For Steve Carlip - Rate of Exponential Decline in Beneficial Sequence Space Ratio
Seanpit
> Seanpit <seanpitnos...@naturalselection.0catch.com> wrote:
> > On Feb 10, 9:06 pm, j.wilki...@uq.edu.au (John Wilkins) wrote:
>
> [...]
>
> >> I don't get your point. If a 10aa mutation can hit a novel function,
> >> then an 11aa muation can hit one.
> >
> > Yes, but the odds of success for a given attempt are exponentially
> > less likely [when the novel function has a greater minimum structural
> > threshold requirement].
>
> "Exponentially less likely" is a phrase I often hear from people who
> don't know very much math. By itself, it doesn't mean anything --
> depending on the "decay constant" in the exponent, an exponential
> relation may be very different from a linear relation, or it may be
> almost indistinguishable from a linear relation. (That is, if a<<1/N,
> then e^{-aN} is very nearly equal to 1-aN.)
>
> Is this just rhetoric, or are you claiming an actual calculation here?
> If the latter, what is the value of the constant in the exponent?
> How, exactly, did you determine (or measure) this value?
How many additional potentially beneficial structures do you think are
added with each additional 1aa structural requirement?
I propose that as one moves up the ladder of minimum structural
threshold requirements, 1aa at a time, the increase in potentially
beneficial sequences approaches a exponent of 1 while the increase in
non-beneficial sequences approaches an exponent of 20.
For example, the total number of meaningful sequences in the English
language system for 1-character sequences is about 3. This produces a
ratio of about 1 in 8 meaningful vs. non-meaningful sequences at this
level. The total number of meaningful 2-character sequences is about
96 or so (a 32 fold increase). The sequence space size for 2
character sequences is 26^2 = 676. This produces a ratio of
meaningful vs. non-meaningful of about 1 in 7. The total number of
meaningful 3-character sequences is about 972 (a 10 fold increase)
while the total sequence space size is 17,576 for a ratio of about 1
in 18. What about meaningful 7-character sequences? Counting
multiword phrases there are probably about 30,000 or so meaningful 7-
character sequences, which produces a ratio of less than 1 in
250,000.
Notice that the "exponential" increase in potentially meaningful
sequences is reduced with each level while the exponential increase in
non-meaningful sequences is increased toward and exponential of 26.
Adding the additional requirement that the sequence be not only
meaningful but beneficial as well only speeds up this process more
quickly so that the disparity between the increase in beneficial vs.
non-beneficial is accentuated more dramatically at lower levels.
The same basic pattern is present in all language/information systems,
to include genetics and protein-based functions.
How many 1aa systems are potentially beneficial from the perspective
of a given life form? 100% - right? The same is almost certainly
true of 2aa sequences. However, this pattern doesn't last long. The
increase in potentially beneficial sequences rapidly declines as one
moves up the ladder of specifically arranged residues 1aa at a time.
By the time the 100aa level is reached, the ratio of potentially
beneficial vs. non-beneficial is around 1e-40 to 1e-60 depending on
the degree of specificity one is considering (Sauer, Olsen, Yockey,
Musgrave, etc). This ratio continues to drop dramatically with
beneficial sequences being outpaced by non-beneficial sequences by
more than 10 fold given a specificity of 1e-40 per 100aa. As one
continues to move up the ladder the increase of non-beneficial
sequences outpaces the increase of potentially beneficial sequences
more and more, approaching a 20 fold differential (likely more than 20
fold given different potential 3D arrangements of the same sequence
residues).
At this point, the exponential declining ratio is clearly problematic
because it is such a severe decline. The only potentially valid
argument left is one of clustering of potentially beneficial sequences
within sequence space in such a way that evolution can progress
because these sequences are not evenly distributed throughout sequence
space. However, as long as there is at lease some distribution and
all the beneficial sequences are not simply clustered in one tiny
corner of sequence space, the degree of the exponential decline in the
ratio will rip apart the islands of beneficial sequences and make them
extremely isolated from each other very quickly at relatively low
levels of minimum structural threshold requirements.
> Steve Carlip
Sean Pitman
www.DetectingDesign.com
Von R. Smith
>
> - Show quoted text -
To answer Steve's question more concisely: It is just rhetoric, and
no, there is no actual calculation here.
Seanpit
>
> > - Show quoted text -
>
> To answer Steve's question more concisely: It is just rhetoric, and
> no, there is no actual calculation here.
Are you actually arguing that the rate of increase for potentially
beneficial sequences with each increase in the minimum structural
threshold requirement keeps even remotely close pace with the increase
in non-beneficial sequences? Do you have any evidence whatsoever to
support this notion?
Sean Pitman
www.DetectingDesign.com
richardal...@googlemail.com
>
> > > - Show quoted text -
>
> > To answer Steve's question more concisely: It is just rhetoric, and
> > no, there is no actual calculation here.
>
> Are you actually arguing that the rate of increase for potentially
> beneficial sequences with each increase in the minimum structural
> threshold requirement keeps even remotely close pace with the increase
> in non-beneficial sequences? Do you have any evidence whatsoever to
> support this notion?
>
> Sean Pitmanwww.DetectingDesign.com
So you don't have any calculations.
You have a model of evolution you have devised for no reason other
than to falsify it.
You have no evidence support your model, and the only prediction of
your model - that there are discontinuities in the nested hierarchy of
living organisms - is not supported by the evidence. This falsifies
your model.
Your "explanation" for this lack of evidence is "common design" or
"hierachical design" or "intelligent design", none of which have any
predictive value whatsoever, and none of which are supported by any
evidence whatsoever. You cannot, for example, show that the works of
any individual designer use any such principle - contrary to your
assertion that this is "common practice".
Inventing things as you go along when your argument is demolished may
provide you with some facile satisfaction, but it is not exactly
honest, is it?
RF
Seanpit
> So you don't have any calculations.
I presented several calculations and the basis for the degree of the
decline in the ratio of beneficial vs. non-beneficial. If you
actually think beneficial sequences increase at a significantly
greater rate than I propose, please do provide your reasons. I'd be
most interested.
< snip >
Sean Pitman
www.DetectingDesign.com
Tracy P. Hamilton
>
> > > > - Show quoted text -
>
> > > To answer Steve's question more concisely: It is just rhetoric, and
> > > no, there is no actual calculation here.
>
> > Are you actually arguing that the rate of increase for potentially
> > beneficial sequences with each increase in the minimum structural
> > threshold requirement keeps even remotely close pace with the increase
> > in non-beneficial sequences? Do you have any evidence whatsoever to
> > support this notion?
>
> > Sean Pitmanwww.DetectingDesign.com
>
> So you don't have any calculations.
>
> You have a model of evolution you have devised for no reason other
> than to falsify it.
> You have no evidence support your model, and the only prediction of
> your model - that there are discontinuities in the nested hierarchy of
> living organisms - is not supported by the evidence. This falsifies
> your model.
The last sentence is erroneous, because Sean Pitman has no model.
[snip]
Tracy P. Hamilton
Von R. Smith
>
> > > - Show quoted text -
>
> > To answer Steve's question more concisely: It is just rhetoric, and
> > no, there is no actual calculation here.
>
> Are you actually arguing that the rate of increase for potentially
> beneficial sequences with each increase in the minimum structural
> threshold requirement keeps even remotely close pace with the increase
> in non-beneficial sequences?
No, I am pointing out that your argument is just rhetoric with no
actual calcuation.
> Do you have any evidence whatsoever to
> support this notion?
Practically every post you write, including this last one, is ample
evidence that your argument is all just rhetoric with no actual
calculation of the parameters you say are important to your model.
Here's an experiment to test that hypothesis:
How many fairly-specified residues are there in the enzyme dntD?
Prediction: "blah blah blah blah 7-letter words blah blah blah blah
go ahead and prove me wrong blah blah blah are you seriously trying to
argue blah blah blah evolution really does simply stall out blah blah
blah the probability of two independent events is their sum blah blah
blah...[...etc.]"
Seanpit
wrote:
> > You have no evidence support your model, and the only prediction of
> > your model - that there are discontinuities in the nested hierarchy of
> > living organisms - is not supported by the evidence. This falsifies
> > your model.
>
> The last sentence is erroneous, becauseSeanPitmanhas no model.
No evolutionary model that is - - Intelligent design certainly is a
potential model. There is no fundamental difference here compared to
what SETI scientists are looking for.
In any case, one doesn't need a model before the validity of the
prevailing model can be adequately challenged.
> Tracy P. Hamilton
Sean Pitman
www.DetectingDesign.com
hersheyh
0catch.com> wrote:
> On Feb 15, 10:57 am, carlip-nos...@physics.ucdavis.edu wrote:
>
>
>
> > Seanpit <seanpitnos...@naturalselection.0catch.com> wrote:
> > > On Feb 10, 9:06 pm, j.wilki...@uq.edu.au (John Wilkins) wrote:
>
> > [...]
>
> > >> I don't get your point. If a 10aa mutation can hit a novel function,
> > >> then an 11aa muation can hit one.
>
> > > Yes, but the odds of success for a given attempt are exponentially
> > > less likely [when the novel function has a greater minimum structural
> > > threshold requirement].
>
> > "Exponentially less likely" is a phrase I often hear from people who
> > don't know very much math. By itself, it doesn't mean anything --
> > depending on the "decay constant" in the exponent, an exponential
> > relation may be very different from a linear relation, or it may be
> > almost indistinguishable from a linear relation. (That is, if a<<1/N,
> > then e^{-aN} is very nearly equal to 1-aN.)
>
> > Is this just rhetoric, or are you claiming an actual calculation here?
> > If the latter, what is the value of the constant in the exponent?
> > How, exactly, did you determine (or measure) this value?
>
> How many additional potentially beneficial structures do you think are
> added with each additional 1aa structural requirement?
"Structural requirement" for what? Is your model of evolution the one
you keep claiming you are NOT presenting? That evolution works by
starting with some random sequence and adds amino acids one by one in
a completely random process?
> I propose that as one moves up the ladder of minimum structural
> threshold requirements, 1aa at a time, the increase in potentially
> beneficial sequences approaches a exponent of 1 while the increase in
> non-beneficial sequences approaches an exponent of 20.
Isn't that making the false assumption that one and only one aa can
produce a particular functional protein for each and every one of your
hypothetical 1001 sites? The number of aa's for which one and only
one aa is compatible with a particular function can almost always be
counted on the fingers of one hand.
> For example, the total number of meaningful sequences in the English
> language system for 1-character sequences is about 3. This produces a
> ratio of about 1 in 8 meaningful vs. non-meaningful sequences at this
> level.
A model based on English is inappropriate in this context. English is
a much more fragile code related to function than proteins are.
English words, unlike proteins, usually completely loses its current
meaning by a single letter change. A protein, in contrast, only
occasionally completely loses its current meaning with a change in
aa. Any math based on such a bogus assumption about how proteins work
is not worth the electrons its written on. Any model, like the ones
you present (mathematically), that assumes that evolution works by
starting with some random sequence *maximally* distant (that is, all
1000 or whatever hypothetical number of aa's you arbitrarily posit)
away from some specified end goal is a bogus strawman.
Until you can mathematically generate a valid measure of the *minimum*
"gap distance" from your hypothetical arbitrary size number of 1000,
you got nothing.
> The total number of meaningful 2-character sequences is about
> 96 or so (a 32 fold increase). The sequence space size for 2
> character sequences is 26^2 = 676. This produces a ratio of
> meaningful vs. non-meaningful of about 1 in 7. The total number of
> meaningful 3-character sequences is about 972 (a 10 fold increase)
> while the total sequence space size is 17,576 for a ratio of about 1
> in 18. What about meaningful 7-character sequences? Counting
> multiword phrases there are probably about 30,000 or so meaningful 7-
> character sequences, which produces a ratio of less than 1 in
> 250,000.
>
> Notice that the "exponential" increase in potentially meaningful
> sequences is reduced with each level while the exponential increase in
> non-meaningful sequences is increased toward and exponential of 26.
Notice the assumptions in sequence space. Sean assumes that words are
invented in English by plucking out random letters or starting with a
random sequence and reaching the end point by a random walk. Hell, he
should know that that is not *even* true for English words. According
to Sean, the word 'bullshit' is reached by starting with the random 8-
letter sequence of 'xymnufsd' and reaching the end goal by a random
walk rather than in a single step from the pre-existing words 'bull'
and 'shit' thus producing a word that has a modified (non-literal)
meaning from either starting point. He should also know that words
can change meaning without changing sequence, or he would be less than
willing to get a 'gift'.
> Adding the additional requirement that the sequence be not only
> meaningful but beneficial as well only speeds up this process more
> quickly so that the disparity between the increase in beneficial vs.
> non-beneficial is accentuated more dramatically at lower levels.
>
> The same basic pattern is present in all language/information systems,
> to include genetics and protein-based functions.
And the mechanism you propose for evolution is not one that is used in
inventing new 'words' in any language.
> How many 1aa systems are potentially beneficial from the perspective
> of a given life form? 100% - right? The same is almost certainly
> true of 2aa sequences. However, this pattern doesn't last long. The
> increase in potentially beneficial sequences rapidly declines as one
> moves up the ladder of specifically arranged residues 1aa at a time.
> By the time the 100aa level is reached, the ratio of potentially
> beneficial vs. non-beneficial is around 1e-40 to 1e-60 depending on
> the degree of specificity one is considering (Sauer, Olsen, Yockey,
> Musgrave, etc).
Only if one makes certain assumptions that we know are not true. You
assume that cytochrome c is a 'typical' protein rather than one that
has a higher degree of sequence stringency than most (but still less
than your designation of 'fairly specified aa residues' implies). You
assume that there is a single *function* of cytochrome c rather than a
cluster of *functions*. You assume that the one function you identify
is "the" function of cytochrome c, when it actually isn't (cytochrome
c is a heme-binding protein; electron transport is entirely due to the
heme moiety). You assume that only proteins related to cytochrome c
could, even in principle, possibly have that function when we know
that, even in mitochondria, the *function* can be and is performed by
a non-protein *in a different context*.
> This ratio continues to drop dramatically with
> beneficial sequences being outpaced by non-beneficial sequences by
> more than 10 fold given a specificity of 1e-40 per 100aa. As one
> continues to move up the ladder the increase of non-beneficial
> sequences outpaces the increase of potentially beneficial sequences
> more and more, approaching a 20 fold differential (likely more than 20
> fold given different potential 3D arrangements of the same sequence
> residues).
>
> At this point, the exponential declining ratio is clearly problematic
> because it is such a severe decline. The only potentially valid
> argument left is one of clustering of potentially beneficial sequences
> within sequence space in such a way that evolution can progress
> because these sequences are not evenly distributed throughout sequence
> space. However, as long as there is at lease some distribution and
> all the beneficial sequences are not simply clustered in one tiny
> corner of sequence space, the degree of the exponential decline in the
> ratio will rip apart the islands of beneficial sequences and make them
> extremely isolated from each other very quickly at relatively low
> levels of minimum structural threshold requirements.
What matters is the *minimum* number of mutational steps between
functional structures. You have no way to calculate that. Your
calculations are simply 'bullshit' (in its non-literal meaning).
Short answer to the relevant question, "Is this just rhetoric, or are
you claiming an actual calculation here?", is that it is just rhetoric
clouded by the smoke and mirrors of pseudomath.
> > Steve Carlip
>
> Sean Pitmanwww.DetectingDesign.com
Free Lunch
"Seanpit" <seanpi...@naturalselection.0catch.com> wrote in
<1171653689....@m58g2000cwm.googlegroups.com>:
Hypothetically true, but you don't actually think you have managed to
challenge it adequately, do you?
>> Tracy P. Hamilton
>
>Sean Pitman
>www.DetectingDesign.com
There is no design. Live with it.
richardal...@googlemail.com
0catch.com> wrote:
> On Feb 16, 9:58 am, richardalanforr...@googlemail.com wrote:
>
> > So you don't have any calculations.
>
> I presented several calculations and the basis for the degree of the
> decline in the ratio of beneficial vs. non-beneficial.
And several people pointed out that your lack of knowledge of even
basic statistics makes your calculations meaningless.
If think that they are meaningful, please post them again.
> If you
> actually think beneficial sequences increase at a significantly
> greater rate than I propose, please do provide your reasons. I'd be
> most interested.
>
You have a model of evolution you have devised for no reason other
than to falsify it.
You have no evidence support your model, and the only prediction of
your model - that there are discontinuities in the nested hierarchy of
living organisms - is not supported by the evidence. This falsifies
your model.
Your "explanation" for this lack of evidence is "common design" or
"hierachical design" or "intelligent design", none of which have any
predictive value whatsoever, and none of which are supported by any
evidence whatsoever. You cannot, for example, show that the works of
any individual designer use any such principle - contrary to your
assertion that this is "common practice".
Inventing things as you go along when your argument is demolished may
provide you with some facile satisfaction, but it is not exactly
honest, is it?
RF
> < snip >
>
> Sean Pitmanwww.DetectingDesign.com
richardal...@googlemail.com
But you have not offered any challenge to the prevailing model.
You have offered a model which bears little resemblance to any model
ever proposed by any evolutionary scientist and assert that because it
doesn't work beyond an arbitrary limit of change you have invented
evolution does not occur beyond that level. The evidence from the
natural world shows clearly that it does, so your model is falsified.
How does this challenge any other model?
RF
>
> > Tracy P. Hamilton
>
> Sean Pitmanwww.DetectingDesign.com
Seanpit
> > In any case, one doesn't need a model before the validity of the
> > prevailing model can be adequately challenged.
>
> But you have not offered any challenge to the prevailing model.
>
> You have offered a model which bears little resemblance to any model
> ever proposed by any evolutionary scientist and assert that because it
> doesn't work beyond an arbitrary limit of change you have invented
> evolution does not occur beyond that level. The evidence from the
> natural world shows clearly that it does, so your model is falsified.
I've presented an observation that evolution that can be observed "in
action" is very common and fast when functional systems requiring only
a few dozen loosely arranged residues are involved, that evolution
becomes much less common when a few hundred residues are required, and
that it doesn't happen at all when more than 1000 specifically
arranged residues are required.
This isn't a hypothesis or model of evolution Forrest. This is an
observation of your proposed mechanism of evolution "in action". The
process of evolution you describe demonstrably stalls out well before
the 1000aa level is reached. Again, this is an observation, not a
hypothesis or model. This is in fact what is happening.
Now come the hypotheses and models. You have no hypothesis or model
to explain this observation. None at all. I, on the other hand, do
have a hypothesized model to explain this very real observation.
> How does this challenge any other model?
Your evolutionary model does not take this stalling effect, which is
quite real, into account. It is not explained in any published paper
or textbook. This observation isn't even described. Yet, it cannot
be rationally denied. It does happen. Period. And, this observation
directly undermines the standard evolutionary model of how the
evolutionary mechanism is supposed to work without stalling out as it
climbs the ladder of functional complexity. What is your explanation
for this stalling effect?
> RF
Sean Pitman
www.DetectingDesign.com
Seanpit
> > How many additional potentially beneficial structures do you think are
> > added with each additional 1aa structural requirement?
>
> "Structural requirement" for what?
For the minimum structural threshold requirement of a higher level
novel functional system. Do I have to explain to you, yet again, that
different types of functional systems require different minimum
structural threshold requirements? Some have lower, some higher,
minimum threshold requirements? Remember?
> Is your model of evolution the one
> you keep claiming you are NOT presenting? That evolution works by
> starting with some random sequence and adds amino acids one by one in
> a completely random process?
Not at all. Start with any sequence/structure you want. Finding
novel beneficial functional systems within sequence/structure space
gets many fold harder when looking for functional systems that have a
single additional specific structural residue requirement.
> > I propose that as one moves up the ladder of minimum structural
> > threshold requirements, 1aa at a time, the increase in potentially
> > beneficial sequences approaches a exponent of 1 while the increase in
> > non-beneficial sequences approaches an exponent of 20.
>
> Isn't that making the false assumption that one and only one aa can
> produce a particular functional protein for each and every one of your
> hypothetical 1001 sites?
Not at all. Many different protein sequences could produce a fairly
specified system with a particular higher-level function. It is just
that this seemingly large number, like 1e60, is dwarfed by the much
larger number of sequences that could not produce the function in
question to any selectable degree, like 1e130 (at the level of 100aa
systems). Again, the discrepancy in ratio is problematic here and
becomes many fold more problematic with each additional specified
residue requirement.
> The number of aa's for which one and only
> one aa is compatible with a particular function can almost always be
> counted on the fingers of one hand.
That's not my argument and you know it. Why build this strawman yet
again?
> > For example, the total number of meaningful sequences in the English
> > language system for 1-character sequences is about 3. This produces a
> > ratio of about 1 in 8 meaningful vs. non-meaningful sequences at this
> > level.
>
> A model based on English is inappropriate in this context. English is
> a much more fragile code related to function than proteins are.
> English words, unlike proteins, usually completely loses its current
> meaning by a single letter change.
Not true. You can read an English phrase or paragraph with a great
many character changes without a complete loss of meaning/function.
> A protein, in contrast, only
> occasionally completely loses its current meaning with a change in
> aa. Any math based on such a bogus assumption about how proteins work
> is not worth the electrons its written on. Any model, like the ones
> you present (mathematically), that assumes that evolution works by
> starting with some random sequence *maximally* distant (that is, all
> 1000 or whatever hypothetical number of aa's you arbitrarily posit)
> away from some specified end goal is a bogus strawman.
>
> Until you can mathematically generate a valid measure of the *minimum*
> "gap distance" from your hypothetical arbitrary size number of 1000,
> you got nothing.
The point of the English-language illustration is to demonstrate what
happens to the ratio of beneficial vs. non-beneficial sequences with
increasing minimum sequence requirements at whatever constant level of
specificity you desire. Say the sequence can change 80% of the
characters between at least 50% of the character options per
position. Do you think that would help your position out to any
significant degree? Think again. The very same problem would quickly
develop.
> > The total number of meaningful 2-character sequences is about
> > 96 or so (a 32 fold increase). The sequence space size for 2
> > character sequences is 26^2 = 676. This produces a ratio of
> > meaningful vs. non-meaningful of about 1 in 7. The total number of
> > meaningful 3-character sequences is about 972 (a 10 fold increase)
> > while the total sequence space size is 17,576 for a ratio of about 1
> > in 18. What about meaningful 7-character sequences? Counting
> > multiword phrases there are probably about 30,000 or so meaningful 7-
> > character sequences, which produces a ratio of less than 1 in
> > 250,000.
>
> > Notice that the "exponential" increase in potentially meaningful
> > sequences is reduced with each level while the exponential increase in
> > non-meaningful sequences is increased toward and exponential of 26.
