perhaps never really grasped, is the concept that
the minimum structural threshold requirements for a system (i.e., like
1,000 specifically arranged residues) is not the same thing as the gap
distance. Increasing the threshold does increase the gap distance,
but they are not the same thing.
What Ron and others like Howard Hershey don't seem to realize is that
tiny gap distances that are only 1 or 2 or 3 mutational changes wide
are not always the most likely minimum gap distance at every level of
minimum structural threshold requirements. The likely minimum gap
distances increase, in a linear manner, with each increase in the
structural threshold requirements. So, by the time the requirements
are over 1,000aa, the odds that the gap distance between what is
beneficial and what might be beneficial is only a handful of changes
wide is next to impossible. The actual gap distance at such levels
tends to follow a Poisson distribution making a gap of dozens of
changes much more likely to be the true gap distance at the 1000aa
minimum threshold.
This concept is what no one who frequents this forum, not Ron Okimoto,
Howard Hershey, Von Smith, Richard Baldwin, Richard Forrest, or anyone
else, has ever come close to explaining or even addressing without
giving up and resorting to the old standbys of endless pejoratives and
strawman mischaracterizations (many of which Ron just listed off
here).
< snip rest >
> Ron Okimoto
Sean Pitman
www.DetectingDesign.com
Frank J
Sean, feel free to jump in the other 2 threads where I ask for the
whats and whens of the last design events. I'm particularly interested
in the last one necessary for the origin of modern humans, and whether
it is also responsible for other species.
Also feel free to debate Behe on your answers, since you and he seem
to have radically different ideas about when such events occurred, and
whether or not they occurred in-vivo. If you think your ideas are
truly scientific, you should be at least as interested in challenging
Behe as you ar in challenging "Darwinists." Behe doesn't have that
"prior commitment to 'naturalism' " so you should have an easier time
sticking to the science.
Seanpit
> > I'm not talking about changes Ron. I'm talking about an absolute
> > number of amino acid residues that have to be in a specified
> > arrangement before a particular type of function can be realized at
> > all.
>
> IOW, evolution is not about *change*. It is about *size*.
It's about both. It is about changes producing functional systems
that have different minimum structural size and specificity
requirements.
> It is
> about manufacturing, for a teleological goal that Sean gets to define,
> a protein that performs that teleological function *from scratch* by a
> mechanism that does not allow any intermediate functionality or
> utility. There, now I have said it again. And now Sean will deny
> what he just said, "I'm not talking about changes...I'm talking about
> an absolute number of amino acid residues that have to be in a
> specified arrangement before a particular type of function can be
> realized at all." He will claim that one can start wherever in
> sequence space one wants to and his argument still holds true.
The only "goal" here is to explain how evolution can actually work to
produce functional systems that have larger and larger minimum
structural threshold requirements. You may argue that evolution
doesn't require this to happen and that's true. However, you
evolutionists believe that it happened very commonly throughout a span
of only 4 billion years or so. How could systems with very high
minimum structural threshold requirements have evolved? You simply
state that when evolution happens it happens because the gaps were
small. I couldn't agree more. The problem is with your notion that
small gaps sizes could easily exist with minimum structural threshold
requirements at 1,000aa and far beyond. That's the problem. You
think the *likely* gap size is the smallest possible gap size (i.e.
"one") regardless of the minimum structural threshold requirement for
the functional system in question.
That notion of yours is clearly mistaken as anyone can prove by simply
doing a BLAST search. Systems with larger minimum structural
requirements than 1 or 2k amino acid residues are not just one or two
residue changes away from any other uniquely functional system. And,
as the minimum requirements grow, so does the number of differences
one sees between it and the next closest uniquely functional system.
There is in fact a linear relationship between the minimum structural
threshold requirement of a system and its likely gap distance. This
is a demonstrable fact. Prove me wrong if you think otherwise.
> > For example, flagellar motility requires a minimum of at least
> > 10,000 residues for the motility part of the function to be realized.
>
> That, however, is not the relevant number for evolution. The relevant
> number for evolution is the minimum number of mutations it takes to
> *change* *existing* (at least potentially) *functional* sequences so
> that they are *modified* to produce a *new* or *novel* function of
> rotary motion of a whip.
>
> The answer to that question has been answered. The answer, in
> principle (and in reality) is one.
Yeah - "In principle" the minimum gap size is just one mutational
change. Again, what are the odds that the minimum possible gap size
will actually exist when you start looking at higher and higher
minimum structural threshold requirements? That's the real question.
The odds do not stay the same. That's the problem. They decrease
dramatically with each increase in the minimum structural threshold -
along a Poisson distribution.
< snip rest >
Sean Pitman
www.DetectingDesign.com
hersheyh
0catch.com> wrote:
> On Aug 23, 1:49 pm, hersheyh <hershe...@yahoo.com> wrote:
>
> > > I'm not talking about changes Ron. I'm talking about an absolute
> > > number of amino acid residues that have to be in a specified
> > > arrangement before a particular type of function can be realized at
> > > all.
>
> > IOW, evolution is not about *change*. It is about *size*.
>
> It's about both. It is about changes producing functional systems
> that have different minimum structural size and specificity
> requirements.
No. Evolution is about change, not size. Change in *function*.
Generation of new *function*. The fact is that evolution is highly
conservative of *structure* and *size* and *specificity* when it
generates new *function*.
Not that larger sized proteins are all that hard to make in single
mutational steps. They are not made, as you seem to think, by adding
one aa at a time to some non-functional imaginary protein. They are
made by the generation of chimeric fusion products due to deletion,
inversion, translocation, or an error in recombination producing a
chimeric protein. Not only does this produce a larger protein, it
often produces one with added new *functional* moieties that were not
present in these particular combinations before. [In fact, a sizeable
percentage of duplicates that are retained in eovlution are chimeric
in nature rather than simple duplication with a few added point
mutations.] I gave you an example of how a deletion can produce a
chimeric protein (but not necessarily one larger than its parent
proteins) that can, in a single step, produce a *new* way of
generating rotational motility in bacteria that lacked that *function*
although they had structures that were similar *strucutrually and
functionally* to TTSS and to motor structures that also exist in
bacteria not as part of the flagellar system. Larger proteins can
also be produced by endoduplication and also mutation of the usual
stop codon or a change in the intron border sequences (which can
produce alternate sized proteins from the same gene).
But you really don't seem happy with the fact that most proteins are
too small, so you then look at aggregations of proteins (such as
ribosomes or flagella) and treat them as if they were a single
protein. The fact is that duplication and divergence (especially
subfunctionalization, which only requires loss of function) are common
events. Once one has duplicates that have either become subfunctional
or neofunctional, the size of the complex would, according to you have
doubled. But without any *change* but a duplication and a different
*loss* of partial function in both of the genes. Over time, of
course, such subfunctionalization can lead to irreducible complexity.
But, of course, you have a teleological mindset and assume that
proteins can only do one thing, their teleological function. You hold
that despite knowing that a flagella which is immotile can still
transport proteins outside the bacteria.
> > It is
> > about manufacturing, for a teleological goal that Sean gets to define,
> > a protein that performs that teleological function *from scratch* by a
> > mechanism that does not allow any intermediate functionality or
> > utility. There, now I have said it again. And now Sean will deny
> > what he just said, "I'm not talking about changes...I'm talking about
> > an absolute number of amino acid residues that have to be in a
> > specified arrangement before a particular type of function can be
> > realized at all." He will claim that one can start wherever in
> > sequence space one wants to and his argument still holds true.
>
> The only "goal" here is to explain how evolution can actually work to
> produce functional systems that have larger and larger minimum
> structural threshold requirements.
You always exaggerate what evolution must do to get a new function.
Increasing the size of a protein or the number of proteins in a
complex is not accomplished by any mechanism where the "structural
threshold" (aka size) gets changed in one aa increments. Why do you
think that even Darwin described evolution as "descent with (and by)
modification". No system in any organism was made by a mechanism
where the size of the structural threshold was relevant. The only
relevant feature, as far as evolution is concerned, is the *size of
the gap*.
You have repeatedly claimed that I think you mean that 1000 aa is the
size of the gap (see quote below). I don't. But if 1000 aa is the
only number you present (and one that you seem to *think* is related
to the number you *really* need, the size of the gap, it is my duty,
as an honest person, to remind you *time after time after time* that
the 1000aa number is irrelevant *unless* you can present a formula by
which one can calculate the number you do need: the minimum size of
the gap, or, at a minimum, and far less useful, the average gap +/- a
variance. Yet you never do anything but assert without evidence that
there is a mathematical (either linear or exponential) relationship of
some sort between the size of the protein (or system) in aa and the
number you do need. Do you realize how frustrating it is to have to
keep reminding you of a fact that you readily admit to? That the
number you need, but never present in your arguments, is the gap
size. And that merely handwaving (or pulling a number out of yer
arse) is no substitute for a real mathematically precise and tested
hypothesis linking total size and gap size.
**********Sean speaking*****
Talk about strawman building and obfuscation - - The 1,000aa
threshold is NOT a measure of any "change" or "gap size". You and
Howard Hershey constantly build this strawman no matter how many times
I've corrected you both on this otherwise elementary concept.
*********End Sean*******
Since I am not making that strawman, but merely reminding you (time
after time after time) that the 1000 number is irrelevant and that the
number you really need is never presented except by waving it into
existence, I feel agrieved and insulted.
> You may argue that evolution
> doesn't require this to happen and that's true. However, you
> evolutionists believe that it happened very commonly throughout a span
> of only 4 billion years or so. How could systems with very high
> minimum structural threshold requirements have evolved?
I've told you how larger proteins can be made. Proteins *like* to
interact with each other, so explaining aggregation of proteins is not
too difficult. Most interactions vary in strength.
> You simply
> state that when evolution happens it happens because the gaps were
> small. I couldn't agree more. The problem is with your notion that
> small gaps sizes could easily exist with minimum structural threshold
> requirements at 1,000aa and far beyond. That's the problem. You
> think the *likely* gap size is the smallest possible gap size (i.e.
> "one") regardless of the minimum structural threshold requirement for
> the functional system in question.
Yes. That is the problem. But as I see it, the problem is that you
have not presented any evidence to support the hypothesis that the
systems that have evolved and that new functionality in particular,
regardless of the size of the protein(s) involved, did so or needed to
do so by crossing large gaps.
You keep asserting that there is a mathematical relationship between
total size and gap size. I have yet to see that equation nor any
evidence supporting the hypothesis.
> That notion of yours is clearly mistaken as anyone can prove by simply
> doing a BLAST search. Systems with larger minimum structural
> requirements than 1 or 2k amino acid residues are not just one or two
> residue changes away from any other uniquely functional system.
Examples? And how long since the system diverged? That is crucial
because a lot of both selective and non-selective changes will occur
in sequences over long periods of time. And these changes would not
necessarily affect the basic *function*; they would optimize it.
Again, a mutation that produces the loss of rotary motility (a single
point mutation can do this) does not necessarily affect the ability to
transport proteins by the flagellin tube, some of which still do
function for this purpose as well as being a flagella. Again, you
seem to think that flagella only has a single function rather than
having proteins that each have an independent function that is still
there if another protein has mutated.
> And,
> as the minimum requirements grow, so does the number of differences
> one sees between it and the next closest uniquely functional system.
So you keep asserting.
> There is in fact a linear relationship between the minimum structural
> threshold requirement of a system and its likely gap distance. This
> is a demonstrable fact. Prove me wrong if you think otherwise.
Show me the math and the logic and evidence that allowed you to
generate it. [I ask for the last because you have a habit of
producing formulas that are supposed to be descriptive of empirical
reality that mean nothing or don't mean what you say they do. Just
like you call what is basically "total size" a "minimum structural
threshold"]
> > > For example, flagellar motility requires a minimum of at least
> > > 10,000 residues for the motility part of the function to be realized.
>
> > That, however, is not the relevant number for evolution. The relevant
> > number for evolution is the minimum number of mutations it takes to
> > *change* *existing* (at least potentially) *functional* sequences so
> > that they are *modified* to produce a *new* or *novel* function of
> > rotary motion of a whip.
>
> > The answer to that question has been answered. The answer, in
> > principle (and in reality) is one.
>
> Yeah - "In principle" the minimum gap size is just one mutational
> change.
And always will be. But there are cases of *real* proteins where more
than one site needed to *selectively* mutate to produce a changed
function (possibly the conversion of a cortisol receptor to an
aldosterone receptor). But the protein actually has some level of
both functions. It is hardly unusual for proteins to have more than
one possible substrate.
> Again, what are the odds that the minimum possible gap size
> will actually exist when you start looking at higher and higher
> minimum structural threshold requirements? That's the real question.
> The odds do not stay the same. That's the problem. They decrease
> dramatically with each increase in the minimum structural threshold -
> along a Poisson distribution.
Show me the math. So far I have seen no formula linking total size
(aka "minimum structural threshold") and gap size. And certainly no
test of its validity, which I seriously doubt, given that gap size is
vastly more a function of an organism's past history and present
protein sequences than a function of the size of the protein.
>
> < snip rest >
>
> Sean Pitmanwww.DetectingDesign.com
Ron O
Why do you do this?
Go find my response in the original thread that this double post came
from.
Ron Okimoto
richardal...@googlemail.com
You know that his argument is invalid and already demolished on
numerous occasions.
Every participant on this forum who has an open mind and the ability
to think, let alone the ability to seek out the many threads in which
this argument was demolished knows that this argument is a load of
bulshit.
Pitman knows that his argument is invalid and has been demolished.
He posts it again so that he can give the impression to other
creationists that he is a scientist making valid scientific arguments
which "evolutionists" cannot falsify. He knows the creationists are so
ignorant of science that they have neither the ability nor the will to
form an objective judgement of the validity of his argument, and will
not bother to read back through the numerous threads in which it has
been demolished.
So basically, he reposts it so that he can gain status in the
creationist camp, and is relying on the ignorance and gullibility of
creationists to get away with the blatant dishonesty he displays by
ignoring the numerous postings which have demolished his assertions.
I think that this shows contempt for his own side in the argument. I
urge any creationist who has any desire to learn the truth of this
matter to read the numerous postings in which Sean's assertions have
been demolished, and try to form an objective view on whether or not
they have any validity.
RF
Gene Poole
0catch.com> wrote:
> On Aug 23, 1:49 pm, hersheyh <hershe...@yahoo.com> wrote:
>
> > > I'm not talking about changes Ron. I'm talking about an absolute
> > > number of amino acid residues that have to be in a specified
> > > arrangement before a particular type of function can be realized at
> > > all.
>
> > IOW, evolution is not about *change*. It is about *size*.
>
> It's about both. It is about changes producing functional systems
> that have different minimum structural size and specificity
> requirements.
Blah blah...
How many gaps between penguins and chickens?
Are penguins even related to chickens?
<http://groups.google.com/group/talk.origins/msg/293f0c8f63f16d3d?
dmode=source&hl=en>
Tiny Bulcher
The problem with that hypothesis is that if this were so, he is posting
in the wrong place. Who is it who reads t.o. he is trying to impress?
Very few creationists hang out here, really, and nearly all of those are
pathetic loonies and/or meatheads whom Sean would be very unlikely to
want to impress. Nearly all of the cleverer creationists avoid places
where they might have to debate actual scientists like the proverbial
infectious disease, and concentrate their efforts on preaching to the
choir.
My own hypothesis, FWIW, (and I freely confess that the arguments
bandied about in Pitman threads are largely beyond my ken) is that he is
primarily trying to convince himself.
Seanpit
> SNIP the worthless bull pucky:
>
> Why do you do this?
So others won't have to wade through a long thread to see something
that might be interesting. You guys start new threads like this all
the time. I never complain about it when you or Richard Forrest or
Howard Hershey do it. Why should you?
> Go find my response in the original thread that this double post came
> from.
Here it is:
> Aren't you just admitting that you are just blowing smoke about any
> claims that I may have made? Aren't you just lying about me having a
> problem with any claim that you have made?
>
> Why do you have to settle for the obfuscation scam?
>
> What happened to the gap distance bogousity? If you aren't talking
> about the gap bogousity than you aren't talking about anything
> relevant to evolutionary biology. No one claims that a protein has to
> evolve from scratch. You know for a fact that whenever we look it is
> some existing protein changing to something else. If that is your
> argument then you have none.
I'm not suggesting that a protein-based system has to evolve from
scratch either. Start with whatever starting point you want. Novel
protein-based systems that require a threshold of at least 1000
specifically arranged amino acid residues will not be able to evolve
from any gene pool you choose in existence today even given trillions
of years of time. Why not? Because, the 1000aa threshold, although
not the gap distance itself, creates a gap that is several dozens of
mutations wide.
Again, the 1000aa threshold is NOT the gap distance. However, it is
associated with a minimum gap distance for populations of even
billions of individuals that is dozens of mutations wide. It is the
linear increase in the gap distance with each increase in the minimum
structural threshold requirements that creates the problem for the
proposed evolutionary mechanism. Each linear increase in the minimum
gap distance translates into an exponential increase in the average
number of mutational steps needed to cross the gap.
> > > Then you made the bogus jump to 1000 when you couldn't even
> > > justify claims of 10.
>
> > You are very confused Ron. This is because you really haven't spent
> > any time with the arguments at hand and still don't grasp the concept
> > that the 1000aa structural threshold requirement is not the same thing
> > as the gap distance.
>
> If it isn't then the argument is so lame that even you probably know
> that you are just blowing smoke. Name anyone that believes that you
> have to assemble a thousand amino acids to evolve some protein
> function. Anyone except the creationist scam artists that you have to
> admit lied to you about the science of ID.
I never said that you have to assemble 1000aa from scratch. That is
why the 1000aa is not the same thing as the gap distance. Again, the
1000aa is a threshold that defines certain types of functional systems
that require at least 1000 specifically arranged amino acid residues
to work at all. Much of the 1000aa requirement may already exist
preformed within a given gene pool. However, odds are that at least a
few dozen mutations would be needed before the minimum structural
threshold requirements of a new unique system with threshold
requirements at or beyond this limitation could be realized. It is
this few dozen needed mutations that is the "gap distance".
The minimum possible gap distance is, of course, always one. This is
true regardless of the minimum structural threshold requirements under
consideration. The problem is that this minimum possible gap distance
is not always the most likely gap distance. It is all about the odds
that the gap distance will be small - like one or two steps wide.
These odds drop, quite dramatically, along a Poisson distribution as
one considers functional systems with greater and greater minimum
structural threshold requirements. Very quickly the likely minimum
gap distance is no longer just one mutation wide - but dozens of
mutations wide. By the time such a minimum gap distance is produced,
the average time required to evolve something new at such a level of
minimum structural threshold requirements has moved into trillions
upon trillions of years of average time.
> > > I claim that there isn't a single instance of
> > > where 12 changes were required because we've haven't found any that
> > > required 12. Demonstrate differently. You never could, now it is
> > > suddenly my fault that you can't come up with an example of 12 changes
> > > being required? What kind of bogus argument is that?
>
> > The demonstration here is found in the exponential decline of
> > evolvability with increasing minimum structural threshold requirements
> > until evolution completely stalls out well shy of the 1000aa
> > threshold. You haven't presented any counter arguments or
> > explanations to explain how this very real phenomenon might be the
> > result of some other cause beside the linear expanding gap problem
> > I've been proposing for many years now.
>
> Now you seem to be mixing gap with your bogus assertion about how
> proteins evolve. Face it Sean the thousand amino acids essentially
> already existed. Small changes in the protein structure would have
> accounted for the evolution of the proteins needed for flagellar
> structure. Why can we tell what proteins a lot of the flagellar
> proteins evolved from if this were not true? Where did the ATPases
> come from? They didn't evolve denovo did they?
The question here is "how small" are the changes that are required
Ron? For systems that have a minimum structural threshold requirement
of only a few hundred loosely specified residues, the minimum number
of changes for at least one member of a huge population of bacteria is
most likely just a handful of mutations. However, when you start
talking about minimum threshold requirements of over 1000aa, the
minimum number of changes is no longer just a handful. Rather, it is
on the order of dozens of mutations.
Look it up and see if you do not discover a pattern - a pattern of
increased minimum differences for higher and higher level systems that
increases in a linear manner with each increase in the minimum
structural threshold requirements of the systems in question.
> > > Remember the Hall junk that you used to claim meant something? He
> > > found that only 1 change was required to change ebg to having beta gal
> > > activity. Two changes made it even better. He found this in an
> > > organism with only around 2000 protein genes. Only 2000 chances for a
> > > sequence to be close enough to the desired activity to get there in 1
> > > or two mutations. Halls experimental methodology limited the number
> > > of mutations required because it was a single step selection and at
> > > best he could expect to select for double mutations. He even repeated
> > > it with other species of bacteria. I believe your own references
> > > cited 2 or 3 other bacteria that he could get to evolve beta gal
> > > activity, but he might not have figured out which genes had been
> > > altered in them. Like he had in identifying the ebg gene in E. coli.
>
> > You continually forget that the minimum structural requirement for
> > lactase activity is only 400 or so fairly specified amino acid
> > residues. That's the whole point Ron. The E. coli in Hall's
> > experiment were successful because the functional system in question
> > has a relatively low minimum structural threshold requirement - not
> > even close to the 1,000 level. The same thing is true of the famous
> > nylonase example that evolutionists love to quote. As it turns out,
> > nylonase requires less of a structural threshold than the lactase
> > enzyme - only 280 or so residues.
>
> And you know that it higher for something else, how? Who claimed that
> 400 specified amino acids were required?
Do a BLAST search Ron. See if you can find a useful lactase enzyme
(in a bacterial colony) that uses significantly less than 400 or so
amino acid residues. Every type of functional system has a minimum
structural threshold requirement that, if not reached, will not
provide a reproductive advantage to a particular type of life form -
such as a bacterial life form. For the lactase function in bacteria,
it turns out that this minimum requirement is around 400aa.
> Lame unsupported assertions
> are just that, lame unsupported assertions. Back it up. How do you
> know that lactase requires 400? Do you have any evidence that lactase
> needs at least 400? E. coli Beta gal (Lac Z) is around 1000 amino
> acids,
That isn't the most trimmed down version available. Much smaller
lactases can be used to at least some advantage. But, the limit
appears to be at around 400aa (380aa is the smallest one I've been
able to find).
> but you are probably going by the size of the EBG gene that
> evolved beta gal activity that was half the size.
The product of the ebg-gene is was also around 1000aa. Again though,
this isn't the minimum requirement. It is the minimum structural
requirement that is statistically important here.
> Why couldn't beta
> gal activity evolve in a smaller protein?
Because lactase activity has a minimum structural threshold
requirement just like all functional systems have. Different types of
systems have different minimum requirements. It turns out that the
lactase system in bacteria have a threshold requirement that appears
to be around 400aa.
> Do you really know the lower size limit?
To a useful approximation . . .
> What does that limit matter?
The limit matters because those systems with smaller limits are much
easier to evolve than are those systems with larger limits. Why?
Because, statistically, a smaller limit will have much greater odds of
being close to pre-existing sequences in a large gene pool.
> You are cooked by
> your own argument. There weren't a thousand specified anythings, just
> one protein sequence evolving a new activity by just two amino acid
> changes. Not only that, but it was accomplished in an organism with
> only around 2000 protein genes that might have evolved the activity.
> Not only that, but more than one species could evolve the activity
> with the same sized genome as raw material for evolution.
Rather, it was a relatively simple single protein enzyme with fairly
loose specificity requirements and a minimum structural size
requirement of only 400 or so amino acid residues. That doesn't come
even close to the 1000aa threshold.
> Why does the flagellum require 1000?
The flagellar motility function requires more like 10,000aa. There is
no way you could get a working flagellar motility system to a useful
selective advantage with just 3,000 codons of DNA (i.e., a 1000aa
equivalent).
> > > Your bogus argument fell apart and you finally did some off the cuff
> > > calculations using expected evolutionary assumptions like mutation
> > > selection balance and figured out that jumping short gaps of 2 or 3
> > > were not as rare as you thought.
>
> > I never argued that jumping gaps of only 2 or 3 residues changes would
> > be hard for a bacterial colony at all. I've always argued that
> > crossing such small gaps would be very easy in a very short period of
> > time - far more quickly than Hall's own calculations seemed to
> > indicate. The problem's come when such small gap distances are no
> > longer likely to be present - i.e., when structural threshold's start
> > moving beyond minimum requirements of just a few hundred to over
> > 1,000aa.
>
> I think that if we pulled up the relavent posts that this would be
> found to be not quite correct. You were the one that was claiming for
> a very long series of posts that a gap of more than 2 was too
> difficult to cross because the Hall experiment could not cross it when
> they removed the EBG gene.
Not true. I never made this claim. I've always argued that Hall was
mistaken in this particular view of his. A gap of just 2 or 3
mutations could easily be crossed by a bacterial population of just a
few billion within just a few generations (i.e., a few days for E.
coli at most).
> You finally had to face the fact (that I
> had to inform you of) that the Hall experiment was only a single step
> selection experiment that would not be expected to identify proteins
> that needed more than two changes, and that in the real world a
> population wasn't a clone and could be expected to have a boat load of
> genetic variation. Your own calculations led you to give up that
> argument. That you are trying to deny that you made it is pretty
> pathetic.
Look it up Ron. I never made this argument.
> What do you think that you were trying to obfuscate by
> using the Hall experiment to demonstrate your point?
I've always used Hall's experiment to support my point of an expanding
non-beneficial gap and I still do use this experiment. It is an
excellent experiment proving what I've been arguing all along - i.e.,
that the minimum likely gap distances do not stay at the minimum
possible distance as minimum structural threshold requirements under
consideration increase. Hall clearly demonstrated this when he
deleted the ebg-gene and the E. coli under consideration could no
longer evolve the lactase function back again despite observation for
almost 50,000 generations. Hall finally gave up in frustration and
argued that his double mutant E. coli had "limited evolutionary
potential".
What was it that "limited" the evolutionary potential of a huge
population with very high mutation rates and over 4 million base pairs
of DNA to evolve a relatively simple enzymatic function like lactase?
Obviously, it was a non-beneficial gap between what existed in such a
gene-pool, a pool that was no longer "clonal" by the way, and any of
the trillions of potential lactases that exist in sequence space.
> Face it you
> found out that your argument was bogus and you gave it up for the gap
> inflation and now your 1000 aa bunk. No one would believe that you
> were using the Hall experiment as an example of how evolution works.
> You were using it to claim that proteins with those activities were
> difficult to evolve and you know it. Your tune changed only after you
> had to give up that bogus argument and the gap inflation started. I'm
> sure that you recall when the gap moved from 3 to 40.
The gap distance do indeed change Ron. They don't stay the same. The
gap distances increase from a minimum of just a handful to dozens of
mutations, even more than 40, as one moves from just a few hundred
residues and beyond the 1000aa threshold to consider mulitprotein
systems like the flagellar motility system.
> > > For those that don't know what that
> > > is it just means that populations that exist for any length of time
> > > would expect to reach mutation selection balance where the genetic
> > > variation of a population would reach an equilibrium with new
> > > mutations equalling the loss of existing mutations from the
> > > population. Populations have an amazing amount of genetic variation.
> > > They don't have to rely on multiple simultaneous mutations.
>
> > Hall's bacteria actually did have to undergo at least 2 mutations
> > before the beneficial function of lactase activity could be realized.
> > Population variation did not come into play because Hall set up the
> > experiment based on a clonal population where the original genetic
> > sequence was already known as was identical at the start of the
> > experiment.
>
> No, one change was sufficient to be selectable, but the second
> mutation followed very rapidly because Hall selected for growth and
> two mutations would grow faster than the individual singles. In fact
> either single mutation could occur before the other. That is my
> recollection from reading the papers, but if you have evidence to the
> contrary, put it forward. It is my recollection that he found
> examples of each single. He could not have done that unless he could
> select them. In one paper he gave the relative activities of each
> single compared to the double.
Not true. Both mutations had to be there at the same time for the
beneficial effect to be realized. In fact, Hall thought that this was
so mysterious to have happened that he proposed a sort of non-random
almost magical process to realize such a double mutation within just
one or two generations. Why? Because Hall thought that such a double
mutant would require over 100,000 years for his colony to achieve. Of
course, Hall's calculations weren't correct, but that is in fact what
he originally proposed.
< snip repetitive >
> > What Ron and others like Howard Hershey don't seem to realize is that
> > tiny gap distances that are only 1 or 2 or 3 mutational changes wide
> > are not always the most likely minimum gap distance at every level of
> > minimum structural threshold requirements. The likely minimum gap
> > distances increase, in a linear manner, with each increase in the
> > structural threshold requirements. So, by the time the requirements
> > are over 1,000aa, the odds that the gap distance between what is
> > beneficial and what might be beneficial is only a handful of changes
> > wide is next to impossible. The actual gap distance at such levels
> > tends to follow a Poisson distribution making a gap of dozens of
> > changes much more likely to be the true gap distance at the 1000aa
> > minimum threshold.
>
> And you know this how? Why haven't you written a paper on your
> wonderous discoveries. The protein biochemists will all be bowing at
> your feet. Behe might even kiss your hand.
He might indeed! ; )
All you have to do is look it up by doing a simple homology
comparison. You'll quickly see that I'm right. Systems with greater
minimum structural threshold requirements are much more widely
separated in sequence space, as a measure of the Hamming Distance
between nearest neighbors, than are systems with lesser minimum
structural threshold requirements. The concept is not a difficult one
to grasp or to demonstrate quite easily.
> > This concept is what no one who frequents this forum, not Ron Okimoto,
> > Howard Hershey, Von Smith, Richard Baldwin, Richard Forrest, or anyone
> > else, has ever come close to explaining or even addressing without
> > giving up and resorting to the old standbys of endless pejoratives and
> > strawman mischaracterizations (many of which Ron just listed off
> > here).
>
> No. Not true, when you come up with an argument that has to be
> countered someone would have to counter it. As it is, you can't even
> demonstrate that 1000 anythings was needed to evolve the flagellum.
> If you can, do it. Stop pretending and just do it. Put up the
> evolutionary pathway and demonstrate that 1000 anythings had to happen
> all at once to get the job done.
This is a perfect example of strawman building. I never said that the
flagellum had to have 1000 changes to evolve from whatever might have
come before. What I said was that the flagellar motility system
requires a minimum of at least 10,000 fairly specified amino acid
residues coded for by at least 30,000 bp of DNA. This minimum
structural threshold produces a likely minimum gap distance in a very
large colony of bacteria (like the size of all the bacteria on Earth)
that is probably well over a hundred mutations wide between most of
the evolutionary steppingstones proposed by you evolutionists. Such a
gap is simply uncrossable even given many trillions of years of time.
> Now that I've put up with your bull pucky once again, why not put up
> what you claimed that you could put forward. Everyone would like to
> see your alternative to common descent and the evidence for it that
> was just as good as the evidence science has. You might also put
> forward what you claimed to have to teach about the science of
> intelligent design.
Obviously, the alternative to common descent is common design.
> You actually made those claims I don't have to make up junk about what
> you haven't done. You know where you come up short.
But you obviously don't know where you come up short . . . You spend
almost all your time on worthless pejoratives without really getting
into any real consideration of the actual arguments dealing with the
topic at hand. I must say though that this particular series is the
closest you've come to a real meaningful discussion in a very long
time. Keep up the good work! ; )
richardal...@googlemail.com
wrote:
> On Aug 23, 6:41 pm, Ron O <rokim...@cox.net> wrote:
>
> > SNIP the worthless bull pucky:
>
> > Why do you do this?
>
> So others won't have to wade through a long thread to see something
> that might be interesting. You guys start new threads like this all
> the time. I never complain about it when you or Richard Forrest or
> Howard Hershey do it. Why should you?
I don't start new threads in the pretense that my postings have not
been refuted.
When I start new threads asking you questions it is because you have
repeatedly failed to answer a question. Perhaps you miss pertinent
questions in all the tangled sub-threads, so I am only posting
questions as a new thread to give you the opportunity of answering
them.
So let's watch you evade once again, shall we Sean? I know you won't
address this, because you are a moral and intellectual coward, so I
post it merely to demonstrate that fact rather than in the expectation
of a meaningful response. Please note that I have asked you this
question six times, and you have always ignored it.
You go on and on about the exceptional preservation of the Santana
formation fish fossils, though you carefully avoid reading any of the
scientific literature on the subject. It doesn't matter if the fish
were preserved in a matter of hours, days, weeks or years. We have
good experimental evidence that preservation of soft tissues of this
kind can occur in timescales of days. Such preservation is *not*
achieved simply by "sudden burial, as in a flood".
However, the overwhelmingly vast majority of the fossil record is NOT*
preserved in lagerstatten such as the Crato Formation. It's logically
incoherent to offer exceptional preservation in a single, limited
locality as evidence for a global flood when most of the fossil record
is *NOT* exceptionally well-preserved.
Your have stated that: "most fossils show clear evidence of rapid
burial or other forms of relatively rapid or even catastrophic
preservation leaving little time for predation or bioturbation)"
This is plainly ridiculous, as anyone who has ever collected fossils
can tell you. Mike Benton, in the reference which I have provided,
writes
"Animal and plant remains are typically buried after a great deal of
scavenging, decay, breakage and transport."
What do you know that Mike Benton doesn't?
RF
<remained snipped>
Ron O
See this is just more bogus obfuscation about your lying about what I
have claimed. Who can't see that? You obviously can see it or you
wouldn't do it so consistently.
Defend the 1000aa threshold. You have never been able to do it, so
why do you think that it exists? Even if it exists, does it negate
your dishonesty? Why do you keep doing this junk? Don't you wish
that you really had an argument so you wouldn't have to depend on
something that you can't even determine exists? Face it, you just
made up this 1000aa threshold, and you can't back it up in any
meaningful way, so why keep pretending?
>
> Again, the 1000aa threshold is NOT the gap distance. However, it is
> associated with a minimum gap distance for populations of even
> billions of individuals that is dozens of mutations wide. It is the
> linear increase in the gap distance with each increase in the minimum
> structural threshold requirements that creates the problem for the
> proposed evolutionary mechanism. Each linear increase in the minimum
> gap distance translates into an exponential increase in the average
> number of mutational steps needed to cross the gap.
Again it doesn't matter what you think it is, what matters is what it
is, and it is just unsupported assertion based on nothing that you can
demonstrate. Not a gap, but associated with a gap and you treat it
like a gap, but it isn't really a gap. What a crock. Do you actually
read the junk that you write? Does it matter? Just do something
simple and demonstrate that your 1000aa threshold means anything.
There must be some research that you have done and calculations that
you have made so lay out the details. Unsupported assertion is not
laying out any details. You can't just claim that it must be this
way, you have to be able to demonstrate it. Not only that, but you
have to be able to demonstrate that whatever this 1000aa threshold
turns out to be that it is at all relevant to the argument that you
are trying to make.
>
> > > > Then you made the bogus jump to 1000 when you couldn't even
> > > > justify claims of 10.
>
> > > You are very confused Ron. This is because you really haven't spent
> > > any time with the arguments at hand and still don't grasp the concept
> > > that the 1000aa structural threshold requirement is not the same thing
> > > as the gap distance.
>
> > If it isn't then the argument is so lame that even you probably know
> > that you are just blowing smoke. Name anyone that believes that you
> > have to assemble a thousand amino acids to evolve some protein
> > function. Anyone except the creationist scam artists that you have to
> > admit lied to you about the science of ID.
>
> I never said that you have to assemble 1000aa from scratch. That is
> why the 1000aa is not the same thing as the gap distance. Again, the
> 1000aa is a threshold that defines certain types of functional systems
> that require at least 1000 specifically arranged amino acid residues
> to work at all. Much of the 1000aa requirement may already exist
> preformed within a given gene pool. However, odds are that at least a
> few dozen mutations would be needed before the minimum structural
> threshold requirements of a new unique system with threshold
> requirements at or beyond this limitation could be realized. It is
> this few dozen needed mutations that is the "gap distance".
Demonstrate it. Show that a dozen mutations have had to be crossed in
one step to get a selectable function. Why can't you do that? Why do
you think that you have a valid argument when you can't do that.
Don't you even keep track of the ID claptrap. They have faced this
same problem for over a decade. Don't you know what they admit about
it? They admit that they have to demonstrate that every possible
evolutionary pathway to a certain selectable function is too
improbable for their argument to hold water. Since they don't even
know what all the possible evolutionary pathways are they gave up.
Dembski promised to do it, but all he came up with was the stupid
tornado through a junk yard probability argument that he admitted was
not biologically relevant. To make the biologically relevant argument
you have to determine what existed and the probability that it could
change to the new function. You can't even start to do that. The
other ID scam artists didn't even try. So what does that say about
this worthless argument?
>
> The minimum possible gap distance is, of course, always one. This is
> true regardless of the minimum structural threshold requirements under
> consideration. The problem is that this minimum possible gap distance
> is not always the most likely gap distance. It is all about the odds
> that the gap distance will be small - like one or two steps wide.
> These odds drop, quite dramatically, along a Poisson distribution as
> one considers functional systems with greater and greater minimum
> structural threshold requirements. Very quickly the likely minimum
> gap distance is no longer just one mutation wide - but dozens of
> mutations wide. By the time such a minimum gap distance is produced,
> the average time required to evolve something new at such a level of
> minimum structural threshold requirements has moved into trillions
> upon trillions of years of average time.
I thought that we weren't talking about gaps. There seems to be a big
gap somewhere, but it isn't in protein sequence space.
Face it you can't back this up and the only evidence that you have
says that you are wrong. How does your immune system work to keep you
alive if this were even close to being true? Why can you develop
enzyme activities in antibodies, and antibodies can be made to
synthetic antigens that have not been seen in nature before. You just
claim that this isn't the type of gap that you are talking about, but
you don't know that. You can't even demonstrate it. You just assert
it because your argument doesn't hold water in the face of reality.
This is protein sequence evolution on a rapid scale and if it had to
cross your exponential gaps you would be probably be dead.
For a specific system, tell us the minimum and then demonstrate that
it didn't exist. Show us the protein sequences and how they would
have had to evolve to get the job done. Put up or shut up. Just do
what you have to do to make this argument valid. You can't just make
baseless claims. There has to be some supporting evidence, so put it
up. You know what you need so put it forward.
>
> Look it up and see if you do not discover a pattern - a pattern of
> increased minimum differences for higher and higher level systems that
> increases in a linear manner with each increase in the minimum
> structural threshold requirements of the systems in question.
>
Demonstrate it. Put up the starting material and demonstrate what you
have just claimed. Why can't you do that? Make it biologically
relevant. Take the flagellar ATPase and figure out the ATPase that it
evolved from, and the ancestral sequence and demonstrate that there
was too large of a gap for this protein to cross to gain the
selectable function leading to its incorporation into the flagellar
system.
You have to figure out the progenitor sequence, the sequence that it
evolved into. You will have to develop a scenario for the evolution
of the flagellum that doesn't exist in any form that you can use at
this time. So go for it. You will become world famous after you can
demonstrate it all. It might take a decade or two, but a lot of
protein sequence is coming in, but it turns out that the flagellum is
likely several billion years old and you know what happens to proteins
in that amount of time. Reconstruction is going to be a pain in the
butt if not already impossible, but go for it and report back when you
have something worth reporting.
The simple point is that you can't tell anyone that there was a gap
when you can't tell anyone what the gap was.
That doesn't mean jack and you know it. About as pathetic as I
expected. Evolution is descent with modification. We see the winners
and they don't have to have the best or most efficient gene, just the
gene that does the job and enough of a head start to make it difficult
for anyother lifeform to follow them into the niche.
You have a gene Duschenes muscular dystrophe gene that has a
transcript length of over a million base-pairs in length. Fugu have
reduced their genome size to 1/10 the size of humans, but the same
gene is still over 300 million base-pairs in length. It only needs to
be 14,000 bp (the final transcript size, the coding size is even
less). When can we expect the gene to evolve down to its minimum and
most efficient size? The answer is that it might never get there.
All evolution is interested is in the survival of the species. There
are many other things about an organism obviously more important than
reducing the overly large size of some genes. They work well enough
to get the job done, and cutting them down to size doesn't seem to
give the organism enough selective advantage to matter.
>
> > Lame unsupported assertions
> > are just that, lame unsupported assertions. Back it up. How do you
> > know that lactase requires 400? Do you have any evidence that lactase
> > needs at least 400? E. coli Beta gal (Lac Z) is around 1000 amino
> > acids,
>
> That isn't the most trimmed down version available. Much smaller
> lactases can be used to at least some advantage. But, the limit
> appears to be at around 400aa (380aa is the smallest one I've been
> able to find).
Those are partial fragments used in cloning vectors. I've used plenty
of them. The smaller the junk you needed in the cloning vector the
more DNA you could expect to shove in. Little pUC was only 2.7 kb
long and had Lac Z and ampicillin resistance stuffed into it. Lac Z
as a color indicator of insertion and amp as a selectable marker. The
whole vector was shorter than the original Lac Z gene. They are the
functional bits that we figured out could work well enough by cutting
up the original gene. They are not works from scratch nor have we
even attempted to figure out the minimum protein sequence that would
do the job. We just lopped off pieces and observed what still worked.
>
> > but you are probably going by the size of the EBG gene that
> > evolved beta gal activity that was half the size.
>
> The product of the ebg-gene is was also around 1000aa. Again though,
> this isn't the minimum requirement. It is the minimum structural
> requirement that is statistically important here.
You don't know the minimum anything. You can't even tell how many
different 400 aa sequence can have beta gal activity, let alone how
many 1000 aa sequence. You have to admit that you don't even know if
a smaller sequence could have beta gal activity. It is all for squat
anyways because you can't tell if any protein sequence was far enough
away from anything that had to evolve to produce the flagellum to
qualify as a gap large enough to worry about. Out of only 2000
proteins one was only 2 aa subs from pretty good beta gal activity.
The same could be said about two or three other bacterial species.
Just demonstrate that your gaps existed. I know that you aren't
supposed to be talking about gaps, but we are and you know that your
1000aa bullpucky depends on these gaps even if they aren't really gaps
etc, etc,, but just demonstrate that one such gap existed that was
part of your 1000aa gap or threshold or whatever you want to call it.
>
> > Why couldn't beta
> > gal activity evolve in a smaller protein?
>
> Because lactase activity has a minimum structural threshold
> requirement just like all functional systems have. Different types of
> systems have different minimum requirements. It turns out that the
> lactase system in bacteria have a threshold requirement that appears
> to be around 400aa.
400 aa from the Lac Z starting sequence. How many possible starting
sequences are there? Your assertion doesn't mean jack about the
minimum size does it? I'll even give you this. Beta gal activity is
one of the rarer types of activities that we observe in enzymes, but
it doesn't mean squat about the minimum size of the chain that will
give it to you. Larger proteins have more chance to evolve such a
function simply because they have a larger surface area, but you could
try more smaller sequences to compensate for that search factor. Beta
gal activity is one of the ones they evolved using antibodies. I
believe that they specifically looked for it because they thought that
it might be difficult to evolve it.
>
> > Do you really know the lower size limit?
>
> To a useful approximation . . .
Prove it. Put forward one example where flagella had to cross such a
gap. Just one.
>
> > What does that limit matter?
>
> The limit matters because those systems with smaller limits are much
> easier to evolve than are those systems with larger limits. Why?
> Because, statistically, a smaller limit will have much greater odds of
> being close to pre-existing sequences in a large gene pool.
No one claims that the flagellum evolved all at once. Put forward
your scenario and get science to agree with it. Go for it.
>
>
>
> > You are cooked by
> > your own argument. There weren't a thousand specified
>
> ...
Still running. Why not face the facts. Where is your alternative to
common descent and the evidence to back it up? Where is the science
of intelligent design that you were going to teach in the science
class? By your above obfuscation you are admitting that I never made
the claims that you claim I came up short on, but you know for a fact
that you did make the claims about common descient and ID, but you
will not make good on them. How is that at all honest? Just
pretending and running away doesn't do you any good because you are
warped enough to keep coming back with some bogus obfuscation
twaddle. You know that is all bogus if you can't make good on the
basic claims that you have made. You have no viable alternative to
common descent, and even the perps that ran the ID bait and switch
scam are admitting that they never had the science to back up the
scam. If you believe that those statements are not true, demonstrate
it.
Ron Okimoto
richardal...@googlemail.com
> ลพus cwฤลก richardalanforr...@googlemail.com :
My reading of Pitman's character is that he is quite content to
impress the loonies and meatheads.
RF
hersheyh
0catch.com> wrote:
> On Aug 23, 6:41 pm, Ron O <rokim...@cox.net> wrote:
>
> > SNIP the worthless bull pucky:
>
> > Why do you do this?
>
> So others won't have to wade through a long thread to see something
> that might be interesting. You guys start new threads like this all
> the time. I never complain about it when you or Richard Forrest or
> Howard Hershey do it. Why should you?
I *rarely* start new threads. I mostly reply to presented bullshit by
bullmerde artistes.
> > Go find my response in the original thread that this double post came
> > from.
>
> Here it is:
>
> > Aren't you just admitting that you are just blowing smoke about any
> > claims that I may have made? Aren't you just lying about me having a
> > problem with any claim that you have made?
>
> > Why do you have to settle for the obfuscation scam?
>
> > What happened to the gap distance bogousity? If you aren't talking
> > about the gap bogousity than you aren't talking about anything
> > relevant to evolutionary biology. No one claims that a protein has to
> > evolve from scratch. You know for a fact that whenever we look it is
> > some existing protein changing to something else. If that is your
> > argument then you have none.
>
> I'm not suggesting that a protein-based system has to evolve from
> scratch either. Start with whatever starting point you want.
Unless, of course, the starting point is merely a single mutational
step or two or three away from a new function.
> Novel
> protein-based systems that require a threshold of at least 1000
> specifically arranged amino acid residues will not be able to evolve
> from any gene pool you choose in existence today even given trillions
> of years of time. Why not? Because, the 1000aa threshold, although
> not the gap distance itself, creates a gap that is several dozens of
> mutations wide.
And where is your evidence for this *assertion*? I keep asking you to
provide this *crucial-to-your-argument* mathematical relationship and
you keep either *ignoring* my repeated pleas for evidence or you do as
you do here and merely hand-wave a number into existence.
> Again, the 1000aa threshold is NOT the gap distance.
We *know* that. We also *know* that you keep tossing out that number
as if it had some relevance to calculating the gap distance. But you
never present the argument that show us that it is.
> However, it is
> associated with a minimum gap distance for populations of even
> billions of individuals that is dozens of mutations wide.
More hand-waving assertion of the *supposed* relationship between
total size and gap size. No evidence. No support at all. Pure
assertion.
> It is the
> linear increase in the gap distance with each increase in the minimum
> structural threshold requirements that creates the problem for the
> proposed evolutionary mechanism. Each linear increase in the minimum
> gap distance translates into an exponential increase in the average
> number of mutational steps needed to cross the gap.
Before you can make a claim that a linear increase in gap size
translates into an exponential increase in average number of
mutational steps needed to cross the gap, you have to demonstrate that
there *actually* is a linear increase in gap size with increasing
total size. I haven't seen that evidence at all. But if one assumes
that your hand-waving number that you apparently pulled out of yer
arse is 60 mutational steps for a protein of size of 1000 [your hand-
waving number was "several dozen", which is too vague to be useful, so
I chose the maximum number for "several" as 5], what you seem to be
saying is that, on average, for a new function to arise, about 6% of
any (the average?) existing ancestral protein's sequence *must* change
in a completely neutral fashion, with intermediate states having no
functional utility at all, to produce a protein that has any sort of
useful altered function. [You can correct me if I am wrong, but since
you have repeatedly and repeatedly and repeatedly failed to actually
discuss this hypothetical and crucial relationship, I must.] Is this
correct? And what empirical evidence do you have that it is correct?
Of course, we both know that this *average* protein would not be the
one that evolution uses as the starting point. But you must at least
start with some sort of argument.
> > > > Then you made the bogus jump to 1000 when you couldn't even
> > > > justify claims of 10.
>
> > > You are very confused Ron. This is because you really haven't spent
> > > any time with the arguments at hand and still don't grasp the concept
> > > that the 1000aa structural threshold requirement is not the same thing
> > > as the gap distance.
>
> > If it isn't then the argument is so lame that even you probably know
> > that you are just blowing smoke. Name anyone that believes that you
> > have to assemble a thousand amino acids to evolve some protein
> > function. Anyone except the creationist scam artists that you have to
> > admit lied to you about the science of ID.
>
> I never said that you have to assemble 1000aa from scratch. That is
> why the 1000aa is not the same thing as the gap distance.
But you *do* keep asserting, without ever presenting supporting
evidence or an actual equation, that there is a linear correlation of
some sort between total size of a protein and the number of mutational
steps needed to evolve a "new" function (which you haven't defined
adequately -- does acquiring a "new" function mean that the "old"
function must cease to exist? At what point does modification of
function equal "new"? Can functions 'emerge' from quantitative
changes? Is a change of optimum to a secondary substrate a "new"
function?).
