David Dryden - Searching All of Sequence Space
Seanpit
http://rsif.royalsocietypublishing.org/content/5/25/953.long
On May 2, 7:54 am, david.dry...@ed.ac.uk wrote:
> Hello, I’m David Dryden, the main author of the paper which has
> generated all of this discussion. Steven Litvintchouk has asked me to
> comment on the analysis of my paper performed by Sean Pitman and this
> is appended at the end of this text. I must say that I am a bit
> surprised at the amount of interest and discussion that has arisen
> from the little paper by myself and two colleagues. However, I am
> pleased that it has done so and that my decision to pay for it to be
> an “open access” paper has been justified. It is my hope that within
> 10 years all professional peer-reviewed science will be freely
> available.
That would be a huge step forward indeed!
> I have skimmed through many of the other comments and noted one
> disparaging comment concerning our acknowledgement of discussion with
> Simon Conway Morris. I would like to briefly explain why we did this.
> I attended a lecture by him in which he discussed convergence at
> length and briefly mentioned the big numbers problem. I started
> corresponding with him and have met him on numerous occasions now for
> further discussions on these two topics. (Inevitably we have also
> talked about his religious views plus his view of creationism/ID. His
> negative views on creationism and ID fully concur with my own.) He is
> a highly respected biologist and palaeontologist and his ideas on
> convergence in organisms would appear to tally with many ideas on
> convergence at the molecular level, my area of interest. He was
> essentially a catalyst in getting me to seriously research the big
> numbers issue so it is perfectly normal practice in science for him to
> be acknowledged. The comment also assumed we were chemists but in
> addition to having worked in chemistry and physics, we have many years
> of practical experience in genetics, molecular biology and
> biochemistry. Not obvious from our address of course.
>
> I am probably going to write far too much but if you want the
> conclusion, it is that Sean Pitman is completely and utterly wrong in
> everything he says in his comments and displays a great ignorance of
> proteins and their structure and function. However, I do hope he will
> read on.
I think you simply don't understand my argument, or the nature of the
concept of increasing levels of functional complexity. It seems like
your understanding of functional complexity is based on how
interesting you think the function in question is. My definition of
functional complexity, in comparison, is not based on how interesting
various systems may or may not be, but in the minimum structural
threshold requirements needed to build a system so that it will work
to at a selectable level of usefulness.
> He has failed to recognise that we wished to establish limits on the
> amount of sequence space explored.
But I do recognize and even agree with your estimates on the limits of
the amount of sequence space that can be explored over a given time
limit. But that isn't the main problem here. The main problem is how
much time it takes to actually find novel beneficial sequences that go
beyond the very very low levels of minimum structural threshold
requirements noted in your paper. You only deal with systems that
have, at minimum, very very low level structural thershold
requirements - less than 100aa or "characters" at minimum.
> Defining limits is a standard
> scientific procedure, though often forgotten, and prevents a lot of
> time wasting as long as one does not initially restrict the
> calculation unnecessarily. Hence, these upper and lower limits are as
> generous as possible based upon current knowledge. They may be out by
> a few powers of ten but this is negligible and as research proceeds
> the limits are likely to come closer together narrowing the range of
> possibilities.
I agree . . .
> In our graph, we overlaid the limits on top of the
> number of different sequences possible for a given pool of letters.
> The letters may total up to 20 in number but it’s just a number. If
> these letters are considered to be amino acids, then we can group the
> 20 amino acids into a smaller number of categories related to their
> physical chemical properties. As soon as you state that the symbols
> you use in the calculation of these big numbers represent physical
> entities then you cannot ignore their physical properties. Such
> groupings are well known to be valid in experiment and are the basis
> for computer-driven sequence analysis. It is unfortunate that such
> computer analysis has been carried too far by some people especially
> those who wish to push the ID complexity agenda and that sight has
> been lost of the fact that proteins do not exist in silico.
I'm not sure I know anyone who is prominent within the ID camp who
would argue otherwise. Of course protein-based systems "do not exist
in silico".
> What follows below is a “lecture” on protein structure for Sean
> Pitman’s benefit. He could of course read a book such as the excellent
> “Introduction to protein structure” by Branden and Tooze and
> accessible to all audiences. I apologise to the rest of you if it gets
> boring but it will eventually lead back to discussing Pitman’s
> comments. Also please do not feel that I am talking “down” to you
> expecting you to believe the expert, I just wish to bring some of the
> latest research and some well established data to you. Also, the
> formality in the writing is just to keep it precise and to exclude, if
> possible, more than one interpretation though given the haste in which
> I have had to write this, it is not perfect.
>
> In the real world of protein structure and function, it is well
> established that many amino acids can be changed with little or no
> effect on function
This is only true if you are talking about changing amino acids one at
a time. It becomes exponentially less and less true when you start
talking about changing more and more amino acids at the same time.
Consider the following quotes from Bloom et al:
"Our theory predicts that for large numbers of substitutions the
probability that a protein retains its structure will decline
exponentially with the number of substitutions, with the severity of
this decline determined by properties of the structure. . . Our work
unifies observations about the clustering of functional proteins in
sequence space. . . " 1
Bloom goes on to point out:
"Experiments have demonstrated that proteins can be extremely
tolerant to single substitutions; for example, 84% of single-residue
mutants of T4 lysozyme and 65% of single-residue mutants of lac
repressor were scored as functional. For multiple substitutions, the
fraction of functional proteins decreases roughly exponentially with
the number of substitutions, although the severity of this decline
varies among proteins." 2
1. Jesse D. Bloom, Alpan Raval, and Claus O. Wilke, Thermodynamics of
Neutral Protein Evolution, Genetics. 2007 January; 175(1): ( Link -
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1775007)
2. Jesse D. Bloom, Jonathan J. Silberg, Claus O. Wilke, D. Allan
Drummond, Christoph Adami, and Frances H. Arnold, Thermodynamic
prediction of protein neutrality, Proc Natl Acad Sci U S A. 2005
January 18; 102(3): 606-611. ( Link -
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=15644440)
> (there are only two “functions” for a protein: to
> bind and control another object or to bind another object and catalyse
> a reaction on that object-and this latter includes proton pumping to
> rotate a flagellum). The catalytic chemical mechanisms performed by
> enzymes and ribozymes fall into only 6 categories of well understood
> chemical reactions (a rather small reaction space). All of
> biochemistry is built upon them. Those mutations that do change
> function usually define an active site (for function) or a crucial
> folding region. It is known that proteins are built up from the
> repetitive use of smaller peptide sequences being joined together by
> gene duplication and recombination in the DNA coding. A general
> consensus seems to be that amino acid sequences of length about 20 or
> 30 really start to get interesting in terms of function but even
> smaller folding units are being proposed as progenitors (see work if
> possible by Edward N Trifonov and also note that even single amino
> acids are capable of catalysing reactions). The joining of these
> 20-30mers (via the gene), which fold into “super-secondary” structure
> units, rapidly leads to a folded “domain” of 50-150 amino acids. These
> domains are small folded units. This domain size is essentially
> universal. You do not find examples of a 1000 amino acid domain but it
> will instead comprise around 10 smaller domains.
Correct.
> It is very important
> to note that in many cases such folding does not require complete
> specification of the sequence but only maintenance of the pattern of
> amino acid categories (polar, non-polar etc). Many domains do
> interesting things but a recurring theme is to then bring collections
> of the domains together either as separate subunits to form quaternary
> structure or to string them together into one single chain by making
> them via a single gene. This latter process is how one makes a 1000
> amino acid protein. Nature takes the domain modules and puts them
> together to make novel structures and functions. (Note that very few
> long protein chains are found as their synthesis is tricky due to
> increasing chances of errors in gene replication, transcription or
> translation. These problems were recognised by Francis Crick if I
> recall correctly in the 1960’s. The average protein size is around 500
> amino acids.) The number of domains with unique folds appears to be
> limited to around 1000 to 10,000 (certainly less than a million) and
> it is becoming rare for science to find new ones. This means that
> whatever sequence you have, you get one of these folds
Good so far.
> (but note that
> there is a relatively new discovery of “natively-unfolded” proteins
> which are unfolded until they bind to their target molecule at which
> point they fold up. How much of sequence space is occupied by these
> fully functional proteins is unknown).
While it is true that the exact ratio of functional vs. non-functional
proteins is not known, an upper limit on the ratio can be determined
to a useful degree of certainty based on the idea that the vast
majority of potential protein folds are not stable and therefore would
not make viable proteins. This ratio of potentially viable vs. non-
viable folds decreases exponentially with each increase in the size of
the protein sequence under consideration.
> The number of protein types in
> any organism also appears to be very limited from several hundred in
> the bacteria with very small genomes to perhaps of the order of 10,000
> in multicellular organisms. These proteins still contain the same
> domains. These limited numbers of proteins perform a limited number of
> reactions (again totalling hundreds to thousands of such reactions as
> detailed in standard biochemistry textbooks). The important thing to
> produce different species is how all these reactions are controlled
> (mostly) by proteins each built using the same structural principles
> as already detailed. This area of control is often referred to as part
> of EvoDevo or evolutionary development and it is where the real
> discussions of complexity are going on. That’s not my speciality so I
> will return now to proteins.
So far so good . . .
> Hopefully it is clear that we have considerable understanding of
> protein structure and how they function and that they are not so
> complex that we cannot possibly explain them (and even design them
> ourselves. David S Goodsell has published an excellent book on
> “Bionanotechnology” showing what Nature has achieved and how our
> understanding of it lets us design new experiments). We could if we
> wished define a structural space and a functional space in the same
> way as a sequence space. From the foregoing, it should be clear that
> neither of these spaces is particularly large when compared to the
> possible size of sequence space.
This is because you are only dealing with sequence spaces for protein-
based systems that are made up of single proteins - and small ones at
that. The real problems come when you start considering multi-protein
systems where all the protein parts, and therefore all of their
individual residues, are required to be in a fairly specific
arrangement relative to each other at the same time for the function
in question to be realized.
> Given the small sizes of the spaces of domain structure, chemical
> reactivity, and biochemical function, or perhaps I could refer to them
> as toolboxes, it does not seem to be too much of a guess that the last
> common ancestor of all life on earth would be equipped with all of
> these toolboxes. This is why we decided to determine the limits of use
> of these toolboxes and calculate the upper and lower limits starting
> from way back in time. The tools may not have been fully utilised or
> explored by that stage (or even by bacteria today), but later when
> multicellular organisms appeared, these tools were ready to be used
> and even reconfigured.
>
> So we return to the problem of how big is sequence space? It is not 20
> raised to the power of the number of amino acids in the sequence but
> much less as we discussed in our paper. There is no need to have 20
> different types of amino acid each with unique properties or sequence
> lengths greater than around 100. This is due to the physical
> similarities between amino acids and the limited range of folded
> structures. Only a few amino acids in any protein are crucial for its
> function. Changing these ones will sometimes do almost nothing to the
> function. However, some will change the function to something new
> while maintaining structure, and a very few will change the protein
> structure (and hence its original function) altogether but in all
> probability still confer a new function. Even if the original
> structure is destroyed by a mutation and the protein does not fold,
> the possibility of a new function is not lost as evidenced by the
> discovery of natively unfolded proteins which acquire fold and
> function upon binding to a target.
It is very clear that protein-based systems do indeed contain a degree
of flexibility where many mutations can be tolerated without a
significant loss of the function in question. It is also agreed that
a smaller alphabet of amino acids would be able to do the job.
However, there are several problems with the assumptions behind this
argument. One problem is the assumption that the minimum size
requirement for a system would not increase given a smaller alphabet.
One might be able to build a flagellar motility system with an
alphabet of only two characters, but most likely the system would
require far more characters, at minimum, than if a 20-character
alphabet were used.
It is like the difference between the English language system of 28-
characters (letters, spaces and periods) and a computer language that
is based on just two characters. Given these two systems, consider a
problem of transmitting the information on a blueprint to build a
particular kind of house. Do you really think it would take the same
number of characters in both language systems to code for the same
particular structure? I don't think so. A few more characters would
be needed, at minimum, for the two-character system vs. the 28-
character system.
> Sequence space when proposed was quickly recognised as a silly
> “paradox” by protein scientists (though not unfortunately by some
> other scientists) rather like the silly Levinthal “paradox” of protein
> folding. Sequence space may be large but that does not mean it is
> complex. I hope the above short essay on protein structure and
> function is useful even to Sean Pitman who needs to stop being
> obsessed with computer-based numerology and do some reading and talk
> to some practical protein scientists. I also hope that he will realise
> that proteins are not relevant to religion and that they as well as
> other macromolecules provide absolutely no foundation for ID.
This has nothing to do with any particular "religion" - unless you
want to call science a form of religion.
> Some short specific replies to the critique by Sean Pitman
>
> "The authors argue that because some types of functional proteins are
> smaller than 100aa [amino acids], and because some types of proteins
> have very low sequence specificity requirements, that pretty much all
> of sequence space could have been searched in just a few billion
> years.
>
> "What these authors fail to realize is that not all protein-based
> systems are created equal. Some systems do indeed require very few
> amino acid building blocks and little sequence specificity. These, of
> course, are on very low levels of functional complexity. Other
> systems, however, require far more than the 100aa systems discussed by
> the authors - at minimum. And, many of these systems require a
> significant degree of specificity. These systems are on a much higher
> level of functional complexity and therefore occupy much much larger
> sequence spaces and also have exponentially lower ratios of
> potentially beneficial vs. non-beneficial at these higher levels.”
>
> Reply: With nearly 50 years of biological and chemical research shared
> between the authors, we really do understand that not all molecules
> are the same.
Great! ; )
> We are not saying only a few specified amino acids are
> available but a few types of amino acids- polar, non-polar, negative,
> positive and so on. For example, any one of the polar ones might do at
> a particular site. All you need to specify is polarity.
That's correct. That's what makes protein-based systems fairly
flexible with regard to tolerance of mutations - especially those that
occur one at a time.
It is much like the English language system where pretty much any
letter in this paragraph could be mutated, one at a time, without a
significant loss of meaning of the paragraph as a whole. The very
same thing is true of protein-based systems. There is a degree of
mutational tolerance. However, reducing the number of characters
doesn't help solve the problem of searching sequence space for higher
and higher level systems. This is because a reduction in the number
of characters would only increase the overall specificity requirements
of the system in question in line the the reduction of the number of
character options in the alphabet. In short, the larger sequence
space only means that the functional islands within that space are
larger. Reducing the overall size of sequence space doesn't change
the ratio of potentially beneficial vs. non-beneficial since the size
of the beneficial islands is also reduced to the same degree as the
reduction of sequence space.
> Since this is
> the entire basis of using sequence comparisons to group proteins into
> functional families and these computer methods are used by supporters
> of ID, they should know this. Small proteins are not necessarily
> functionally simple nor are big proteins necessarily complex in
> function (in fact some a remarkably boring).