>
> Notice the assumptions in sequence space. Seanassumes that words are
> invented in English by plucking out random letters or starting with a
> random sequence and reaching the end point by a random walk. Hell, he
> should know that that is not *even* true for English words. According
> toSean, the word 'bullshit' is reached by starting with the random 8-
> letter sequence of 'xymnufsd' and reaching the end goal by a random
> walk rather than in a single step from the pre-existing words 'bull'
> and 'shit' thus producing a word that has a modified (non-literal)
> meaning from either starting point. He should also know that words
> can change meaning without changing sequence, or he would be less than
> willing to get a 'gift'.
You just don't get it. Start with whatever sequence you want. At low
levels, comparable to 3-letter words, there is a very high degree of
interconnectedness were any potentially beneficial sequence can be
reached via a series of short single character changes that are each
sequentially beneficial. However, this is not so easy as one moves up
the ladder because of the dramatic decline in the ratio of beneficial
vs. non-beneficial sequences - REGARDLESS of your starting point(s).
> > Adding the additional requirement that the sequence be not only
> > meaningful but beneficial as well only speeds up this process more
> > quickly so that the disparity between the increase in beneficial vs.
> > non-beneficial is accentuated more dramatically at lower levels.
>
> > The same basic pattern is present in all language/information systems,
> > to include genetics and protein-based functions.
>
> And the mechanism you propose for evolution is not one that is used in
> inventing new 'words' in any language.
I'm not asking for the invention of new words. I'm asking for the
finding of potentially beneficial sequences in sequence space at
higher and higher levels where the ratio of beneficial vs. non-
beneficial drops dramatically with each step up the ladder of
functional complexity.
> > How many 1aa systems are potentially beneficial from the perspective
> > of a given life form? 100% - right? The same is almost certainly
> > true of 2aa sequences. However, this pattern doesn't last long. The
> > increase in potentially beneficial sequences rapidly declines as one
> > moves up the ladder of specifically arranged residues 1aa at a time.
> > By the time the 100aa level is reached, the ratio of potentially
> > beneficial vs. non-beneficial is around 1e-40 to 1e-60 depending on
> > the degree of specificity one is considering (Sauer, Olsen, Yockey,
> > Musgrave, etc).
>
> Only if one makes certain assumptions that we know are not true. You
> assume that cytochrome c is a 'typical' protein rather than one that
> has a higher degree of sequence stringency than most (but still less
> than your designation of 'fairly specified aa residues' implies). You
> assume that there is a single *function* of cytochrome c rather than a
> cluster of *functions*. You assume that the one function you identify
> is "the" function of cytochrome c, when it actually isn't (cytochrome
> c is a heme-binding protein; electron transport is entirely due to the
> heme moiety). You assume that only proteins related to cytochrome c
> could, even in principle, possibly have that function when we know
> that, even in mitochondria, the *function* can be and is performed by
> a non-protein *in a different context*.
None of this removes the fact that the ratio for fairly specified
functional systems, to include all of the different types of
structures that could produce a given function or all types of
potentially beneficial functions, declines dramatically with each step
up the ladder of minimum structural threshold requirements. These
potentially beneficial functional systems simply are not clustered in
one tiny corner of sequence space like you imagine. That's pure
fantasy.
> > This ratio continues to drop dramatically with
> > beneficial sequences being outpaced by non-beneficial sequences by
> > more than 10 fold given a specificity of 1e-40 per 100aa. As one
> > continues to move up the ladder the increase of non-beneficial
> > sequences outpaces the increase of potentially beneficial sequences
> > more and more, approaching a 20 fold differential (likely more than 20
> > fold given different potential 3D arrangements of the same sequence
> > residues).
>
> > At this point, the exponential declining ratio is clearly problematic
> > because it is such a severe decline. The only potentially valid
> > argument left is one of clustering of potentially beneficial sequences
> > within sequence space in such a way that evolution can progress
> > because these sequences are not evenly distributed throughout sequence
> > space. However, as long as there is at lease some distribution and
> > all the beneficial sequences are not simply clustered in one tiny
> > corner of sequence space, the degree of the exponential decline in the
> > ratio will rip apart the islands of beneficial sequences and make them
> > extremely isolated from each other very quickly at relatively low
> > levels of minimum structural threshold requirements.
>
> What matters is the *minimum* number of mutational steps between
> functional structures. You have no way to calculate that. Your
> calculations are simply 'bullshit' (in its non-literal meaning).
The minimum number of mutational steps is exactly what matters - you
are most certainly right in this regard. Where you go wrong is in
thinking that the minimum possible distance is always the most likely
distance regardless of the level of minimum structural threshold
requirements under consideration. That notion is mistaken. The odds
that the minimum possible distance will be the true distance drops
many fold (maximum of 20 fold) with each increase in the minimum
structural threshold requirements.
> Short answer to the relevant question, "Is this just rhetoric, or are
> you claiming an actual calculation here?", is that it is just rhetoric
> clouded by the smoke and mirrors of pseudomath.
Your assumption that the minimum possible distance is always the most
likely distance is your key mistaken in this whole thing. The math
involved is simple and it clearly counters your position.
Sorry . . . you are backing a statistically untenable notion.
Sean Pitman
www.DetectingDesign.com
ruthf...@gmail.com
0catch.com> wrote:
> On Feb 16, 11:40 am, richardalanforr...@googlemail.com wrote:
>
> > > In any case, one doesn't need a model before the validity of the
> > > prevailing model can be adequately challenged.
>
> > But you have not offered any challenge to the prevailing model.
>
> > You have offered a model which bears little resemblance to any model
> > ever proposed by any evolutionary scientist and assert that because it
> > doesn't work beyond an arbitrary limit of change you have invented
> > evolution does not occur beyond that level. The evidence from the
> > natural world shows clearly that it does, so your model is falsified.
>
> I've presented an observation that evolution that can be observed "in
> action" is very common and fast when functional systems requiring only
> a few dozen loosely arranged residues are involved, that evolution
> becomes much less common when a few hundred residues are required, and
> that it doesn't happen at all when more than 1000 specifically
> arranged residues are required.
>
> This isn't a hypothesis or model of evolution Forrest. This is an
> observation of your proposed mechanism of evolution "in action".
1) Your model of evolution assumes that the adaptive landscape consist
of a series of isolated peaks.
2) Your model assumes that the phase space occupied by the proteins
used by biological systems is far greater than research has shown;
3) It assumes that evolution is directional.
4) It assumes that evolution is goal-oriented.
5) IIr assumes that the proteins used in biological systems are far
more specific in their function that research shows to be the case.
So it is rather a long way from "my" model of evolutioln.
> The
> process of evolution you describe demonstrably stalls out well before
> the 1000aa level is reached. Again, this is an observation, not a
> hypothesis or model. This is in fact what is happening.
>
No this is not a fact, it is a prediction of your model, which differs
considerably from that of evolutionary theory.
Where are the discontinuities on the hierarchy of living organisms
which your model predicts?
> Now come the hypotheses and models. You have no hypothesis or model
> to explain this observation. None at all. I, on the other hand, do
> have a hypothesized model to explain this very real observation.
>
> > How does this challenge any other model?
>
> Your evolutionary model does not take this stalling effect, which is
> quite real, into account. It is not explained in any published paper
> or textbook. This observation isn't even described.
This is because it does not exist. It is a prediction of your flawed
model of evolution.
If you think that iit exists, I suggest that you demonstrate its
existence with eviodence rather than unfounded assertions.
> Yet, it cannot
> be rationally denied. It does happen. Period.
As all you have is nothing but unfounded assertions. it is perfectly
rational to deny it.
> And, this observation
> directly undermines the standard evolutionary model of how the
> evolutionary mechanism is supposed to work without stalling out as it
> climbs the ladder of functional complexity. What is your explanation
> for this stalling effect?
>
Show me evidence that such a stalling effect occurs.
RF
> > RF
>
> Sean Pitmanwww.DetectingDesign.com
Seanpit
> 1) Your model of evolution assumes that the adaptive landscape consist
> of a series of isolated peaks.
More like islands - - But yes, these islands are indeed very isolated
at levels of functional complexity where the potential beneficial
target sequences require a minimum of over 1000 specifically arranged
amino acid residues.
> 2) Your model assumes that the phase space occupied by the proteins
> used by biological systems is far greater than research has shown;
I beg to differ. The known protein universe is widely distributed
throughout sequence space at all levels of minimum structural
threshold requirements.
> 3) It assumes that evolution is directional.
Evolutionary mechanisms may find any one of many different potentially
beneficial target sequences that exist in sequence space. However, if
no beneficial sequences are found via random mutations, then
functional evolution will not occur - period.
> 4) It assumes that evolution is goal-oriented.
Again, although no specific beneficial target is required to be found,
evolution is goal oriented in that it has to find novel beneficial
sequences in order for evolution to take place. Unless it finds at
least one of these, functional evolution doesn't happen.
> 5) IIr assumes that the proteins used in biological systems are far
> more specific in their function that research shows to be the case.
Not true at all. I assume a fair degree of protein flexibility for
protein-based systems. Even with a great deal of protein-system
flexibility, the problem of many fold exponential decline of
potentially beneficial sequences quickly becomes a significant issue
as one moves up the ladder of functional complexity.
> So it is rather a long way from "my" model of evolutioln.
Not at all. You just don't seem to understand that my model is right
in line with known evolutionary parameters, some of which you don't
seem to understand.
> > The
> > process of evolution you describe demonstrably stalls out well before
> > the 1000aa level is reached. Again, this is an observation, not a
> > hypothesis or model. This is in fact what is happening.
>
> No this is not a fact, it is a prediction of your model, which differs
> considerably from that of evolutionary theory.
It is an observation, not a prediction Richard. My model explains the
observation - the very real observation that you simply cannot
discount.
> Where are the discontinuities on the hierarchy of living organisms
> which your model predicts?
My model does not predict hierarchical discontinuities. It only
predicts expanding non-beneficial gaps as being responsible for the
observed stalling-out effect of evolutionary processes.
> > Now come the hypotheses and models. You have no hypothesis or model
> > to explain this observation. None at all. I, on the other hand, do
> > have a hypothesized model to explain this very real observation.
>
> > > How does this challenge any other model?
>
> > Your evolutionary model does not take this stalling effect, which is
> > quite real, into account. It is not explained in any published paper
> > or textbook. This observation isn't even described.
>
> This is because it does not exist. It is a prediction of your flawed
> model of evolution.
It does exist Richard or there'd be all kinds of real time examples of
evolution in action at levels below and about the 1000aa threshold.
> If you think that iit exists, I suggest that you demonstrate its
> existence with eviodence rather than unfounded assertions.
I have demonstrated the existence of the stalling out effect.
Observe, Richard, that evolution happens quickly and rapidly below
100aa, much less commonly between 200 and 400aa, and not at all above
the 1000aa threshold. That is a fact. There is simply no argument
here. It is a real observation regardless of if anyone has officially
noticed it.
> > Yet, it cannot
> > be rationally denied. It does happen. Period.
>
> As all you have is nothing but unfounded assertions. it is perfectly
> rational to deny it.
Rather it is you who are asserting that a very clear observation
doesn't actually exist. I'm not quite sure of your sanity here. How
can you possibly deny the fact that evolution slows down at higher and
higher levels and has never been observed to happen "in action" beyond
the 1000aa threshold when you have no examples to the contrary?
> > And, this observation
> > directly undermines the standard evolutionary model of how the
> > evolutionary mechanism is supposed to work without stalling out as it
> > climbs the ladder of functional complexity. What is your explanation
> > for this stalling effect?
>
> Show me evidence that such a stalling effect occurs.
What do you want Richard? The fact that evolution is less and less
common and then disappears completely well shy of the 1000aa marks is
the evidence! How can you not see that?
> RF
Sean Pitman
www.DetectingDesign.com
Bobby Bryant
"Seanpit" <seanpi...@naturalselection.0catch.com> writes:
> Intelligent design certainly is a potential model.
So is slhanrt[ainewrgaskfgyxzlrt ns
--
Bobby Bryant
Reno, Nevada
Remove your hat to reply by e-mail.
Bobby Bryant
"Von R. Smith" <trak...@gmail.com> writes:
> Practically every post you write, including this last one, is ample
> evidence that your argument is all just rhetoric with no actual
> calculation of the parameters you say are important to your model.
>
> Here's an experiment to test that hypothesis:
>
> How many fairly-specified residues are there in the enzyme dntD?
Fairly many, of course.
R. Baldwin
news:hLtBh.15206$O02...@newssvr11.news.prodigy.net...
> In article <1171652703.3...@v33g2000cwv.googlegroups.com>,
> "Von R. Smith" <trak...@gmail.com> writes:
>
>> Practically every post you write, including this last one, is ample
>> evidence that your argument is all just rhetoric with no actual
>> calculation of the parameters you say are important to your model.
>>
>> Here's an experiment to test that hypothesis:
>>
>> How many fairly-specified residues are there in the enzyme dntD?
>
> Fairly many, of course.
>
I think that is most unfair.
Von R. Smith
Hey, I have an hypothesis. I even posted it, together with something
it predicted, in this very thread:
[quote]
Practically every post you write, including this last one, is ample
evidence that your argument is all just rhetoric with no actual
calculation of the parameters you say are important to your model.
Here's an experiment to test that hypothesis:
How many fairly-specified residues are there in the enzyme dntD?
Prediction: "blah blah blah blah 7-letter words blah blah blah blah
go ahead and prove me wrong blah blah blah are you seriously trying
to
argue blah blah blah evolution really does simply stall out blah blah
blah the probability of two independent events is their sum blah
blah
blah...[...etc.]"
[/quote]
You've posted this post and two others like it without bothering to
respond to mine. Looks like a confirmation to me.
richardal...@googlemail.com
0catch.com> wrote:
> On Feb 16, 1:43 pm, ruthforr...@gmail.com wrote:
>
> > 1) Your model of evolution assumes that the adaptive landscape consist
> > of a series of isolated peaks.
>
> More like islands - - But yes, these islands are indeed very isolated
> at levels of functional complexity where the potential beneficial
> target sequences require a minimum of over 1000 specifically arranged
> amino acid residues.
Well, this is not the model of the adaptive landscape in evolutionary
theory.
>
> > 2) Your model assumes that the phase space occupied by the proteins
> > used by biological systems is far greater than research has shown;
>
> I beg to differ. The known protein universe is widely distributed
> throughout sequence space at all levels of minimum structural
> threshold requirements.
>
Which part of "used by biological systems" do you not understand?
The fact that such proteins are clustered closely together in the huge
potential phase space is good evidence for evolution.
> > 3) It assumes that evolution is directional.
>
> Evolutionary mechanisms may find any one of many different potentially
> beneficial target sequences that exist in sequence space. However, if
> no beneficial sequences are found via random mutations, then
> functional evolution will not occur - period.
>
Which does not make it directional as you seem to think in your use of
terms such as "higher".
> > 4) It assumes that evolution is goal-oriented.
>
> Again, although no specific beneficial target is required to be found,
> evolution is goal oriented in that it has to find novel beneficial
> sequences in order for evolution to take place. Unless it finds at
> least one of these, functional evolution doesn't happen.
>
The poorly formulated statistical argument which you are so fond of
using works only if evolution is driven towards specific goals.
> > 5) IIr assumes that the proteins used in biological systems are far
> > more specific in their function that research shows to be the case.
>
> Not true at all. I assume a fair degree of protein flexibility for
> protein-based systems. Even with a great deal of protein-system
> flexibility, the problem of many fold exponential decline of
> potentially beneficial sequences quickly becomes a significant issue
> as one moves up the ladder of functional complexity.
>
...which is no more than a empty assertion not supported by evidence.
> > So it is rather a long way from "my" model of evolutioln.
>
> Not at all. You just don't seem to understand that my model is right
> in line with known evolutionary parameters, some of which you don't
> seem to understand.
Your model differs from evolutionary theory as understood by
biologists in several rather significant areas. You have accepted
this. Why persist in your insistence that it doesn't?
Where in the scientific literature do you find the adaptive landscape
described as a adaptive archipelago, for example? This is a very
significant difference, and is one you rely on very heavily to falsify
your model.
>
> > > The
> > > process of evolution you describe demonstrably stalls out well before
> > > the 1000aa level is reached. Again, this is an observation, not a
> > > hypothesis or model. This is in fact what is happening.
>
> > No this is not a fact, it is a prediction of your model, which differs
> > considerably from that of evolutionary theory.
>
> It is an observation, not a prediction Richard. My model explains the
> observation - the very real observation that you simply cannot
> discount.
So please cite the papers in the scientific literature which conclude
that evolution "stalls out" well before the "1000aa level" is reached.
If this is a fact, one would imagine that the researchers who study
the phenomenon would be aware of it.
>
> > Where are the discontinuities on the hierarchy of living organisms
> > which your model predicts?
>
> My model does not predict hierarchical discontinuities. It only
> predicts expanding non-beneficial gaps as being responsible for the
> observed stalling-out effect of evolutionary processes.
Which sounds to me very like discontinuities in the nested hierarchy
of living organisms.
Where is this "observed stalling-out effect" recorded in the
scientific literature, by the way? None of the evolutionary biologists
I know seem to be aware of such a phenomenon.
>
> > > Now come the hypotheses and models. You have no hypothesis or model
> > > to explain this observation. None at all. I, on the other hand, do
> > > have a hypothesized model to explain this very real observation.
>
> > > > How does this challenge any other model?
>
> > > Your evolutionary model does not take this stalling effect, which is
> > > quite real, into account. It is not explained in any published paper
> > > or textbook. This observation isn't even described.
>
> > This is because it does not exist. It is a prediction of your flawed
> > model of evolution.
>
> It does exist Richard or there'd be all kinds of real time examples of
> evolution in action at levels below and about the 1000aa threshold.
>
If it exists, perhaps you could post a few links to scientific
publications which record a "stalling effect".
> > If you think that iit exists, I suggest that you demonstrate its
> > existence with eviodence rather than unfounded assertions.
>
> I have demonstrated the existence of the stalling out effect.
> Observe, Richard, that evolution happens quickly and rapidly below
> 100aa, much less commonly between 200 and 400aa, and not at all above
> the 1000aa threshold. That is a fact. There is simply no argument
> here. It is a real observation regardless of if anyone has officially
> noticed it.
It's a fact that more complex systems take more time to evolve. Why is
this a problem for evolutionary theory?
>
> > > Yet, it cannot
> > > be rationally denied. It does happen. Period.
>
> > As all you have is nothing but unfounded assertions. it is perfectly
> > rational to deny it.
>
> Rather it is you who are asserting that a very clear observation
> doesn't actually exist. I'm not quite sure of your sanity here. How
> can you possibly deny the fact that evolution slows down at higher and
> higher levels and has never been observed to happen "in action" beyond
> the 1000aa threshold when you have no examples to the contrary?
>
I've provided examples of evolution beyond such limits, as in the
origin of the mammalian ear. You deny that this is evidence on the
grounds that it was not observed in "real time", but refuse to offer
any alternative explanation for the evidence.
Mere denial of evidence is not acceptable in science.
> > > And, this observation
> > > directly undermines the standard evolutionary model of how the
> > > evolutionary mechanism is supposed to work without stalling out as it
> > > climbs the ladder of functional complexity. What is your explanation
> > > for this stalling effect?
>
> > Show me evidence that such a stalling effect occurs.
>
> What do you want Richard? The fact that evolution is less and less
> common and then disappears completely well shy of the 1000aa marks is
> the evidence! How can you not see that?
>
Sean, no matter how many times you repeat this assertion, it is not
evidence.
If you think that this is a real phenomenon and not just a prediction
of your deliberately flawed model of evolutionary processes, please
provide a citation to the scientific papers which describes this
phenomenon.
The fossil record, genetics and comparitive anatomy provides a vast
amount of evidence best explained by the theory that living organisms
have evolved from a common ancestor. This involves evolution way, way
beyond the "1000aa" mark you insist is so significant. It also
provides robust predictions which have been confirmed time and time
again.
So what hypothesis are you offering which can be tested against the
same evidence and which has equal or better predictive value? Science
does not offer ultimate truths. It seeks the best explanation for the
evidence. The best explanation for a vast amount of evidence is that
all living organism on earth have evolved from a common ancestor. As
is the case with all theories in science, it is not complete, and
there are areas of how evolution works which we are only beginning to
understand.
Why we should abandon all this because you have devised a deliberately
flawed model of evolutionary processes for no reason other than to
falsify it?
RF
> > RF
>
> Sean Pitmanwww.DetectingDesign.com
Klaus
<snip>
> Notice the assumptions in sequence space. Sean assumes that words are
> invented in English by plucking out random letters or starting with a
> random sequence and reaching the end point by a random walk. Hell, he
> should know that that is not *even* true for English words. According
> to Sean, the word 'bullshit' is reached by starting with the random 8-
> letter sequence of 'xymnufsd' and reaching the end goal by a random
> walk rather than in a single step from the pre-existing words 'bull'
> and 'shit' thus producing a word that has a modified (non-literal)
> meaning from either starting point. He should also know that words
> can change meaning without changing sequence, or he would be less than
> willing to get a 'gift'.
Did you mean "gift" in the German sense?
Klaus
<snip>
John Wilkins
One man's meat is another man's poisson.
--
John S. Wilkins, Postdoctoral Research Fellow, Biohumanities Project
University of Queensland - Blog: scienceblogs.com/evolvingthoughts
"He used... sarcasm. He knew all the tricks, dramatic irony, metaphor,
bathos, puns, parody, litotes and... satire. He was vicious."
Seanpit
> > invented in English by plucking out random letters or starting with a
> > random sequence and reaching the end point by a random walk. Hell, he
> > should know that that is not *even* true for English words. According
> > letter sequence of 'xymnufsd' and reaching the end goal by a random
> > walk rather than in a single step from the pre-existing words 'bull'
> > and 'shit' thus producing a word that has a modified (non-literal)
> > meaning from either starting point. He should also know that words
> > can change meaning without changing sequence, or he would be less than
> > willing to get a 'gift'.
You do realize that the same thing happens in genetics. The very same
gene and protein can do very different functions as part of different
systems.
The use of English here is to illustrate the distribution of
meaningful sequences in sequence space. Regardless of how you think
one information system vs. any other actually came into being, the
distribution of beneficial and potentially beneficial sequences within
sequence space is the same. These beneficial sequences are not
clustered together in one tiny corner like you claim. Anyone with any
interest in this topic should simply go look at the sequence data of
existing protein-based systems and note that they are not all
clustered together at any level - not even close.
> Did you mean "gift" in the German sense?
> Klaus
I'm sure he does.
Sean Pitman
www.DetectingDesign.com
Seanpit
> On Feb 16, 10:37 pm, "Seanpit" <seanpitnos...@naturalselection.
>
> 0catch.com> wrote:
> > On Feb 16, 1:43 pm, ruthforr...@gmail.com wrote:
>
> > > 1) Your model of evolution assumes that the adaptive landscape consist
> > > of a series of isolated peaks.
>
> > More like islands - - But yes, these islands are indeed very isolated
> > at levels of functional complexity where the potential beneficial
> > target sequences require a minimum of over 1000 specifically arranged
> > amino acid residues.