This is real simple math even you should be able to do: You claim
that there is an equation of the form y = bn (I am assuming that the y
intercept is 0 when n = 0), where y is the gap size, n is the size of
the "minimum threshold" or total size, and b is the linear
relationship between total size and gap size. b should be obtainable
by looking at real data for the evolution of "new" functions from old
proteins. But you don't seem to actually present this equation nor
the evidence that you use to determine b (which you *repeatedly* claim
exists).
> Again, the
> 1000aa is a threshold that defines certain types of functional systems
> that require at least 1000 specifically arranged amino acid residues
> to work at all. Much of the 1000aa requirement may already exist
> preformed within a given gene pool. However, odds are that at least a
> few dozen mutations would be needed before the minimum structural
> threshold requirements of a new unique system with threshold
> requirements at or beyond this limitation could be realized. It is
> this few dozen needed mutations that is the "gap distance".
Yet, as you say, what really matters wrt whether something can or
cannot evolve is what proteins (particularly *structure* more than
*sequence*) actually exists in any given cell, not any hypothetical
*average* gap distance.
> The minimum possible gap distance is, of course, always one. This is
> true regardless of the minimum structural threshold requirements under
> consideration. The problem is that this minimum possible gap distance
> is not always the most likely gap distance.
Evolution is not teleological in nature.
> It is all about the odds
> that the gap distance will be small - like one or two steps wide.
> These odds drop, quite dramatically, along a Poisson distribution as
> one considers functional systems with greater and greater minimum
> structural threshold requirements.
This does assume that the hypothetical linear relationship exists as a
linear relationship regardless of the total size. And it does assume
that evolution is teleological in that it produces *functions*
regardless of the size of the gap needed to produce that function.
Instead most people think that evolution only happens when the size of
any gap between useful functions is relatively small. IOW, the
average gap size in a theoretical sequence space is irrelevant when
the only events that actually happened are those that are on a tail
end. And one consequence of such a non-average evolution is that
structures of life (structure is a better indicator of function than
sequence) should be clustered and appear in those clusters as organic
outgrowth rather than random scatter.
> Very quickly the likely minimum
> gap distance is no longer just one mutation wide - but dozens of
> mutations wide. By the time such a minimum gap distance is produced,
Now you have switched from the *average* gap distance to the "likely
minimum gap distance". As *you* pointed out the "minimum gap
distance" is always one. And evolution almost always works by the
smallest *available* gap distance between functional states and is non-
teleological. Wouldn't that merely mean that the evolution that *did*
happen happened when the "minimum gap distance" is small enough to
cross. I have no idea how you calculate the "likely" minimum gap size
as anything more than one. At what point does one become "unlikely"
even if the *average* gap size is 60 (as, if you accept my numbers, it
would be for a total size of 1000)? Does that mean that you think
there is a very small variance? How did you calculate that variance?
Given that there are thousands of species and millions of years, at
what % of all possible likelihoods is the probability of 1 (or less
than, say, three) too small to be possible even if the *average* gap
size is 60?
> the average time required to evolve something new at such a level of
> minimum structural threshold requirements has moved into trillions
> upon trillions of years of average time.
So you keep asserting. But I certainly have seen no actual argument
that wasn't bogus (based on *maximum* or *average* gap numbers that
were essentially pulled out of yer arse) where you have presented such
an argument.
> > > > I claim that there isn't a single instance of
> > > > where 12 changes were required because we've haven't found any that
> > > > required 12. Demonstrate differently. You never could, now it is
> > > > suddenly my fault that you can't come up with an example of 12 changes
> > > > being required? What kind of bogus argument is that?
>
> > > The demonstration here is found in the exponential decline of
> > > evolvability with increasing minimum structural threshold requirements
> > > until evolution completely stalls out well shy of the 1000aa
> > > threshold. You haven't presented any counter arguments or
> > > explanations to explain how this very real phenomenon might be the
> > > result of some other cause beside the linear expanding gap problem
> > > I've been proposing for many years now.
All your argument does is restrict that which has evolved to being
modifications that don't cross large gaps from pre-existing proteins
or moieties. IOW, it restricts evolution to "descent with and by
modification", although sometimes the modification involves chimeric
protein formation or duplication and divergence. I have no problem
with accepting such a limitation.
> > Now you seem to be mixing gap with your bogus assertion about how
> > proteins evolve. Face it Sean the thousand amino acids essentially
> > already existed. Small changes in the protein structure would have
> > accounted for the evolution of the proteins needed for flagellar
> > structure. Why can we tell what proteins a lot of the flagellar
> > proteins evolved from if this were not true? Where did the ATPases
> > come from? They didn't evolve denovo did they?
>
> The question here is "how small" are the changes that are required
> Ron? For systems that have a minimum structural threshold requirement
> of only a few hundred loosely specified residues, the minimum number
> of changes for at least one member of a huge population of bacteria is
> most likely just a handful of mutations.
You need to distinguish between the number of mutations that produces
a selectable level of a particular function, the mutations that, once
one has a selectable level of function, lead to quantitative and
qualitative optimization of that function, and mutations that are
selectively neutral but accumulate over geological time. You seem to
lump any *difference* between proteins as evidence of the first type
of mutation even though the *evidence* is that most differences are of
the last kind, many are of the second kind, and the first type of
mutation is actually quite rare wrt accounting for differences.
> However, when you start
> talking about minimum threshold requirements of over 1000aa, the
> minimum number of changes is no longer just a handful. Rather, it is
> on the order of dozens of mutations.
>
> Look it up and see if you do not discover a pattern - a pattern of
> increased minimum differences for higher and higher level systems that
> increases in a linear manner with each increase in the minimum
> structural threshold requirements of the systems in question.
I see no such pattern. Where do you? I have seen you *repeatedlly*
assert that such a pattern exists. But never come up with actual
evidence that was relevant.
> > > > Remember the Hall junk that you used to claim meant something? He
> > > > found that only 1 change was required to change ebg to having beta gal
> > > > activity. Two changes made it even better. He found this in an
> > > > organism with only around 2000 protein genes. Only 2000 chances for a
> > > > sequence to be close enough to the desired activity to get there in 1
> > > > or two mutations. Halls experimental methodology limited the number
> > > > of mutations required because it was a single step selection and at
> > > > best he could expect to select for double mutations. He even repeated
> > > > it with other species of bacteria. I believe your own references
> > > > cited 2 or 3 other bacteria that he could get to evolve beta gal
> > > > activity, but he might not have figured out which genes had been
> > > > altered in them. Like he had in identifying the ebg gene in E. coli.
>
> > > You continually forget that the minimum structural requirement for
> > > lactase activity is only 400 or so fairly specified amino acid
> > > residues. That's the whole point Ron. The E. coli in Hall's
> > > experiment were successful because the functional system in question
> > > has a relatively low minimum structural threshold requirement - not
> > > even close to the 1,000 level. The same thing is true of the famous
> > > nylonase example that evolutionists love to quote. As it turns out,
> > > nylonase requires less of a structural threshold than the lactase
> > > enzyme - only 280 or so residues.
With a linear relationship between total size and gap size, I would
expect that the gap size for lactases should be about 24 selectively
neutral mutations (0.4 * 60, which is the value for a protein of 1000
aas). Yet there it is, a gap of 1 or 2 actually existing in a real
organism. Does that mean that the "likely minimum gap size" for a
protein of 1000 should be around 6? And why would that be the "likely
minimum gap size" rather than one? Or perhaps there simply is no
linear relationship between total size and gap size? Perhaps gap size
is a function of other features and not total size to any significant
extent at all?
>
> > And you know that it higher for something else, how? Who claimed that
> > 400 specified amino acids were required?
>
> Do a BLAST search Ron. See if you can find a useful lactase enzyme
> (in a bacterial colony) that uses significantly less than 400 or so
> amino acid residues.
Not relevant and not what BLAST does.
> Every type of functional system has a minimum
> structural threshold requirement that, if not reached, will not
> provide a reproductive advantage to a particular type of life form -
> such as a bacterial life form. For the lactase function in bacteria,
> it turns out that this minimum requirement is around 400aa.
And what makes you think that this is the minimum possible size? It
may be the minimum size that nature has discovered to date. That
doesn't make it the absolute minimum size.
> > Lame unsupported assertions
> > are just that, lame unsupported assertions. Back it up. How do you
> > know that lactase requires 400? Do you have any evidence that lactase
> > needs at least 400? E. coli Beta gal (Lac Z) is around 1000 amino
> > acids,
>
> That isn't the most trimmed down version available. Much smaller
> lactases can be used to at least some advantage. But, the limit
> appears to be at around 400aa (380aa is the smallest one I've been
> able to find).
>
> > but you are probably going by the size of the EBG gene that
> > evolved beta gal activity that was half the size.
>
> The product of the ebg-gene is was also around 1000aa. Again though,
> this isn't the minimum requirement. It is the minimum structural
> requirement that is statistically important here.
Why?
> > Why couldn't beta
> > gal activity evolve in a smaller protein?
>
> Because lactase activity has a minimum structural threshold
> requirement just like all functional systems have. Different types of
> systems have different minimum requirements. It turns out that the
> lactase system in bacteria have a threshold requirement that appears
> to be around 400aa.
>
> > Do you really know the lower size limit?
>
> To a useful approximation . . .
>
> > What does that limit matter?
>
> The limit matters because those systems with smaller limits are much
> easier to evolve than are those systems with larger limits. Why?
> Because, statistically, a smaller limit will have much greater odds of
> being close to pre-existing sequences in a large gene pool.
>
> > You are cooked by
> > your own argument. There weren't a thousand specified
>
> ...
>
> read more ยป
Tiny Bulcher
Well, it won't work, then. The loonies and meatheads we get here are all
obsessives with their own agendas ... they are not interested in others'
obsessions. I bet they don't even /read/ his threads.
R. Baldwin
news:1188016705....@q4g2000prc.googlegroups.com...
> On Aug 23, 6:41 pm, Ron O <rokim...@cox.net> wrote:
>> SNIP the worthless bull pucky:
>>
>> Why do you do this?
>
> So others won't have to wade through a long thread to see something
> that might be interesting. You guys start new threads like this all
> the time. I never complain about it when you or Richard Forrest or
> Howard Hershey do it. Why should you?
>
Howard Hershey doesn't do this.
I suggest that the larger probem is you post the same thing in two threads,
causing your correspondents to curse audibly after posting a long point by
point response in the first thread only to discover you've started a new
one. If you want to split to a new thread, why don't you say so in the old
thread?
Seanpit
< snip >
> > > Why couldn't beta
> > > gal activity evolve in a smaller protein?
>
> > Because lactase activity has a minimum structural threshold
> > requirement just like all functional systems have. Different types of
> > systems have different minimum requirements. It turns out that the
> > lactase system in bacteria have a threshold requirement that appears
> > to be around 400aa.
>
> 400 aa from the Lac Z starting sequence.
You still don't get it. The minimum structural threshold requirement
isn't relative to some other sequence. It isn't "from" any starting
sequence. The ebg sequence didn't evolve from a LacZ sequence. It
was a unique sequence that happened to be close to one of a great many
potential lactase sequences in the vastness of sequence space at the
400aa minimum level.
> How many possible starting sequences are there?
The number of starting points is the number of genetic sequences of a
given length in a particular gene pool. That number is far more
limited than the number of potential sequences of a given length.
For example, E. coli have access to around 4e6 bp of genetic real
estate. Even given a population the size of all bacteria on Earth
(around 1e30), the total size of available genetic real estate would
only be around 1e36. This is a far cry from the size of 400aa
sequence space of about 1e520. So, the odds that anything in the gene
pool would be within one or two mutations of any sequence with a
lactase function depends upon the ratio of lactase sequences in 400aa
sequence space.
As it turns out, there have been several scientists who have published
rough estimates for such ratios when it comes to specific types of
single-protein functions - Yockey, Sauer, Olsen, Choi and Kim to name
just a few. Choi and Kim's paper is especially interesting:
http://www.pnas.org/content/vol103/issue38/images/large/zpq0370634700004.jpeg
Notice in the above listed image that the smaller proteins mapped from
hyperdimensional sequence space onto three dimensions have a much
closer average distance as compared to the larger proteins. This
means that the likely minimum distance from any given starting point
or points does not remain at the minimum possible distance (i.e., one)
as you and those like Howard Hershey often parrot. Rather, the likely
minimum distance increases in a linear manner as the minimum size and/
or specificity threshold requirements increase.
> Your assertion doesn't mean jack about the
> minimum size does it? I'll even give you this. Beta gal activity is
> one of the rarer types of activities that we observe in enzymes, but
> it doesn't mean squat about the minimum size of the chain that will
> give it to you.
Oh really? Then it would be possible to build a useful lactase enzyme
(useful from the perspective of a bacterium) with just 10aa? How about
100aa? Have any evidence for this? If so, I'd really like to see
it . . .
> Larger proteins have more chance to evolve such a
> function simply because they have a larger surface area, but you could
> try more smaller sequences to compensate for that search factor. Beta
> gal activity is one of the ones they evolved using antibodies. I
> believe that they specifically looked for it because they thought that
> it might be difficult to evolve it.
If you look into the matter of antibodies with lactase activity, you
will find that none of these had significantly fewer than 400aa
residues. I've pointed this observation out many times now in this
forum, yet it keeps surfacing as if it somehow means something . . .
In short, larger proteins are more likely to evolve the lactase
function because they are more likely to have the 400aa minimum in
place. No matter how you arrange the residues, a 50aa protein just
won't be able to do the job.
You and those like Howard have this strange notion that all protein
systems are created equal - that there is no such thing as different
minimum structural threshold requirements. This notion of yours is
simply ludicrous. It is overwhelmingly obvious to anyone with a
candid mind that different types of functional systems have different
minimum structural threshold requirements. Those with larger minimum
requirements are exponentially harder for a particular gene pool to
evolve. The obvious reason for this is because of the expanding non-
beneficial gap problem - i.e., the exponential decline in the odds
that the real minimum gap distance will actually be the minimum
possible gap distance.
> > > Do you really know the lower size limit?
>
> > To a useful approximation . . .
>
> Prove it. Put forward one example where flagella had to cross such a
> gap. Just one.
Show me just one of the proposed steppingstones in flagellar evolution
where just one or two mutations would have done the job. Such a
notion of small gaps between the supposed steppingstones is based on
nothing more than wishful thinking Ron. All of the proposed steps in
the flagellar evolution pathway are separated from each other by
dozens of required changes or mutations. Yet, no one really talks
about this. It is just assumed that evolution did the job somehow and
no one feels the need to do any sort of real statistical evaluation to
see if such an assertion makes rational statistical sense.
If you want further details of the gaps involved in the proposed steps
of flagellar evolution see:
http://www.detectingdesign.com/flagellum.html
> > > What does that limit matter?
>
> > The limit matters because those systems with smaller limits are much
> > easier to evolve than are those systems with larger limits. Why?
> > Because, statistically, a smaller limit will have much greater odds of
> > being close to pre-existing sequences in a large gene pool.
>
> No one claims that the flagellum evolved all at once. Put forward
> your scenario and get science to agree with it. Go for it.
You claim that the flagellum evolved in a stepwise manner from what
was already there before. That's great. Show me how these proposed
steps of yours where all smaller than one or two mutations wide . . .
each step being more functionally beneficial than what came before.
That's what you evolutionists are up against Ron. You come up with
these fantastic stories about how the steps were so small without
really looking into the details to discover that a gap of just a few
dozen steps is fundamentally lethal to your theory.
> > > You are cooked by
> > > your own argument. There weren't a thousand specified
>
> > ...
>
> Still running. Why not face the facts. Where is your alternative to
> common descent and the evidence to back it up? Where is the science
> of intelligent design that you were going to teach in the science
> class? By your above obfuscation you are admitting that I never made
> the claims that you claim I came up short on, but you know for a fact
> that you did make the claims about common descient and ID, but you
> will not make good on them. How is that at all honest? Just
> pretending and running away doesn't do you any good because you are
> warped enough to keep coming back with some bogus obfuscation
> twaddle. You know that is all bogus if you can't make good on the
> basic claims that you have made. You have no viable alternative to
> common descent, and even the perps that ran the ID bait and switch
> scam are admitting that they never had the science to back up the
> scam. If you believe that those statements are not true, demonstrate
> it.
I've yet to see you or anyone else in this forum present any
reasonable evidence for your wild notion that the minimum possible gap
distance (i.e., one mutation) is always the likely gap distance
regardless of the minimum structural threshold requirements for
different types of systems. This notion is obviously mistaken and is
never honestly evaluated by the evolutionists in this forum. You just
wave your hands over this problem and pretend that it doesn't exist.
Your theory isn't really based in scientific evaluation and
statistical analysis. Rather, it is based exclusively on the
assumption that your proposed method did the job without actually
putting your proposed mechanism to the test.
One more thing, no one has to present any alternative to a proposed
hypothesis before the proposed hypothesis can be adequately questioned
and falsified.
Seanpit
> รพus cwรฆรฐ richardalanforr...@googlemail.com :
>
>
>
>
>
> > On 24 Aug, 18:36, "Tiny Bulcher" <alycid...@btinternet.com> wrote:
> >> รพus cwรฆรฐ richardalanforr...@googlemail.com :
>
> >>> On 24 Aug, 02:41, Ron O <rokim...@cox.net> wrote:
> >>>> SNIP the worthless bull pucky:
>
> >>>> Why do you do this?
>
> >>>> Go find my response in the original thread that this double post
> >>>> came from.
>
> >>>> Ron Okimoto
>
> >>> You know that his argument is invalid and already demolished on
> >>> numerous occasions.
>
> >>> Every participant on this forum who has an open mind and the ability
> >>> to think, let alone the ability to seek out the many threads in
> >>> which this argument was demolished knows that this argument is a
> >>> load of bulshit.
>
>
> >>> He posts it again so that he can give the impression to other
> >>> creationists that he is a scientist making valid scientific
> >>> arguments which "evolutionists" cannot falsify. He knows the
> >>> creationists are so ignorant of science that they have neither the
> >>> ability nor the will to form an objective judgement of the validity
> >>> of his argument, and will not bother to read back through the
> >>> numerous threads in which it has been demolished.
>
> >>> So basically, he reposts it so that he can gain status in the
> >>> creationist camp, and is relying on the ignorance and gullibility of
> >>> creationists to get away with the blatant dishonesty he displays by
> >>> ignoring the numerous postings which have demolished his assertions.
>
> >>> I think that this shows contempt for his own side in the argument. I
> >>> urge any creationist who has any desire to learn the truth of this
> >>> been demolished, and try to form an objective view on whether or not
> >>> they have any validity.
>
> >> The problem with that hypothesis is that if this were so, he is
> >> posting in the wrong place. Who is it who reads t.o. he is trying to
> >> impress? Very few creationists hang out here, really, and nearly all
> >> very unlikely to want to impress. Nearly all of the cleverer
> >> creationists avoid places where they might have to debate actual
> >> scientists like the proverbial infectious disease, and concentrate
> >> their efforts on preaching to the choir.
>
> >> My own hypothesis, FWIW, (and I freely confess that the arguments
> >> he is primarily trying to convince himself.
>
> > impress the loonies and meatheads.
>
> Well, it won't work, then. The loonies and meatheads we get here are all
> obsessives with their own agendas ... they are not interested in others'
> obsessions. I bet they don't even /read/ his threads.
Richard can't understand why any sincere creationist would come to a
forum like this? He can't comprehend that I'm not here to convince
anyone - certainly not the creationists in this forum or even the
evolutionists. Most of the creationists who frequent this forum have
no more clue than the evolutionists - in my opinion.
In short, I'm here for myself. To test my own ideas to see if anyone
in even the most adversarial forums, has anything that remotely
challenges my ideas in a way that actually makes sense to me.
To be honest, I've had to modify or completely discard a number of
points. But, so far, these have been relatively minor. My main
points regarding the evidence for intelligent design and how to detect
it continue to gain ground and have withstood almost 10 years of
challenges by members of this forum - some a bit brighter than Richard
and his constant strawman misrepresentations.
Sean Pitman
www.DetectingDesign.com
Ron O
wrote:
> On Aug 25, 6:18 am, Ron O <rokim...@cox.net> wrote:
>
> < snip >
>
> > > > Why couldn't beta
> > > > gal activity evolve in a smaller protein?
>
> > > Because lactase activity has a minimum structural threshold
> > > requirement just like all functional systems have. Different types of
> > > systems have different minimum requirements. It turns out that the
> > > lactase system in bacteria have a threshold requirement that appears
> > > to be around 400aa.
>
> > 400 aa from the Lac Z starting sequence.
>
> You still don't get it. The minimum structural threshold requirement
> isn't relative to some other sequence. It isn't "from" any starting
> sequence. The ebg sequence didn't evolve from a LacZ sequence. It
> was a unique sequence that happened to be close to one of a great many
> potential lactase sequences in the vastness of sequence space at the
> 400aa minimum level.
You are getting some kind of message, but you are mixing it up with
bogus bull pucky about some 400 minimum. The whole point is that
there are sequences close to what is needed and that you can't keep
them from existing.
Your 400 minimum is something that you just made up. Admit it. Where
did it come from?
>
> > How many possible starting sequences are there?
>
> The number of starting points is the number of genetic sequences of a
> given length in a particular gene pool. That number is far more
> limited than the number of potential sequences of a given length.
>
> For example, E. coli have access to around 4e6 bp of genetic real
> estate. Even given a population the size of all bacteria on Earth
> (around 1e30), the total size of available genetic real estate would
> only be around 1e36. This is a far cry from the size of 400aa
> sequence space of about 1e520. So, the odds that anything in the gene
> pool would be within one or two mutations of any sequence with a
> lactase function depends upon the ratio of lactase sequences in 400aa
> sequence space.
Just imagine if you were right. Why was E. coli close enough to get
the job done? Something is obviously wrong with your argument because
Hall got it to work with 2 or 3 other species out of whatever number
he tested, and I bet that it was less than 50 species tested.
Some how the impossible happens too often for your argument to
possibly be corect.
>
> As it turns out, there have been several scientists who have published
> rough estimates for such ratios when it comes to specific types of
> single-protein functions - Yockey, Sauer, Olsen, Choi and Kim to name
> just a few. Choi and Kim's paper is especially interesting:
>
> http://www.pnas.org/content/vol103/issue38/images/large/zpq0370634700...
>
> Notice in the above listed image that the smaller proteins mapped from
> hyperdimensional sequence space onto three dimensions have a much
> closer average distance as compared to the larger proteins. This
> means that the likely minimum distance from any given starting point
> or points does not remain at the minimum possible distance (i.e., one)
> as you and those like Howard Hershey often parrot. Rather, the likely
> minimum distance increases in a linear manner as the minimum size and/
> or specificity threshold requirements increase.
Your reference is pathetically inadequate and you should give a proper
reference and not just to some stupid figure. This seems to be
calculations from a given point. This is stupid. How many starting
points are there? What does reality tell you? Choi and Kim can't
even predict how close any sequence is. They have to estimate what it
would take to move a certain distance, but they can't tell you how
many existing sequences are already closer than that. Would they have
been able to tell you that EBG was only one substitution away from
beta gal activity? I doubt it.
>
> > Your assertion doesn't mean jack about the
> > minimum size does it? I'll even give you this. Beta gal activity is
> > one of the rarer types of activities that we observe in enzymes, but
> > it doesn't mean squat about the minimum size of the chain that will
> > give it to you.
>
> Oh really? Then it would be possible to build a useful lactase enzyme
> (useful from the perspective of a bacterium) with just 10aa? How about
> 100aa? Have any evidence for this? If so, I'd really like to see
> it . . .
Once someone tries you might get your answer. Until then you are just
blowing smoke so why make yourself look so stupid?
>
> > Larger proteins have more chance to evolve such a
> > function simply because they have a larger surface area, but you could
> > try more smaller sequences to compensate for that search factor. Beta
> > gal activity is one of the ones they evolved using antibodies. I
> > believe that they specifically looked for it because they thought that
> > it might be difficult to evolve it.
>
> If you look into the matter of antibodies with lactase activity, you
> will find that none of these had significantly fewer than 400aa
> residues. I've pointed this observation out many times now in this
> forum, yet it keeps surfacing as if it somehow means something . . .
You know that this doesn't mean jack because most of the antibody
sequence isn't involved in creating the beta gal activity most of it
is use to produce the antibody structure. Again, this is stupid.
I'm going to SNIP the rest and skip to the real point that you keep
avoiding because it isn't worth my time to keep repeating how bogus
your arguments are, when you have to know that something like your
above argument counts for squat.
SNIP:
Still running. That is a fact and you know it. Why do you have to
run? Why do you consider this to be even close to an honest
response? Who the heck cares about the minimum gap distance to
anything when you can't even demonstrate that the gaps you need exist?
Just put up or shut up. It should be that simple. Put up your best
shot at what you claimed to have. Just do it and stop pretending.
This is so sad that no one can miss how badly off you must be. What
do you think that you are accomplishing with obfuscation and utter
bogousity when you know that you don't have an argument. If you think
that you do have an argument demonstrate it.
>
> One more thing, no one has to present any alternative to a proposed
> hypothesis before the proposed hypothesis can be adequately questioned
> and falsified.
That isn't what you claimed. You claimed that you had an alternative
to common descent and evidence to back it up that was just as good as
the evidence that you don't. You claimed that you had some science to
teach about intelligent design. These were your claims and you have
just been running from them for years. Why?
Why do you have to obfuscate the issue instead of address it?
Why is your web page still catering to the rubes too stupid to know
that intelligent design was just a dishonest scam? If it wasn't a
scam, you could demonstrate it by putting up the ID science you
claimed existed, but I guess that would mean that it wasn't a
dishonest scam, and you seem to be happy admitting that it always was
one.
Ron Okimoto
>
> > Ron Okimoto
>
> Sean Pitmanwww.DetectingDesign.com- Hide quoted text -
>
> - Show quoted text -
Frank J
If I had an alternative to common descent, the first people I'd want
to pitch it to would be the DI, particularly Behe. Unless of course I
really didn't have any confidence in the data to back it up.
> You claimed that you had some science to
> teach about intelligent design. These were your claims and you have
> just been running from them for years. Why?
>
> Why do you have to obfuscate the issue instead of address it?
Note in particular his ignoring of my Aug 23 request (in this thread)
to answer the simple questions about the last design actuation event.
>
> Why is your web page still catering to the rubes too stupid to know
> that intelligent design was just a dishonest scam? If it wasn't a
> scam, you could demonstrate it by putting up the ID science you
> claimed existed, but I guess that would mean that it wasn't a
> dishonest scam, and you seem to be happy admitting that it always was
> one.
Not all rubes are stupid, or even ignorant. Many (most?) are just
misled or hopelessly compartmentalized. Admit it. If you didn't have
to answer to a higher authority (no Sean, I mean God, not Dawkins), it
would be fun to exploit them.
Seanpit
> > > 400 aa from the Lac Z starting sequence.
>
> > You still don't get it. The minimum structural threshold requirement
> > isn't relative to some other sequence. It isn't "from" any starting
> > sequence. The ebg sequence didn't evolve from a LacZ sequence. It
> > was a unique sequence that happened to be close to one of a great many
> > potential lactase sequences in the vastness of sequence space at the
> > 400aa minimum level.
>
> You are getting some kind of message, but you are mixing it up with
> bogus bull pucky about some 400 minimum. The whole point is that
> there are sequences close to what is needed and that you can't keep
> them from existing.
>
> Your 400 minimum is something that you just made up. Admit it. Where
> did it come from?
Again, I'd be very interested in any reference suggesting a
significantly smaller beneficial lactase. Your example of lac+
antibodies doesn't count because the antibodies in question were
larger than 400aa.
> > > How many possible starting sequences are there?
>
> > The number of starting points is the number of genetic sequences of a
> > given length in a particular gene pool. That number is far more
> > limited than the number of potential sequences of a given length.
>
> > For example, E. coli have access to around 4e6 bp of genetic real
> > estate. Even given a population the size of all bacteria on Earth
> > (around 1e30), the total size of available genetic real estate would
> > only be around 1e36. This is a far cry from the size of 400aa
> > sequence space of about 1e520. So, the odds that anything in the gene
> > pool would be within one or two mutations of any sequence with a
> > lactase function depends upon the ratio of lactase sequences in 400aa
> > sequence space.
>
> Just imagine if you were right. Why was E. coli close enough to get
> the job done?
Because of the minimum sequence specificity wasn't high enough. But,
it was still fairly high considering that a colony of 100 billion E.
coli were not able to evolve the lactase function in over 40,000
generations once the ebg gene was deleted. This shows that the
lactase function has a density of less than 1 in 1e24.
> Something is obviously wrong with your argument because
> Hall got it to work with 2 or 3 other species out of whatever number
> he tested, and I bet that it was less than 50 species tested.
This is not true. Hall's experiment did not work with other species.
In fact, there are species of bacteria that have been observed for
over a million generations without being able to evolve the lactase
function - despite the reproductive advantage that would be gained if
they did happen to evolve this function.
> Some how the impossible happens too often for your argument to
> possibly be corect.
You need to read up on this experiment. Beyond this, I never said
that evolution at this level couldn't happen on a regular basis. It
obvious does happen and there are many examples of it happening at
this level. It is just that the relative number of examples at this
level is far less than the number of lower-level examples and far far
more than higher level examples. In fact, there are no examples of
evolution very far beyond this level - not a single example beyond the
1000aa threshold in all of literature.
This brings us back to my original question for you. How do you
explain this observation? The complete lack of evolution beyond the
1000aa threshold? I've yet to see you even try to answer this
question. . .
> > As it turns out, there have been several scientists who have published
> > rough estimates for such ratios when it comes to specific types of
> > single-protein functions - Yockey, Sauer, Olsen, Choi and Kim to name
> > just a few. Choi and Kim's paper is especially interesting:
>
> >http://www.pnas.org/content/vol103/issue38/images/large/zpq0370634700...
>
> > Notice in the above listed image that the smaller proteins mapped from
> > hyperdimensional sequence space onto three dimensions have a much
> > closer average distance as compared to the larger proteins. This
> > means that the likely minimum distance from any given starting point
> > or points does not remain at the minimum possible distance (i.e., one)
> > as you and those like Howard Hershey often parrot. Rather, the likely
> > minimum distance increases in a linear manner as the minimum size and/
> > or specificity threshold requirements increase.
>
> Your reference is pathetically inadequate and you should give a proper
> reference and not just to some stupid figure. This seems to be
> calculations from a given point. This is stupid. How many starting
> points are there? What does reality tell you? Choi and Kim can't
> even predict how close any sequence is. They have to estimate what it
> would take to move a certain distance, but they can't tell you how
> many existing sequences are already closer than that. Would they have
> been able to tell you that EBG was only one substitution away from
> beta gal activity? I doubt it.
You don't seem to grasp the concept. Higher-level systems are much
much less clustered together in sequence space compared to lower level
systems that have fewer minimum structural threshold requirements.
That's the point. Choi and Kim also do NOT base their calculations
relative to any starting point. The proteins analyzed are placed in
sequence space without regard to any reference. It is just that the
smaller proteins tend to be far more clustered than the larger
proteins - for obvious reasons that should be self-evident to you.
The overall trend gives you an idea as to what happens to all existing
sequences relative to all potentially beneficial sequences. They get
farther and farther apart with each increase in the minimum size and
specificity requirements.
As far as the "proper reference" is concerned, don't tell me that you
had problems finding the paper from the information I gave you? Come
on now . . . Here is the link to the full paper which I've already
listed many times in this forum in threads that you yourself have
responded to several times.
http://www.pnas.org/cgi/content/full/103/38/14056
> > > Your assertion doesn't mean jack about the
> > > minimum size does it? I'll even give you this. Beta gal activity is
> > > one of the rarer types of activities that we observe in enzymes, but
> > > it doesn't mean squat about the minimum size of the chain that will
> > > give it to you.
>
> > Oh really? Then it would be possible to build a useful lactase enzyme
> > (useful from the perspective of a bacterium) with just 10aa? How about
> > 100aa? Have any evidence for this? If so, I'd really like to see
> > it . . .
>
> Once someone tries you might get your answer. Until then you are just
> blowing smoke so why make yourself look so stupid?
Science is based on the best currently available evidence - not some
evidence which might come along in the future. Until then it is you
who are blowing smoke with your bravado notions that there are no
minimum structural threshold difference between different types of
functional systems. And you are calling me "stupid"? ; ) What do
you have to disprove my position? I'm still waiting . . .
> > > Larger proteins have more chance to evolve such a
> > > function simply because they have a larger surface area, but you could
> > > try more smaller sequences to compensate for that search factor. Beta
> > > gal activity is one of the ones they evolved using antibodies. I
> > > believe that they specifically looked for it because they thought that
> > > it might be difficult to evolve it.
>
> > If you look into the matter of antibodies with lactase activity, you
> > will find that none of these had significantly fewer than 400aa
> > residues. I've pointed this observation out many times now in this
> > forum, yet it keeps surfacing as if it somehow means something . . .
>
> You know that this doesn't mean jack because most of the antibody
> sequence isn't involved in creating the beta gal activity most of it
> is use to produce the antibody structure. Again, this is stupid.
Oh really? Then please do present a smaller portion of an antibody
sequence or any other protein sequence that still maintains useful
lactase activity from the perspective of any bacterium.
< snip repetitions >
richardal...@googlemail.com
wrote:
If you are a "sincere creationist", why do you lie about the
statistical method you claim to have applied to granite objects? It is
clear to anyone with even a few functioning brain cells that you have
done no such thing, yet you persist in claiming that you have done so.
> He can't comprehend that I'm not here to convince
> anyone - certainly not the creationists in this forum or even the
> evolutionists.
I understand very well why you are here. You are preaching to the
choir of other creationists and are trying to raise your profile in
the creationist community by pretending that you are a knowledgable
scientist in fields other than your own in which you evidently have
little knowledge or understanding.
> Most of the creationists who frequent this forum have
> no more clue than the evolutionists - in my opinion.
Do you think the scientists who have studied the subjects of
palaeontology, geology and so on don't have a clue? Some contribute to
this forum.
>
> In short, I'm here for myself. To test my own ideas to see if anyone
> in even the most adversarial forums, has anything that remotely
> challenges my ideas in a way that actually makes sense to me.
So why do you not address questions which challenge your views?
>
> To be honest, I've had to modify or completely discard a number of
> points. But, so far, these have been relatively minor. My main
> points regarding the evidence for intelligent design and how to detect
> it continue to gain ground and have withstood almost 10 years of
> challenges by members of this forum - some a bit brighter than Richard
> and his constant strawman misrepresentations.
If I have ever misrepresented you, Sean, please post a link to where I
did so.
I do not think that I have, and have challenged you on this matter
previously. As is usually the case, you failed to respond to any post
which asks you to substantiate your assertions.
>
> Sean Pitmanwww.DetectingDesign.com
Sean, I don't misrepresent you, though you frequently misrepresent
me.
Furthermore, I don't lie about the evidence for my position, as you do
in respect of the statistical tests for detecting "deliberate action"
in granite forms It is perfectly clear that you have not carried out
any such analysis in spite of your repeated claims to have done so.
I also do no ignore questions. For example, I have posed this question
several times:
You go on and on about the exceptional preservation of the Santana
formation fish fossils, though you carefully avoid reading any of the
scientific literature on the subject. It doesn't matter if the fish
were preserved in a matter of hours, days, weeks or years. We have
good experimental evidence that preservation of soft tissues of this
kind can occur in timescales of days. Such preservation is *not*
achieved simply by "sudden burial, as in a flood".
However, the overwhelmingly vast majority of the fossil record is NOT*
preserved in lagerstatten such as the Crato Formation. It's logically
incoherent to offer exceptional preservation in a single, limited
locality as evidence for a global flood when most of the fossil record
is *NOT* exceptionally well-preserved.
Your have stated that: "most fossils show clear evidence of rapid
burial or other forms of relatively rapid or even catastrophic
preservation leaving little time for predation or bioturbation)"
This is plainly ridiculous, as anyone who has ever collected fossils
can tell you. Mike Benton, in the reference which I have provided,
writes
"Animal and plant remains are typically buried after a great deal of
scavenging, decay, breakage and transport."
What do you know that Mike Benton doesn't?
You may consider evidence which completely demolishes your assertions,
and therefore your arguments as being a "relatively minor point", but
no scientist would, and your blatant avoidance shows your lack of
integrity.
I have no problem with this. After all, as I have written on many
occasions, one of my reasons for posting here is to expose the
dishonesty of creationists. Your help is greatly appreciated.
RF
TomS
<1188692102....@57g2000hsv.googlegroups.com>, Ron O stated..."
[...snip...]
>That isn't what you claimed. You claimed that you had an alternative
>to common descent and evidence to back it up that was just as good as
>the evidence that you don't. You claimed that you had some science to
>teach about intelligent design. These were your claims and you have
>just been running from them for years. Why?
>
>Why do you have to obfuscate the issue instead of address it?
Someone is claiming to have an alternative to common descent?
The only alternative that I've seen to common descent depends
on something like these:
* The designer was working within the limitations of the material.
* The designer had similar intentions.
I'd be interested to discuss those points.
--
---Tom S.
"... to call in a special or miraculous act of creation reduces every
conceivable world to accident."
Jacob Bronowski, in "American Scholar" v.43 (1974) page 400
Ron O
wrote:
> On Sep 1, 5:15 pm, Ron O <rokim...@cox.net> wrote:
>
>
>
>
>
> > > > 400 aa from the Lac Z starting sequence.
>
> > > You still don't get it. The minimum structural threshold requirement
> > > isn't relative to some other sequence. It isn't "from" any starting
> > > sequence. The ebg sequence didn't evolve from a LacZ sequence. It
> > > was a unique sequence that happened to be close to one of a great many
> > > potential lactase sequences in the vastness of sequence space at the
> > > 400aa minimum level.
>
> > You are getting some kind of message, but you are mixing it up with
> > bogus bull pucky about some 400 minimum. The whole point is that
> > there are sequences close to what is needed and that you can't keep
> > them from existing.
>
> > Your 400 minimum is something that you just made up. Admit it. Where
> > did it come from?
>
> Again, I'd be very interested in any reference suggesting a
> significantly smaller beneficial lactase. Your example of lac+
> antibodies doesn't count because the antibodies in question were
> larger than 400aa.
>
Has anyone ever made a very extensive push to develop lactase function
and determine the minimum? No. So what does it mean when you try and
use that argument to claim some minimum. Not only that, but even if
the minimum was 400 your argument still doesn't work because of Hall's
work and his success. Not his failures, but his sucesses. Why did he
ever succeed if you are right about 400 anythings?
>
> > > > How many possible starting sequences are there?
>
> > > The number of starting points is the number of genetic sequences of a
> > > given length in a particular gene pool. That number is far more
> > > limited than the number of potential sequences of a given length.
>
> > > For example, E. coli have access to around 4e6 bp of genetic real
> > > estate. Even given a population the size of all bacteria on Earth
> > > (around 1e30), the total size of available genetic real estate would
> > > only be around 1e36. This is a far cry from the size of 400aa
> > > sequence space of about 1e520. So, the odds that anything in the gene
> > > pool would be within one or two mutations of any sequence with a
> > > lactase function depends upon the ratio of lactase sequences in 400aa
> > > sequence space.
>
> > Just imagine if you were right. Why was E. coli close enough to get
> > the job done?
>
> Because of the minimum sequence specificity wasn't high enough. But,
> it was still fairly high considering that a colony of 100 billion E.
> coli were not able to evolve the lactase function in over 40,000
> generations once the ebg gene was deleted. This shows that the
> lactase function has a density of less than 1 in 1e24.
I don't know where you are getting this 40,000 generation stuff. None
of the references that you ever put up did such an experiment. Even
growing at full speed that would be 2 years of constant growth for
some population (20-30 minute generation length), and to select for
lactase function the generation length would have to be calculated on
a minimal carbon source like glycerol so that you could select for the
ones that could grow faster. When we used glyscerol as a carbon
source the generation length went from around 25 minutes to 120
minutes. So you might be talking about 8 years of constant growth.
Where is the citation for this work? All you ever put forward were
plate experiments. You can't get this kind of estimate from such
experiments and you know it.
>
> > Something is obviously wrong with your argument because
> > Hall got it to work with 2 or 3 other species out of whatever number
> > he tested, and I bet that it was less than 50 species tested.
>
> This is not true. Hall's experiment did not work with other species.
> In fact, there are species of bacteria that have been observed for
> over a million generations without being able to evolve the lactase
> function - despite the reproductive advantage that would be gained if
> they did happen to evolve this function.
I'm not going to look it up, but I believe that you recall your own
references and this seems to be just a blatant lie. Admit it. There
was a reference that we discussed where he tried several different
species and he found 2 or 3 that his same single step selection
strategy worked. It was in the abstract of the paper. I couldn't get
the paper, but the abstract was available on PubMed. The abstract did
not say how many species were tried, just how many worked.
>
> > Some how the impossible happens too often for your argument to
> > possibly be corect.
>
> You need to read up on this experiment. Beyond this, I never said
> that evolution at this level couldn't happen on a regular basis. It
> obvious does happen and there are many examples of it happening at
> this level. It is just that the relative number of examples at this
> level is far less than the number of lower-level examples and far far
> more than higher level examples. In fact, there are no examples of
> evolution very far beyond this level - not a single example beyond the
> 1000aa threshold in all of literature.
And you know that the relative number of successes is not enough
because....
You can't just make this junk up. You have to be able to demonstrate
it, and you can't even demonstrate that your 1000 aa threshold even
exists. Just do it. produce your numbers. Determine that such a gap
existed. Since you can't do that, what are you making noises about?
>
> This brings us back to my original question for you. How do you
> explain this observation? The complete lack of evolution beyond the
> 1000aa threshold? I've yet to see you even try to answer this
> question. . .
>
Bogus obfuscation is just bogus obfuscation. Until you can even
demonstrate that some 1000aa threshold even exists you have no
argument. There is no observation to explain until you can tell us
what the 1000aa threshold is and demonstrate that it had to be crossed
at some point in such a way that descent with modification and
selection would not have been able to cross such a threshold in a
biologically relevant fashion.
Just demonstrate one problem step in getting past your fictional
1000aa threshold in the evolution of the flagellum. Present the
sequences and tell us where the gap is and why it could not be
crossed.
No one is going to answer any stupid questions about this fictional
1000aa threshold until you can demonstrate that it actually exists and
that there is something to explain.
You know that this bogus argument is the same as the IC bogousity that
the IDiots tried for years. What did they finally have to admit about
calculating the probability of evolving the flagellum? Tell us in
your own words why they were not able to calculate that probability
with any sense of accuracy and why they had to give up on that bogus
argument. You are just putting some number on the system that they
were trying to estimate the probability of evolving with your 1000aa
threshold. They didn't even try to limit it to 1000 anythings. They
knew that they didn't have the knowledge of the systems to put such a
refined number on it. You don't either. Their argument still failed,
so you tell us why it failed and why your argument is better. You
have to admit that your argument is just a bogus probability argument,
so tell us why your bogousity rates higher than theirs.
I put in Choi and Kim in a search and came up with a bunch of papers
that I wasn't about to sort through since you didn't even give the
date of publication.
I'll promise this. As soon as you make good on your claims and
present your alternative to common descent and the evidence that is
just as good as the evidence for common descent that you don't think
is good enough, and you put up the science of intelligent design that
you claimed existed to teach to children, I will put up my evaluation
of the paper and what it means.
I have a copy of the paper, now. I will present my evaluation of it
if you make good on your past claims that you are constantly running
from.
Put up or shut up.
>
> > > > Your assertion doesn't mean jack about the
> > > > minimum size does it? I'll even give you this. Beta gal activity is
> > > > one of the rarer types of activities that we observe in enzymes, but
> > > > it doesn't mean squat about the minimum size of the chain that will
> > > > give it to you.
>
> > > Oh really? Then it would be possible to build a useful lactase enzyme
> > > (useful from the perspective of a bacterium) with just 10aa? How about
> > > 100aa? Have any evidence for this? If so, I'd really like to see
> > > it . . .
>
> > Once someone tries you might get your answer. Until then you are just
> > blowing smoke so why make yourself look so stupid?
>
> Science is based on the best currently available evidence - not some
> evidence which might come along in the future. Until then it is you
> who are blowing smoke with your bravado notions that there are no
> minimum structural threshold difference between different types of
> functional systems. And you are calling me "stupid"? ; ) What do
> you have to disprove my position? I'm still waiting . . .
You have to demonstrate that your functional threshold existed in a
way that is meaningful to your argument. To do this you have to be
able to determine what the threshold actually is. Until you can do
that you can't make your bogus claims. That is how science works.
Claim all that you want, but no one has to take you seriously until
you can verify what you are claiming. Have you forgotten the testing
part of science? How did you test your notion? Why do you think that
it is valid? You have to get other people to agree with you and to do
that they have to be able to repeat your work and get the same
answers. So how do we repeat it? It has to be actually accomplished
in order to repeat something. So demonstrate that your 1000aa
threshold exists.
>
> > > > Larger proteins have more chance to evolve such a
> > > > function simply because they have a larger surface area, but you could
> > > > try more smaller sequences to compensate for that search factor. Beta
> > > > gal activity is one of the ones they evolved using antibodies. I
> > > > believe that they specifically looked for it because they thought that
> > > > it might be difficult to evolve it.
>
> > > If you look into the matter of antibodies with lactase activity, you
> > > will find that none of these had significantly fewer than 400aa
> > > residues. I've pointed this observation out many times now in this
> > > forum, yet it keeps surfacing as if it somehow means something . . .
>
> > You know that this doesn't mean jack because most of the antibody
> > sequence isn't involved in creating the beta gal activity most of it
> > is use to produce the antibody structure. Again, this is stupid.
>
> Oh really? Then please do present a smaller portion of an antibody
> sequence or any other protein sequence that still maintains useful
> lactase activity from the perspective of any bacterium.
Well for one thing you can cut the number of aa residues about in half
by just cutting off the common tail and retaining the two active
ends. These constructs work quite often and I don't see why it
wouldn't work for lactase function. I don't know how much of the
variable parts can be deleted because it is dependent on a lot of
factors that can't be calculated, but if you have the data that it
can't be done. Let's see it. Not only that, but you are talking
about a specific start point. You haven't ruled out other start
points using even smaller numbers of residues. The starting point was
from the antibody sequence. I've seen no experiments to minimize the
structural components, and even if they had been done, how many
starting sequences would they have tried? It isn't the same thing to
cut something down as it would be to build it from the ground up.
>
> < snip repetitions >
Run away and pretend. Pretending is what you do best, but it doesn't
work in science because someone always asks for verification.
Really, put up what you have claimed in the past and I will evaluate
your paper. Go for it or admit that the paper doesn't support your
assertions and your past claims have been bogus. They aren't just
stupid claims about fictional 1000aa thresholds, they are claims about
your ID science and your alternative to common descent. Why is it so
hard to make good on those claims if your argument is at all valid?
After all these years of bogus arguing, shouldn't you have an
alternative? It would be insane just to be arguing to be arguing. If
you really have any science worth teaching to kids about this
claptrap, shouldn't you be able to produce what you claimed to have
wanted to teach to them? You must have had something worth teaching
or you wouldn't have wanted to teach it, so what was the science of ID
that you would have taught?
If you don't get it. Dishonestly ignoring your past claims and
running from them is an admission that they were not valid claims.
You made the claims. You don't even try to deny it. You just snip
and pretend. What does that say about you?
Ron Okimoto
Ron O
> "On Sat, 01 Sep 2007 17:15:02 -0700, in article
The claims were more than just the usual Sean blather. He actually
claimed to have an alternative to common descent and the evidence to
back it up. He pretends that if he doesn't acknowledge that claim
that it never really existed. Probably, no more dishonest than his
usual junk.
He actually made the claims about having science to teach about
intelligent design after the Discovery Institute ran the bait and
switch on the Ohio rubes that had bought into the ID scam. The Ohio
rubes wanted to teach ID, but all they got from the ID scam artists
was the bogus switch scam that didn't even mention that ID ever
existed. Sean couldn't give up on ID so he claimed that he had the
science to teach to school kids and that he could have done better
than the ID scam artists that had perpetrated the dishonest ID scam
for years. He got pretty incoherant trying to defend that claim,
while not putting any ID science forward, and then he just quit
trying.
Now, he just pretends that he never made the claims. He doesn't even
try to deny that he made them. He seems to operate on the false
assumption that denying that he made the claims would be lying, while
just pretending that he never made the claims is somehow more honests
and acceptable. It is pretty sad.
Ron Okimoto
Seanpit
> > Richard can't understand why any sincere creationist would come to a
> > forum like this?
>
> If you are a "sincere creationist", why do you lie about the
> statistical method you claim to have applied to granite objects? It is
> clear to anyone with even a few functioning brain cells that you have
> done no such thing, yet you persist in claiming that you have done so.
Anyone who has observed the material of granite as it interacts with
natural forces to the even limited degree that I have would clearly
know that a highly symmetrical polished 1m granite cube (to within
0.01% tolerance) would be clear evidence of artifact - even if found
on an alien planet with nothing else around. The statistics do not
have to be highly refined to know that no naturally produced granite
stone comes or could come remotely close to such a degree of
symmetry. I have no idea what you point might be by now or how you
can honestly suggest any dishonesty here. I've been very open for
years now about the granite cube illustration. Only someone as dense
as you apparently are would still be so confused.