This is also correct. I think you are not understanding my argument
here. I'm not talking about just any large protein-based system. Not
all large proteins are created equal either. Some require more
specificity than do other proteins. My argument is that given a
specific degree of required sequence specificity, increasing the
minimum size requirement ends up producing a exponential decrease in
the ratio of sequences in sequence space able to produce a beneficial
function at that level of minimum structural threshold requirements.
So, you see, I'm not just talking about any large protein here. Many
large proteins have very little specificity requirements and therefore
their attached functionality can be achieved by a great many more
proteins in sequence space. In other words, the ratio of these types
of functions is relatively high in sequence space.
> "The authors of this paper do not even address the concept of
> different levels of functional complexity. They only point out the
> obvious that some types of functional systems are very very low level
> systems. Well duh! What about those systems that are on much much
> higher levels of minimum size and/or specificity requirements?...”
>
> Reply:These increasing degrees of functional complexity are a mirage.
> Just because a flagellum spins and looks fancy does not mean it is
> more complex than something smaller. The much smaller wonderful
> machines involved in manipulating DNA, making cell walls or
> cytoskeletons during the cell’s lifecycle do far more complex and
> varied things including switching between functions. Even a small
> serine protease has a much harder job than the flagellum. The
> flagellum just spins and spins and yawn…
You're mistaken here. You have to consider the minimum structural
threshold requirement needed to produce a particular type of
functionality. A serine protease is a single protein enzyme that
requires no more than a few hundred fairly specified amino acid
residues, at minimum, to work to a useful level of activity. This is
simply not true of a multiprotein system like a rotary flagellar
motility system. There is no way that you could produce such a system
with only a few hundred coded residue positions regardless of their
arrangement in sequence space. At minimum such a system requires
several thousand amino acid residues working together at the same time
in a fairly specified arrangement.
I'm sorry, but your attempt to argue that a single-protein enzyme is
just as functionally complex as a flagellar motility system is simply
ludicrous. The fact that you are bored with the functionality of the
flagellar system, arguing that it does nothing more than go round and
round, "yawn", has nothing to do with what it takes to make this
"boring" function actually work - at minimum.
> "The evidence shows that the distances [in sequence space] between
> higher and higher level beneficial sequences with novel functions
> increases in a linear manner."
>
> Reply: What evidence? And if importance of function scales with
> sequence length and the scaling is linear then I am afraid that 20^100
> is essentially identical to 2 x 20^100. Also a novel function is not a
> new function but just one we stumble upon in doing the hard work in
> the lab. It’s been there a long time…
The functional island has been there all along in sequence space. It
is just as matter of discovering it - as you note. The very same
thing is true of the evolutionary mechanism of RM/NS for a living
organism or population of organisms. The average time needed for the
mechanism of evolution to find a novel functional system in sequence
space depends on the average distance between potentially beneficial
islands of sequences in overall sequence space. It is this ratio that
determines the likely minimum distance between anything in the
existing gene pool of options and the closet potential target (i.e.,
beneficial sequence with a novel beneficial function) in sequence
space.
As it turns out, as the minimum size and/or specificity requirements
of systems under consideration increase in a linear manner, the ratio
of potentially beneficial vs. non-beneficial systems decrease in an
exponential manner. This is true regardless of the size of your
alphabet. As the ratio decreases exponentially, the average distance
between potentially beneficial islands in sequence space increases in
a linear manner. And, with each linear increase in the distance to
the closest potentially beneficial island the average number of
mutations needed to reach that island (or any other beneficial island)
increases exponentially as well.
That is the problem for the mechanism of RM/NS in a nutshell. And, it
is this very problem that your paper does not address - and neither
does any other paper in mainstream literature.
For a more detailed review of this problem see:
http://www.detectingdesign.com/flagellum.html#Calculation
In any case, I do thank you for the time you took to present your
thoughts. I don't think you actually understand my position, however,
or the problem of exponentially decreasing ratios of beneficial vs.
non-beneficial with increasing levels of functional complexity. Your
paper basically treats all protein-based systems as if they were on
the same level - a very very low level of functional complexity that,
by definition, has a relatively high ratio of potentially beneficial
vs. non-beneficial systems. Certainly searching out practically all
of such low levels of functional complexity is no problem for the
mechanism of RM/NS within a few billion years. That's a no brainer.
The problems come when you move up the ladder a few steps to consider
systems that require at least 1000 fairly specified amino acid
residues (or characters in whatever alphabet you want to consider)
working together at the same time (as in systems that require multiple
specified proteins to work - not just single-protein systems).
Sean Pitman
www.DetectingDesign.com
wf3h
> Regarding the following paper by David Dryden:
>
>
> based systems that are made up of single proteins - and small ones at
> that. The real problems come when you start considering multi-protein
> systems where all the protein parts, and therefore all of their
> individual residues, are required to be in a fairly specific
> arrangement relative to each other at the same time for the function
> in question to be realized.
really? is this true? because it seems sean has admitted proteins of
<300 aa evolve all the time. his argument hinges on the need for
SIMULTANEOUS evolution. is this a requirement for systems to evolve?
that everything has to happen at once?
i haven't seen it.
and, again, one needs to ask how his creationist views solve this
problem. absent the presence of any method to EXCLUDE natural
processes, we'r'e left with the unknown...rather than ID.
it looks like sean isn't addressing the argument here. dryden argues
that smaller systems are flexible in terms of function. sean says
that smaller systems can't do the job and 'most likely' would need
more 'letters' in the alphabet
IOW he doesnt care what the evidence says...he's gonna put his own
premise into the argument to make sure his argument is circular.
> >
> > Sequence space when proposed was quickly recognised as a silly
> > “paradox” by protein scientists (though not unfortunately by some
> > other scientists) rather like the silly Levinthal “paradox” of protein
> > folding. Sequence space may be large but that does not mean it is
> > complex. I hope the above short essay on protein structure and
> > function is useful even to Sean Pitman who needs to stop being
> > obsessed with computer-based numerology and do some reading and talk
> > to some practical protein scientists. I also hope that he will realise
> > that proteins are not relevant to religion and that they as well as
> > other macromolecules provide absolutely no foundation for ID.
>
> This has nothing to do with any particular "religion" - unless you
> want to call science a form of religion.
?? uh sean...NO ONE believes you when you say you're not arguing
religion. since your argument is wrong, the only reason to keep making
it is BECAUSE of reigion. i've said this many times, and now dryden
has as well..
did it ever occur to you that objective observers, aware of science,
AND of the history of creationism, see your argument differently than
you do because of your religious bias?
>
> > Reply:These increasing degrees of functional complexity are a mirage.
> > Just because a flagellum spins and looks fancy does not mean it is
> > more complex than something smaller. The much smaller wonderful
> > machines involved in manipulating DNA, making cell walls or
> > cytoskeletons during the cell’s lifecycle do far more complex and
> > varied things including switching between functions. Even a small
> > serine protease has a much harder job than the flagellum. The
> > flagellum just spins and spins and yawn…
>
> You're mistaken here.
ah. sean talks about functional complexity of long chains. when shown
that this is a fabrication he immediately says no one understands
their own arguments except sean. functional complexity means what sean
says it does; no more, no less.
You have to consider the minimum structural
> threshold requirement needed to produce a particular type of
> functionality. A serine protease is a single protein enzyme that
> requires no more than a few hundred fairly specified amino acid
> residues, at minimum, to work to a useful level of activity. This is
> simply not true of a multiprotein system like a rotary flagellar
> motility system.
and IF the system that creates a rotary flagellar system is VERY
flexible, and if almost ANY sequence of amino acids can work, then
functional complexity is the WRONG way to view this argument as dryden
points out.
IOW sean's whole argument, based on LENGTH and FUNCTIONALITY is simply
wrong.
sean, it seems, doesn't understand his own work! isn't THAT ironic!
There is no way that you could produce such a system
> with only a few hundred coded residue positions regardless of their
> arrangement in sequence space. At minimum such a system requires
> several thousand amino acid residues working together at the same time
> in a fairly specified arrangement.
and if it doesn't matter what the sequence of these amino acids is,
then sean's argument is irrelevant. again it seems he doesn't
understand his own argument.
>
> I'm sorry, but your attempt to argue that a single-protein enzyme is
> just as functionally complex as a flagellar motility system is simply
> ludicrous.
ROFLMAO!! sean your whole argument is a house of cards! your
assumptions are not based on empirical evidence.
>
> As it turns out, as the minimum size and/or specificity requirements
> of systems under consideration increase in a linear manner, the ratio
> of potentially beneficial vs. non-beneficial systems decrease in an
> exponential manner. \
seems again, sean doesn't understand his own work. he thinks size
ALWAYS correlates to COMPLEXITY. there's no reason to assume this is
true. a wrist watch is more complex than a gallon of water even though
the watch is smaller.
so sean is caught trying to make an ex post facto justification of
creationist nonsense based on wrong premises he assumes are true. this
is a classic circular argument.
This is true regardless of the size of your
> alphabet. As the ratio decreases exponentially, the average distance
> between potentially beneficial islands in sequence space increases in
> a linear manner.
and again, the size vs complexity argument rears its head. is this
justified? if so, why? evidence?
oh. he has none.
sean's argument seems to be:
1. there is, deterministically, a relationship between SIZE of a
protein and its functional complexity (whatever that is)
2. the longer the protein or the more proteins involved in a system
the more deterministically functional it is; you can change almost
NOTHING in such a system
but, it appears, neither of these is true. and if they are NOT true,
the only reason to make such a wrong argument must be for reasons not
associated with science....IOW religion...
which is what a bunch of folks have been telling sean all along.
GCPAXS...@spammotel.com
> Regarding the following paper by David Dryden:
>
> http://rsif.royalsocietypublishing.org/content/5/25/953.long
>
Sean, was it too much trouble to answer Dryden
where he posted his stuff? And are you going
to start a new thread after each answer of his?
Just curious.
Regards,
Karel
--
If knowledge can create problems,
it is not through ignorance that we
can solve them (Asimov)
Seanpit
> On May 4, 7:26 pm, Seanpit <sean...@gmail.com> wrote:> Regarding the following paper by DavidDryden:
>
> >http://rsif.royalsocietypublishing.org/content/5/25/953.long
>
> [snip discussion]
>
> Sean, was it too much trouble to answerDryden
> where he posted his stuff? And are you going
> to start a new thread after each answer of his?
> Just curious.
The original thread was too garbled by a large number of nonsense or
irrelevant posts and a great many title changes so that the thread was
becoming hard to follow. I put a link in the other similar threads to
this one.
> Regards,
>
> Karel
>
> --
> If knowledge can create problems,
> it is not through ignorance that we
> can solve them (Asimov)
Sean Pitman
www.DetectingDesign.com
Seanpit
> On May 4, 1:26 pm, Seanpit <sean...@gmail.com> wrote:
>
> > Regarding the following paper by DavidDryden:
>
> > This is because you are only dealing with sequence spaces for protein-
> > based systems that are made up of single proteins - and small ones at
> > that. The real problems come when you start considering multi-protein
> > systems where all the protein parts, and therefore all of their
> > individual residues, are required to be in a fairly specific
> > arrangement relative to each other at the same time for the function
> > in question to be realized.
>
> really? is this true? because it seems sean has admitted proteins of
> <300 aa evolve all the time. his argument hinges on the need for
> SIMULTANEOUS evolution. is this a requirement for systems to evolve?
> that everything has to happen at once?
Systems that require less than 300 fairly specified amino acid
residues (fsaars) do evolve all the time - often quite rapidly. The
reason that systems with minimum requirements over 1000 fsaars
(usually involving systems with multiple proteins) is not that the
entire system must evolve from scratch. That's not true. It is true,
however, that until the minimum threshold requirement is reached, the
higher level system will not work to any useful degree at all. That
requirement must be in place first before the system can work at all.
The gap between what exists in the genome and this minimum threshold
requirement of the higher level system is what creates the need for
time for the mechanism of RM/NS to cross the gap. Each linear
increase in this gap distance translates into an exponential increase
in the average amount of time required to cross the gap.
> i haven't seen it.
No one has seen evolution at all beyond the 1000 fsaar threshold even
though the starting points within existing genomes are far closer than
a Hamming Distance of 1000 mutational changes. The likely minimum
Hamming gap distances at the 1000 fsaar level of functional complexity
is no more than a couple hundred or so mutational changes, but very
likely more than 50 differences.
That's the problem in nutshell. The minimum likely Hamming gap
distance increases linearly with each step up the ladder of functional
complexity. Therefore, the average number of mutations needed to
cross the gap increases exponentially.
> and, again, one needs to ask how his creationist views solve this
> problem. absent the presence of any method to EXCLUDE natural
> processes, we'r'e left with the unknown...rather than ID.
While this is completely irrelevant to the question at hand, at least
human-level ID is a natural process.
> > > function is useful even to SeanPitmanwho needs to stop being
NA Sides
wrote:
It is clear from your responses to this newsgroup that *you* do not
understand your own claims about "functional complexity" and "structural
complexity." You can't define functional informational complexity in any
meaningful way. You can't measure it. You equate it with the length of
polypeptide chains, but you lack any clue as to how this metric links
with any real biological functions. David Dryden has completely
demolished your pretence that any such relationship exists.
>> He has failed to recognise that we wished to establish limits on the
>> amount of sequence space explored.
>
>But I do recognize and even agree with your estimates on the limits of
>the amount of sequence space that can be explored over a given time
>limit. But that isn't the main problem here. The main problem is how
>much time it takes to actually find novel beneficial sequences that go
>beyond the very very low levels of minimum structural threshold
>requirements noted in your paper. You only deal with systems that
>have, at minimum, very very low level structural thershold
>requirements - less than 100aa or "characters" at minimum.
Evolution apparently doesn't go searching for these large novel aa
sequences. It makes do with what's available at any given time in the
history of life on earth. You apparently doubt that organisms evolve
through the gradual modification of pre-existing structures. Therefore,
according to you, huge evolutionary leaps, or intelligent intervention,
is required.
<snip>
>So far so good . . .
>
>> Hopefully it is clear that we have considerable understanding of
>> protein structure and how they function and that they are not so
>> complex that we cannot possibly explain them (and even design them
>> ourselves. David S Goodsell has published an excellent book on
>> “Bionanotechnology” showing what Nature has achieved and how our
>> understanding of it lets us design new experiments). We could if we
>> wished define a structural space and a functional space in the same
>> way as a sequence space. From the foregoing, it should be clear that
>> neither of these spaces is particularly large when compared to the
>> possible size of sequence space.
>
>This is because you are only dealing with sequence spaces for protein-
>based systems that are made up of single proteins - and small ones at
>that. The real problems come when you start considering multi-protein
>systems where all the protein parts, and therefore all of their
>individual residues, are required to be in a fairly specific
>arrangement relative to each other at the same time for the function
>in question to be realized.
Ha! Multi-protein based systems don't even figure in your bogus
definition of "functional informational complexity." How would you
calculate the odds that a hemoglobin molecule's alpha and beta subunits
will spontaneously fall together?