>
> Well, this is not the model of the adaptive landscape in evolutionary
> theory.
I know. That is why evolutionary thinking is wrong. If there were no
gaps in sequence space regardless of the level of functional
complexity under consideration, there would be no slowing effect as
one move up the ladder. There is a clear slowing effect of
evolutionary progress. So, your model of how sequence space actually
looks is mistaken.
It doesn't fit what is observed in either real time observations of
evolution in action or in observations of functional sequence gaps
between functional systems.
> > > 2) Your model assumes that the phase space occupied by the proteins
> > > used by biological systems is far greater than research has shown;
>
> > I beg to differ. The known protein universe is widely distributed
> > throughout sequence space at all levels of minimum structural
> > threshold requirements.
>
> Which part of "used by biological systems" do you not understand?
> The fact that such proteins are clustered closely together in the huge
> potential phase space is good evidence for evolution.
That's just it. The protein systems that *are* used by biological
systems are not closely clustered together is sequence space. They are
widely distributed throughout. Those who claim otherwise, like Howard
Hershey, don't know what they are talking about. The sequence data
clearly shows a wide distribution of existing protein-systems
throughout. I've listed several papers demonstrating this effect even
at low very low levels - such as the level of basic protein fold
"families". At higher and higher levels, the overall distribution is
still there, it is just that the individual beneficial islands become
more and more widely separated.
> > > 3) It assumes that evolution is directional.
>
> > Evolutionary mechanisms may find any one of many different potentially
> > beneficial target sequences that exist in sequence space. However, if
> > no beneficial sequences are found via random mutations, then
> > functional evolution will not occur - period.
>
> Which does not make it directional as you seem to think in your use of
> terms such as "higher".
Higher-level targets do indeed exist within sequence space. If
evolution never found any of these, no higher-level systems would
exist today. Of course, evolution does have to find higher-level
targets. However, if you want to explain how higher-level evolution
occurs, you have to explain the odds of what it takes to find higher-
level targets.
> > > 4) It assumes that evolution is goal-oriented.
>
> > Again, although no specific beneficial target is required to be found,
> > evolution is goal oriented in that it has to find novel beneficial
> > sequences in order for evolution to take place. Unless it finds at
> > least one of these, functional evolution doesn't happen.
>
> The poorly formulated statistical argument which you are so fond of
> using works only if evolution is driven towards specific goals.
Not true at all. The odds of finding different types of targets are
indeed different. Rather, it is your position that the different
minimum requirements of different types of systems don't make any
difference with regard to the time it takes to find them. That's what
is truly ludicrous.
> > > 5) IIr assumes that the proteins used in biological systems are far
> > > more specific in their function that research shows to be the case.
>
> > Not true at all. I assume a fair degree of protein flexibility for
> > protein-based systems. Even with a great deal of protein-system
> > flexibility, the problem of many fold exponential decline of
> > potentially beneficial sequences quickly becomes a significant issue
> > as one moves up the ladder of functional complexity.
>
> ...which is no more than a empty assertion not supported by evidence.
It is backed up both by real observation as well as clear statistical
analysis. Your notion that protein-system flexibility solves any
significant problems at all is clearly mistaken. Increasing the
flexibility of a target only increases the volume of the island within
sequence space. However, if you have any limitation whatsoever to the
size of the island, the increase in the non-beneficial ocean of
surrounding sequences still increases at many fold times the rate of
the increase in the number of islands. The end result is the same.
Evolutionary processes stall out at a dramatic rate at relatively low
levels of functional complexity.
> > > So it is rather a long way from "my" model of evolutioln.
>
> > Not at all. You just don't seem to understand that my model is right
> > in line with known evolutionary parameters, some of which you don't
> > seem to understand.
>
> Your model differs from evolutionary theory as understood by
> biologists in several rather significant areas. You have accepted
> this. Why persist in your insistence that it doesn't?
If my explanation for observed phenomena and statistical problems were
the same as yours, we wouldn't have a disagreement now would we? The
problem is that your explanation for real observations just doesn't
fit. You have no statistical basis behind your position. You don't
understand how random mutation and natural selection could possible do
the job you claim it does without making extraordinary claims about
the appearance of sequence space that are clearly untenable.
> Where in the scientific literature do you find the adaptive landscape
> described as a adaptive archipelago, for example? This is a very
> significant difference, and is one you rely on very heavily to falsify
> your model.
That's just it. Your notion of how sequence space looks doesn't match
what we actually see in the real world - either in sequence analysis
of existing protein systems or in real life observations of evolution
in action. Your model of sequence space is wrong.
> > > > The
> > > > process of evolution you describe demonstrably stalls out well before
> > > > the 1000aa level is reached. Again, this is an observation, not a
> > > > hypothesis or model. This is in fact what is happening.
>
> > > No this is not a fact, it is a prediction of your model, which differs
> > > considerably from that of evolutionary theory.
>
> > It is an observation, not a prediction Richard. My model explains the
> > observation - the very real observation that you simply cannot
> > discount.
>
> So please cite the papers in the scientific literature which conclude
> that evolution "stalls out" well before the "1000aa level" is reached.
No one talks about this phenomenon in literature. That doesn't make it
any less clear as a demonstrable fact. Just because a fact has been
ignored doesn't mean that it isn't real - and clearly so.
> If this is a fact, one would imagine that the researchers who study
> the phenomenon would be aware of it.
Are you unable to recognize something until someone else does? Can't
you think for yourself at all?
> > > Where are the discontinuities on the hierarchy of living organisms
> > > which your model predicts?
>
> > My model does not predict hierarchical discontinuities. It only
> > predicts expanding non-beneficial gaps as being responsible for the
> > observed stalling-out effect of evolutionary processes.
>
> Which sounds to me very like discontinuities in the nested hierarchy
> of living organisms.
A nested pattern can have gaps within itself. Gaps within the overall
pattern doesn't make the overall pattern sequence non-hierarchical.
> Where is this "observed stalling-out effect" recorded in the
> scientific literature, by the way? None of the evolutionary biologists
> I know seem to be aware of such a phenomenon.
It is recorded in the actual data. Lots of evolution at low levels,
few examples at higher levels, no examples beyond the 1000aa level.
It doesn't matter that no one has pointed out this fact in
literature. The data speaks for itself.
> > > > Now come the hypotheses and models. You have no hypothesis or model
> > > > to explain this observation. None at all. I, on the other hand, do
> > > > have a hypothesized model to explain this very real observation.
>
> > > > > How does this challenge any other model?
>
> > > > Your evolutionary model does not take this stalling effect, which is
> > > > quite real, into account. It is not explained in any published paper
> > > > or textbook. This observation isn't even described.
>
> > > This is because it does not exist. It is a prediction of your flawed
> > > model of evolution.
>
> > It does exist Richard or there'd be all kinds of real time examples of
> > evolution in action at levels below and above the 1000aa threshold.
>
> If it exists, perhaps you could post a few links to scientific
> publications which record a "stalling effect".
The data speaks for itself Richard. Do you really need someone else
to recognize a fact before you can see it for yourself?
> > > If you think that iit exists, I suggest that you demonstrate its
> > > existence with eviodence rather than unfounded assertions.
>
> > I have demonstrated the existence of the stalling out effect.
> > Observe, Richard, that evolution happens quickly and rapidly below
> > 100aa, much less commonly between 200 and 400aa, and not at all above
> > the 1000aa threshold. That is a fact. There is simply no argument
> > here. It is a real observation regardless of if anyone has officially
> > noticed it.
>
> It's a fact that more complex systems take more time to evolve. Why is
> this a problem for evolutionary theory?
Why does it take more time Richard? How much more time does it take
for every increase in minimum structural requirements? If there were
no increase in gaps for each increase in level, more time would NOT be
required. That's the whole point.
> > > > Yet, it cannot
> > > > be rationally denied. It does happen. Period.
>
> > > As all you have is nothing but unfounded assertions. it is perfectly
> > > rational to deny it.
>
> > Rather it is you who are asserting that a very clear observation
> > doesn't actually exist. I'm not quite sure of your sanity here. How
> > can you possibly deny the fact that evolution slows down at higher and
> > higher levels and has never been observed to happen "in action" beyond
> > the 1000aa threshold when you have no examples to the contrary?
>
> I've provided examples of evolution beyond such limits, as in the
> origin of the mammalian ear. You deny that this is evidence on the
> grounds that it was not observed in "real time", but refuse to offer
> any alternative explanation for the evidence.
>
> Mere denial of evidence is not acceptable in science.
Mere assertion is not acceptable science either. You assert that
sequence similarities or morphologic similarities must be the result
of common ancestry and evolutionary mechanisms. Based on what? Where
is your statistical analysis with regard to your proposed mechanism?
You argue that science doesn't need statistical analysis. That's the
first clue that you don't know what you are talking about. Without
statistical analysis regarding your mechanism, your mechanism has no
scientific backing or predictive value.
<snip >
> RF
Sean Pitman
www.DetectingDesign.com
Walter Bushell
j.wil...@uq.edu.au (John Wilkins) wrote:
> Klaus <khel...@sbcglobal.net> wrote:
>
> > hersheyh wrote:
> > <snip>
> > > Notice the assumptions in sequence space. Sean assumes that words are
> > > invented in English by plucking out random letters or starting with a
> > > random sequence and reaching the end point by a random walk. Hell, he
> > > should know that that is not *even* true for English words. According
> > > to Sean, the word 'bullshit' is reached by starting with the random 8-
> > > letter sequence of 'xymnufsd' and reaching the end goal by a random
> > > walk rather than in a single step from the pre-existing words 'bull'
> > > and 'shit' thus producing a word that has a modified (non-literal)
> > > meaning from either starting point. He should also know that words
> > > can change meaning without changing sequence, or he would be less than
> > > willing to get a 'gift'.
> >
> > Did you mean "gift" in the German sense?
>
> One man's meat is another man's poisson.
There is something fishy about that epigram.
--
"The power of the Executive to cast a man into prison without formulating any
charge known to the law, and particularly to deny him the judgement of his
peers, is in the highest degree odious and is the foundation of all totali-
tarian government whether Nazi or Communist." -- W. Churchill, Nov 21, 1943
richardal...@googlemail.com
0catch.com> wrote:
> On Feb 17, 2:16 am, richardalanforr...@googlemail.com wrote:
>
> > On Feb 16, 10:37 pm, "Seanpit" <seanpitnos...@naturalselection.
>
> > 0catch.com> wrote:
> > > On Feb 16, 1:43 pm, ruthforr...@gmail.com wrote:
>
> > > > 1) Your model of evolution assumes that the adaptive landscape consist
> > > > of a series of isolated peaks.
>
> > > More like islands - - But yes, these islands are indeed very isolated
> > > at levels of functional complexity where the potential beneficial
> > > target sequences require a minimum of over 1000 specifically arranged
> > > amino acid residues.
>
> > Well, this is not the model of the adaptive landscape in evolutionary
> > theory.
>
> I know. That is why evolutionary thinking is wrong.
Which rather contradicts your assertion that your model represents
evolutionary theory acurately!
Unfortunately it requires rather more than your unfounded assertion to
demonstrate that it is wrong, however.
> If there were no
> gaps in sequence space regardless of the level of functional
> complexity under consideration, there would be no slowing effect as
> one move up the ladder.
"Moving up the ladder" is something else which evolutionary scientists
don't consider to be a model of evolution.
> There is a clear slowing effect of
> evolutionary progress. So, your model of how sequence space actually
> looks is mistaken.
So please demonstrate from the evidence that such an effect occurs.
> It doesn't fit what is observed in either real time observations of
> evolution in action or in observations of functional sequence gaps
> between functional systems.
Since when has observation in "real time" been a requirement for
science?
Evolutionary theory predicts than major evolutionary changes will take
hundreds of thousands, if not millions of years to take place.
Do you understand that your insistence that unless we observe such
changes in "real time" evolutionary theory falsified is a bit
unreasonable?
>
> > > > 2) Your model assumes that the phase space occupied by the proteins
> > > > used by biological systems is far greater than research has shown;
>
> > > I beg to differ. The known protein universe is widely distributed
> > > throughout sequence space at all levels of minimum structural
> > > threshold requirements.
>
> > Which part of "used by biological systems" do you not understand?
> > The fact that such proteins are clustered closely together in the huge
> > potential phase space is good evidence for evolution.
>
> That's just it. The protein systems that *are* used by biological
> systems are not closely clustered together is sequence space. They are
> widely distributed throughout. Those who claim otherwise, like Howard
> Hershey, don't know what they are talking about.
I presume that you include the authors of the paper you cited as not
knowing what they are talking about as well in this case.
Who do you think actually knows about this subject? You, or the people
who have actually studied the material and published their research?
> The sequence data
> clearly shows a wide distribution of existing protein-systems
> throughout.
"The protein structure space is sparsely populated, and all of the
proteins of known structures cluster mostly into four elongated
regions, which correspond approximately to four SCOP classes (all-
{alpha}, all-beta, {alpha}+beta, and {alpha}/beta) of protein
structures indicated by red, yellow, purple, and cyan spheres,
respectively"
Funny, the authors of this paper don't seem to agree with you.
What do you know that they don't?
You do understand what "sparsely populated" means?
> I've listed several papers demonstrating this effect even
> at low very low levels - such as the level of basic protein fold
> "families". At higher and higher levels, the overall distribution is
> still there, it is just that the individual beneficial islands become
> more and more widely separated.
As has been pointed out so many times, your cherry-picking of these
papers to find quotations which you can use out of context in the
pretence that they support your assertions is not very convincing.
As for "islands", what do you think is meant by this:
"The fact that most of proteins are structured and that the protein
structure space is very sparsely populated and restricted mostly to
the four elongated regions suggest that mutations in genes encoding
proteins have been constrained to those resulting in a structurally
viable protein occupying one of the four allowed regions of the
protein structure space: structural selection or "designability" "
Oh, and please don't wet your pants over the use of the term
"designability". It's in quote marks.
>
> > > > 3) It assumes that evolution is directional.
>
> > > Evolutionary mechanisms may find any one of many different potentially
> > > beneficial target sequences that exist in sequence space. However, if
> > > no beneficial sequences are found via random mutations, then
> > > functional evolution will not occur - period.
>
> > Which does not make it directional as you seem to think in your use of
> > terms such as "higher".
>
> Higher-level targets do indeed exist within sequence space.
> If
> evolution never found any of these, no higher-level systems would
> exist today. Of course, evolution does have to find higher-level
> targets. However, if you want to explain how higher-level evolution
> occurs, you have to explain the odds of what it takes to find higher-
> level targets.
How do you recognise a "higher level target"? What metric of "level"
are you using? Is the acquisition of "milk" in cockroaches reaching a
"higher level target", and if not, why not?
>
> > > > 4) It assumes that evolution is goal-oriented.
>
> > > Again, although no specific beneficial target is required to be found,
> > > evolution is goal oriented in that it has to find novel beneficial
> > > sequences in order for evolution to take place. Unless it finds at
> > > least one of these, functional evolution doesn't happen.
>
> > The poorly formulated statistical argument which you are so fond of
> > using works only if evolution is driven towards specific goals.
>
> Not true at all. The odds of finding different types of targets are
> indeed different. Rather, it is your position that the different
> minimum requirements of different types of systems don't make any
> difference with regard to the time it takes to find them. That's what
> is truly ludicrous.
Where have I ever made such a statement?
It take more time to evolve more complex systems.
This is what evolutionary theory predicts.
Such complex systems evolve in a series of small incremental steps.
>
> > > > 5) IIr assumes that the proteins used in biological systems are far
> > > > more specific in their function that research shows to be the case.
>
> > > Not true at all. I assume a fair degree of protein flexibility for
> > > protein-based systems. Even with a great deal of protein-system
> > > flexibility, the problem of many fold exponential decline of
> > > potentially beneficial sequences quickly becomes a significant issue
> > > as one moves up the ladder of functional complexity.
>
> > ...which is no more than a empty assertion not supported by evidence.
>
> It is backed up both by real observation as well as clear statistical
> analysis.
So where has this observation and statistical analysis been
published?
And please don't refer me to your pathetic web site. The fact that
you refuse to educate yourself on the subjects you pontificate about -
such a taphonomy - makes it a very unreliable source of information.
> Your notion that protein-system flexibility solves any
> significant problems at all is clearly mistaken. Increasing the
> flexibility of a target only increases the volume of the island within
> sequence space.
"The fact that most of proteins are structured and that the protein
structure space is very sparsely populated and restricted mostly to
the four elongated regions suggest that mutations in genes encoding
proteins have been constrained to those resulting in a structurally
viable protein occupying one of the four allowed regions of the
protein structure space: structural selection or "designability".
Do you think that "island" is a good description of "four elongated
regions"?
> However, if you have any limitation whatsoever to the
> size of the island, the increase in the non-beneficial ocean of
> surrounding sequences still increases at many fold times the rate of
> the increase in the number of islands. The end result is the same.
> Evolutionary processes stall out at a dramatic rate at relatively low
> levels of functional complexity.
>
And your evidence that evolutionary processes stall out is.....?
> > > > So it is rather a long way from "my" model of evolutioln.
>
> > > Not at all. You just don't seem to understand that my model is right
> > > in line with known evolutionary parameters, some of which you don't
> > > seem to understand.
>
> > Your model differs from evolutionary theory as understood by
> > biologists in several rather significant areas. You have accepted
> > this. Why persist in your insistence that it doesn't?
>
> If my explanation for observed phenomena and statistical problems were
> the same as yours, we wouldn't have a disagreement now would we?
Then why state that your model represents that of evolutionary theory?
Perhaps you can explain why your model should supercede that of the
scientists who has done research in evolutionary biology?
> The
> problem is that your explanation for real observations just doesn't
> fit.
You mean the fact that we observe evolution action, that the records
of comparitive anatomy, genetic, the fossil record and so on match the
predictions of evolutionary theory, that we can make predictions which
we can and have tested exhaustively and all the rest is not good
enough?
I wonder what you *would* accept as evidence in that case?
Are you insisting that unless we observe the evolution of a major new
function in "real time" you refuse to accept the other evidence that
evolution has occured?
Setting impossible standards of evidence seems to be all you can do.
> You have no statistical basis behind your position.
You haven't explained either why a statistical basis is necessary, or
how one would carry out such an analysis.
> You don't
> understand how random mutation and natural selection could possible do
> the job you claim it does without making extraordinary claims about
> the appearance of sequence space that are clearly untenable.
>
Well, the people who have researched the distribution of proteins in
sequence space (of which, just to remind you, proteins used by
biological systems occupy a very small part) disagree with you.
What do you know that they don't?
> > Where in the scientific literature do you find the adaptive landscape
> > described as a adaptive archipelago, for example? This is a very
> > significant difference, and is one you rely on very heavily to falsify
> > your model.
>
> That's just it.
So your model of evolution doesn't match that of the evolutionary
scientists. Why did you say that it did?
>Your notion of how sequence space looks doesn't match
> what we actually see in the real world - either in sequence analysis
> of existing protein systems or in real life observations of evolution
> in action. Your model of sequence space is wrong.
>
....as is the model of sequence space which the researchers into
biological proteins have produced.
So what do you know that they don't?
> > > > > The
> > > > > process of evolution you describe demonstrably stalls out well before
> > > > > the 1000aa level is reached. Again, this is an observation, not a
> > > > > hypothesis or model. This is in fact what is happening.
>
> > > > No this is not a fact, it is a prediction of your model, which differs
> > > > considerably from that of evolutionary theory.
>
> > > It is an observation, not a prediction Richard. My model explains the
> > > observation - the very real observation that you simply cannot
> > > discount.
>
> > So please cite the papers in the scientific literature which conclude
> > that evolution "stalls out" well before the "1000aa level" is reached.
>
> No one talks about this phenomenon in literature.
If it were so obvious, don't you think someone other than you might
have noticed it?
> That doesn't make it
> any less clear as a demonstrable fact.
A "demonstrable fact" which nobody other than you has noticed?
I need rather more evidence than a flawed model of evolution (which I
presume you now conceede does not match that of evolutionary
biologists) and your empty assertions.
> Just because a fact has been
> ignored doesn't mean that it isn't real - and clearly so.
>
So now you are asserting that the scientist involved in the research
are ignoring this "fact" which only you have recognised?
> > If this is a fact, one would imagine that the researchers who study
> > the phenomenon would be aware of it.
>
> Are you unable to recognize something until someone else does? Can't
> you think for yourself at all?
I'm quite capable of thinking for myself. Universities don't allow
people who can't think for themselves study for PhDs. As someone who
is perfectly capable of thinking for myself, I see no reason why I
should accept as fact something which only you can see, especially
when your assertions are contradicted by the scientists who actually
work in the field, your evolutionary model is deliberately flawed, and
the level of scholarship and academic integrity you demonstrate here
and on your web site is appallingly low.
>
> > > > Where are the discontinuities on the hierarchy of living organisms
> > > > which your model predicts?
>
> > > My model does not predict hierarchical discontinuities. It only
> > > predicts expanding non-beneficial gaps as being responsible for the
> > > observed stalling-out effect of evolutionary processes.
>
> > Which sounds to me very like discontinuities in the nested hierarchy
> > of living organisms.
>
> A nested pattern can have gaps within itself. Gaps within the overall
> pattern doesn't make the overall pattern sequence non-hierarchical.
>
Gaps are not discontities.
> > Where is this "observed stalling-out effect" recorded in the
> > scientific literature, by the way? None of the evolutionary biologists
> > I know seem to be aware of such a phenomenon.
>
> It is recorded in the actual data. Lots of evolution at low levels,
> few examples at higher levels, no examples beyond the 1000aa level.
> It doesn't matter that no one has pointed out this fact in
> literature. The data speaks for itself.
>
You mean the fact that evolutionary theory predicts that more complex
functions (call them "higher level" if you want) take longer to evolve
that less complex functions?
What the data - which comes from the genetic and fossil record - tells
us is that such functions take millions of years to evolve. This makes
your demand that we should be able to observe them in "real time"
somewhat unreasonable.
Of course, if you have a better explanation for the genetic and fossil
record (by which I mean, of course, one which yields testable
predictions), please feel free to offer it.
>
>
> > > > > Now come the hypotheses and models. You have no hypothesis or model
> > > > > to explain this observation. None at all. I, on the other hand, do
> > > > > have a hypothesized model to explain this very real observation.
>
> > > > > > How does this challenge any other model?
>
> > > > > Your evolutionary model does not take this stalling effect, which is
> > > > > quite real, into account. It is not explained in any published paper
> > > > > or textbook. This observation isn't even described.
>
> > > > This is because it does not exist. It is a prediction of your flawed
> > > > model of evolution.
>
> > > It does exist Richard or there'd be all kinds of real time examples of
> > > evolution in action at levels below and above the 1000aa threshold.