This is only to be expected from someone who still denies that a
statue like Michelangelo's David shows little if any symmetry. You
have argued that since David's eye's are not perfectly lined up that
the face isn't symmetrical. You don't seem to grasp the concept that
while David's face is not perfectly symmetrical (and no one said it
was) it is indeed very highly symmetrical with regard to a large
number of surface irregularities - high enough to obviously be judged
as being the result of deliberate artifact over that of any humanoid
natural carving of granite or marble rock found anywhere in nature.
You argue that the statue of David as a whole shows no symmetry at all
because the limbs and torso of the statue are in different relative
positions in space. That notion is absolute nonsense. It is quite
clear that the statue has bilateral symmetry regardless of the
different positions of the limbs in space. You also don't seem to
grasp the concept of "rotoreflection" symmetry or the symmetry of
"improper rotation".
Yes, I know, you argue that, "In 3D, rotoreflection or improper
rotation in the strict sense is rotation about an axis, combined with
reflection in a plane perpendicular to that axis. No elements of
"David" show such a symmetry."
That's simply not true. The arm or forearm or finger joint on one
side of the statue has its rotoreflection on the other side that is a
very near match - about a shared axis. Sure, the axis of rotation may
be different for the arm vs. the forearm. But that doesn't matter.
Pick any part on one side and there will be an axis of rotation that
produces a very close rotoreflection match with a part on the other
side of the statue. Even a child can recognize the match of one side
to the other. Yet, you are trying desperately to deny the obvious
Richard. Why is that?
What is really funny is the following exchange where you argued that
you couldn't "rotate" the parts of the statue because it was "marble".
_________
> > > Rotate the limbs so that they are in the same orientation in space.
> > You can't. It's a freaking lump of marble!
> Are you saying that something made out of marble can't express
> rotoreflection symmetry because marble can be "rotated" to match up
> both sides?
I'm saying that you can't take elements of a marble statue and rotate
them!
> Neither side of a granite cube can be easily "rotated"
> either, yet it expresses "rotational" symmetry.
So what? You don't have to take a part of that cube and "virtually
rotate" it!
____________
Interesting that you finally figured out the concept of "virtual
rotation". ; )
Yet, you go on to argue:
****
"Why on earth has "virtual rotation" to do with anything? One could
take almost *any* marble or granite object and "virtually rotate"
parts of it so that it shows some form of symmetry, and almost
certainly to a greater degree than the limbs of "David" which, as you
would know if you had bothered to read the link I have provided, are
not only anatomically different because Michaelangelo knew the ways in
which the muscles under the skin change outline as the limbs move, but
that they are of different sizes."
****
You seem again to be confused by thinking I'm trying to achieve
perfect symmetry or identity. I'm not. My whole point is that the
high degree of symmetry exhibited by something like the statue of
David, symmetry with regard to many closely matching surface
irregularities in the same object, is far beyond anything that has
been or could be achieved by non-deliberate natural processes. This
point is overwhelmingly obvious to anyone who has observed and
mentally carried out even a rough evaluation of the material of
granite as it interacts with non-deliberate forces of nature.
> > He can't comprehend that I'm not here to convince
> > anyone - certainly not the creationists in this forum or even the
> > evolutionists.
>
> I understand very well why you are here. You are preaching to the
> choir of other creationists and are trying to raise your profile in
> the creationist community by pretending that you are a knowledgable
> scientist in fields other than your own in which you evidently have
> little knowledge or understanding.
If I was preaching to the choir, I wouldn't be here.
> > Most of the creationists who frequent this forum have
> > no more clue than the evolutionists - in my opinion.
>
> Do you think the scientists who have studied the subjects of
> palaeontology, geology and so on don't have a clue? Some contribute to
> this forum.
I think mainstream science is way off base when it comes to
understanding the meaning of both the geologic column and the fossil
record.
> > In short, I'm here for myself. To test my own ideas to see if anyone
> > in even the most adversarial forums, has anything that remotely
> > challenges my ideas in a way that actually makes sense to me.
>
> So why do you not address questions which challenge your views?
You think that if a person doesn't agree with your arguments that they
haven't "addressed" the issues or questions you've raised. The fact
is that I've answered all of your questions many times. You just don't
like or agree with my answers.
> > To be honest, I've had to modify or completely discard a number of
> > points. But, so far, these have been relatively minor. My main
> > points regarding the evidence for intelligent design and how to detect
> > it continue to gain ground and have withstood almost 10 years of
> > challenges by members of this forum - some a bit brighter than Richard
> > and his constant strawman misrepresentations.
>
> If I have ever misrepresented you, Sean, please post a link to where I
> did so.
You misrepresent me constantly Richard. You deliberately misinterpret
statements of mine to suggest that I said or claimed things I never
did. You say I've never responded to questions of yours for which
I've responded dozens of times. You say that I've never presented an
argument or methodology for detecting artifact in objects like granite
cubes when I've gone into significant detail over hundreds of posts.
You constantly suggest that I claim rapid burial as the only means of
fossilization when I've presented the Santana formation to you many
many times as an example of rapid catastrophic fossilization that was
not the result of rapid burial. You also say over and over again that
I've never discussed the findings of the Santana formation when I've
done so at least 50 times. You argue that I misrepresent the findings
of the scientific community regarding the Santana formation when all
I've done is presented evidence of very rapid preservation of the
fossil fish that had to be achieved within a few hours at most
(preserved cellular turgidity). And on and on and on . . .
> I do not think that I have, and have challenged you on this matter
> previously. As is usually the case, you failed to respond to any post
> which asks you to substantiate your assertions.
Again, if you disagree with someone's response, it evidently doesn't
count as a true "response" - is that it?
> > Sean Pitmanwww.DetectingDesign.com
>
> Sean, I don't misrepresent you, though you frequently misrepresent
> me.
Really? How so?
> Furthermore, I don't lie about the evidence for my position, as you do
> in respect of the statistical tests for detecting "deliberate action"
> in granite forms It is perfectly clear that you have not carried out
> any such analysis in spite of your repeated claims to have done so.
I have carried out analysis of the material of granite to at least a
rough degree of certainty. So have you. This is why you yourself can
recognize artifact without having any other information regarding
materials or methods as soon as you see such a highly symmetrical
granite object - even if you were on an alien planet.
Of course, I've pointed this little concept out to you many times
before, but you still argue that this type of "analysis" is not real
analysis - regardless of the fact that it is in fact quite useful as
it stands.
> I also do no ignore questions. For example, I have posed this question
> several times:
>
> You go on and on about the exceptional preservation of the Santana
> formation fish fossils, though you carefully avoid reading any of the
> scientific literature on the subject. It doesn't matter if the fish
> were preserved in a matter of hours, days, weeks or years. We have
> good experimental evidence that preservation of soft tissues of this
> kind can occur in timescales of days. Such preservation is *not*
> achieved simply by "sudden burial, as in a flood".
I've answered this false misrepresentation many times Richard. It is
just a mystery why you feel the need to keep presenting this argument
as if it had not been refuted over and over again? I never said that
the Santana formation was the result of rapid burial. I said that the
Santana formation was the result of a sudden catastrophe. It was you
who initially argued that the preservation of the creatures in this
formation need not have been very rapid, as in a few hours, but could
have been achieved by much slower processes of non-catastrophic
fossilization.
> However, the overwhelmingly vast majority of the fossil record is NOT*
> preserved in lagerstatten such as the Crato Formation. It's logically
> incoherent to offer exceptional preservation in a single, limited
> locality as evidence for a global flood when most of the fossil record
> is *NOT* exceptionally well-preserved.
The exceptional preservation isn't the only evidence of shortly spaced
catastrophes in the fossil record Richard. It is just that this
particular example of the Santana formation, which you originally
brought up to challenge the concept of catastrophic fossilization and/
or preservation, does nothing of the sort.
> Your have stated that: "most fossils show clear evidence of rapid
> burial or other forms of relatively rapid or even catastrophic
> preservation leaving little time for predation or bioturbation)"
>
> This is plainly ridiculous, as anyone who has ever collected fossils
> can tell you. Mike Benton, in the reference which I have provided,
> writes
>
> "Animal and plant remains are typically buried after a great deal of
> scavenging, decay, breakage and transport."
>
> What do you know that Mike Benton doesn't?
I agree that a great deal of breakage and transport is the norm, as is
a bit of scavenging. However, without rapid burial as a general rule,
the fine lines of lamination and preservation of such organically rich
material would not have been preserved due to continued scavenging and
bioturbation.
> You may consider evidence which completely demolishes your assertions,
> and therefore your arguments as being a "relatively minor point", but
> no scientist would, and your blatant avoidance shows your lack of
> integrity.
Anyone who disagrees with you lacks integrity I guess? No one can be
honestly wrong I suppose? It's like my view of you. I think you are
way off base in much of your thinking, but I don't stoop to challenge
your integrity. I think you honestly believe at least most of what
you say. Yet, you don't seem to be able to extend me the same benefit
of the doubt?
> I have no problem with this. After all, as I have written on many
> occasions, one of my reasons for posting here is to expose the
> dishonesty of creationists. Your help is greatly appreciated.
For the candid reader, all you've done is exposed your own desperation
- your need to paint all who disagree with you as debased, dishonest,
and morally corrupt. That is a generalization that just doesn't hold
water. Most evolutionists are good honest sincere people who really
believe in what they are doing and saying. The same thing is true of
creationists and those who believe in intelligent design. Sure, one
or the other is wrong, but that by no means supports the ludicrous
notion that all those who have been mislead are dishonest or in any
sense evil.
> RF
Sean Pitman
www.DetectingDesign.com
TomS
<1188745913.8...@w3g2000hsg.googlegroups.com>, Ron O stated..."
Myself, I don't much care whether Sean made that claim. I know that
anti-evolutionists have, several times, made the claim that "common
design" of some kind or other, along the lines that I mentioned, are
enough to account for the same things that common descent does.
But it has always puzzled me that anyone would be so desperate, or
so oblivious to the implications, that they would make a claim like
that.
Of course, the evidence for common descent is *not* just that there
are similarities, but rather that there is a pattern to the similarities,
the "tree of life". I don't expect that anyone has thought up anything
to account for that particular complexity, other than common
descent.
Von R. Smith
What I find interesting is that Sean thinks that it is perfectly OK
for him to assume that the smallest known lactase enzyme is also the
smallest possible, but for some reason does not apply the same
reasoning to, say, the fastest known erosion rates, the fastest known
nuclear decay rates, the fastest known deposition and uplift rates,
etc. Suddenly, this becomes an unwarranted uniformitarian assumption.
richardal...@googlemail.com
wrote:
> On Sep 2, 2:31 am, richardalanforr...@googlemail.com wrote:
>
> > > Richard can't understand why any sincere creationist would come to a
> > > forum like this?
>
> > If you are a "sincere creationist", why do you lie about the
> > statistical method you claim to have applied to granite objects? It is
> > clear to anyone with even a few functioning brain cells that you have
> > done no such thing, yet you persist in claiming that you have done so.
>
> Anyone who has observed the material of granite as it interacts with
> natural forces to the even limited degree that I have would clearly
> know that a highly symmetrical polished 1m granite cube (to within
> 0.01% tolerance) would be clear evidence of artifact - even if found
> on an alien planet with nothing else around. The statistics do not
> have to be highly refined to know that no naturally produced granite
> stone comes or could come remotely close to such a degree of
> symmetry. I have no idea what you point might be by now or how you
> can honestly suggest any dishonesty here. I've been very open for
> years now about the granite cube illustration. Only someone as dense
> as you apparently are would still be so confused.
The point, Sean, is that you claim not only to have a **STATISTICAL**
method for detecting such symmetries and regularities, but to have
applied it to granite objects.
As you have been unable to tell us how you have assembled your data
set, which statistical tools you are using, how you have made your
measurements, how many objects you have measured, how you have
selected the objects you have measured, how you have selected your
control sample or any of the other factors which are an essential part
of carrying out such a study, I can only conclude that you are lying
when you claim to have carried out such a study.
>
> This is only to be expected from someone who still denies that a
> statue like Michelangelo's David shows little if any symmetry.
You are misrepresenting me again, Sean.
Let's repost something (typing error and all):
"I am not, and have never claimed that there is no symetry in the face
on the stature."
(http://groups.google.co.uk/group/talk.origins/msg/8be4811c61c86bd2?
dmode=source&hl=en)
*YOU* claim to have an statistical method which can detect such
symmetry.
You don't.
Hand-waving about "reflective symmetry", or whichever other form of
symmetry you have discovered by googling is *NOT* a statistical method
for detecting symmetry.
> You
> have argued that since David's eye's are not perfectly lined up that
> the face isn't symmetrical.
Which part of "I am not, and have never claimed that there is no
symetry in the face on the stature" do you not understand?
What is at issue is your false claim to have a statistical method to
detect symmetries.
It is a simple matter of fact that the face of Michaelangelo's David
is deliberately *NOT* symmetrical.
> You don't seem to grasp the concept that
> while David's face is not perfectly symmetrical (and no one said it
> was)
You have asserted that is shows an "extremely high degree" of
symmetry, a "very high degree" of symmetry, that it is
"extraordinarily symmetrical" and that the face has "near perfect
symmetry" . Here are some of your posts on the subject:
"David's face has an extremely high degree of measurable reflective
symmetry."
"You will notice, if you can actually admit it, that the features on
one side of the face are reflectively identical to those on the
other." (by the way, if they are actually identical you are claiming
perfect symmetry)
(http://groups.google.co.uk/group/talk.origins/msg/8b7dac9646e94c07?
dmode=source&hl=en)
" However, the face of Michelangelo's David is extraordinarily
symmetrical."
(http://groups.google.co.uk/group/talk.origins/msg/8e766c555a5aa40e?
dmode=source&hl=en)
" You yourself can see the very high degree of symmetry in David's
face and body "
"Are you seriously trying to tell me that just because this is a
marble statue that you cannot see the near perfect symmetry of that
face?"
> it is indeed very highly symmetrical with regard to a large
> number of surface irregularities - high enough to obviously be judged
> as being the result of deliberate artifact over that of any humanoid
> natural carving of granite or marble rock found anywhere in nature.
We know that it is an artifact because we know not only how it was
made, but when it was made, who made it, who commissioned it, who paid
for it, and the various places it has stood for the past few
centuries.
You claim to have a *STATISTICAL* method for detecting that it is an
artifact.
I think you are lying.
>
> You argue that the statue of David as a whole shows no symmetry at all
> because the limbs and torso of the statue are in different relative
> positions in space. That notion is absolute nonsense. It is quite
> clear that the statue has bilateral symmetry regardless of the
> different positions of the limbs in space. You also don't seem to
> grasp the concept of "rotoreflection" symmetry or the symmetry of
> "improper rotation"
I suspect (hell, I KNOW) that I have a better grasp of such concepts
that you do, Sean. I am not the one claiming falsely to have a
*STATISTICAL* method for detecting such symmetries.
You are.
It's not my honesty which is at issue.
It's yours.
.
>
> Yes, I know, you argue that, "In 3D, rotoreflection or improper
> rotation in the strict sense is rotation about an axis, combined with
> reflection in a plane perpendicular to that axis. No elements of
> "David" show such a symmetry."
>
> That's simply not true. The arm or forearm or finger joint on one
> side of the statue has its rotoreflection on the other side that is a
> very near match - about a shared axis. Sure, the axis of rotation may
> be different for the arm vs. the forearm. But that doesn't matter.
> Pick any part on one side and there will be an axis of rotation that
> produces a very close rotoreflection match with a part on the other
> side of the statue. Even a child can recognize the match of one side
> to the other. Yet, you are trying desperately to deny the obvious
> Richard. Why is that?
>
> What is really funny is the following exchange where you argued that
> you couldn't "rotate" the parts of the statue because it was "marble".
>
Can you rotate parts of a marble statue?
Perhaps you can explain how you do that.
Then perhaps you can explain why you can't take *any* marble object
and rotate parts of it until it shows some degree of symmetry.
What you are claiming, Sean, is to have a ***STATISTICAL*** method for
detecting such symmetries.
I think you are lying.
>
> > > He can't comprehend that I'm not here to convince
> > > anyone - certainly not the creationists in this forum or even the
> > > evolutionists.
>
> > I understand very well why you are here. You are preaching to the
> > choir of other creationists and are trying to raise your profile in
> > the creationist community by pretending that you are a knowledgable
> > scientist in fields other than your own in which you evidently have
> > little knowledge or understanding.
>
> If I was preaching to the choir, I wouldn't be here.
Are you claiming that there are no creationists on this forum, or that
your web sites are not targeted at other creationists?
>
> > > Most of the creationists who frequent this forum have
> > > no more clue than the evolutionists - in my opinion.
>
> > Do you think the scientists who have studied the subjects of
> > palaeontology, geology and so on don't have a clue? Some contribute to
> > this forum.
>
> I think mainstream science is way off base when it comes to
> understanding the meaning of both the geologic column and the fossil
> record.
Why on earth should anyone care what you think? You have demonstrated
that you are dishonest, that you won't address the evidence which
demolishes your claims, and that most of your arguments are based on
unfounded assertions.
>
> > > In short, I'm here for myself. To test my own ideas to see if anyone
> > > in even the most adversarial forums, has anything that remotely
> > > challenges my ideas in a way that actually makes sense to me.
>
> > So why do you not address questions which challenge your views?
>
> You think that if a person doesn't agree with your arguments that they
> haven't "addressed" the issues or questions you've raised. The fact
> is that I've answered all of your questions many times. You just don't
> like or agree with my answers.
Another outright lie, Sean.
I've posted this question *SEVEN* times and you have yet to answer it:
Your have stated that: "most fossils show clear evidence of rapid
burial or other forms of relatively rapid or even catastrophic
preservation leaving little time for predation or bioturbation)"
This is plainly ridiculous, as anyone who has ever collected fossils
can tell you. Mike Benton, in the reference which I have provided,
writes
"Animal and plant remains are typically buried after a great deal of
scavenging, decay, breakage and transport."
What do you know that Mike Benton doesn't?
>
> > > To be honest, I've had to modify or completely discard a number of
> > > points. But, so far, these have been relatively minor. My main
> > > points regarding the evidence for intelligent design and how to detect
> > > it continue to gain ground and have withstood almost 10 years of
> > > challenges by members of this forum - some a bit brighter than Richard
> > > and his constant strawman misrepresentations.
>
> > If I have ever misrepresented you, Sean, please post a link to where I
> > did so.
>
> You misrepresent me constantly Richard.
I've identified in this post an instance in which you have
misrepresented me. You claimed that I was misrepresening you, yet I am
able to produce several posts which support my position.
If you think I have misrepresented you, please post a link to
somewhere I have done so.
> You deliberately misinterpret
> statements of mine to suggest that I said or claimed things I never
> did. You say I've never responded to questions of yours for which
> I've responded dozens of times. You say that I've never presented an
> argument or methodology for detecting artifact in objects like granite
> cubes when I've gone into significant detail over hundreds of posts.
You have never given us *ANY* details of your methodology.
Reposting the same empty assertions is *NOT* going into any
significant detail.
> You constantly suggest that I claim rapid burial as the only means of
> fossilization when I've presented the Santana formation to you many
> many times as an example of rapid catastrophic fossilization that was
> not the result of rapid burial.
Your web site included the sentence "For fossilization to occur,
burial must be very rapid."
You seem to have removed it now, but you still make the repeated
assertion that rapid burial is necessary for the preservation of large
vertebrates.
There is extensive literature which shows that this is not necessarily
the case. I've posted the references many times.
> You also say over and over again that
> I've never discussed the findings of the Santana formation when I've
> done so at least 50 times.
Where have I made that assertion? What I have said about the Santana
fish, and the issue which you refuse to address is this. By the way,
this is at least the seventh time I have posted this, and you have yet
to address the question:
It doesn't matter if the fish
were preserved in a matter of hours, days, weeks or years. We have
good experimental evidence that preservation of soft tissues of this
kind can occur in timescales of days. Such preservation is *not*
achieved simply by "sudden burial, as in a flood".
However, the overwhelmingly vast majority of the fossil record is NOT*
preserved in lagerstatten such as the Crato Formation. It's logically
incoherent to offer exceptional preservation in a single, limited
locality as evidence for a global flood when most of the fossil record
is *NOT* exceptionally well-preserved.
Your have stated that: "most fossils show clear evidence of rapid
burial or other forms of relatively rapid or even catastrophic
preservation leaving little time for predation or bioturbation)"
This is plainly ridiculous, as anyone who has ever collected fossils
can tell you. Mike Benton, in the reference which I have provided,
writes
"Animal and plant remains are typically buried after a great deal of
scavenging, decay, breakage and transport."
What do you know that Mike Benton doesn't?
> You argue that I misrepresent the findings
> of the scientific community regarding the Santana formation when all
> I've done is presented evidence of very rapid preservation of the
> fossil fish that had to be achieved within a few hours at most
> (preserved cellular turgidity). And on and on and on . . .
I've posted the links for you to the experimental and taphonomic
evidence that such preservation can be achieved quickly several times!
We are learning more all the processes of fossilization all the time.
Yet you avoid the main issue, which is that such preservation is *NOT*
typical.
It doesn't matter if the fish
were preserved in a matter of hours, days, weeks or years. We have
good experimental evidence that preservation of soft tissues of this
kind can occur in timescales of days. Such preservation is *not*
achieved simply by "sudden burial, as in a flood".
However, the overwhelmingly vast majority of the fossil record is NOT*
preserved in lagerstatten such as the Crato Formation. It's logically
incoherent to offer exceptional preservation in a single, limited
locality as evidence for a global flood when most of the fossil record
is *NOT* exceptionally well-preserved.
Your have stated that: "most fossils show clear evidence of rapid
burial or other forms of relatively rapid or even catastrophic
preservation leaving little time for predation or bioturbation)"
This is plainly ridiculous, as anyone who has ever collected fossils
can tell you. Mike Benton, in the reference which I have provided,
writes
"Animal and plant remains are typically buried after a great deal of
scavenging, decay, breakage and transport."
What do you know that Mike Benton doesn't?
>
> > I do not think that I have, and have challenged you on this matter
> > previously. As is usually the case, you failed to respond to any post
> > which asks you to substantiate your assertions.
>
> Again, if you disagree with someone's response, it evidently doesn't
> count as a true "response" - is that it?
>
> > > Sean Pitmanwww.DetectingDesign.com
>
> > Sean, I don't misrepresent you, though you frequently misrepresent
> > me.
>
> Really? How so?
You've done so at least twice in this post!
1) You misrepresent what I have said about the symmetry of "David".
2) You misrepresent my position on the preservation of the Sanatana
fish
>
> > Furthermore, I don't lie about the evidence for my position, as you do
> > in respect of the statistical tests for detecting "deliberate action"
> > in granite forms It is perfectly clear that you have not carried out
> > any such analysis in spite of your repeated claims to have done so.
>
> I have carried out analysis of the material of granite to at least a
> rough degree of certainty.
You have not carried out the statistical tests you claim to have done.
> So have you.
No I haven't. In any case, I'm not claiming to have a statistical
method for analysing granite objects.
> This is why you yourself can
> recognize artifact without having any other information regarding
> materials or methods as soon as you see such a highly symmetrical
> granite object - even if you were on an alien planet.
I've explained to you on numerous occasions how I and other scientists
recognise that an object is an artifact. It's by testing hypotheses of
manufacture.
>
> Of course, I've pointed this little concept out to you many times
> before, but you still argue that this type of "analysis" is not real
> analysis - regardless of the fact that it is in fact quite useful as
> it stands.
You claim to have a ****STATISTICAL****
Seanpit
> On Sep 1, 9:30 pm, Seanpit <seanpitnos...@naturalselection.0catch.com>
> wrote:> On Sep 1, 5:15 pm, Ron O <rokim...@cox.net> wrote:
>
> > > > > 400 aa from the Lac Z starting sequence.
>
> > > > You still don't get it. The minimum structural threshold requirement
> > > > isn't relative to some other sequence. It isn't "from" any starting
> > > > sequence. The ebg sequence didn't evolve from a LacZ sequence. It
> > > > was a unique sequence that happened to be close to one of a great many
> > > > potential lactase sequences in the vastness of sequence space at the
> > > > 400aa minimum level.
>
> > > You are getting some kind of message, but you are mixing it up with
> > > bogus bull pucky about some 400 minimum. The whole point is that
> > > there are sequences close to what is needed and that you can't keep
> > > them from existing.
>
> > > Your 400 minimum is something that you just made up. Admit it. Where
> > > did it come from?
>
> > Again, I'd be very interested in any reference suggesting a
> > significantly smaller beneficial lactase. Your example of lac+
> > antibodies doesn't count because the antibodies in question were
> > larger than 400aa.
>
> And again, the fact that such a reference does not exist means what?
It means that based on the information that does exist, the hypothesis
of a 400aa threshold has the most support. You may argue that future
information is likely to reveal a much smaller threshold. That isn't
science Ron. That's an unsupported hypothesis that isn't even
falsifiable this side of eternity. You could always argue that this
or that hypothesis could be wrong given some future discovery. That's
always a possibility in science.
> Has anyone ever made a very extensive push to develop lactase function
> and determine the minimum? No. So what does it mean when you try and
> use that argument to claim some minimum. Not only that, but even if
> the minimum was 400 your argument still doesn't work because of Hall's
> work and his success. Not his failures, but his sucesses. Why did he
> ever succeed if you are right about 400 anythings?
I've already told you. The 400aa size requirement isn't the only
aspect of the equation. The minimum specificity of amino acid residue
arrangement is also in play. Proteins, to include those that have the
lactase function, are not perfectly ridged structures. A certain
degree of sequence flexibility is available without a complete loss of
the function in question - i.e., lactase in this case. However, all
protein based systems have a certain limit to the degree of
flexibility beyond which the function in question cannot be realized
at all - not even a little bit.
In the case of lactase, Hall's experiments proved that the degree of
flexibility is in fact quite limited. The evolution of lactase is
extremely rare in living systems, even when it comes to large colonies
over tens of thousands of generations under extreme conditions (i.e.,
high mutation rates and a highly selective environment favoring
lactase evolution). The lack of evolution in most gene pools observed
in Hall's experiments support the notion that the average distance
between lactase islands is well over a dozen mutations wide. Of
course, this is just the average distance for most types of bacteria.
The minimum distance is obviously one. On occasion, rare colonies of
bacteria will be within just one or two mutations of at least one of
the potential lactase islands that exist in sequence space. However,
the number of colonies or types of bacteria that will be this close is
extremely limited compared to all types of bacterial gene pools -
along a Poisson distribution.
Now, when it comes to higher level functional systems, the average
distance is even greater (i.e., several dozen mutations wide). The
odds that any bacteria will be within just one or two mutations of
success drops off dramatically - along a Poisson distribution. This
concept is supported by papers like the one published by Choi and Kim.
http://www.pnas.org/cgi/content/full/103/38/14056
> > > Just imagine if you were right. Why was E. coli close enough to get
> > > the job done?
>
> > Because of the minimum sequence specificity wasn't high enough. But,
> > it was still fairly high considering that a colony of 100 billion E.
> > coli were not able to evolve the lactase function in over 40,000
> > generations once the ebg gene was deleted. This shows that the
> > lactase function has a density of less than 1 in 1e24.
>
> I don't know where you are getting this 40,000 generation stuff. None
> of the references that you ever put up did such an experiment. Even
> growing at full speed that would be 2 years of constant growth for
> some population (20-30 minute generation length), and to select for
> lactase function the generation length would have to be calculated on
> a minimal carbon source like glycerol so that you could select for the
> ones that could grow faster. When we used glyscerol as a carbon
> source the generation length went from around 25 minutes to 120
> minutes. So you might be talking about 8 years of constant growth.
> Where is the citation for this work? All you ever put forward were
> plate experiments. You can't get this kind of estimate from such
> experiments and you know it.
Hall studied K12 E. coli and the evolution of lactase from ebg for
over 25 years. If you want to argue that the reproductive rate was
lower, on the order of 2 hours, that's fine. The number of
generations studied are still plenty for the purposes of this
discussion.
> > > Something is obviously wrong with your argument because
> > > Hall got it to work with 2 or 3 other species out of whatever number
> > > he tested, and I bet that it was less than 50 species tested.
>
> > This is not true. Hall's experiment did not work with other species.
> > In fact, there are species of bacteria that have been observed for
> > over a million generations without being able to evolve the lactase
> > function - despite the reproductive advantage that would be gained if
> > they did happen to evolve this function.
>
> I'm not going to look it up, but I believe that you recall your own
> references and this seems to be just a blatant lie. Admit it. There
> was a reference that we discussed where he tried several different
> species and he found 2 or 3 that his same single step selection
> strategy worked. It was in the abstract of the paper. I couldn't get
> the paper, but the abstract was available on PubMed. The abstract did
> not say how many species were tried, just how many worked.
As far as I am aware lactase evolution was not achieved in any other
species besides E. coli. If you do have a reference to the contrary,
please list it here. Where is this abstract you remember reading? I
don't remember any such abstract.
> > > Some how the impossible happens too often for your argument to
> > > possibly be corect.
>
> > You need to read up on this experiment. Beyond this, I never said
> > that evolution at this level couldn't happen on a regular basis. It
> > obvious does happen and there are many examples of it happening at
> > this level. It is just that the relative number of examples at this
> > level is far less than the number of lower-level examples and far far
> > more than higher level examples. In fact, there are no examples of
> > evolution very far beyond this level - not a single example beyond the
> > 1000aa threshold in all of literature.
>
> And you know that the relative number of successes is not enough
> because....
There isn't even one example beyond this level.
> You can't just make this junk up.
Anyone can look it up and see that I'm right. There aren't any
examples beyond the 1000aa minimum threshold.
> You have to be able to demonstrate
> it, and you can't even demonstrate that your 1000 aa threshold even
> exists. Just do it. produce your numbers. Determine that such a gap
> existed. Since you can't do that, what are you making noises about?
There are a great many protein-based systems that require well over
1000 fairly specified amino acid residues. A system of 1000 residues
requires at least 3,000 codons of genetic real estate. Do you think
you could produce a flagellar motility system with just 3000 codons?
Think again. Flagellar motility requires at least 30,000 codons of
genetic real estate at minimum.
There are many other such examples as well - such as the minimum
structural threshold it takes to code for the functional system
responsible for DNA transcription or RNA translation - to name just a
couple more examples of higher-level functions.
> > This brings us back to my original question for you. How do you
> > explain this observation? The complete lack of evolution beyond the
> > 1000aa threshold? I've yet to see you even try to answer this
> > question. . .
>
> Bogus obfuscation is just bogus obfuscation. Until you can even
> demonstrate that some 1000aa threshold even exists you have no
> argument. There is no observation to explain until you can tell us
> what the 1000aa threshold is and demonstrate that it had to be crossed
> at some point in such a way that descent with modification and
> selection would not have been able to cross such a threshold in a
> biologically relevant fashion.
I've provided you with this information over and over again. The
flagellar motility system requires over 30,000 codons of genetic real
estate. Obviously, this threshold had to be crossed or this type of
motility system would not exist. None of the proposed steppingstones
in flagellar evolution are narrower than a few dozen mutations. How
then were they crossed and why are there no examples of any system
beyond the 1000aa evolving?
> Just demonstrate one problem step in getting past your fictional
> 1000aa threshold in the evolution of the flagellum. Present the
> sequences and tell us where the gap is and why it could not be
> crossed.
All the steps in the proposed model of flagellar evolution are beyond
the 1000aa threshold. None of them have ever been demonstrated to
actually evolve outside of the wild imagination of evolutionists.
> No one is going to answer any stupid questions about this fictional
> 1000aa threshold until you can demonstrate that it actually exists and
> that there is something to explain.
It is obvious that this threshold exists. What is not so obvious,
from the evolutionary perspective anyway, is why nothing beyond the
1000aa threshold actually evolves. Why isn't there even one example
when there are lots of examples of lower-level evolution that require
a minimum structural threshold no more than a few hundred fairly
specified amino acid residues? Why do relatively small single
protein systems, like lactase and nylonase, occasionally evolve while
higher level systems that require more than a few hundred residues
never evolve?
It's a simple and obvious question Ron. What's your answer?
< snip >
> > As far as the "proper reference" is concerned, don't tell me that you
> > had problems finding the paper from the information I gave you? Come
> > on now . . . Here is the link to the full paper which I've already
> > listed many times in this forum in threads that you yourself have
> > responded to several times.
>
> >http://www.pnas.org/cgi/content/full/103/38/14056
>
> I put in Choi and Kim in a search and came up with a bunch of papers
> that I wasn't about to sort through since you didn't even give the
> date of publication.
>
> I'll promise this. As soon as you make good on your claims and
> present your alternative to common descent and the evidence that is
> just as good as the evidence for common descent that you don't think
> is good enough, and you put up the science of intelligent design that
> you claimed existed to teach to children, I will put up my evaluation
> of the paper and what it means.
>
> I have a copy of the paper, now. I will present my evaluation of it
> if you make good on your past claims that you are constantly running
> from.
>
> Put up or shut up.
LOL - The paper in your hands is evidence of exactly what I've been
explaining to you for years now. If I'm right about what I've been
saying, the proposed evolutionary mechanism is incapable of doing what
you evolutionists say it did. That is a fact regardless of any other
explanation that might be put forward as an explanation.
Again, one does not need any other hypothesis before the hypothesis at
hand can be successfully questioned and falsified.
Beyond this, the presentation of good evidence of the lack of non-
deliberate natural processes to produce a given phenomenon is the very
basis of hypothesizing deliberate artifact - even when it comes to
various mainstream sciences like forensics, anthropology, and SETI.
< snip repetitive >
> > > You know that this doesn't mean jack because most of the antibody
> > > sequence isn't involved in creating the beta gal activity most of it
> > > is use to produce the antibody structure. Again, this is stupid.
>
> > Oh really? Then please do present a smaller portion of an antibody
> > sequence or any other protein sequence that still maintains useful
> > lactase activity from the perspective of any bacterium.
>
> Well for one thing you can cut the number of aa residues about in half
> by just cutting off the common tail and retaining the two active
> ends. These constructs work quite often and I don't see why it
> wouldn't work for lactase function.
Present an actual paper that shows that it does work for the lactase
function. So far this has not been demonstrated. Regardless of your
notion that it should work, it hasn't been done. The best
experimental evidence that we actually have doesn't go significantly
less than 400aa residues for a useful lactase function.
> I don't know how much of the
> variable parts can be deleted because it is dependent on a lot of
> factors that can't be calculated, but if you have the data that it
> can't be done. Let's see it.
Again, science is based on the best available experimental data - not
wishful thinking.
> Not only that, but you are talking
> about a specific start point.
No I'm not. I'm talking about using any living thing with the entire
available genome as a vast host of starting points.
> You haven't ruled out other start
> points using even smaller numbers of residues.
That's fine - present this evidence if you have it. I don't care what
pre-existing starting point you choose. So far, I don't see that it
exists outside of your bald speculations.
> The starting point was
> from the antibody sequence. I've seen no experiments to minimize the
> structural components, and even if they had been done, how many
> starting sequences would they have tried? It isn't the same thing to
> cut something down as it would be to build it from the ground up.
It doesn't matter Ron. If a smaller lactase could have been used, the
odds would have been exponentially better than Hall's E. coli would
have evolved it. The fact that they didn't evolve a smaller lactase,
and no one has ever seen a smaller lactase in action with any
experiment (not even antibody lactases) is strong indication that
smaller lactases than 400aa either don't exist or are extremely rare
in comparison.
If you think otherwise, present some actual evidence that goes beyond
your guesswork and hunches.
You do understand, don't you, that even if you found a lactase of only
200aa, that wouldn't remove the problem. You do understand that -
right? The fact that different types of functional systems have
different minimum structural threshold requirements would still be
there. The fact that those systems with greater minimum thresholds
are exponentially harder to evolve would also remain as a real problem
for the ToE.
< snip >
Seanpit
> > And again, the fact that such a reference does not exist means what?
> > Has anyone ever made a very extensive push to develop lactase function
> > and determine the minimum? No. So what does it mean when you try and
> > use that argument to claim some minimum. Not only that, but even if
> > the minimum was 400 your argument still doesn't work because of Hall's
> > work and his success. Not his failures, but his sucesses. Why did he
> > ever succeed if you are right about 400 anythings?
>
> What I find interesting is that Sean thinks that it is perfectly OK
> for him to assume that the smallest known lactase enzyme is also the
> smallest possible, but for some reason does not apply the same
> reasoning to, say, the fastest known erosion rates, the fastest known
> nuclear decay rates, the fastest known deposition and uplift rates,
> etc. Suddenly, this becomes an unwarranted uniformitarian assumption.
For erosion rates, I don't use the highest number in my estimates, but
the minimum reasonably possible erosion rate extrapolated over tens
and hundreds of millions of years. You do understand the difference?
- right? This isn't a uniformitarian argument. This is an argument
that assumes the likely minimum rate of erosion.
Also, I do not assume any difference in radiometric decay rates over
time. I know other IDists and creationists have used such arguments,
but I have not.
Sean Pitman
www.DetectingDesign.com
Frank J
> "On Sat, 01 Sep 2007 17:15:02 -0700, in article
> [...snip...]>That isn't what you claimed. You claimed that you had an alternative
> >to common descent and evidence to back it up that was just as good as
> >the evidence that you don't. You claimed that you had some science to
> >teach about intelligent design. These were your claims and you have
> >just been running from them for years. Why?
>
> >Why do you have to obfuscate the issue instead of address it?
>
> [...snip...]
>
> Someone is claiming to have an alternative to common descent?
>
> The only alternative that I've seen to common descent depends
> on something like these:
>
> * The designer was working within the limitations of the material.
>
> * The designer had similar intentions.
>
> I'd be interested to discuss those points.
Don't forget Schwabe and Senapathy, who at least don't invoke the
"designer or evolution" false dichotomy. Of course they too base their
alternative mostly on what they think evolution can't do. But it's
interesting how they confront common descent directly, while the usual
suspects, if they address it at all, do it only as an afterthought.
Bobby Bryant
Seanpit <seanpi...@naturalselection.0catch.com> writes:
> This is only to be expected from someone who still denies that a
> statue like Michelangelo's David shows little if any symmetry.
So, how do you know that _David_ is designed and snowflakes aren't?
(Or do you think snowflakes are designed as well?)
Your whole symmetry thing is just a post hoc rationalization for your
IKIWISI design detection kit.
--
Bobby Bryant
Reno, Nevada
Remove your hat to reply by e-mail.
Bobby Bryant
Seanpit <seanpi...@naturalselection.0catch.com> writes:
> I think mainstream science is way off base when it comes to
> understanding the meaning of both the geologic column and the fossil
> record.
<snicker> I wonder how you respond when some quack claims that
physicians don't know diddly about the human body and how it operates.
richardal...@googlemail.com
> On 2 Sep, 16:50, Seanpit <seanpitnos...@naturalselection.0catch.com>
> wrote:
>
> Of course, I've pointed this little concept out to you many times
> before, but you still argue that this type of "analysis" is not real
> analysis - regardless of the fact that it is in fact quite useful as
> it stands.
As nobody including you has ever carried out such an analysis (i.e. a
**STATISTICAL** analysis of shape to determine artificiality), how on
earth can you claim this?
>
> > I also do no ignore questions. For example, I have posed this question
> > several times:
>
> > You go on and on about the exceptional preservation of the Santana
> > formation fish fossils, though you carefully avoid reading any of the
> > scientific literature on the subject. It doesn't matter if the fish
> > were preserved in a matter of hours, days, weeks or years. We have
> > good experimental evidence that preservation of soft tissues of this
> > kind can occur in timescales of days. Such preservation is *not*
> > achieved simply by "sudden burial, as in a flood".
>
> I've answered this false misrepresentation many times Richard. It is
> just a mystery why you feel the need to keep presenting this argument
> as if it had not been refuted over and over again? I never said that
> the Santana formation was the result of rapid burial.
What is at issue is "as in a flood". The characteristics of the very
fine sediments which buried the fish are *NOT* characteristic of a
flood.
> I said that the
> Santana formation was the result of a sudden catastrophe. It was you
> who initially argued that the preservation of the creatures in this
> formation need not have been very rapid, as in a few hours, but could
> have been achieved by much slower processes of non-catastrophic
> fossilization.
You are misrepresenting me again. I have never made any such
statement. In fact, I have posted several links to papers which
demonstrate that the *lower* limit on the time required for such
preservation is a few hours, not "within an hour" as you originally
claimed.
>
> > However, the overwhelmingly vast majority of the fossil record is NOT*
> > preserved in lagerstatten such as the Crato Formation. It's logically
> > incoherent to offer exceptional preservation in a single, limited
> > locality as evidence for a global flood when most of the fossil record
> > is *NOT* exceptionally well-preserved.
>
> The exceptional preservation isn't the only evidence of shortly spaced
> catastrophes in the fossil record Richard. It is just that this
> particular example of the Santana formation, which you originally
> brought up to challenge the concept of catastrophic fossilization and/
> or preservation, does nothing of the sort.
Once again you are misrepresenting me. *You* brought up the Santana
fish, not me. I have never argued that they were not fossilised
rapidly. Bearing in mind that the papers to which I have posted links
on numerous occasions describe the processes whereby fossilisation in
some exceptional cases may be very rapid, why do you think that such
phenomena pose any threat to the views of scientists in this matter?
Incidentally, what the hell do you mean by "catastrophic fossilization
and/or preservation"? It's not a term which appears anywhere in the
scientific literature, which is no surprise as it is pretty well
meaningless. Why do you feel the need to invent terms in a vain
pretence that you have knowledge of the subject?
>
> > Your have stated that: "most fossils show clear evidence of rapid
> > burial or other forms of relatively rapid or even catastrophic
> > preservation leaving little time for predation or bioturbation)"
>
> > This is plainly ridiculous, as anyone who has ever collected fossils
> > can tell you. Mike Benton, in the reference which I have provided,
> > writes
>
> > "Animal and plant remains are typically buried after a great deal of
> > scavenging, decay, breakage and transport."
>
> > What do you know that Mike Benton doesn't?
>
> I agree that a great deal of breakage and transport is the norm, as is
> a bit of scavenging.
This flatly contradicts your statement that ""most fossils show clear
evidence of rapid burial or other forms of relatively rapid or even
catastrophic preservation leaving little time for predation or
bioturbation"
Which is it? And will you change your web site to make it clear that
you have changed your position on this matter?
> However, without rapid burial as a general rule,
> the fine lines of lamination and preservation of such organically rich
> material would not have been preserved due to continued scavenging and
> bioturbation.
Most of the fossils I study show extensive signs of scavenging by
vertebrates and invertebrates, and in the main these fossils come from
formation showing very good or exceptional preservation. These are far
better preserved than most fossils, as they come from the "soupy
substrate" deposits in which bioturbation is generally limited or
lacking. On the other hand, most sedimentary structures show some
degree of bioturbation.
"Fine lines of lamination" are lacking in most sedimentary formations
by the way.
Most fossils are invertebrate skeletons which are not "organically
rich".
Many sedimentary structures, such as chalks, are composed almost
entirely from invertebrate skeletons. The Oxford Clay Formation, which
I have studied intensively, is formed from the fecal pellets of
shrimps.
Why not expand your education on such structures as carbonate
platforms and their formation. Then explain to us how they can be
created by rapid burial.
>
> > You may consider evidence which completely demolishes your assertions,
> > and therefore your arguments as being a "relatively minor point", but
> > no scientist would, and your blatant avoidance shows your lack of
> > integrity.
>
> Anyone who disagrees with you lacks integrity I guess?
No, but people who lie about what they have done do.
I have accused you of lacking integrity because:
1) You misrepresent others. Your change of heading on this post is a
clear example. I have *never* said that "All creationists are evil
liars", and have been very reluctant to label *any* creationist as a
liar unless there is very clear evidence that they are lying.
2) You claim to have carried through a methodology which it is
patently clear that you have not.
3) You evade or ignore any question which demonstrates the vacuousness
of your assertions.
4) You persist in arguments founded on unsubstantiated assertions but
never address the validity of those assertions.
5) You foster the pretence that you have scientific knowledge by
inventing terms such as "catastrophic fossilisation" which are
essentially meaningless and have never been used in any scientific
context.
6) Rather than address the issue of your own integrity you try to cast
doubts on the integrity of others.
> No one can be
> honestly wrong I suppose?
Of course they can. However, when you are making statement you know to
be false with the intent to deceive, you are not being honesty wrong.
You are lying. You claim to have carried through a STATISTICAL
methodology for detecting artifacts. You quite blatantly haven't. The
only puzzling aspect of this is why you persist in this falsehood
after it has been exposed.
> It's like my view of you. I think you are
> way off base in much of your thinking, but I don't stoop to challenge
> your integrity.
I've given you no reason to challenge my integrity.
You have given ample reason to challenge yours, such as your habit of
making things up as you go along, persisting in falsehoods about what
methodologies you have applied, misrepresenting me and others (as I
have identified on several occasions in this post alone), and evading
questions which you don't want to answer as the only honest answer
would blow your arguments apart.
> I think you honestly believe at least most of what
> you say. Yet, you don't seem to be able to extend me the same benefit
> of the doubt?
No, because it is quite evident that you have made statements which
you know to be false.
>
> > I have no problem with this. After all, as I have written on many
> > occasions, one of my reasons for posting here is to expose the
> > dishonesty of creationists. Your help is greatly appreciated.
>
> For the candid reader, all you've done is exposed your own desperation
> - your need to paint all who disagree with you as debased, dishonest,
> and morally corrupt.
I suggest that the "candid reader" is the best judge of that, Sean,
not you.
> That is a generalization that just doesn't hold
> water.
Quite so, and I have never made any such generalisation. It is blatant
misrepresentation on your part to claim that I have done so. I have
been very careful not to call creationists liars unless there is clear
and compelling evidence that they are lying. I have even withdrawn my
labeling of Ray Martinez as a liar after consideration on the grounds
that he is apparently suffering from mental illness. I see no reason
to think that you are mentally ill, by the way. I just think that you
are dishonest.
> Most evolutionists are good honest sincere people who really
> believe in what they are doing and saying. The same thing is true of
> creationists and those who believe in intelligent design.
Why do they have to resort to dishonest arguments in that case?
No creationist has every been able to identify a creationist web site
which is free of misrepresentation, distortion or outright falsehood.
If you think that such a site exists, by all means post the link.
If you can't it rather proves my point.
> Sure, one
> or the other is wrong, but that by no means supports the ludicrous
> notion that all those who have been mislead are dishonest or in any
> sense evil.
I'm not talking about those who have been misled, and have made this
clear on many occasions. I have never labeled anyone as "evil". I have
specifically labeled *you* as dishonest because you have made
assertions which I think you know to be false, and persist in making
such assertions.
Why do you need to misrepresent me in this way? And rather than
posting a snappy answer, why not ask *yourself* that question?
RF
>
> > RF
>
> Sean Pitmanwww.DetectingDesign.com
Ron O
This is stupid. The whole point is that no one has systematically
looked for the lower limit so you can't claim 400aa with any degree of
certainty worth spit. It doesn't matter what people haven't done it
is what they have done and the conclusions that you can make from
those studies. You can't go on about some minimum when they haven't
looked for it.
>
> > Has anyone ever made a very extensive push to develop lactase function
> > and determine the minimum? No. So what does it mean when you try and
> > use that argument to claim some minimum. Not only that, but even if
> > the minimum was 400 your argument still doesn't work because of Hall's
> > work and his success. Not his failures, but his sucesses. Why did he
> > ever succeed if you are right about 400 anythings?
>
> I've already told you. The 400aa size requirement isn't the only
> aspect of the equation. The minimum specificity of amino acid residue
> arrangement is also in play. Proteins, to include those that have the
> lactase function, are not perfectly ridged structures. A certain
> degree of sequence flexibility is available without a complete loss of
> the function in question - i.e., lactase in this case. However, all
> protein based systems have a certain limit to the degree of
> flexibility beyond which the function in question cannot be realized
> at all - not even a little bit.
Demonstrate that this means that functions can't evolve. Why can't
you? How do antibodies work if you are right? Why does your immune
system work nearly every time? Why can you generate antibodies to
synthetic antigens that have never been seen in nature and do it
consistently? You obviously don't know what you are talking about and
your limits aren't the biological limits or you would probably be dead
of some disease by now.
>
> In the case of lactase, Hall's experiments proved that the degree of
> flexibility is in fact quite limited. The evolution of lactase is
> extremely rare in living systems, even when it comes to large colonies
> over tens of thousands of generations under extreme conditions (i.e.,
> high mutation rates and a highly selective environment favoring
> lactase evolution). The lack of evolution in most gene pools observed
> in Hall's experiments support the notion that the average distance
> between lactase islands is well over a dozen mutations wide. Of
> course, this is just the average distance for most types of bacteria.
> The minimum distance is obviously one. On occasion, rare colonies of
> bacteria will be within just one or two mutations of at least one of
> the potential lactase islands that exist in sequence space. However,
> the number of colonies or types of bacteria that will be this close is
> extremely limited compared to all types of bacterial gene pools -
> along a Poisson distribution.