<snip>
>> We are not saying only a few specified amino acids are
>> available but a few types of amino acids- polar, non-polar, negative,
>> positive and so on. For example, any one of the polar ones might do at
>> a particular site. All you need to specify is polarity.
>
>That's correct. That's what makes protein-based systems fairly
>flexible with regard to tolerance of mutations - especially those that
>occur one at a time.
>
>It is much like the English language system where pretty much any
>letter in this paragraph could be mutated, one at a time, without a
>significant loss of meaning of the paragraph as a whole. The very
>same thing is true of protein-based systems. There is a degree of
>mutational tolerance. However, reducing the number of characters
>doesn't help solve the problem of searching sequence space for higher
>and higher level systems. This is because a reduction in the number
>of characters would only increase the overall specificity requirements
>of the system in question in line the the reduction of the number of
>character options in the alphabet. In short, the larger sequence
>space only means that the functional islands within that space are
>larger. Reducing the overall size of sequence space doesn't change
>the ratio of potentially beneficial vs. non-beneficial since the size
>of the beneficial islands is also reduced to the same degree as the
>reduction of sequence space.
Evolution doesn't make these blind one in ten to the zillionth power
searches, it just modifies existing structures. Is that so difficult to
understand?
>> Since this is
>> the entire basis of using sequence comparisons to group proteins into
>> functional families and these computer methods are used by supporters
>> of ID, they should know this. Small proteins are not necessarily
>> functionally simple nor are big proteins necessarily complex in
>> function (in fact some a remarkably boring).
>
>This is also correct. I think you are not understanding my argument
>here. I'm not talking about just any large protein-based system. Not
>all large proteins are created equal either. Some require more
>specificity than do other proteins. My argument is that given a
>specific degree of required sequence specificity, increasing the
>minimum size requirement ends up producing a exponential decrease in
>the ratio of sequences in sequence space able to produce a beneficial
>function at that level of minimum structural threshold requirements.
Which is only relevant for organisms that have no ancestors. So your
argument would only be valid for the very first organism. I don't know
what that organism looked like, but I don't think it had a bacterial
flagellum.
But the function itself isn't complex, and once you have any kind of
rotary motion, natural selection can work to add functionality. You need
to get it through your head that organisms have ancestors that bequeath
to them structures that can be modified in small ways. That's apparently
how evolution works.
>I'm sorry, but your attempt to argue that a single-protein enzyme is
>just as functionally complex as a flagellar motility system is simply
>ludicrous. The fact that you are bored with the functionality of the
>flagellar system, arguing that it does nothing more than go round and
>round, "yawn", has nothing to do with what it takes to make this
>"boring" function actually work - at minimum.
Well, I don't think he's assuming, as you are, that the whole system
just fell together at once from random molecular components.
<snip>
NAS
>Sean Pitman
>www.DetectingDesign.com
wf3h
> On May 4, 11:17 am, wf3h <w...@vsswireless.net> wrote:
>
>
>
>
>
> > On May 4, 1:26 pm, Seanpit <sean...@gmail.com> wrote:
>
> > > Regarding the following paper by DavidDryden:
>
> > > This is because you are only dealing with sequence spaces for protein-
> > > based systems that are made up of single proteins - and small ones at
> > > that. The real problems come when you start considering multi-protein
> > > systems where all the protein parts, and therefore all of their
> > > individual residues, are required to be in a fairly specific
> > > arrangement relative to each other at the same time for the function
> > > in question to be realized.
>
> > really? is this true? because it seems sean has admitted proteins of
> > <300 aa evolve all the time. his argument hinges on the need for
> > SIMULTANEOUS evolution. is this a requirement for systems to evolve?
> > that everything has to happen at once?
>
> Systems that require less than 300 fairly specified amino acid
> residues (fsaars) do evolve all the time - often quite rapidly. The
> reason that systems with minimum requirements over 1000 fsaars
> (usually involving systems with multiple proteins) is not that the
> entire system must evolve from scratch.
?? who says? and if the system is so flexible in terms of structure vs
function, then it doesn't matter WHAT the structure is.
That's not true. It is true,
> however, that until the minimum threshold requirement is reached, the
> higher level system will not work to any useful degree at all.
i don't know what this means. as gould once pointed out, a partially
functioning system...such as a light sensitive spot...is better than
no eye at all, for example. i don't know what you mean by 'any useful
degree' and i suspect it's a bogus term
That
> requirement must be in place first before the system can work at all.
> The gap between what exists in the genome and this minimum threshold
> requirement of the higher level system is what creates the need for
> time for the mechanism of RM/NS to cross the gap. Each linear
> increase in this gap distance translates into an exponential increase
> in the average amount of time required to cross the gap.
and if size has NO relationship to functionality...a 1000aa system
composed of 1 structure working as well as another, then it doesn't
matter how 'hard' it is to get there. if all roads lead to rome it
doesnt matter what road i take.
and creationism has no answer for this.
>
> > i haven't seen it.
>
> No one has seen evolution at all beyond the 1000 fsaar threshold even
> though the starting points within existing genomes are far closer than
> a Hamming Distance of 1000 mutational changes.
well now you've confused yourself.
when i've asked you about this before, regarding the structure of
FUNCTIONAL parts of proteins (the folding areas) which are often
<300aa in length, you go off on a tangent about MULTIPLE protein
systems. so which is it? is it 1000 fsar or multiple proteins that you
say can't evolve?
because it seems neither is relevant. if proteins >1000aa in length
are so functionally flexible then it doesnt matter what road evolution
takes. any solution will work (if there is one). and if evolution
procedes by 'tinkering' (as it often does) then the reason systems of
1000aa don't evolve 'all at once' is that the solution to get to a
1000aa system is irrelevant. evolution builds simpler systems and
combines them in systems of <1000aa at a time.
the reason such systems are not 'observed to evolve' is because
evolution doesn't work the way you think it does. that appears to be
what dryden is saying when he points out how functionally flexible
large protein systems are regarding the associated structure.
you, of course, casually dismiss his work, saying he doesn't
understand his own work (a staple response of yours to ANY scientist
who disagrees with you) AND saying that such systems MUST evolve the
way YOU say they do. neither argument is valid.
>
> > and, again, one needs to ask how his creationist views solve this
> > problem. absent the presence of any method to EXCLUDE natural
> > processes, we'r'e left with the unknown...rather than ID.
>
> While this is completely irrelevant to the question at hand, at least
> human-level ID is a natural process.
not if it doesnt exist in nature it's not. and you haven't presented
any information proving it's logical to exclude natural processes.
it's another 'just so story' in a series of stories told by
creationists over a 2000 year history of failure.
your argument hinges on how poorly scientists understand science and
how well creationists DO understand nature. if that were the case, we
would have had antibiotics 2000 years ago. the very non-existence of
virtually ANY understanding of nature, based on the creationist model,
means that model is fatally flawed.
'Rev Dr' Lenny Flank
> I don't think you actually understand my position, however,
> or the problem of exponentially decreasing ratios of beneficial vs.
> non-beneficial with increasing levels of functional complexity.
Gee, Sean, it seems that NBOBODY understands your position except
you. Odd, isn't it, that everyone you've shown your world-shattering
sciency mathy stuff to, thinks it's full of shit because, as you put
it, "they don'[t understand it". Very odd.
How does that always happen, Sean? is it because you're just too dumb
and incompetent to explain your paradigm-shattering scientificf
discovery of the millenium to in such a way that they bcan understand
it and grasp your genius?
Or do they actually understand it all too well and just think that you
are full of shit?
Which of those is most likely, Sean . . . . . . ?
(snicker) (giggle)
Yes, Sean, I am laughing at you. Again.
================================================
Lenny Flank
"There are no loose threads in the web of life"
Editor, Red and Black Publishers
http://www.RedandBlackPublishers.com
Seanpit
> On May 4, 4:22 pm, Seanpit <sean...@gmail.com> wrote:
>
>
>
> > On May 4, 11:17 am, wf3h <w...@vsswireless.net> wrote:
>
> > > On May 4, 1:26 pm, Seanpit <sean...@gmail.com> wrote:
>
> > > > Regarding the following paper by DavidDryden:
>
> > > > This is because you are only dealing with sequence spaces for protein-
> > > > based systems that are made up of single proteins - and small ones at
> > > > that. The real problems come when you start considering multi-protein
> > > > systems where all the protein parts, and therefore all of their
> > > > individual residues, are required to be in a fairly specific
> > > > arrangement relative to each other at the same time for the function
> > > > in question to be realized.
>
> > > really? is this true? because it seems sean has admitted proteins of
> > > <300 aa evolve all the time. his argument hinges on the need for
> > > SIMULTANEOUS evolution. is this a requirement for systems to evolve?
> > > that everything has to happen at once?
>
> > Systems that require less than 300 fairly specified amino acid
> > residues (fsaars) do evolve all the time - often quite rapidly. The
> > reason that systems with minimum requirements over 1000 fsaars
> > (usually involving systems with multiple proteins) is not that the
> > entire system must evolve from scratch.
>
> ?? who says? and if the system is so flexible in terms of structure vs
> function, then it doesn't matter WHAT the structure is.
The system has a degree of flexibility with regard to structure, but
it also has a fair degree of specificity. Therefore, it does matter
what the structure is. Not just any structure will work to do a
particular type of function.
> > That's not true. It is true,
> > however, that until the minimum threshold requirement is reached, the
> > higher level system will not work to any useful degree at all.
>
> i don't know what this means. as gould once pointed out, a partially
> functioning system...such as a light sensitive spot...is better than
> no eye at all, for example. i don't know what you mean by 'any useful
> degree' and i suspect it's a bogus term
A useful degree of functionality means that the level of functionality
has reached a point where it will pay for the energy needed to
preserve it and replicate it over time. Take, for instance, a lactase
enzyme. Not just any level of lactase activity will be selectably
advantageous for a particular type of bacterium in a particular type
of environment. The level of activity of the enzyme must reach a
certain threshold level before it will be functionally advantageous.
This level can only be reached with a certain minimum size AND
specificity requirement. Until this threshold is reached, that gene
pool has no selectable level of lactase activity whatsoever - not even
a little bit.
> > That
> > requirement must be in place first before the system can work at all.
> > The gap between what exists in the genome and this minimum threshold
> > requirement of the higher level system is what creates the need for
> > time for the mechanism of RM/NS to cross the gap. Each linear
> > increase in this gap distance translates into an exponential increase
> > in the average amount of time required to cross the gap.
>
> and if size has NO relationship to functionality...a 1000aa system
> composed of 1 structure working as well as another, then it doesn't
> matter how 'hard' it is to get there. if all roads lead to rome it
> doesnt matter what road i take. and creationism has no answer for this.
Functionalities do indeed have a relationship to both size and
specificity. That's the whole point. Some types of functional
systems have minimum size requirements that are very low - like less
than 100aa with very low specificity limitations on sequence
arrangements. These are very low level functions and can and do
evolve often and quite rapidly. Other types of functional systems are
much more complex in that they have much greater minimum size and
specificity requirements - well beyond the 1000 fsaar threshold of
functional complexity.
And therefore, it does matter which road you take because most roads
possible roads at the level of 1000 fsaar systems are extremely long -
requiring trillions of years before you "reach Rome" - so to speak.
That's the whole problem. The average time to success is very much
dependent upon the average gap distance between what exists and what
might exist within a given gene pool at a particular level of
functional complexity.
> > > i haven't seen it.
>
> > No one has seen evolution at all beyond the 1000 fsaar threshold even
> > though the starting points within existing genomes are far closer than
> > a Hamming Distance of 1000 mutational changes.
>
> well now you've confused yourself.
>
> when i've asked you about this before, regarding the structure of
> FUNCTIONAL parts of proteins (the folding areas) which are often
> <300aa in length, you go off on a tangent about MULTIPLE protein
> systems. so which is it? is it 1000 fsar or multiple proteins that you
> say can't evolve?
It is the total number of amino acid residues required, at minimum, in
all parts of the system. For multi-protein systems, that means adding
up all the amino acid parts in all of the different proteins in the
system - all of which must work together in a specific arrangement at
the same time (as in a flagellar motility system).
> because it seems neither is relevant. if proteins >1000aa in length
> are so functionally flexible then it doesnt matter what road evolution
> takes. any solution will work (if there is one). and if evolution
> procedes by 'tinkering' (as it often does) then the reason systems of
> 1000aa don't evolve 'all at once' is that the solution to get to a
> 1000aa system is irrelevant. evolution builds simpler systems and
> combines them in systems of <1000aa at a time.
I'm not talking about 1000aa proteins, but about 1000 fsaar systems.
There's difference. And yes, 1000+ fsaar systems can be fairly
specified - as is the case for the flagellar motility system.
> the reason such systems are not 'observed to evolve' is because
> evolution doesn't work the way you think it does. that appears to be
> what dry denis saying when he points out how functionally flexible
> large protein systems are regarding the associated structure.
Dryden was talking about large single-proteins - not systems of
proteins where there is much greater specificity for the system as a
whole with regard to the arrangement of its basic building block
residues. Large proteins that have very low specificity requirements
are not more complex than much smaller proteins with higher
specificity requirements. In order to increase the level of
functional complexity, you have to compare apples with apples with
regard to the same degree of sequence specificity at various minimum
size requirements.
> you, of course, casually dismiss his work, saying he doesn't
> understand his own work (a staple response of yours to ANY scientist
> who disagrees with you) AND saying that such systems MUST evolve the
> way YOU say they do. neither argument is valid.
The mechanism under discussion isn't my mechanism Bob. The mechanism
is RM/NS. That's it. The only question left concerns the nature of
sequence space - Does sequence space show an exponential decline in
the ratio of potentially beneficial sequences with increasing
functional complexity or not? That really is the only question under
discussion here.
And no, Dryden does not understand the concept of levels of functional
complexity. He doesn't seem to grasp that concept at all. His entire
paper deals only with very low level examples of functional complexity
that don't remotely approach the 1000 fsaar level. That is why he
thinks he has been so successful. What he has actually done is to
show that it is easy to completely search out sequence space for all
sequences of less than a few dozen characters. That's obvious true,
but it doesn't remotely address the question as to how the mechanism
of RM/NS can produce higher and higher levels of functional complexity
without the exponential stalling out effect? He doesn't answer that
question at all. He doesn't even address it.
> > > and, again, one needs to ask how his creationist views solve this
> > > problem. absent the presence of any method to EXCLUDE natural
> > > processes, we'r'e left with the unknown...rather than ID.
>
> > While this is completely irrelevant to the question at hand, at least
> > human-level ID is a natural process.
>
> not if it doesnt exist in nature it's not.
We've already been over this Bob. Human-level intelligence does exist
in nature. You exist in nature - right?
> and you haven't presented
> any information proving it's logical to exclude natural processes.
> it's another 'just so story' in a series of stories told by
> creationists over a 2000 year history of failure.