>
> > If it exists, perhaps you could post a few links to scientific
> > publications which record a "stalling effect".
>
> The data speaks for itself Richard. Do you really need someone else
> to recognize a fact before you can see it for yourself?
>
I need rather more than your unfounded assertion, Sean, especially in
light of the fact that you refuse to educate yourself in the subjects
you pontificate about and refuse to address the copious evidence that
you are wrong.
Have you read "Paleobiology" yet? Just the chapters on Lagerstatten
will do.
RF
> > > > If you think that iit exists, I suggest that you demonstrate its
> > > > existence with eviodence rather than unfounded assertions.
>
> > > I have demonstrated the existence of the stalling out effect.
> > > Observe, Richard, that evolution happens quickly and rapidly below
> > > 100aa, much less commonly between 200 and 400aa, and not at all above
> > > the 1000aa threshold. That is a fact. There is simply no argument
> > > here. It is a real observation regardless of if anyone has officially
>
> ...
>
> read more »
Seanpit
> > I know. That is why evolutionary thinking is wrong.
>
> Which rather contradicts your assertion that your model represents
> evolutionary theory acurately!
I didn't say that my model was the same as yours! Hello! What I said
was that I was not misrepresenting your model. I use your model
accurately. It is just that your model does not adequately explain
the observed data. My model is a much better explanation of the facts
at hand.
> Unfortunately it requires rather more than your unfounded assertion to
> demonstrate that it is wrong, however.
You offer nothing but assertions in favor of your model. You have no
statistical analysis or predictive power whatsoever regarding your
proposed mechanism. You simply assert that it must work. That's
it!
> > If there were no
> > gaps in sequence space regardless of the level of functional
> > complexity under consideration, there would be no slowing effect as
> > one move up the ladder.
>
> "Moving up the ladder" is something else which evolutionary scientists
> don't consider to be a model of evolution.
Not true. Evolutionists strongly believe that the proposed
evolutionary mechanism can and has moved up the ladder of functional
complexity.
> > There is a clear slowing effect of
> > evolutionary progress. So, your model of how sequence space actually
> > looks is mistaken.
>
> So please demonstrate from the evidence that such an effect occurs.
You yourself admit that this effect occurs. You've even offered an
explanation for this slowing effect - arguing that it requires more
time because of a need to build up smaller changes.
> > It doesn't fit what is observed in either real time observations of
> > evolution in action or in observations of functional sequence gaps
> > between functional systems.
>
> Since when has observation in "real time" been a requirement for
> science?
>
> Evolutionary theory predicts than major evolutionary changes will take
> hundreds of thousands, if not millions of years to take place.
>
> Do you understand that your insistence that unless we observe such
> changes in "real time" evolutionary theory falsified is a bit
> unreasonable?
We are not looking at very high levels here. Real time evolution
drops off rather dramatically at the level of very small molecular
machines. There is no reason for this drop off in rate if there were
in fact no non-beneficial gaps.
> > > > > 2) Your model assumes that the phase space occupied by the proteins
> > > > > used by biological systems is far greater than research has shown;
>
> > > > I beg to differ. The known protein universe is widely distributed
> > > > throughout sequence space at all levels of minimum structural
> > > > threshold requirements.
>
> > > Which part of "used by biological systems" do you not understand?
> > > The fact that such proteins are clustered closely together in the huge
> > > potential phase space is good evidence for evolution.
>
> > That's just it. The protein systems that *are* used by biological
> > systems are not closely clustered together is sequence space. They are
> > widely distributed throughout. Those who claim otherwise, like Howard
> > Hershey, don't know what they are talking about.
>
> I presume that you include the authors of the paper you cited as not
> knowing what they are talking about as well in this case.
>
> Who do you think actually knows about this subject? You, or the people
> who have actually studied the material and published their research?
You don't seem to understand the statements of the authors - and
neither does Howard.
> > The sequence data
> > clearly shows a wide distribution of existing protein-systems
> > throughout.
>
> "The protein structure space is sparsely populated, and all of the
> proteins of known structures cluster mostly into four elongated
> regions, which correspond approximately to four SCOP classes (all-
> {alpha}, all-beta, {alpha}+beta, and {alpha}/beta) of protein
> structures indicated by red, yellow, purple, and cyan spheres,
> respectively"
>
> Funny, the authors of this paper don't seem to agree with you.
> What do you know that they don't?
>
> You do understand what "sparsely populated" means?
Do you? Of course sequence space is sparsely populated by potentially
beneficial sequences! That's one of my main points. And, it gets
more and more sparsely populated by many fold with each increase in
the structural threshold requirements. Beyond this, these extremely
outnumbered "target" sequences are NOT clustered in one tiny corner of
sequence space, even at this very low level of useable protein-folds
> > I've listed several papers demonstrating this effect even
> > at low very low levels - such as the level of basic protein fold
> > "families". At higher and higher levels, the overall distribution is
> > still there, it is just that the individual beneficial islands become
> > more and more widely separated.
>
> As has been pointed out so many times, your cherry-picking of these
> papers to find quotations which you can use out of context in the
> pretence that they support your assertions is not very convincing.
You don't have the first clue as to what you are reading in these
papers. They do indeed directly undermine your most fundamental
contentions.
> As for "islands", what do you think is meant by this:
> "The fact that most of proteins are structured and that the protein
> structure space is very sparsely populated and restricted mostly to
> the four elongated regions suggest that mutations in genes encoding
> proteins have been constrained to those resulting in a structurally
> viable protein occupying one of the four allowed regions of the
> protein structure space: structural selection or "designability" "
>
> Oh, and please don't wet your pants over the use of the term
> "designability". It's in quote marks.
Look at the actual 3D projection of sequence space presented by these
authors. The fold-types are NOT clustered together at all in one
corner of sequence space. Sure, they are loosely arranged in 4
broadly defined families. However, note that these families traverse
the entire breadth of sequence space in four loosely recognizable
directions.
Again, this directly undermines the assertion that potentially
beneficial proteins are closely clustered in one tiny corner of
sequence space. This simply isn't true, even at this very low level of
functional complexity. And, it is even less true at higher and higher
levels where family groups multiply many fold at each level of
increased structural complexity. These families are NOT all clustered
together in one tiny corner without large gaps in between. They are
indeed separated in sequence space and they become dramatically more
and more separated with each step up the ladder.
> > Higher-level targets do indeed exist within sequence space.
> > If evolution never found any of these,
> > no higher-level systems would
> > exist today. Of course, evolution does have to find higher-level
> > targets. However, if you want to explain how higher-level evolution
> > occurs, you have to explain the odds of what it takes to find higher-
> > level targets.
>
> How do you recognise a "higher level target"? What metric of "level"
> are you using? Is the acquisition of "milk" in cockroaches reaching a
> "higher level target", and if not, why not?
As I've explain dozens of times to you, a higher-level target is one
that requires a greater minimum structural threshold requirement.
Cockroach milk only requires 200 or so loosely arranged amino acid
residues. While this requirement may be at a higher level compared to
a functional system that only requires 20 loosely arranged residues,
it doesn't even come close to my challenge of crossing the 1000aa
threshold. Again, the 1000aa level is a target because it is clearly
well beyond any example of evolution in action that has ever been
observed - to include this favorite example of yours (which isn't even
a real time example).
> > > > > 4) It assumes that evolution is goal-oriented.
>
> > > > Again, although no specific beneficial target is required to be found,
> > > > evolution is goal oriented in that it has to find novel beneficial
> > > > sequences in order for evolution to take place. Unless it finds at
> > > > least one of these, functional evolution doesn't happen.
>
> > > The poorly formulated statistical argument which you are so fond of
> > > using works only if evolution is driven towards specific goals.
>
> > Not true at all. The odds of finding different types of targets are
> > indeed different. Rather, it is your position that the different
> > minimum requirements of different types of systems don't make any
> > difference with regard to the time it takes to find them. That's what
> > is truly ludicrous.
>
> Where have I ever made such a statement?
> It take more time to evolve more complex systems.
> This is what evolutionary theory predicts.
> Such complex systems evolve in a series of small incremental steps.
If there were no non-beneficial gaps between more complex systems and
other complex systems or lower level systems, more time would NOT be
required to evolve higher-level systems. You are very confused on
this point. Without non-beneficial gaps, higher-level systems would
evolve just as quickly as lower-level systems. Set up your own
simulation and you'll see that I'm correct here.
< snip >
> > Your notion that protein-system flexibility solves any
> > significant problems at all is clearly mistaken. Increasing the
> > flexibility of a target only increases the volume of the island within
> > sequence space.
>
> "The fact that most of proteins are structured and that the protein
> structure space is very sparsely populated and restricted mostly to
> the four elongated regions suggest that mutations in genes encoding
> proteins have been constrained to those resulting in a structurally
> viable protein occupying one of the four allowed regions of the
> protein structure space: structural selection or "designability".
>
> Do you think that "island" is a good description of "four elongated
> regions"?
The four elongated regions are made up of a loosely arranged
collection of island folds Richard. The reason why the individual
islands are relatively close to their neighbors is because the level
of functional complexity described here is very low indeed, involving
only a few dozen residues for each structural fold type.
> > However, if you have any limitation whatsoever to the
> > size of the island, the increase in the non-beneficial ocean of
> > surrounding sequences still increases at many fold times the rate of
> > the increase in the number of islands. The end result is the same.
> > Evolutionary processes stall out at a dramatic rate at relatively low
> > levels of functional complexity.
>
> And your evidence that evolutionary processes stall out is.....?
Real time observation and required sequence differences that do in
fact exist between higher and higher-level novel functional systems
that are already in existence.
> > > > > So it is rather a long way from "my" model of evolutioln.
>
> > > > Not at all. You just don't seem to understand that my model is right
> > > > in line with known evolutionary parameters, some of which you don't
> > > > seem to understand.
>
> > > Your model differs from evolutionary theory as understood by
> > > biologists in several rather significant areas. You have accepted
> > > this. Why persist in your insistence that it doesn't?
>
> > If my explanation for observed phenomena and statistical problems were
> > the same as yours, we wouldn't have a disagreement now would we?
>
> Then why state that your model represents that of evolutionary theory?
I never said that. I said that I accurately presented your model of
evolutionary theory. The model I present as an explanation of the
observed phenomena, clearly, is quite different than yours. It is also
far more consistent with the evidence than is your model.
> Perhaps you can explain why your model should supercede that of the
> scientists who has done research in evolutionary biology?
Because my model actually explains the evidence whereas the popular
evolution model does not explain the stalling out effect that is
clearly evident in the observed data.
> > The
> > problem is that your explanation for real observations just doesn't
> > fit.
>
> You mean the fact that we observe evolution action, that the records
> of comparitive anatomy, genetic, the fossil record and so on match the
> predictions of evolutionary theory, that we can make predictions which
> we can and have tested exhaustively and all the rest is not good
> enough?
You don't observe evolution "in action" beyond very low levels of
functional complexity - i.e., well below the 1000aa threshold. There
is a clear stalling out effect of evolution "in action" as one
approaches this 1000aa threshold. Growing non-benefical gaps are also
clearly evident in sequence data between higher-level systems that are
already in existence. These systems are NOT clustered together in one
tiny corner of sequence space.
Your theory does not explain this stalling out effect of evolution in
action nor does it explain how the clearly evident non-beneficial gaps
can be crossed in what anyone would call a reasonable amount of time.
Your theory has absolutely no predictive value when it comes to
understanding how your proposed mechanism actually works. This simply
isn't science. It just just-so story telling. It is nothing but bold
assertion independent of statistical value.
< snip rest >
Sean Pitman
www.DetectingDesign.com
Seanpit
wrote:
> "Bobby Bryant" <bdbry...@wherever.ur> wrote in message
>
> news:hLtBh.15206$O02...@newssvr11.news.prodigy.net...
>
> > In article <1171652703.316902.232...@v33g2000cwv.googlegroups.com>,
> > "Von R. Smith" <trakl...@gmail.com> writes:
>
> >> Practically every post you write, including this last one, is ample
> >> evidence that your argument is all just rhetoric with no actual
> >> calculation of the parameters you say are important to your model.
>
> >> Here's an experiment to test that hypothesis:
>
> >> How many fairly-specified residues are there in the enzyme dntD?
>
> > Fairly many, of course.
>
> I think that is most unfair.
It's not unfair at all. The answer is that there are far less than
1000. I really don't see there being any argument here.
Sean Pitman
www.DetectingDesign.com
Frank J
> On Feb 16, 6:24 pm, "Seanpit" <seanpitnos...@naturalselection.
>
> 0catch.com> wrote:
> > On Feb 16, 9:58 am, richardalanforr...@googlemail.com wrote:
>
> > > So you don't have any calculations.
>
> > I presented several calculations and the basis for the degree of the
> > decline in the ratio of beneficial vs. non-beneficial.
>
> And several people pointed out that your lack of knowledge of even
> basic statistics makes your calculations meaningless.
>
> If think that they are meaningful, please post them again.
>
> > If you
> > actually think beneficial sequences increase at a significantly
> > greater rate than I propose, please do provide your reasons. I'd be
> > most interested.
>
> You have a model of evolution you have devised for no reason other
> than to falsify it.
> You have no evidence support your model, and the only prediction of
> your model - that there are discontinuities in the nested hierarchy of
> living organisms - is not supported by the evidence. This falsifies
> your model.
Can we even call that a "model"? If he really thinks that two lineages
are truly unrelated by "descent with evolutionary modification" (& I
strongly suspect that he does *not*), why is he not proposing a
testable hypothesis of saltation (or "descent with 'revolutionary'
modification), or independent abiogenesis?
>
> Your "explanation" for this lack of evidence is "common design" or
> "hierachical design" or "intelligent design",
IOW weasel words.
> none of which have any
> predictive value whatsoever, and none of which are supported by any
> evidence whatsoever. You cannot, for example, show that the works of
> any individual designer use any such principle - contrary to your
> assertion that this is "common practice".
>
> Inventing things as you go along when your argument is demolished may
> provide you with some facile satisfaction, but it is not exactly
> honest, is it?
Especially when all that "inventing" serves only to promote
incredulity about evolution, and says absolutely nothing to support
any potential alternative - that he knows cannot be supported.
>
> RF
>
>
>
> > < snip >
>
> > Sean Pitmanwww.DetectingDesign.com- Hide quoted text -
richardal...@googlemail.com
0catch.com> wrote:
> On Feb 17, 11:22 am, richardalanforr...@googlemail.com wrote:
>
> > > I know. That is why evolutionary thinking is wrong.
>
> > Which rather contradicts your assertion that your model represents
> > evolutionary theory acurately!
>
> I didn't say that my model was the same as yours! Hello! What I said
> was that I was not misrepresenting your model.
You quite categorically did! The adaptive landscape of evolutionary
theory is *NOT* a series of isolated islands. So you *DID*
mispreresent "my" model.
> I use your model
> accurately.
That is quite frankly a bald-faced lie.
The adaptive landscape of evolutionary theory is *NOT* a series of
isolated islands.
> It is just that your model does not adequately explain
> the observed data. My model is a much better explanation of the facts
> at hand.
And which facts are those, Sean? The "facts" which you claim that all
those evolutionary scientists are studiously ignoring, and which only
you seem to be aware of?
>
> > Unfortunately it requires rather more than your unfounded assertion to
> > demonstrate that it is wrong, however.
>
> You offer nothing but assertions in favor of your model.
How do you explain the series of fossils which palaeontologists
interpret as the evolution of the mammalian ear from elements of the
reptilian jaw, for example?
This is evidence which I have presented on several occasions, which
makes this another outright lie.
I've suggested that you educate yourself in evolutionary biology. I've
offered plenty of evidence, but you refuse to address it or provide
any alternative explanation.;
> You have no
> statistical analysis or predictive power whatsoever regarding your
> proposed mechanism. You simply assert that it must work. That's
> it!
>
I gave you the example of the discovery of Tiktaalik. This involved
prediction of both the morphology and geographical location of the
specimens.l
So this is another lie, Sean.
You have not explained why a statistical analysis is a requirement in
any case, and I have explained why such an analysis is neither
applicable nor possible.
> > > If there were no
> > > gaps in sequence space regardless of the level of functional
> > > complexity under consideration, there would be no slowing effect as
> > > one move up the ladder.
>
> > "Moving up the ladder" is something else which evolutionary scientists
> > don't consider to be a model of evolution.
>
> Not true. Evolutionists strongly believe that the proposed
> evolutionary mechanism can and has moved up the ladder of functional
> complexity.
I can only suggest that you educate yourself in evolutionary theory.
The idea of a "ladder of complexity" is an apparent reference to the
great chain of being, a concept abandoned by science well over a
century ago. Evolutionary scientists are *very* careful to avoid
language which implies "higher" or "lower" organisms, or a direction
to evolution.
I suggest that you educate yourself on the metabolism of temperature
regulatory mechanisms in lizards, and compare that to the temperature
control systems in mammals. Mammals have a far less complex system.
>
> > > There is a clear slowing effect of
> > > evolutionary progress. So, your model of how sequence space actually
> > > looks is mistaken.
>
> > So please demonstrate from the evidence that such an effect occurs.
>
> You yourself admit that this effect occurs. You've even offered an
> explanation for this slowing effect - arguing that it requires more
> time because of a need to build up smaller changes.
What is wrong with this explanation?
>
> > > It doesn't fit what is observed in either real time observations of
> > > evolution in action or in observations of functional sequence gaps
> > > between functional systems.
>
> > Since when has observation in "real time" been a requirement for
> > science?
>
> > Evolutionary theory predicts than major evolutionary changes will take
> > hundreds of thousands, if not millions of years to take place.
>
> > Do you understand that your insistence that unless we observe such
> > changes in "real time" evolutionary theory falsified is a bit
> > unreasonable?
>
> We are not looking at very high levels here.
You are specifically demanding "higher levels", Sean.
Another lie, I'm afraid.
> Real time evolution
> drops off rather dramatically at the level of very small molecular
> machines.
Another unfounded assertion, Sean.
> There is no reason for this drop off in rate if there were
> in fact no non-beneficial gaps.
A conclusion drawn from an unfounded assertion.
>
>
>
> > > > > > 2) Your model assumes that the phase space occupied by the proteins
> > > > > > used by biological systems is far greater than research has shown;
>
> > > > > I beg to differ. The known protein universe is widely distributed
> > > > > throughout sequence space at all levels of minimum structural
> > > > > threshold requirements.
>
> > > > Which part of "used by biological systems" do you not understand?
> > > > The fact that such proteins are clustered closely together in the huge
> > > > potential phase space is good evidence for evolution.
>
> > > That's just it. The protein systems that *are* used by biological
> > > systems are not closely clustered together is sequence space. They are
> > > widely distributed throughout. Those who claim otherwise, like Howard
> > > Hershey, don't know what they are talking about.
>
> > I presume that you include the authors of the paper you cited as not
> > knowing what they are talking about as well in this case.
>
> > Who do you think actually knows about this subject? You, or the people
> > who have actually studied the material and published their research?
>
> You don't seem to understand the statements of the authors - and
> neither does Howard.
Oh I see. But you do.
Could you explain why the authors of this paper use these protein
data to reconstruct evolutionary relationships in this case? Evidently
they do *not* agree with your assertion that evolution "stalls out" at
"higher levels of complexity", so I fail to see how you can claim
that they support your views.
>
> > > The sequence data
> > > clearly shows a wide distribution of existing protein-systems
> > > throughout.
>
> > "The protein structure space is sparsely populated, and all of the
> > proteins of known structures cluster mostly into four elongated
> > regions, which correspond approximately to four SCOP classes (all-
> > {alpha}, all-beta, {alpha}+beta, and {alpha}/beta) of protein
> > structures indicated by red, yellow, purple, and cyan spheres,
> > respectively"
>
> > Funny, the authors of this paper don't seem to agree with you.
> > What do you know that they don't?
>
> > You do understand what "sparsely populated" means?
>
> Do you? Of course sequence space is sparsely populated by potentially
> beneficial sequences!
No, Sean.
Either you are unable to read for comprehension or you are lying
again.
They are talking about the proteins used by biological systems, not
"potentially beneficial sequences"
> That's one of my main points.
...and as you have either failed to understand the paper to which this
refers, or are deliberately misrepresenting it, your argument rather
falls apart, doesn't it?
> And, it gets
> more and more sparsely populated by many fold with each increase in
> the structural threshold requirements. Beyond this, these extremely
> outnumbered "target" sequences are NOT clustered in one tiny corner of
> sequence space, even at this very low level of useable protein-folds
There is no reference whatsoever in this paper to "target sequences".
>
> > > I've listed several papers demonstrating this effect even
> > > at low very low levels - such as the level of basic protein fold
> > > "families". At higher and higher levels, the overall distribution is
> > > still there, it is just that the individual beneficial islands become
> > > more and more widely separated.
>
> > As has been pointed out so many times, your cherry-picking of these
> > papers to find quotations which you can use out of context in the
> > pretence that they support your assertions is not very convincing.
>
> You don't have the first clue as to what you are reading in these
> papers. They do indeed directly undermine your most fundamental
> contentions.
So a paper in which the authors draw conclusions of evolutionary
relationships and timing of divergence of lineages from a study of the
distribution of the proteins used in biological systems "undermines"
my "fundamental contentions"?
>
> > As for "islands", what do you think is meant by this:
> > "The fact that most of proteins are structured and that the protein
> > structure space is very sparsely populated and restricted mostly to
> > the four elongated regions suggest that mutations in genes encoding
> > proteins have been constrained to those resulting in a structurally
> > viable protein occupying one of the four allowed regions of the
> > protein structure space: structural selection or "designability" "
>
> > Oh, and please don't wet your pants over the use of the term
> > "designability". It's in quote marks.
>
> Look at the actual 3D projection of sequence space presented by these
> authors. The fold-types are NOT clustered together at all in one
> corner of sequence space. Sure, they are loosely arranged in 4
> broadly defined families. However, note that these families traverse
> the entire breadth of sequence space in four loosely recognizable
> directions.
The graphs only illustrate the portion of sequence space occupied by
biological proteins! Where on earth do you get the notion that they
"traverse the entire breadth of sequence space"?
>
> Again, this directly undermines the assertion that potentially
> beneficial proteins are closely clustered in one tiny corner of
> sequence space. This simply isn't true, even at this very low level of
> functional complexity. And, it is even less true at higher and higher
> levels where family groups multiply many fold at each level of
> increased structural complexity. These families are NOT all clustered
> together in one tiny corner without large gaps in between. They are
> indeed separated in sequence space and they become dramatically more
> and more separated with each step up the ladder.
>
Sean, learn to read and understand graphs.
> > > Higher-level targets do indeed exist within sequence space.
> > > If evolution never found any of these,
> > > no higher-level systems would
> > > exist today. Of course, evolution does have to find higher-level
> > > targets. However, if you want to explain how higher-level evolution
> > > occurs, you have to explain the odds of what it takes to find higher-
> > > level targets.