We have been over this. Present the evidence that Hall ever did the
experiment where he let a population evolve over 10,000 generations.
10,000 generations from a clonal start point in a series of single
step selection experiments will not demonstrate what you claim. You
already did the calculations yourself and even if you are a couple of
orders of magnitude off you know that if you let the population come
to mutation selection balance, as a population would in due time (not
instantly from a clone) that you needed your gap inflation suddenly to
jump from 3 to 40. If Hall ever made the claim he was just wrong. He
backed adaptive mutation for years, and was wrong about that, so he
isn't perfect, and you know it.
>
> Now, when it comes to higher level functional systems, the average
> distance is even greater (i.e., several dozen mutations wide). The
> odds that any bacteria will be within just one or two mutations of
> success drops off dramatically - along a Poisson distribution. This
> concept is supported by papers like the one published by Choi and Kim.
>
> http://www.pnas.org/cgi/content/full/103/38/14056
Like I said, I'll discuss this paper when you make good on the claims
you made years ago.
Just think if you could demonstrate what you claim. Why would the
other dishonest ID scam artists have had to quit and go with another
scam? A replacement scam that can't even mention that ID ever
existed. How sad is that, and what does it tell you about your
argument?
>
> > > > Just imagine if you were right. Why was E. coli close enough to get
> > > > the job done?
>
> > > Because of the minimum sequence specificity wasn't high enough. But,
> > > it was still fairly high considering that a colony of 100 billion E.
> > > coli were not able to evolve the lactase function in over 40,000
> > > generations once the ebg gene was deleted. This shows that the
> > > lactase function has a density of less than 1 in 1e24.
>
> > I don't know where you are getting this 40,000 generation stuff. None
> > of the references that you ever put up did such an experiment. Even
> > growing at full speed that would be 2 years of constant growth for
> > some population (20-30 minute generation length), and to select for
> > lactase function the generation length would have to be calculated on
> > a minimal carbon source like glycerol so that you could select for the
> > ones that could grow faster. When we used glyscerol as a carbon
> > source the generation length went from around 25 minutes to 120
> > minutes. So you might be talking about 8 years of constant growth.
> > Where is the citation for this work? All you ever put forward were
> > plate experiments. You can't get this kind of estimate from such
> > experiments and you know it.
>
> Hall studied K12 E. coli and the evolution of lactase from ebg for
> over 25 years. If you want to argue that the reproductive rate was
> lower, on the order of 2 hours, that's fine. The number of
> generations studied are still plenty for the purposes of this
> discussion.
Actually I found out that the doubling time for the experiment was 30
to 50 hours so Hall wasn't using a very good (or low concentration)
carbon source, at least not one as good as glycerol and glycerol is
pretty poor.
Demonstrate that Hall did the experiment that you are claiming that he
did. You, know letting a population evolve for 10,000 generations.
You wouldn't be trying to pull a fast one and make claims about what
he did that aren't supported by the actual work, would you?
>
> > > > Something is obviously wrong with your argument because
> > > > Hall got it to work with 2 or 3 other species out of whatever number
> > > > he tested, and I bet that it was less than 50 species tested.
>
> > > This is not true. Hall's experiment did not work with other species.
> > > In fact, there are species of bacteria that have been observed for
> > > over a million generations without being able to evolve the lactase
> > > function - despite the reproductive advantage that would be gained if
> > > they did happen to evolve this function.
>
> > I'm not going to look it up, but I believe that you recall your own
> > references and this seems to be just a blatant lie. Admit it. There
> > was a reference that we discussed where he tried several different
> > species and he found 2 or 3 that his same single step selection
> > strategy worked. It was in the abstract of the paper. I couldn't get
> > the paper, but the abstract was available on PubMed. The abstract did
> > not say how many species were tried, just how many worked.
>
> As far as I am aware lactase evolution was not achieved in any other
> species besides E. coli. If you do have a reference to the contrary,
> please list it here. Where is this abstract you remember reading? I
> don't remember any such abstract.
It was your reference that I looked up, and you have never contested
this claim from the first time that I made it years ago after seeing
the abstract, so why now? This is about as tragic as any argument
should get. What do you expect to gain by stooping to something like
this. I looked up Hall BG in PubMed and got this reference on
Klebsiella where he got the lactase function and figured out what gene
was mutating and it wasn't the same one as in E. coli. It was related
to ebg, but not the same. In other papers it seems that the whole
family diverged about 2 billion years ago. Do you agree with Hall's
divergence estimate? So here is a definite example. Do I have to
search for the reference that I recall? It might not have been a Hall
paper, but written by someone else you might have cited.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=110764
>
> > > > Some how the impossible happens too often for your argument to
> > > > possibly be corect.
>
> > > You need to read up on this experiment. Beyond this, I never said
> > > that evolution at this level couldn't happen on a regular basis. It
> > > obvious does happen and there are many examples of it happening at
> > > this level. It is just that the relative number of examples at this
> > > level is far less than the number of lower-level examples and far far
> > > more than higher level examples. In fact, there are no examples of
> > > evolution very far beyond this level - not a single example beyond the
> > > 1000aa threshold in all of literature.
>
> > And you know that the relative number of successes is not enough
> > because....
>
> There isn't even one example beyond this level.
>
> > You can't just make this junk up.
>
> Anyone can look it up and see that I'm right. There aren't any
> examples beyond the 1000aa minimum threshold.
What are you babbling about? You have to first tell us what this
threshold is and demonstrate that it exists before anyone can see
anything.
>
> > You have to be able to demonstrate
> > it, and you can't even demonstrate that your 1000 aa threshold even
> > exists. Just do it. produce your numbers. Determine that such a gap
> > existed. Since you can't do that, what are you making noises about?
>
> There are a great many protein-based systems that require well over
> 1000 fairly specified amino acid residues. A system of 1000 residues
> requires at least 3,000 codons of genetic real estate. Do you think
> you could produce a flagellar motility system with just 3000 codons?
> Think again. Flagellar motility requires at least 30,000 codons of
> genetic real estate at minimum.
First the average size of a protein is only around 300 amino acids.
There are larger ones, but the minimum is obviously zero so there
aren't too many really big ones.
All you have to do is determine what threshold you are talking about
for the 30,000 codons of the flagella, and why that threshold could
not be crossed by biological evolution. Go for it. What were the
sequences as they were evolving? What systems evolved first? What
were the selective conditions? It obviously doesn't matter how many
amino acids make up a protein or are needed to specify function if
there are proteins around only 1 or 2 substitutions away from getting
that function. Your own examples tell you that, so what is your
beef? Demonstrate that what you call a threshold means anything.
Why did the similar IDiot scam artist claims fail? What makes your
argument better than theirs, and why have they given up and gone with
a stupid obfuscation scam if you have such a great argument?
>
> There are many other such examples as well - such as the minimum
> structural threshold it takes to code for the functional system
> responsible for DNA transcription or RNA translation - to name just a
> couple more examples of higher-level functions.
I predicted that the IDiots would keep falling back until they hit
some really old systems that it is nearly impossible to figure out how
they evolved. The flagellum evolved over 2 billion years ago, and has
changed so much that it is going to take a lot of hard work to even
attempt an answer as to how it evolved, but we can still tell what
proteins are related to, at least, some of them. What chance to we
have of something that evolved over 3.5 billion years ago? The sword
cuts both ways. To claim that it was impossible to evolve such a
system you have to figure out every possible way it could have
happened and determine that it didn't happen that way. Go for it, but
I think you realize that your great grand children will still be
working on the problem with as much success as you can hope to
achieve, unless they invent time travel.
>
> > > This brings us back to my original question for you. How do you
> > > explain this observation? The complete lack of evolution beyond the
> > > 1000aa threshold? I've yet to see you even try to answer this
> > > question. . .
>
> > Bogus obfuscation is just bogus obfuscation. Until you can even
> > demonstrate that some 1000aa threshold even exists you have no
> > argument. There is no observation to explain until you can tell us
> > what the 1000aa threshold is and demonstrate that it had to be crossed
> > at some point in such a way that descent with modification and
> > selection would not have been able to cross such a threshold in a
> > biologically relevant fashion.
>
> I've provided you with this information over and over again. The
> flagellar motility system requires over 30,000 codons of genetic real
> estate. Obviously, this threshold had to be crossed or this type of
> motility system would not exist. None of the proposed steppingstones
> in flagellar evolution are narrower than a few dozen mutations. How
> then were they crossed and why are there no examples of any system
> beyond the 1000aa evolving?
>
You provided nothing but baseless assertion with no credible arguments
to back up the assertions. You have to tell us what the 1000 aa are
before we can tell you how they were crossed. You also have to
provide the starting material because I don't have a crystal ball.
>
> > Just demonstrate one problem step in getting past your fictional
> > 1000aa threshold in the evolution of the flagellum. Present the
> > sequences and tell us where
>
> ...
>
For some reason Google cut off your post here. I'll have to go back
and see if I can bring up the entire post.
Ron Okimoto
Ron O
0catch.com> wrote:
> On Sep 2, 7:56 am, Ron O <rokim...@cox.net> wrote:
>
> > On Sep 1, 9:30 pm, Seanpit <seanpitnos...@naturalselection.0catch.com>
> > wrote:> On Sep 1, 5:15 pm, Ron O <rokim...@cox.net> wrote:
>
> > Just demonstrate one problem step in getting past your fictional
> > 1000aa threshold in the evolution of the flagellum. Present the
> > sequences and tell us where the gap is and why it could not be
> > crossed.
>
> All the steps in the proposed model of flagellar evolution are beyond
> the 1000aa threshold. None of them have ever been demonstrated to
> actually evolve outside of the wild imagination of evolutionists.
Where and when did this 1000 aa threshold exist? Just give some
specific example like when the ATPases were evolving to function in
their role, or how the tail proteins evolved. Just take the proteins
that they are related too and try and demonstrate that there was some
threshold that they had to cross, but couldn't. You don't seem to get
it, but you haven't even established that there was a 1000 aa
threshold to cross.
>
> > No one is going to answer any stupid questions about this fictional
> > 1000aa threshold until you can demonstrate that it actually exists and
> > that there is something to explain.
>
> It is obvious that this threshold exists. What is not so obvious,
> from the evolutionary perspective anyway, is why nothing beyond the
> 1000aa threshold actually evolves. Why isn't there even one example
> when there are lots of examples of lower-level evolution that require
> a minimum structural threshold no more than a few hundred fairly
> specified amino acid residues? Why do relatively small single
> protein systems, like lactase and nylonase, occasionally evolve while
> higher level systems that require more than a few hundred residues
> never evolve?
So obvious that you can't even tell us what the threshold was.
>
> It's a simple and obvious question Ron. What's your answer?
Because evolution doesn't work that way. Complex systems are not
expect to evolve de novo all at once. That would be closer to special
creation than biological evolution and you know it. They are expected
to evolve from existing systems already doing something else, and it
might take some time and intermediate steps that have nothing to do
with the final function, but did have some other function. Why can we
determine that related proteins to those found in the flagellum are
doing other things in the cell? What is your answer to that? Why can
Hall claim that the ebg genes diverged from the Lac genes over 2
billion years ago, but that they had a common origin?
Put up or shut up. So far all you have been doing is obfuscating and
blowing smoke. So put up or shut up.
You know that I'll keep my promise, so back up the claims that you
made if you think that I can't.
>
> Again, one does not need any other hypothesis before the hypothesis at
> hand can be successfully questioned and falsified.
Again. That is not what you claimed. You claimed that you had some
science to teach about intelligent design. You claimed that you could
back up teaching the claptrap. You claimed to have an alternative to
common descent and the evidence to back it up that was just as good as
the evidence that you don't think is good enough to support the
scientific explanation.
This is just a dishonest ploy. You have degenerated into lying, but
you probably have some insane notion that as long as you just
misrepresent something that it isn't lying. You know what your claims
were. So put up or shut up.
>
> Beyond this, the presentation of good evidence of the lack of non-
> deliberate natural processes to produce a given phenomenon is the very
> basis of hypothesizing deliberate artifact - even when it comes to
> various mainstream sciences like forensics, anthropology, and SETI.
>
> < snip repetitive >
SNIP what you can't deal with. Pretending is dishonest. Some little
bug in your brain probably whispers that in your ear, but you refuse
to heed it. Just think if you could make good on your claims. You
wouldn't need bogus arguments about 1000 aa bull pucky. You could
actually have an argument.
>
> > > > You know that this doesn't mean jack because most of the antibody
> > > > sequence isn't involved in creating the beta gal activity most of it
> > > > is use to produce the antibody structure. Again, this is stupid.
>
> > > Oh really? Then please do present a smaller portion of an antibody
> > > sequence or any other protein sequence that still maintains useful
> > > lactase activity from the perspective of any bacterium.
>
> > Well for one thing you can cut the number of aa residues about in half
> > by just cutting off the common tail and retaining the two active
> > ends. These constructs work quite often and I don't see why it
> > wouldn't work for lactase function.
>
> Present an actual paper that shows that it does work for the lactase
> function. So far this has not been demonstrated. Regardless of your
> notion that it should work, it hasn't been done. The best
> experimental evidence that we actually have doesn't go significantly
> less than 400aa residues for a useful lactase function.
No one has done it, so what? Did I claim that it had been done for
lactase? They have gotten it to work for other abzymes. Just look it
up for yourself. You know that you don't even have to look it up.
That is what makes this challenge so sad. Just think if you had an
honest argument, would you have to stoop this low?
>
> > I don't know how much of the
> > variable parts can be deleted because it is dependent on a lot of
> > factors that can't be calculated, but if you have the data that it
> > can't be done. Let's see it.
>
> Again, science is based on the best available experimental data - not
> wishful thinking.
Yeah, but science is also based on what has already been done and you
can't make your claims from what has been done. Admit it and move on.
>
> > Not only that, but you are talking
> > about a specific start point.
>
> No I'm not. I'm talking about using any living thing with the entire
> available genome as a vast host of starting points.
What happens in that case? It works. Lactase function evolves. It
might not happen in every genome, but it does happen. How often does
it have to happen from a starting point of a couple thousand proteins?
>
> > You haven't ruled out other start
> > points using even smaller numbers of residues.
>
> That's fine - present this evidence if you have it. I don't care what
> pre-existing starting point you choose. So far, I don't see that it
> exists outside of your bald speculations.
>
> > The starting point was
> > from the antibody sequence. I've seen no experiments to minimize the
> > structural components, and even if they had been done, how many
> > starting sequences would they have tried? It isn't the same thing to
> > cut something down as it would be to build it from the ground up.
>
> It doesn't matter Ron. If a smaller lactase could have been used, the
> odds would have been exponentially better than Hall's E. coli would
> have evolved it. The fact that they didn't evolve a smaller lactase,
> and no one has ever seen a smaller lactase in action with any
> experiment (not even antibody lactases) is strong indication that
> smaller lactases than 400aa either don't exist or are extremely rare
> in comparison.
This seems to be coming out of left field. What was the starting
material? Why would you expect the smallest protein to evolve a new
function to be present in any experiment? Wouldn't a protein with
more surface area be a more likely candidate? Has the smallest
possible protein with lactase activity been determined? Yes or no?
>
> If you think otherwise, present some actual evidence that goes beyond
> your guesswork and hunches.
I laugh at this openly. How did you determine that your 1000 aa
threshold existed? Got any actual evidence?
>
> You do understand, don't you, that even if you found a lactase of only
> 200aa, that wouldn't remove the problem. You do understand that -
> right? The fact that different types of functional systems have
> different minimum structural threshold requirements would still be
> there. The fact that those systems with greater minimum thresholds
> are exponentially harder to evolve would also remain as a real problem
> for the ToE.
It doesn't really matter, what matters is that you can't make your
argument work no matter how large or small the minimum lactase enzyme
would be. It obviously isn't as large as nature created it. It can
be reduced in size from over a 1000 aa to less than 400. All
biological evolution claims is that it will use what works. What is
your counter claim? The intelligent design made it bigger than it had
to be because he wanted lifeforms to waste energy in making junk that
they don't need? Why didn't he make it smaller for humans? Why is it
the same size for chimps and humans?
>
> < snip >
Pretend and run away. Snipping doesn't change reality. I just
thought that I'd tell you that if you have really convinced yourself
otherwise. Pathetic dishonesty, is just that, pathetic dishonesty.
I'll just put it back in so that everyone will get a sense of how
pathetic. Snipping a response to a snip is pretty pathetic. Why not
just make good on your claims. You made them.
[replaced material]
> < snip repetitions >
Run away and pretend. Pretending is what you do best, but it doesn't
work in science because someone always asks for verification.
Really, put up what you have claimed in the past and I will evaluate
your paper. Go for it or admit that the paper doesn't support your
assertions and your past claims have been bogus. They aren't just
stupid claims about fictional 1000aa thresholds, they are claims
about
your ID science and your alternative to common descent. Why is it so
hard to make good on those claims if your argument is at all valid?
After all these years of bogus arguing, shouldn't you have an
alternative? It would be insane just to be arguing to be arguing.
If
you really have any science worth teaching to kids about this
claptrap, shouldn't you be able to produce what you claimed to have
wanted to teach to them? You must have had something worth teaching
or you wouldn't have wanted to teach it, so what was the science of
ID
that you would have taught?
If you don't get it. Dishonestly ignoring your past claims and
running from them is an admission that they were not valid claims.
You made the claims. You don't even try to deny it. You just snip
and pretend. What does that say about you?
[end replaced material]
>
> > Ron Okimoto
>
> Sean Pitmanwww.DetectingDesign.com
Just think if intelligent design hadn't been a dishonest scam you
might actually have a valid argument.
Put up or shut up.
If you keep running away and pretending, you are just lying to
yourself.
Ron Okimoto
Seanpit
> In article <1188748245.326427.67...@w3g2000hsg.googlegroups.com>,
> Seanpit <seanpitnos...@naturalselection.0catch.com> writes:
>
> > This is only to be expected from someone who still denies that a
> > statue like Michelangelo's David shows little if any symmetry.
>
> So, how do you know that _David_ is designed and snowflakes aren't?
> (Or do you think snowflakes are designed as well?)
Snowflakes aren't made out of granite or marble, materials that do not
naturally tend toward highly symmetrical self-assembly.
Again, you have to have prior experience with the *material* in
question and how it interacts with non-deliberate forces of nature
before you can begin to reasonably detect artifact.
Take, for instance, SETI scientists. If they had absolutely no
experience with radiowaves they wouldn't be able to say if this or
that pattern was or was not likely to be the result of artifact. It
is only because of their prior experience with radiowaves that they
can in fact suggest features that would likely be artifactual if they
were ever discovered in radiowaves.
> Your whole symmetry thing is just a post hoc rationalization for your
> IKIWISI design detection kit.
You do have to have prior knowledge gained through experience with the
material in question before you can reliably "know it when you see
it".
Tell me Bobby, what methodology would you use to hypothesize
artifact? Please explain how you would go about it. Richard says
that it cannot be done without some sort of evidence for manufacture.
The problem with this notion is that SETI scientists think they can
detect artifact without detecting anything other than a particular
type of radiosignal - no need for knowing how such a signal was
actually made. The same thing is true of a highly symmetrical
polished granite cube. Such a cube is clearly artifactual in nature
regardless of how it was actually "manufactured".
So, Bobby, how would you be able to detect artifact when you see it?
Can you put into words or into a method how you "know it when you see
it"? There has to be some sort of reason or you would not be able to
"KIWYSI" - right?
> Bobby Bryant
> Reno, Nevada
Sean Pitman
www.DetectingDesign.com
Seanpit
Before responding to this post in detail, you still don't seem to have
grasped the difference between a minimum structural threshold
requirement and a gap distance. They are not the same thing. A
minimum structural threshold is NOT related to any starting point
either. It is what it is. A system requires a certain minimum
structural form before it can work regardless of how it came to be.
If that structure is realized, the system will work. Otherwise, it
will not work. The greater this minimum structural requirement, the
less the odds are that this requirement will be within one or two
mutations of what already exists within any gene pool. Sure,
increasing the size of the gene pool will help, but for every increase
in the minimum structural threshold requirements, the needed increase
in gene pool size to keep the gap size the same is an exponential
increase. Pretty soon, the environment cannot support the needed
population increase and so the minimum gap size starts to increase in
a linear manner with each increase in the minimum structural threshold
requirements. This means that the gap size will always be smaller
than the threshold size.
And, there you have it. Although the gap size and the threshold size
are not the same, they are related to each other. You will not
understand my position until you are able to grasp these basis
concepts:
1. The minimum structural threshold size is the minimum structural
requirements needed to produce a particular type of functional system
2. The minimum gap size is the mutational distance between what exists
in a gene pool and what might exist as a beneficial system if it were
ever found by random mutation.
3. The gap size is always smaller than the threshold size.
4. The average gap size increases with each increase in structural
threshold requirements.
5. The minimum gap size does not increase until the population size
remains static and until the number of genetic elements within just
one mutation of a beneficial target drop to one. At this point, the
increase in the gap distance follows a linear relationship to the
increase in the minimum structural threshold requirements.
> > > And again, the fact that such a reference does not exist means what?
>
> > It means that based on the information that does exist, the hypothesis
> > of a 400aa threshold has the most support. You may argue that future
> > information is likely to reveal a much smaller threshold. That isn't
> > science Ron. That's an unsupported hypothesis that isn't even
> > falsifiable this side of eternity. You could always argue that this
> > or that hypothesis could be wrong given some future discovery. That's
> > always a possibility in science.
>
> This is stupid. The whole point is that no one has systematically
> looked for the lower limit so you can't claim 400aa with any degree of
> certainty worth spit. It doesn't matter what people haven't done it
> is what they have done and the conclusions that you can make from
> those studies. You can't go on about some minimum when they haven't
> looked for it.
You can certainly get a rough idea that different types of systems
have very different minimum structural threshold limitations and that
those with larger minimum requirements are much harder to evolve.
What you are trying to do is deny everything based on some lame notion
that because these limitations have not been exhaustively defined that
the whole concept is completely meaningless. You're just trying to
ignore the obvious. It is overwhelmingly clear that different types
of functionally beneficial systems have different minimum
requirements. It is also overwhelmingly clear that evolution works
very well to produce systems with very low minimums (i.e., a few dozen
fairly specified residues or less), much less commonly for systems
that require at least a few hundred fairly specified residues (i.e.,
lactase, nylonase, etc), and not at all for systems that require over
1,000 fairly specified residues (flagellar motility, DNA
transcription, etc).
> > > Has anyone ever made a very extensive push to develop lactase function
> > > and determine the minimum? No. So what does it mean when you try and
> > > use that argument to claim some minimum. Not only that, but even if
> > > the minimum was 400 your argument still doesn't work because of Hall's
> > > work and his success. Not his failures, but his sucesses. Why did he
> > > ever succeed if you are right about 400 anythings?
>
> > I've already told you. The 400aa size requirement isn't the only
> > aspect of the equation. The minimum specificity of amino acid residue
> > arrangement is also in play. Proteins, to include those that have the
> > lactase function, are not perfectly ridged structures. A certain
> > degree of sequence flexibility is available without a complete loss of
> > the function in question - i.e., lactase in this case. However, all
> > protein based systems have a certain limit to the degree of
> > flexibility beyond which the function in question cannot be realized
> > at all - not even a little bit.
>
> Demonstrate that this means that functions can't evolve. Why can't
> you? How do antibodies work if you are right? Why does your immune
> system work nearly every time? Why can you generate antibodies to
> synthetic antigens that have never been seen in nature and do it
> consistently? You obviously don't know what you are talking about and
> your limits aren't the biological limits or you would probably be dead
> of some disease by now.
You do understand how antibodies work - right? Antibodies almost
always work because the size of sequence space which must be covered
to produce a highly effective immune system is relatively small. As
far as antigens are concerned, the total number of possible epitopes
is 20^B since there are 20 different amino acids. Well, the typical
length of an antigen epitope ("B" in the preceding formula) is about
20 amino acid residues. So, the total number of possible antigen
epitopes is about 20^20 or 104,857,600,000,000,000,000,000,000 or
~100 trillion trillion.
That sounds like a big number doesn't it? Since there are trillions
of different possible antigen epitopes, how does one's immune system
cope with such a variety of potential enemies? Well, there are many
immune cells produced by the body. In humans, in particular, about
10^12 lymphocytes are present at any given time.
Not all the T-cells have different Y-shaped receptors, but many of
them do. Chances are that if enough non-self enemies get into the
body at least one of the immune cells will recognize the non-self
marker sequences or "antigens" located on this invader as "foreign" to
at least some useful degree. The odds that a single T-cell will
recognize a random epitope to at least some useful degree is about 1
in 10^12. So, does this mean it would take a trillion different T-
cells to cover all possible invaders? Well, no. The reason is
because an average cell or foreign invader "bug" has about 10^12
different epitopes. So, on average, a single T-cell will recognize at
least one of the potential antigen epitopes of a foreign invader.
That is how the immune system works in a nutshell. And, that is why
immune system "evolution" really isn't very high level. It is working
in a relatively small "sequence space" of just 20^20. This is not
true when you start talking about sequence spaces greater than
20^1000.
For further information concerning immune system "evolution" see:
http://www.detectingdesign.com/immunesystem.html
> > In the case of lactase, Hall's experiments proved that the degree of
> > flexibility is in fact quite limited. The evolution of lactase is
> > extremely rare in living systems, even when it comes to large colonies
> > over tens of thousands of generations under extreme conditions (i.e.,
> > high mutation rates and a highly selective environment favoring
> > lactase evolution). The lack of evolution in most gene pools observed
> > in Hall's experiments support the notion that the average distance
> > between lactase islands is well over a dozen mutations wide. Of
> > course, this is just the average distance for most types of bacteria.
> > The minimum distance is obviously one. On occasion, rare colonies of
> > bacteria will be within just one or two mutations of at least one of
> > the potential lactase islands that exist in sequence space. However,
> > the number of colonies or types of bacteria that will be this close is
> > extremely limited compared to all types of bacterial gene pools -
> > along a Poisson distribution.
>
> We have been over this. Present the evidence that Hall ever did the
> experiment where he let a population evolve over 10,000 generations.
> 10,000 generations from a clonal start point in a series of single
> step selection experiments will not demonstrate what you claim. You
> already did the calculations yourself and even if you are a couple of
> orders of magnitude off you know that if you let the population come
> to mutation selection balance, as a population would in due time (not
> instantly from a clone) that you needed your gap inflation suddenly to
> jump from 3 to 40. If Hall ever made the claim he was just wrong. He
> backed adaptive mutation for years, and was wrong about that, so he
> isn't perfect, and you know it.
You still don't seem to understand that the gap between lactases and a
given genome, like that of E. coli, is never going to be 40 mutations
wide at minimum. Rather, it is probably not going to be more than 10
or 12 mutations wide at minimum. However, although seemingly small, a
gap of just 10 or 12 mutations is more than enough to explain the
results of Hall's experiment - the "limited evolutionary potential" he
describes for his ebg- E. coli. It is also enough to explain the
complete lack of lactase evolution not only in E. coli, but in other
types of bacteria that have been observed for several decades now
without ever evolving this enzymatic function - a function that would
be reproductively useful for them if they ever did happen to evolve
it.
> > Now, when it comes to higher level functional systems, the average
> > distance is even greater (i.e., several dozen mutations wide). The
> > odds that any bacteria will be within just one or two mutations of
> > success drops off dramatically - along a Poisson distribution. This
> > concept is supported by papers like the one published by Choi and Kim.
>
> >http://www.pnas.org/cgi/content/full/103/38/14056
>
> Like I said, I'll discuss this paper when you make good on the claims
> you made years ago.
>
> Just think if you could demonstrate what you claim. Why would the
> other dishonest ID scam artists have had to quit and go with another
> scam? A replacement scam that can't even mention that ID ever
> existed. How sad is that, and what does it tell you about your
> argument?
What are you talking about? You are the one making bald claims about
something I supposedly said years ago - something I never said.
Present the reference Ron. Otherwise, you just avoiding the
obvious.
> > Hall studied K12 E. coli and the evolution of lactase from ebg for
> > over 25 years. If you want to argue that the reproductive rate was
> > lower, on the order of 2 hours, that's fine. The number of
> > generations studied are still plenty for the purposes of this
> > discussion.
>
> Actually I found out that the doubling time for the experiment was 30
> to 50 hours so Hall wasn't using a very good (or low concentration)
> carbon source, at least not one as good as glycerol and glycerol is
> pretty poor.
>
> Demonstrate that Hall did the experiment that you are claiming that he
> did. You, know letting a population evolve for 10,000 generations.
> You wouldn't be trying to pull a fast one and make claims about what
> he did that aren't supported by the actual work, would you?
He used the same clone as a basis for his work for over 25 years Ron.
What more do you need?
> > As far as I am aware lactase evolution was not achieved in any other
> > species besides E. coli. If you do have a reference to the contrary,
> > please list it here. Where is this abstract you remember reading? I
> > don't remember any such abstract.
>
> It was your reference that I looked up, and you have never contested
> this claim from the first time that I made it years ago after seeing
> the abstract, so why now? This is about as tragic as any argument
> should get. What do you expect to gain by stooping to something like
> this. I looked up Hall BG in PubMed and got this reference on
> Klebsiella where he got the lactase function and figured out what gene
> was mutating and it wasn't the same one as in E. coli. It was related
> to ebg, but not the same. In other papers it seems that the whole
> family diverged about 2 billion years ago. Do you agree with Hall's
> divergence estimate? So here is a definite example. Do I have to
> search for the reference that I recall? It might not have been a Hall
> paper, but written by someone else you might have cited.
>
> http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubme...
Present the actual reference, along with a quote, where any other
bacteria evolved the lactase function. As far as I am aware, this
experiment was not performed by Barry Hall or anyone else.
< snip >
> > > You have to be able to demonstrate
> > > it, and you can't even demonstrate that your 1000 aa threshold even
> > > exists. Just do it. produce your numbers. Determine that such a gap
> > > existed. Since you can't do that, what are you making noises about?
>
> > There are a great many protein-based systems that require well over
> > 1000 fairly specified amino acid residues. A system of 1000 residues
> > requires at least 3,000 codons of genetic real estate. Do you think
> > you could produce a flagellar motility system with just 3000 codons?
> > Think again. Flagellar motility requires at least 30,000 codons of
> > genetic real estate at minimum.
>
> First the average size of a protein is only around 300 amino acids.
> There are larger ones, but the minimum is obviously zero so there
> aren't too many really big ones.
That's true for single protein systems.
> All you have to do is determine what threshold you are talking about
> for the 30,000 codons of the flagella, and why that threshold could
> not be crossed by biological evolution. Go for it.
The 30,000 codons IS the threshold Ron. Without all of these 30,000
codons in place in a fairly specified arrangement the function of
flagellar motility could not be realized at all - not even a little
bit. The 30,000 number is NOT calculated in regard to some
reference. It is its own reference. Regardless of how it is achieved,
flagellar motility cannot be realized until this threshold is crossed
- by small steps or deliberate design. Whatever method was used, it
had to achieve this 30,000 codon threshold limitation.
> What were the
> sequences as they were evolving? What systems evolved first? What
> were the selective conditions? It obviously doesn't matter how many
> amino acids make up a protein or are needed to specify function if
> there are proteins around only 1 or 2 substitutions away from getting
> that function. Your own examples tell you that, so what is your
> beef? Demonstrate that what you call a threshold means anything.
My "beef" is that all of your proposed steppingstones in the evolution
of flagellar motility are separated from each other, not by 1 or 2
mutations, but by dozens of mutations. That's the "beef" Ron. Higher
level systems like this have gaps between the subsystem steppingstones
that are much wider than one or two mutations. And, there is a linear
relationship between the likely minimum gap size and the minimum
structural threshold size. They aren't the same thing, but they are
certainly related to each other.
Again, you need to look carefully at the Choi and Kim paper I
referenced.
> Why did the similar IDiot scam artist claims fail? What makes your
> argument better than theirs, and why have they given up and gone with
> a stupid obfuscation scam if you have such a great argument?
As far as I am aware, my argument is rather unique. No one else is
presenting quite what I'm presenting.
In any case, you're talking to me now - not someone else. How can you
counter my observation and hypothesis? That's the only relevant
question here.
> > There are many other such examples as well - such as the minimum
> > structural threshold it takes to code for the functional system
> > responsible for DNA transcription or RNA translation - to name just a
> > couple more examples of higher-level functions.
>
> I predicted that the IDiots would keep falling back until they hit
> some really old systems that it is nearly impossible to figure out how
> they evolved. The flagellum evolved over 2 billion years ago, and has
> changed so much that it is going to take a lot of hard work to even
> attempt an answer as to how it evolved, but we can still tell what
> proteins are related to, at least, some of them. What chance to we
> have of something that evolved over 3.5 billion years ago? The sword
> cuts both ways. To claim that it was impossible to evolve such a
> system you have to figure out every possible way it could have
> happened and determine that it didn't happen that way. Go for it, but
> I think you realize that your great grand children will still be
> working on the problem with as much success as you can hope to
> achieve, unless they invent time travel.
Pick any molecular system you want, modern or ancient. If it requires
over 1000aa a minimum to function it doesn't evolve in real time and,
statistically, it couldn't have evolved in trillions of years.
> > > > This brings us back to my original question for you. How do you
> > > > explain this observation? The complete lack of evolution beyond the
> > > > 1000aa threshold? I've yet to see you even try to answer this
> > > > question. . .
>
> > > Bogus obfuscation is just bogus obfuscation. Until you can even
> > > demonstrate that some 1000aa threshold even exists you have no
> > > argument. There is no observation to explain until you can tell us
> > > what the 1000aa threshold is and demonstrate that it had to be crossed
> > > at some point in such a way that descent with modification and
> > > selection would not have been able to cross such a threshold in a
> > > biologically relevant fashion.
>
> > I've provided you with this information over and over again. The
> > flagellar motility system requires over 30,000 codons of genetic real
> > estate. Obviously, this threshold had to be crossed or this type of
> > motility system would not exist. None of the proposed steppingstones
> > in flagellar evolution are narrower than a few dozen mutations. How
> > then were they crossed and why are there no examples of any system
> > beyond the 1000aa evolving?
>
> You provided nothing but baseless assertion with no credible arguments
> to back up the assertions. You have to tell us what the 1000 aa are
> before we can tell you how they were crossed. You also have to
> provide the starting material because I don't have a crystal ball.
What don't you get about the 1000aa threshold? How can you ask "what
the 1000aa are?" They are amino acid residues Ron. Any and every
system that requires at least 1000 fairly specified amino acid
residues to achieve its particular type of function, doesn't evolve
via random mutation and natural selection. There are a lot of systems
that require more than this minimum. Most of these are indeed made up
of multiple proteins working together - like the flagellar motility
system. Their total specified amino acid requirement, as reflected in
the minimum amount of DNA that is required to code for them, is the
minimum threshold requirement. This minimum threshold requirement is
NOT the gap size. That is a different but related measure. How can
you not grasp that concept?
> > > Just demonstrate one problem step in getting past your fictional
> > > 1000aa threshold in the evolution of the flagellum. Present the
> > > sequences and tell us where the gap is and why it could not be
> > > crossed.
>
> > All the steps in the proposed model of flagellar evolution are beyond
> > the 1000aa threshold. None of them have ever been demonstrated to
> > actually evolve outside of the wild imagination of evolutionists.
>
> Where and when did this 1000 aa threshold exist?
It exists whenever a functional system requires at least this many
fairly specified residues. Again, the flagellar system requires
upward of 10,000 codons (30,000 bp) or the equivalent of 10,000aa.
That is a threshold limitation that is 10 times more than the 1000aa
threshold. The TTSS system requires about 3,000 codons - about 3
times more than the 1000aa threshold. The relatively simple P-pilus
also requires well over 1000 codons. None of these systems have or can
evolve from anything pre-existing within any gene pool.
> Just give some
> specific example like when the ATPases were evolving to function in
> their role, or how the tail proteins evolved. Just take the proteins
> that they are related too and try and demonstrate that there was some
> threshold that they had to cross, but couldn't. You don't seem to get
> it, but you haven't even established that there was a 1000 aa
> threshold to cross.
You don't seem to get the idea that the 1000aa isn't the gap
distance. The gap distance is always much smaller than the minimum
structural threshold requirements. How many times do I have to
explain this before you'll grasp this seemingly simply concept?
< snip redundant >
> > It's a simple and obvious question Ron. What's your answer?
>
> Because evolution doesn't work that way. Complex systems are not
> expect to evolve de novo all at once. That would be closer to special
> creation than biological evolution and you know it. They are expected
> to evolve from existing systems already doing something else, and it
> might take some time and intermediate steps that have nothing to do
> with the final function, but did have some other function. Why can we
> determine that related proteins to those found in the flagellum are
> doing other things in the cell? What is your answer to that? Why can
> Hall claim that the ebg genes diverged from the Lac genes over 2
> billion years ago, but that they had a common origin?
If evolution happened, it obviously happened by co-opting pre-existing
structures to do unique functions. The problem, Ron, is that when
minimum structural threshold requirements (not the gap distance) go
beyond the 1000aa level, the gap distance between what exist in a gene
pool and what might exist as a beneficial co-opted function grows in a
linear manner. It does not remain at the minimum possible gap
distance of just 1 or 2 mutations. The gap distance increases, even
for very large populations, in line with each increase in the minimum
structural threshold requirements of different types of potentially
beneficial systems.
In short, non of your proposed steppingstones for the evolution of the
flagellum are likely to be within a few dozen mutations of each other
- not one. Look it up and you'll see that I'm correct. The needed
subsystems would require too many modifications to be fit together
properly to form the next step in the flagellar evolution pathway. It
just wouldn't have worked even given trillions of years of time.
If you think otherwise, present a model for flagellar evolution where
the gaps between one beneficial system and the next is only a handful
of mutations wide. No one has been able to do that for any high-level
system to include the flagellar motility system. All that exist are
assertions that the gaps are small and that they could have been
crossed by evolutionary mechanisms given millions of years. No actual
statistical calculations or real mathematical evaluations have been
published to support these otherwise baseless assumptions. That
leaves them with the status of "just-so story telling" - not science.
< snip >
> > > Well for one thing you can cut the number of aa residues about in half
> > > by just cutting off the common tail and retaining the two active
> > > ends. These constructs work quite often and I don't see why it
> > > wouldn't work for lactase function.
>
> > Present an actual paper that shows that it does work for the lactase
> > function. So far this has not been demonstrated. Regardless of your
> > notion that it should work, it hasn't been done. The best
> > experimental evidence that we actually have doesn't go significantly
> > less than 400aa residues for a useful lactase function.
>
> No one has done it, so what? Did I claim that it had been done for
> lactase? They have gotten it to work for other abzymes. Just look it
> up for yourself. You know that you don't even have to look it up.
> That is what makes this challenge so sad. Just think if you had an
> honest argument, would you have to stoop this low?
So, you think all enzymatic functions have the same minimum structural
threshold requirements? Think again Ron. This is utter nonsense.
Obviously, some types of enzymes have far more structural threshold
requirements than others have. Those that have more requirements are
exponentially less likely to evolve. That's the whole point.
> > > I don't know how much of the
> > > variable parts can be deleted because it is dependent on a lot of
> > > factors that can't be calculated, but if you have the data that it
> > > can't be done. Let's see it.
>
> > Again, science is based on the best available experimental data - not
> > wishful thinking.
>
> Yeah, but science is also based on what has already been done and you
> can't make your claims from what has been done. Admit it and move on.
What has been done clearly supports my position, not yours. Admit it
and at least try to consider the implications.
> > > Not only that, but you are talking
> > > about a specific start point.
>
> > No I'm not. I'm talking about using any living thing with the entire
> > available genome as a vast host of starting points.
>
> What happens in that case? It works. Lactase function evolves.
That's right. Lactase functions as well as many other relatively
small single protein functions evolve all the time. The point is that
none of these examples of novel system evolution end up producing
anything with a minimum structural threshold requirement of more than
a few hundred amino acid residues. Nothing evolves beyond the 1000aa
threshold.
> It
> might not happen in every genome, but it does happen. How often does
> it have to happen from a starting point of a couple thousand proteins?
It is the pattern of evolution that is interesting here Ron. Lower
level systems evolve exponentially more common than higher level
systems. This exponential decline in evolvability demonstrably stalls
out well before the 1000aa structural threshold is reached. Nothing
evolves at all beyond this threshold in observable time. That
observation is very interesting and can only be explained by an
expansion of the non-beneficial gap between potentially beneficial
steppingstone functions in sequence/structure space.
> > > You haven't ruled out other start
> > > points using even smaller numbers of residues.
>
> > That's fine - present this evidence if you have it. I don't care what
> > pre-existing starting point you choose. So far, I don't see that it
> > exists outside of your bald speculations.
>
> > > The starting point was
> > > from the antibody sequence. I've seen no experiments to minimize the
> > > structural components, and even if they had been done, how many
> > > starting sequences would they have tried? It isn't the same thing to
> > > cut something down as it would be to build it from the ground up.
>
> > It doesn't matter Ron. If a smaller lactase could have been used, the
> > odds would have been exponentially better than Hall's E. coli would
> > have evolved it. The fact that they didn't evolve a smaller lactase,
> > and no one has ever seen a smaller lactase in action with any
> > experiment (not even antibody lactases) is strong indication that
> > smaller lactases than 400aa either don't exist or are extremely rare
> > in comparison.
>
> This seems to be coming out of left field. What was the starting
> material?
Any gene pool you want - as I've pointed out many times now.
> Why would you expect the smallest protein to evolve a new
> function to be present in any experiment?
You do understand that a large protein can evolve a novel function
that only requires a much smaller portion of itself to achieve? If
function X only requires 10aa and you start with 10,000 proteins all
over 500aa in size, fX can evolve as a subpart of any one of the
larger proteins - and it will still work. Later, the larger redundant
or vestigial parts of the system that aren't needed can be easily
trimmed down to the ideal size.
In this way, odds are that a novel beneficial system that requires
only a few specifically arranged residues will already exist largely
pre-formed in the gene pool to produce a very small gap size (i.e.,
two, one, or even zero mutations).
> Wouldn't a protein with
> more surface area be a more likely candidate?
Again, it doesn't matter what you start with. It matters what the
minimum target requirements are to achieve a novel beneficial
function. If the beneficial function requires a greater structural
threshold, odds are that the gap between what already exists in the
gene pool and this potentially beneficial system will not be just one
or two mutations.
> Has the smallest
> possible protein with lactase activity been determined? Yes or no?
To a rough degree of usefulness, yes. So far, you've presented no
real evidence beyond your imagination to think otherwise.
> > If you think otherwise, present some actual evidence that goes beyond
> > your guesswork and hunches.
>
> I laugh at this openly. How did you determine that your 1000 aa
> threshold existed? Got any actual evidence?
The evidence is obvious. Evolution clearly stalls out well before the
1000aa is reached. That is why the 1000aa threshold is so
interesting. Evolution just doesn't work beyond this threshold. Why
not?
> > You do understand, don't you, that even if you found a lactase of only
> > 200aa, that wouldn't remove the problem. You do understand that -
> > right? The fact that different types of functional systems have
> > different minimum structural threshold requirements would still be
> > there. The fact that those systems with greater minimum thresholds
> > are exponentially harder to evolve would also remain as a real problem
> > for the ToE.
>
> It doesn't really matter, what matters is that you can't make your
> argument work no matter how large or small the minimum lactase enzyme
> would be. It obviously isn't as large as nature created it. It can
> be reduced in size from over a 1000 aa to less than 400. All
> biological evolution claims is that it will use what works. What is
> your counter claim? The intelligent design made it bigger than it had
> to be because he wanted lifeforms to waste energy in making junk that
> they don't need? Why didn't he make it smaller for humans? Why is it
> the same size for chimps and humans?
Once the minimum structural threshold is reached, the mechanism of
random mutation and natural selection is perfectly capable of
modifying a system to include making it larger or smaller as needed.
This can be done very rapidly in fact. Therefore, modification is a
problem for your mechanism. The problem is achieving the minimum
structural threshold to begin with. That's the fundamental problem
for the ToE.
< snip useless pejoratives >
Bobby Bryant
Seanpit <seanpi...@naturalselection.0catch.com> writes:
> On Sep 2, 12:35 pm, bdbry...@wherever.ur (Bobby Bryant) wrote:
>> In article <1188748245.326427.67...@w3g2000hsg.googlegroups.com>,
>> Seanpit <seanpitnos...@naturalselection.0catch.com> writes:
>>
>> > This is only to be expected from someone who still denies that a
>> > statue like Michelangelo's David shows little if any symmetry.
>>
>> So, how do you know that _David_ is designed and snowflakes aren't?
>> (Or do you think snowflakes are designed as well?)
>
> Snowflakes aren't made out of granite or marble, materials that do not
> naturally tend toward highly symmetrical self-assembly.
So for all your claims, you're still nowhere near an ability to detect
design in biology?
> Again, you have to have prior experience with the *material* in
> question and how it interacts with non-deliberate forces of nature
> before you can begin to reasonably detect artifact.
>
> Take, for instance, SETI scientists. If they had absolutely no
> experience with radiowaves they wouldn't be able to say if this or
> that pattern was or was not likely to be the result of artifact. It
> is only because of their prior experience with radiowaves that they
> can in fact suggest features that would likely be artifactual if they
> were ever discovered in radiowaves.
>
>> Your whole symmetry thing is just a post hoc rationalization for your
>> IKIWISI design detection kit.
>
> You do have to have prior knowledge gained through experience with the
> material in question before you can reliably "know it when you see
> it".
>
> Tell me Bobby, what methodology would you use to hypothesize
> artifact?
I doubt that any such methodology exists.
> Please explain how you would go about it. Richard says
> that it cannot be done without some sort of evidence for manufacture.
> The problem with this notion is that SETI scientists think they can
> detect artifact without detecting anything other than a particular
> type of radiosignal - no need for knowing how such a signal was
> actually made.
Like other ID apologists, you stop your ears when we tell you how
SETI actually works. SETI is simply looking for an observation that
would confirm a specific hypothesis.
Does ID have any hypotheses that make predictions we can look for?
> The same thing is true of a highly symmetrical
> polished granite cube. Such a cube is clearly artifactual in nature
> regardless of how it was actually "manufactured".
>
> So, Bobby, how would you be able to detect artifact when you see it?
> Can you put into words or into a method how you "know it when you see
> it"? There has to be some sort of reason or you would not be able to
> "KIWYSI" - right?
IKIWISI is merely an opinion, and thus does not imply the existence of
any actual characteristic or technique for detecting it. I very
seriously doubt that any such mechanism exists.
Look how many times IKIWISI has proven wrong when people thought they
were seeing intelligent design. From Europeans first encounter of
bower bird's bowers (unless of course you consider birds intelligent
by ID standards) to UFO kooks claims about the the Eltanin antenna, and
lots of stuff in between. IKIWISI simply isn't reliable.
hersheyh
wrote:
> On Sep 2, 7:56 am, Ron O <rokim...@cox.net> wrote:
>
>
>
> > On Sep 1, 9:30 pm, Seanpit <seanpitnos...@naturalselection.0catch.com>
> > wrote:> On Sep 1, 5:15 pm, Ron O <rokim...@cox.net> wrote:
>
> > > > > > 400 aa from the Lac Z starting sequence.
>
> > > > > You still don't get it. The minimum structural threshold requirement
> > > > > isn't relative to some other sequence. It isn't "from" any starting
> > > > > sequence. The ebg sequence didn't evolve from a LacZ sequence. It
> > > > > was a unique sequence that happened to be close to one of a great many
> > > > > potential lactase sequences in the vastness of sequence space at the
> > > > > 400aa minimum level.
Actually it is probable that ebg *was* evolved from either from one of
the many, many, sequences that have lactase activity or from the even
more numerous ancestral proteins that have related functionality.
What evidence do you have that ebg was due to pure chance aggregation
of 400 or so aa's completely independently from the proteins that are
related to lactases? I cannot think of a single person who would
believe that nonsense, so the idea that the "ebg sequence didn't
evolve from a LacZ sequence. It was a unique sequence that happened
to be close to one of a great many potential lactase sequences in the
vastness of sequence space at the 400aa minimum level" is a strawman
idea that no one who thinks in terms of evolution would accept.
> > > > You are getting some kind of message, but you are mixing it up with
> > > > bogus bull pucky about some 400 minimum. The whole point is that
> > > > there are sequences close to what is needed and that you can't keep
> > > > them from existing.
>
> > > > Your 400 minimum is something that you just made up. Admit it. Where
> > > > did it come from?
>
> > > Again, I'd be very interested in any reference suggesting a
> > > significantly smaller beneficial lactase.
The size of the smallest *known* lactase is irrelevant to how it
arose. You are *falsely* assuming that each and every lactase must
arise *from scratch* in some magical poof of aggregating aa's.
Actually that is the *creationist* argument; it is not the
*evolutionary* argument. The evolutionary argument would be that the
lactase *function* would arise from modification of a protein that has
other *functions* that are related. Or it could arise, like the
antibody lactases, independently because antibody proteins, *like many
proteins*, function to produce a cleft that binds a small segment of a
molecule via a very small subset of the protein's aa's.