I'm not excluding natural processes Bob. Human-level intelligence is
a natural process. What I'm excluding are certain types of natural
processes - namely mindless natural processes.
> your argument hinges on how poorly scientists understand science and
> how well creationists DO understand nature. if that were the case, we
> would have had antibiotics 2000 years ago. the very non-existence of
> virtually ANY understanding of nature, based on the creationist model,
> means that model is fatally flawed.
The fathers of the various scientific disciplines, to include most of
the various branches of modern science, were pioneered by
creationists. Science, good science, is not limited to those who
attribute everything to mindless forces of nature. Sorry. Even those
who believe in God can do very good science without always having to
impose their religion onto their science.
Sean Pitman
www.DetectingDesign.com
Seanpit
> On Mon, 4 May 2009 10:26:32 -0700 (PDT), Seanpit <sean...@gmail.com>
> wrote:
>
>
>
> >Regarding the following paper by DavidDryden:
>
> >http://rsif.royalsocietypublishing.org/content/5/25/953.long
>
> >On May 2, 7:54 am, david.dry...@ed.ac.uk wrote:
> >> generated all of this discussion. Steven Litvintchouk has asked me to
> >> everything he says in his comments and displays a great ignorance of
> >> proteins and their structure and function. However, I do hope he will
> >> read on.
>
> >I think you simply don't understand my argument, or the nature of the
> >concept of increasing levels of functional complexity. It seems like
> >your understanding of functional complexity is based on how
> >interesting you think the function in question is. My definition of
> >functional complexity, in comparison, is not based on how interesting
> >various systems may or may not be, but in the minimum structural
> >threshold requirements needed to build a system so that it will work
> >to at a selectable level of usefulness.
>
> It is clear from your responses to this newsgroup that *you* do not
> understand your own claims about "functional complexity" and "structural
> complexity." You can't define functional informational complexity in any
> meaningful way. You can't measure it. You equate it with the length of
> polypeptide chains, but you lack any clue as to how this metric links
> with any real biological functions. David Dryden has completely
> demolished your pretence that any such relationship exists.
Not remotely. He himself recognizes that different types of systems
are not all created equal. Different types of functional systems do
in fact have different minimum structural threshold requirements.
This is a fact. There really is no argument here. Levels of
functional complexity can clearly defined with regard to the minimum
structural threshold requirements needed to achieve them to their most
basic useful level of functionality. To suggest otherwise is to
remove any semblance of a scientific basis from your "theory". You
remove the ability to make useful predictions about the progress of
your mechanism of RM/NS into the future - predictions which are
actually testable in a falsifiable manner. You also remove any basis
for statistical analysis of your mechanism and how likely it is to be
able to succeed at various levels of functional complexity. How is
that? Well, because neither you nor Dryden has defined this concept.
Dryden has no clue how to define a level of functional complexity. He
certain doesn't address this concept in his paper nor does he seem
able to grasp this idea so far in this forum.
>
> >> He has failed to recognise that we wished to establish limits on the
> >> amount of sequence space explored.
>
> >But I do recognize and even agree with your estimates on the limits of
> >the amount of sequence space that can be explored over a given time
> >limit. But that isn't the main problem here. The main problem is how
> >much time it takes to actually find novel beneficial sequences that go
> >beyond the very very low levels of minimum structural threshold
> >requirements noted in your paper. You only deal with systems that
> >have, at minimum, very very low level structural thershold
> >requirements - less than 100aa or "characters" at minimum.
>
> Evolution apparently doesn't go searching for these large novel aa
> sequences. It makes do with what's available at any given time in the
> history of life on earth. You apparently doubt that organisms evolve
> through the gradual modification of pre-existing structures. Therefore,
> according to you, huge evolutionary leaps, or intelligent intervention,
> is required.
Gradual modification can only occur if the gap distance between what
currently exists and what might exist to some benefit are small enough
to cross in a reasonable amount of time. For very low level systems,
requiring no more than a few hundred fairly specified building blocks
at minimum, these gaps are indeed small enough to cross in very short
order. However, the average gap distances do not stay the same as one
moves up the ladder of functional complexity. They do in fact grow in
size, increasing in a linear manner with each increase in the minimum
structural threshold requirements for higher and higher levels of
functional complexity.
This is in fact why we often see evolution "in action" producing
systems that require no more than a few hundred fairly specified
residues working together at the same time, but we never ever see any
novel system of function evolving which requires at least 1000 fsaars
at minimum (even for multiprotein systems).
I ask you, what is it that limits the evolutionary progress of the
mechanism of RM/NS so that there are no examples evolution in action
beyond such very low levels of functional complexity? - not a single
example in all of literature?
< snip rest >
Sean Pitman
www.DetectingDesign.com
'Rev Dr' Lenny Flank
>And no, Dryden does not understand the concept of levels of functional
complexity.
Gee, who DOES, Sean? Other than you, I mean . . . .
Why does NOBODY, absolutely NOBODY, ever seem to understand your
awesome world-shattering mathy sciency argument, Sean? Why does
EVERBODY who hears it, absolutely EVERYBODY, think it's a load of
bullshit?
Is it because
1. everybody but you is engaged in a vast international atheistic
conspiracy against you, Sean? or
2. you are just too stupid and incompetent to explain your wonder
science to people so they can understand it? or
3. your mathy sciency stuff really is just bullshit?
Which is it?
That's a simple question, Sean. Why are you so reluctant to answer
it?
>Human-level intelligence does exist
in nature. You exist in nature - right?
But you are NOT claiming that humans are the intelligent designers
that designed humans, are you Sean. So why do you keep tossing out
his evasive bullshit?
If the designer is "human-level", and if humans weren't around when
humans were designed, then WHO THE FUCK DO YOU THINK THE INTELLIGENT
DESIGNER WAS, Sean? Space aliens? Time-travelling humans?
Why are you so reluctant to answer that simple question?
>
> The fathers of the various scientific disciplines, to include most of
> the various branches of modern science, were pioneered by
> creationists.
So what. The fathers of chemistry were alchemists. But alchemy is
still full of shit. (shrug)
Anyway, I thougth IDers weren't creationists. Isn't that what they
all testified to, under oath, in open court? Or were they just
bullshitting us about that, too . . . . Of course, you ARE just a
creationist, aren't you, Sean. A young-earth Seventh-Day Adventist
cultist who hides behind ID "theory" because his own "creation
science" got eviscerated in court, repeatedly. Right?
You are a bullshitter, Sean. Nothing more, nothing less, nothing
else.
'Rev Dr' Lenny Flank
> It is the total number of amino acid residues required, at minimum, in
> all parts of the system. For multi-protein systems, that means adding
> up all the amino acid parts in all of the different proteins in the
> system - all of which must work together in a specific arrangement at
> the same time (as in a flagellar motility system).
So we're back once more to the old creationist "747 forming in a
junkyard during a tornado" bullshit . . .
(sigh)
Sean, Sean, Sean . . . you know just as well as we do that this
bullshit is not how evolution works. Evolution does not POOF big
complex things into existence all at once intact in one fell swoop
from a collection of random parts. Evolution works by cobbling
together things using bits and pieces of whatever other unrelated
things happen to already be available.
747's didn't appear all at once from random parts in a junkyard
assembled by a tornado. 747's came from earlier airplanes. And those
airplanes came from even earlier airplanes. And airplanes came from
bicycle parts.
Which means all of your 747-tornado mathy stuff, is bullshit. Pure
unadulterated unvarnished bullshit.
But of course you already knew that, since everybody that you have
sprung your 1000-fs-whatever bullshit upon -- absolutely everybody
without exception -- has pointed out that it's bullshit.
NA Sides
wrote:
>On May 4, 1:28 pm, NA Sides <nongo1...@sonic.net> wrote:
Natural selection can be observed and tested. Predictions can be made
about how populations will acquire immunity to antibiotics or acquire an
ability to metabolize nutrients. You, on the other hand, can't even
define "functional information complexity" in any meaningful way. You
equate it with polypeptide length and claim, without any evidence, that
this is a useful measure of biological function. You can't tell us what
this functionality is. And in this very paragraph you have the gall to
pretend that no one can define what a mutation is, or how it relates to
natural selection. And to top it off, you boast that no one can define a
level of "functional complexity." I don't suppose it ever occurred to
you that's because, as you use it, it's a completely indefinable and
useless concept. If you can't meaningfully define it, no one else is
going to do it for you.
You've presented no evidence that evolution *ever* requires complex
systems to fall together from random molecular components. You *claim*
there exist thresholds of functional complexity that can't be crossed by
random mutation and natural selection, but the claim is based on nothing
more than your own refusal to acknowledge that organisms descend, with
slight modifications, from similar ancestors.
>This is in fact why we often see evolution "in action" producing
>systems that require no more than a few hundred fairly specified
>residues working together at the same time, but we never ever see any
>novel system of function evolving which requires at least 1000 fsaars
>at minimum (even for multiprotein systems).
You'll never see these huge jumps because they don't happen and
evolution doesn't need them. You imagine they must happen because you
simply can't accept that the entire process involves slight progressive
modifications of pre-existing structures and processes.
>I ask you, what is it that limits the evolutionary progress of the
>mechanism of RM/NS so that there are no examples evolution in action
>beyond such very low levels of functional complexity? - not a single
>example in all of literature?
It's because these huge jumps don't occur and are not needed. Complex
biological systems develop from slightly modified precursors. There's
not a lick of evidence, so far as I can tell, that your molecular
saltations have ever occurred. So you don't really need an intelligent
designer to account for them.
NAS
>Sean Pitman
>www.DetectingDesign.com
Rodjk #613
> On Mon, 4 May 2009 10:26:32 -0700 (PDT), Seanpit <sean...@gmail.com>
Like the all of the creationist con-men, Sean does not have to make
sense.
He just has to make his comments long enough and confusing enough so
that the 'man on the street' is convinced that there is some
complicated discussion going on, and therefore creationism is not
treated fairly as science.
Since that man on the street is most likely religious and wants to
believe in creationism anyway, Sean and his like really have a pretty
easy time of it.
Rodjk #613
wf3h
>
> I ask you, what is it that limits the evolutionary progress of the
> mechanism of RM/NS so that there are no examples evolution in action
> beyond such very low levels of functional complexity? - not a single
> example in all of literature?
and in 2000 years why are there no examples of a mind based process in
nature?
why are there no minds apart from brains?
why are all brains composed of matter?
if sean's view of nature is right, then brainless minds should be
predominant in nature, and should be causing all KINDS of processes
but we've never seen a single one. his idea is useless
wf3h
> On May 4, 1:51 pm, wf3h <w...@vsswireless.net> wrote:
> >
>
> >
> > ?? who says? and if the system is so flexible in terms of structure vs
> > function, then it doesn't matter WHAT the structure is.
>
> The system has a degree of flexibility with regard to structure, but
> it also has a fair degree of specificity. Therefore, it does matter
> what the structure is. Not just any structure will work to do a
> particular type of function.
>
which is certainly NOT a scientific rationale for your argument. if
function is NOT related to structure deterministically then your
argument fails.
it's another just-so-story of creationism.
> > > That's not true. It is true,
> > > however, that until the minimum threshold requirement is reached, the
> > > higher level system will not work to any useful degree at all.
>
> > i don't know what this means. as gould once pointed out, a partially
> > functioning system...such as a light sensitive spot...is better than
> > no eye at all, for example. i don't know what you mean by 'any useful
> > degree' and i suspect it's a bogus term
>
> A useful degree of functionality means that the level of functionality
> has reached a point where it will pay for the energy needed to
> preserve it and replicate it over time. Take, for instance, a lactase
> enzyme. Not just any level of lactase activity will be selectably
> advantageous for a particular type of bacterium in a particular type
> of environment. The level of activity of the enzyme must reach a
> certain threshold level before it will be functionally advantageous.
> This level can only be reached with a certain minimum size AND
> specificity requirement. Until this threshold is reached, that gene
> pool has no selectable level of lactase activity whatsoever - not even
> a little bit.
and 'even a little bit' works as i pointed out for the eye. again
your argument fails. you haven't established
1. the lack of functionality of a partially functioning system
2. the need for a completely functioning system and a
deterministically related structure...IOW if there are ALOT of
structures that will work then 'complexity' is irrelevant.
again your argument fails.
>
> > and if size has NO relationship to functionality...a 1000aa system
> > composed of 1 structure working as well as another, then it doesn't
> > matter how 'hard' it is to get there. if all roads lead to rome it
> > doesnt matter what road i take. and creationism has no answer for this.
>
> Functionalities do indeed have a relationship to both size and
> specificity. That's the whole point.
so you say. prove it. dryden seems to be making the argument...and
you've implicitly agreed...that structure is largely irrelevant to
function. a large protein has a functionality determined by a VERY
SMALL percentage of amino acids. thus, again, your argument fails.
Some types of functional
> systems have minimum size requirements that are very low - like less
> than 100aa with very low specificity limitations on sequence
> arrangements. These are very low level functions and can and do
> evolve often and quite rapidly. Other types of functional systems are
> much more complex in that they have much greater minimum size and
> specificity requirements - well beyond the 1000 fsaar threshold of
> functional complexity.
the 1000aa is a red herring. there is apparently no relationship
between
1. the size of a protein and its complexity of function
2. the size of a protein and its evolutionary history (all roads lead
to rome)
thus creationism is not only the WRONG explanation, it's an UNNEEDED
explanation since evolution is quite capable of explaining the needed
evoltuionary history..
>
> > when i've asked you about this before, regarding the structure of
> > FUNCTIONAL parts of proteins (the folding areas) which are often
> > <300aa in length, you go off on a tangent about MULTIPLE protein
> > systems. so which is it? is it 1000 fsar or multiple proteins that you
> > say can't evolve?
>
> It is the total number of amino acid residues required, at minimum, in
> all parts of the system. For multi-protein systems, that means adding
> up all the amino acid parts in all of the different proteins in the
> system - all of which must work together in a specific arrangement at
> the same time (as in a flagellar motility system).
and, again, if the FUNCTIONAL complexity is determined by a very SMALL
group of amino acids...several hundred...then your argument fails. and
this seems to be the case. so, again, your argument is wrong.
>
> > the reason such systems are not 'observed to evolve' is because
> > evolution doesn't work the way you think it does. that appears to be
> > what dry denis saying when he points out how functionally flexible
> > large protein systems are regarding the associated structure.
>
> Dryden was talking about large single-proteins - not systems of
> proteins where there is much greater specificity for the system as a
> whole with regard to the arrangement of its basic building block
> residues. Large proteins that have very low specificity requirements
> are not more complex than much smaller proteins with higher
> specificity requirements. In order to increase the level of
> functional complexity, you have to compare apples with apples with
> regard to the same degree of sequence specificity at various minimum
> size requirements.
and, as dryden pointed out, the FUNCTIONALITY of a protein is largely
independent of its size. some VERY SMALL proteins are VERY
functionally complex. thus the same is true of a multi protein
system.
you just dont understand your argument.