>
> > How do you recognise a "higher level target"? What metric of "level"
> > are you using? Is the acquisition of "milk" in cockroaches reaching a
> > "higher level target", and if not, why not?
>
> As I've explain dozens of times to you, a higher-level target is one
> that requires a greater minimum structural threshold requirement.
So what metric of "level" defines a "higher level target"?
Repeating assertions is not explaining anything. Answering questions
is.
> Cockroach milk only requires 200 or so loosely arranged amino acid
> residues.
So on what metric have you established that this is not a "higher
level function"?
> While this requirement may be at a higher level compared to
> a functional system that only requires 20 loosely arranged residues,
> it doesn't even come close to my challenge of crossing the 1000aa
> threshold. Again, the 1000aa level is a target because it is clearly
> well beyond any example of evolution in action that has ever been
> observed - to include this favorite example of yours (which isn't even
> a real time example).
So what you are telling us is that a "higher level function" is
defined only in terms of the arbitrary "1000aa level".
Perhaps you can explain why.
>
>
>
> > > > > > 4) It assumes that evolution is goal-oriented.
>
> > > > > Again, although no specific beneficial target is required to be found,
> > > > > evolution is goal oriented in that it has to find novel beneficial
> > > > > sequences in order for evolution to take place. Unless it finds at
> > > > > least one of these, functional evolution doesn't happen.
>
> > > > The poorly formulated statistical argument which you are so fond of
> > > > using works only if evolution is driven towards specific goals.
>
> > > Not true at all. The odds of finding different types of targets are
> > > indeed different. Rather, it is your position that the different
> > > minimum requirements of different types of systems don't make any
> > > difference with regard to the time it takes to find them. That's what
> > > is truly ludicrous.
>
> > Where have I ever made such a statement?
> > It take more time to evolve more complex systems.
> > This is what evolutionary theory predicts.
> > Such complex systems evolve in a series of small incremental steps.
>
> If there were no non-beneficial gaps between more complex systems and
> other complex systems or lower level systems, more time would NOT be
> required to evolve higher-level systems.
Oh, please!
Walk ten paces, and time yourself.
Walk a hundred paces and time yourself.
Which takes longer?
> You are very confused on
> this point. Without non-beneficial gaps, higher-level systems would
> evolve just as quickly as lower-level systems. Set up your own
> simulation and you'll see that I'm correct here.
>
> < snip >
>
> > > Your notion that protein-system flexibility solves any
> > > significant problems at all is clearly mistaken. Increasing the
> > > flexibility of a target only increases the volume of the island within
> > > sequence space.
>
> > "The fact that most of proteins are structured and that the protein
> > structure space is very sparsely populated and restricted mostly to
> > the four elongated regions suggest that mutations in genes encoding
> > proteins have been constrained to those resulting in a
>
> ...
>
> read more »
Let's restore just some of what you snipped, Sean.
What's the matter? Are you embarrased by the number of questions you
are evading?
R. Baldwin
news:1171821342.1...@a75g2000cwd.googlegroups.com...
This was a joke, Sean.
Bobby Bryant
"Seanpit" <seanpi...@naturalselection.0catch.com> writes:
> Not true. Evolutionists strongly believe that the proposed
> evolutionary mechanism can and has moved up the ladder of functional
> complexity.
So let's get this clear... Do you admit that evolution has happened,
and merely reject the proposed mechanism? Or do you reject the fact
as well as the explanation?
> You don't seem to understand the statements of the authors - and
> neither does Howard.
8<
> You don't have the first clue as to what you are reading in these
> papers. They do indeed directly undermine your most fundamental
> contentions.
Sean, when have you *ever* posted *anything* here that would make
*anyone* think you were qualified to interpret a scientific paper?
Whenever you drop in on topics I know something about, you've shown
yourself to be clueless about the most basic of concepts, and yet
you're absolutely dogmatic that the results of that field refute
evolution. And whenever you get onto other topics, the people who
have actually studied those topics also say that you show yourself to
be clueless about the most basic of concepts, but still you're
absolutely dogmatic that the results of that field refute evolution.
And when people show you to be wrong, you start introducing undefined
terms into your argument.
Why should I give even the briefest consideration to your claim that
you understand the papers better than Steve and Howard do?
Has it ever crossed your mind that you simply aren't qualified to
argue against evolution, even if it happened to be wrong?
carlip...@physics.ucdavis.edu
> On Feb 15, 10:57 am, carlip-nos...@physics.ucdavis.edu wrote:
>> Seanpit <seanpitnos...@naturalselection.0catch.com> wrote:
>> > Yes, but the odds of success for a given attempt are exponentially
>> > less likely [when the novel function has a greater minimum structural
>> > threshold requirement].
>> "Exponentially less likely" is a phrase I often hear from people who
>> don't know very much math. By itself, it doesn't mean anything --
>> depending on the "decay constant" in the exponent, an exponential
>> relation may be very different from a linear relation, or it may be
>> almost indistinguishable from a linear relation. (That is, if a<<1/N,
>> then e^{-aN} is very nearly equal to 1-aN.)
>> Is this just rhetoric, or are you claiming an actual calculation here?
>> If the latter, what is the value of the constant in the exponent?
>> How, exactly, did you determine (or measure) this value?
> How many additional potentially beneficial structures do you think are
> added with each additional 1aa structural requirement?
I asked you how you determined your claim. I don't see how "What do
you think?" is a responsive answer.
In any case, it seems unlikely to me that your question makes sense.
In particular:
** Why do you think the answer should be the same from protein to protein?
Note that you must assume this if you want to justify your "exponential."
An average of exponential functions is not an exponential function, and
can, in fact, be just about anything. (Look up the Laplace transform.)
** Why do you think the answer is independent of the number of previous
"1aa structural requirement[s]"? Again, if it is not, you will not get
anything like exponential behavior.
> I propose that as one moves up the ladder of minimum structural
> threshold requirements, 1aa at a time, the increase in potentially
> beneficial sequences approaches a exponent of 1 while the increase in
> non-beneficial sequences approaches an exponent of 20.
OK, that's your proposal. Please recall that my question was, "How,
exactly, did you determine (or measure) this value?"
Have you done, or can you cite, specific theoretical calculations --
as a first step, for example, a computation of the number of
biologically distinct protein foldings -- that has led you to these
numbers? Have you done, or can you cite, systematic experimental
results that lead to these numbers? If so, could you please give me
the citations, and identify specifically where the numbers "1" and
"20" appear?
Why 1 and not, say, 5? Why 20 and not, say, 12, or 30?
Why a single number, and not, say, "20 for the first 15 steps; then
5 for the next ten steps because the number of protein geometries
suddenly increases, then 30 for the next five steps, then 2 for a
couple of steps..."? Why not "20 for proteins A and B, 30 for
protein C, 100 for protein D, and 5 for protein E?"
Note that I am not advocating a particular alternative here, so a
repeat of "What do you think" is not an appropriate answer. You are
making a proposal, with a specific mathematical form and, now, some
specific numbers. I am asking for *your* *evidence* for your proposal.
> For example, the total number of meaningful sequences in the English
> language system for 1-character sequences is about 3. This produces a
> ratio of about 1 in 8 meaningful vs. non-meaningful sequences at this
> level.
So your mathematical claim is based on a metaphor?
[...]
> How many 1aa systems are potentially beneficial from the perspective
> of a given life form? 100% - right? The same is almost certainly
> true of 2aa sequences. However, this pattern doesn't last long. The
> increase in potentially beneficial sequences rapidly declines as one
> moves up the ladder of specifically arranged residues 1aa at a time.
Exponentially? Citation, please.
> By the time the 100aa level is reached, the ratio of potentially
> beneficial vs. non-beneficial is around 1e-40 to 1e-60 depending on
> the degree of specificity one is considering (Sauer, Olsen, Yockey,
> Musgrave, etc).
Specific citation, and precise definition of "degree of specificity,"
please. Again, you are making a fairly exact mathematical claim;
please provide citations in which I can see the math.
> This ratio continues to drop dramatically with
> beneficial sequences being outpaced by non-beneficial sequences by
> more than 10 fold given a specificity of 1e-40 per 100aa. As one
> continues to move up the ladder the increase of non-beneficial
> sequences outpaces the increase of potentially beneficial sequences
> more and more, approaching a 20 fold differential (likely more than 20
> fold given different potential 3D arrangements of the same sequence
> residues).
Again, are you claiming this as an experimental result? As a
theoretical prediction? Please give a citation, or a calculation,
from which I can see these numbers you are using.
Steve Carlip
Seanpit
wrote:
> "Seanpit" <seanpitnos...@naturalselection.0catch.com> wrote in message
Good one! ; )
Seanpit
> I asked you how you determined your claim. I don't see how "What do
> you think?" is a responsive answer.
>
> In any case, it seems unlikely to me that your question makes sense.
Then that's progress. This question must make sense before there is
any further basis of discussion. So, lets work on that first . . .
> In particular:
>
> ** Why do you think the answer should be the same from protein to protein?
I don't think I suggested that the answer would be the same from
protein to protein. Different types of protein-based systems have
different minimum structural threshold requirements. Some types of
functional systems require a greater number of specifically arranged
amino acid residues while other types require fewer before at least a
minimum selective advantage will be gained.
For example, the lactase function seems to require a minimum of at
least 380 fairly specifically arranged amino acid residues. Nylonase,
on the other hand, seems to require about 200aa. The insulin function
seems to require no more than 50 or so residues at minimum.
So, you see, it is the type of function that has minimum structural
threshold requirements.
These different minimums are what I call "levels of functional
complexity" or "minimum structural threshold requirements".
> Note that you must assume this if you want to justify your "exponential."
Not quite true since I'm not looking at the proteins themselves but at
different types of protein-based systems that have different minimum
structural threshold requirements.
> An average of exponential functions is not an exponential function, and
> can, in fact, be just about anything. (Look up the Laplace transform.)
I'm not looking at an average of exponential functions. I'm looking
at a specific exponential that is roughly identifiable to at least a
useful degree for a given level of minimum structural threshold
requirements (which includes a measure of the minimum number of
residues and degree of specificity of their arrangement before a
particular type of function can be realized to a useful degree).
> ** Why do you think the answer is
> independent of the number of previous
> "1aa structural requirement[s]"?
> Again, if it is not, you will not get
> anything like exponential behavior.
Again, consider the English-language analogy. Each increase in the
minimum size requirement for a meaningful sequence by a single
character does indeed exponentially increase the number of non-
meaningful sequences many times faster than the increase of meaningful
sequences. I propose that exactly the same thing happens in genetic
information systems and protein-based functional systems. If you
understand the basis for the marked exponential difference in one, the
other is also clear.
> > I propose that as one moves up the ladder of minimum structural
> > threshold requirements, 1aa at a time, the increase in potentially
> > beneficial sequences approaches a exponent of 1 while the increase in
> > non-beneficial sequences approaches an exponent of 20.
>
> OK, that's your proposal. Please recall that my question was, "How,
> exactly, did you determine (or measure) this value?"
>
> Have you done, or can you cite, specific theoretical calculations --
> as a first step, for example, a computation of the number of
> biologically distinct protein foldings -- that has led you to these
> numbers? Have you done, or can you cite, systematic experimental
> results that lead to these numbers?
As far as distinct protein folds, it seems clear that there is a
limited number of viable folds - "about ten thousand distinctly
different types of folds." This is a tiny fraction of the total
number of possible proteins within the size of protein-fold space.
For example, the size of sequence space for protein fold sequences of
25aa or less is 20^25 or about 1e32.
"A recent study, based solely on objective similarity among the 3D
structures represented by C-alpha atoms and using a much larger
structure database and multidimensional scaling, revealed that all of
the known protein folds and protein structures cluster into four
elongated regions in the very sparsely populated protein structure
space."
Note that functions or beneficial sequences that only require a
minimum of 25 fairly specifically arranged residues is a very low
level function the overall ladder of functional complexity. Functions
at this level, even though "sparse" are really not that sparse
relatively speaking. This means they are (though distributed across
the entire breadth of sequence space) fairly closely arranged relative
to each other with very small gaps between the boarders of one and the
next closest viable/beneficial structure in structural space.
http://www.lbl.gov/Science-Articles/Archive/PBD-Universe-map-Kim.html
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1560931
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1560931&rendertype=figure&id=F2
> If so, could you please give me
> the citations, and identify specifically where the numbers "1" and
> "20" appear?
The number 20 is the theoretical maximum increase in sequence/
structural space size with each additional amino acid residue
requirement. This limitation is due to the fact that there are only
20 commonly used amino acid residues in living things. For example,
the sequence/structural space size for a sequence of 5aa is 20^5 or
3,200,000. Compare this to the sequence space size for a sequence of
6aa, which is 20^6 or 64,000,000.
If the "level" of complexity in question required complete specificity
of sequence, the
> Why 1 and not, say, 5? Why 20 and not, say, 12, or 30?
Actually, I think the increase in potentially beneficial sequences
would approach an exponent of 0 instead of 1.
> Why a single number, and not, say, "20 for the first 15 steps; then
> 5 for the next ten steps because the number of protein geometries
> suddenly increases, then 30 for the next five steps, then 2 for a
> couple of steps..."? Why not "20 for proteins A and B, 30 for
> protein C, 100 for protein D, and 5 for protein E?"
Again, I'm not talking about proteins here, but levels of functional
complexity; How many potentially beneficial sequences/structures vs.
non-beneficial sequences/structures exist at a given level of
structural threshold requirements? That number is a specific number
even if this number is not absolutely known. In any case, I think
this number can be roughly approximated even if it cannot be fully
known.
> Note that I am not advocating a particular alternative here, so a
> repeat of "What do you think" is not an appropriate answer. You are
> making a proposal, with a specific mathematical form and, now, some
> specific numbers. I am asking for *your* *evidence* for your proposal.
Certainly I'm the one making a proposal here, but is it completely out
of the question for me to ask what others might think regarding this
particular problem? Do you have absolutely no personal thoughts or
even hunches on this topic?
> > For example, the total number of meaningful sequences in the English
> > language system for 1-character sequences is about 3. This produces a
> > ratio of about 1 in 8 meaningful vs. non-meaningful sequences at this
> > level.
>
> So your mathematical claim is based on a metaphor?
As it turns out, this metaphor isn't really a metaphor. All
information systems share some basic features to include a very
similar exponential decay in the ratio between beneficial vs. non-
beneficial sequences as one moves up the ladder of functional
complexity. This is true of the English language, computer code, and
genetic information, among many others.
> > How many 1aa systems are potentially beneficial from the perspective
> > of a given life form? 100% - right? The same is almost certainly
> > true of 2aa sequences. However, this pattern doesn't last long. The
> > increase in potentially beneficial sequences rapidly declines as one
> > moves up the ladder of specifically arranged residues 1aa at a time.
>
> Exponentially? Citation, please.
>
> > By the time the 100aa level is reached, the ratio of potentially
> > beneficial vs. non-beneficial is around 1e-40 to 1e-60 depending on
> > the degree of specificity one is considering (Sauer, Olsen, Yockey,
> > Musgrave, etc).
>
> Specific citation, and precise definition of "degree of specificity,"
> please. Again, you are making a fairly exact mathematical claim;
> please provide citations in which I can see the math.
The definition of "specificity" is the degree of change that can be
tolerated before a complete lack of beneficial function of a certain
type is realized. Some protein-based functions cannot tolerate very
much change in sequence/structure at all before a complete loss of
that type of function while other functions can tolerate a great deal
of change. The greater the degree of change that can be tolerated,
the greater the absolute number of sequences in sequence space that
can produce the function in question.
It seems that in 1978 Yockey calculated the ratio of cytochrome c
sequences in sequence space via phylogenetic sequence comparisons and
then published an article in the Journal of Theoretical Biology
(Yockey, 1981, J Theor Biol, 91) suggesting that the ratio of
functional cytochrome c sequences in sequence space of about 100aa
would probably be around 1 in 1e65.
In this light, it is interesting to consider the work of "Robert T.
Sauer and his M.I.T. team of biologists who undertook the scientific
research of substituting the 20 different types amino acids in two
different proteins. After each substitution, the protein sequence was
reinserted into bacteria to be tested for function. They discovered
that in some locations of the protein's amino acid chains, up to 15
different amino acids may be substituted while at other locations
their was a tolerance of only a few, and yet other locations could not
tolerate even one substitution of any other amino acid. One of the
proteins they chose was the 92-residue lambda repressor. Sauer et. al.
calculated that:
"... there should be about 10^57 different allowed sequences for the
entire 92 residue domain. ... the calculation does indicate in a
qualitative way the tremendous degeneracy in the information that does
specifies a particular protein fold. Nevertheless, the estimated
number of sequences capable of adopting the lambda repressor fold is
still an exceedingly small fraction, about 1 in 10^63, of the total
possible 92 residue sequences."
Sauer et. al. go on to highlight that "Yockey (1978) had obtained
similar result for cytochrome C."
Biologists R.T. Sauer, James U Bowie, John F.R. Olson, and Wendall A.
Lim, 1989, 'Proceedings of the National Academy of Science's USA 86,
2152-2156. and 1990, March 16, Science, 247; and, John F. Reidhaar-
Olson and Robert T. Sauer, "Functionally Acceptable Substitutions in
Two a-Helical regions of the [lambda] Repressor", Proteins: Structure,
Function, and Genetics 7:306-316, 1990.
Then, in 1992, Yockey revised this estimate to 1 in 1e36 (see
reference). However, this revised estimate does not negate the work
by Sauer et al showing that some types of ~100aa functions do indeed
have ratios as low as 1 in 1e60 in sequence space. These functions are
obviously quite specified. Even a function with a ratio of 1 in 1e36
is fairly specified - wouldn't you say?
Yockey HP, "Information Theory and Molecular Biology", Cambridge
University Press, 1992
> > This ratio continues to drop dramatically with
> > beneficial sequences being outpaced by non-beneficial sequences by
> > more than 10 fold given a specificity of 1e-40 per 100aa. As one
> > continues to move up the ladder the increase of non-beneficial
> > sequences outpaces the increase of potentially beneficial sequences
> > more and more, approaching a 20 fold differential (likely more than 20
> > fold given different potential 3D arrangements of the same sequence
> > residues).
>
> Again, are you claiming this as an experimental result? As a
> theoretical prediction? Please give a citation, or a calculation,
> from which I can see these numbers you are using.
Both. I think there is a good deal of experimental evidence to form
an good inductive basis for theoretical predictions.
> Steve Carlip
Sean Pitman
www.DetectingDesign.com
Seanpit
> In article <1171821119.373860.183...@v45g2000cwv.googlegroups.com>,
> "Seanpit" <seanpitnos...@naturalselection.0catch.com> writes:
>
> > Not true. Evolutionists strongly believe that the proposed
> > evolutionary mechanism can and has moved up the ladder of functional
> > complexity.
>
> So let's get this clear... Do you admit that evolution has happened,
> and merely reject the proposed mechanism? Or do you reject the fact
> as well as the explanation?
Without the mechanism, there is no evolution. Evolution, by
definition, is change over time by use of random mutation and natural
selection. Any other mechanism isn't "evolution".
> > You don't seem to understand the statements of the authors - and
> > neither does Howard.
>
> 8<
>
> > You don't have the first clue as to what you are reading in these
> > papers. They do indeed directly undermine your most fundamental
> > contentions.
>
> Sean, when have you *ever* posted *anything* here that would make
> *anyone* think you were qualified to interpret a scientific paper?
>
> Whenever you drop in on topics I know something about, you've shown
> yourself to be clueless about the most basic of concepts, and yet
> you're absolutely dogmatic that the results of that field refute
> evolution. And whenever you get onto other topics, the people who
> have actually studied those topics also say that you show yourself to
> be clueless about the most basic of concepts, but still you're
> absolutely dogmatic that the results of that field refute evolution.
>
> And when people show you to be wrong, you start introducing undefined
> terms into your argument.
>
> Why should I give even the briefest consideration to your claim that
> you understand the papers better than Steve and Howard do?
>
> Has it ever crossed your mind that you simply aren't qualified to
> argue against evolution, even if it happened to be wrong?
LOL - oh please! Where are these arguments that have clearly proved
me wrong on any significant aspect of my position? - Or where have I
introduced undefined terms that you just can't seem to figure out?
This is like Pres. Clinton asking for the definition of "is". Also,
I'm not the only one who has studied genetics in some detail who
remains "confused" about how the proposed mechanism of evolution could
actually do what you guys confidently assert that it does - a bald
assertion without any statistical predictive power I might add.
> Bobby Bryant
> Reno, Nevada
Sean Pitman
www.DetectingDesign.com
Sean Pitman
www.DetectingDesign.com
Bobby Bryant
"Seanpit" <seanpi...@naturalselection.0catch.com> writes:
> On Feb 18, 1:23 pm, bdbry...@wherever.ur (Bobby Bryant) wrote:
>> In article <1171821119.373860.183...@v45g2000cwv.googlegroups.com>,
>> "Seanpit" <seanpitnos...@naturalselection.0catch.com> writes:
>>
>> > Not true. Evolutionists strongly believe that the proposed
>> > evolutionary mechanism can and has moved up the ladder of functional
>> > complexity.
>>
>> So let's get this clear... Do you admit that evolution has happened,
>> and merely reject the proposed mechanism? Or do you reject the fact
>> as well as the explanation?
>
> Without the mechanism, there is no evolution. Evolution, by
> definition, is change over time by use of random mutation and natural
> selection. Any other mechanism isn't "evolution".
No, you're mistaking the explanation for the thing explained.
We knew about evolution before Charles Darwin was born.
>> > You don't seem to understand the statements of the authors - and
>> > neither does Howard.
>>
>> 8<
>>
>> > You don't have the first clue as to what you are reading in these
>> > papers. They do indeed directly undermine your most fundamental
>> > contentions.
>>
>> Sean, when have you *ever* posted *anything* here that would make
>> *anyone* think you were qualified to interpret a scientific paper?
>>
>> Whenever you drop in on topics I know something about, you've shown
>> yourself to be clueless about the most basic of concepts, and yet
>> you're absolutely dogmatic that the results of that field refute
>> evolution. And whenever you get onto other topics, the people who
>> have actually studied those topics also say that you show yourself to
>> be clueless about the most basic of concepts, but still you're
>> absolutely dogmatic that the results of that field refute evolution.
>>
>> And when people show you to be wrong, you start introducing undefined
>> terms into your argument.
>>
>> Why should I give even the briefest consideration to your claim that
>> you understand the papers better than Steve and Howard do?
>>
>> Has it ever crossed your mind that you simply aren't qualified to
>> argue against evolution, even if it happened to be wrong?
>
> LOL - oh please! Where are these arguments that have clearly proved
> me wrong on any significant aspect of my position?
Do you want me to look up your idiotic entropy post that you've asked
me not to rub your nose in?
> - Or where have I introduced undefined terms that you just can't
> seem to figure out?