> > > Your example of lac+
> > > antibodies doesn't count because the antibodies in question were
> > > larger than 400aa.
But it *clearly* points out the way that *new* protein function
*arises*. The vast majority of the aa's in the antibody protein that
has lactase activity are unchanged from their role in the antibody
binding function that they performed. Only a very small subset of
aa's needed to change to *modify* an antibody to become an enzyme.
The vast majority of aa's do not need to change. The number that do
need to change is uncorrelated with the size of the end product.
And that is where your entire house of cards falls into illogic. You
keep making the claim that the number of aa's that need to change (the
gap) *increases* exponentially or linearly or somehow with total size
of the end product. And that simply is not true.
BTW, the size distribution of proteins can largely be described as 500
+/- 300 aa, with a few outlier proteins of very large (mostly compound
or endoduplicated) or very small size. One reason that no one can
meet your 1000 aa challenge is that there are so few proteins that
qualify.
> > And again, the fact that such a reference does not exist means what?
>
> It means that based on the information that does exist, the hypothesis
> of a 400aa threshold has the most support.
Only if you have the mistaken and silly idea that every aa in every
protein were absolutely necessary for function and that parsimony were
the relevant feature of protein production in that proteins were
somehow made from scratch by adding one aa at a time until somehow the
minimum size that has lactase activity was found and that existing
lactases were made from that size. If, OTOH, lactases were modified
from previously existing proteins, the fact that the size produced was
unnecessarily large would be irrelevant. Evolution selects for
*function*, not minimum size. In fact, when one looks at sequence
homologous proteins with the same function one of the variants that
often occurs involves both small to medium deletions and/or insertions
that do not greatly affect the overall structure of the enzyme.
> You may argue that future
> information is likely to reveal a much smaller threshold. That isn't
> science Ron. That's an unsupported hypothesis that isn't even
> falsifiable this side of eternity.
Evolution selects for *function*, not size. That is why one of the
electron transport systems involves a small non-protein and another
involves cytochrome c with the transport being done by a bound small
non-protein.
> You could always argue that this
> or that hypothesis could be wrong given some future discovery. That's
> always a possibility in science.
>
> > Has anyone ever made a very extensive push to develop lactase function
> > and determine the minimum? No. So what does it mean when you try and
> > use that argument to claim some minimum. Not only that, but even if
> > the minimum was 400 your argument still doesn't work because of Hall's
> > work and his success. Not his failures, but his sucesses. Why did he
> > ever succeed if you are right about 400 anythings?
>
> I've already told you. The 400aa size requirement isn't the only
> aspect of the equation.
There is no frigging equation. You are merely pushing size, not any
damned equation that takes anything else into consideration.
> The minimum specificity of amino acid residue
> arrangement is also in play.
And you completely ignore this. Because you have no frigging equation
that includes it.
> Proteins, to include those that have the
> lactase function, are not perfectly ridged structures. A certain
> degree of sequence flexibility is available without a complete loss of
> the function in question - i.e., lactase in this case.
And, as has been pointed out, that degree of sequence flexibility is
huge, to the point where two proteins with sequences so different that
they cannot be recognized as homologous by looking at *sequence* can
perform the same *function* and have the same *structure*. In
addition, of course, there can also be independently evolved
*structures* that serve the same *function*. In short, the
relationship between *sequence* and *function* is *much* weaker than
the relationship between *structure* and *function*. And even that
doesn't rule out that different *structures* can evolve the same
*function*. For example, the antibody lactase and several other
lactases. Or the two different rotary motility flagella.
> However, all
> protein based systems have a certain limit to the degree of
> flexibility beyond which the function in question cannot be realized
> at all - not even a little bit.
Of course. But the question is, how much is "not a bit". There are,
I am sure, proteins that have a very low level of lactase activity but
that actually perform a different role in the cell. One of your false
assumptions is the idea that proteins only have a single function and
do not have secondary activities. And there may be other proteins
that play a role in lactose synthesis that could be changed to favor
the reverse activity.
> In the case of lactase, Hall's experiments proved that the degree of
> flexibility is in fact quite limited.
No he didn't in those experiments. What he showed is that the
evolution of a new lactase *function* from some other protein in the
E. coli depends on the proteins present at the time. The way to
demonstrate the flexibility of a protein to evolve new sequences that
perform the same function is to do a search of homologous sequences in
many different organisms. In fact, one should also look for proteins
that do not have detectable sequence homology but do have structure
(and function) homology.
> The evolution of lactase is
> extremely rare in living systems, even when it comes to large colonies
> over tens of thousands of generations under extreme conditions (i.e.,
> high mutation rates and a highly selective environment favoring
> lactase evolution). The lack of evolution in most gene pools observed
> in Hall's experiments support the notion that the average distance
> between lactase islands is well over a dozen mutations wide.
It does no such thing. This is another example of a flat-out
misinterpretation of the evidence.
> Of
> course, this is just the average distance for most types of bacteria.
> The minimum distance is obviously one.
And the minimum distance is the relevant distance for evolution.
Functions do not arise *independently* in different organisms. They
arise rarely and spread largely by vertical (common) descent and (more
rarely) horizontal transmission.
> On occasion, rare colonies of
> bacteria will be within just one or two mutations of at least one of
> the potential lactase islands that exist in sequence space. However,
> the number of colonies or types of bacteria that will be this close is
> extremely limited compared to all types of bacterial gene pools -
> along a Poisson distribution.
Again, SFW? In evolution, it is the bacteria who, by good luck, has
the ebg (or its equivalent) that wins the evolutionary race for
function. *It's* progeny will be the ones able to use the resource.
The losers go extinct or are limited to environments where the new
resource is not crucial.
> Now, when it comes to higher level functional systems, the average
> distance is even greater (i.e., several dozen mutations wide).
So you keep asserting. But I still haven't seen how you determined
this. You assert that there is a linear correlation between the gap
size (what you really need to determine) and total size (which you
call minimum threshold). That is, the relationship is g (gap size) =
b (undetermined functional relationship) * N (minimum threshold). I
have yet to see how you determined b from the available data. Yet
that *is* your argument.
> The
> odds that any bacteria will be within just one or two mutations of
> success drops off dramatically - along a Poisson distribution. This
> concept is supported by papers like the one published by Choi and Kim.
>
> http://www.pnas.org/cgi/content/full/103/38/14056
Yet another article you mangle in your incompetent interpretation of
it.
[snip]
> > You can't just make this junk up.
>
> Anyone can look it up and see that I'm right. There aren't any
> examples beyond the 1000aa minimum threshold.
And how many proteins reach this threshold. AIR, you tended to
eliminate all the *real* examples because they clearly were complex
proteins with multiple function or had internal duplications. In
fact, for examples of what you mean, you have had to go to "systems"
like the eubacterial flagella, despite the fact that these "systems"
are obviously composed of *functional* subsystems that have potential
(and sometimes actual) independent utility. Yet, even here you
continue the *unwarranted assertion* that there is g = bN, with not a
shred of evidence to support this assertion or tell us what b is
numerically and how it was calculated.
> > You have to be able to demonstrate
> > it, and you can't even demonstrate that your 1000 aa threshold even
> > exists. Just do it. produce your numbers. Determine that such a gap
> > existed. Since you can't do that, what are you making noises about?
>
> There are a great many protein-based systems that require well over
> 1000 fairly specified amino acid residues.
Such as? That are not actually complexes of proteins, but actual
single function proteins?
> A system of 1000 residues
> requires at least 3,000 codons of genetic real estate.
You are aware, are you not, that there is even more flexibility in DNA
sequence than there is in protein sequence derived from it? That is,
just as there are multiple protein sequence that determine the same
structure, there are multiple DNA sequences that can determine the
same protein sequence. By and large it is protein *structure* that
determines protein *function* most directly, with only a few aa
residues being absolutely crucial to function. And even then, more
than one *structure* have been known to produce the same *function*,
and, since protein structures are not found randomly scattered in
total structure space, so there is no indication that life *had to*
(nor *did*) search all of structure space to find them.
> Do you think
> you could produce a flagellar motility system with just 3000 codons?
> Think again. Flagellar motility requires at least 30,000 codons of
> genetic real estate at minimum.
Do you think you can produce the *function* of rotary motility from a
pore-based whip structure and a membrane-fixed motor that converts a
source of energy into motion?
Ask the wrong question and you get the wrong answer. Your question
assumes that flagella must be invented from scratch with no
intermediate utility possible. That, you will now claim, is not what
you mean. It is merely a filthy, insidious insinuation that you keep
making. The right question is what structures that cells already
have, could be minimally *modified* to produce rotary motility. And
how many *changes* are needed to do this, at minimum. [Of course, if
you can tell us how to calculate b, I might have to reconsider.]
Average number is irrelevant. The rotary motility only needs to
evolve once. In fact, of course, it evolved independently at least
twice, with both examples differing in precisely the way that
indicates that the question asked just above is the right question and
that your question is brain dead ignorant.
> There are many other such examples as well - such as the minimum
> structural threshold it takes to code for the functional system
> responsible for DNA transcription or RNA translation - to name just a
> couple more examples of higher-level functions.
Those are multiprotein systems. And, in the case of the ribosome, it
is clear that it is the RNA that is enzymatically crucial and the
proteins are merely "helpers" making the process more efficient.
> > > This brings us back to my original question for you. How do you
> > > explain this observation? The complete lack of evolution beyond the
> > > 1000aa threshold? I've yet to see you even try to answer this
> > > question. . .
>
> > Bogus obfuscation is just bogus obfuscation. Until you can even
> > demonstrate that some 1000aa threshold even exists you have no
> > argument. There is no observation to explain until you can tell us
> > what the 1000aa threshold is and demonstrate that it had to be crossed
> > at some point in such a way that descent with modification and
> > selection would not have been able to cross such a threshold in a
> > biologically relevant fashion.
>
> I've provided you with this information over and over again. The
> flagellar motility system requires over 30,000 codons of genetic real
> estate.
The obfustication is still obfustication. The question still implies
that the way that rotary motility is obtained is by starting from
scratch and producing the function in one fell swoop of blindly and
randomly aggregating aa's together (BTW, a codon is 3 nt long, so you
are talking about a system with 30,000 aa's; I suspect the term you
wnat is nucleotide pair and not codon). Yet you keep admitting that
the number you really need is the gap between functional states, and
you assert (without any evidence at all) that there is a linear
relationship between the gap size and the total size (or a large
percentage of it) of the end product. Yet if the flagella arises by
interaction of two pre-existing useful systems (as indicated by actual
experiment of a model system), I fail to see how the size of the two
components added together gives us a clue about how many mutational
steps are required to link the two components together to produce a
novel *function*. Can you give us the math?
> Obviously, this threshold had to be crossed or this type of
> motility system would not exist. None of the proposed steppingstones
> in flagellar evolution are narrower than a few dozen mutations.
Shouldn't that depend on the size of the end system, in a linear
fashion? Which would mean that the smaller steps would be quite
likely? I am having trouble seeing how all the gaps can be a few
dozen mutations, if it is the last step that would be the biggest
'gap'?
> How
> then were they crossed and why are there no examples of any system
> beyond the 1000aa evolving?
>
> > Just demonstrate one problem step in getting past your fictional
> > 1000aa threshold in the evolution of the flagellum. Present the
> > sequences and tell us where
>
> ...
>
> read more ยป
TomS
<TyXCi.1030$7P7...@newssvr19.news.prodigy.net>, Bobby Bryant stated..."
>
>In article <1188830321.5...@d55g2000hsg.googlegroups.com>,
> Seanpit <seanpi...@naturalselection.0catch.com> writes:
>> Tell me Bobby, what methodology would you use to hypothesize
>> artifact?
>
>I doubt that any such methodology exists.
How about:
Means, Opportunity, and Motive
hersheyh
Which you have no way to actually calculate, so you use total size in
aa of some existing protein that performs the *function* (which you
use as if a protein only had one possible function) as a rough
measure.
Things wrong with this are: 1) *Function* is determined by what an
observer considers to be important. *Function* of a protein can vary,
depending upon conditions. For example, in most cell types, the
effect of insulin (via its binding to a receptor) is to release
sugar. In other cell types, the effect of insulin is to store sugar.
So, what exactly is the "function" of insulin? Is it merely to bind
to an insulin receptor? Or is its function somehow related to sugar
metabolism? What is the "function" of cytochrome c? Most people
would say it is involved in electron transport. But actually, the
electrons are transported solely by the heme that cytochrome c binds
to. So is cytochrome c merely a "heme-binding" protein?
2) It assumes, implicitly, that "function" is a unitary feature, with
each protein having one and only one function and that function cannot
be subdivided into subfunctions. In fact, most proteins have
independent moieties that are independently involved in different
aspects of function. Moreover, most proteins have secondary functions
and different activities with secondary substrates. The aa's involved
in binding lactose does not actually recognize the glucose moiety at
all. It only recognizes the b-galactosidase bond. Other aa's are
involved in recognizing the galactose residue by a few key features.
That is why lacZ, in addition to cleaving lactose, can also cleave (at
different rates) other b-galactoside bonds.
3) Although Sean pretends that his calculation takes into
consideration the fact that aa's can be rather widely substituted for
without affecting function, in reality, the only aa's he considers to
not be a part of his "minimum threshold size" are those that have
absolutely no constraints on aa replacement, not even proline (which
causes breaks in secondary structures). The *fact* is that different
aa's can allow widely different degrees of substitutability. Only a
few sites (if any!) are absolutely unsubstitutable. Many aas can
actually be deleted. Sometimes it can be deleted, but cannot be
replaced by proline (or, for a hydrophobic aa, by a hydrophilic aa).
He has no way to include this in his calculations, yet it is precisely
this that makes sequence such a poor substitute for structure in
determining function.
> 2. The minimum gap size is the mutational distance between what exists
> in a gene pool and what might exist as a beneficial system if it were
> ever found by random mutation.
This, of course, is the number that Sean needs to be presenting *all*
the time, not just when I remind him that the number he does present,
his minimum threshold size, is utterly without relevance to the number
he does need.
> 3. The gap size is always smaller than the threshold size.
Ah. But how much smaller? And is there any correlation between gap
size and minimum threshold size? And is evolution more a matter of
whether or not an organism has an already useful functional precursor
that can be *modified* to produce the end function in a reasonable
matter of steps. Or whether or not functionally relevant moieties can
be linked together (covalently or by other association) to produce a
novel function? None of that has any relevance to the minimum
threshold size that I can see.
Sean *asserts* that there is a linear relationship between 'gap size'
and 'minimum threshold size' of the end product, but he never seems to
be able to actually present the crucial constant for such a linear
relationship. Namely the ratio "gap size units" per "minimum
threshold size units", aka, the slope of the linear line. [I am
assuming that the y intercept is at 0 and that the relationship is
only valid for positive values of x).
> 4. The average gap size increases with each increase in structural
> threshold requirements.
This is an unwarranted assertion that appears to be contradictory to
the evidence I know about. How did you determine this without
assuming a mechanism for how structural threshold requirements can be
increased? The only way that I can even think is that you assume that
increases in size are done by adding one aa at a time followed by a
random walk in total sequence space.
> 5. The minimum gap size does not increase until the population size
> remains static and until the number of genetic elements within just
> one mutation of a beneficial target drop to one.
This doesn't make any sense at all. What population size are you
talking about? And why are you assuming that when there is only be
one genetic element (do you mean genes?) within one mutation of a
beneficial target that the minimum gap size would *increase*? Could
you try re-phrasing this into English?
> At this point, the
> increase in the gap distance follows a linear relationship to the
> increase in the minimum structural threshold requirements.
At that point, wouldn't the gap distance be one?
>
[snip]
Seanpit
> On 2 Sep, 18:11, richardalanforr...@googlemail.com wrote:> On 2 Sep, 16:50, Seanpit <seanpitnos...@naturalselection.0catch.com>
> > wrote:
>
> <snipped as usenet seems to have lost half my post. Here's the rest:
>
> > Of course, I've pointed this little concept out to you many times
> > before, but you still argue that this type of "analysis" is not real
> > analysis - regardless of the fact that it is in fact quite useful as
> > it stands.
>
> As nobody including you has ever carried out such an analysis (i.e. a
> **STATISTICAL** analysis of shape to determine artificiality), how on
> earth can you claim this?
That's not true Richard. Even you have carried out an analysis of the
various forms of naturally produced granite forms that allows you to
understand, with a very high degree of STATISTICAL certainty that a
highly symmetrical polished granite cube is very unlikely to be the
result of any non-deliberate non-artifactual process of nature. If
you had no statistical idea, you would be unable to make any such
approximation with any reasonable certainty.
You just don't understand that rough statistical analysis can be
achieved without taking very detailed measurements or writing them
down on paper and yet still achieve a very useful degree of certainty.
It is via use of this very same analysis that I can predict, with a
very high degree of confidence, that no cow can jump farther than 100
feet. That is based on rough analysis of the jumping ability of cows
that I have so far evaluated to a rough degree of certainty that is
plenty accurate enough for me to make this "prediction".
How can you not grasp such a simple and otherwise obvious concept?
< snip >
> > I said that the
> > Santana formation was the result of a sudden catastrophe. It was you
> > who initially argued that the preservation of the creatures in this
> > formation need not have been very rapid, as in a few hours, but could
> > have been achieved by much slower processes of non-catastrophic
> > fossilization.
>
> You are misrepresenting me again. I have never made any such
> statement. In fact, I have posted several links to papers which
> demonstrate that the *lower* limit on the time required for such
> preservation is a few hours, not "within an hour" as you originally
> claimed.
You originally fought long and hard arguing that the preservation of
fish in the Santana formation was the result of autolithifying
bacteria that preserved the fish and other creatures in a non-
catastrophic manner as part of some anoxic lagoon. This notion is
mistaken because of the evidence for much more rapid preservation of
cellular detail that can be explained by autolithifying bacteria. In
particular, as I've noted for you many times, the preservation of
cellular turgidity is inconsistent with autolithifying bacteria in
that its preservation requires much more sudden crystallization - to
"within one hour". Why is that? Because, cellular turgidity rapidly
declines after death and is gone within one or two hours at most.
> > > However, the overwhelmingly vast majority of the fossil record is NOT*
> > > preserved in lagerstatten such as the Crato Formation. It's logically
> > > incoherent to offer exceptional preservation in a single, limited
> > > locality as evidence for a global flood when most of the fossil record
> > > is *NOT* exceptionally well-preserved.
>
> > The exceptional preservation isn't the only evidence of shortly spaced
> > catastrophes in the fossil record Richard. It is just that this
> > particular example of the Santana formation, which you originally
> > brought up to challenge the concept of catastrophic fossilization and/
> > or preservation, does nothing of the sort.
>
> Once again you are misrepresenting me. *You* brought up the Santana
> fish, not me.
You brought up the Lagoa Vermelha fish and then argued that the
Santana formation was the result of similar activity - i.e.,
autolithifying bacteria. In other words, you originally argued that
the Santana formation was not the result of sudden catastrophe.
> I have never argued that they were not fossilised
> rapidly.
I guess that depends on your definition of "rapid" doesn't it? When I
wrote that the fossilization of the fish and other creatures in the
Santana formation was "lightening quick", you responded by saying that
it "took months, possibly years".
You wrote:
"The taphonomy [of the Santana Formation] is more consistent with
immersion in soft substrates [i.e., with non-catastrophic anoxic
conditions]. High levels of salinity create some of the conditions in
which autolithifying bacteria can live. The bottom can be soft
allowing dehydrated fish to be submerged in the substrate. . .
"Lightning quick" is an exaggeration. It is a process which probably
took months, possibly years.
> Bearing in mind that the papers to which I have posted links
> on numerous occasions describe the processes whereby fossilisation in
> some exceptional cases may be very rapid, why do you think that such
> phenomena pose any threat to the views of scientists in this matter?
What it doesn't do is pose a threat to my theory of a very rapid
formation of the geologic column via a series of closely space
catastrophic events. This fossil evidence is consistent with my
theory. The evidence that is inconsistent with the long-age model is
largely in the form of erosion problems (i.e., the general lack of the
expected uneven erosion of exposed surfaces over millions of years of
time).
> Incidentally, what the hell do you mean by "catastrophic fossilization
> and/or preservation"? It's not a term which appears anywhere in the
> scientific literature, which is no surprise as it is pretty well
> meaningless. Why do you feel the need to invent terms in a vain
> pretence that you have knowledge of the subject?
Obviously, catastrophic fossilization is fossilization that is the
direct result of sudden catastrophic conditions. I really don't know
why I have to constantly define the obvious for you.
> > > Your have stated that: "most fossils show clear evidence of rapid
> > > burial or other forms of relatively rapid or even catastrophic
> > > preservation leaving little time for predation or bioturbation)"
>
> > > This is plainly ridiculous, as anyone who has ever collected fossils
> > > can tell you. Mike Benton, in the reference which I have provided,
> > > writes
>
> > > "Animal and plant remains are typically buried after a great deal of
> > > scavenging, decay, breakage and transport."
>
> > > What do you know that Mike Benton doesn't?
>
> > I agree that a great deal of breakage and transport is the norm, as is
> > a bit of scavenging.
>
> This flatly contradicts your statement that "most fossils show clear
> evidence of rapid burial or other forms of relatively rapid or even
> catastrophic preservation leaving little time for predation or
> bioturbation"
Not true. Scavenging can occur during catastrophic conditions or
during brief episodes of calm between shortly spaced catastrophes.
> Which is it? And will you change your web site to make it clear that
> you have changed your position on this matter?
I have not changed my position on this matter. It is just that you
misrepresent my position on this matter - despite repetitive
correction.
> > However, without rapid burial as a general rule,
> > the fine lines of lamination and preservation of such organically rich
> > material would not have been preserved due to continued scavenging and
> > bioturbation.
>
> Most of the fossils I study show extensive signs of scavenging by
> vertebrates and invertebrates, and in the main these fossils come from
> formation showing very good or exceptional preservation. These are far
> better preserved than most fossils, as they come from the "soupy
> substrate" deposits in which bioturbation is generally limited or
> lacking. On the other hand, most sedimentary structures show some
> degree of bioturbation.
Not true. Most sedimentary structures do not show nearly the degree
of bioturbation that would be expected if they formed slowly over
millions of years. Take the Yesnaby Sea Stacks shale beds for
example. These shale beds did not form slowly by the annual or
subannual accumulation of sedimentary layers. Rather, they give clear
evidence of very rapid, even catastrophic, formation. The same thing
is true of your anoxic lake bottoms and lagoons. No such place is
present in the world today preserving anything like what we find in
the fossil record - like the Santana formation etc. Large creatures
in particular are not preserved today without near complete scavenging
and bioturbation over a relatively short period of time.
http://www.detectingdesign.com/geologiccolumn.html#Shale%20Beds
< snip >
> > > You may consider evidence which completely demolishes your assertions,
> > > and therefore your arguments as being a "relatively minor point", but
> > > no scientist would, and your blatant avoidance shows your lack of
> > > integrity.
>
> > Anyone who disagrees with you lacks integrity I guess?
>
> No, but people who lie about what they have done do.
> I have accused you of lacking integrity because:
> 1) You misrepresent others. Your change of heading on this post is a
> clear example. I have *never* said that "All creationists are evil
> liars", and have been very reluctant to label *any* creationist as a
> liar unless there is very clear evidence that they are lying.
You have said several times that you haven't found any honest
creationist. You have also said several times that it is your whole
purpose to expose this as a fact to those who frequent this forum -
that no honest creationists exist.
You've wrote:
"I've invited creationists on numerous occasions to point out any
mistakes I have made in assesing statements on those sites as false,
and even offered to humiliate myself in public if even a small number
can be found. No creationist has tried to take up this challenge.
Their only responses have been to ignore the challenge completely, or
to resort to ad hominem attacks. I can only assume that creationists
are liars."
Again Richard, I've challenged many of your notions many times. Yet,
because you are not convinced by my arguments you don't just say that
you think I'm wrong or even way off base. Rather, you feel the need
to go even farther and judge my motive by calling me a liar? Why the
need to paint those who disagree with you as evil lying slimebags?
Why not just call them stupid or pathetically ignorant and give them
the benefit of the doubt?
> 2) You claim to have carried through a methodology which it is
> patently clear that you have not.
You just don't understand that a "methodology" isn't as restrictive as
you make it out to be. You yourself have carried out the same
methodology as I have. That is why you know I'm right - even if you
won't admit it.
> 3) You evade or ignore any question which demonstrates the vacuousness
> of your assertions.
I don't have the time to keep up with your oft repeated questions
Richard. I've certainly answered as many as I've had the time to
answer and I dare say far more time than any other creationists has
given you in this forum.
> 4) You persist in arguments founded on unsubstantiated assertions but
> never address the validity of those assertions.
I think the same thing about your arguments - most of which are based
on plenty of smoke and hand-waving with little substance. This
"point" of yours is nothing more than a difference of opinion on what
constitutes useful or weighty evidence.
> 5) You foster the pretence that you have scientific knowledge by
> inventing terms such as "catastrophic fossilisation" which are
> essentially meaningless and have never been used in any scientific
> context.
This is like former Pres. Clinton asking for the definition of "is".
If you don't understand what the term "catastrophic fossilization"
might mean, there really is no point in discussing much of anything
with you.
> 6) Rather than address the issue of your own integrity you try to cast
> doubts on the integrity of others.
I do not doubt your integrity. I've said that repeatedly whenever
you've called me a liar. I don't think you are deliberately lying -
thought often you do misrepresent me. What I do doubt is your ability
to think critically and rationally on your own.
> > No one can be
> > honestly wrong I suppose?
>
> Of course they can. However, when you are making statement you know to
> be false with the intent to deceive, you are not being honesty wrong.
I've never made statements I know to be false nor with any intent to
deceive. You may find that hard to believe, as hard to believe as it
is hard for me to believe that you have honestly mischaracterized my
position yet again. But, it's the truth.
> You are lying. You claim to have carried through a STATISTICAL
> methodology for detecting artifacts. You quite blatantly haven't. The
> only puzzling aspect of this is why you persist in this falsehood
> after it has been exposed.
Again, you just don't understand the concept here. That is why you
and I have a misunderstanding over terminology in this case. This is
not a lie. It is just that you defined certain terms and concepts
very differently and in a way I consider to be way off base.
< snip repetitive >
> > > I have no problem with this. After all, as I have written on many
> > > occasions, one of my reasons for posting here is to expose the
> > > dishonesty of creationists. Your help is greatly appreciated.
>
> > For the candid reader, all you've done is exposed your own desperation
> > - your need to paint all who disagree with you as debased, dishonest,
> > and morally corrupt.
>
> I suggest that the "candid reader" is the best judge of that, Sean,
> not you.
Obviously, that is what I just recommended myself . . .
Sean Pitman
www.DetectingDesign.com
Seanpit
>
> > Tell me Bobby, what methodology would you use to hypothesize
> > artifact?
>
> I doubt that any such methodology exists.
Then SETI science is pretty much bunkem I guess . . . along with
forensics and anthropology for that matter.
Arguing that SETI is looking for something that "matches a hypothesis"
is the methodolgy Bobby. The hypothesis itself is what is interesting
here. How does one make a useful hypothesis of what to expect from
deliberate artifact vs. non-deliberate natural production?
< snip >
Sean Pitman
www.DetectingDesign.com
richardal...@googlemail.com
wrote:
> On Sep 3, 1:46 am, richardalanforr...@googlemail.com wrote:
>
> > On 2 Sep, 18:11, richardalanforr...@googlemail.com wrote:> On 2 Sep, 16:50, Seanpit <seanpitnos...@naturalselection.0catch.com>
> > > wrote:
>
> > <snipped as usenet seems to have lost half my post. Here's the rest:
>
> > > Of course, I've pointed this little concept out to you many times
> > > before, but you still argue that this type of "analysis" is not real
> > > analysis - regardless of the fact that it is in fact quite useful as
> > > it stands.
>
> > As nobody including you has ever carried out such an analysis (i.e. a
> > **STATISTICAL** analysis of shape to determine artificiality), how on
> > earth can you claim this?
>
> That's not true Richard. Even you have carried out an analysis of the
> various forms of naturally produced granite forms that allows you to
> understand, with a very high degree of STATISTICAL certainty that a
> highly symmetrical polished granite cube is very unlikely to be the
> result of any non-deliberate non-artifactual process of nature.
So now you are claiming that you can calculate statistical
probabilities without numbers.
I suggest that you announce this amazing feat to the statisticians of
the world. They will be astonished.
> If
> you had no statistical idea, you would be unable to make any such
> approximation with any reasonable certainty.
If you have no data set of numbers, you can't calculate any
statistics.
Period.
End of story.
Arm waving is no substitute for mathematical calculation.
>
> You just don't understand that rough statistical analysis can be
> achieved without taking very detailed measurements or writing them
> down on paper and yet still achieve a very useful degree of certainty.
No, I don't, because it is fundamentally and blatantly untrue.
Nobody can do even a rough statistical analysis without a data set of
numbers.
> It is via use of this very same analysis that I can predict, with a
> very high degree of confidence, that no cow can jump farther than 100
> feet.
That is not a statistical analysis.
> That is based on rough analysis of the jumping ability of cows
> that I have so far evaluated to a rough degree of certainty that is
> plenty accurate enough for me to make this "prediction".
It's not a statistical analysis.
>
> How can you not grasp such a simple and otherwise obvious concept?
The simple and obvious concept you need to grasp is that you need a
data set of numbers to carry out any form of statistical analysis.
>
> < snip >
>
> > > I said that the
> > > Santana formation was the result of a sudden catastrophe. It was you
> > > who initially argued that the preservation of the creatures in this
> > > formation need not have been very rapid, as in a few hours, but could
> > > have been achieved by much slower processes of non-catastrophic
> > > fossilization.
>
> > You are misrepresenting me again. I have never made any such
> > statement. In fact, I have posted several links to papers which
> > demonstrate that the *lower* limit on the time required for such
> > preservation is a few hours, not "within an hour" as you originally
> > claimed.
>
> You originally fought long and hard arguing that the preservation of
> fish in the Santana formation was the result of autolithifying
> bacteria that preserved the fish and other creatures in a non-
> catastrophic manner as part of some anoxic lagoon.
The preservation of the Santana fish *IS* the result of autolithifying
bacteria!
Didn't you read the papers which I cited?
> This notion is
> mistaken because of the evidence for much more rapid preservation of
> cellular detail that can be explained by autolithifying bacteria.
What evidence? You haven't read the papers and now you know what
evidence is described there?
> In
> particular, as I've noted for you many times, the preservation of
> cellular turgidity is inconsistent with autolithifying bacteria in
> that its preservation requires much more sudden crystallization - to
> "within one hour".
The preservation of cellular turgidity is a consequence of osmotic
pressure in a hypersaline fluid which allow time for the
autolithifying bacteria to deposit carbonates.
Didn't you read the papers I have recommended?
And what the hell has crystalisation to do with it? Crystalisation
*destroys* fine structures! It's the fact that the bacteria control
the size of the crystals which allows such fine structures to be
preseved!
> Why is that? Because, cellular turgidity rapidly
> declines after death and is gone within one or two hours at most.
I see.
You haven't read the papers on the subject.
You know nothing about taphonomic processes.
You apparently do not understand the difference between a hypersaline
and a supersaturated solution
You have apparently never heard of osmotic pressure.
(You're a pathologist, for crying out loud! How the hell did you
manage to miss that much basic science?)
So, please tell us: if it is not the processes which have been studied
in fossils and replicated in the laboratory and have been described by
the scientists who have actually done the research which produced this
exceptional fossilisation, what do you think caused it?
And please, don't imagine for one moment that "A flood" is any sort of
explanation. Floods produce turbulence which oxygenates the water, and
encourages the growth of bacteria which digest organic remains from
the water and from the sediments churned up by the flood. That's why
your home stinks to high heaven after it has been flooded. It's all
those bacteria busily feasting on anything they can find. It's why
turbidites - which is what geologists (you know, the scientists who
actually *study* geology rather than making it up as they go along)
call deposits laid down by floods - are rarely fossilferous. Floods
simply don't create suitable conditions.
> > > > However, the overwhelmingly vast majority of the fossil record is NOT*
> > > > preserved in lagerstatten such as the Crato Formation. It's logically
> > > > incoherent to offer exceptional preservation in a single, limited
> > > > locality as evidence for a global flood when most of the fossil record
> > > > is *NOT* exceptionally well-preserved.
>
> > > The exceptional preservation isn't the only evidence of shortly spaced
> > > catastrophes in the fossil record Richard. It is just that this
> > > particular example of the Santana formation, which you originally
> > > brought up to challenge the concept of catastrophic fossilization and/
> > > or preservation, does nothing of the sort.
>
> > Once again you are misrepresenting me. *You* brought up the Santana
> > fish, not me.
>
> You brought up the Lagoa Vermelha fish
Excuse me? I have never mentioned any "Lagoa Vermelha fish". Why do
you have this need blatantly to misrepresent me? Or are you so much in
the habit of making things up as you go along that you don't know that
you are doing it?
> and then argued that the
> Santana formation was the result of similar activity - i.e.,
> autolithifying bacteria. In other words, you originally argued that
> the Santana formation was not the result of sudden catastrophe.
I have never argued that the Santana fish were not the product of a
sudden catastrophe. Once again you are misrepresenting me. All I have
done is correct you mistaken idea that fossilisation ocured "within an
hour", which was based on an inadequate knowledge of the literature.
You have apparently accepted that it took rather longer than that.
Fine. There is no argument.
However, quite how the fact that the Sanatana fish were preserved
rapidly adds anything at all to your assertion that there was a global
flood is beyond my comprehension.
>
> > I have never argued that they were not fossilised
> > rapidly.
>
> I guess that depends on your definition of "rapid" doesn't it? When I
> wrote that the fossilization of the fish and other creatures in the
> Santana formation was "lightening quick", you responded by saying that
> it "took months, possibly years".
>
> You wrote:
>
> "The taphonomy [of the Santana Formation] is more consistent with
> immersion in soft substrates [i.e., with non-catastrophic anoxic
> conditions]. High levels of salinity create some of the conditions in
> which autolithifying bacteria can live. The bottom can be soft
> allowing dehydrated fish to be submerged in the substrate. . .
> "Lightning quick" is an exaggeration. It is a process which probably
> took months, possibly years.
Quite so, and that is the conclusion formed in the most recent studies
of the phenomenon. The lower limit is a few hours, but it probably
took much longer.
I've provided references to the relevant literature. Why not read it?
>
> > Bearing in mind that the papers to which I have posted links
> > on numerous occasions describe the processes whereby fossilisation in
> > some exceptional cases may be very rapid, why do you think that such
> > phenomena pose any threat to the views of scientists in this matter?
>
> What it doesn't do is pose a threat to my theory of a very rapid
> formation of the geologic column via a series of closely space
> catastrophic events.
The fact that most fossils are not exceptional, and that many
sedimentary structures could only have been laid down over very long
periods of time demolishes your theory. Then there is the radiometric
dating, the palaeobiological data, the astronomical data, the simple
Laws of Physics and most of the rest of modern science.
> This fossil evidence is consistent with my
> theory.
Well, the palaeontologist who have actually studied the fossils don't
think so.
What do you know that they don't?
> The evidence that is inconsistent with the long-age model is
> largely in the form of erosion problems (i.e., the general lack of the
> expected uneven erosion of exposed surfaces over millions of years of
> time).
The "evidence" you have invented, you mean?
The geological record is *full* of erosion surfaces. They are
ubiquitous. They are found all over the world in virtually every
formation.
There are three in this small part of Siccar Point alone:
http://www.winona.edu/geology/dynamicearth/Images/SiccarPointCloseup.jpg
Making things up as you go along, as you do, is no substitute for
learning about a subject.
>
> > Incidentally, what the hell do you mean by "catastrophic fossilization
> > and/or preservation"? It's not a term which appears anywhere in the
> > scientific literature, which is no surprise as it is pretty well
> > meaningless. Why do you feel the need to invent terms in a vain
> > pretence that you have knowledge of the subject?
>
> Obviously, catastrophic fossilization is fossilization that is the
> direct result of sudden catastrophic conditions. I really don't know
> why I have to constantly define the obvious for you.
As this is a term you have invented, it's up to you to define what you
mean by it.
Fossilisation does not generally occur as a result of a catastrophic
conditions.
Floods don't produce many fossils, and certainly not well preserved
ones.
Asteroid impacts do not produce fossils. Being vaporised is generally
not a good start.
Volcanic erruptions sometimes produce fossils, but as volcanic
deposits tend to be highly acidic, in most cases all organic material
is destroyed leaving mouldic fossils such as the human bodies found in
Pompei.
Hurricanes don't produce many fossils.
Tidal waves don't produce many fossils.
Droughts can produce good fossils if mummified corpses are buried in
fine, windbourne sand, but these are very rare.
So which types of "catastrophic conditions" result in exceptionally
preserved fossils?
>
> > > > Your have stated that: "most fossils show clear evidence of rapid
> > > > burial or other forms of relatively rapid or even catastrophic
> > > > preservation leaving little time for predation or bioturbation)"
>
> > > > This is plainly ridiculous, as anyone who has ever collected fossils
> > > > can tell you. Mike Benton, in the reference which I have provided,
> > > > writes
>
> > > > "Animal and plant remains are typically buried after a great deal of
> > > > scavenging, decay, breakage and transport."
>
> > > > What do you know that Mike Benton doesn't?
>
> > > I agree that a great deal of breakage and transport is the norm, as is
> > > a bit of scavenging.
>
> > This flatly contradicts your statement that "most fossils show clear
> > evidence of rapid burial or other forms of relatively rapid or even
> > catastrophic preservation leaving little time for predation or
> > bioturbation"
>
> Not true. Scavenging can occur during catastrophic conditions or
> during brief episodes of calm between shortly spaced catastrophes.
>
So how do you explain the fact that most fossils come from deposits
which show a great deal of bioturbation, and that the overwhelming
majority are broken, damaged, worn and fragmented?
> > Which is it? And will you change your web site to make it clear that
> > you have changed your position on this matter?
>
> I have not changed my position on this matter. It is just that you
> misrepresent my position on this matter - despite repetitive
> correction.
As I have quoted you verbatim in a clear context, and not presented
your words in a misleading way, this is flatly untrue.
Your position on this has changed, as it has on the time scale over
which Sanatana fish preservation took place.
>
> > > However, without rapid burial as a general rule,
> > > the fine lines of lamination and preservation of such organically rich
> > > material would not have been preserved due to continued scavenging and
> > > bioturbation.
>
> > Most of the fossils I study show extensive signs of scavenging by
> > vertebrates and invertebrates, and in the main these fossils come from
> > formation showing very good or exceptional preservation. These are far
> > better preserved than most fossils, as they come from the "soupy
> > substrate" deposits in which bioturbation is generally limited or
> > lacking. On the other hand, most sedimentary structures show some
> > degree of bioturbation.
>
> Not true.
I'm sorry, but why should we believe you? You know bugger all about
geology.
Any textbook on geology will tell you that bioturbation to some degree
is present in almost all sedimentary rocks.
> Most sedimentary structures do not show nearly the degree
> of bioturbation that would be expected if they formed slowly over
> millions of years.
I'm sorry, but why should we believe you? You know bugger all about
geology.
> Take the Yesnaby Sea Stacks shale beds for
> example.
Why? Are they typical of sedimentary structures? Have you studied
them?
> These shale beds did not form slowly by the annual or
> subannual accumulation of sedimentary layers.
And your evidence for this is....? Or are we simply expected to take
your word for it?
> Rather, they give clear
> evidence of very rapid, even catastrophic, formation.
And your evidence for this is....? Or are we simply expected to take
your word for it?
> The same thing
> is true of your anoxic lake bottoms and lagoons. No such place is
> present in the world today preserving anything like what we find in
> the fossil record - like the Santana formation etc.
Why should we expect to? It was an exceptional event leading to
exceptional preservation.
> Large creatures
> in particular are not preserved today without near complete scavenging
> and bioturbation over a relatively short period of time.
Large creatures in the fossil record almost always show some degree of
scavenging, and the overwhelmingly vast majority are disarticulated
skeletal components.
By the way, fossils don't show bioturbation. Sediments do. For someone
pontificating on geology this is a rather elementary error.
You have not tried to show that the statements I identify on those
sites as false are not false.
> Yet,
> because you are not convinced by my arguments you don't just say that
> you think I'm wrong or even way off base. Rather, you feel the need
> to go even farther and judge my motive by calling me a liar?
I call you a liar because you make statements which you must know to
be false with the intent to deceive.
Or do you expect me to believe that a pathologist who has co-authored
scientific papers is so ignorant that he thinks that one carry out as
statistical study without a data set of numbers?
> Why the
> need to paint those who disagree with you as evil lying slimebags?
I don't. I have not done so, and once again you have misrepresented
me.
I have never called you evil.
I have never called you a slimebag.
I have called you a liar not because you disagree with me, but because
I think you are lying.
The fact that I have had exchanges with other creationists which have
been heated at times and have not called them liars, not labelled them
as evil, and not called them "slimebags (your word, not mine) is proof
of this.
> Why not just call them stupid or pathetically ignorant and give them
> the benefit of the doubt?
Because in your case I don't think that you *are* ignorant.
The others I give the benefit of the doubt.
>
> > 2) You claim to have carried through a methodology which it is
> > patently clear that you have not.
>
> You just don't understand that a "methodology" isn't as restrictive as
> you make it out to be.
Utter bullshit. A methodology is precisely that: a restrictive and
precise way of collecting and analysing data.
You know that, or you could not have attained the qualifications you
have.
I know that.
> You yourself have carried out the same
> methodology as I have.
No I haven't. Please stop telling me what I have and have not done.
Looking at a pile of rocks and getting a gut feeling about how they
were formed is not a methodology.
> That is why you know I'm right - even if you
> won't admit it.
Sean, I know that you are wrong. You know that you are wrong for that
matter.
>
> > 3) You evade or ignore any question which demonstrates the vacuousness
> > of your assertions.
>
> I don't have the time to keep up with your oft repeated questions
> Richard. I've certainly answered as many as I've had the time to
> answer and I dare say far more time than any other creationists has
> given you in this forum.
I would not have to repeat my questions so many times if you answered
them.
>
> > 4) You persist in arguments founded on unsubstantiated assertions but
> > never address the validity of those assertions.
>
> I think the same thing about your arguments - most of which are based
> on plenty of smoke and hand-waving with little substance.
So where are the flaws in the numerous papers I have cited in support
of my arguments?
Which of my arguments are not backed up with solid evidence?
> This
> "point" of yours is nothing more than a difference of opinion on what
> constitutes useful or weighty evidence.
No, it's not a difference of opinion. It's a fact. When it comes down
to it, you have nothing other than unfounded assertion to support your
arguments.
>
> > 5) You foster the pretence that you have scientific knowledge by
> > inventing terms such as "catastrophic fossilisation" which are
> > essentially meaningless and have never been used in any scientific
> > context.
>
> This is like former Pres. Clinton asking for the definition of "is".
> If you don't understand what the term "catastrophic fossilization"
> might mean, there really is no point in discussing much of anything
> with you.
As it is a term you have invented (and if I am wrong, please provide a
citation from the scientific literature which uses it), it's meaning
is by no means clear. As catastrophic conditions are *not* in general
suitable for fossilisation to occur, and that there are numerous
different ways in which fossils can be formed, none of which is
particularly associated with catastrophic conditions, it is perfectly
valid to call the term meaningless.
>
> > 6) Rather than address the issue of your own integrity you try to cast
> > doubts on the integrity of others.
>
> I do not doubt your integrity. I've said that repeatedly whenever
> you've called me a liar. I don't think you are deliberately lying -
> thought often you do misrepresent me.
I do not believe that I have ever misrepresented you, Sean, though as
you constantly change your position and then try to pretend that you
haven't it can be hard to know just what you mean at times.
It's worth pointing out that you have misrepresented me several times
in this post alone.
> What I do doubt is your ability
> to think critically and rationally on your own.
Well, the academic staff of Leicester University who allowed me to
study for my PhD don't, and neither do the editors of the scientific
journals in which I have published my research findings. Nor do the
palaeontologists who have attended symposia at which I have presented
by findings. In fact, several have said that they enjoy my talks
because they contain original ideas which make them think differently
about what they are doing.
What do you know that they don't?
>
> > > No one can be
> > > honestly wrong I suppose?
>
> > Of course they can. However, when you are making statement you know to
> > be false with the intent to deceive, you are not being honesty wrong.
>
> I've never made statements I know to be false nor with any intent to
> deceive.
So why do you claim to have carried out a statistical methodology
which you quite clearly have not?
If you were simply an uneducated creationist parroting the AiG party
line I would not be calling you a liar.
However, you are a pathologist who has co-authored several academic
papers. I find it impossible to believe that you can be in such a
position and not know that one needs numbers to do statistics.
> You may find that hard to believe, as hard to believe as it
> is hard for me to believe that you have honestly mischaracterized my
> position yet again. But, it's the truth.
>
> > You are lying. You claim to have carried through a STATISTICAL
> > methodology for detecting artifacts. You quite blatantly haven't. The
> > only puzzling aspect of this is why you persist in this falsehood
> > after it has been exposed.
>
> Again, you just don't understand the concept here.
I understand that one can't do statistics without a data set of
numbers.
> That is why you
> and I have a misunderstanding over terminology in this case. This is
> not a lie. It is just that you defined certain terms and concepts
> very differently and in a way I consider to be way off base.
Are you now redefining the whole mathematical field of statistics in
such a way that one does *not* need a data set of numbers to do
statistics?
You'd better advise the statisticians in that case.
>
> < snip repetitive >
>
> > > > I have no problem with this. After all, as I have written on many
> > > > occasions, one of my reasons for posting here is to expose the
> > > > dishonesty of creationists. Your help is greatly appreciated.
>
> > > For the candid reader, all you've done is exposed your own desperation
> > > - your need to paint all who disagree with you as debased, dishonest,
> > > and morally corrupt.
>
> > I suggest that the "candid reader" is the best judge of that, Sean,
> > not you.
>
> Obviously, that is what I just recommended myself . . .
>
> Sean Pitmanwww.DetectingDesign.com
...so let's just put back the parts you snipped without marking, shall
we Sean? Why is that?
R. Baldwin
news:1188844325....@r34g2000hsd.googlegroups.com...
> On Sep 3, 1:46 am, richardalanforr...@googlemail.com wrote:
>> On 2 Sep, 18:11, richardalanforr...@googlemail.com wrote:> On 2 Sep,
>> 16:50, Seanpit <seanpitnos...@naturalselection.0catch.com>
>> > wrote:
>>
>> <snipped as usenet seems to have lost half my post. Here's the rest:
>>
>> > Of course, I've pointed this little concept out to you many times
>> > before, but you still argue that this type of "analysis" is not real
>> > analysis - regardless of the fact that it is in fact quite useful as
>> > it stands.
>>
>> As nobody including you has ever carried out such an analysis (i.e. a
>> **STATISTICAL** analysis of shape to determine artificiality), how on
>> earth can you claim this?
>
> That's not true Richard. Even you have carried out an analysis of the
> various forms of naturally produced granite forms that allows you to
> understand, with a very high degree of STATISTICAL certainty that a
> highly symmetrical polished granite cube is very unlikely to be the
> result of any non-deliberate non-artifactual process of nature. If
> you had no statistical idea, you would be unable to make any such
> approximation with any reasonable certainty.
>
> You just don't understand that rough statistical analysis can be
> achieved without taking very detailed measurements or writing them
> down on paper and yet still achieve a very useful degree of certainty.
This is puffed up bloviating. You made overreaching, exaggerated claims
about having some numerical analysis method that you had used, and got
called for it. Then you kept changing your mind about what the method was,
and never provided any data showing that the method had been tested at all.
The decent thing to do is retract the claim.
[snip]
R. Baldwin
> On Sep 2, 12:35 pm, bdbry...@wherever.ur (Bobby Bryant) wrote:
>> In article <1188748245.326427.67...@w3g2000hsg.googlegroups.com>,
>> Seanpit <seanpitnos...@naturalselection.0catch.com> writes:
>>
>> > This is only to be expected from someone who still denies that a
>> > statue like Michelangelo's David shows little if any symmetry.
>>
>> So, how do you know that _David_ is designed and snowflakes aren't?
>> (Or do you think snowflakes are designed as well?)
>
> Snowflakes aren't made out of granite or marble, materials that do not
> naturally tend toward highly symmetrical self-assembly.
>
> Again, you have to have prior experience with the *material* in
> question and how it interacts with non-deliberate forces of nature
> before you can begin to reasonably detect artifact.
>
> Take, for instance, SETI scientists. If they had absolutely no
> experience with radiowaves they wouldn't be able to say if this or
> that pattern was or was not likely to be the result of artifact. It
> is only because of their prior experience with radiowaves that they
> can in fact suggest features that would likely be artifactual if they
> were ever discovered in radiowaves.
Now, this much I agree with. How does it help you in biology?