>
> And no, Dryden does not understand the concept of levels of functional
> complexity.
he certainly does because he demonstrates such a concept is unneeded
in evaluating evoltuion. since complexity, functionality and structure
are not related your argument is useless. the entire basis of your
argument is not needed.
He doesn't seem to grasp that concept at all. His entire
> paper deals only with very low level examples of functional complexity
> that don't remotely approach the 1000 fsaar level.
he grasps that you've constructed a strawman...a non existent
relationship between SIZE and functionality. as freud pointed out,
size is not all that important.
That is why he
> thinks he has been so successful. What he has actually done is to
> show that it is easy to completely search out sequence space for all
> sequences of less than a few dozen characters. That's obvious true,
> but it doesn't remotely address the question as to how the mechanism
> of RM/NS can produce higher and higher levels of functional complexity
> without the exponential stalling out effect? He doesn't answer that
> question at all. He doesn't even address it.
he certainly does address it by showing it's a useless and baseless
argument. and he addresses it by showing that your argument is simply
wrong. creationism can't explain ANY features of proteins from 1 amino
acid up. it's useless.
>
> > > > and, again, one needs to ask how his creationist views solve this
> > > > problem. absent the presence of any method to EXCLUDE natural
> > > > processes, we'r'e left with the unknown...rather than ID.
>
> > > While this is completely irrelevant to the question at hand, at least
> > > human-level ID is a natural process.
>
> > not if it doesnt exist in nature it's not.
>
> We've already been over this Bob. Human-level intelligence does exist
> in nature. You exist in nature - right?
and you seem to ignore EVERY intelligence is related to brains. IF
'intelligence' can cause what is not seen in the literature, then it's
ALSO true that the ONLY Intelligence seen 'in the literature' is due
to material brains
are you saying that? it's a FACT that, just as no '1000 aas' proteins
evolve, NO intelligences exist apart from material brains built from
lipoproteins.
are you willing to say that? because it's a fact.
> > your argument hinges on how poorly scientists understand science and
> > how well creationists DO understand nature. if that were the case, we
> > would have had antibiotics 2000 years ago. the very non-existence of
> > virtually ANY understanding of nature, based on the creationist model,
> > means that model is fatally flawed.
>
> The fathers of the various scientific disciplines, to include most of
> the various branches of modern science, were pioneered by
> creationists.
uh...sean...here's a fact for you:
NONE of them used creationism. not a single one. not newton. not
pasteur. if their work was based on creationism you'd never know it
because it does not appear in their work. again you're fairly
uneducated in science, so think that something like F=MA is a
'statistical observation' which is meanignless.
there is no 'mind' in newton's laws. and the ONLY time he DID try to
use ID he was proven wrong. so go ahead, sean. tell us how useful ID
is when it's ALWAYS been wrong and it has NEVER been used
successfully. go ahead. prove your case
where in the entire HISTORY of science can we see SUCCESSFUL
intelligent design? it's your whole argument. in 2000 years there
must be at least ONE case, right?
where is it??
Science, good science, is not limited to those who
> attribute everything to mindless forces of nature.
fine. you go find me a mindful process in nature. go ahead sean. find
one. from any science.
go find me a mind that is NOT composed of matter.
proteins...fats...neurotransmitters. find me such a mind, sean. you
say it exists.
tell me where, sean. even ONE example would destroy evolution. a
SINGLE case would do so....in 2000 years where is there a SINGLE
instance??
Sorry. Even those
> who believe in God can do very good science without always having to
> impose their religion onto their science.
IOW ID is science except when it's not. it's science becauase it's
NEVER used. it's ALWAYS wrong and that proves it's science?? is that
your argument?
Seanpit
> On May 4, 7:45 pm, Seanpit <sean...@gmail.com> wrote:
>
> > It is the total number of amino acid residues required, at minimum, in
> > all parts of the system. For multi-protein systems, that means adding
> > up all the amino acid parts in all of the different proteins in the
> > system - all of which must work together in a specific arrangement at
> > the same time (as in a flagellar motility system).
>
> So we're back once more to the old creationist "747 forming in a
> junkyard during a tornado" bullshit . . .
>
> (sigh)
>
> Sean, Sean, Sean . . . you know just as well as we do that this
> bullshit is not how evolution works. Evolution does not POOF big
> complex things into existence all at once intact in one fell swoop
> from a collection of random parts. Evolution works by cobbling
> together things using bits and pieces of whatever other unrelated
> things happen to already be available.
Of course evolution doesn't "poof" big complex things into existence
all at once intact in one fell swoop from a collection of random
parts. Who is suggesting such a thing? Certainly not I. Evolution,
when it does work, does indeed work by cobbling together things using
bits and pieces of whatever other unrelated things happen to already
be available. That's exactly right. You hit it on the head. This is
exactly how the mechanism of RM/NS works when it works. You're right
on base here.
It is just that this method is only able to produce novel systems of
function which themselves require no more than a few hundred fairly
specified residues at minimum to work. The cobbling process takes
what exists and stick them together in various ways and what turns out
is almost always detrimental. It is like randomly putting pieces and
parts of phrases together and seeing if something meaningful results.
Occasionally it does turn out something beneficial. But, when this
happens the beneficial product is always at a low level of functional
complexity itself - always far less than 1000 fsaars for its minimum
structural threshold requirement. There isn't a single example of
evolution in action producing a higher level system by your above
listed method - not one example.
Now, there's a reason for that. It is the linearly expanding non-
beneficial gap problem. That's the reason why your evolutionary
mechanism stalls out at such low levels of functional complexity. It
isn't a 747-in-a-junkyard problem. However, it is an expanding non-
beneficial gap problem.
> 747's didn't appear all at once from random parts in a junkyard
> assembled by a tornado. 747's came from earlier airplanes. And those
> airplanes came from even earlier airplanes. And airplanes came from
> bicycle parts.
>
> Which means all of your 747-tornado mathy stuff, is bullshit. Pure
> unadulterated unvarnished bullshit.
>
> But of course you already knew that, since everybody that you have
> sprung your 1000-fs-whatever bullshit upon -- absolutely everybody
> without exception -- has pointed out that it's bullshit.
Not with anything other than the old tired lame arguments you've just
used - along with plenty of just-so stories without any statistical
analysis or predictive value whatsoever.
>
> ================================================
> Lenny Flank
> "There are no loose threads in the web of life"
>
> Editor, Red and Black Publishershttp://www.RedandBlackPublishers.com
Sean Pitman
www.DetectingDesign.com
Seanpit
>
> >> It is clear from your responses to this newsgroup that *you* do not
> >> understand your own claims about "functional complexity" and "structural
> >> complexity." You can't define functional informational complexity in any
> >> meaningful way. You can't measure it. You equate it with the length of
> >> polypeptide chains, but you lack any clue as to how this metric links
> >> with any real biological functions. David Dryden has completely
> >> demolished your pretence that any such relationship exists.
>
> >Not remotely. He himself recognizes that different types of systems
> >are not all created equal. Different types of functional systems do
> >in fact have different minimum structural threshold requirements.
> >This is a fact. There really is no argument here. Levels of
> >functional complexity can clearly defined with regard to the minimum
> >structural threshold requirements needed to achieve them to their most
> >basic useful level of functionality. To suggest otherwise is to
> >remove any semblance of a scientific basis from your "theory". You
> >remove the ability to make useful predictions about the progress of
> >your mechanism of RM/NS into the future - predictions which are
> >actually testable in a falsifiable manner. You also remove any basis
> >for statistical analysis of your mechanism and how likely it is to be
> >able to succeed at various levels of functional complexity. How is
> >that? Well, because neither you norDrydenhas defined this concept.
> >certain doesn't address this concept in his paper nor does he seem
> >able to grasp this idea so far in this forum.
>
> Natural selection can be observed and tested.
Absolutely! NS is a real force of nature. It works very very well.
However, it is primarily a force of preservation, not a creative
force. It doesn't solve the problem of producing functional
complexity beyond very very low levels of functional complexity.
> Predictions can be made
> about how populations will acquire immunity to antibiotics or acquire an
> ability to metabolize nutrients.
Of course. That's because most forms of antibiotic resistance are
based on a loss of a pre-established system or interaction - not a
gain of a novel structural system with an independent action which is
not dependent upon the loss or disruption of a pre-established system
or interaction. Remember, like the children's story of Humpty Dumpty,
it is very easy to break something that's already there. It is another
matter entirely to produce something structurally and functionally
new.
> You, on the other hand, can't even
> define "functional information complexity" in any meaningful way.
Sure I can. It is the minimum structural threshold requirement needed
to achieve a particular type of functional system. In other words,
there are different minimum size and specificity requirements for
different types of systems. Those with greater minimum size and
specificity requirements are on higher levels of functional
complexity.
This concept isn't really that hard to define or to understand - - or
apply.
> You
> equate it with polypeptide length and claim, without any evidence, that
> this is a useful measure of biological function.
It isn't a measure of length alone. It is based on the minimum size
AND specificity requirements of the system in question.
> You can't tell us what
> this functionality is.
You start with the functionality and then determine the minimum
structural threshold requirements. So, yes, I can tell you want the
functionality is.
> And in this very paragraph you have the gall to
> pretend that no one can define what a mutation is, or how it relates to
> natural selection.
Where do you get that from anything I've said? Mutations are very
easy to define as is their relation to the force of NS. Mutations
happen all the time. They are very common. The definition for a
mutation is very simple. Mutations are simply random character
changes to a pre-existing sequence. It just so happens that the odds
that such random character changes will end up producing something
beneficial drop exponentially when it comes to producing higher and
higher levels of functional complexity.
> And to top it off, you boast that no one can define a
> level of "functional complexity."
What? Of course the concept of functional complexity can be defined.
I've just defined it for you. You, on the other hand, don't seem to
be able to define it yourself in any other rational or useful way than
how I've already defined it.
> I don't suppose it ever occurred to
> you that's because, as you use it, it's a completely indefinable and
> useless concept. If you can't meaningfully define it, no one else is
> going to do it for you.
My definition is easy, straightforward, and useful. What other
definition did you have in mind? If you have no other definition, how
then can you be so sure that your method of RM/NS can produce it so
easily regardless of the level of functional complexity under
consideration? If you don't have your own definition of this concept
that is significantly different from the one I've given you, how on
Earth can you say that you're concept of the mechanism of RM/NS is
remotely scientific? Where is your statistical analysis and
predictive value?
That's not my argument. The components are not random. The mutations
are random. That's a big difference. Bringing together non-random
components via a random process of mutations into a meaningful product
is a huge problem when it comes to producing higher level products -
i.e., beyond the 1000 fsaar threshold of functional complexity.
> You *claim*
> there exist thresholds of functional complexity that can't be crossed by
> random mutation and natural selection, but the claim is based on nothing
> more than your own refusal to acknowledge that organisms descend, with
> slight modifications, from similar ancestors.
Ok, have any examples of this? - beyond your just-so stories that such
a thing actually happens via the specific mechanism of RM/NS? Produce
a single example of your mechanism producing a novel functional system
that requires at least 1000 fsaars to work. For example, the rotary
flagellar motility system requires several thousand fairly specified
coded residue positions, at minimum, to work as a motility system.
Care to provide any statistical basis for how long it should take your
mechanism to produce such a system starting with any historically non-
flagellate gene pool? Good luck.
If you are successful in this, you will be the first. Certainly there
are no such observations of evolution in action and there are no
relevant statistical predictions either - regarding the creative power
of the mechanism of RM/NS. There are assumptions along these lines
and many just-so stories, but none are based on real statistical
analysis or predictive value. They are just fairytales, not
science.
> >This is in fact why we often see evolution "in action" producing
> >systems that require no more than a few hundred fairly specified
> >residues working together at the same time, but we never ever see any
> >novel system of function evolving which requires at least 1000 fsaars
> >at minimum (even for multiprotein systems).
>
> You'll never see these huge jumps because they don't happen and
> evolution doesn't need them. You imagine they must happen because you
> simply can't accept that the entire process involves slight progressive
> modifications of pre-existing structures and processes.
I'm not asking for huge jumps. Show me any system that is close
enough to any other novel system beyond the 1000 fsaar threshold. In
other words, show me two novel systems of function that are
qualitatively unique in function, both require at least 1000 fsaar to
work, and yet are within only a handful of mutational differences from
each other. Do you know of any such examples? Or, show me any other
system that is within dozens of mutational differences from a
flagellar system. Or, show me any subsystem or proposed steppingstone
system within the proposed evolutionary pathway of the flagellar
system where any two steppingstones are within striking distance of
your evolutionary mechanism - i.e., this side of trillions of years of
time on average.
If you can show me any such examples, you will effectively falsify my
position. Good luck!
> >I ask you, what is it that limits the evolutionary progress of the
> >mechanism of RM/NS so that there are no examples evolution in action
> >beyond such very low levels of functional complexity? - not a single
> >example in all of literature?
>
> It's because these huge jumps don't occur and are not needed.
Again, I'm not proposing huge steps. The 1000 fsaar threshold isn't a
mutational step. It is a description of the final product. If your
staring point happens to be within one point mutation of such a
system, then evolution across this threshold would be very easy. All
you have to do now is to find that such a small gap between what
exists in any genome and what might exist to some beneficial level is
actually a very small gap size. That's your goal here.
> Complex
> biological systems develop from slightly modified precursors.
That's a lovely story. Prove it. Or, at least produce some
statistical basis for this bald assertion beyond very very low levels
of functional complexity.
> There's
> not a lick of evidence, so far as I can tell, that your molecular
> saltations have ever occurred. So you don't really need an intelligent
> designer to account for them.
Large molecular mutations do occur - quite often. It is just that
they don't ever end up producing higher level systems of function.
> NAS
Sean Pitman
www.DetectingDesign.com
'Rev Dr' Lenny Flank
Says you. (shrug)
> The cobbling process takes
> what exists and stick them together in various ways and what turns out
> is almost always detrimental. It is like randomly putting pieces and
> parts of phrases together and seeing if something meaningful results.
So we're now back, yet again, to the "747 in a tornado" bullshit.
(yawn)
You need to learn some new chords, Sean. Your song and dance is
boring.
> Occasionally it does turn out something beneficial. But, when this
> happens the beneficial product is always at a low level of functional
> complexity itself - always far less than 1000 fsaars for its minimum
> structural threshold requirement. There isn't a single example of
> evolution in action producing a higher level system by your above
> listed method - not one example.
Tell me again how, as you stupidly believe, the bacterial flagellum
got pulled out of some bacterium's ass and managed to get utilized in
the totally unrelated and functionally-not-even-remotely-close
secretaory system, Sean.
>
> Now, there's a reason for that. It is the linearly expanding non-
> beneficial gap problem. That's the reason why your evolutionary
> mechanism stalls out at such low levels of functional complexity. It
> isn't a 747-in-a-junkyard problem. However, it is an expanding non-
> beneficial gap problem.