Does "fairly specified" ring a bell?
> This is like Pres. Clinton asking for the definition of "is". Also,
> I'm not the only one who has studied genetics in some detail who
> remains "confused" about how the proposed mechanism of evolution
> could actually do what you guys confidently assert that it does - a
> bald assertion without any statistical predictive power I might add.
Funny that only creationists and their political suck-ups have any
trouble understanding it.
richardal...@googlemail.com
0catch.com> wrote:
> On Feb 18, 1:23 pm, bdbry...@wherever.ur (Bobby Bryant) wrote:
>
> > In article <1171821119.373860.183...@v45g2000cwv.googlegroups.com>,
> > "Seanpit" <seanpitnos...@naturalselection.0catch.com> writes:
>
> > > Not true. Evolutionists strongly believe that the proposed
> > > evolutionary mechanism can and has moved up the ladder of functional
> > > complexity.
>
> > So let's get this clear... Do you admit that evolution has happened,
> > and merely reject the proposed mechanism? Or do you reject the fact
> > as well as the explanation?
>
> Without the mechanism, there is no evolution. Evolution, by
> definition, is change over time by use of random mutation and natural
> selection. Any other mechanism isn't "evolution".
>
This is the sort of posting which truly demonstrates your willful
ignorance of evolutionary science.
1) Evolution is, by definition, changes in the genetic make-up of
organisms over time. It is a fact that evolution occurs.
2) It doesn't matter what mechanism drives evolution, it's still
evolution. It could be driven by the direct intervention of little
green goblins from Mars, and it would still be evolution.
3) Evolutionary theory proposes that the mechanism which drives
evolution is natural selection acting on the variation produced by
random mutations in the geneomes of populations of organisms. This
theory has been extensively tested over a century and a half, and to
date has not been falsified. It is the ruling paradigm in biology not
because a gang of atheist thugs got together in a smoke-filled room
and decided to promote it because of their atheist convictions, but
because it has enormous explanatory power.
>
>
> > > You don't seem to understand the statements of the authors - and
> > > neither does Howard.
>
> > 8<
>
> > > You don't have the first clue as to what you are reading in these
> > > papers. They do indeed directly undermine your most fundamental
> > > contentions.
>
> > Sean, when have you *ever* posted *anything* here that would make
> > *anyone* think you were qualified to interpret a scientific paper?
>
> > Whenever you drop in on topics I know something about, you've shown
> > yourself to be clueless about the most basic of concepts, and yet
> > you're absolutely dogmatic that the results of that field refute
> > evolution. And whenever you get onto other topics, the people who
> > have actually studied those topics also say that you show yourself to
> > be clueless about the most basic of concepts, but still you're
> > absolutely dogmatic that the results of that field refute evolution.
>
> > And when people show you to be wrong, you start introducing undefined
> > terms into your argument.
>
> > Why should I give even the briefest consideration to your claim that
> > you understand the papers better than Steve and Howard do?
>
> > Has it ever crossed your mind that you simply aren't qualified to
> > argue against evolution, even if it happened to be wrong?
>
> LOL - oh please! Where are these arguments that have clearly proved
> me wrong on any significant aspect of my position? - Or where have I
> introduced undefined terms that you just can't seem to figure out?
1) What do you mean by "common design"
2) what evidence do you have that any designer has ever used such a
principle?
3) What do you mean by "fairly specifed" and how can one measure it?
4) On what basis have you determined that only functions involving
changes to proteins above your "1000aa threshold" are "higher level
functions"?
5) Why do you insist on an adaptive archipelago rather than an
adaptive landscape?
6) ** Why do you think the answer should be the same from protein to
protein?
Note that you must assume this if you want to justify your
"exponential."
An average of exponential functions is not an exponential function,
and
can, in fact, be just about anything. (Look up the Laplace
transform.)
7) ** Why do you think the answer is independent of the number of
previous
"1aa structural requirement[s]"? Again, if it is not, you will not
get
anything like exponential behavior.
8) > Many functional systems exist that require a minimum structural
> threshold of many more than 1000 specified residues.
So? List them and tell us how you calculated that they require a
"minimum structural threshold of more than 1000 specified residues"?
9) How do you determine what level of substitution is required to
define
a residue as "specified"?
10) > How can you possibly argue, with any
> seriousness, that is not an obvious stalling out effect?
Because any stalling out effect is due to an increase in the size of
the minimal gap (in mutational steps) rather than the size of the end
protein in aa's or specified aa's. I see no way to predict the size
of the former from knowledge of the latter. What is the mathematical
relationship you see and what *real* material evidence do you have to
support such a relationship?
11) What makes you think that the total size
is relevant?
12) Or are you claiming that, if a protein has a minimum gap
size of 1000 mutational steps between functionally useful structures,
that anyone thinks that such a protein would evolve?
13) What makes you
think that anyone is proposing a gap of 1000 mutational steps between
functionally useful states?
14) And what does that have to do with how evolution by mutation of
pre-
existing structures to modify them to new selectable functions works?
15) > Yes, but the odds of success for a given attempt are
exponentially
> less likely.
Have you done these calculations? I mean by this that you have
computed
how many functional alternatives there are, and worked out how many
generations and individuals are need at realistic mutation rates to
figure out that the likelihood of getting *any* large functional
novelty
is too low to be acceptable?
16) And have you included parallel processing, so to speak, of
multiple
muations in a population (i.e., recombination of independently
assorting
alleles due to sex)?
17) > The odds decrease exponentially with the needed number of
character
> changes. The threshold is the point at which the mechanism clearly
> looses ability to act in any sort of meaningful way. Statistically the
> evolutionary mechanism just isn't believable any more as a creative
> force beyond the 1000aa level; even for an extremely large population
> of living things.
So this is about what you find credible? I ask, because maths make
some
unintuitive outcomes very likely indeed. So have you done the math?
18) > That's true as long as you can increase the population's size
> exponentially with each step of the structural threshold ladder. It
> is just that population sizes have limits that are far too small to
> cross the 1000aa threshold this side of a practical eternity of time.
Please show me how that works. I promise I will try to work through
the
math, like I haven't since I was in school.
19) > If you think this estimate is significnatly off based, then by
all
> means, do present your own estimate of the likely minimum structural
> requirements. I'd be most interested.
I'd be most interested in an answer to a question that I asked you a
few weeks ago that you never answered:
20) How many "fairly specified" residues are there in each of the
proteins
in the 2,4-DNT cascade? And again, please show your work.
21) However, this closeness of the potential steppingstones rapidly
> expands as one moves up the ladder of minimum structural threshold
> requirements.
Interesting assertion. Any backup for it - it's not in the papers
discussed
here.
22) > Cascades are not the same
> as systems of function where all the parts have to be in a specific
> arrangement relative to each other at the same time. Cascades are
> therefore much much less specified; no more functionally complex then
> the most complex single part that does require all its residues to be
> in specific orientation at the same time.
Right now, I am not asking you about the overall complexity of the
cascade; I am asking you about how many fairly specified residues
there are in each protein. Where are the numbers?
22) Where is your work?
23) > One cannot simply focus on one aspect of a phenomenon and
> make a conclusive hypothesis about mindless or mindful origin. One
> must consider all aspects of the phenomenon before a reliable
> hypothesis can be established. While the nested pattern observed in
> living things can indeed be explained by mindless evolutionary
> processes, the functional aspects of living things, as they move
> beyond very low levels of minimum structural threshold requirements,
> are exponentially harder and harder to explain via mindless
> evolutionary processes.
You keep repeating this, but what is this exponential structural
threshold requirement and how do you know that it exists in biological
systems?
24) > Certainly a structure can be modified with a corresponding
> modification in the degree of function of a pre-established system.
> However, the likelihood that a novel system of function can be found
> in this manner is unlikely and becomes exponentially more and more
> unlikely as one considers higher and higher minimum structural
> threshold requirements.
Where do you get that from this paper? Any limited number of
sequences is going to have large gaps between them in sequence space.
What you need to know is how many of those sequences can provide the
functions that life needs. They do not appear to provide this answer
in the paper. Where is it?
Just demonstrate that your gaps exist, and then look at your
demonstration and compare it to what is wrong with your model and tell
us which one comes up short.
26) Why keep obfuscating when you could nail
everyone with your model and evidence?
27) > There are no real time
> examples - period. Not one. Those functions that do evolve require
> only a few hundred specified residues - like your cockroach milk
> evolution example (only about 200 or so loosely specified residues
> needed), which isn't even an observed example.
What utter nonsense! If you have a better explanation for the evidence
presented by the authors of the paper, feel free to offer it. Their
conclusions are firmly based on that evidence.
28) You have yet to explain why your "1000aa threshold" is of any
significance. Novel beneficial functions evolved with changes well
below this threshold.
What is so special about novel beneficial functions above this
arbitrary threshold?
29) What mechanism prevents the accumulation of beneficial functions
at
levels of change well below your arbitrary threshold?
30) Since when has observation in "real time" been a
requirement in science?
31) How many more years of denial, dishonest obfuscation, and evasion
are
we going to get out of you, Sean?
32) Just give me one good reason why I should tell you how lame your
current argument is, when you have found out how lame all your others
were?
33) You don't even deny the facts you just evade them, so you know
that
you aren't on the up and up. You can't possibly call it honest, so
how do you justify it?
34) Professor Pitman, how many aa are involved in the bacterial
flagella ?
Accurate count, please.
35) Give me a
metric. *One* metric that you will agree to apply consistently
throughout the discussion without trying to change the subject to
Bernoulli trials. Then, after we have nailed down the metric, we can
discuss the issue. Until then, I'm not going to waste my time with
your hand-wavings.
36) How many specified residues are there in each protein of the 2,4-
DNT
cascade?
37) You mean that *each* protein in this cascade requires less than
1000
of whatever you mean by aa, don't you? Or do you mean the total in
all of the proteins of the cascade?
And that hand-waving smoke-and-mirrors number of 1000 is not the
answer that was asked for. He asked "How many specified residues are
there in each protein of the 2,4-DNT cascade? To answer that, you
have to come up with a specific number for each of the proteins (or
one for all of the proteins of the cascade). And you have to tell us
how you calculated that specific number.
39) You say that you have already answered this question "many many"
times. Since an answer to the question would consist of a number for
each protein, you are claiming to have posted these numbers for each
protein many many times. So show me one post where you have actually
done what you claimed.
40) "Exponentially less likely" is a phrase I often hear from people
who
don't know very much math. By itself, it doesn't mean anything --
depending on the "decay constant" in the exponent, an exponential
relation may be very different from a linear relation, or it may be
almost indistinguishable from a linear relation. (That is, if a<<1/N,
then e^{-aN} is very nearly equal to 1-aN.)
Is this just rhetoric, or are you claiming an actual calculation
here?
If the latter, what is the value of the constant in the exponent?
How,
exactly, did you determine (or measure) this value?
41) Wat are the precise structural size and complete specificity
requirements of the bacterial flagellae ?
42) Now, Sean, show me how it's done. Show me a table with how many
Fairly
Specificated AAs each of the 42 or so proteins has, and how much is
the Pitman Fidge Factor you throw on top. And why.
43) So, in mitochondria, the cascades that are represented by
complexes
(proteins that adhere to one another and thereby increase the
efficiency of electron transfer within the complex) are evolutionarily
impossible because they adhere to one another whereas if they (less
efficiently) performed the same sequence as a cascade, they would be
"much much less specified"?
44) How many mutational steps do you think
are necessary to cause proteins to adhere to one another to some
extent?
45) Isn't this number simply the total number of aa residues in some
specific bacterial flagella or some arbitrary large fraction thereof?
46) How do you calculate the number of "fairly specified" aa residues
in
this *specific* case?
47) How do you calculate the gap size from that
number of "fairly specified" aa residues?
48) How do you deal with
mutations that produce chimeric proteins rather than point mutations?
49) How do you deal with proteins/protein structures in the
eubacterial
flagella that have alternative useful *functions* that do not rely on
it being a part of a flagella?
50) There are many *subfunctions* of parts
of different proteins in flagella; why do you focus entirely on a
single function of rotary motility?
51) Given that one can, in principle
and also in practice, generate the *function* of rotary motility from
structures that have potential (and real) independent utilities in one
or a very few mutational step(s), why is the total number of aa
residues relevant to producing that *function*?
52) Given that the
*function* of rotary motility can be generated by a similar linking of
pre-existing motor (but not the same one that eubacteria use) and
whip-
containing pore (but not the same one that eubacteria use) in
archaebacteria and that there are even massive modifications of the
eubacterial flagella in different eubacteria (e.g. spirochaetes), why
do you think that the eubacterial flagella had to start from a random
useless sequence to produce the end result?
> This is like Pres. Clinton asking for the definition of "is". Also,
> I'm not the only one who has studied genetics in some detail who
> remains "confused" about how the proposed mechanism of evolution could
> actually do what you guys confidently assert that it does - a bald
> assertion without any statistical predictive power I might add.
So why not start by demonstrating your sincerity by answering the list
of unanswered questions. This is just from one thread, by the way.
There are numerous others which you have not answered in spite of
having been asked many times. Have you read the chapters on the
taphonomy of Lagerstatten in "Palaeobiology", for example.
Of course, you won't address the questions, you won't reconsider your
position, you won't educate yourself in the subject, you won't remove
from your web site statements which are demonstrably false, or do any
of the things we would expect of an honest scientist.
RF
Seanpit
> >> So let's get this clear... Do you admit that evolution has happened,
> >> and merely reject the proposed mechanism? Or do you reject the fact
> >> as well as the explanation?
>
> > Without the mechanism, there is no evolution. Evolution, by
> > definition, is change over time by use of random mutation and natural
> > selection. Any other mechanism isn't "evolution".
>
> No, you're mistaking the explanation for the thing explained.
What is your definition of evolution? Change over time? Slow
creation via intelligent design is change over time. Is that
therefore "evolution". Not really - that isn't what is generally
meant when someone refers to something like the "evolution of life".
> We knew about evolution before Charles Darwin was born.
That's true. The concepts of small changes or mutations and natural
selection were both around before Darwin popularized them.
> >> Why should I give even the briefest consideration to your claim that
> >> you understand the papers better than Steve and Howard do?
>
> >> Has it ever crossed your mind that you simply aren't qualified to
> >> argue against evolution, even if it happened to be wrong?
>
> > LOL - oh please! Where are these arguments that have clearly proved
> > me wrong on any significant aspect of my position?
>
> Do you want me to look up your idiotic entropy post that you've asked
> me not to rub your nose in?
Oh, please do! And please do explain to me again how the concept of
informational entropy is all wet . . . As I recall, your arguments
here were exceptionally lame.
> > - Or where have I introduced undefined terms that you just can't
> > seem to figure out?
>
> Does "fairly specified" ring a bell?
Does the definition of a ratio of 1e-40 per 100aa ring a bell? How
can I define it any more specifically than that?
> > This is like Pres. Clinton asking for the definition of "is". Also,
> > I'm not the only one who has studied genetics in some detail who
> > remains "confused" about how the proposed mechanism of evolution
> > could actually do what you guys confidently assert that it does - a
> > bald assertion without any statistical predictive power I might add.
>
> Funny that only creationists and their political suck-ups have any
> trouble understanding it.
Funny how that is . . .
Seanpit
> > Without the mechanism, there is no evolution. Evolution, by
> > definition, is change over time by use of random mutation and natural
> > selection. Any other mechanism isn't "evolution".
>
> This is the sort of posting which truly demonstrates your willful
> ignorance of evolutionary science.
>
> 1) Evolution is, by definition, changes in the genetic make-up of
> organisms over time. It is a fact that evolution occurs.
Genetic changes could be and are often (these days anyway) the result
of deliberate human design. Ever hear of designer genes? Is a
deliberate change in the makeup of a living thing by some scientist in
a lab somewhere "evolution". Not by most people's understanding of
the term "evolution of life". Evolution is generally understood to be
a non-intelligent process. In other words, the definition of
"evolution" is tied up in its proposed mechanism.
> 2) It doesn't matter what mechanism drives evolution, it's still
> evolution. It could be driven by the direct intervention of little
> green goblins from Mars, and it would still be evolution.
Not true. This is a description of slow creation - not evolution.
> 3) Evolutionary theory proposes that the mechanism which drives
> evolution is natural selection acting on the variation produced by
> random mutations in the geneomes of populations of organisms. This
> theory has been extensively tested over a century and a half, and to
> date has not been falsified. It is the ruling paradigm in biology not
> because a gang of atheist thugs got together in a smoke-filled room
> and decided to promote it because of their atheist convictions, but
> because it has enormous explanatory power.
Not beyond extremely low levels of functional complexity. Beyond the
1000aa level, it has no explanatory or predictive power regarding the
proposed mechanism at all. All that exist beyond this level are bold
statements and statistically baseless assumptions - otherwise known as
just-so-stores.
< snip >
Sean Pitman
www.DetectingDesign.com
Seanpit
> > > > I know. That is why evolutionary thinking is wrong.
>
> > > Which rather contradicts your assertion that your model represents
> > > evolutionary theory acurately!
>
> > I didn't say that my model was the same as yours! Hello! What I said
> > was that I was not misrepresenting your model.
>
> You quite categorically did! The adaptive landscape of evolutionary
> theory is *NOT* a series of isolated islands. So you *DID*
> mispreresent "my" model.
I never said that your model of sequence space proposed a series of
extremely isolated islands. That certainly is not *your* model - It's
MY model. Sheesh!
Your model proposes that the islands are extremely close together and
even overlapping - that there are no expanding non-beneficial gaps at
higher and higher levels of structural threshold requirements. That's
your model. I propose that this model of YOURS is wrong. I believe
that MY model, the model that does actually propose that the islands
of potentially beneficial sequences are indeed isolated and that they
become dramatically more and more isolated with each step up the
ladder of minimum structural threshold requirements, is correct.
Do you see the difference? I think that your model, your real model
without any strawman misrepresentations, is mistaken. I'm not
presenting my model as your model. Have you lost your mind Richard?
Obviously, my model is my model. It is very much different than your
view of what the proper model looks like. Clearly that is why we have
a disagreement here. You think my model is wrong and I think your
model is wrong. Where have I come close to giving you credit for my
model?
> > I use your model
> > accurately.
>
> That is quite frankly a bald-faced lie.
> The adaptive landscape of evolutionary
> theory is *NOT* a series of
> isolated islands.
Again Richard, that's my model, not yours. I use your model as a
contrast to my model - to show the striking difference between the
two. Your model is nothing like my model. They are very very
different.
> > It is just that your model does not adequately explain
> > the observed data. My model is a much better explanation of the facts
> > at hand.
>
> And which facts are those, Sean? The "facts" which you claim that all
> those evolutionary scientists are studiously ignoring, and which only
> you seem to be aware of?
We've gone over this dozens of times already Richard. The facts are
that observed rates of evolution slow down dramatically at higher and
higher levels of minimum structural threshold requirements. Even you
admit this. You just provide an untenable explanation for this very
real observation.
< snip >
> > > "Moving up the ladder" is something else which evolutionary scientists
> > > don't consider to be a model of evolution.
>
> > Not true. Evolutionists strongly believe that the proposed
> > evolutionary mechanism can and has moved up the ladder of functional
> > complexity.
>
> I can only suggest that you educate yourself in evolutionary theory.
> The idea of a "ladder of complexity" is an apparent reference to the
> great chain of being, a concept abandoned by science well over a
> century ago. Evolutionary scientists are *very* careful to avoid
> language which implies "higher" or "lower" organisms, or a direction
> to evolution.
Evolutionary scientists talking about higher and lower levels of
functional complexity all the time - about the concept of "emergent"
functional systems that require greater minimum structural
thresholds. This concept is not at all foreign to mainstream science.
> I suggest that you educate yourself on the metabolism of temperature
> regulatory mechanisms in lizards, and compare that to the temperature
> control systems in mammals. Mammals have a far less complex system.
There you go. Right there you just admit a difference in functional
complexity. Different types of systems do indeed require different
minimums in order to be achieved to a selectable level of usefulness.
> > > > There is a clear slowing effect of
> > > > evolutionary progress. So, your model of how sequence space actually
> > > > looks is mistaken.
>
> > > So please demonstrate from the evidence that such an effect occurs.
>
> > You yourself admit that this effect occurs. You've even offered an
> > explanation for this slowing effect - arguing that it requires more
> > time because of a need to build up smaller changes.
>
> What is wrong with this explanation?
Because a gene pool that already contains a range of higher and lower
level functional systems would have something just about ready to
cross a higher-level threshold if in fact no significant non-
beneficial gaps existed in sequence space between higher and lower
levels. The rate of evolution of higher-level systems would not be
any less than the rate of evolution of novel lower-level systems.
They would all evolve at the same rate and commonality if your model
of sequence space were actually correct.
> > > > It doesn't fit what is observed in either real time observations of
> > > > evolution in action or in observations of functional sequence gaps
> > > > between functional systems.
>
> > > Since when has observation in "real time" been a requirement for
> > > science?
>
> > > Evolutionary theory predicts than major evolutionary changes will take
> > > hundreds of thousands, if not millions of years to take place.
>
> > > Do you understand that your insistence that unless we observe such
> > > changes in "real time" evolutionary theory falsified is a bit
> > > unreasonable?
>
> > We are not looking at very high levels here.
>
> You are specifically demanding "higher levels", Sean.
> Another lie, I'm afraid.
My proposed 1000aa threshold is indeed "higher" than functions that
require a minimum of only 100aa, but the 1000aa threshold is extremely
low level relative to much higher level systems that exist within all
living things - systems that require many thousands of specifically
arranged residues working together at the same time.
> > Real time evolution
> > drops off rather dramatically at the level of very small molecular
> > machines.
>
> Another unfounded assertion, Sean.
Give me an example then of evolution "in action" beyond the 1000aa
level. Again, I'm not talking about the type of change needed here.
I'm just talking about an example of evolution producing a novel
system of function that requires a minimum of 1000 specifically
arranged residues. This system could evolve by any series of small or
large steps. I don't care as long as a novel system is produced in
real time beyond this threshold.
< snip >
> > > Who do you think actually knows about this subject? You, or the people
> > > who have actually studied the material and published their research?
>
> > You don't seem to understand the statements of the authors - and
> > neither does Howard.
>
> Oh I see. But you do.
> Could you explain why the authors of this paper use these protein
> data to reconstruct evolutionary relationships in this case? Evidently
> they do *not* agree with your assertion that evolution "stalls out" at
> "higher levels of complexity", so I fail to see how you can claim
> that they support your views.
The authors don't even discuss the mechanism of evolution as it
relates to the time need to get from one viable fold type to the next
closest viable fold. However, did you notice in Fig. 2 that the
shorter protein folds (green dots) are the most closely spaced? Those
proteins that have multiple domains (black dots) are much more widely
spaced. Notice that the author's proposed "origin" for evolution stars
out with the smallest protein folds and moves on toward the larger and
more complex protein folds. Notice that this trend also demonstrates
a progression from more closely spaced dots to more widely spaced dots
within sequence space.