[snip]
R. Baldwin
> On Sep 3, 6:16 am, Ron O <rokim...@cox.net> wrote:
>
> Before responding to this post in detail, you still don't seem to have
> grasped the difference between a minimum structural threshold
> requirement and a gap distance. They are not the same thing. A
> minimum structural threshold is NOT related to any starting point
> either. It is what it is. A system requires a certain minimum
> structural form before it can work regardless of how it came to be.
> If that structure is realized, the system will work. Otherwise, it
> will not work.
Would it not be more correct to say, "Otherwise it will do something else"?
Because "it will not work" is a teleological concept, implying the system
has some goal. I think this has much to do with why your whole argument is
rejected. A biological system doesn't need to have some goal. It simply is.
[snip]
Seanpit
>
> > You just don't understand that rough statistical analysis can be
> > achieved without taking very detailed measurements or writing them
> > down on paper and yet still achieve a very useful degree of certainty.
>
> This is puffed up bloviating. You made overreaching, exaggerated claims
> about having some numerical analysis method that you had used, and got
> called for it. Then you kept changing your mind about what the method was,
> and never provided any data showing that the method had been tested at all.
> The decent thing to do is retract the claim.
The claim is valid and it is useful. Nothing in nature comes remotely
close to producing the degree of symmetry of the polished granite cube
I described to you and you know it. This is why you yourself can
recognize such a granite cube as being artifactual right away - even
if you happened to find it on an alien planet. The statistics
provided by your own experience tell you that this is true when it
comes to this particular degree of symmetry in the material of granite
(i.e., within 0.01%).
Sean Pitman
www.DetectingDesign.com
hersheyh
0catch.com> wrote:
> On Sep 2, 12:35 pm, bdbry...@wherever.ur (Bobby Bryant) wrote:
>
> > In article <1188748245.326427.67...@w3g2000hsg.googlegroups.com>,
> > Seanpit <seanpitnos...@naturalselection.0catch.com> writes:
>
> > > This is only to be expected from someone who still denies that a
> > > statue like Michelangelo's David shows little if any symmetry.
>
> > So, how do you know that _David_ is designed and snowflakes aren't?
> > (Or do you think snowflakes are designed as well?)
>
> Snowflakes aren't made out of granite or marble, materials that do not
> naturally tend toward highly symmetrical self-assembly.
The question is not whether or not you can identify the "occasional"
object as being designed and come up with a post hoc rationalization
for declaring it "designed". After all, an analog stopped clock is
right twice a day. It is whether or not you have a *systematic*
procedure that can identify an object as "designed" or "not designed".
Below is a series of objects that contain the material granite. Many
of them have been manipulated by an intelligent designer. Others have
not. Your task is to use your criteria for distinguishing between
designed and non-designed objects to systematically determine which of
these objects meet *your* criteria for being designed and which don't.
Some of the objects have symmetry. Some don't. Some are polished.
Some are not. Obviously some of them are identified as sculpture or
material worked by human hands. Others are identified as natural.
But your claim is that you can consistently use your criteria to
distinguish between designed and non-designed objects. So you have to
give your reason for classifying the objects herein.
Of course *any IDiot* can use post hoc reasoning to identify a *small
select group* of objects as designed. But you need to do so
consistently and with high levels of accuracy. Go to it.
http://www.peterrandall-page.com/recent_projects/artwork/Give_and_Take.jpg
http://www.weltonrotz.com/wrbird2.jpg
http://www.soldwedelsculptures.com/images/lono-b85.jpg
http://www.soldwedelsculptures.com/stone_sculpture_pamela_soldwedel.html
http://www.artcol.stir.ac.uk/rock.jpg
http://www.sculpturalpursuit.com/media/Products/book_cover.jpg
http://www.cmsgardens.co.uk/images/heissner/F31143AA.jpg
http://www.dreamdesignstrading.com/images/products/granite_countertops_03.jpg
http://www.made-in-china.com/image/2f0j00beztYAJlZRqcM/Paving-Stone-Granite-.jpg
http://www.stone-essentials.co.uk/Images/grey_granite_headstone.jpg
http://www.alfaisalmarble.com/finalpics/landscapping_pebbles_14big.jpg
http://www.bowlandstone.com/images/agg_large/granite_setts.jpg
http://www.earth.ox.ac.uk/~oesis/field/medium/granite1.jpg
>
> Again, you have to have prior experience with the *material* in
> question and how it interacts with non-deliberate forces of nature
> before you can begin to reasonably detect artifact.
[snip]
Seanpit
> "Seanpit" <seanpitnos...@naturalselection.0catch.com> wrote in message
>
> > Before responding to this post in detail, you still don't seem to have
> > grasped the difference between a minimum structural threshold
> > requirement and a gap distance. They are not the same thing. A
> > minimum structural threshold is NOT related to any starting point
> > either. It is what it is. A system requires a certain minimum
> > structural form before it can work regardless of how it came to be.
> > If that structure is realized, the system will work. Otherwise, it
> > will not work.
>
> Would it not be more correct to say, "Otherwise it will do something else"?
> Because "it will not work" is a teleological concept, implying the system
> has some goal. I think this has much to do with why your whole argument is
> rejected. A biological system doesn't need to have some goal. It simply is.
A biological system that is does not produce some sort of beneficial
function will not be in existence for very long. It will be lost
because nature will not select to maintain it. Those that remain in
the gene pool remain because the produce some sort of reproductive
advantage. Different types of potentially beneficial systems have
different minimum structural requirements without which they cannot be
realized in the gene pool at all.
For example, despite the fact that a lactase enzyme might be useful in
a particular gene pool in a particular environment, that function will
not exist with any arrangement of just 40 or 50 residues . . . or even
100 residues. The same thing is true of flagellar motility. This
type of function cannot be realized with the use of just a 400 or 500
or even 1000 codons of DNA - regardless of arrangement.
*All* potentially beneficial systems that have higher minimum
requirements will be more widely seperated in sequence space compared
to lower level functions - much much more widely seperated (on
average). That means, the evolution of any novel beneficial system at
higher level requires many more mutations, on average, from the
perspective of any given gene pool.
Sean Pitman
www.DetectingDesign.com
Seanpit
>
> > > As nobody including you has ever carried out such an analysis (i.e. a
> > > **STATISTICAL** analysis of shape to determine artificiality), how on
> > > earth can you claim this?
>
> > That's not true Richard. Even you have carried out an analysis of the
> > various forms of naturally produced granite forms that allows you to
> > understand, with a very high degree of STATISTICAL certainty that a
> > highly symmetrical polished granite cube is very unlikely to be the
> > result of any non-deliberate non-artifactual process of nature.
>
> So now you are claiming that you can calculate statistical
> probabilities without numbers.
I did you numbers Richard. As I've explained to you many times now, I
can eyeball a rock to at least a useful degree of measure -
centimeters or inches (depending on the size of the rock). And, so
can you. You don't have to right down all of these observations
either before you can recognize a developing trend with regard to
symmetry in the material of granite. The trend is actually based on
roughly estimated measurements that you have averaged in your head.
That is how you know that a very high degree of symmetry, like that
shown by a polished granite cube with a variance of less than 0.01%,
is not remotely approached by any non-deliberate force of nature. You
know this because no naturally produced granite form has even come
close to your ability to recognize it as non-symmetrical to the rough
degree that you are able to eyeball symmetry.
Again, you argue that this is not what anyone would call "statistical
analysis". But, it actually is. If you had absolutely no idea how to
eyeball anything to any degree of certainty or measurement, you
wouldn't be able to instantly recognize a highly symmetrical polished
granite cube as artifactual. You'd have to go around actually
measuring everything before you could detect artifact. For close call
cases you might have to do this. You don't have to do this when the
degree of certainty is so extreme that you can instantly tell just by
looking at the object or phenomenon.
< snip rest >
Sean Pitman
www.DetectingDesign.com
Seanpit
> > > **STATISTICAL** analysis of shape to determine artificiality), how on
> > > earth can you claim this?
>
> > That's not true Richard. Even you have carried out an analysis of the
> > various forms of naturally produced granite forms that allows you to
> > understand, with a very high degree of STATISTICAL certainty that a
> > highly symmetrical polished granite cube is very unlikely to be the
> > result of any non-deliberate non-artifactual process of nature.
>
> So now you are claiming that you can calculate statistical
> probabilities without numbers.
I did use numbers Richard. As I've explained to you many times now, I
can eyeball a rock to at least a useful degree of measure -
centimeters or inches or meters, etc (depending on the size of the
rock). And, so can you. You don't have to write down all of these
observations either before you can recognize a developing trend with
regard to symmetry in the material of granite. The trend is actually
based on roughly estimated measurements that you have averaged in your
head. That is how you know that a very high degree of symmetry, like
Seanpit
>
> > 1. The minimum structural threshold size is the minimum structural
> > requirements needed to produce a particular type of functional system
>
> Which you have no way to actually calculate, so you use total size in
> aa of some existing protein that performs the *function* (which you
> use as if a protein only had one possible function) as a rough
> measure.
As I've explained to you several times before, the same protein can
have many different functions as parts of different larger systems
within a living thing. This fact has absolutely nothing to do with
the concept that a particular type of function has a minimum
structural threshold requirement. It doesn't matter one lick what
other functions a particular protein can do. If it doesn't have the
needed minimum threshold requirements it will no be able to achieve
the function in question to a beneficial degree.
> Things wrong with this are: 1) *Function* is determined by what an
> observer considers to be important.
What? Function is determined by what the protein actually does
regardless of if you or I think it is "important". The "beneficial"
nature of the function is also determined by the organism itself as it
interacts with its current environment.
> *Function* of a protein can vary,
> depending upon conditions.
This is true, but completely irrelevant.
>For example, in most cell types, the
> effect of insulin (via its binding to a receptor) is to release
> sugar. In other cell types, the effect of insulin is to store sugar.
> So, what exactly is the "function" of insulin?
It depends upon the cell in question and how it is set up to use
recognize and use the insulin signal.
> Is it merely to bind
> to an insulin receptor? Or is its function somehow related to sugar
> metabolism? What is the "function" of cytochrome c? Most people
> would say it is involved in electron transport. But actually, the
> electrons are transported solely by the heme that cytochrome c binds
> to. So is cytochrome c merely a "heme-binding" protein?
The heme molecule, by itself, would not function effectively in the
electron transport chain. It also would not function effectively if
the cytochrome c sequence were changed too much. In other words, not
just any heme binding protein, like hemoglobin, could do the job that
cytochrome c does.
> 2) It assumes, implicitly, that "function" is a unitary feature, with
> each protein having one and only one function and that function cannot
> be subdivided into subfunctions.
Not true at all. Again, it doesn't matter what else a particular
protein can do. The function in question still has its own minimum
structural threshold requirement given the current cellular and
extracellular environment. This includes the currently available parts
in the cell and how they are already arranged.
> In fact, most proteins have
> independent moieties that are independently involved in different
> aspects of function. Moreover, most proteins have secondary functions
> and different activities with secondary substrates. The aa's involved
> in binding lactose does not actually recognize the glucose moiety at
> all. It only recognizes the b-galactosidase bond. Other aa's are
> involved in recognizing the galactose residue by a few key features.
> That is why lacZ, in addition to cleaving lactose, can also cleave (at
> different rates) other b-galactoside bonds.
That's true, but again, completely irrelevant.
> 3) Although Sean pretends that his calculation takes into
> consideration the fact that aa's can be rather widely substituted for
> without affecting function, in reality, the only aa's he considers to
> not be a part of his "minimum threshold size" are those that have
> absolutely no constraints on aa replacement, not even proline (which
> causes breaks in secondary structures). The *fact* is that different
> aa's can allow widely different degrees of substitutability. Only a
> few sites (if any!) are absolutely unsubstitutable. Many aas can
> actually be deleted. Sometimes it can be deleted, but cannot be
> replaced by proline (or, for a hydrophobic aa, by a hydrophilic aa).
> He has no way to include this in his calculations, yet it is precisely
> this that makes sequence such a poor substitute for structure in
> determining function.
All of this is taken into consideration. It is very much like the
English language system. Many letters in this paragraph can be
changed or deleted without a complete loss of its original meaning/
function. However, delete too many or change too many at the same
time, beyond a certain minimum threshold, and all the original meaning/
function will be lost. The same thing is true of all beneficial
biosystems. They all have a minimum size and specificity requirement
beyond which just one more deletion or substitution will completely
remove that type of function below a beneficial level of utility.
> > 2. The minimum gap size is the mutational distance between what exists
> > in a gene pool and what might exist as a beneficial system if it were
> > ever found by random mutation.
>
> This, of course, is the number that Sean needs to be presenting *all*
> the time, not just when I remind him that the number he does present,
> his minimum threshold size, is utterly without relevance to the number
> he does need.
The minimum threshold size is very much related to the minimum gap
size. That's the whole point. Your notion that the likely minimum
gap size stays the same regardless of the minimum structural threshold
requirements is simply wrong. This is a fact provable to anyone who
cares to do a little investigation into the distances that exist
between beneficial sequences in sequence space at different structural
requirements. A pretty good illustration of this can be found in the
Choi and Kim paper I've presented many times now.
http://www.pnas.org/cgi/content/full/103/38/14056
> > 3. The gap size is always smaller than the threshold size.
>
> Ah. But how much smaller?
That depends upon the size of the gene pool. A smaller gene pool will
likely have a larger minimum gap size. And, if one could have an
infinitely large gene pool, the gap size would always be zero.
> And is there any correlation between gap
> size and minimum threshold size?
Yes, there is . . .
> And is evolution more a matter of
> whether or not an organism has an already useful functional precursor
> that can be *modified* to produce the end function in a reasonable
> matter of steps.
That is exactly what evolution is dependent upon. The problem is that
the odds of having a precursor that is only one or two mutations away
drop dramatically with each increase in the minimum threshold size
under consideration.
> Or whether or not functionally relevant moieties can
> be linked together (covalently or by other association) to produce a
> novel function? None of that has any relevance to the minimum
> threshold size that I can see.
All of these factors are affected by the threshold size. The larger
the threshold size, the markedly less likely anything will exist that
can easily be linked together to produced any higher threshold
function with just one or two mutations.
> Sean *asserts* that there is a linear relationship between 'gap size'
> and 'minimum threshold size' of the end product, but he never seems to
> be able to actually present the crucial constant for such a linear
> relationship. Namely the ratio "gap size units" per "minimum
> threshold size units", aka, the slope of the linear line. [I am
> assuming that the y intercept is at 0 and that the relationship is
> only valid for positive values of x).
The slope is affected by the size of the population. But, given a
static population size, the slope can be roughly estimated.
> > 4. The average gap size increases with each increase in structural
> > threshold requirements.
>
> This is an unwarranted assertion that appears to be contradictory to
> the evidence I know about. How did you determine this without
> assuming a mechanism for how structural threshold requirements can be
> increased? The only way that I can even think is that you assume that
> increases in size are done by adding one aa at a time followed by a
> random walk in total sequence space.
The threshold requirement is independent of how it is achieved
Howard. It is what it is regardless. For example, the minimum
threshold requirement for flagellar motility is always going to be
more than 10,000 codons or 30,000 bp of genetic real estate period.
There are other types of systems that also occupy this level and they
do so regardless of how they came to be.
Now, finding such potentially beneficial systems is where random walk
or selection via various kinds of mutations comes into play. For
those potentially beneficial islands in sequence/structure space that
have higher threshold requirements, any and all kinds of random
searches into space will exponentially greater amounts of time to find
any one of them.
> > 5. The minimum gap size does not increase until the population size
> > remains static and until the number of genetic elements within just
> > one mutation of a beneficial target drop to one.
>
> This doesn't make any sense at all. What population size are you
> talking about?
The population that makes up the gene pool. The bigger the
population, the greater the odds are that a genetic sequence within
the gene pool will be within one or two mutations from a novel
beneficial system at a particular threshold minimum.
> And why are you assuming that when there is only be
> one genetic element (do you mean genes?) within one mutation of a
> beneficial target that the minimum gap size would *increase*? Could
> you try re-phrasing this into English?
The odds that there will be at least one genetic element within one
mutation of any potentially beneficial target at a particular
threshold level improve by increasing the number of genetic elements
available in the gene pool. However, given even a very large gene
pool that is static in size, the minimum gap distance will eventually
go beyond the minimum possible distance of one. At this point, the
ability of this gene pool to evolve even higher level systems will
drop in an exponential manner. Why? Because, it is at this point
that the odds of the minimum gap distance staying at the minimum
possible distance drop off along a Poisson distribution with each
increase in the minimum threshold requirements of the potentially
beneficial target sequences/structures.
> > At this point, the
> > increase in the gap distance follows a linear relationship to the
> > increase in the minimum structural threshold requirements.
>
> At that point, wouldn't the gap distance be one?
Imagine a Poisson distribution curve. For potentially beneficial
systems that have low structural threshold requirements the curve is
shifted so that a large number of genetic sequences in a large gene
pool are within just one mutation of many such potentially beneficial
structures/systems. However, as the threshold requirements under
consideration are increased, the Poisson curve is shifted so that far
fewer existing sequences are within just one mutation of any of the
many potentially beneficial sequences in sequence/structure space.
Raise the threshold requirements under consideration again and the
number of existing sequences that is within one mutation of any of the
even higher level potentially beneficial sequences drops off even more
dramatically - down to just one existing genetic element being within
one mutation of any potentially beneficial sequence with the higher
threshold requirements. Raise the bar again and the odds that any
existing genetic sequence will still be within one mutation of any
potentially beneficial sequence drop dramatically - again along a
Poisson distribution.
Understand now?
Sean Pitman
www.DetectingDesign.com
Seanpit
> > requirements needed to produce a particular type of functional system
>
> Which you have no way to actually calculate, so you use total size in
> aa of some existing protein that performs the *function* (which you
> use as if a protein only had one possible function) as a rough
> measure.
As I've explained to you several times before, the same protein can
have many different functions as parts of different larger systems
within a living thing. This fact has absolutely nothing to do with
the concept that a particular type of function has a minimum
structural threshold requirement. It doesn't matter one lick what
other functions a particular protein can do. If it doesn't have the
needed minimum threshold requirements it will no be able to achieve
the function in question to a beneficial degree.
> Things wrong with this are: 1) *Function* is determined by what an
> observer considers to be important.
What? Function is determined by what the protein actually does
regardless of if you or I think it is "important". The "beneficial"
nature of the function is also determined by the organism itself as it
interacts with its current environment.
> *Function* of a protein can vary,
> depending upon conditions.
This is true, but completely irrelevant.
>For example, in most cell types, the
> effect of insulin (via its binding to a receptor) is to release
> sugar. In other cell types, the effect of insulin is to store sugar.
> So, what exactly is the "function" of insulin?
It depends upon the cell in question and how it is set up to use
recognize and use the insulin signal.
> Is it merely to bind
> to an insulin receptor? Or is its function somehow related to sugar
> metabolism? What is the "function" of cytochrome c? Most people
> would say it is involved in electron transport. But actually, the
> electrons are transported solely by the heme that cytochrome c binds
> to. So is cytochrome c merely a "heme-binding" protein?
The heme molecule, by itself, would not function effectively in the
electron transport chain. It also would not function effectively if
the cytochrome c sequence were changed too much. In other words, not
just any heme binding protein, like hemoglobin, could do the job that
cytochrome c does.
> 2) It assumes, implicitly, that "function" is a unitary feature, with
> each protein having one and only one function and that function cannot
> be subdivided into subfunctions.
Not true at all. Again, it doesn't matter what else a particular
protein can do. The function in question still has its own minimum
structural threshold requirement given the current cellular and
extracellular environment. This includes the currently available parts
in the cell and how they are already arranged.
> In fact, most proteins have
> independent moieties that are independently involved in different
> aspects of function. Moreover, most proteins have secondary functions
> and different activities with secondary substrates. The aa's involved
> in binding lactose does not actually recognize the glucose moiety at
> all. It only recognizes the b-galactosidase bond. Other aa's are
> involved in recognizing the galactose residue by a few key features.
> That is why lacZ, in addition to cleaving lactose, can also cleave (at
> different rates) other b-galactoside bonds.
That's true, but again, completely irrelevant.
> 3) Although Sean pretends that his calculation takes into
> consideration the fact that aa's can be rather widely substituted for
> without affecting function, in reality, the only aa's he considers to
> not be a part of his "minimum threshold size" are those that have
> absolutely no constraints on aa replacement, not even proline (which
> causes breaks in secondary structures). The *fact* is that different
> aa's can allow widely different degrees of substitutability. Only a
> few sites (if any!) are absolutely unsubstitutable. Many aas can
> actually be deleted. Sometimes it can be deleted, but cannot be
> replaced by proline (or, for a hydrophobic aa, by a hydrophilic aa).
> He has no way to include this in his calculations, yet it is precisely
> this that makes sequence such a poor substitute for structure in
> determining function.
All of this is taken into consideration. It is very much like the
English language system. Many letters in this paragraph can be
changed or deleted without a complete loss of its original meaning/
function. However, delete too many or change too many at the same
time, beyond a certain minimum threshold, and all the original meaning/
function will be lost. The same thing is true of all beneficial
biosystems. They all have a minimum size and specificity requirement
beyond which just one more deletion or substitution will completely
remove that type of function below a beneficial level of utility.
> > 2. The minimum gap size is the mutational distance between what exists
> > in a gene pool and what might exist as a beneficial system if it were
> > ever found by random mutation.
>
> This, of course, is the number that Sean needs to be presenting *all*
> the time, not just when I remind him that the number he does present,
> his minimum threshold size, is utterly without relevance to the number
> he does need.
The minimum threshold size is very much related to the minimum gap
size. That's the whole point. Your notion that the likely minimum
gap size stays the same regardless of the minimum structural threshold
requirements is simply wrong. This is a fact provable to anyone who
cares to do a little investigation into the distances that exist
between beneficial sequences in sequence space at different structural
requirements. A pretty good illustration of this can be found in the
Choi and Kim paper I've presented many times now.
http://www.pnas.org/cgi/content/full/103/38/14056
> > 3. The gap size is always smaller than the threshold size.
>
> Ah. But how much smaller?
That depends upon the size of the gene pool. A smaller gene pool will
likely have a larger minimum gap size. And, if one could have an
infinitely large gene pool, the gap size would always be zero.
> And is there any correlation between gap
> size and minimum threshold size?
Yes, there is . . .
> And is evolution more a matter of
> whether or not an organism has an already useful functional precursor
> that can be *modified* to produce the end function in a reasonable
> matter of steps.
That is exactly what evolution is dependent upon. The problem is that
the odds of having a precursor that is only one or two mutations away
drop dramatically with each increase in the minimum threshold size
under consideration.
> Or whether or not functionally relevant moieties can
> be linked together (covalently or by other association) to produce a
> novel function? None of that has any relevance to the minimum
> threshold size that I can see.
All of these factors are affected by the threshold size. The larger
the threshold size, the markedly less likely anything will exist that
can easily be linked together to produced any higher threshold
function with just one or two mutations.
> Sean *asserts* that there is a linear relationship between 'gap size'
> and 'minimum threshold size' of the end product, but he never seems to
> be able to actually present the crucial constant for such a linear
> relationship. Namely the ratio "gap size units" per "minimum
> threshold size units", aka, the slope of the linear line. [I am
> assuming that the y intercept is at 0 and that the relationship is
> only valid for positive values of x).
The slope is affected by the size of the population. But, given a
static population size, the slope can be roughly estimated.
> > 4. The average gap size increases with each increase in structural
> > threshold requirements.
>
> This is an unwarranted assertion that appears to be contradictory to
> the evidence I know about. How did you determine this without
> assuming a mechanism for how structural threshold requirements can be
> increased? The only way that I can even think is that you assume that
> increases in size are done by adding one aa at a time followed by a
> random walk in total sequence space.
The threshold requirement is independent of how it is achieved
Howard. It is what it is regardless. For example, the minimum
threshold requirement for flagellar motility is always going to be
more than 10,000 codons or 30,000 bp of genetic real estate period.
There are other types of systems that also occupy this level and they
do so regardless of how they came to be.
Now, finding such potentially beneficial systems is where random walk
or selection via various kinds of mutations comes into play. For
those potentially beneficial islands in sequence/structure space that
have higher threshold requirements, any and all kinds of random
searches into space will exponentially greater amounts of time to find
any one of them.
> > 5. The minimum gap size does not increase until the population size
> > remains static and until the number of genetic elements within just
> > one mutation of a beneficial target drop to one.
>
> This doesn't make any sense at all. What population size are you
> talking about?
The population that makes up the gene pool. The bigger the
population, the greater the odds are that a genetic sequence within
the gene pool will be within one or two mutations from a novel
beneficial system at a particular threshold minimum.
> And why are you assuming that when there is only be
> one genetic element (do you mean genes?) within one mutation of a
> beneficial target that the minimum gap size would *increase*? Could
> you try re-phrasing this into English?
The odds that there will be at least one genetic element within one
mutation of any potentially beneficial target at a particular
threshold level improve by increasing the number of genetic elements
available in the gene pool. However, given even a very large gene
pool that is static in size, the minimum gap distance will eventually
go beyond the minimum possible distance of one. At this point, the
ability of this gene pool to evolve even higher level systems will
drop in an exponential manner. Why? Because, it is at this point
that the odds of the minimum gap distance staying at the minimum
possible distance drop off along a Poisson distribution with each
increase in the minimum threshold requirements of the potentially
beneficial target sequences/structures.
> > At this point, the
> > increase in the gap distance follows a linear relationship to the
> > increase in the minimum structural threshold requirements.
>
> At that point, wouldn't the gap distance be one?
Imagine a Poisson distribution curve. For potentially beneficial
R. Baldwin
The invalid claim is about having a METHOD. Nobody disputes being able to
identify polished granite cubes as artifacts at a glance.
R. Baldwin
> On Sep 3, 5:20 pm, "R. Baldwin" <res0k...@nozirevBACKWARDS.net> wrote:
>> "Seanpit" <seanpitnos...@naturalselection.0catch.com> wrote in message
>>
>> > Before responding to this post in detail, you still don't seem to have
>> > grasped the difference between a minimum structural threshold
>> > requirement and a gap distance. They are not the same thing. A
>> > minimum structural threshold is NOT related to any starting point
>> > either. It is what it is. A system requires a certain minimum
>> > structural form before it can work regardless of how it came to be.
>> > If that structure is realized, the system will work. Otherwise, it
>> > will not work.
>>
>> Would it not be more correct to say, "Otherwise it will do something
>> else"?
>> Because "it will not work" is a teleological concept, implying the system
>> has some goal. I think this has much to do with why your whole argument
>> is
>> rejected. A biological system doesn't need to have some goal. It simply
>> is.
>
> A biological system that is does not produce some sort of beneficial
> function will not be in existence for very long. It will be lost
> because nature will not select to maintain it. Those that remain in
> the gene pool remain because the produce some sort of reproductive
> advantage. Different types of potentially beneficial systems have
> different minimum structural requirements without which they cannot be
> realized in the gene pool at all.
I can see no reason that a neutral bit of tissue must be selected against.
>
> For example, despite the fact that a lactase enzyme might be useful in
> a particular gene pool in a particular environment, that function will
> not exist with any arrangement of just 40 or 50 residues . . . or even
> 100 residues. The same thing is true of flagellar motility. This
> type of function cannot be realized with the use of just a 400 or 500
> or even 1000 codons of DNA - regardless of arrangement.
So what? Perhaps some other non-harmful function can be realized with fewer
codons.
>
> *All* potentially beneficial systems that have higher minimum
> requirements will be more widely seperated in sequence space compared
> to lower level functions - much much more widely seperated (on
> average). That means, the evolution of any novel beneficial system at
> higher level requires many more mutations, on average, from the
> perspective of any given gene pool.
>
You have not demonstrated that there are *any* systems that have minimum
requirements for being either (a) beneficial, or (b) not harmful.
hersheyh
> > > 2. The minimum gap size is the mutational distance between what exists
> > > in a gene pool and what might exist as a beneficial system if it were
> > > ever found by random mutation.
>
> > This, of course, is the number that Sean needs to be presenting *all*
> > the time, not just when I remind him that the number he does present,
> > his minimum threshold size, is utterly without relevance to the number
> > he does need.
>
> The minimum threshold size is very much related to the minimum gap
> size. That's the whole point.
Yes, that is the assertion you keep implying is true without ever
presenting *any* supporting evidence and certainly never presenting
the requisite data that allowed you to determine that the relationship
is linear. That data would also have let you determine the value of
b, the slope of the line in your linear relationship between y (the
number of units of gap size) and x (the number of units of minimum
threshold size) which, necessarily, must be an empirically determined
value.
I notice, as does everyone else, that you continue to evade, mince,
and hide from presenting the necessary evidence for your repeated
assertion.
> Your notion that the likely minimum
> gap size stays the same regardless of the minimum structural threshold
> requirements is simply wrong.
No. My claim is that the number of mutational steps (not aa's, but
mutational steps) required to generate a new *function* is
idiosyncratic and is unrelated (i.e., uncorrelated) to the size of the
end product. That is *because* evolution requires that new functions
arise by modification of pre-existing functional proteins and not
every cell or every organism will have the requisite conditions.
*New* or *novel* function generation is an exceedingly rare event and
usually is the result of linking of pre-existing subsystems, proteins,
or protein moieties, or is the result of a significant change in the
regulation of pre-existing proteins. I am quite sure that any change
that could arise by a single point mutation would not be considered to
be *novel* by you, even if it changed the substrate being used.
> This is a fact provable to anyone who
> cares to do a little investigation into the distances that exist
> between beneficial sequences in sequence space at different structural
> requirements. A pretty good illustration of this can be found in the
> Choi and Kim paper I've presented many times now.
Bullshit. The Choi and Kim paper says no such thing. I have
repeatedly told you that you clearly do not understand their paper and
what the data mean. Your interpretation of their data is ignorance
personified. You are so ignorant that you repeatedly ignore the fact
that they only presented a *sample* (a small one at that) of the
universe of proteins. A plot with the entire universe of proteins
would shrink all the gaps. You also fail to understand that the
*fact* that the data they present is organically linked means that no
search through total structure space was performed. You also continue
to ignore and conflate the distinction and reality of the differences
between structure, sequence, and function and act as if they were all
the same thing.
> http://www.pnas.org/cgi/content/full/103/38/14056
>
> > > 3. The gap size is always smaller than the threshold size.
>
> > Ah. But how much smaller?
>
> That depends upon the size of the gene pool.
Don't you mean the size and *nature* of the organism's pre-existing
genome? You would be wrong in either case, but you should at least
look at the right thing. The number of organisms with a particular
genome (within biological reason) would not affect the size of the
minimum gap size more than by a mutation or two. The precise nature
of the genome, OTOH, would affect the gap size.
> A smaller gene pool will
> likely have a larger minimum gap size. And, if one could have an
> infinitely large gene pool, the gap size would always be zero.
The availability of the appropriate pre-existing proteins is
idiosyncratic and is based on the past evolutionary history of the
organism. The number of organisms would have an insignificant effect
in comparison. Again, a very large population might mean that one
would not have to wait quite so long for a specific point mutation (on
average), but would have little effect on the frequency of specific
deletions, translocations, inversions, etc., that might generate some
new combination of functional moieties that already exist in the
organism.
> > And is there any correlation between gap
> > size and minimum threshold size?
>
> Yes, there is . . .
And that correlation is...? Please present the linear relationship
you claim exists and the evidence for it. I notice that you have
avoided doing so once again. If I were a cynical person, I might
assume that you do so because you are simply bullshitting. What the
heck, I AM that cynical when it comes to you.
> > And is evolution more a matter of
> > whether or not an organism has an already useful functional precursor
> > that can be *modified* to produce the end function in a reasonable
> > matter of steps.
>
> That is exactly what evolution is dependent upon. The problem is that
> the odds of having a precursor that is only one or two mutations away
> drop dramatically with each increase in the minimum threshold size
> under consideration.
So you keep asserting, again without presenting any evidence or any
actual equation, despite your claim that the relationship is both
known, tested, and true. I, of course, will believe that you are not
bullshitting when you actually come up with the equation, the value
for the slope determined empirically, and the evidence you used to
generate it. Until then, you are simply bullshitting.
> > Or whether or not functionally relevant moieties can
> > be linked together (covalently or by other association) to produce a
> > novel function? None of that has any relevance to the minimum
> > threshold size that I can see.
>
> All of these factors are affected by the threshold size. The larger
> the threshold size, the markedly less likely anything will exist that
> can easily be linked together to produced any higher threshold
> function with just one or two mutations.
That is empirically not true. I have presented evidence that the
function of rotary motility by a *new* mechanism can be accomplished
by at least two different single mutational events (with different
results) in a model system that lacked that function, but had all the
requisite precursor features to produce such a function. This was
accomplished by producing a chimeric protein that did not previously
exist either in the original rotary flagella nor, most likely, in the
ancestral protein that produced the original rotary flagella. And the
rotary motility function of the eubacterial flagella was *your*
example of function that could not possibly be produced by linking
functional subunits that lacked that emergent function.
> > Sean *asserts* that there is a linear relationship between 'gap size'
> > and 'minimum threshold size' of the end product, but he never seems to
> > be able to actually present the crucial constant for such a linear
> > relationship. Namely the ratio "gap size units" per "minimum
> > threshold size units", aka, the slope of the linear line. [I am
> > assuming that the y intercept is at 0 and that the relationship is
> > only valid for positive values of x).
>
> The slope is affected by the size of the population. But, given a
> static population size, the slope can be roughly estimated.
Then frigging do so. But first explain why you think the slope is
affected by the size of the population. I see no reason why it would
be significantly affected by any reasonable biological population
size. But choose a population if you think it would affect the size
of the gap significantly (rather than merely by one or, at most, two
mutational steps).
> > > 4. The average gap size increases with each increase in structural
> > > threshold requirements.
>
> > This is an unwarranted assertion that appears to be contradictory to
> > the evidence I know about. How did you determine this without
> > assuming a mechanism for how structural threshold requirements can be
> > increased? The only way that I can even think is that you assume that
> > increases in size are done by adding one aa at a time followed by a
> > random walk in total sequence space.
>
> The threshold requirement is independent of how it is achieved
> Howard.
Evidence that the *number of mutational steps* is the same for
producing a protein with a minimum threshold (aka total size) of 400
if that protein can be produced by linking two different pre-existing
functional moieties relative to the only way to produce the new
protein is by adding one aa at a time to some random unrelated
sequence completely randomly? It certainly seems to me that the
first, given that the pre-existing functional moieties are actually
present in the cell and that there exists actual mechanisms that can
link them together in various ways would require fewer steps than if
there were no pre-existing moieties and one must generate the entire
sequence by randomly adding aa's one at a time by an unknown mechanism
(there is no known mechanism that works like this in cells) completely
randomly. But perhaps you can explain why you think this?
> It is what it is regardless. For example, the minimum
> threshold requirement for flagellar motility is always going to be
> more than 10,000 codons or 30,000 bp
Well, you do learn at least some things. Now that you have learned
the difference between codons and bp's, perhaps you could present that
equation I keep asking you for?
> of genetic real estate period.
But why does this tell us how many mutational steps are required to
produce that *from the closest functional subsystems*? Not from
scratch. From the closest functional subsystems.
> There are other types of systems that also occupy this level and they
> do so regardless of how they came to be.
SFW? Unless you are claiming that these systems cannot arise by
direct linkage of pre-existing smaller subunits, but instead are
produced by producing some arbitrarily random sequence of a given size
and then that random sequence must wander around total sequence space
until it reaches some telelological end point.
> Now, finding such potentially beneficial systems is where random walk
> or selection via various kinds of mutations comes into play. For
> those potentially beneficial islands in sequence/structure space that
> have higher threshold requirements, any and all kinds of random
> searches into space will exponentially greater amounts of time to find
> any one of them.
IOW, you DO claim that evolution works by first producing some sort of
average random sequence of a given size that then must wander total
sequence space until it some teleological end point that is some
average distance away (although you often falsely imply that the
distance is the minimum threshold size rather than the gap size by
continuing to never present your actual method for determining gap
size).
> > > 5. The minimum gap size does not increase until the population size
> > > remains static and until the number of genetic elements within just
> > > one mutation of a beneficial target drop to one.
>
> > This doesn't make any sense at all. What population size are you
> > talking about?
>
> The population that makes up the gene pool. The bigger the
> population, the greater the odds are that a genetic sequence within
> the gene pool will be within one or two mutations from a novel
> beneficial system at a particular threshold minimum.
This would, at best, be a minor effect and one that would be
evolutionarily pretty much irrelevant compared to the nature of the
proteins and genes that were present. Unless, of course, one were so
ignorant as to think that evolution works by producing some random
sequence of a given length that then wandered total sequence space
until it hit a teleological goal. Oh, did I just describe what you
think?
> > And why are you assuming that when there is only be
> > one genetic element (do you mean genes?) within one mutation of a
> > beneficial target that the minimum gap size would *increase*? Could
> > you try re-phrasing this into English?
>
> The odds that there will be at least one genetic element within one
> mutation of any potentially beneficial target at a particular
> threshold level ...
>
> read more ยป
hersheyh
Not true assuming that this apparently hypothetical cell is like real
cells. Real cells in real populations do not contain any significant
(if any) number of DNA sequences that produce random non-functional
proteins of *any* given size. There may be a few pseudogenes which
produce truncated useless proteins and a few proteins that used to be
useful but no longer are, but by and large, all the real genes in a
cell are producing functional proteins of various degrees of utility.
There is no significant population of random genes of a given size
that produce random protein sequences by wandering randomly through
total sequence space. Nor does evolution assume that. Instead
evolution assumes that any new *function* that arises will do so by
modification of pre-existing sequences in that particular species.
And for any new and useful function that *does* arise in such a cell,
the number of mutational steps that produces it will be relatively
small. That is, evolution is constrained primarily by past history
and not by average gap distances.
> However, as the threshold requirements under
> consideration are increased, the Poisson curve is shifted so that far
> fewer existing sequences are within just one mutation of any of the
> many potentially beneficial sequences in sequence/structure space.
Perhaps that explains why proteins are largely 300 +/- 200 aa long and
most of the longer ones involve internal repeats or are compound
complex functionalities formed by joining pre-existing sequences
(which can take a mere one mutational step linking the pre-existing
moieties). But I suspect that you mean to imply that the Poisson
curve (presumably of the gap size?) is meant to imply a model of new
protein generation that simply does not exist in real cells; namely
the hypothetical generation of some hypothetical average random
sequence that wanders total sequence space to find a new function.
There is no such mechanism at work in cells and evolution does not
call upon such a mechanism. That mechanism is your fantasy, not
biological reality.
> Raise the threshold requirements under consideration again and the
> number of existing sequences that is within one mutation of any of the
> even higher level potentially beneficial sequences drops off even more
> dramatically - down to just one existing genetic element being within
> one mutation of any potentially beneficial sequence with the higher
> threshold requirements.
No matter how much you increase the threshold size, the number of
*possible* protein sequences that are within one mutational step
(assuming only point mutations) of any specific (usually functional)
protein sequence that actually exists in a cell is n^20, not one.
But, of course, the reality is that many, but not all, of those n^20
variants will *also* be functional and probably equally functional
(others will have various quantitative and qualitative differences in
function -- which, of course, is the feature that is relevant to
evolution by point mutation), as will also be many sequences with
various small internal or end deletions. This is amply evident from
the reality of sequence differences in different existing species
where the different sequences perform the same function.
> Raise the bar again and the odds that any
> existing genetic sequence will still be within one mutation of any
> potentially beneficial sequence drop dramatically - again along a
> Poisson distribution.
>
> Understand now?
No. Your argument has no empirical reality in how genomes and
evolution works. And is mathematically ignorant besides.
>
> Sean Pitmanwww.DetectingDesign.com
Seanpit
> "Seanpit" <seanpitnos...@naturalselection.0catch.com> wrote in message
There is no way to identify highly symmetrical polished granite cubes
as "artifactual" at a glance *unless* one has some sort of prior
experience and a *method* of analyzing and interpreting that
experience with regard to the range of granite forms produced by non-
artifactual processes.
In other words, one must have some sort of methodological basis for
determining the likely limits of this range of non-artifactual
production - a range beyond which one can be reasonably confident of
artifactual production. It doesn't matter how rough the methodology
allows one's estimate to be. There must be at least some experiencial
basis with statistical relevance before anyone can be remotely able to
recognize even a very highly symmetrical polished granite cube as
artifactual at all much less at a glance.
Sean Pitman
www.DetectingDesign.com
Seanpit
>
> >> So, how do you know that _David_ is designed and snowflakes aren't?
> >> (Or do you think snowflakes are designed as well?)
>
> > Snowflakes aren't made out of granite or marble, materials that do not
> > naturally tend toward highly symmetrical self-assembly.
>
> > Again, you have to have prior experience with the *material* in
> > question and how it interacts with non-deliberate forces of nature
> > before you can begin to reasonably detect artifact.
>
> > Take, for instance, SETI scientists. If they had absolutely no
> > experience with radiowaves they wouldn't be able to say if this or
> > that pattern was or was not likely to be the result of artifact. It
> > is only because of their prior experience with radiowaves that they
> > can in fact suggest features that would likely be artifactual if they
> > were ever discovered in radiowaves.
>
> Now, this much I agree with.
Well, it's good that at least someone has come this far. It is more
than I can say for most in this forum!
> How does it help you in biology?
Non-artifactual processes always have a certain limited range in how
they affect a given material - whatever that material may be. If one
can identify this range to a useful degree of confidence, one can use
this information to detect artifact whenever this range is crossed to
a significant degree.
When it comes to biology and living things, non-deliberate natural
processes do have a significant impact when it comes to modifying both
form and function over time. However, there seems to be a very clear
range beyond which non-deliberate forces simply do not and evidently
cannot go. One particular parameter is most striking. That is, the
evolution of novel beneficially functional biosystems. The non-
deliberate mechanism of random mutation and function-based selection
(otherwise known as natural selection) is able to evolve new systems
very commonly and often very rapidly whenever they are needed - like
during rapid environmental changes or the addition of a new nutrient
or toxin to the environment. What is interesting though is that out
of all the cases where novel systems have been observed to evolve,
those systems with novel functions that evolve most commonly and most
rapidly have few size and/or sequence specificity requirements (i.e.,
less than 100 fairly specified residues). Those systems that have
minimum structural requirements of a few hundred amino acid residues
evolve much less commonly. And, amazingly, systems that require a
minimum of more than 1000 fairly specified amino acid residues (or an
equivalent of 1000 codons of DNA) have never actually been observed to
evolve. There isn't a single reported case in all of scientific
literature beyond the 1000aa level.
The whole pattern demonstrates a clear exponential decline in
evolvability with increasing minimum structural threshold requirements
until the non-deliberate non-artifactual evolutionary mechanism
completely stalls out well shy of the 1000aa threshold. I find that
most intriguing because there are a large number of biosystems that
require far more than a minimum of 1000 codons of DNA to be realized.
The flagellar motility system, for example, requires over 10,000
codons of genetic real estate at minimum before the motility function
can be realized at all. None of the proposed steppingstones along the
pathway of flagellar evolution have ever been demonstrated to evolve
in the laboratory or anywhere else. And, what is most interesting, is
that all of the proposed steppingstones are separated from each other
by differences that would require several dozen mutations, at minimum,
to link them up properly to achieve the next beneficial step in the
flagellar evolution pathway.
While a gap of just 30 or 40 non-beneficial, even neutral, mutations
might not seem like a big deal, such a gap would take a population the
size of all the bacteria on Earth trillions of years to cross - on
average. Clearly then, the existence of such a system seems well
beyond the abilities of any known non-deliberate process of nature to
explain. This suggests that it is at least reasonable to consider the
potential of deliberate artifact in the construction of the flagellar
motility system as well as all other systems that require more than
1000 fairly specified codons at minimum.
Sean Pitman
www.DetectingDesign.com
Seanpit
> On Aug 23, 7:02 pm, Seanpit <seanpitnos...@naturalselection.
>
> 0catch.com> wrote:
> > On Aug 23, 1:49 pm, hersheyh <hershe...@yahoo.com> wrote:
>
> > > > I'm not talking about changes Ron. I'm talking about an absolute
> > > > number of amino acid residues that have to be in a specified
> > > > arrangement before a particular type of function can be realized at
> > > > all.
>
> > > IOW, evolution is not about *change*. It is about *size*.
>
> > It's about both. It is about changes producing functional systems
> > that have different minimum structural size and specificity
> > requirements.
>
> No. Evolution is about change, not size. Change in *function*.
> Generation of new *function*. The fact is that evolution is highly
> conservative of *structure* and *size* and *specificity* when it
> generates new *function*.
We are talking about evolving functional systems that require greater
minimum size requirements. What are the odds that any such
potentially beneficial larger system would be evolvable? Are the odds
the same as they are for smaller potentially beneficial systems?
That's the question at hand here - as you already know.
> Not that larger sized proteins are all that hard to make in single
> mutational steps. They are not made, as you seem to think, by adding
> one aa at a time to some non-functional imaginary protein.
You're building the strawman you always build - yet again. Why do I
have to constantly remind you that I do not suggest that larger
systems need to be built one amino acid at a time? Use any type of
mutation and pre-existing system available. The odds of success are
exactly the same as a random walk of just one amino acid change at a
time. There is no advantage in blindly taking large vs. small steps
into sequence/structure space. All that matters is the relative
density of potentially beneficial targets in that space. That is the
only thing that determines the average number of mutations needed to
achieve success.
As it turns out, the density of potentially beneficial sequences and
structures declines exponentially when one considers larger minimum
structural threshold requirements.
< snip >
> But you really don't seem happy with the fact that most proteins are
> too small, so you then look at aggregations of proteins (such as
> ribosomes or flagella) and treat them as if they were a single
> protein.
I treat such systems as if they were a single system whose function is
dependent upon a minimum number of them being in a particular
location.
> The fact is that duplication and divergence (especially
> subfunctionalization, which only requires loss of function) are common
> events. Once one has duplicates that have either become subfunctional
> or neofunctional, the size of the complex would, according to you have
> doubled.
But the minimum requirements would not have doubled. Once the minimum
threshold requirement is reached, further modifications are not a
problem.
> But without any *change* but a duplication and a different
> *loss* of partial function in both of the genes. Over time, of
> course, such subfunctionalization can lead to irreducible complexity.
> But, of course, you have a teleological mindset and assume that
> proteins can only do one thing, their teleological function. You hold
> that despite knowing that a flagella which is immotile can still
> transport proteins outside the bacteria.
The transport function has a far smaller minimum threshold requirement
compared to the flagellar motility function. Maintaining subfunction
does not remove the fact that the flagellar motility function is still
irreducibly complex in that it still requires a much higher minimum
structural threshold to work as a system of flagellar *motility*.
Kenneth Miller also makes this very same mistake. He thinks that
showing intact subsystems means that the flagellar motility system is
therefore "reducible". It isn't. It still requires the same minimum
threshold that it ever did. This key "argument" of Miller is just
silly and I'm very surprised that so many people fall for this blatant
nonsense. It is like suggesting that the motility function of a car
is "reducible" by showing that the lights still work when the engine
and drive shaft are removed.
< snip >
> > You may argue that evolution
> > doesn't require this to happen and that's true. However, you
> > evolutionists believe that it happened very commonly throughout a span
> > of only 4 billion years or so. How could systems with very high
> > minimum structural threshold requirements have evolved?
>
> I've told you how larger proteins can be made. Proteins *like* to
> interact with each other, so explaining aggregation of proteins is not
> too difficult. Most interactions vary in strength.
The problem isn't getting proteins to stick together to form larger
protein complexes. The problem is in getting them to stick together
properly so that a higher-level system is produced in the union - a
system that has a larger minimum structural threshold requirement.
> > You simply
> > state that when evolution happens it happens because the gaps were
> > small. I couldn't agree more. The problem is with your notion that
> > small gaps sizes could easily exist with minimum structural threshold
> > requirements at 1,000aa and far beyond. That's the problem. You
> > think the *likely* gap size is the smallest possible gap size (i.e.
> > "one") regardless of the minimum structural threshold requirement for
> > the functional system in question.
>
> Yes. That is the problem. But as I see it, the problem is that you
> have not presented any evidence to support the hypothesis that the
> systems that have evolved and that new functionality in particular,
> regardless of the size of the protein(s) involved, did so or needed to
> do so by crossing large gaps.
None of the proposed steps in larger systems, like the flagellar
motility system, are smaller than a few dozen mutations. If your
notion of gaps of only one or two mutations were remotely correct, all
the steps in the flagellar system should be able to be evolved by all
kinds of different bacteria within a handful of generations - i.e.,
just a few days for some types of bacteria. Try again . . .
> You keep asserting that there is a mathematical relationship between
> total size and gap size. I have yet to see that equation nor any
> evidence supporting the hypothesis.
Look at the Choi and Kim paper again. Or, do your own search and
sequence comparisons of higher level systems. They aren't remotely as
close together as you seem to imagine - not even close to your oft
repeated minimum of just one mutation apart. That's clearly mistaken
for anyone who cares to actually look into the matter instead of
blindly waving a hand over the obvious.