Sorry, Sean, your bullshit doesn't impress me.
>
> > 747's didn't appear all at once from random parts in a junkyard
> > assembled by a tornado. 747's came from earlier airplanes. And those
> > airplanes came from even earlier airplanes. And airplanes came from
> > bicycle parts.
>
> > Which means all of your 747-tornado mathy stuff, is bullshit. Pure
> > unadulterated unvarnished bullshit.
>
> > But of course you already knew that, since everybody that you have
> > sprung your 1000-fs-whatever bullshit upon -- absolutely everybody
> > without exception -- has pointed out that it's bullshit.
>
> Not with anything other than the old tired lame arguments you've just
> used - along with plenty of just-so stories without any statistical
> analysis or predictive value whatsoever.
>
Speaking of whcih, Sean:
What mechanism for ID are you proposing, Sean? You've said it
involves a
"human-level intelligence". That rules out any supernatural or
divine
influence, right? No God required, right? No need for anything that
plain old ordinary humans can't do, right? "Design theory" is just
as athiestic and godless as Darwinism is, right, Sean?
So what WAS involved, Sean, if it wasn't god. Space aliens? Time-
travelling human biologists from the future? Where did THEY come
from,
Sean? Did they evolve natgurally? Or were THEY designed by some
OTHER human-level intelligence, and where did THAT come from?
And what did this human-level designer DO, Sean? How did it make new
genetic sequencies? What mechanisms did it use? Where can we see it
using similar mechanisms today to do . . . well . . . anything?
You declared that the IDer manipulates natural forces and materials to
accomplish its design. Show us. WHat natural forces and materials
has the ID manipulated? What mechanisms did it use to manipulate
them? Where can we se it using any mechanisms to manipulate anything
today?
Oh, and hey-- you said that your "ID theory" is testable. Show me.
How can I go about testing the, uh, hypothesis that "an unknown thing
did an unknown thing at an unknown time using unknown methods" . . ?
How could anyone falsify your, uh, hypothesis, Sean -- how could
anyone show that an unknown thing did NOT do an unknown thing at an
unknown time using unknown methods? Do you think there are things
that God -- uh, I mean "the unknown intelligent designer" -- could not
have done, Sean?
And if you don't have one single scientific reason -- none at all
whatsoever -- that humans didn't evolve from apes, why do you conclude
anyway that hominids required a designer (a really really smart one)?
Just your religious opinion, Sean? Telling stories again, Sean?
And, since every time someone mentions "designer", you burp up your
SETI bullshit -- SETI doesn't say "We think a designer did this. But,
ya know, we're really not interested, at all, in finding out what that
designer is, what it did, how it did it, or what it's doing today."
Why does ID "science" say that, Sean?
Can you think of any OTHER area of science which concludes "We think
something happened here, but we're not remotely interested in finding
out what it was or what did it."
Why does ID "science" say that, Sean? Is there some non-science
reason for that? A legal strategy, perhaps . . . ?
Oh, and would you mind pointing to an example of any scientific
discovery, of any note, in any area of science, that has resulted
from
the hypothesis "Godiddit!!!!" . . .?
Your bullshit is boring, Sean.
Kent Paul Dolan
Not a single claim in that paragraph is true, well
defined, or meaningful. All of it is made up
handwaving by you to pretend you are doing science
when all you are doing is making meaningless
assertions with no facts to back them up.
Your arguments have been obliterated by someone who
unlike you has the training and the talent to do the
math. You aren't going to restore your arguments by
just repeating more loudly and unchanged.
xanthian.
'Rev Dr' Lenny Flank
> NS is a real force of nature. It works very very well.
> However, it is primarily a force of preservation, not a creative
> force.
Oh, Jesus H Christ, Sean -- ICR was passing this bullshit around **40
years ago**.
What will you be telling us next, Sean -- evolution violates the
second law of thermodynamics? Short-period comets prove the earth is
young? Bomby the bombardier beetle?
(sigh)
No WONDER nobody takes anything you say seriously.
But instead of boring us with half-century-old creationist crapola,
why don't you tell us all what year the Seventh-Day Adventists are
predicting the world will end THIS time? That at least could be
mildly entertaining . . . . and heck, if we're lucky, some of us might
not even need to pay off our mortgages.
(snicker) (giggle) <---- yes, Sean, I am laughing at you. Again.
R. Baldwin
news:47c29c43-bfe4-4c16...@f41g2000pra.googlegroups.com:
> Regarding the following paper by David Dryden:
>
> http://rsif.royalsocietypublishing.org/content/5/25/953.long
>
[snip]
>>
>> I am probably going to write far too much but if you want the
>> conclusion, it is that Sean Pitman is completely and utterly wrong in
>> everything he says in his comments and displays a great ignorance of
>> proteins and their structure and function. However, I do hope he will
>> read on.
>
> I think you simply don't understand my argument, or the nature of the
> concept of increasing levels of functional complexity. It seems like
> your understanding of functional complexity is based on how
> interesting you think the function in question is. My definition of
> functional complexity, in comparison, is not based on how interesting
> various systems may or may not be, but in the minimum structural
> threshold requirements needed to build a system so that it will work
> to at a selectable level of usefulness.
It seemed clear that Dryden understood and dismissed your argument as
vacuous. ORFs reach a "selectable level of usefulness" at far shorter
lengths than 1000 aa. Since there is no goal, there is no minimum
structural threshold to worry about. A flagellar motility system isn't a
goal. It just happens to be where things ended up for a particular
genome. A sequence either does something biologically interesting, or it
doesn't. Your functional complexity concept is meaningless.
>
>> He has failed to recognise that we wished to establish limits on the
>> amount of sequence space explored.
>
> But I do recognize and even agree with your estimates on the limits of
> the amount of sequence space that can be explored over a given time
> limit. But that isn't the main problem here. The main problem is how
> much time it takes to actually find novel beneficial sequences that go
> beyond the very very low levels of minimum structural threshold
> requirements noted in your paper. You only deal with systems that
> have, at minimum, very very low level structural thershold
> requirements - less than 100aa or "characters" at minimum.
If you paid attention to his explanation, you would understand why
systems having short sequences sufficient.You should have focused on
"Nature takes the domain modules and puts them together to make novel
structures and functions," and contemplated what that means with respect
to your model. Evolution is not exploring a space the size of 20^N when
combining domain modules. You should consider the subspace defined by
the combinations of domain modules.
[snip]
How many non-stable sequences do you really need to worry about if you
are combining stable domain modules to form a larger stable sequence?
Who cares about the "function in question"? There IS no function in
question. An ensemble of proteins either has a combined function, or
not. This teleological goal of finding a particular function exists only
in your mind.
You seem to have made an assumption that most of the characters in the
sequence are contributing to what the function of the protein actually
is. Otherwise, you could easily accept Dryden's explanation which is
based on what the molecles are actually doing. What is the basis for
your assumption? WHY do you believe that all those characters are vital?
>
> It is like the difference between the English language system of 28-
> characters (letters, spaces and periods) and a computer language that
> is based on just two characters. Given these two systems, consider a
> problem of transmitting the information on a blueprint to build a
> particular kind of house. Do you really think it would take the same
> number of characters in both language systems to code for the same
> particular structure? I don't think so. A few more characters would
> be needed, at minimum, for the two-character system vs. the 28-
> character system.
Such a comparison is not warranted. It makes an unjustified assumption
about the structure of an ORF - to wit, that the coding has anything to
do with efficient representation of information, as written English
roughly does.
>
>> Sequence space when proposed was quickly recognised as a silly
>> �paradox� by protein scientists (though not unfortunately by some
>> other scientists) rather like the silly Levinthal �paradox� of protei
> n
>> folding. Sequence space may be large but that does not mean it is
>> complex. I hope the above short essay on protein structure and
>> function is useful even to Sean Pitman who needs to stop being
>> obsessed with computer-based numerology and do some reading and talk
>> to some practical protein scientists. I also hope that he will
>> realise that proteins are not relevant to religion and that they as
>> well as other macromolecules provide absolutely no foundation for ID.
>
> This has nothing to do with any particular "religion" - unless you
> want to call science a form of religion.
ID clearly has to do with religion. The Wedge Document made that plain
years ago.
[snip]
>
>> We are not saying only a few specified amino acids are
>> available but a few types of amino acids- polar, non-polar,
>> negative, positive and so on. For example, any one of the polar ones
>> might do at a particular site. All you need to specify is polarity.
>
> That's correct. That's what makes protein-based systems fairly
> flexible with regard to tolerance of mutations - especially those that
> occur one at a time.
>
> It is much like the English language system where pretty much any
> letter in this paragraph could be mutated, one at a time, without a
> significant loss of meaning of the paragraph as a whole. The very
> same thing is true of protein-based systems. There is a degree of
> mutational tolerance. However, reducing the number of characters
> doesn't help solve the problem of searching sequence space for higher
> and higher level systems. This is because a reduction in the number
> of characters would only increase the overall specificity requirements
> of the system in question in line the the reduction of the number of
> character options in the alphabet. In short, the larger sequence
> space only means that the functional islands within that space are
> larger. Reducing the overall size of sequence space doesn't change
> the ratio of potentially beneficial vs. non-beneficial since the size
> of the beneficial islands is also reduced to the same degree as the
> reduction of sequence space.
With an alphabet of folds to play with, who cares about the overall size
of sequence space?
>
>> Since this is
>> the entire basis of using sequence comparisons to group proteins into
>> functional families and these computer methods are used by supporters
>> of ID, they should know this. Small proteins are not necessarily
>> functionally simple nor are big proteins necessarily complex in
>> function (in fact some a remarkably boring).
>
> This is also correct. I think you are not understanding my argument
> here. I'm not talking about just any large protein-based system. Not
> all large proteins are created equal either. Some require more
> specificity than do other proteins. My argument is that given a
> specific degree of required sequence specificity, increasing the
> minimum size requirement ends up producing a exponential decrease in
> the ratio of sequences in sequence space able to produce a beneficial
> function at that level of minimum structural threshold requirements.
>
> So, you see, I'm not just talking about any large protein here. Many
> large proteins have very little specificity requirements and therefore
> their attached functionality can be achieved by a great many more
> proteins in sequence space. In other words, the ratio of these types
> of functions is relatively high in sequence space.
Your argument is not based on what the molecules actually do.
How do you know what that minimum is, Sean? By assertion?
>
>> "The evidence shows that the distances [in sequence space] between
>> higher and higher level beneficial sequences with novel functions
>> increases in a linear manner."
>>
>> Reply: What evidence? And if importance of function scales with
>> sequence length and the scaling is linear then I am afraid that
>> 20^100 is essentially identical to 2 x 20^100. Also a novel function
>> is not a new function but just one we stumble upon in doing the hard
>> work in the lab. It�s been there a long time�
>
> The functional island has been there all along in sequence space. It
> is just as matter of discovering it - as you note. The very same
> thing is true of the evolutionary mechanism of RM/NS for a living
> organism or population of organisms. The average time needed for the
> mechanism of evolution to find a novel functional system in sequence
> space depends on the average distance between potentially beneficial
> islands of sequences in overall sequence space. It is this ratio that
> determines the likely minimum distance between anything in the
> existing gene pool of options and the closet potential target (i.e.,
> beneficial sequence with a novel beneficial function) in sequence
> space.
No, because your "model" is not based on what actually happens.
>
> As it turns out, as the minimum size and/or specificity requirements
> of systems under consideration increase in a linear manner, the ratio
> of potentially beneficial vs. non-beneficial systems decrease in an
> exponential manner. This is true regardless of the size of your
> alphabet. As the ratio decreases exponentially, the average distance
> between potentially beneficial islands in sequence space increases in
> a linear manner. And, with each linear increase in the distance to
> the closest potentially beneficial island the average number of
> mutations needed to reach that island (or any other beneficial island)
> increases exponentially as well.
The number of long nonsense sequences that could be reached through
successive point mutation is not relevant when the process is
combination of domain modules.
[snip]
NA Sides
wrote:
>On May 4, 5:51 pm, NA Sides <nongo1...@sonic.net> wrote:
You're merely asserting that NS is primarily a force of preservation.
Evidence, including the evolution of new capabilities, such as the
ability to digest nylon, says something different. Or do you think an
intelligent designer bestowed such capabilities?
>> Predictions can be made
>> about how populations will acquire immunity to antibiotics or acquire an
>> ability to metabolize nutrients.
>
>Of course. That's because most forms of antibiotic resistance are
>based on a loss of a pre-established system or interaction - not a
>gain of a novel structural system with an independent action which is
>not dependent upon the loss or disruption of a pre-established system
>or interaction. Remember, like the children's story of Humpty Dumpty,
>it is very easy to break something that's already there. It is another
>matter entirely to produce something structurally and functionally
>new.
So you think that the ability to digest nylon is a loss of the ability
to *not* digest nylon?
>> You, on the other hand, can't even
>> define "functional information complexity" in any meaningful way.
>
>Sure I can. It is the minimum structural threshold requirement needed
>to achieve a particular type of functional system. In other words,
>there are different minimum size and specificity requirements for
>different types of systems. Those with greater minimum size and
>specificity requirements are on higher levels of functional
>complexity.
You're assuming that the bacterial flagellum had to appear fully
developed before motile bacteria could exist. You have no evidence to
support this assertion and there's no reason to suppose you're correct.
>This concept isn't really that hard to define or to understand - - or
>apply.
>
>> You
>> equate it with polypeptide length and claim, without any evidence, that
>> this is a useful measure of biological function.
>
>It isn't a measure of length alone. It is based on the minimum size
>AND specificity requirements of the system in question.
Neither of which you can specify. Small proteins can have complex
functions and specificity requirements, expect at the active site, are
apparently often quite low.
>> You can't tell us what
>> this functionality is.
>
>You start with the functionality and then determine the minimum
>structural threshold requirements. So, yes, I can tell you want the
>functionality is.
Once again you're just making a post-hoc assertion that the smallest
known system that performs some function must, in every case, represent
a "functional threshold" for that function. It's just another of your
unsupported assertions. You can't define any general relationship
between the length of polypeptide chains and functionality. If you
really did know of any such relationship you could define it and show
evidence that it exists.
>> And in this very paragraph you have the gall to
>> pretend that no one can define what a mutation is, or how it relates to
>> natural selection.
>
>Where do you get that from anything I've said? Mutations are very
>easy to define as is their relation to the force of NS. Mutations
>happen all the time. They are very common. The definition for a
>mutation is very simple. Mutations are simply random character
>changes to a pre-existing sequence. It just so happens that the odds
>that such random character changes will end up producing something
>beneficial drop exponentially when it comes to producing higher and
>higher levels of functional complexity.
"Functional complexity" is a term you still haven't defined
*meaningfully.* You claimed it is polypeptide length, then you claimed
it's "the minimum threshold requirement" to perform some function. In
neither case do you have a scientifically useful concept. All you have
is your ridiculous claim that complex structures like the bacterial
flagellum must appear all at once, without functional precursors.