> > > You do understand what "sparsely populated" means?
>
> > Do you? Of course sequence space is sparsely populated by potentially
> > beneficial sequences!
>
> No, Sean.
> Either you are unable to read for
> comprehension or you are lying
> again. They are talking about the proteins
> used by biological systems, not
> "potentially beneficial sequences"
The authors extrapolate based on known protein sequences and
structures. Based on the 1e4 known fold domains the authors estimate
1e5 structural families.
In any case, given the extreme sparsely of existing beneficial
proteins within sequence space, even at such low levels of structural
threshold requirements (only a few hundred specified residues at
minimum) do you honestly think the number of potentially beneficial
sequences that are yet to be found is significantly greater at any
given level of structural complexity?
> > That's one of my main points.
>
> ...and as you have either failed to understand the paper to which this
> refers, or are deliberately misrepresenting it, your argument rather
> falls apart, doesn't it?
Not at all since it is you who doesn't seem to grasp the implications
of the paper.
> > And, it gets
> > more and more sparsely populated by many fold with each increase in
> > the structural threshold requirements. Beyond this, these extremely
> > outnumbered "target" sequences are NOT clustered in one tiny corner of
> > sequence space, even at this very low level of useable protein-folds
>
> There is no reference whatsoever in this paper to "target sequences".
Any novel viable beneficial protein fold/sequence/structure is a
"target".
< snip >
> > > As for "islands", what do you think is meant by this:
> > > "The fact that most of proteins are structured and that the protein
> > > structure space is very sparsely populated and restricted mostly to
> > > the four elongated regions suggest that mutations in genes encoding
> > > proteins have been constrained to those resulting in a structurally
> > > viable protein occupying one of the four allowed regions of the
> > > protein structure space: structural selection or "designability" "
>
> > > Oh, and please don't wet your pants over the use of the term
> > > "designability". It's in quote marks.
>
> > Look at the actual 3D projection of sequence space presented by these
> > authors. The fold-types are NOT clustered together at all in one
> > corner of sequence space. Sure, they are loosely arranged in 4
> > broadly defined families. However, note that these families traverse
> > the entire breadth of sequence space in four loosely recognizable
> > directions.
>
> The graphs only illustrate the portion of sequence space occupied by
> biological proteins! Where on earth do you get the notion that they
> "traverse the entire breadth of sequence space"?
Look up the actual sequences of 100aa+ existing protein sequences and
you will see that those on opposing ends of those illustrated are very
far apart in sequence space. They are not clustered together in one
concentrated corner as you and Howard have been suggesting.
> > Again, this directly undermines the assertion that potentially
> > beneficial proteins are closely clustered in one tiny corner of
> > sequence space. This simply isn't true, even at this very low level of
> > functional complexity. And, it is even less true at higher and higher
> > levels where family groups multiply many fold at each level of
> > increased structural complexity. These families are NOT all clustered
> > together in one tiny corner without large gaps in between. They are
> > indeed separated in sequence space and they become dramatically more
> > and more separated with each step up the ladder.
>
> Sean, learn to read and understand graphs.
Learn to read and understand the range of sequence differences between
existing beneficial protein-based systems and the implications of
location that these differences indicate regarding sequence space
positioning.
> > > > Higher-level targets do indeed exist within sequence space.
> > > > If evolution never found any of these,
> > > > no higher-level systems would
> > > > exist today. Of course, evolution does have to find higher-level
> > > > targets. However, if you want to explain how higher-level evolution
> > > > occurs, you have to explain the odds of what it takes to find higher-
> > > > level targets.
>
> > > How do you recognise a "higher level target"? What metric of "level"
> > > are you using? Is the acquisition of "milk" in cockroaches reaching a
> > > "higher level target", and if not, why not?
>
> > As I've explain dozens of times to you, a higher-level target is one
> > that requires a greater minimum structural threshold requirement.
>
> So what metric of "level" defines a "higher level target"?
> Repeating assertions is not explaining anything. Answering questions
> is.
I just gave you the metric Richard! A higher-level target is one that
has a greater minimum structural threshold requirement - i.e., greater
number of specifically arranged residues before a particular type of
function can be realized. That's the metric Richard. I'm not sure
how it can be made clearer than that.
Now, your cockroach milk example is at a "higher-level" than those
functions that require lower-level structural thresholds (i.e., less
than 200 loosely arranged residues). However, 200 very loosely
arranged residues isn't a very high level at all relatively speaking.
Just because one may be able to find lower-level functional systems
does not mean that you've demonstrated how evolution can work at
higher and higher levels without a dramatic drop in rate of
evolutionary progress.
Again, functions that only require a few hundred loosely or even
fairly specified residues can and often do evolve in real time.
However, they evolve much less commonly then do those functions at
even lower levels. Demonstrating the progression, those functions
that require a few more hundred specified residues don't evolve in
real time at all. There's not a single example beyond the 1000aa
level - which, obviously, is an even "higher" level than the 200aa
example you've presented.
Of course, there are far far higher levels than the 1000aa level.
These are far far more beyond the reach of evolutionary progress than
the 1000aa level - many times more for each additional structural
threshold requirement.
> > Cockroach milk only requires 200 or so loosely arranged amino acid
> > residues.
>
> So on what metric have you established that this is not a "higher
> level function"?
See above . . .
> > While this requirement may be at a higher level compared to
> > a functional system that only requires 20 loosely arranged residues,
> > it doesn't even come close to my challenge of crossing the 1000aa
> > threshold. Again, the 1000aa level is a target because it is clearly
> > well beyond any example of evolution in action that has ever been
> > observed - to include this favorite example of yours (which isn't even
> > a real time example).
>
> So what you are telling us is that a "higher level function" is
> defined only in terms of the arbitrary "1000aa level".
>
> Perhaps you can explain why.
A higher-level function is a relative term. Even very low-level
functions are at a "higher level" than even lower level functions.
This is obvious stuff Richard. The 1000aa threshold is simply that
level at which evolution doesn't even come close when it comes to
"evolution in action". The reason for this stalling out effect is
clearly the result of linearly expanding non-beneficial gaps between
potentially beneficial islands in sequence space.
> > If there were no non-beneficial gaps between more complex systems and
> > other complex systems or lower level systems, more time would NOT be
> > required to evolve higher-level systems.
>
> Oh, please!
> Walk ten paces, and time yourself.
> Walk a hundred paces and time yourself.
> Which takes longer?
Have a whole bunch of individual searchers all spread out along the
line between 0 and 100 paces. How long does it take at least one
member of a population to find, via random walk, at least one of many
evenly distributed targets that is 1 pace from you vs. 100 paces from
you? The same amount of time - on average.
Now, set up an uneven distribution of many potential targets with the
greatest concentration of targets per unit area closet to you and a 10
fold decrease in the number of targets per unit area as one moves away
from you. Now, get a whole bunch of individual searchers staring at
different target points from 1 pace to 100 paces from you. Which
targets will be found at a greater rate? The answer is that the
targets in the area of greatest concentration will be found at a
greater rate.
> > You are very confused on
> > this point. Without non-beneficial gaps, higher-level systems would
> > evolve just as quickly as lower-level systems. Set up your own
> > simulation and you'll see that I'm correct here.
Did you try to set up such a simulation?
hersheyh
have been successfully posted to this group, yet never appear. It's
frustrating because unlike Sean, I am not merely cutting and pasting
responses using tired meaningless word salad that I don't have to
think about.
On Feb 18, 12:51 pm, "Seanpit" <seanpitnos...@naturalselection.
0catch.com> wrote:
> On Feb 17, 11:22 am, richardalanforr...@googlemail.com wrote:
>
> > > I know. That is why evolutionary thinking is wrong.
>
> > Which rather contradicts your assertion that your model represents
> > evolutionary theory acurately!
>
> I didn't say that my model was the same as yours! Hello! What I said
> was that I was not misrepresenting your model.
Read for comprehension. The model that you are presenting and
pretending that it represents the real world is not anything of the
sort. It is a purely hypothetical model and you claim that, by
falsifying the possibility that evolution can occur *in the context
and assumptions of this purely hypothetical model*, you have falsified
evoluton. That is, you have constructed a hypothetical model of
reality with all sorts of hidden strawman assumptions that every
biologist recognizes has little connection to our knowledge of the
real empirical world. And you then claim that by asserting that
evolution would not be possible in your hypothetical, magical strawman
world (and I agree; *if* evolution had to occur in your hypothetical
world, it would be unlikely) it is not possible in the real world.
> I use your model
> accurately. It is just that your model does not adequately explain
> the observed data. My model is a much better explanation of the facts
> at hand.
Your model is a hypothetical strawman model that has little connection
to the real empirical world of observation. It has little connection
to observed data; it is a purely mathematical hypothetical
construction.
Just to give a small example of your unwarranted assumptions, your
model *assumes* that there is a linear (or, if you think you can get
away with it, exponential) correlation between the "level of
functional [sic] complexity" measured as the number of "fairly specied
aa residues" or "number of structurally relevant aa residues" and the
unstated and unmeasured and uncalculated *real* number you need (the
number of mutational steps between functional structures in biological
systems). Yet the *evidence* from the rate of fixation of mutations
over geological timeframes tells a different story. As the size of
proteins increase, in general, there is a greater rate of fixation of
variant aa's per unit time. The rate of fixation of variant aa
residues, unlike your pseudocalculated number for "fairly specified aa
residues", is a reasonably good measure of the interchangeability of
aa's in any particular functional protein since it largely records
selectively neutral changes. Let's take two extremes, histone H4 and
the fibrinogen peptide. Histone H4 is an extremely strongly conserved
protein over geological time because nearly every aa is in contact
with the substrate it binds. So the aa residues in histone H4 change
quite slowly. Remember that all the variants retain pretty much full
histone H4 function, so we are not talking about changes that affect
function here. We are talking about changes that have either
individually have no functional consequence or complementary changes
that counteract a selective defect for one or both of the individual
effects. Such changes are rare for histone H4. In contrast, the
fibrinogen peptide sequence is pretty much irrelevant. Except for the
site where cleavage of this peptide off of fibrinogen to produce
fibrin for clotting, essentially no aa specificity is required. This
sequence, needless to say, in evolution exhibits a rapid rate of
change in aa sequence due to simple neutral fixation.
The protein which you base your pseudocalculation of the amount of
"fairly specified aa residues", the small heme-binding protein
cytochrome c, is, in fact, much closer in rate to histone H4 than it
is to fibrinogen peptide. If the rate of change of cytochrome c were
*standard* or *typical*, that might not matter. But it isn't. You
are, in fact, intentionally biasing the number of "fairly specified aa
residues" in favor of your hypothesis. That means that your measure
of "level of functional [sic] complexity" (which is nothing more than
a hand-waved pseudocalculation that is a large fraction of total size)
gets more and more bogus as total size increases. Rather than a
linear increase in your "fairly specified aa level" size as total size
increases, there is, by and large in the real world of proteins, a
*decrease* in the fraction of "fairly specified aa residues" as
protein size increases. For example, the heme-binding hemoglobin
alpha is 141 aa long compared to the 104 for the heme-binding
cytochrome c, yet the rate of aa change in hemoglobin is about 18% per
100 million years whereas cytochrome c's rate of aa change is about 5%
per 100 million years. Fibrinogen peptide's rate of change is about
100% per 100 million years and histone H4 is around 0.5%. Notice that
these rates of change, which measures the substitutability of aa
residues and are thus a *real* measure of the substitutability of
sites are NOT a function of size. The real correlation is that rate
of change is a function of the amount of a protein that is in contact
with substrate or required in active sites. In order to determine the
real number of "fairly specified aa residues" one cannot simply
extrapolate from some ratio in cytochrome c.
That the number of "fairly specified aa residues" is NOT, in general,
a large fraction of total size is also confirmed by the *fact* that
there exist very old enzymes that retain both function and structure
but NOT sequence. That is, unless we observed that the structures
were the same, we could not tell, based solely on sequence analysis,
that the two proteins were homologous (derived by descent) rather than
analogous (independently arrived at). There are analogous enzymes
(cellulase, for example, has been invented at least three times) and
analogous protein systems (the two bacterial rotary flagellae).
Analogous proteins are, naturally enough, rare because evolution
typically favors a "to the winner (first organism to produce a useful
trait) goes the spoils (avoidance of extinction)" mechanism. That
they do exist (and activities done by homologous enzymes in living
organisms can be created artifically as well, as in the immunoglobin-
based betagalactosidase) tells us that life has not found all the
possible ways to have a particular function). Not surprising since
the *clustering* of proteins in structure space show that only a
fraction of total structure space has been explored.
In summary, this *actual real evidence* clearly shows that your
assumption that the number of "fairly specified aa residues" increases
linearly as some fixed large fraction of total number of aa residues
is completely *unsupported* by the evidence. Because the number of
"fairly specified aa residues" actually, in general, decreases and
sometimes significantly decreases with total size.
> > Unfortunately it requires rather more than your unfounded assertion to
> > demonstrate that it is wrong, however.
>
> You offer nothing but assertions in favor of your model. You have no
> statistical analysis or predictive power whatsoever regarding your
> proposed mechanism. You simply assert that it must work. That's
> it!
If this gets through, I will contine to try to respond to Sean's so-
called arguments and point out how far divorced from empirical reality
Sean's hypothetical model of "sequence space" is.
[snip]
richardal...@googlemail.com
0catch.com> wrote:
> On Feb 19, 9:20 am, richardalanforr...@googlemail.com wrote:
>
> > > Without the mechanism, there is no evolution. Evolution, by
> > > definition, is change over time by use of random mutation and natural
> > > selection. Any other mechanism isn't "evolution".
>
> > This is the sort of posting which truly demonstrates your willful
> > ignorance of evolutionary science.
>
> > 1) Evolution is, by definition, changes in the genetic make-up of
> > organisms over time. It is a fact that evolution occurs.
>
> Genetic changes could be and are often (these days anyway) the result
> of deliberate human design.
So what?
> Ever hear of designer genes? Is a
> deliberate change in the makeup of a living thing by some scientist in
> a lab somewhere "evolution".
Yes. It's just that the mechanisms is human intervention. It's still a
change in the genetic makeup of organisms over time.
> Not by most people's understanding of
> the term "evolution of life".
It is evolution by the definition used by evolutionary biologists.
> Evolution is generally understood to be
> a non-intelligent process.
So what?
> In other words, the definition of
> "evolution" is tied up in its proposed mechanism.
Not in the way the term is used by scientists.
There is a clear distinction between the fact that evolution occurs,
and the theory of how it occurs.
>
> > 2) It doesn't matter what mechanism drives evolution, it's still
> > evolution. It could be driven by the direct intervention of little
> > green goblins from Mars, and it would still be evolution.
>
> Not true. This is a description of slow creation - not evolution.
No, it's a description of evolution. It's just that the mechanism is
not natural selection.
>
> > 3) Evolutionary theory proposes that the mechanism which drives
> > evolution is natural selection acting on the variation produced by
> > random mutations in the geneomes of populations of organisms. This
> > theory has been extensively tested over a century and a half, and to
> > date has not been falsified. It is the ruling paradigm in biology not
> > because a gang of atheist thugs got together in a smoke-filled room
> > and decided to promote it because of their atheist convictions, but
> > because it has enormous explanatory power.
>
> Not beyond extremely low levels of functional complexity.
UNfounded assertion.
The evidence shows very clearly that evolution *does* occur "beyond
low levels of functional complexity. I have given the example of the
fossil series in which the jaw bones of a reptile migrate to become
the ear bones of mammals, and this is only one of an large number of
such transistional series.
So far you have ignored all my requests to address this evidence and
provide a better, testable theory as to why these fossils exist.
> Beyond the
> 1000aa level, it has no explanatory or predictive power regarding the
> proposed mechanism at all.
Unfounded assertion.
> All that exist beyond this level are bold
> statements and statistically baseless assumptions - otherwise known as
> just-so-stores.
No, it's known as evolutionary theory, and contrary to your assertions
it is a lot more that "just so stories".
I have given you the example of the discovery of Tiktaalilk to show
how evolutionary theory can make predictions which can be tested
against the evidence, but as ever you ignore anything which shows that
your assertions are categorically false.
Theories which make predictions which can be tested against the
evidence are not "just so stories". They are the foundation of
science.
>
> < snip >
Running away from the mess of undefined terms you pretend you don't
use, and the numerous questions you don't answer again.
Tell me, Sean. Do you think that this makes you look honest?
RF
>
> Sean Pitmanwww.DetectingDesign.com
Desertphile
<seanpi...@naturalselection.0catch.com> wrote:
> On Feb 19, 9:11 am, bdbry...@wherever.ur (Bobby Bryant) wrote:
>
> > >> So let's get this clear... Do you admit that evolution has happened,
> > >> and merely reject the proposed mechanism? Or do you reject the fact
> > >> as well as the explanation?
> >
> > > Without the mechanism, there is no evolution. Evolution, by
> > > definition, is change over time by use of random mutation and natural
> > > selection. Any other mechanism isn't "evolution".
> >
> > No, you're mistaking the explanation for the thing explained.
> What is your definition of evolution? Change over time? Slow
> creation via intelligent design is change over time. Is that
> therefore "evolution". Not really - that isn't what is generally
> meant when someone refers to something like the "evolution of life".
You have been corrected on this mistake of yours dozens and dozens
of times. Evolution is not "change over time." It is differential
reproductive success coupled with natural selection: you can claim
your gods ("intelligent designers") run the show, but there is no
reason to add them.
I think you deliberaltely obfuscate the issue by swapping the fact
with the theory: that is very Creationist of you.
> > We knew about evolution before Charles Darwin was born.
> That's true. The concepts of small changes or mutations and natural
> selection were both around before Darwin popularized them.
Er, no. Evolution was known to have happened at least two hundred
years before Darwin correctly explained how it happens.
--
"Nope! Nope! No pictures, no X-rays. I got things in there I
don't want seen. Dark thoughts and evil plans." --- Kolchak
hersheyh
Simple. Tell us how you got from the ratio of 1e-40 per 100aa (the
ratio derived under certain assumptions about the ratio of functional
cytochrome c molecules to total molecules of 100 aa in length, as if
that were relevant to how cytochrome c first evolved; btw, Yockey's
first guess was 1e-65 so he must have changed some of his assumptions)
to the ratio of 80 fairly specified aa residues out of 104 in
cytochrome c.
hersheyh
0catch.com> wrote:
> On Feb 18, 4:15 pm, carlip-nos...@physics.ucdavis.edu wrote:
>
> > I asked you how you determined your claim. I don't see how "What do
> > you think?" is a responsive answer.
>
> > In any case, it seems unlikely to me that your question makes sense.
>
> Then that's progress. This question must make sense before there is
> any further basis of discussion. So, lets work on that first . . .
>
> > In particular:
>
>
> protein to protein. Different types of protein-based systems have
> different minimum structural threshold requirements. Some types of
> functional systems require a greater number of specifically arranged
> amino acid residues while other types require fewer before at least a
> minimum selective advantage will be gained.
Except that you seem to merely be choosing the smallest known protein
that produces a particular function and then multiplying that number
by about 0.8, which you somehow concluded was the fraction of the 104
aa's in cytochrome c that were "fairly specified". You did this based
somehow on Yockey's ratio of 1e-39 for the ratio of 'functional'
cytochrome c's of 100 aa to the total number of possible proteins of
length 100. Or at least that *appears* to be the method you use to
determine the number of "fairly specifically arranged amino acid
residues". You could, of course, disabuse me of that notion by telling
me how you actually do specify the numbers below individually for each
function.
But, it must also be remembered that 'function' in your model does not
mean actual refer to "function". Rather "level of function" is merely
an alternate statement of the size values you give below. Thus any
protein of size 200 "fairly specifically arranged amino acids" by
whatever manipulation of total size you used (which looks to me like a
simple multiplication by the large fraction (about 0.8) that you
somehow derived for the number of such aa's in cytochrome c, somehow
by manipulating 10e-39. Or, of course, these numbers could simply be
hand-waving bullshit numbers.
> For example, the lactase function seems to require a minimum of at
> least 380 fairly specifically arranged amino acid residues. Nylonase,
> on the other hand, seems to require about 200aa. The insulin function
> seems to require no more than 50 or so residues at minimum.
>
> So, you see, it is the type of function that has minimum structural
> threshold requirements.
Rather it seems to be the total size (or the large fraction thereof
that you call "fairly specified aa residues) that determines level of
function. That is how you measure "level of function", isn't it?
> These different minimums are what I call "levels of functional
> complexity" or "minimum structural threshold requirements".
See. It is the size that determines "level of functional [sic]
complexity" rather than the level of functional complexity (where you
actually have a measure of *function* that measures the complexity of
*function*) that determines size.
> > Note that you must assume this if you want to justify your "exponential."
>
> Not quite true since I'm not looking at the proteins themselves but at
> different types of protein-based systems that have different minimum
> structural threshold requirements.
Rather necessary, since there are so few single proteins that are 1000
aa's in size. And so many of those have obvious internal
duplications. But then, you also add the criteria that the proteins
interact by binding with other proteins to form a complex rather than
a non-complexed cascade, even if they were to perform the same
function. You must somehow think that complexing proteins together
must involve very tight linkages along large stretches of the
individual proteins rather than being at one diffuse end of a
continuum of protein interaction. Of course, you have very many
strange ideas about proteins.
In fact, your criteria are so strange, I am hard put to find
structures or complexes that actually meet them without those
structures or complexes having subcomponents of independently useful
activity.
> > An average of exponential functions is not an exponential function, and
> > can, in fact, be just about anything. (Look up the Laplace transform.)
>
> I'm not looking at an average of exponential functions. I'm looking
> at a specific exponential that is roughly identifiable to at least a
> useful degree for a given level of minimum structural threshold
> requirements (which includes a measure of the minimum number of
> residues and degree of specificity of their arrangement before a
> particular type of function can be realized to a useful degree).
Actually, in the sequence space of a protein with a given level of
"functional [sic] complexity", aka size, ALL the sequences in that
space have the same level of "functional complexity" since they all
have the same size. Even if they don't have any useful function at
all. That means that the number that you do need is not the number
that you keep giving (the level of functional [sic] complexity or the
minimum threshold requirement or the number of fairly specified aa
residues or whatever other code name you want to use for "large
fraction of total size" of the smallest known molecule that has the
one activity you regard as *the* activity).
What you need, for any given level of "size" (and size is what all
your Newspeak verbiage amounts to) is to show us how to calculate the
number of mutational steps from the nearest functional neighbor that
lacks significant levels of *the* activity you regard as important.
You claim to be able to calculate this number purely from your
knowledge of the "level of functional [sic] complexity" or size. You
vary between saying that the "gap size" increases linearly with your
"large fraction of total size" and that it increases exponentially.
Usually, it is that the "gap size" increases linearly while the time
taken to cross it increases exponentially.