> > That notion of yours is clearly mistaken as anyone can prove by simply
> > doing a BLAST search. Systems with larger minimum structural
> > requirements than 1 or 2k amino acid residues are not just one or two
> > residue changes away from any other uniquely functional system.
>
> Examples?
I've given you many examples already Howard. Why do you need more?
> And how long since the system diverged?
This is completely irrelevant since times of divergence are not based
on analysis of how long it would take to cross the non-beneficial
chasm that is obviously dozens of mutations wide.
> That is crucial
> because a lot of both selective and non-selective changes will occur
> in sequences over long periods of time.
That's the whole problem. Neutral drift takes too long to cross gaps
of just a few dozen mutations. Your suggestion that the changes were
somehow directed by natural selection along a beneficial pathway is
completely unfounded. There is absolutely no evidence to support this
beyond wishful thinking.
> And these changes would not
> necessarily affect the basic *function*; they would optimize it.
Optimization of a pre-existing function is not the issue here. That's
not the problem. Getting an entirely new unique function to at least
some degree of usefulness is the problem.
> Again, a mutation that produces the loss of rotary motility (a single
> point mutation can do this) does not necessarily affect the ability to
> transport proteins by the flagellin tube, some of which still do
> function for this purpose as well as being a flagella. Again, you
> seem to think that flagella only has a single function rather than
> having proteins that each have an independent function that is still
> there if another protein has mutated.
It is one thing to remove a pre-existing function with a single
mutation. It is quite another thing to be just one mutation away from
a novel high-level system that has never existed before. For example,
some cavefish without eyes have lost their eye as the result of a
single point mutation. These eyes will actually grow back if this
point mutation is corrected. Does this mean then that getting eyes to
evolve de novo in fish that never had eyes before is likely to be
achieved with a single point mutation? Not even close.
> > And,
> > as the minimum requirements grow, so does the number of differences
> > one sees between it and the next closest uniquely functional system.
>
> So you keep asserting.
So you keep denying - denying the obvious. Just look it up Howard.
Look up the differences in the Hamming distances between higher level
systems compared to lower level systems. See if you don't recognize a
trend . . . the same trend illustrated by Choi and Kim.
< snip >
> > > The answer to that question has been answered. The answer, in
> > > principle (and in reality) is one.
>
> > Yeah - "In principle" the minimum gap size is just one mutational
> > change.
>
> And always will be.
This is true only in principle, but it is very unlikely to be true in
reality for higher level systems - - to an exponential degree.
> But there are cases of *real* proteins where more
> than one site needed to *selectively* mutate to produce a changed
> function (possibly the conversion of a cortisol receptor to an
> aldosterone receptor). But the protein actually has some level of
> both functions. It is hardly unusual for proteins to have more than
> one possible substrate.
Again, if a protein already has at least some beneficial level of a
given function, further modification isn't a problem. This isn't the
type of "evolution" we are talking about Howard. The type of
evolution that is problematic is the type where a truly novel system
of function that was NOT already there to any beneficial degree is
evolved using what is already there.
< snip >
Sean Pitman
www.DetectingDesign.com
Seanpit
>
> > A biological system that is does not produce some sort of beneficial
> > function will not be in existence for very long. It will be lost
> > because nature will not select to maintain it. Those that remain in
> > the gene pool remain because the produce some sort of reproductive
> > advantage. Different types of potentially beneficial systems have
> > different minimum structural requirements without which they cannot be
> > realized in the gene pool at all.
>
> I can see no reason that a neutral bit of tissue must be selected against.
It cost energy to maintain DNA. Therefore, DNA that isn't providing
any benefit to the creature will eventually be discarded. Besides,
this discussion is about the time it takes to find useful genetic
elements with different minimum size and specificity requirements.
Neutral evolution or "random walk" doesn't really help, statistically,
to find potentially beneficial islands in the vastness of sequence
space any faster that any other search algorithm.
> > For example, despite the fact that a lactase enzyme might be useful in
> > a particular gene pool in a particular environment, that function will
> > not exist with any arrangement of just 40 or 50 residues . . . or even
> > 100 residues. The same thing is true of flagellar motility. This
> > type of function cannot be realized with the use of just a 400 or 500
> > or even 1000 codons of DNA - regardless of arrangement.
>
> So what? Perhaps some other non-harmful function can be realized with fewer
> codons.
That's fine. If all that existed where functions that required no
more than a few hundred fairly specified residues, the ToE would be a
perfectly reasonable explanation. The problem is that functional
systems exist that require very large minimum threshold requirements.
The question is, can the proposed evolutionary mechanism explain these
higher level systems? Sure, evolution doesn't have to produce higher
level systems, but can it? That's the question. Could the
evolutionary mechanism move beyond systems that have very low minimum
threshold requirements to come up with higher level systems?
> > *All* potentially beneficial systems that have higher minimum
> > requirements will be more widely separated in sequence space compared
> > to lower level functions - much much more widely separated (on
> > average). That means, the evolution of any novel beneficial system at
> > higher level requires many more mutations, on average, from the
> > perspective of any given gene pool.
>
> You have not demonstrated that there are *any* systems that have minimum
> requirements for being either (a) beneficial, or (b) not harmful.
There are lots of beneficial systems, like flagellar motility, that
also have very high minimum structural threshold requirements coded
for by a minimum of well over 10,000 codons, or 30,000 bp, of DNA.
Again, the argument that such systems didn't have to evolve doesn't
address the question of if they could have evolved via random mutation
and function-based selection.
Sean Pitman
www.DetectingDesign.com
richardal...@googlemail.com
> "Seanpit" <seanpitnos...@naturalselection.0catch.com> wrote in message
Sean's "method" reminds me of an old joke.
Two men sitting in a train compartment.
One of them is reading a newspaper. Every so often, he rips out a
page, crumples it up and throws it out of the window.
Eventually (this is England, after all, and we English are naturally
reticent) the other man asks him why he is doing it.
"It keeps the elephants away"
"But there aren't any elephants here!"
"Yes. It's very effective".
RF
richardal...@googlemail.com
wrote:
> On Sep 3, 1:28 pm, richardalanforr...@googlemail.com wrote:
>
>
>
> > > > As nobody including you has ever carried out such an analysis (i.e. a
> > > > **STATISTICAL** analysis of shape to determine artificiality), how on
> > > > earth can you claim this?
>
> > > That's not true Richard. Even you have carried out an analysis of the
> > > various forms of naturally produced granite forms that allows you to
> > > understand, with a very high degree of STATISTICAL certainty that a
> > > highly symmetrical polished granite cube is very unlikely to be the
> > > result of any non-deliberate non-artifactual process of nature.
>
> > So now you are claiming that you can calculate statistical
> > probabilities without numbers.
>
> I did you numbers Richard. As I've explained to you many times now, I
> can eyeball a rock to at least a useful degree of measure -
> centimeters or inches (depending on the size of the rock).
So you can tell roughly how big a lump of rock is by looking at it.
What the hell has that to do with determining if it's an artifact?
> And, so
> can you.
Quite. What I don't do, however, is to claim that these eyeball
measurements tell me anything about the artificiality of the object
I'm looking at.
You do.
> You don't have to right down all of these observations
> either before you can recognize a developing trend with regard to
> symmetry in the material of granite.
As one would need many accurate measurements to define the shape of an
object, I fail to see how one could do any meaningful statistical
analysis *without* both measuring the objects and recording the
results.
> The trend is actually based on
> roughly estimated measurements that you have averaged in your head.
So now you are trying to tell us that a few rough estimates of size
alone are enough to tell us if an object is an artifact.
> That is how you know that a very high degree of symmetry, like that
> shown by a polished granite cube with a variance of less than 0.01%,
> is not remotely approached by any non-deliberate force of nature.
It is in crystals. Or had you forgotten that?
More to the point, this explanatory filter of yours rules out
virtually every manufactured object man has ever made, even reference
cubes of granite made as accurately as possible.
> You
> know this because no naturally produced granite form has even come
> close to your ability to recognize it as non-symmetrical to the rough
> degree that you are able to eyeball symmetry.
There are many pebbles which do. But then you exclude any object which
proves you wrong, don't you?
>
> Again, you argue that this is not what anyone would call "statistical
> analysis".
No statistician, or anyone with even a passing familiarity with
statistic would call it that.
> But, it actually is. If you had absolutely no idea how to
> eyeball anything to any degree of certainty or measurement, you
> wouldn't be able to instantly recognize a highly symmetrical polished
> granite cube as artifactual.
You mean in the way people have recognised large pyrite crystals as
artifacts?
This has nothing whatsoever to do with statistics. It's about shape
recognition, something humans are rather good at.
> You'd have to go around actually
> measuring everything before you could detect artifact.
You have to examine objects closely and test hypotheses of manufacture
before you can identify an unfamilar object as an artifact.
Measurement has little to do with it.
> For close call
> cases you might have to do this. You don't have to do this when the
> degree of certainty is so extreme that you can instantly tell just by
> looking at the object or phenomenon.
>
Oh, please!
So you memorize all the numbers (which numbers, by the way?) from all
those objects (1000 objects, as I recall) which define it's shape in
great detail (for otherwise how would you be able to measure the high
degrees of accuracy you witter on about), and then perform statistical
calculations on them, and all in your head.
In a word, bullshit.
If you would like me to expand on that, complete and utter bullshit
which wouldn't fool a five-year old of moderate intelligence.
RF
> < snip rest >
>
> Sean Pitmanwww.DetectingDesign.com
richardal...@googlemail.com
And as an addendum to my last post, let's restore the parts you
snipped, shall we?
Why is that? Ashamed of your dishonesty and constant misrepresentation
of my position?
Seanpit
>
> > Imagine a Poisson distribution curve. For potentially beneficial
> > systems that have low structural threshold requirements the curve is
> > shifted so that a large number of genetic sequences in a large gene
> > pool are within just one mutation of many such potentially beneficial
> > structures/systems.
>
> Not true assuming that this apparently hypothetical cell is like real
> cells. Real cells in real populations do not contain any significant
> (if any) number of DNA sequences that produce random non-functional
> proteins of *any* given size.
The proteins don't have to be non-functional in order to be close to a
new type of potentially beneficial sequence/structure. Remember your
own mantra Howard, protein systems can have multiple functions and the
underlying genetics can undergo duplication mutations to free up a
copy for even further evolutionary modification under the appropriate
selective environment.
< snip rest of non-argument >
> > However, as the threshold requirements under
> > consideration are increased, the Poisson curve is shifted so that far
> > fewer existing sequences are within just one mutation of any of the
> > many potentially beneficial sequences in sequence/structure space.
>
> Perhaps that explains why proteins are largely 300 +/- 200 aa long and
> most of the longer ones involve internal repeats or are compound
> complex functionalities formed by joining pre-existing sequences
> (which can take a mere one mutational step linking the pre-existing
> moieties). But I suspect that you mean to imply that the Poisson
> curve (presumably of the gap size?) is meant to imply a model of new
> protein generation that simply does not exist in real cells; namely
> the hypothetical generation of some hypothetical average random
> sequence that wanders total sequence space to find a new function.
> There is no such mechanism at work in cells and evolution does not
> call upon such a mechanism. That mechanism is your fantasy, not
> biological reality.
What is fantasy here is your notion that any kind of mutation will
have better odds of finding a novel beneficial sequence/structure over
a random walk of single amino acid additions, subtractions, or
substitutions. The odds of success are exactly the same Howard. The
odds of hitting upon a new beneficial system by linking up large pre-
existing moieties are essentially the same as the odds that a single
point mutation will do the trick. I know you haven't figured this out
yet, but look into it. There is no significant statistical advantage
for one method over any other. Use any type of mutation you want.
The odds are always going to be essentially the same.
> > Raise the threshold requirements under consideration again and the
> > number of existing sequences that is within one mutation of any of the
> > even higher level potentially beneficial sequences drops off even more
> > dramatically - down to just one existing genetic element being within
> > one mutation of any potentially beneficial sequence with the higher
> > threshold requirements.
>
> No matter how much you increase the threshold size, the number of
> *possible* protein sequences that are within one mutational step
> (assuming only point mutations) of any specific (usually functional)
> protein sequence that actually exists in a cell is n^20, not one.
You have several concepts all messed up here. First off, we aren't
talking about one specific protein sequence here. We are talking
about a function here that can be realized by a fairly large number of
different protein sequences that form an island cluster (i.e., only
"fair" protein specificity - not perfect specificity like you are
suggesting). Hitting upon any one of these sequences will equal
success. This means that a large pre-existing gene pool is more
likely to be within one or two mutations of at least one member of a
potentially beneficial island in sequence space when the number of
islands per unit area (i.e., the density of islands) is increased.
This happens when one considers systems with lower minimum structural
threshold requirements. Higher threshold limitations equal an
exponential reduction in the density of potentially beneficial
sequences in sequence space along with a reduction in the odds that
any existing sequence in the gene pool will be within one mutation of
any member of any potentially beneficial island cluster.
> But, of course, the reality is that many, but not all, of those n^20
> variants will *also* be functional and probably equally functional
> (others will have various quantitative and qualitative differences in
> function -- which, of course, is the feature that is relevant to
> evolution by point mutation), as will also be many sequences with
> various small internal or end deletions. This is amply evident from
> the reality of sequence differences in different existing species
> where the different sequences perform the same function.
This is completely irrelevant - as noted in the extensive portion of
the previous post which you snipped.
> > Raise the bar again and the odds that any
> > existing genetic sequence will still be within one mutation of any
> > potentially beneficial sequence drop dramatically - again along a
> > Poisson distribution.
>
> > Understand now?
>
> No. Your argument has no empirical reality in how genomes and
> evolution works. And is mathematically ignorant besides.
I understand quite well how genomes work and how evolution is supposed
to work. Your problem is that you think that certain types of
mutations have a statistical advantage over other types of mutations
when it comes to finding novel beneficial sequences/structures in
sequence/structure space. This notion is false. There is no
significant advantage using multicharacter mutations or combinations
of pre-existing sequences over single character mutations when it
comes to finding novel beneficial systems.
Sean Pitman
www.DetectingDesign.com
Seanpit
Ah, but how do you know that there are no elephants in England? What
"method" did you use to arive at this conclusion? ; )
Likewise, what "method" do you and Baldwin use to quickly conclude
artifact when you see a highly symmetrical polished granite cube? You
have to have some sort of basis before you can make such a rapid
conclusion - do you not? How did you establish this basis? How do
you know it is a reliable conclusion if you used absolutely no method
or even cursory statistical analysis?
Sometimes I don't think you English know why you do or think the way
you do. You just do and think out of habbit without really thinking
about it.
> RF
Sean Pitman
www.DetectingDesign.com
Seanpit
> On 4 Sep, 02:00, Seanpit <seanpitnos...@naturalselection.0catch.com>
>
> > > probabilities without numbers.
>
> > can eyeball a rock to at least a useful degree of measure -
> > centimeters or inches (depending on the size of the rock).
>
> So you can tell roughly how big a lump of rock is by looking at it.
> What the hell has that to do with determining if it's an artifact?
I can also roughly judge symmetry by looking at a rock. After looking
at a great many rocks, I can tell you, with a great deal of
confidence, that naturally produced rocks never come even close to
producing high level symmetry in the form of a polished granite cube
with less than 0.01% variance. This is a clear indication that such a
degree of symmetry is evidence of artifact.
> > And, so
> > can you.
>
> Quite. What I don't do, however, is to claim that these eyeball
> measurements tell me anything about the artificiality of the object
> I'm looking at.
>
> You do.
Hmmmm . . . Interesting that you are so limited in your ability to
recognize artifact on sight given certain features in certain
materials - like a highly symmetrical polished granite cube. Even
Baldwin says he would quickly recognize such a cube as artifactual on
sight.
Baldwin argues, "Nobody disputes being able to identify polished
granite cubes as artifacts at a glance."
Evidently he hasn't considered someone like you?
> > You don't have to right down all of these observations
> > either before you can recognize a developing trend with regard to
> > symmetry in the material of granite.
>
> As one would need many accurate measurements to define the shape of an
> object, I fail to see how one could do any meaningful statistical
> analysis *without* both measuring the objects and recording the
> results.
That's complete BS. Even you have done enough meaningful analysis by
simply making a mental notes of the various forms produced by natural
processes with the material of granite to come up with some very
useful data that you yourself have analyzed in such a way that you
would no doubt be able to quickly recognized a highly symmetrical
granite cube as artifactual on sight without the need for any
additional information such as how it was actually "manufactured".
> > The trend is actually based on
> > roughly estimated measurements that you have averaged in your head.
>
> So now you are trying to tell us that a few rough estimates of size
> alone are enough to tell us if an object is an artifact.
Size and shape - yes. That's all.
> > That is how you know that a very high degree of symmetry, like that
> > shown by a polished granite cube with a variance of less than 0.01%,
> > is not remotely approached by any non-deliberate force of nature.
>
> It is in crystals. Or had you forgotten that?
Have you forgotten my oft-repeated statement that one must have
experience with the particular material in question before the
hypothesis of artifact can be adequately proposed? Very high level
symmetry, with regard to surface irregularities, is found in lots of
materials in nature, but not in granite. Have you forgotten my
discussions with you about snowflakes, pyrite, and other natural
crystalline structures already?
> More to the point, this explanatory filter of yours rules out
> virtually every manufactured object man has ever made, even reference
> cubes of granite made as accurately as possible.
I've just presented a starting point with parameters so overwhelmingly
clear as to make the point as obvious as possible. Even then it has
been extremely difficult to get you and others to actually admit the
obvious truth of this extreme example. However, once this extreme
example is accepted, the method used to achieve it is quite easily
modified to detect a much wider range of "artifacts". Simply relaxing
the tolerance levels a bit would include quite a few artifacts.
Including different forms of symmetry would allow the detection of
many more - - and so on.
> > You
> > know this because no naturally produced granite form has even come
> > close to your ability to recognize it as non-symmetrical to the rough
> > degree that you are able to eyeball symmetry.
>
> There are many pebbles which do. But then you exclude any object which
> proves you wrong, don't you?
I've gone over the use of symmetry many times Richard. Rounded
pebbles are not symmetrical with regard to surface irregularities -
i.e., angular projections with sharply defined edges and corners
etc.
Obviously, when one is setting up a useful method for detecting
artifact, one has to be careful to avoid the obvious pitfalls. That
means excluding those things that would produce false positives right
off the bat. Why else do you think I used a cube instead of an oval
or a sphere for my primary example?
> > Again, you argue that this is not what anyone would call "statistical
> > analysis".
>
> No statistician, or anyone with even a passing familiarity with
> statistic would call it that.
Sure they would. Anyone who has any reliable or useful idea about
anything uses at least some form of statistical analysis. Without
such analysis to any degree, one could not have any opinion about
anything to any useful or reliable degree whatsoever.
> > But, it actually is. If you had absolutely no idea how to
> > eyeball anything to any degree of certainty or measurement, you
> > wouldn't be able to instantly recognize a highly symmetrical polished
> > granite cube as artifactual.
>
> You mean in the way people have recognised large pyrite crystals as
> artifacts?
As you know, I've gone over this many times now. Pyrite is not
granite. The same shape that wouldn't be evidence of artifact in
pyrite would be instantly recognized as artifact in granite.
> This has nothing whatsoever to do with statistics. It's about shape
> recognition, something humans are rather good at.
It isn't just about shape recognition. It is about the idea that
certain shapes, when recognized in certain materials, are not the
result of non-artifactual processes.
> > You'd have to go around actually
> > measuring everything before you could detect artifact.
>
> You have to examine objects closely and test hypotheses of manufacture
> before you can identify an unfamilar object as an artifact.
> Measurement has little to do with it.
Not true. A highly symmetrical polished granite cube is instantly
recognizable as artifactual without the need for any additional
knowledge regarding manufacture or anything else. All that is needed
is some prior experience with the material of granite as it relates to
various non-deliberate forces of nature.
> > For close call
> > cases you might have to do this. You don't have to do this when the
> > degree of certainty is so extreme that you can instantly tell just by
> > looking at the object or phenomenon.
>
> Oh, please!
> So you memorize all the numbers (which numbers, by the way?) from all
> those objects (1000 objects, as I recall) which define it's shape in
> great detail (for otherwise how would you be able to measure the high
> degrees of accuracy you witter on about), and then perform statistical
> calculations on them, and all in your head.
>
> In a word, bullshit.
> If you would like me to expand on that, complete and utter bullshit
> which wouldn't fool a five-year old of moderate intelligence.
You're simply denying the obvious Richard. You yourself have done the
necessary observations and analysis in your own head to know that I'm
right. Perhaps you should ask Baldwin to explain how he is able to
instantly recognized highly symmetrical polished granite cubes as
artifactual?
> RF
Sean Pitman
www.DetectingDesign.com
Seanpit
>
> > > You are misrepresenting me again. I have never made any such
> > > statement. In fact, I have posted several links to papers which
> > > demonstrate that the *lower* limit on the time required for such
> > > preservation is a few hours, not "within an hour" as you originally
> > > claimed.
> > You originally fought long and hard arguing that the preservation of
> > fish in the Santana formation was the result of autolithifying
> > bacteria that preserved the fish and other creatures in a non-
> > catastrophic manner as part of some anoxic lagoon.
>
> The preservation of the Santana fish *IS* the result of autolithifying
> bacteria!
>
> Didn't you read the papers which I cited?
Nothing that you have cited explains how cellular turgidity could be
preserved by autolithifying bacteria. You argue that osmotic pressure
does the job. How do you think osmotic pressure is maintained in fish
gills after death? The loss of osmotic pressure is very rapid after
death. That's the whole reason why preservation must be so rapid if
turgid cells are to be preserved in their turgid state.
< snip rest, I don't have time for this >
Sean Pitman
www.DetectingDesign.com
richardal...@googlemail.com
wrote:
> On Sep 4, 12:42 am, richardalanforr...@googlemail.com wrote:
>
> > On 4 Sep, 02:00, Seanpit <seanpitnos...@naturalselection.0catch.com>
>
> > > > So now you are claiming that you can calculate statistical
> > > > probabilities without numbers.
>
> > > I did use numbers Richard. As I've explained to you many times now, I
> > > can eyeball a rock to at least a useful degree of measure -
> > > centimeters or inches (depending on the size of the rock).
>
> > So you can tell roughly how big a lump of rock is by looking at it.
> > What the hell has that to do with determining if it's an artifact?
>
> I can also roughly judge symmetry by looking at a rock.
Your "methodology" for detecting artifact demands an extraordinary
degree of precision in determining symmetry.
You can't do that by eye.
> After looking
> at a great many rocks, I can tell you, with a great deal of
> confidence, that naturally produced rocks never come even close to
> producing high level symmetry in the form of a polished granite cube
> with less than 0.01% variance.
What has that to do with any sort of statistical test?
> This is a clear indication that such a
> degree of symmetry is evidence of artifact.
But only if you exclude objects such as river cobbles which might show
a high degree of symmetry.
>
> > > And, so
> > > can you.
>
> > Quite. What I don't do, however, is to claim that these eyeball
> > measurements tell me anything about the artificiality of the object
> > I'm looking at.
>
> > You do.
>
> Hmmmm . . . Interesting that you are so limited in your ability to
> recognize artifact on sight given certain features in certain
> materials - like a highly symmetrical polished granite cube.
Oh dear, Sean. Resorting to misrepresentation again. Why add more
evidence of dishonesty when it's your honesty which is in question?
I recognise a granite cube as being an artifact because it belongs to
a class of objects I know to be artifacts.
I don't do it on the basis of eyeball measurements of symmetry.
I don't do it on the basis of any form of statistical analysis.
I do it on the basis of pattern recognition.
If there were any doubts as to whether or not a granite object was
natural or artificial, I would try to make that determination by
testing hypotheses of how it was made.
I've explained this to you many times before, yet you insist on
misrepresenting me.
> Even
> Baldwin says he would quickly recognize such a cube as artifactual on
> sight.
Nobody has ever denied this.
However, your claim is to have a statistical method which determines
whether or not it is an artifact.
>
> Baldwin argues, "Nobody disputes being able to identify polished
> granite cubes as artifacts at a glance."
>
> Evidently he hasn't considered someone like you?
You're misrepresenting me once again, Sean. Do you not read my posts,
or are you being deliberately dishonest in an attempt to deceive the
lurkers?
>
> > > You don't have to right down all of these observations
> > > either before you can recognize a developing trend with regard to
> > > symmetry in the material of granite.
>
> > As one would need many accurate measurements to define the shape of an
> > object, I fail to see how one could do any meaningful statistical
> > analysis *without* both measuring the objects and recording the
> > results.
>
> That's complete BS. Even you have done enough meaningful analysis by
> simply making a mental notes of the various forms produced by natural
> processes with the material of granite to come up with some very
> useful data that you yourself have analyzed in such a way that you
> would no doubt be able to quickly recognized a highly symmetrical
> granite cube as artifactual on sight without the need for any
> additional information such as how it was actually "manufactured".
That's not a statistical test.
>
> > > The trend is actually based on
> > > roughly estimated measurements that you have averaged in your head.
>
> > So now you are trying to tell us that a few rough estimates of size
> > alone are enough to tell us if an object is an artifact.
>
> Size and shape - yes. That's all.
Your "method" insists on very high degrees of accuracy in measurement
to determine if an object is an artifact, as well as criteria of
symmetry which few manufactured objects exhibit.
Are you seriously telling us that you can judge all that by eye?
>
> > > That is how you know that a very high degree of symmetry, like that
> > > shown by a polished granite cube with a variance of less than 0.01%,
> > > is not remotely approached by any non-deliberate force of nature.
>
> > It is in crystals. Or had you forgotten that?
>
> Have you forgotten my oft-repeated statement that one must have
> experience with the particular material in question before the
> hypothesis of artifact can be adequately proposed?
Well, yes.
But then your method consists of pulling criteria out of the air and
then excluding any naturally formed object without any justification.
Why exclude pyrite crystals?
By the way, to which types of granite does your method apply? Granites
are formed by the cooling of molten rock over varying time periods
(all far longer that 6,000 years, by the way), so there is a wide
range of granites each with different physical properties.
> Very high level
> symmetry, with regard to surface irregularities, is found in lots of
> materials in nature, but not in granite. Have you forgotten my
> discussions with you about snowflakes, pyrite, and other natural
> crystalline structures already?
I haven't forgotten them, Sean. Mind you, as they are all post hoc
justification I don't place much weight in them.
> > More to the point, this explanatory filter of yours rules out
> > virtually every manufactured object man has ever made, even reference
> > cubes of granite made as accurately as possible.
>
> I've just presented a starting point with parameters so overwhelmingly
> clear as to make the point as obvious as possible.
When you first stated your parameters, they excluded even highly
engineered granite reference cubes. In fact, there was *no* artifact
which met your standards. Of course, you changed your parameters to
accommodate this uncomfortable reality, but as you claim to have
established these parameters by a statistical analysis this merely
demonstrates that you are simply pulling numbers out of the air. If
you had done any form of statistical analysis you would have been able
to justify your parameters.
> Even then it has
> been extremely difficult to get you and others to actually admit the
> obvious truth of this extreme example.
You mean that an object made to standards of precision higher than
anything we have been able to achieve were found we would recognise it
as an artifact?
You have a great method for determining if non-existent objects are
artificial.
> However, once this extreme
> example is accepted, the method used to achieve it is quite easily
> modified to detect a much wider range of "artifacts". Simply relaxing
> the tolerance levels a bit would include quite a few artifacts.
> Including different forms of symmetry would allow the detection of
> many more - - and so on.
So when your method is shown to be absolutely useless, you are
modifying it in the vain pretence that it has anything useful to
offer.
By the way, as your "method" stands, it would not detect that a
granite reference cube with a makers name engraved on it is an
artifact. Or a granite grave marker for than matter. Or even a square
granite plaque with a perfectly symmetrical engraving on it if the
sides of the pattern are cut at 45 degrees rather than square.
Perhaps you can explain again why such a method is useful.
>
> > > You
> > > know this because no naturally produced granite form has even come
> > > close to your ability to recognize it as non-symmetrical to the rough
> > > degree that you are able to eyeball symmetry.
>
> > There are many pebbles which do. But then you exclude any object which
> > proves you wrong, don't you?
>
> I've gone over the use of symmetry many times Richard. Rounded
> pebbles are not symmetrical with regard to surface irregularities -
> i.e., angular projections with sharply defined edges and corners
> etc.
In the way you have defined "surface irregularities", neither is
lettering cut into a gravestone. You've forgotten your additional
criterion that the edges of these "surface irregularities" must be at
right angles to the surface.
>
> Obviously, when one is setting up a useful method for detecting
> artifact, one has to be careful to avoid the obvious pitfalls. That
> means excluding those things that would produce false positives right
> off the bat. Why else do you think I used a cube instead of an oval
> or a sphere for my primary example?
Can you provide an example of *any* object meeting your criteria which
could not be excluded by something as simple as carving your name onto
it?
>
> > > Again, you argue that this is not what anyone would call "statistical
> > > analysis".
>
> > No statistician, or anyone with even a passing familiarity with
> > statistic would call it that.
>
> Sure they would.
Provide a reference in that case. Or ask a statistician.
> Anyone who has any reliable or useful idea about
> anything uses at least some form of statistical analysis. Without
> such analysis to any degree, one could not have any opinion about
> anything to any useful or reliable degree whatsoever.
Go and get an education in statistics. This is pure and unmitigated
bullshit.
>
> > > But, it actually is. If you had absolutely no idea how to
> > > eyeball anything to any degree of certainty or measurement, you
> > > wouldn't be able to instantly recognize a highly symmetrical polished
> > > granite cube as artifactual.
>
> > You mean in the way people have recognised large pyrite crystals as
> > artifacts?
>
> As you know, I've gone over this many times now. Pyrite is not
> granite. The same shape that wouldn't be evidence of artifact in
> pyrite would be instantly recognized as artifact in granite.
So basically your "method" can recognise as artificial anything we
know in advance to be artificial.
You still haven't explained why such a method is of any practical
value.
>
> > This has nothing whatsoever to do with statistics. It's about shape
> > recognition, something humans are rather good at.
>
> It isn't just about shape recognition. It is about the idea that
> certain shapes, when recognized in certain materials, are not the
> result of non-artifactual processes.
So it's about shape recognition, not statistics.
>
> > > You'd have to go around actually
> > > measuring everything before you could detect artifact.
>
> > You have to examine objects closely and test hypotheses of manufacture
> > before you can identify an unfamilar object as an artifact.
> > Measurement has little to do with it.
>
> Not true. A highly symmetrical polished granite cube is instantly
> recognizable as artifactual without the need for any additional
> knowledge regarding manufacture or anything else.
How do you test this conclusion?
> All that is needed
> is some prior experience with the material of granite as it relates to
> various non-deliberate forces of nature.
And how do you test this conclusion?
>
> > > For close call
> > > cases you might have to do this. You don't have to do this when the
> > > degree of certainty is so extreme that you can instantly tell just by
> > > looking at the object or phenomenon.
>
> > Oh, please!
> > So you memorize all the numbers (which numbers, by the way?) from all
> > those objects (1000 objects, as I recall) which define it's shape in
> > great detail (for otherwise how would you be able to measure the high
> > degrees of accuracy you witter on about), and then perform statistical
> > calculations on them, and all in your head.
>
> > In a word, bullshit.
> > If you would like me to expand on that, complete and utter bullshit
> > which wouldn't fool a five-year old of moderate intelligence.
>
> You're simply denying the obvious Richard. You yourself have done the
> necessary observations and analysis in your own head to know that I'm
> right.
No, I haven't, and it's time you stopped misrepresenting me.
Do you think that I don't know how I decide if an object is an
artifact or not? I've explained it to you numerous times, but
evidently you either fail to understand, or are deliberately
misrepresenting me to deceive the lurkers.
Do you lack the ability to read, or are you simply dishonest?
> Perhaps you should ask Baldwin to explain how he is able to
> instantly recognized highly symmetrical polished granite cubes as
> artifactual?
He doesn't use your "method" either.
RF
>
> > RF
>
> Sean Pitmanwww.DetectingDesign.com
richardal...@googlemail.com
wrote:
> On Sep 4, 12:41 am, richardalanforr...@googlemail.com wrote:
>
> > On 4 Sep, 03:36, "R. Baldwin" <res0k...@nozirevBACKWARDS.net> wrote:
> > > The invalid claim is about having a METHOD. Nobody disputes being able to
> > > identify polished granite cubes as artifacts at a glance.
>
> > Sean's "method" reminds me of an old joke.
>
> > Two men sitting in a train compartment.
> > One of them is reading a newspaper. Every so often, he rips out a
> > page, crumples it up and throws it out of the window.
> > Eventually (this is England, after all, and we English are naturally
> > reticent) the other man asks him why he is doing it.
> > "It keeps the elephants away"
> > "But there aren't any elephants here!"
> > "Yes. It's very effective".
>
> Ah, but how do you know that there are no elephants in England? What
> "method" did you use to arive at this conclusion? ; )
>
> Likewise, what "method" do you and Baldwin use to quickly conclude
> artifact when you see a highly symmetrical polished granite cube?
Because it is an object of a class we know to be artificial.
Which part of that don't you understand?
> You
> have to have some sort of basis before you can make such a rapid
> conclusion - do you not?
Yes, it's membership of a class of objects we know to be artificial.
> How did you establish this basis?
>From a familiarity of objects of this class.
> How do
> you know it is a reliable conclusion if you used absolutely no method
> or even cursory statistical analysis?
This is not a case in which statistical methods are appropriate.
The recognition that they are members of a class of objects we know to
be artifacts is good enough. If there is any doubt, one can test
hypotheses of manufacture.
This has all been explained to you over and over again. What parts do
you not follow?
>
> Sometimes I don't think you English know why you do or think the way
> you do. You just do and think out of habbit without really thinking
> about it.
You think? There's a turn-up for the books.
Mind you, you evidently can't read, and have to rely on
misrepresentation to defend an indefensible position.
RF
>
> > RF
>
> Sean Pitmanwww.DetectingDesign.com
richardal...@googlemail.com
wrote:
> On Sep 4, 12:45 am, richardalanforr...@googlemail.com wrote:
>
>
>
> > > > You are misrepresenting me again. I have never made any such
> > > > statement. In fact, I have posted several links to papers which
> > > > demonstrate that the *lower* limit on the time required for such
> > > > preservation is a few hours, not "within an hour" as you originally
> > > > claimed.
> > > You originally fought long and hard arguing that the preservation of
> > > fish in the Santana formation was the result of autolithifying
> > > bacteria that preserved the fish and other creatures in a non-
> > > catastrophic manner as part of some anoxic lagoon.
>
> > The preservation of the Santana fish *IS* the result of autolithifying
> > bacteria!
>
> > Didn't you read the papers which I cited?
>
> Nothing that you have cited explains how cellular turgidity could be
> preserved by autolithifying bacteria.
Quite so.
> You argue that osmotic pressure
> does the job. How do you think osmotic pressure is maintained in fish
> gills after death? The loss of osmotic pressure is very rapid after
> death. That's the whole reason why preservation must be so rapid if
> turgid cells are to be preserved in their turgid state.
So you don't know what osmotic pressure is either.
UNANSWERED QUESTION #1
I suggest that you read the papers I have cited, and provide an
alternative model which explains the evidence better.
By the way, you have not provided *your* explanation for this
phenomenon. "Rapid burial, as in a flood" (or whichever variation on
that you are using at the moment) is *not* an explanation. If you
don't believe me, take a recently dead fish and dump a load of mud on
it Then check how well it is preserved after a few days.
You may need a gas mask.
>
> < snip rest, I don't have time for this >
That figures.
Running away again like the moral and intellectual coward you are.
I'll just put back some of the main points this time.
You haven't read the papers on the subject.
You know nothing about taphonomic processes.
You apparently do not understand the difference between a hypersaline
and a supersaturated solution
You have apparently never heard of osmotic pressure.
(You're a pathologist, for crying out loud! How the hell did you
manage to miss that much basic science?)
UNANSWERED QUESTION #2
So, please tell us: if it is not the processes which have been studied
in fossils and replicated in the laboratory and have been described by
the scientists who have actually done the research which produced this
exceptional fossilisation, what do you think caused it?
And please, don't imagine for one moment that "A flood" is any sort of
explanation. Floods produce turbulence which oxygenates the water, and
encourages the growth of bacteria which digest organic remains from
the water and from the sediments churned up by the flood. That's why
your home stinks to high heaven after it has been flooded. It's all
those bacteria busily feasting on anything they can find. It's why
turbidites - which is what geologists (you know, the scientists who
actually *study* geology rather than making it up as they go along)
call deposits laid down by floods - are rarely fossilferous. Floods
simply don't create suitable conditions.
MISREPRESENTATION ALERT!!!
> You brought up the Lagoa Vermelha fish
UNANSWERED QUESTION #3
Excuse me? I have never mentioned any "Lagoa Vermelha fish". Why do
you have this need blatantly to misrepresent me? Or are you so much in
the habit of making things up as you go along that you don't know that
you are doing it?
MISREPRESENTATION ALERT!!!
> and then argued that the
> Santana formation was the result of similar activity - i.e.,
> autolithifying bacteria. In other words, you originally argued that
> the Santana formation was not the result of sudden catastrophe.
I have never argued that the Santana fish were not the product of a
sudden catastrophe. Once again you are misrepresenting me. All I have
done is correct you mistaken idea that fossilisation ocured "within an
hour", which was based on an inadequate knowledge of the literature.
You have apparently accepted that it took rather longer than that.
Fine. There is no argument.
However, quite how the fact that the Sanatana fish were preserved
rapidly adds anything at all to your assertion that there was a global
flood is beyond my comprehension.
> What it doesn't do is pose a threat to my theory of a very rapid
> formation of the geologic column via a series of closely space
> catastrophic events.
The fact that most fossils are not exceptional, and that many
sedimentary structures could only have been laid down over very long
periods of time demolishes your theory. Then there is the radiometric
dating, the palaeobiological data, the astronomical data, the simple
Laws of Physics and most of the rest of modern science.
ARGUMENT FROM IGNORANCE ALERT!!!
> The evidence that is inconsistent with the long-age model is
> largely in the form of erosion problems (i.e., the general lack of the
> expected uneven erosion of exposed surfaces over millions of years of
> time).
The "evidence" you have invented, you mean?
The geological record is *full* of erosion surfaces. They are
ubiquitous. They are found all over the world in virtually every
formation.
There are three in this small part of Siccar Point alone:
http://www.winona.edu/geology/dynamicearth/Images/SiccarPointCloseup.jpg
Making things up as you go along, as you do, is no substitute for
learning about a subject.
ARGUMENT FROM IGNORANCE ALERT!!!
> Obviously, catastrophic fossilization is fossilization that is the
> direct result of sudden catastrophic conditions. I really don't know
> why I have to constantly define the obvious for you.
As this is a term you have invented, it's up to you to define what you
mean by it.
Fossilisation does not generally occur as a result of a catastrophic
conditions.
Floods don't produce many fossils, and certainly not well preserved
ones.
Asteroid impacts do not produce fossils. Being vaporised is generally
not a good start.
Volcanic erruptions sometimes produce fossils, but as volcanic
deposits tend to be highly acidic, in most cases all organic material
is destroyed leaving mouldic fossils such as the human bodies found in
Pompei.
Hurricanes don't produce many fossils.
Tidal waves don't produce many fossils.
Droughts can produce good fossils if mummified corpses are buried in
fine, windbourne sand, but these are very rare.
UNANSWERED QUESTION #4
So which types of "catastrophic conditions" result in exceptionally
preserved fossils?
UNFOUNDED ASSERTION ALERT!!
> Not true. Scavenging can occur during catastrophic conditions or
> during brief episodes of calm between shortly spaced catastrophes.
UNANSWERED QUESTION #5
So how do you explain the fact that most fossils come from deposits
which show a great deal of bioturbation, and that the overwhelming
majority are broken, damaged, worn and fragmented?
OUTRIGHT FALSEHOOD ALERT!!
> I have not changed my position on this matter. It is just that you
> misrepresent my position on this matter - despite repetitive
> correction.
As I have quoted you verbatim in a clear context, and not presented
your words in a misleading way, this is flatly untrue.
Your position on this has changed, as it has on the time scale over
which Sanatana fish preservation took place.
UNFOUNDED ASSERTION ALERT!!
>>On the other hand, most sedimentary structures show some
> > degree of bioturbation.
> Not true.
I'm sorry, but why should we believe you? You know bugger all about
geology.
Any textbook on geology will tell you that bioturbation to some degree
is present in almost all sedimentary rocks.
UNFOUNDED ASSERTION ALERT!!
> Most sedimentary structures do not show nearly the degree
> of bioturbation that would be expected if they formed slowly over
> millions of years.
I'm sorry, but why should we believe you? You know bugger all about
geology.
UNFOUNDED ASSERTION ALERT!!
> These shale beds did not form slowly by the annual or
> subannual accumulation of sedimentary layers.
And your evidence for this is....? Or are we simply expected to take
your word for it?
UNFOUNDED ASSERTION ALERT!!
> Rather, they give clear
> evidence of very rapid, even catastrophic, formation.
And your evidence for this is....? Or are we simply expected to take
your word for it?
UNFOUNDED ASSERTION ALERT!!
> The same thing
> is true of your anoxic lake bottoms and lagoons.
UNFOUNDED ASSERTION ALERT!!
> No such place is
> present in the world today preserving anything like what we find in
> the fossil record - like the Santana formation etc.
Why should we expect to? It was an exceptional event leading to
exceptional preservation.
UNFOUNDED ASSERTION ALERT!! AND
DISPLAY OF IGNORANCE ALERT!!
> Large creatures
> in particular are not preserved today without near complete scavenging
> and bioturbation over a relatively short period of time.
Large creatures in the fossil record almost always show some degree of
scavenging, and the overwhelmingly vast majority are disarticulated
skeletal components.
By the way, fossils don't show bioturbation. Sediments do. For someone
pontificating on geology this is a rather elementary error.
EVASION OF ISSUE ALERT!!
> You've wrote:
> "I've invited creationists on numerous occasions to point out any
> mistakes I have made in assesing statements on those sites as false,
> and even offered to humiliate myself in public if even a small number
> can be found. No creationist has tried to take up this challenge.
> Their only responses have been to ignore the challenge completely, or
> to resort to ad hominem attacks. I can only assume that creationists
> are liars."
> Again Richard, I've challenged many of your notions many times.
You have not tried to show that the statements I identify on those
sites as false are not false.
MISREPRESENTATION ALERT!!
> Yet,
> because you are not convinced by my arguments you don't just say that
> you think I'm wrong or even way off base. Rather, you feel the need
> to go even farther and judge my motive by calling me a liar?
I call you a liar because you make statements which you must know to
be false with the intent to deceive.
Or do you expect me to believe that a pathologist who has co-authored
scientific papers is so ignorant that he thinks that one carry out as
statistical study without a data set of numbers?
OUTRIGHT FALSEHOOD ALERT!!
> Why the
> need to paint those who disagree with you as evil lying slimebags?
I don't. I have not done so, and once again you have misrepresented
me.
I have never called you evil.
I have never called you a slimebag.
I have called you a liar not because you disagree with me, but because
I think you are lying.
The fact that I have had exchanges with other creationists which have
been heated at times and have not called them liars, not labelled them
as evil, and not called them "slimebags (your word, not mine) is proof
of this.
OUTRIGHT FALSEHOOD ALERT!!
> You yourself have carried out the same
> methodology as I have.
No I haven't. Please stop telling me what I have and have not done.
Looking at a pile of rocks and getting a gut feeling about how they
were formed is not a methodology.
UNSUPPORTED ASSERTION ALERT!!
> I think the same thing about your arguments - most of which are
based
> on plenty of smoke and hand-waving with little substance.
So where are the flaws in the numerous papers I have cited in support
of my arguments?
Which of my arguments are not backed up with solid evidence?
OUTRIGHT FALSEHOOD ALERT!!
> This
> "point" of yours is nothing more than a difference of opinion on what
> constitutes useful or weighty evidence.
No, it's not a difference of opinion. It's a fact. When it comes down
to it, you have nothing other than unfounded assertion to support your
arguments.
PATHETIC ATTEMPT AT EVASION ALERT!!
> This is like former Pres. Clinton asking for the definition of
"is".
> If you don't understand what the term "catastrophic fossilization"
> might mean, there really is no point in discussing much of anything
> with you.
As it is a term you have invented (and if I am wrong, please provide a
citation from the scientific literature which uses it), it's meaning
is by no means clear. As catastrophic conditions are *not* in general
suitable for fossilisation to occur, and that there are numerous
different ways in which fossils can be formed, none of which is
particularly associated with catastrophic conditions, it is perfectly
valid to call the term meaningless.
UNANSWERED QUESTION #7!
> What I do doubt is your ability
> to think critically and rationally on your own.
Well, the academic staff of Leicester University who allowed me to
study for my PhD don't, and neither do the editors of the scientific
journals in which I have published my research findings. Nor do the
palaeontologists who have attended symposia at which I have presented
by findings. In fact, several have said that they enjoy my talks
because they contain original ideas which make them think differently
about what they are doing.
What do you know that they don't?
EVASION, MISREPRESENTATION AND OUTRIGHT FALSEHOOD ALERT!!
> Sure, one
> or the other is wrong, but that by no means supports the ludicrous
> notion that all those who have been mislead are dishonest or in any
> sense evil.
I'm not talking about those who have been misled, and have made this
clear on many occasions. I have never labeled anyone as "evil". I have
specifically labeled *you* as dishonest because you have made
assertions which I think you know to be false, and persist in making
such assertions.
Why do you need to misrepresent me in this way? And rather than
posting a snappy answer, why not ask *yourself* that question?
> Sean Pitmanwww.DetectingDesign.com
RF
Ron O
0catch.com> wrote:
Did you really respond to my post in detail? All the little lies just
keep rolling along, don't they? Wouldn't you just rather have an
argument instead of having to lie about it constantly? What happened
to owning up to your claims? Snipping and pretending isn't answering
anything in detail is it?
>you still don't seem to have
> grasped the difference between a minimum structural threshold
> requirement and a gap distance. They are not the same thing. A
> minimum structural threshold is NOT related to any starting point
> either. It is what it is. A system requires a certain minimum
> structural form before it can work regardless of how it came to be.
> If that structure is realized, the system will work. Otherwise, it
> will not work. The greater this minimum structural requirement, the
> less the odds are that this requirement will be within one or two
> mutations of what already exists within any gene pool. Sure,
> increasing the size of the gene pool will help, but for every increase
> in the minimum structural threshold requirements, the needed increase
> in gene pool size to keep the gap size the same is an exponential
> increase. Pretty soon, the environment cannot support the needed
> population increase and so the minimum gap size starts to increase in
> a linear manner with each increase in the minimum structural threshold
> requirements. This means that the gap size will always be smaller
> than the threshold size.
What Sean means here is that he doesn't know what his argument is. It
isn't a gap, but it is a gap, but no it isn't a gap, but it relies on
all the little gaps that have to be crossed to get the final system up
and functioning.
Just face it Sean this is just a stupid rendition of Behe's bogus IC
argument. In the end Behe couldn't tell anyone what IC was, but it
looks a lot like your threshold argument. All the parts have to work
together, they all have to have a certain sequence or minimum "fit" so
that they are "well matched." Behe calls the flagellum IC doesn't
he? He can't tell anyone why it is IC, but it just is. You claim
that the flagellum has a 1000 aa threshold that can't be crossed, but
you can't tell anyone what this threshold is and it seems to devolve
into the stupid probability argument that IC became. Behe even tried
to claim that the more parts a system had the more IC it was, but he
never could tell anyone how many parts were needed to make it his kind
of IC. Why isn't your argument just the stupid creationist
probability argument, except for the fact that you don't know what you
are trying to calculate the probability for?
When you try and explain this threshold it turns out to be all the
little gaps needed to join the complex together, but you can't tell
anyone what the gaps are or if they even existed for a specific
sequence at the time the flagellum was evolving. You might claim that
it is all the gaps needed to have the final product and that it isn't
the same as jumping single gaps because all the parts have to work
together, but isn't that just Behe's failed IC argument? IC did fail
and you know it because you never put it up as part of the science
that you would have taught to school kids. It turned out to be either
a stupid mistake or just something to scam the rubes with to get them
in line to support other dishonest political bull pucky.
Tell us why Behe's argument failed and why yours is better than that
failure.
>
> And, there you have it. Although the gap size and the threshold size
> are not the same, they are related to each other. You will not
> understand my position until you are able to grasp these basis
> concepts:
Sure they aren't the same, the threshold is just all the gaps strung
together. So what kind of threshold is it? You claim that all 1000
aa do not have to evolve all at once, so why is this a problem for
biological evolution? This is just the stupid creationist probability
argument with an arbitrary number of 1000 tacked onto it and you can't
even tell anyone what the probability of getting those 1000 residues
together is. It is just a very low number to you. Just like 1000
sounds big enough to do the job of obfuscating the issue. It just
doesn't fly
What was the gap that had to be crossed as part of this threshold for
the ATPase to function in the flagellum or its precursor? Demonstrate
that you can tell anyone that this gap existed, and why crossing it is
a problem for biological evolution. Then go to the next gap of how
the tail structure formed. What gaps are part of your threshold and
when did they exist?