>> And to top it off, you boast that no one can define a
>> level of "functional complexity."
>
>What? Of course the concept of functional complexity can be defined.
>I've just defined it for you. You, on the other hand, don't seem to
>be able to define it yourself in any other rational or useful way than
>how I've already defined it.
You've done nothing but claim that polypeptide length has some general
relationship to biological functionality - a claim that appears from all
evidence to be false. You also claim that the smallest known system to
perform some function is the smallest system that *can* perform that
function, and you say that this unsupported assumption is your
definition of functional complexity. You apparently think that a viable
theory can be based on unsupported assertions in place of meaningful
definitions and physical evidence.
>> I don't suppose it ever occurred to
>> you that's because, as you use it, it's a completely indefinable and
>> useless concept. If you can't meaningfully define it, no one else is
>> going to do it for you.
>
>My definition is easy, straightforward, and useful. What other
>definition did you have in mind? If you have no other definition, how
>then can you be so sure that your method of RM/NS can produce it so
>easily regardless of the level of functional complexity under
>consideration? If you don't have your own definition of this concept
>that is significantly different from the one I've given you, how on
>Earth can you say that you're concept of the mechanism of RM/NS is
>remotely scientific? Where is your statistical analysis and
>predictive value?
Mutation and natural selection are *observed* to occur. On the other
hand, your own assertions about the existence of "informational
complexity" thresholds are not observations. You have no evidence
whatever that simpler systems couldn't have some degree of similar
functionality. You assert your assumptions as facts.
If the precursor components are not random, but instead consist of fully
developed and functional systems similar to the modified systems that
develop from them, then evolution *never* has to make any of your
impossible leaps. Your probability estimates aren't based on
observations of how evolution actually works, but on your refusal to
acknowledge that new functions and structures arise from similar
precursors.
>> You *claim*
>> there exist thresholds of functional complexity that can't be crossed by
>> random mutation and natural selection, but the claim is based on nothing
>> more than your own refusal to acknowledge that organisms descend, with
>> slight modifications, from similar ancestors.
>
>Ok, have any examples of this? - beyond your just-so stories that such
>a thing actually happens via the specific mechanism of RM/NS? Produce
>a single example of your mechanism producing a novel functional system
>that requires at least 1000 fsaars to work. For example, the rotary
>flagellar motility system requires several thousand fairly specified
>coded residue positions, at minimum, to work as a motility system.
>Care to provide any statistical basis for how long it should take your
>mechanism to produce such a system starting with any historically non-
>flagellate gene pool? Good luck.
Do I have any examples of *what*? There are numerous examples of
organisms acquiring new capabilities by means of slight modifications of
existing structures and processes. Are you really demanding that I
produce an example of something that *you* claim must occur, but for
which you can't marshal a single scrap of evidence? I don't think *any*
systems have ever required one of your imaginary great leaps. It's all
just a figment of your own imagination that such leaps are required.
Evolution proceeds by small, adaptively useful modifications of existing
structures and processes. I've told you this before but it just goes in
one of your ears and out the other.
>If you are successful in this, you will be the first. Certainly there
>are no such observations of evolution in action and there are no
>relevant statistical predictions either - regarding the creative power
>of the mechanism of RM/NS. There are assumptions along these lines
>and many just-so stories, but none are based on real statistical
>analysis or predictive value. They are just fairytales, not
>science.
Nobody will ever be *successful* in demonstrating to you the existence
of your molecular saltations. They never happened. The evolutionary
process got along just fine without them. You're like a child demanding
that we demonstrate the existence of the Easter Bunny.
>> >This is in fact why we often see evolution "in action" producing
>> >systems that require no more than a few hundred fairly specified
>> >residues working together at the same time, but we never ever see any
>> >novel system of function evolving which requires at least 1000 fsaars
>> >at minimum (even for multiprotein systems).
>>
>> You'll never see these huge jumps because they don't happen and
>> evolution doesn't need them. You imagine they must happen because you
>> simply can't accept that the entire process involves slight progressive
>> modifications of pre-existing structures and processes.
>
>I'm not asking for huge jumps. Show me any system that is close
>enough to any other novel system beyond the 1000 fsaar threshold. In
>other words, show me two novel systems of function that are
>qualitatively unique in function, both require at least 1000 fsaar to
>work, and yet are within only a handful of mutational differences from
>each other. Do you know of any such examples? Or, show me any other
>system that is within dozens of mutational differences from a
>flagellar system. Or, show me any subsystem or proposed steppingstone
>system within the proposed evolutionary pathway of the flagellar
>system where any two steppingstones are within striking distance of
>your evolutionary mechanism - i.e., this side of trillions of years of
>time on average.
Let me see now. Molecules don't fossilize. Therefore we don't have
fossils of the evolutionary precursors to the bacterial flagellum. We do
have numerous fossils of organisms that *do* fossilize, and they all
pretty much seem to indicate that evolution proceeds by a long series of
small changes to structures and processes. We also know of existing
systems like the type three secretion system that have similar
functionality. But there's no fossilized flagella. You ignore the fact
that molecules don't fossilize and that therefore it's completely
fatuous to conclude from this fact that the flagellum had no similar
precursors. You conclude that there were no precursors. You deduce that,
in the absence of evolutionary precursors, an intelligent designer must
have created the flagellum completely de novo. You regard your procedure
as scientifically valid. Others regard it as God of the gaps.
>If you can show me any such examples, you will effectively falsify my
>position. Good luck!
No thanks. I'm not, like you, assuming that organisms have no closely
similar ancestors. If they have similar ancestors, they don't require
your molecular saltations.
>> >I ask you, what is it that limits the evolutionary progress of the
>> >mechanism of RM/NS so that there are no examples evolution in action
>> >beyond such very low levels of functional complexity? - not a single
>> >example in all of literature?
>>
>> It's because these huge jumps don't occur and are not needed.
>
>Again, I'm not proposing huge steps. The 1000 fsaar threshold isn't a
>mutational step. It is a description of the final product. If your
>staring point happens to be within one point mutation of such a
>system, then evolution across this threshold would be very easy. All
>you have to do now is to find that such a small gap between what
>exists in any genome and what might exist to some beneficial level is
>actually a very small gap size. That's your goal here.
No, it's not my goal, Sean. You see, I don't share your view that
evolution is shooting at specified targets within some vast universe of
potential functions. It's just stepping from one functional system to
another that may be slightly different. Over great spans of time the
little changes sometimes add up to something substantially different,
but there never was any improbable "search."
>> Complex
>> biological systems develop from slightly modified precursors.
>
>That's a lovely story. Prove it. Or, at least produce some
>statistical basis for this bald assertion beyond very very low levels
>of functional complexity.
Go ahead and ignore the entire fossil record. Ignore the nested
hierarchy of species which conforms to the pattern generated by
branching evolutionary processes. Ignore it all and then demand proof
that such evidence exists. Stick with your own claims, although you
can't adduce a scrap of evidence to support their validity or relevance.
Heck, it's your life; you can do with it as you please.
>> There's
>> not a lick of evidence, so far as I can tell, that your molecular
>> saltations have ever occurred. So you don't really need an intelligent
>> designer to account for them.
>
>Large molecular mutations do occur - quite often. It is just that
>they don't ever end up producing higher level systems of function.
Well, genes get duplicated sometimes, producing a redundant gene that
may then undergo slight modifications that eventually alter its
function. As for "higher levels of function," I don't think you have any
more idea what that means than I do.
NAS
>Sean Pitman
>www.DetectingDesign.com
Ernest Major
<83516b7c-f621-4126...@y6g2000prf.googlegroups.com>,
Seanpit <sea...@gmail.com> writes
>
>This is in fact why we often see evolution "in action" producing
>systems that require no more than a few hundred fairly specified
>residues working together at the same time, but we never ever see any
>novel system of function evolving which requires at least 1000 fsaars
>at minimum (even for multiprotein systems).
>
>I ask you, what is it that limits the evolutionary progress of the
>mechanism of RM/NS so that there are no examples evolution in action
>beyond such very low levels of functional complexity? - not a single
>example in all of literature?
>
you don't believe your own argument.
It should be self-evident that there will a level of protein evolution
which will not have been observed in the last 50 years (as an estimate
as to how long we've had the technology that would have allowed us to
notice it happen). You may have set your goalposts safely beyond reach,
but since your goalposts are inadequately defined (how does one
objectively ascertain how many fsaars are present in a protein?) whether
you have done so isn't even of academic interest.
--
alias Ernest Major
Seanpit
First off, why do you highlight every single one of your posts by
changing the topic heading? It is very annoying . . .
Beyond this, where is your own definition of levels of functional
complexity? Or, better yet, where has Dryden produced his own
definition? He and you seem to talk as if all functional systems are
created equal - that everything is on the same level of functional
complexity. Well, Mr. Dolan, that simply isn't true. Your position
simply isn't scientific because of it. You have no statistical basis
for your just-so stories. They are just made up fairytales about what
is possible without any idea about what is remotely likely. That, I'm
afraid, is the extent of the "science" of the mechanism of RM/NS
coming from Dryden - nothing more.
> xanthian.
Sean Pitman
www.DetectingDesign.com
Seanpit
wrote:
> Seanpit <sean...@gmail.com> wrote innews:47c29c43-bfe4-4c16...@f41g2000pra.googlegroups.com:
>
>
>
>
>
> > Regarding the following paper by David Dryden:
>
> >http://rsif.royalsocietypublishing.org/content/5/25/953.long
>
> [snip]
>
> >> I am probably going to write far too much but if you want the
> >> conclusion, it is that Sean Pitman is completely and utterly wrong in
> >> everything he says in his comments and displays a great ignorance of
> >> proteins and their structure and function. However, I do hope he will
> >> read on.
>
> > I think you simply don't understand my argument, or the nature of the
> > concept of increasing levels of functional complexity. It seems like
> > your understanding of functional complexity is based on how
> > interesting you think the function in question is. My definition of
> > functional complexity, in comparison, is not based on how interesting
> > various systems may or may not be, but in the minimum structural
> > threshold requirements needed to build a system so that it will work
> > to at a selectable level of usefulness.
>
> It seemed clear that Dryden understood and dismissed your argument as
> vacuous. ORFs reach a "selectable level of usefulness" at far shorter
> lengths than 1000 aa.
Of course, that is because they don't have a minimum structural
threshold requirement that is greater than 1000 fsaars. That is why
they are in fact on a lower level of functional complexity.
How do you not understand this concept? The definition of a level of
functional complexity is defined as the *minimum* structural threshold
requirement for a system to work. If you find that the minimum
requirement for a particular system is far less than 1000 fsaars, then
that system is on a far low level of functional complexity.
Your argument here makes it very clear that both you and Dryden
misunderstand the very concept of levels of functional complexity.
You just don't get it - even after all of this time. Yet, it is such
a simple concept. How is it that you cannot seem to grasp it?
> Since there is no goal, there is no minimum
> structural threshold to worry about. A flagellar motility system isn't a
> goal. It just happens to be where things ended up for a particular
> genome. A sequence either does something biologically interesting, or it
> doesn't. Your functional complexity concept is meaningless.
There is a goal for evolutionary progress - and that is to actually
find novel beneficial systems. If the system in question has a very
low minimum structural threshold requirement it is exponentially more
likely to be found vs. a system that has a higher minimum structural
threshold requirement. That is why single protein enzymes which
require no more than a few hundred fairly specified amino acid
residues are found all the time by RM/NS. Yet, no system, to include
multi-protein systems, which have more than a 1000 fsaar minimum
structural threshold requirement are ever found by RM/NS - regardless
of the starting points within any gene pool you wish to consider. It
just doesn't happen, has never happened, and statistically is
extremely unlikely to happen this side of trillions of years of
time.
> >> He has failed to recognise that we wished to establish limits on the
> >> amount of sequence space explored.
>
> > But I do recognize and even agree with your estimates on the limits of
> > the amount of sequence space that can be explored over a given time
> > limit. But that isn't the main problem here. The main problem is how
> > much time it takes to actually find novel beneficial sequences that go
> > beyond the very very low levels of minimum structural threshold
> > requirements noted in your paper. You only deal with systems that
> > have, at minimum, very very low level structural thershold
> > requirements - less than 100aa or "characters" at minimum.
>
> If you paid attention to his explanation, you would understand why
> systems having short sequences sufficient.You should have focused on
> "Nature takes the domain modules and puts them together to make novel
> structures and functions," and contemplated what that means with respect
> to your model. Evolution is not exploring a space the size of 20^N when
> combining domain modules. You should consider the subspace defined by
> the combinations of domain modules.
You're mistaken. A combination of domain modules does in fact explore
a larger sequence space and has the potential to land upon a system
that is on a higher level of functional complexity - i.e., a system
with greater minimum size and specificity requirements. It is just
that the odds of this actually happening are exponentially lower than
the odds of such a combination landing upon a lower level system. The
reason for this is due to the exponentially reduced ratio of higher
level vs. lower level system in sequence space.
I've already explained to you that the vast majority of possible
combinations of stable domains will be unstable. How do you not grasp
this concept? It is like trying to randomly combine meaningful words
and phrases and expecting the majority of combinations to be
meaningfully beneficial as well. That's a ludicrous assumption and is
demonstrably false when it comes to protein combinations.
It is not a teleological goal as far as a specific type of function is
concerned. However, if no novel functionally beneficial sequences are
ever discovered by RM/NS evolution does not occur. While it is true
that evolution doesn't have to occur at any level of functional
complexity, that isn't the issue. The issue is what it takes for
evolution to occur at various levels of functional complexity - what
are the odds? What is the predicted time that it should take to find
any type of functional system at any given *level* of functional
complexity. That's the question here.
Most of the characters in the sequence are contributing to at least
some degree. That's a fact. This is the reason why that each
additional character change that is realized at the same time produces
an exponentially increased risk of a total loss of functionality of
the system in question.
< all I have time for today >
Sean Pitman
www.DetectingDesign.com
wf3h
. .
>
> Beyond this, where is your own definition of levels of functional
> complexity? Or, better yet, where has Dryden produced his own
> definition? He and you seem to talk as if all functional systems are
> created equal - that everything is on the same level of functional
> complexity. Well, Mr. Dolan, that simply isn't true. Your position
> simply isn't scientific because of it. You have no statistical basis
> for your just-so stories. They are just made up fairytales about what
> is possible without any idea about what is remotely likely. That, I'm
> afraid, is the extent of the "science" of the mechanism of RM/NS
> coming from Dryden - nothing more.
>
more of the same....'dryden doesn't understand his own work...blah
blah blah'
'no one agrees with me but i'm right on evolution even though there's
no literature support to show i'm right...blah blah blah'
sean erected a strawman to, sotto voce, justify creationism. his
argument was quickly shown to be a sham, and his motivations regarding
his illiterate church theology were exposed. no wonder he's
frustrated.
wf3h
> On May 5, 12:04 am, "R. Baldwin" <res0k...@nozirevBACKWARDS.net>
> wrote:
> >
> > It seemed clear that Dryden understood and dismissed your argument as
> > vacuous. ORFs reach a "selectable level of usefulness" at far shorter
> > lengths than 1000 aa.