>
> > ** Why do you think the answer is
> > independent of the number of previous
> > "1aa structural requirement[s]"?
> > Again, if it is not, you will not get
> > anything like exponential behavior.
Again, we are not talking about adding aa's one by one to build a
protein in our sequence space model, we are talking about *changing*
amino acids to cross gaps. Under those conditions, the *only* way
that you would get a 20-fold anything is by assuming that at each
amino acid site, one and only one amino acid will lead to a functional
protein.
> Again, consider the English-language analogy. Each increase in the
> minimum size requirement for a meaningful sequence by a single
> character does indeed exponentially increase the number of non-
> meaningful sequences many times faster than the increase of meaningful
> sequences. I propose that exactly the same thing happens in genetic
> information systems and protein-based functional systems. If you
> understand the basis for the marked exponential difference in one, the
> other is also clear.
>
> > > I propose that as one moves up the ladder of minimum structural
> > > threshold requirements, 1aa at a time, the increase in potentially
> > > beneficial sequences approaches a exponent of 1 while the increase in
> > > non-beneficial sequences approaches an exponent of 20.
Here we have you giving the *worst case* scenario as if it were
typical. But that may depend upon what you mean by "fairly specified
aa residue". If to be "fairly specified" a residue can be one and
only one aa, then how can you possibly say that cytochrome c has 80
"fairly specified aa residues"? Surely even you know that that is
contradicted by the evidence.
>
[snip]
>
> The number 20 is the theoretical maximum increase in sequence/
> structural space size with each additional amino acid residue
> requirement. This limitation is due to the fact that there are only
> 20 commonly used amino acid residues in living things. For example,
> the sequence/structural space size for a sequence of 5aa is 20^5 or
> 3,200,000. Compare this to the sequence space size for a sequence of
> 6aa, which is 20^6 or 64,000,000.
But knowing that tells us nothing about the size of functionaly
useless gaps between the nearest functional structures of the same
size that have different functions, as far as I can tell. Or, let's
just say that you haven't justified the assumption that increasing
total sequence space necessarily affects the *minimum* size (in terms
of number of mutational steps, which, by your hypothetical model, you
have limited to point mutations and exchange of equal sized functional
moieties (protein construction is often modular) between functional
states with different (but often related) functions.
The FACT that the proteins found in the biosphere are NOT randomly
distributed in total *structure* [and I am tired of your continually
replacing the word 'structure' with 'sequence' as if you were ignorant
of the distinction] space. Life's proteins are *clustered* in
structure space. Maybe, to your mind, the fact that they are not all
clustered "in one tiny corner" is significant. But the important
feature is that *because* they are clustered rather than randomly
distributed, this necessarily means that the size of the minimum
'gap' (in mutational steps) between proteins that have useful
functions is smaller than they would be if the proteins of life really
were randomly scattered in total structure space.
Not surpisingly, this lack of scatter is evidenced in the frequent
ability to identify *sequence* similarity between proteins that
perform different functions. Proteins tend to exist in extensive
families rather than in random isolation. In short, the structure and
sequence of existing proteins tells us that your assumption that
functions *must* be randomly distributed in total sequence space is
not true.
> If the "level" of complexity in question required complete specificity
> of sequence, the
>
> > Why 1 and not, say, 5? Why 20 and not, say, 12, or 30?
>
> Actually, I think the increase in potentially beneficial sequences
> would approach an exponent of 0 instead of 1.
If you start with a functional protein and add an amino acid to either
end (or even in the middle), the odds favor that protein remaining
"beneficial". Whether or not adding the amino acid has any effect,
modifies the function, or produces a novel interaction is
idiosyncratic.
>
> > Why a single number, and not, say, "20 for the first 15 steps; then
> > 5 for the next ten steps because the number of protein geometries
> > suddenly increases, then 30 for the next five steps, then 2 for a
> > couple of steps..."? Why not "20 for proteins A and B, 30 for
> > protein C, 100 for protein D, and 5 for protein E?"
>
> Again, I'm not talking about proteins here, but levels of functional
> complexity;
Since, by your own admission above, level of functional [sic]
complexity is measured by some (abitrary AFAICT) large fraction of
total sequence size, how are you now distinguishing between "level of
functional complexity" and "proteins"?
> How many potentially beneficial sequences/structures vs.
> non-beneficial sequences/structures exist at a given level of
> structural threshold requirements?
That is rather irrelevant. What you need is a measure of the number
of beneficial sequences/structures within a certain number of
mutational steps in some existing genome. Evolution has no mechanism
for examining total sequence or structure space (which is why
measuring it is a strawman process). Evolution can only examine the
sequence and/or structure space close by some existing genome. And we
have already pointed out that sequence and structure space in existing
genomes is 'clustered'. Thus, if the evolutionary mechanism is at
work, one would expect any "new" or altered or modified function that
arises to have a sequence or structure that would not differ greatly
from some (or hybrid combination) of existing proteins. That is, we
would expect a blood-born O2 transport protein to be more likely to
arise as a modification of an existing O2 binding protein than to
arise from some random sequence. Such a mechanism will produce gene
families (in both sequence and structure). It will produce hybrid
proteins. It will add, modularly, moieties to proteins. It will
endoduplicate moieties. These new genes will be different from, but
still clustered with, the previously existing proteins. In short, we
would expect what is actually observed rather than what one would
expect from a model in which there is your average random walk from
some unspecified random site to some specified site.
> That number is a specific number
> even if this number is not absolutely known.
IOW, the number is a specific number even if I *also* pulled this one
out of my ass. Just like that funny number of "fairly specified aa
residues" in cytochrome c.
> In any case, I think
> this number can be roughly approximated even if it cannot be fully
> known.
It's somewhere between negative infinity and infinity, so it is
"fairly specified"
> > Note that I am not advocating a particular alternative here, so a
> > repeat of "What do you think" is not an appropriate answer. You are
> > making a proposal, with a specific mathematical form and, now, some
> > specific numbers. I am asking for *your* *evidence* for your proposal.
>
> Certainly I'm the one making a proposal here, but is it completely out
> of the question for me to ask what others might think regarding this
> particular problem? Do you have absolutely no personal thoughts or
> even hunches on this topic?
Yes. But I won't mention them in polite company. My personal
thoughts and hunches start with "You are so full of..."
[snip]
bro...@noguchi.mimcom.net
Do you have a model? I do some mathematical modeling, and here is how
it works. You take a simple system, identify the parameters and
relationships you think are important, make a model, maybe using
preliminary data set to estimate parameters, and then test it against
a new data set to see how well it works (and there's a whole lot of
work that goes into quantitating "how well it worked"). Then if you
want to model additional complexities, you add them in one at a time
and keep checking against the data.
Here's what you could do to convince people you know what you're
talking about. Start with Zach's word mutagenator. Consider 4 letter
words. Make a model that accurately predicts the statistical
distribution of numbers of mutational steps required to get from a
given four letter word, or random sequence of four letters, to another
four letter English word. Then model how that distribution changes as
the length of the word increases. By "model how that distribution
changes" I do not mean "it takes more steps" or "it takes
exponentially more steps," I mean derive a specific equation that
shows the relationship between word length and the distribution of
numbers of mutational steps required to get form a specific starting
point to an Engish word of the specified length.
This should be an easy problem. Your fitness landscape is defined by
the dictionary. The sorts of mutational steps allowed can be specified
in advance (you can even decide whether you want to allow
recombination, insertions, deletions). Then test your model equation
against empirical results from Zach's word mutagenator and see whether
your predictions are accurate. If you cannot make an accurate model in
this simple case of short English words, why should we take you
seriously when you say you have a model of protein function evolution?
If you cannot accurately model the sorts of evolutionary change even
you think can happen (random generation of short English words,
antibiotic resistance) why should we take you seriously about things
that are clearly more difficult to model.
Remember "X can happen in a decade but Y would take trillions of
years" is not a model. First you have to show that you can accurately
model the specific less-than-a-decade times for a series of X's before
we start to take you seriously about the Y's. In the meanwhile, all
you have is a very verbose argument from incredulity.
>- Or where have I
> introduced undefined terms that you just can't seem to figure out?
> This is like Pres. Clinton asking for the definition of "is". Also,
> I'm not the only one who has studied genetics in some detail who
> remains "confused" about how the proposed mechanism of evolution could
> actually do what you guys confidently assert that it does - a bald
> assertion without any statistical predictive power I might add.
>
> > Bobby Bryant
> > Reno, Nevada
>
> Sean Pitmanwww.DetectingDesign.com
Bobby Bryant
"Seanpit" <seanpi...@naturalselection.0catch.com> writes:
>> Do you want me to look up your idiotic entropy post that you've asked
>> me not to rub your nose in?
>
> Oh, please do! And please do explain to me again how the concept of
> informational entropy is all wet . . . As I recall, your arguments
> here were exceptionally lame.
I see you have a selective memory. Forget the one where your claim
about Shannon entropy could be shown wrong by math that can be done
in your head?
R. Baldwin
> On Feb 19, 9:11 am, bdbry...@wherever.ur (Bobby Bryant) wrote:
>
>
>> >> Why should I give even the briefest consideration to your claim that
>> >> you understand the papers better than Steve and Howard do?
>>
>> >> Has it ever crossed your mind that you simply aren't qualified to
>> >> argue against evolution, even if it happened to be wrong?
>>
>> > LOL - oh please! Where are these arguments that have clearly proved
>> > me wrong on any significant aspect of my position?
>>
>> Do you want me to look up your idiotic entropy post that you've asked
>> me not to rub your nose in?
>
> Oh, please do! And please do explain to me again how the concept of
> informational entropy is all wet . . . As I recall, your arguments
> here were exceptionally lame.
Sean, there are two *distinct* concepts of informational entropy, neither of
which is all wet, but neither of which will help you.
The Shannon (classical) defnition is the average uncertainty a receiver has
about the messages a transmitter will send. It increases to a maximum when
all possible messages are equiprobable, at which point the most efficient
use of a communication channel can be made.
For Algorithmic Information Theory (Chaitin-Kolmogorov), algorithmic entropy
is another word for Kolmogorov Complexity, the length of the shortest
program on a given Universal Turning Machine that produces a given string.
[snip]
Seanpit
wrote:
> >> Do you want me to look up your idiotic entropy post that you've asked
> >> me not to rub your nose in?
>
> > Oh, please do! And please do explain to me again how the concept of
> > informational entropy is all wet . . . As I recall, your arguments
> > here were exceptionally lame.
>
> Sean, there are two *distinct* concepts of informational entropy, neither of
> which is all wet, but neither of which will help you.
>
> The Shannon (classical) defnition is the average uncertainty a receiver has
> about the messages a transmitter will send. It increases to a maximum when
> all possible messages are equiprobable, at which point the most efficient
> use of a communication channel can be made.
>
> For Algorithmic Information Theory (Chaitin-Kolmogorov), algorithmic entropy
> is another word for Kolmogorov Complexity, the length of the shortest
> program on a given Universal Turning Machine that produces a given string.
KC and Shannon definitions of "information" are not the only ones out
there. I'm talking about meaningful or useful information; not about
a measure of concepts such as randomness or chaos. Meaningful
information also undergoes meaningful informational entropy, which is
related while being distinct at the same time, to KC and Shannon types
of "information".
http://www.detectingdesign.com/meaningfulinformation.html
Sean Pitman
www.DetectingDesign.com
hersheyh
0catch.com> wrote:
> On Feb 19, 11:05 pm, "R. Baldwin" <res0k...@nozirevBACKWARDS.net>
> wrote:
>
> > >> Do you want me to look up your idiotic entropy post that you've asked
> > >> me not to rub your nose in?
>
> > > Oh, please do! And please do explain to me again how the concept of
> > > informational entropy is all wet . . . As I recall, your arguments
> > > here were exceptionally lame.
>
> > Sean, there are two *distinct* concepts of informational entropy, neither of
> > which is all wet, but neither of which will help you.
>
> > The Shannon (classical) defnition is the average uncertainty a receiver has
> > about the messages a transmitter will send. It increases to a maximum when
> > all possible messages are equiprobable, at which point the most efficient
> > use of a communication channel can be made.
>
> > For Algorithmic Information Theory (Chaitin-Kolmogorov), algorithmic entropy
> > is another word for Kolmogorov Complexity, the length of the shortest
> > program on a given Universal Turning Machine that produces a given string.
>
> KC and Shannon definitions of "information" are not the only ones out
> there. I'm talking about meaningful or useful information; not about
> a measure of concepts such as randomness or chaos.
Isn't the "meaningfulness" of information a function of the viewer or
user of that information and, thus, not related to the amount or
nature of the information at all? After all, the word "Duck!" can be
very meaningful if a thrown rock is headed my way. And far less
meaningful in other contexts, such as in the poultry section of the
store. And utterly meaningless (to me) when shouted in the Mandarin
Chinese spoken in Peking.
> Meaningful
> information also undergoes meaningful informational entropy, which is
> related while being distinct at the same time, to KC and Shannon types
> of "information".
So, how do you measure this 'entropy' from a knowledge of the message
without a knowledge of how or whether the recipient views it? I
suspect another load of bovine excrement here.
> http://www.detectingdesign.com/meaningfulinformation.html
>
> Sean Pitmanwww.DetectingDesign.com
R. Baldwin
Twaddle. I seriously doubt you can provide any cites from any credible
Information Theorist that supports any mathematically sound definition for
"meaningful information" or "useful information.," much less "meaningful
information entropy."
Seanpit
> In article <1171908787.503850.118...@m58g2000cwm.googlegroups.com>,
> "Seanpit" <seanpitnos...@naturalselection.0catch.com> writes:
>
> >> Do you want me to look up your idiotic entropy post that you've asked
> >> me not to rub your nose in?
>
> > Oh, please do! And please do explain to me again how the concept of
> > informational entropy is all wet . . . As I recall, your arguments
> > here were exceptionally lame.
>
> I see you have a selective memory. Forget the one where your claim
> about Shannon entropy could be shown wrong by math that can be done
> in your head?
What are you talking about? I *never* claimed that Shannon entropy was
wrong at all. It isn't. Shannon's theory is correct regarding a
certain definition of "information". Please do quote where I said
otherwise.
Seanpit
> > > No, you're mistaking the explanation for the thing explained.
> >
> > What is your definition of evolution? Change over time? Slow
> > creation via intelligent design is change over time. Is that
> > therefore "evolution". Not really - that isn't what is generally
> > meant when someone refers to something like the "evolution of life".
>
> You have been corrected on this mistake of yours dozens and dozens
> of times. Evolution is not "change over time." It is differential
> reproductive success coupled with natural selection: you can claim
> your gods ("intelligent designers") run the show, but there is no
> reason to add them.
LOL - Differential reproductive success coupled with natural
selection? That's the definition of "evolution? You do realize, of
course, that such a differential has been produced by human
manipulation of genetic codes? In other words, this differential you
speak of has been produced by deliberate design. This isn't, at least
according to most, what anyone would call "evolution" - certainly not
in the Darwinian sense of the word.
> I think you deliberaltely obfuscate the issue by swapping the fact
> with the theory: that is very Creationist of you.
Without a viable mechanism the theory of evolution simply isn't
tenable. It is only because there supposedly is a viable mechanism in
the form of random mutation and natural selection that the theory
holds the prominence that it holds today. If this mechanism fell, so
would the theory.
> > > We knew about evolution before Charles Darwin was born.
> >
> > That's true. The concepts of small changes or mutations and natural
> > selection were both around before Darwin popularized them.
>
> Er, no. Evolution was known to have happened at least two hundred
> years before Darwin correctly explained how it happens.
Change over time was known to happen before Darwin. Much of this
"change" is now known to be the result of something quite different
from Darwinian-style evolution. In fact, many of the changes
described by Darwin in support of his theory are now known to be
nothing more than Mendelian-type variation. Mendelian variation is
not "evolution" since the overall gene pool does not gain any novel
functional options. In other words, there would be no way to turn a
reptile into a bird via Mendelian variation alone. Why? Because there
simply is no novel change in functional potential within the gene pool
using Mendelian variation.
Again, real evolution requires a specific type of mechanism - random
mutation and function-based selection. Without this mechanism in
play, there simply is no evolution. Intelligently designed changes
over time are not "evolution" in the Darwinian sense of the term.
Rather, such changes would be best referred to as "slow" or "stepwise
creation" or "stepwise design".
There you have it. If the mechanism of random mutation and function-
based selection was ever conclusively shown to be useless when it
comes to producing higher and higher levels of functional complexity,
then entire field of evolutionary biology would come crumbling down.
> "Nope! Nope! No pictures, no X-rays. I got things in there I
> don't want seen. Dark thoughts and evil plans." --- Kolchak
Sean Pitman
www.DetectingDesign.com
Seanpit
wrote:
> "Seanpit" <seanpitnos...@naturalselection.0catch.com> wrote in message
The definition can at least be reasonably approximated to a useful
degree:
http://necsi.org/projects/baranger/cce.pdf
Sean Pitman
www.DetectingDesign.com
R. Baldwin
Try again. Nowhere in Baranger's article are the terms "meaningful
information," "useful information," or "meaningful information entropy."
The article does not even remotely approach such a subject.
Perhaps you can explain why you think the article is relevant?
Bobby Bryant
I'm not saying that IT is "all wet". Rather, you displayed that your
understanding of it is.
Look it up yourself. You and Pagano can use dejagoogle as well as I
can. I'm tired of playing the ReMine game with you two.
Seanpit
wrote:
"When you look at an elementary mathematical fractal, it may seem to
you very 'complex', but this is not the same meaning of complex as
when saying 'complex systems'. The simple fractal is *chaotic*, it is
not complex. Another example would be the simple gas mentioned
earlier: it is highly chaotic, but it is not complex in the present
sense."
Barranger is using the term "complex system" in the same sense as I am
using the term informational complexity. Shannon entropy and KC are
both dealing with measuring sequence chaos as "complexity". Barranger
notes that there is a significant difference between this type of
"complexity" and what is meant by functional or "system" complexity.
They are very different concepts that unfortunately use the same word.
Sean Pitman
www.DetectingDesign.com
Seanpit
> In article <1172096623.151618.217...@v33g2000cwv.googlegroups.com>,
> "Seanpit" <seanpitnos...@naturalselection.0catch.com> writes:
>
>
>
>
>
> > On Feb 19, 9:16 pm, bdbry...@wherever.ur (Bobby Bryant) wrote:
> >> In article <1171908787.503850.118...@m58g2000cwm.googlegroups.com>,
> >> "Seanpit" <seanpitnos...@naturalselection.0catch.com> writes:
>
> >> >> Do you want me to look up your idiotic entropy post that you've asked
> >> >> me not to rub your nose in?
>
> >> > Oh, please do! And please do explain to me again how the concept of
> >> > informational entropy is all wet . . . As I recall, your arguments
> >> > here were exceptionally lame.
>
> >> I see you have a selective memory. Forget the one where your claim
> >> about Shannon entropy could be shown wrong by math that can be done
> >> in your head?
>
> > What are you talking about? I *never* claimed that Shannon entropy was
> > wrong at all. It isn't. Shannon's theory is correct regarding a
> > certain definition of "information". Please do quote where I said
> > otherwise.
>
> I'm not saying that IT is "all wet". Rather, you displayed that your
> understanding of it is.
> Look it up yourself. You and Pagano can use dejagoogle as well as I
> can. I'm tired of playing the ReMine game with you two.
Let me make it easy for you. I have an essay on my website dealing
with the concepts of Shannon entropy and Kolmogorov/Chaitin complexity
and how they relate to meaningful informational complexity and
entropy. Please do detail were this supposedly significant error of
mine exists in this essay . . .
http://www.detectingdesign.com/meaningfulinformation.html
R. Baldwin
We are still left without definitions for your terms "meaningful
information," "useful information," and "meaningful information entropy." It
appears that you made these terms up without any kind of mathematical basis.
You've also introduced a new undefined term: "sequence chaos".
I would like to correct gross errors in your reply. Shannon entropy does not
measure sequence chaos as "complexity." It does not measure any property of
a sequence. It measures the average information from an information source.
That makes it a measure for a statistical ensemble of messages, not one
message. The content of one message (sequence) allows you to estimate the
entropy of its information source, not measure it - and since the
information source is modeled as Markov, there is no way to tell from the
estimated Shanon entropy whether an output sequence is chaotic or not.
Similarly, Kolmogorov complexity will in no way tell you whether a sequence
is chaotic. It tells you whether a sequence is algorithmically random with
respect to a reference computer. Any finite sequence will be algorithmically
random with respect to some reference computers and algorithmically
non-random with respect to others.
I note that Baranger also writes "At the present time, the notion of complex
system is not precisely delineated yet. This is normal. As people work on
complex systems more and more, they will gain better understanding of their
defining properties. Now, however, the idea is somewhat fuzzy and it differs
from author to author." In other words, this property you call
"informational complexity" and Baranger calls "complex system" has no
definition today, and has no defined properties - so any conclusion you
reach about it is most likely erroneous.
Furthermore, the subititle of his paper is "A physics talk for
non-physicists." It is not a scientific or mathematical paper on which to
draw substance.
Bobby Bryant
"Seanpit" <seanpi...@naturalselection.0catch.com> writes:
> Let me make it easy for you. I have an essay on my website dealing
> with the concepts of Shannon entropy and Kolmogorov/Chaitin complexity
> and how they relate to meaningful informational complexity and
> entropy. Please do detail were this supposedly significant error of
> mine exists in this essay . . .
>
> http://www.detectingdesign.com/meaningfulinformation.html
The error wasn't in your essay, but rather in a t.o. post where you
made some black-and-white statements about the entropy of two extremely
simple systems, and you were flat out wrong. You don't understand
the most rudimentary properties of IT.
Seanpit
> In article <1172173081.555472.111...@v45g2000cwv.googlegroups.com>,
> "Seanpit" <seanpitnos...@naturalselection.0catch.com> writes:
>
> > Let me make it easy for you. I have an essay on my website dealing
> > with the concepts of Shannon entropy and Kolmogorov/Chaitin complexity
> > and how they relate to meaningful informational complexity and
> > entropy. Please do detail were this supposedly significant error of
> > mine exists in this essay . . .
>
> >http://www.detectingdesign.com/meaningfulinformation.html
>
> The error wasn't in your essay, but rather in a t.o. post where you
> made some black-and-white statements about the entropy of two extremely
> simple systems, and you were flat out wrong. You don't understand
> the most rudimentary properties of IT.
Oh please! If you have to dredge up some minor mistatement that
someone made years ago in order to ignor the main thrust of an
argument, you're really reaching. Where in my current essay dealing
with Shannon or algorithmic entropy do I make any significant errors?
I thought you said you had something? Did I miss it? Where is this
stunning rebuttle of yours? I've made lots of minor errors here on
T.O., and I've admitted to them. Which, I might add, is far more than
I can say for most, such as yourself, who frequent this forum.