>
> 1. The minimum structural threshold size is the minimum structural
> requirements needed to produce a particular type of functional system
Sean speak for all the little gaps strung together.
>
> 2. The minimum gap size is the mutational distance between what exists
> in a gene pool and what might exist as a beneficial system if it were
> ever found by random mutation.
But the threshold isn't a gap, it is only a gap when I want it to be a
gap.
>
> 3. The gap size is always smaller than the threshold size.
Because it is just all the small gaps strung together.
>
> 4. The average gap size increases with each increase in structural
> threshold requirements.
Sean speak for I don't know what the threshold is and I'm just bull
shitting so I can make any claim that I want to.
>
> 5. The minimum gap size does not increase until the population size
> remains static and until the number of genetic elements within just
> one mutation of a beneficial target drop to one. At this point, the
> increase in the gap distance follows a linear relationship to the
> increase in the minimum structural threshold requirements.
Sean speak for I know I'm talking about gaps but the threshold isn't a
gap. So who cares? It sounds good so I'll use it to snow anyone
stupid enough to not know the difference.
>
> > > > And again, the fact that such a reference does not exist means what?
>
> > > It means that based on the information that does exist, the hypothesis
> > > of a 400aa threshold has the most support. You may argue that future
> > > information is likely to reveal a much smaller threshold. That isn't
> > > science Ron. That's an unsupported hypothesis that isn't even
> > > falsifiable this side of eternity. You could always argue that this
> > > or that hypothesis could be wrong given some future discovery. That's
> > > always a possibility in science.
>
> > This is stupid. The whole point is that no one has systematically
> > looked for the lower limit so you can't claim 400aa with any degree of
> > certainty worth spit. It doesn't matter what people haven't done it
> > is what they have done and the conclusions that you can make from
> > those studies. You can't go on about some minimum when they haven't
> > looked for it.
>
> You can certainly get a rough idea that different types of systems
> have very different minimum structural threshold limitations and that
> those with larger minimum requirements are much harder to evolve.
> What you are trying to do is deny everything based on some lame notion
> that because these limitations have not been exhaustively defined that
> the whole concept is completely meaningless. You're just trying to
> ignore the obvious. It is overwhelmingly clear that different types
> of functionally beneficial systems have different minimum
> requirements. It is also overwhelmingly clear that evolution works
> very well to produce systems with very low minimums (i.e., a few dozen
> fairly specified residues or less), much less commonly for systems
> that require at least a few hundred fairly specified residues (i.e.,
> lactase, nylonase, etc), and not at all for systems that require over
> 1,000 fairly specified residues (flagellar motility, DNA
> transcription, etc).
Sean speak for I don't know what I'm talking about, but it sounds
good.
What are those 1000 fairly specified residues in the flagellum and why
aren't they gaps? Why don't they all have to evolve at once, but you
treat them like they have to all evolve at once for your argument to
make sense. What happens to this argument if all the 1000 fairly
specified residues come together one or two at a time over a couple
hundred million years?
Why was it that one of the reasons that ID scam artists flagellar
argument failed is that they admitted that to make their argument
valid that they would have to determine that all biologically relevant
pathways to evolving the flagellum were just too improbable to have
occured? Since they couldn't even calculate the probability of a
single biologically relevant evolutionary path the argument became
bogus. They only kept on about the flagellum to shill the rubes so
that they could run the bait and switch on them. Sean found out about
that after Ohio, but he still couldn't bring himself to admit that ID
had just been a bogus scam, and made claims that he had the science to
teach about ID even if the other ID creationist scam artists had given
up.
Sean, why is it that you have never made good on those claims? What
was the science of ID that you would have taught to school kids. You
wouldn't have wanted to lie to them would you?
>
> > > > Has anyone ever made a very extensive push to develop lactase function
> > > > and determine the minimum? No. So what does it mean when you try and
> > > > use that argument to claim some minimum. Not only that, but even if
> > > > the minimum was 400 your argument still doesn't work because of Hall's
> > > > work and his success. Not his failures, but his sucesses. Why did he
> > > > ever succeed if you are right about 400 anythings?
>
> > > I've already told you. The 400aa size requirement isn't the only
> > > aspect of the equation. The minimum specificity of amino acid residue
> > > arrangement is also in play. Proteins, to include those that have the
> > > lactase function, are not perfectly ridged structures. A certain
> > > degree of sequence flexibility is available without a complete loss of
> > > the function in question - i.e., lactase in this case. However, all
> > > protein based systems have a certain limit to the degree of
> > > flexibility beyond which the function in question cannot be realized
> > > at all - not even a little bit.
>
> > Demonstrate that this means that functions can't evolve. Why can't
> > you? How do antibodies work if you are right? Why does your immune
> > system work nearly every time? Why can you generate antibodies to
> > synthetic antigens that have never been seen in nature and do it
> > consistently? You obviously don't know what you are talking about and
> > your limits aren't the biological limits or you would probably be dead
> > of some disease by now.
>
> You do understand how antibodies work - right? Antibodies almost
> always work because the size of sequence space which must be covered
> to produce a highly effective immune system is relatively small. As
> far as antigens are concerned, the total number of possible epitopes
> is 20^B since there are 20 different amino acids. Well, the typical
> length of an antigen epitope ("B" in the preceding formula) is about
> 20 amino acid residues. So, the total number of possible antigen
> epitopes is about 20^20 or 104,857,600,000,000,000,000,000,000 or
> ~100 trillion trillion.
Actually this is an over estimate because the antibodies have specific
start points that are highly variable when they splice all the
possible sequences together, but it isn't even close to this number
that is available to any immune system of a single organism.
>
> That sounds like a big number doesn't it? Since there are trillions
> of different possible antigen epitopes, how does one's immune system
> cope with such a variety of potential enemies? Well, there are many
> immune cells produced by the body. In humans, in particular, about
> 10^12 lymphocytes are present at any given time.
10E12 is just a maximum number of lymphocytes that might have
participated in the immune response over the few days or weeks that it
took to select the final antibody that did the job. It is a serial
selection over several generations of cells placing more mutations in
the sequence that was selected for amplification. This is the maximum
number of sequences that could have possibly been tested.
>
> Not all the T-cells have different Y-shaped receptors, but many of
> them do. Chances are that if enough non-self enemies get into the
> body at least one of the immune cells will recognize the non-self
> marker sequences or "antigens" located on this invader as "foreign" to
> at least some useful degree. The odds that a single T-cell will
> recognize a random epitope to at least some useful degree is about 1
> in 10^12. So, does this mean it would take a trillion different T-
> cells to cover all possible invaders? Well, no. The reason is
> because an average cell or foreign invader "bug" has about 10^12
> different epitopes. So, on average, a single T-cell will recognize at
> least one of the potential antigen epitopes of a foreign invader.
Sean forgets that the immune response doesn't rely on the number of
possible epitopes it works even when a single synthetic antigen is
used to induce the response. Only a single target that may have never
been seen in nature before and it still works.
>
> That is how the immune system works in a nutshell. And, that is why
> immune system "evolution" really isn't very high level. It is working
> in a relatively small "sequence space" of just 20^20. This is not
> true when you start talking about sequence spaces greater than
> 20^1000.
That is Sean in a nutshell. But how can you tell the difference
between a nut and Sean? The point that Sean ignores is that a very
few sequences have to be searched to select for the desired result. A
number so small that it makes Sean's little gaps and sequence of gaps
to create his 1000 pretty insignificant. I'm not saying that it is
all cut and dried, but Sean doesn't have an argument and he knows it.
He just won't admit it.
The amount of sequence space needed to be tested is such a small
number 10E12 max number of sequences that Sean can't even begin to
figure out what his 1000 aa threshold means.
Sean, just do this. Calculate your minimum threshold that has to be
crossed to get antibody function if you can get it in only 10E12
sequences or less. It has to be a threshold that would always be met
in that number of attempts, not just the simple probability of
stringing a minimum number of residues together.
>
> For further information concerning immune system "evolution" see:
>
> http://www.detectingdesign.com/immunesystem.html
And if you believe that you will get anything but obfuscation and crap
out of Sean about it you are dreaming. Do you still have your bogus
emperor with no clothes scam up on the web page? If science has no
clothes what do you have? Where is that evidence for your alternative
to common descent?
I have to go, but I'll just SNIP this junk and go to Sean's best
argument.
> < snip useless pejoratives >
This is all Sean can do. He can't face the issues so he has to
pretend that they don't exist. He has to lie to himself constantly
about it. He has to do it in such a way that no one that knows what
he snipped has to wonder why he won't put up or shut up. He made the
claims, but he has never made good on them. They aren't just any old
claims they are the heart of his existence. His own web site caters
to the intelligent design scam. He took the name when he might have
been clueless enough to believe that it wasn't a scam, but he knows
better, now because he refuses to put forward the science of ID that
he would have taught to school kids. He knows that this science never
existed, but all he can do is snip and pretend.
You'd think that for all the bogus obfuscation Sean attempts that
there must be a reason for his obfuscation, but he claims to have an
alternative to common descent and the evidence to back it up that is
as good as the evidence that science has for common descent, but
somehow he would rather snip and pretend than make good on such a
claim. What is all Sean's bluster for if he doesn't have an
alternative? Does anyone really believe that he is doing it just to
expand the horizons of science? If that is true, why is he still
backing the dishonest ID scam when even the ID creationist perps are
running a new scam?
Such is Sean's dishonesty.
Up this thread Sean posted that all creationists were liars, but that
isn't true. Only some creationists are liars and Sean is in that
group. He knows it, but he'd rather pretend otherwise. In effect he
even has to lie to himself.
Instead of snipping and pretending, why not put up or shut up?
Ron Okimoto
>
> > Ron Okimoto
>
> Sean Pitmanwww.DetectingDesign.com
hersheyh
wrote:
IOW, one must have knowledge, using this particular type of material
and making this particular type of artifact, how a *known* intelligent
agent would manufacture that artifact so that it looks different from
any known process by which nature in the absence of that manufacturer
would work.
Given your complete inability to demonstrate the existence of a
*known* intelligent agent and knowledge of his method of manufacture
for biological systems and your complete inability to even tell us
what size gaps *must* be crossed, you are bullshitting when it comes
to making your obviously flawed argument by analogy.
> It doesn't matter how rough the methodology
> allows one's estimate to be. There must be at least some experiencial
> basis with statistical relevance before anyone can be remotely able to
> recognize even a very highly symmetrical polished granite cube as
> artifactual at all much less at a glance.
IOW, you must already *know* that such artifacts are manufactured
artifacts by known intelligent agents before you can tell they are
artifacts.
>
> Sean Pitmanwww.DetectingDesign.com
hersheyh
wrote:
And how, pray tell, do you calculate that range? You keep asserting
without evidence that there is a linear relationship between gap size
and total size, yet have never (NOT ONCE) presented an equation with
an empirically valid estimate of the slope. That means that the
"clear range" is nothing but a bullshitting hand-waving number that
you plucked out of yer arse. You cannot *even* tell us what
*specific* function cannot possibly arise by evolutionary mechanisms
with enough specificity to make it anything but hand-waved assumption.
> One particular parameter is most striking. That is, the
> evolution of novel beneficially functional biosystems.
Since you explicitly exclude what evolution *really* does, produce
'new' function by *modification* of old structures with related
functions, it is hard to know exactly what you regard as "novel
beneficial functional biosystems". After all, the production of the
function of rotary motility can be accomplished in one step by
formation of a chimeric protein without *any* change in the function
of any of the other subsystems or proteins. The only "new" or "novel"
feature is exactly what is being moved. To change a cortisol receptor
into an aldosterone receptor takes precisely two mutational steps and
can be done with an intermediate that has *both* functions. In fact,
very often evolution produces new function (like the beta globin of
hemoglobin) by duplication and specialization to the point where it
becomes IC. That certainly is the case for the different whip
proteins of the eubacterial flagella.
> The non-
> deliberate mechanism of random mutation and function-based selection
> (otherwise known as natural selection) is able to evolve new systems
> very commonly and often very rapidly whenever they are needed - like
> during rapid environmental changes or the addition of a new nutrient
> or toxin to the environment. What is interesting though is that out
> of all the cases where novel systems have been observed to evolve,
> those systems with novel functions that evolve most commonly and most
> rapidly have few size and/or sequence specificity requirements (i.e.,
> less than 100 fairly specified residues).
Well, duh. That is also exactly what happens in the formation of the
'novel' rotary motility function by formation of a single chimeric
protein linking the pore + whip substructure and the motor
substructure (with neither of these changing their functions except
for the way that they are linked). In fact, such an event produces a
*loss* of information and not a *gain* of information, since the
chimeric protein has fewer aa's than the sum of the two ancestral
proteins it was derived from. One mutational event, large phenotypic
difference with selectable consequences.
And now you suddenly go from describing the entire size as important
to looking at only the parts that interact with the toxin or
substrate. Now the size that is relevant is only that part of the
cortisol receptor that needs to change to modify it into an
aldosterone receptor (without change in any other part). Now it is
only the one aa of the one protein in the ribosome *system* of
thousands of aa's that needs to change to produce resistance to
streptomycin. So that neither of these *modifications* of existing
systems that results in a change in *function* is what *YOU* mean by
'novel'. BTW, the resistance to strep is a perfect example of the
ignorance of your argument. Ribosomes contain thousands of aa's in
its 20 odd associated proteins. Thus it is a *system* that is at
least as complex as the eubacterial flagella. Yet it acquires a new
or novel additional function that it did not have before (resistance
to streptomycin) by a single point mutation in one of the proteins.
And, of course, it can be demonstated that the rRNA has some protein
synthetic ability all by itself; the proteins are merely assisting and
making the process more efficient in a quantitative sense.
Quantitative optimization, of course, is exactly where variation and
selection works best.
> Those systems that have
> minimum structural requirements of a few hundred amino acid residues
> evolve much less commonly. And, amazingly, systems that require a
> minimum of more than 1000 fairly specified amino acid residues (or an
> equivalent of 1000 codons of DNA) have never actually been observed to
> evolve. There isn't a single reported case in all of scientific
> literature beyond the 1000aa level.
>
> The whole pattern demonstrates a clear exponential decline in
> evolvability with increasing minimum structural threshold requirements
> until the non-deliberate non-artifactual evolutionary mechanism
> completely stalls out well shy of the 1000aa threshold. I find that
> most intriguing because there are a large number of biosystems that
> require far more than a minimum of 1000 codons of DNA to be realized.
> The flagellar motility system, for example, requires over 10,000
> codons of genetic real estate at minimum before the motility function
> can be realized at all.
> None of the proposed steppingstones along the
> pathway of flagellar evolution have ever been demonstrated to evolve
> in the laboratory or anywhere else.
And you are wrong about that. I have explicitly proposed that *the*
step that produced the powered rotary motility arose by formation of a
chimeric linker protein between *pre-existing* subsystems and
demonstrated that such a process can be observed *experimentally* in a
model system that includes both a model for the rotatable pore and a
model for the motor. We know for a fact that more than one type of
*pre-existing* rotatable pore can be conscripted into use as a whip
and more than one type of *pre-existing* motor can be conscripted into
use as a motor. And both types have relevant potential linker
proteins. And, *experimentally*, the formation of a linker that is
*different* from the original linker (in fact, during the course of
the experiment, two *different* linkers formed by mutation) that
produced the 'novel' (it did not exist before the mutation) function
of rotary motility occurred. Both involved a single mutational step.
> And, what is most interesting, is
> that all of the proposed steppingstones are separated from each other
> by differences that would require several dozen mutations, at minimum,
> to link them up properly to achieve the next beneficial step in the
> flagellar evolution pathway.
That is flatly false. Not only has a proposed quite relevant
steppingstone to produce the *function* of rotary motility been
proposed that only requires a single step, it has been demonstrated to
be a real potential step by use of a model system that actually
generated the function in a single mutational step.
> While a gap of just 30 or 40 non-beneficial, even neutral, mutations
> might not seem like a big deal, such a gap would take a population the
> size of all the bacteria on Earth trillions of years to cross - on
> average.
If you knew a damned thing about this, you would know that neutral
mutations are essentially irrelevant to generating a new function
unless they, by chance, made subsequent selective mutations useful.
And nothing, not selection or any other process, can prevent the
fixation of different neutral mutations in different lineages. That
may mean that only species A has the potential to produce novel
function X, but, in fact, novel functions are quite rare. Most
functions are transmitted by vertical descent, not by neoformation.
The specific eubacterial flagella's rotary motility *function* only
evolved *once*. It only needed to evolve once. All the different
eubacterial flagellae in existence today were generated by vertical
descent (and probably some horizontal transfer, since these are
bacteria), not by new formation. The niches where such flagella are
functionally selected for have been filled by species that received
their flagella by descent, not by mutation to produce the flagella
once again from scratch.
Given that it can be *experimentally* demonstrated that the minimum
number of mutational steps required to produce the rotary motility
*function* (although not necessarily the *modern* eubacterial flagella
-- subsequent mutation would clearly optimize the function, once a
selectable level of function existed, from its original suboptimal
state) from systems that already exist in eubacteria in a number of
variant forms and that such an event need only happen once in *some*
ancestral bacteria, you need to present more evidence that it cannot
possibly happen.
The fact that the same sort of co-option of similar, but not
identical, subsystems in archae (and possibly even different motors in
eubacteria -- some eubacterial flagellar motors run by Na+ ion
transport rather than H+ ion transport) occurred demonstrates the
nature of the co-option to produce the rotary motility *function*.
And the size or even the structure, much less the sequence, is
irrelevant. All that was required to produce the *function* was the
availability of a rotatable pore and a motor subsystem and conditions
that allowed the formation of a linker protein. That is for *both*
the archaean and eubacterial flagellae. The model system I have
described *experimentally* demonstrates how such a linker can be
formed. That does not mean that every species of bacteria will be
able to do so. The formation of the linker would require
idiosyncratic positioning of genes or unforseeable events like
illegitimate recombination or entry of a partial gene via a virus.
But a requirement that *every* species of bacteria be able to produce
the linker and generate a selectable level of rotary motility is
unnecessary because these systems only need to be produced and (more
importantly) selected for *once*.
> Clearly then, the existence of such a system seems well
> beyond the abilities of any known non-deliberate process of nature to
> explain.
Actually what seems to be beyond your ability to produce is the
reasoning that leads you to think that there is a linear relationship
between total size and the 'gap size' needed to generate the novel or
modified functions that have actually occurred in nature. I still
anxiously await your explanation and evidence for that. BTW, in case
you don't know what a linear relationship is, it is y = bx + a. In
this case, a certainly = 0, so the relationship is really y = bx. b,
the slope of the line that describes the relationship between gap size
(y) and total size, or minimum threshold size, (x). It must be
determined empirically, I believe. You claim to have this
information. Where can I find it?
> This suggests that it is at least reasonable to consider the
> potential of deliberate artifact in the construction of the flagellar
> motility system as well as all other systems that require more than
> 1000 fairly specified codons at minimum.
Now I have just described two such large 'systems' and
'functions' (the ribosome's resistance to streptomycin function and
the eubacterial flagella's rotary motility function that can, in
principle and with experimental evidence to support that idea) that
appear to contradict your assertion. You keep asserting that the
reason my descriptions are impossible is because of the linear
relationship between minimum threshold size and gap size. But I have
yet to see you present any evidence in support of this supposed linear
relationship. Despite my repeated requests. All you do is snip out
those requests.
>
> Sean Pitmanwww.DetectingDesign.com
gregwrld
I noticed Sean also ignored your request to analyze a set of objects
by his
statistical "method".
Seems like Sean's science is all in his head which makes it as good
as any
fantasy can be, no?
Sean doesn't publish because Sean has nothing to publish.
gregwrld
<snip>
hersheyh
wrote:> > On Aug 23, 7:02 pm, Seanpit <seanpitnos...@naturalselection.
>
> > 0catch.com> wrote:
> > > On Aug 23, 1:49 pm, hersheyh <hershe...@yahoo.com> wrote:
>
> > > > > I'm not talking about changes Ron. I'm talking about an absolute
> > > > > number of amino acid residues that have to be in a specified
> > > > > all.
>
> > > > IOW, evolution is not about *change*. It is about *size*.
>
> > > It's about both. It is about changes producing functional systems
> > > that have different minimum structural size and specificity
> > > requirements.
>
> > No. Evolution is about change, not size. Change in *function*.
> > Generation of new *function*. The fact is that evolution is highly
> > conservative of *structure* and *size* and *specificity* when it
> > generates new *function*.
>
> We are talking about evolving functional systems that require greater
> minimum size requirements. What are the odds that any such
> potentially beneficial larger system would be evolvable? Are the odds
> the same as they are for smaller potentially beneficial systems?
> That's the question at hand here - as you already know.
>
> > Not that larger sized proteins are all that hard to make in single
> > mutational steps. They are not made, as you seem to think, by adding
> > one aa at a time to some non-functional imaginary protein.
>
> You're building the strawman you always build - yet again. Why do I
> have to constantly remind you that I do not suggest that larger
> systems need to be built one amino acid at a time? Use any type of
> mutation and pre-existing system available. The odds of success are
> exactly the same as a random walk of just one amino acid change at a
> time.
This is an absurd argument. It basically is saying that *if* one
starts with two functional moieties that are positioned with moiety B
downstream from moiety A such that a single deletion can bring the two
moieties into the same rather than different proteins to produce a new
function (there is often flexibility wrt to how far apart in the
proteins the two moieties can be and still have the new function) that
the odds of producing this single deletion is exactly the same as
generating moiety B (which already exists in the cell) by a random
walk of one aa change at a time. Let's say that to make such a change
one needs to first knock out the stop codon at the end of the protein
that encodes A. Now you have a more or less random sequence of
sufficient length. Then one has to randomly change 20-30 amino acid
sites to get anything close to the function of moiety B (which already
exists elsewhere in the cell). This of course makes perfect
creationist math. One mutation (a single deletion) is the same as
dozens of mutations. 1 change = at least 40 changes in creationist
math and that is even assuming that the 40 changes are each
selectively more useful than the preceding variant.
> There is no advantage in blindly taking large vs. small steps
> into sequence/structure space.
There is a distinct advantage in blindly combining functional moieties
that already exist in an organism into new combinations rather than
inventing them *from scratch* in situ by a completely random process.
You would have to be completely ignorant to claim that the odds of the
two processes are exactly equal. Oh, sorry. You *are* that
ignorant. You *do* make that absurd claim.
> All that matters is the relative
> density of potentially beneficial targets in that space.
That assumes that the targets are reached by a random walk one aa at a
time, not by combination of pre-existing functional elements nor by
searching space near pre-existing functional elements for related
functions. It also assumes, falsely, that only one possible island of
function in total sequence space exists for any given function.
Potentially useful targets not sufficiently nearby simply will not be
found. The functions that *do* exist in life were those that *were*
sufficiently close to be reached by one of the known processes. The
functions that do not exist in life are likely those that cannot be
reached by one of the known processes.
And, again, your argument that combining pre-existing functional
elements or modifying already existing functional elements to produce
new function
> That is the
> only thing that determines the average number of mutations needed to
> achieve success.
Only if one is completely ignorant of the actual mechanisms by which
new proteins have been made. And only if one is so ignorant that he
or she thinks that the *average* number of mutations starting from
some random position in some specified sequence space is relevant.
Oh, sorry. You *are* that ignorant.
> As it turns out, the density of potentially beneficial sequences and
> structures declines exponentially when one considers larger minimum
> structural threshold requirements.
You have no evidence to support this statement. And again, this
statement only makes sense if one assumes that one starts somehow with
some random sequence and procedes randomly to some other sequence by a
random neutral walk.
> < snip >
>
> > But you really don't seem happy with the fact that most proteins are
> > too small, so you then look at aggregations of proteins (such as
> > ribosomes or flagella) and treat them as if they were a single
> > protein.
>
> I treat such systems as if they were a single system whose function is
> dependent upon a minimum number of them being in a particular
> location.
IOW, you are bullshitting us when you talk about function. Every
protein (and even subprotein moieties) in, say, the flagella serves a
*different* function. FliG, for example, serves the function of
linking the motor and the rotatable pore. That is the only function
it performs. I have told you how such a protein, one that links a pre-
existing motor to the rotatable pore, can be produced in a single
mutational step. Proteins do not have a single *function* and its
global function is usually a consequence of different subfunctions.
> > The fact is that duplication and divergence (especially
> > subfunctionalization, which only requires loss of function) are common
> > events. Once one has duplicates that have either become subfunctional
> > or neofunctional, the size of the complex would, according to you have
> > doubled.
>
> But the minimum requirements would not have doubled. Once the minimum
> threshold requirement is reached, further modifications are not a
> problem.
But all the minimum threshold requirement is is the size of the
smallest protein that can perform a function. A subfunctionalized
protein typically requires the same number of aa's as the original
protein. Neofunctionalized proteins typically do.
> > But without any *change* but a duplication and a different
> > *loss* of partial function in both of the genes. Over time, of
> > course, such subfunctionalization can lead to irreducible complexity.
> > But, of course, you have a teleological mindset and assume that
> > proteins can only do one thing, their teleological function. You hold
> > that despite knowing that a flagella which is immotile can still
> > transport proteins outside the bacteria.
>
> The transport function has a far smaller minimum threshold requirement
> compared to the flagellar motility function. Maintaining subfunction
> does not remove the fact that the flagellar motility function is still
> irreducibly complex in that it still requires a much higher minimum
> structural threshold to work as a system of flagellar *motility*.
Which, as has been pointed out, can be acheived by generating a hybrid
linker protein that links the motor and the rotatable pore with the
loss of aa information.
> Kenneth Miller also makes this very same mistake. He thinks that
> showing intact subsystems means that the flagellar motility system is
> therefore "reducible". It isn't. It still requires the same minimum
> threshold that it ever did.
And the way to produce that threshold can be by the loss of existing
informaton in the process of producing a linker protein. Or do you
deny that there is a *single* protein that links the motor subsystem
to the rotatable pore subsystem? One does not need to change
thousands of aa's or even a few dozen to produce that *single* linker
protein. One only needs to modify *existing* proteins.
> This key "argument" of Miller is just
> silly and I'm very surprised that so many people fall for this blatant
> nonsense. It is like suggesting that the motility function of a car
> is "reducible" by showing that the lights still work when the engine
> and drive shaft are removed.
The engine and transmission exists and works. The chasis and wheels
exist and are moveable. All one needs to do is to link the two. That
is, one needs to hook up the drive shaft (which was connected to a
different system).
> < snip >
>
> > > You may argue that evolution
> > > doesn't require this to happen and that's true. However, you
> > > evolutionists believe that it happened very commonly throughout a span
> > > of only 4 billion years or so.
Au contrarie. It happened relatively rarely throughout the span of 4
billion years or so. The number of rotary motility systems produced
by evolution is two (there has been massive subsequent variations on
this system). The number of whip-like cilia/eucaryotic flagella is
one. The number of actin/myosin based sliding contractility motility
is one. In each case, the motility system that evolved did so by
modifying pre-existing systems, not by poofing some entirely new
system into existence. Evolution does not poof things into
existence. That is what *you* creationists claim happened.
> > > How could systems with very high
> > > minimum structural threshold requirements have evolved?
>
> > I've told you how larger proteins can be made. Proteins *like* to
> > interact with each other, so explaining aggregation of proteins is not
> > too difficult. Most interactions vary in strength.
>
> The problem isn't getting proteins to stick together to form larger
> protein complexes. The problem is in getting them to stick together
> properly so that a higher-level system is produced in the union - a
> system that has a larger minimum structural threshold requirement.
When the new mutational variant's sticking together is dysfunctional,
selection will ultimately prevent it. When the new mutational
variant's sticking together is functional (wrt reproductive success),
selection will favor it. What's the problem?
> > > You simply
> > > state that when evolution happens it happens because the gaps were
> > > small. I couldn't agree more. The problem is with your notion that
> > > small gaps sizes could easily exist with minimum structural threshold
> > > requirements at 1,000aa and far beyond. That's the problem. You
> > > think the *likely* gap size is the smallest possible gap size (i.e.
> > > "one") regardless of the minimum structural threshold requirement for
> > > the functional system in question.
>
> > Yes. That is the problem. But as I see it, the problem is that you
> > have not presented any evidence to support the hypothesis that the
> > systems that have evolved and that new functionality in particular,
> > regardless of the size of the protein(s) involved, did so or needed to
> > do so by crossing large gaps.
>
> None of the proposed steps in larger systems, like the flagellar
> motility system, are smaller than a few dozen mutations.
You obviously have the memory of an Alzheimer's patient. I have
repeatedly proposed that *the* crucial step that likely produced the
*function* of rotary motility could occur in as little as a single
mutational step. And presented an experimental model that shows the
feasibility of just that.
> If your
> notion of gaps of only one or two mutations were remotely correct, all
> the steps in the flagellar system should be able to be evolved by all
> kinds of different bacteria within a handful of generations - i.e.,
> just a few days for some types of bacteria. Try again . . .
No. The gap between functional states, *when they occur*, would have
to be small. But I have no illusions that *every* bacteria has the
requisite conditions for such mutation. But I don't need the flagella
to be evolvable in *every* species of bacteria. One, the ancestor to
all current eubacterial flagella, is all that is needed. *You* are
the one that has to explain every species getting its different and
special flagella by magical poofing at some time and some place rather
than by common descent from the one ancestor where the proper mutation
occurred.
> > You keep asserting that there is a mathematical relationship between
> > total size and gap size. I have yet to see that equation nor any
> > evidence supporting the hypothesis.
>
> Look at the Choi and Kim paper again. Or, do your own search and
> sequence comparisons of higher level systems. They aren't remotely as
> close together as you seem to imagine - not even close to your oft
> repeated minimum of just one mutation apart. That's clearly mistaken
> for anyone who cares to actually look into the matter instead of
> blindly waving a hand over the obvious.
And any idiot would understand that the data in the Choi and Kim paper
represents a sampling of all proteins and not the entire population.
And I note that you have again avoided (run away from) actually
presenting the equation and evidence for this hypothetical
mathematical relationship between gap size and total size. The Choi
and Kim paper does not present it.
> > > That notion of yours is clearly mistaken as anyone can prove by simply
> > > doing a BLAST search. Systems with larger minimum structural
> > > requirements than 1 or 2k amino acid residues are not just one or two
> > > residue changes away from any other uniquely functional system.
>
> > Examples?
>
> I've given you many examples already Howard. Why do you need more?
Because you are lying. You have not presented *any* such evidence
that "Systems with larger minimum structural requirements than 1 or 2k
amino acid residues are not just one or two residue changes away from
any other uniquely functional system." unless your definition of
"uniquely functional system" is the equivalent of demanding that
evolution show a dog giving birth to a monkey.
> > And how long since the system diverged?
>
> This is completely irrelevant since times of divergence are not based
> on analysis of how long it would take to cross the non-beneficial
> chasm that is obviously dozens of mutations wide.
>
> > That is crucial
> > because a lot of both selective and non-selective changes will occur
> > in sequences over long periods of time.
>
> That's the whole problem. Neutral drift takes too long to cross gaps
> of just a few dozen mutations. Your suggestion that the changes were
> somehow directed by natural selection along a beneficial pathway is
> completely unfounded. There is absolutely no evidence to support this
> beyond wishful thinking.
You fail to understand. Most of the differences in proteins that
perform the same function in all organisms arose by completely neutral
drift and fixation *after* the ancestor acquired the function.
Essentially all of that occurred *after* the function existed due
primarily to time since divergence from the last common ancestor of
two modern species. Selection for function, when it occurred,
occurred much more rapidly and then selection is subsequently
primarily conservative in nature. Again, in evolution most proteins
in modern organism are acquired by common descent. They are not
reinvented separately in each organism as your creationism requires.
> > And these changes would not
> > necessarily affect the basic *function*; they would optimize it.
>
> Optimization of a pre-existing function is not the issue here. That's
> not the problem. Getting an entirely new unique function to at least
> some degree of usefulness is the problem.
How much difference in a modified protein's function is required for
it to have a "new unique function"? Does a dog have to give birth to
a monkey for you to accept evolution?
>
> > Again, a mutation that produces the loss of rotary motility (a single
> > point mutation can do this) does not necessarily affect the ability to
> > transport proteins by the flagellin tube, some of which still do
> > function for this purpose as well as being a flagella. Again, you
> > seem to think that flagella only has a single function rather than
> > having proteins that each have an independent function that is still
> > there if another protein has mutated.
>
> It is one thing to remove a pre-existing function with a single
> mutation. It is quite another thing to be just one mutation away from
> a novel high-level system that has never existed before. For example,
> some cavefish without eyes have lost their eye as the result of a
> single point mutation. These eyes will actually grow back if this
> point mutation is corrected. Does this mean then that getting eyes to
> evolve de novo in fish that never had eyes before is likely to be
> achieved with a single point mutation? Not even close.
Of course not. And that is precisely why Behe's IC argument is
absurd. It assumes that the mechanisms that produce loss-of-function
has some relevance to how the function came into existence in the
first place.
> > > And,
> > > as the minimum requirements grow, so does the number of differences
> > > one sees between it and the next closest uniquely functional system.
>
> > So you keep asserting.
>
> So you keep denying - denying the obvious. Just look it up Howard.
> Look up the differences in the Hamming distances between higher level
> systems compared to lower level systems. See if you don't recognize a
> trend . . . the same trend illustrated by Choi and Kim.
Yadda. Yadda. Yadda. Now, if you would present *your* linear equation
for the linkage between gap size and total size that you *keep
asserting* exists.
>
> < snip >
>
> > > > The answer to that question has been answered. The answer, in
> > > > principle (and in reality) is one.
>
> > > Yeah - "In principle" the minimum gap size is just one mutational
> > > change.
>
> > And always will be.
>
> This is true only in principle, but it is very unlikely to be true in
> reality for higher level systems - - to an ...
>
> read more ยป
hersheyh
> On Sep 4, 11:18 am, hersheyh <hershe...@yahoo.com> wrote:
>
>
>
> > On Sep 4, 2:29 am, Seanpit <seanpitnos...@naturalselection.0catch.com>
> > wrote:
>
> > > On Sep 3, 5:13 pm, "R. Baldwin" <res0k...@nozirevBACKWARDS.net> wrote:
>
Sean is real good at making assertions. He is not nearly so good at
backing up those assertions with real equations, much less real
evidence, or actually testing his "methodology", such as it is.
>
> gregwrld
>
> <snip>
R. Baldwin
What computational neuroscience research supports the idea that humans use a
"method", as we understand the word in a science and engineering context,
when classifying observed objects?
>
> In other words, one must have some sort of methodological basis for
> determining the likely limits of this range of non-artifactual
> production - a range beyond which one can be reasonably confident of
> artifactual production. It doesn't matter how rough the methodology
> allows one's estimate to be. There must be at least some experiencial
> basis with statistical relevance before anyone can be remotely able to
> recognize even a very highly symmetrical polished granite cube as
> artifactual at all much less at a glance.
>
Why must there must be some sort of methodological basis? Your assertion
doesn't correspond to what I've read about human cognition.
R. Baldwin
> On Sep 3, 5:13 pm, "R. Baldwin" <res0k...@nozirevBACKWARDS.net> wrote:
>>
>> >> So, how do you know that _David_ is designed and snowflakes aren't?
>> >> (Or do you think snowflakes are designed as well?)
>>
>> > Snowflakes aren't made out of granite or marble, materials that do not
>> > naturally tend toward highly symmetrical self-assembly.
>>
>> > Again, you have to have prior experience with the *material* in
>> > question and how it interacts with non-deliberate forces of nature
>> > before you can begin to reasonably detect artifact.
>>
>> > Take, for instance, SETI scientists. If they had absolutely no
>> > experience with radiowaves they wouldn't be able to say if this or
>> > that pattern was or was not likely to be the result of artifact. It
>> > is only because of their prior experience with radiowaves that they
>> > can in fact suggest features that would likely be artifactual if they
>> > were ever discovered in radiowaves.
>>
>> Now, this much I agree with.
>
> Well, it's good that at least someone has come this far. It is more
> than I can say for most in this forum!
>
>> How does it help you in biology?
>
> Non-artifactual processes always have a certain limited range in how
> they affect a given material - whatever that material may be.
Kindly demonstrate that this assertion is correct before we go on. It seems
to be foundational to your argument, and not one that I'm willing to accept
on your say-so. Why should I believe you?
[snip]
R. Baldwin
> On Sep 3, 7:42 pm, "R. Baldwin" <res0k...@nozirevBACKWARDS.net> wrote:
>>
>> > A biological system that is does not produce some sort of beneficial
>> > function will not be in existence for very long. It will be lost
>> > because nature will not select to maintain it. Those that remain in
>> > the gene pool remain because the produce some sort of reproductive
>> > advantage. Different types of potentially beneficial systems have
>> > different minimum structural requirements without which they cannot be
>> > realized in the gene pool at all.
>>
>> I can see no reason that a neutral bit of tissue must be selected
>> against.
>
> It cost energy to maintain DNA. Therefore, DNA that isn't providing
> any benefit to the creature will eventually be discarded.
There seems to be an awful lot of wasteful, do-nothing, layabout DNA in most
organisms. Why is that?
> Besides,
> this discussion is about the time it takes to find useful genetic
> elements with different minimum size and specificity requirements.
I don't accept your bald assertion that there is such a thing as minimum
size and specificity. I'm not alone in this. You need to demonstrate it, if
you want anyone to accept your arguments.
> Neutral evolution or "random walk" doesn't really help, statistically,
> to find potentially beneficial islands in the vastness of sequence
> space any faster that any other search algorithm.
It seems to me this is approaching the problem backwards. There is no
algorithm attempting to find anything. There is no goal. The mutations end
up where they end up. Whatever interesting behavior that happens along the
way is what happens.
>
>> > For example, despite the fact that a lactase enzyme might be useful in
>> > a particular gene pool in a particular environment, that function will
>> > not exist with any arrangement of just 40 or 50 residues . . . or even
>> > 100 residues. The same thing is true of flagellar motility. This
>> > type of function cannot be realized with the use of just a 400 or 500
>> > or even 1000 codons of DNA - regardless of arrangement.
>>
>> So what? Perhaps some other non-harmful function can be realized with
>> fewer
>> codons.
>
> That's fine. If all that existed where functions that required no
> more than a few hundred fairly specified residues, the ToE would be a
> perfectly reasonable explanation. The problem is that functional
> systems exist that require very large minimum threshold requirements.
> The question is, can the proposed evolutionary mechanism explain these
> higher level systems? Sure, evolution doesn't have to produce higher
> level systems, but can it? That's the question. Could the
> evolutionary mechanism move beyond systems that have very low minimum
> threshold requirements to come up with higher level systems?
The idea is that the function evolved from a different one. There need be no
minimum. Why is that so hard to understand?
>
>> > *All* potentially beneficial systems that have higher minimum
>> > requirements will be more widely separated in sequence space compared
>> > to lower level functions - much much more widely separated (on
>> > average). That means, the evolution of any novel beneficial system at
>> > higher level requires many more mutations, on average, from the
>> > perspective of any given gene pool.
>>
>> You have not demonstrated that there are *any* systems that have minimum
>> requirements for being either (a) beneficial, or (b) not harmful.
>
> There are lots of beneficial systems, like flagellar motility, that
> also have very high minimum structural threshold requirements coded
> for by a minimum of well over 10,000 codons, or 30,000 bp, of DNA.
> Again, the argument that such systems didn't have to evolve doesn't
> address the question of if they could have evolved via random mutation
> and function-based selection.
>
What is so difficult about flagellar motility evolving from a similar system
that had a slightly simpler structure and performed a slightly simpler
function?
hersheyh
wrote:
> "Seanpit" <seanpitnos...@naturalselection.0catch.com> wrote in message
>
> news:1188890449.3...@d55g2000hsg.googlegroups.com...
>
> > On Sep 3, 7:42 pm, "R. Baldwin" <res0k...@nozirevBACKWARDS.net> wrote:
>
> >> > A biological system that is does not produce some sort of beneficial
> >> > function will not be in existence for very long. It will be lost
> >> > because nature will not select to maintain it. Those that remain in
> >> > the gene pool remain because the produce some sort of reproductive
> >> > advantage. Different types of potentially beneficial systems have
> >> > different minimum structural requirements without which they cannot be
> >> > realized in the gene pool at all.
>
> >> I can see no reason that a neutral bit of tissue must be selected
> >> against.
>
> > It cost energy to maintain DNA. Therefore, DNA that isn't providing
> > any benefit to the creature will eventually be discarded.
>
> There seems to be an awful lot of wasteful, do-nothing, layabout DNA in most
> organisms. Why is that?
Well, for most eucaryotic organisms and, in particular, multicellular
or large eucaryotes with relatively slow reproductive rates.
Parsimony in DNA appears to be correlated with small size,
unicellularity, and rapid reproduction, as occurs in yeasts and
bacteria. For fat, lazy, slow-growing eucaryotes like humans, the
amount of DNA per cell is not correlated strongly enough with
reproductive success (the only measure that counts) to be a
significant factor. It is also possible that larger amounts of DNA is
one easy way to increase cell size via a feed-back mechanism that
regulates cell size to nuclear size (plant breeders take advantage of
this; most commercial, i.e., big, flowers are polyploid) which has
possible advantages in certain lifestyles or niches. In that case,
carrying a load of otherwise useless "junk" DNA might have some
advantage, but that would NOT be a sequence-dependent use of DNA.
Some 95+% of human DNA is sequence-irrelevant material, to give a more
accurate definition of "junk DNA", of course.
> > Besides,
> > this discussion is about the time it takes to find useful genetic
> > elements with different minimum size and specificity requirements.
>
> I don't accept your bald assertion that there is such a thing as minimum
> size and specificity. I'm not alone in this. You need to demonstrate it, if
> you want anyone to accept your arguments.
And Sean needs to explain how *he* thinks different genes arise (what
natural method -- since only natural methods have natural effects --
was used), when they arose, why they exhibit the pattern of
differences (for a given function) that they do, *and* present the
*material* evidence that this is what actually happened to produce
these results.
We have given him the mechanisms (duplication and divergence, chimera
formation, various forms of mutation), mechanisms that are *actually
known* to occur in nature, that can produce the modified or novel
functions that *have* evolved. We have demonstrated that, given
standard times since divergence of currently living groups from common
ancestors, the pattern of *differences* in proteins with the same
function, is essentially an inevitable consequence of random fixation
of selectively neutral sites (no need to invoke selection at all) and
the rate of such change is well within the *observable* rates at which
such events (selective or neutral fixation) would happen. [All he
would have to do is demonstrate that there actually is consistent
evidence that the earth is only 6000 years old to falsify this. And
to demonstrate why all the current evidence pointing to much longer
time frames is misleading.]
> > Neutral evolution or "random walk" doesn't really help, statistically,
> > to find potentially beneficial islands in the vastness of sequence
> > space any faster that any other search algorithm.
But combinatorial variation does. And finding what functional
variations nearby that can be reached have potential utility does,
since the beneficial island for, say, the aldosterone receptor protein
overlaps with the beneficial island for the cortisol receptor
protein. Such overlapping functionalities are quite common in the
*real* world of *real* enzymes, which almost always have secondary
functionalities and have effects on substrates other than the primary
one in current use.
Duplication and subfunctionalization or neofunctionalization are
common events. For example, this explains the current structure of
hemoglobin in mammals, with its IC structure of two alpha and two beta
globins (as well as the changes in beta globins during development).
Most features of *real* evolutionary change are primarily quantitative
or involve timing in nature. The sequences that regulate gene
expression are short and can be affected in a quantitative rather than
a qualitative way.
Similarly, changes that affect aggregation and interaction of proteins
are also short and can be changed in a *quantitative* way to produce
greater or lesser affinity.
> It seems to me this is approaching the problem backwards. There is no
> algorithm attempting to find anything. There is no goal. The mutations end
> up where they end up. Whatever interesting behavior that happens along the
> way is what happens.
Sean, like all creationists, greatly exaggerates the amount of
"novelty" that exists in nature at the molecular level and assumes
that one cannot reach a current structure by modification of a
previous one(s). He, in particular, assumes, although he denies it,
that the only way to produce a new function that he names is to start
at some random sequence *of the same size* some unknown distance away
and proceed in a single-step manner. In fact, his model of how
"evolution" works is absurd and has no relationship to any real
*evolutionary* model for the generation of new or modified function.
That is why I consider what he is doing numerology rather than
science.
> >> > For example, despite the fact that a lactase enzyme might be useful in
> >> > a particular gene pool in a particular environment, that function will
> >> > not exist with any arrangement of just 40 or 50 residues . . . or even
> >> > 100 residues. The same thing is true of flagellar motility. This
> >> > type of function cannot be realized with the use of just a 400 or 500
> >> > or even 1000 codons of DNA - regardless of arrangement.
>
> >> So what? Perhaps some other non-harmful function can be realized with
> >> fewer
> >> codons.
>
> > That's fine. If all that existed where functions that required no
> > more than a few hundred fairly specified residues, the ToE would be a
> > perfectly reasonable explanation.
The vast majority of proteins are 300 +/- 200 aa in length. And
ICness in multiprotein systems can arise by the initial effect of an
associating protein merely being 'helpful', with subsequent changes
making it 'necessary'. Or, like the eubacterial (and, independently,
the archaean flagella) being the consequence of a linkage of pre-
existing subsystems that do not need to change what they do,
converting the problem to that of producing one particular protein (a
chimeric one at that, and chimeric proteins are not produced by
starting at some random sequence of a random size).
> The problem is that functional
> > systems exist that require very large minimum threshold requirements.
> > The question is, can the proposed evolutionary mechanism explain these
> > higher level systems? Sure, evolution doesn't have to produce higher
> > level systems, but can it? That's the question. Could the
> > evolutionary mechanism move beyond systems that have very low minimum
> > threshold requirements to come up with higher level systems?
Sean, of course, has no idea what he means by "higher level system"
when it comes to *function*.
> The idea is that the function evolved from a different one. There need be no
> minimum. Why is that so hard to understand?
>
>
>
>
>
> >> > *All* potentially beneficial systems that have higher minimum
> >> > requirements will be more widely separated in sequence space compared
> >> > to lower level functions - much much more widely separated (on
> >> > average).
Notice that Sean here is implying a model for how *he* thinks
evolution works. That it has no relationship to how people who
understand evolution and how new proteins in real cells arise doesn't
seem to bother him. He prefers his strawman, because it produces the
numerology he wants. He seems to be fascinated by large numbers and
always works to produce them, even to the point of producing
*probabilities* of 10^23. ;-)
> > > >That means, the evolution of any novel beneficial system at
> >> > higher level requires many more mutations, on average, from the
> >> > perspective of any given gene pool.
>
> >> You have not demonstrated that there are *any* systems that have minimum
> >> requirements for being either (a) beneficial, or (b) not harmful.
>
> > There are lots of beneficial systems, like flagellar motility, that
> > also have very high minimum structural threshold requirements coded
> > for by a minimum of well over 10,000 codons, or 30,000 bp, of DNA.
Originally, of course, this was 30,000 codons. Again, Sean does like
his numbers large, even if the large numbers are irrelevant.
> > Again, the argument that such systems didn't have to evolve doesn't
> > address the question of if they could have evolved via random mutation
> > and function-based selection.
>
> What is so difficult about flagellar motility evolving from a similar system
> that had a slightly simpler structure and performed a slightly simpler
> function?
Or, as has been observed to happen, by the generation of a chimeric
linker that links the motor function and its proteins to the rotatable
pore and its proteins.
Earle Jones
Seanpit <seanpi...@naturalselection.0catch.com> wrote:
> On Sep 2, 12:35 pm, bdbry...@wherever.ur (Bobby Bryant) wrote:
> > In article <1188748245.326427.67...@w3g2000hsg.googlegroups.com>,
> > Seanpit <seanpitnos...@naturalselection.0catch.com> writes:
> >
> > > This is only to be expected from someone who still denies that a
> > > statue like Michelangelo's David shows little if any symmetry.
> >
> > So, how do you know that _David_ is designed and snowflakes aren't?
> > (Or do you think snowflakes are designed as well?)
>
> Snowflakes aren't made out of granite or marble, materials that do not
> naturally tend toward highly symmetrical self-assembly.
*
I invite you to visit the "Devil's Postpile" on the east side of the
Sierra near Mammoth Lakes, CA.
Basalt columns show an amazing near-perfect hexagonal cross section.
See: http://geology.wr.usgs.gov/parks/depo/dpgeol1.html
or https://64.241.25.143/depo/planyourvisit/nearbyattractions.htm
earle
*
_
_/\_\
/\_\/_/
\/_/\_\ earle
\/_/ jones
richardal...@googlemail.com
> In article <1188830321.568255.123...@d55g2000hsg.googlegroups.com>,
You forgot one of the fundamental principles of Sean's "method":
Any observation which falsifies his conclusions is specifically
excluded from analysis.
It's much the same principle as Behe's specific exclusion of the known
evolutionary explanation for the bacterial flagellum from
consideration when demonstrating that it could not have evolved.
RF