>
> Of course, that is because they don't have a minimum structural
> threshold requirement that is greater than 1000 fsaars. That is why
> they are in fact on a lower level of functional complexity.
does anyone know what 'functional complexity' is? a 300aa protein
enzyme that catalyzes complex reactions is somehow 'less' complex than
a flagellum that rotates?
looks like a meaningless distinction.
>
> How do you not understand this concept?
wrong question. how do YOU understand a concept that NO ONE thinks is
valid?
The definition of a level of
> functional complexity is defined as the *minimum* structural threshold
> requirement for a system to work. If you find that the minimum
> requirement for a particular system is far less than 1000 fsaars, then
> that system is on a far low level of functional complexity.
uh...why? if the system WORKS then the LENGTH of the protein is
irrelevant BY YOUR OWN DEFINITION.
sean's argument is a hodgepodge of mis-applied ideas, 7th day
adventist nonsense, distortions of real work and complete disregard
for the methods of science
other than that it's great stuff.
Seanpit
>
> >> Natural selection can be observed and tested.
>
> >Absolutely! NS is a real force of nature. It works very very well.
> >However, it is primarily a force of preservation, not a creative
> >force. It doesn't solve the problem of producing functional
> >complexity beyond very very low levels of functional complexity.
>
> You're merely asserting that NS is primarily a force of preservation.
> Evidence, including the evolution of new capabilities, such as the
> ability to digest nylon, says something different. Or do you think an
> intelligent designer bestowed such capabilities?
How many times do I have to explain to you that RM/NS works very well
at very low levels of functional complexity? - i.e., well below the
level of 1000 fsaars? I ask you, what level do you think single
protein enzymes, like nylonase, are found? Don't you know that
nylonase requires no more than a couple hundred fairly specified
residues working together at the same time? That's a very low level
function - well within the real of the mechanism of RM/NS.
So yes, the mechanism of RM/NS does have a limited creative
potential. However, this potential shows an exponential decline with
each step up the ladder of functional complexity until it is non-
existent well before the level of 1000 fsaars is reached.
> >> Predictions can be made
> >> about how populations will acquire immunity to antibiotics or acquire an
> >> ability to metabolize nutrients.
>
> >Of course. That's because most forms of antibiotic resistance are
> >based on a loss of a pre-established system or interaction - not a
> >gain of a novel structural system with an independent action which is
> >not dependent upon the loss or disruption of a pre-established system
> >or interaction. Remember, like the children's story of Humpty Dumpty,
> >it is very easy to break something that's already there. It is another
> >matter entirely to produce something structurally and functionally
> >new.
>
> So you think that the ability to digest nylon is a loss of the ability
> to *not* digest nylon?
That's different. Nylonase evolution is real evolution in action. It
is based on the discovery of a truly novel structural sequence in
sequence space by random mutations. The only problem with this
example is that the nylonase enzyme is a very low level system of
function - requiring only a couple hundred fsaars.
> >> You, on the other hand, can't even
> >> define "functional information complexity" in any meaningful way.
>
> >Sure I can. It is the minimum structural threshold requirement needed
> >to achieve a particular type of functional system. In other words,
> >there are different minimum size and specificity requirements for
> >different types of systems. Those with greater minimum size and
> >specificity requirements are on higher levels of functional
> >complexity.
>
> You're assuming that the bacterial flagellum had to appear fully
> developed before motile bacteria could exist.
Before rotary flagellar motility could exist, you're exactly right -
there is indeed a minimum structural threshold requirement needed to
produce this type of motility. And, the very same thing is true of
all types of bacterial motility. All of them have minimum structural
threshold requirements - every single one.
> You have no evidence to
> support this assertion and there's no reason to suppose you're correct.
It is a fact. All systems of function, all of them, have minimum
structural threshold requirements below which the function in question
will not work at all - not even a little bit.
> >This concept isn't really that hard to define or to understand - - or
> >apply.
>
> >> You
> >> equate it with polypeptide length and claim, without any evidence, that
> >> this is a useful measure of biological function.
>
> >It isn't a measure of length alone. It is based on the minimum size
> >AND specificity requirements of the system in question.
>
> Neither of which you can specify. Small proteins can have complex
> functions and specificity requirements, expect at the active site, are
> apparently often quite low.
Small proteins do not have "complex" functionality. Small proteins,
like 3-letter words, are structurally simplistic - not complex. It
doesn't matter how many different larger systems they influence. The
complexity of a structure is based on its own minimum size and
specificity requirements. This measurement produces an odds ratio of
how likely such a system is to be found by random searches in sequence
space.
> >> You can't tell us what
> >> this functionality is.
>
> >You start with the functionality and then determine the minimum
> >structural threshold requirements. So, yes, I can tell you want the
> >functionality is.
>
> Once again you're just making a post-hoc assertion that the smallest
> known system that performs some function must, in every case, represent
> a "functional threshold" for that function.
That is the basis of science. Science is only able to deal with what
is currently known - not with what might be known in the future. So,
based on the best currently available data, these measurements can be
performed and they do have a useful degree of predictive value. Could
these hypotheses be falsified with future data? Certainly! That's
what makes them scientific.
> It's just another of your
> unsupported assertions. You can't define any general relationship
> between the length of polypeptide chains and functionality. If you
> really did know of any such relationship you could define it and show
> evidence that it exists.
You're looking at this problem backwards. The relationship is between
the type of function and its minimum structural threshold
requirements. You don't look at a random sequence and determine its
functionality. You look at a system and determine its minimum
structural requirements.
> >> And in this very paragraph you have the gall to
> >> pretend that no one can define what a mutation is, or how it relates to
> >> natural selection.
>
> >Where do you get that from anything I've said? Mutations are very
> >easy to define as is their relation to the force of NS. Mutations
> >happen all the time. They are very common. The definition for a
> >mutation is very simple. Mutations are simply random character
> >changes to a pre-existing sequence. It just so happens that the odds
> >that such random character changes will end up producing something
> >beneficial drop exponentially when it comes to producing higher and
> >higher levels of functional complexity.
>
> "Functional complexity" is a term you still haven't defined
> *meaningfully.* You claimed it is polypeptide length, then you claimed
> it's "the minimum threshold requirement" to perform some function. In
> neither case do you have a scientifically useful concept. All you have
> is your ridiculous claim that complex structures like the bacterial
> flagellum must appear all at once, without functional precursors.
I have never said that the flagellar system must appear all at once
without precursors. That's a strawman misrepresentation of my
position. Obviously there are several potential precursor
steppingstone systems within the potential evolutionary pathway of
flagellar evolution. It is just that none of these steppingstones is
close enough to any of the other steppingstones for RM/NS to cross
from one to the other in a reasonable amount of time - i.e., this side
of trillions of years.
> >> And to top it off, you boast that no one can define a
> >> level of "functional complexity."
>
> >What? Of course the concept of functional complexity can be defined.
> >I've just defined it for you. You, on the other hand, don't seem to
> >be able to define it yourself in any other rational or useful way than
> >how I've already defined it.
>
> You've done nothing but claim that polypeptide length has some general
> relationship to biological functionality - a claim that appears from all
> evidence to be false.
Again, that is not my claim. My actual claim is that different
functional systems have different minimum structural threshold
requirements. That's a fact. Not all systems are created equal.
Those with greater minimum requirements are on higher levels of
functional complexity. It really is a simple concept.
> You also claim that the smallest known system to
> perform some function is the smallest system that *can* perform that
> function,
That is the hypothesis and it is open to potential falsification as is
any valid scientific hypothesis. Good luck falsifying it though.
> and you say that this unsupported assumption is your
> definition of functional complexity.
This assumption or hypothesis is very well supported - by the very
best currently known data.
> You apparently think that a viable
> theory can be based on unsupported assertions in place of meaningful
> definitions and physical evidence.
There is physical evidence. And the very best physical evidence that
is currently known supports my definition of functional complexity.
You, on the other hand, have no definition at all.
> >> I don't suppose it ever occurred to
> >> you that's because, as you use it, it's a completely indefinable and
> >> useless concept. If you can't meaningfully define it, no one else is
> >> going to do it for you.
>
> >My definition is easy, straightforward, and useful. What other
> >definition did you have in mind? If you have no other definition, how
> >then can you be so sure that your method of RM/NS can produce it so
> >easily regardless of the level of functional complexity under
> >consideration? If you don't have your own definition of this concept
> >that is significantly different from the one I've given you, how on
> >Earth can you say that you're concept of the mechanism of RM/NS is
> >remotely scientific? Where is your statistical analysis and
> >predictive value?
>
> Mutation and natural selection are *observed* to occur.
Indeed they are - but they don't come up with anything beyond very low
levels of functional complexity and they show an exponential stalling
out effect with each step up the ladder of functional complexity.
> On the other
> hand, your own assertions about the existence of "informational
> complexity" thresholds are not observations. You have no evidence
> whatever that simpler systems couldn't have some degree of similar
> functionality. You assert your assumptions as facts.
Science cannot prove a negative with absolute certainty. If you could
ever be absolutely certain, you wouldn't need science. It amazes me
how many people in this forum do not grasp this concept. Science is
never about perfection. It is about producing predictive value based
on limited information - the best available limited information.
That's science. Try it sometime. Produce your own testable
potentially falsifiable definition of functional complexity. I'd be
most interested.
> >> You've presented no evidence that evolution *ever* requires complex
> >> systems to fall together from random molecular components.
>
> >That's not my argument. The components are not random. The mutations
> >are random. That's a big difference. Bringing together non-random
> >components via a random process of mutations into a meaningful product
> >is a huge problem when it comes to producing higher level products -
> >i.e., beyond the 1000 fsaar threshold of functional complexity.
>
> If the precursor components are not random, but instead consist of fully
> developed and functional systems similar to the modified systems that
> develop from them, then evolution *never* has to make any of your
> impossible leaps.
The mechanism of RM/NS always makes leaps across gaps of some sort.
The only question is how big of a gap can it cross in a reasonable
amount of time? It is your assumption that if you start with fully
developed systems that it is an easy matter to move up the ladder of
functional complexity indefinitely. You assume this based on your
notion that the starting point(s) will always be close enough to
potential targets regardless of their functional complexity. That's a
mistaken assumption. The minimum likely gap distances do not stay
the same as the levels of functional complexity increase. The gap
distances also increase as the levels of complexity increase. In
other words the odds that your starting systems will in fact be
similar enough to the next closest potentially beneficial systems in
sequence space decline exponentially with increasing levels of
functional complexity.
> Your probability estimates aren't based on
> observations of how evolution actually works, but on your refusal to
> acknowledge that new functions and structures arise from similar
> precursors.
The question concerns the odds that something similar enough to a
higher level system will actually exist, preformed, anywhere within
any gene pool. That's the question. You have no idea about these
odds. You have done no statistical analysis to answer this question.
Therefore you're notions are nothing more than just-so fairytale
stories - not science. You have no idea as to the likelihood that your
notions remotely represent reality beyond very very low levels of
functional complexity. That's why your stories are only "just-so"
stories without any scientific value or relevance.
> >> You *claim*
> >> there exist thresholds of functional complexity that can't be crossed by
> >> random mutation and natural selection, but the claim is based on nothing
> >> more than your own refusal to acknowledge that organisms descend, with
> >> slight modifications, from similar ancestors.
>
> >Ok, have any examples of this? - beyond your just-so stories that such
> >a thing actually happens via the specific mechanism of RM/NS? Produce
> >a single example of your mechanism producing a novel functional system
> >that requires at least 1000 fsaars to work. For example, the rotary
> >flagellar motility system requires several thousand fairly specified
> >coded residue positions, at minimum, to work as a motility system.
> >Care to provide any statistical basis for how long it should take your
> >mechanism to produce such a system starting with any historically non-
> >flagellate gene pool? Good luck.
>
> Do I have any examples of *what*? There are numerous examples of
> organisms acquiring new capabilities by means of slight modifications of
> existing structures and processes.
Yes, but name one that produces a novel system beyond the 1000 fsaar
threshold level. Know of any precursor system that is close enough to
a higher level system, like within a couple of mutations?
> Are you really demanding that I
> produce an example of something that *you* claim must occur, but for
> which you can't marshal a single scrap of evidence? I don't think *any*
> systems have ever required one of your imaginary great leaps.
I'm not asking for a great leap. I'm asking for you to demonstrate
that a small leap is possible beyond the 1000 fsaar threshold level.
The 1000aa system is not the measure of the size of the leap that must
be taken. It is possible to produce such a system with a single point
mutation - the tiniest leap possible. The problem is that the actual
existence of such a small gap distance is extremely unlikely. That is
why there are no such examples in all of literature.
> It's all
> just a figment of your own imagination that such leaps are required.
Again, I'm not asking for large leaps - just larger product minimums
of any kind of leap - small or large.
> Evolution proceeds by small, adaptively useful modifications of existing
> structures and processes. I've told you this before but it just goes in
> one of your ears and out the other.
That's what I'm asking you for. Produce an example of evolution by a
small adaptively useful modification of existing structures and
processes that ends up producing a new system of function that itself
requires at least 1000 fsaar to work - at minimum. I've given you
examples of such higher level systems. Show any precursor system that
is within a small enough step to any one of these higher level
systems. This should be an easy demonstration for you given your
extreme confidence . . .
> >If you are successful in this, you will be the first. Certainly there
> >are no such observations of evolution in action and there are no
> >relevant statistical predictions either - regarding the creative power
> >of the mechanism of RM/NS. There are assumptions along these lines
> >and many just-so stories, but none are based on real statistical
> >analysis or predictive value. They are just fairytales, not
> >science.
>
> Nobody will ever be *successful* in demonstrating to you the existence
> of your molecular saltations. They never happened. The evolutionary
> process got along just fine without them. You're like a child demanding
> that we demonstrate the existence of the Easter Bunny.
Again, I'm not asking for large molecular saltations. I'm asking you
to present an example of your own definition of evolution where the
product itself requires at least 1000 fsaars at minimum. The steps
you demonstrate can be very small indeed. It is theorectically
possible. It is just very very statistically unlikely that you will
be able to find any such small gap size beyond the 1000 fsaar level of
functional complexity.
> >> >This is in fact why we often see evolution "in action" producing
> >> >systems that require no more than a few hundred fairly specified
> >> >residues working together at the same time, but we never ever see any
> >> >novel system of function evolving which requires at least 1000 fsaars
> >> >at minimum (even for multiprotein systems).
>
> >> You'll never see these huge jumps because they don't happen and
> >> evolution doesn't need them. You imagine they must happen because you
> >> simply can't accept that the entire process involves slight progressive
> >> modifications of pre-existing structures and processes.
>
> >I'm not asking for huge jumps. Show me any system that is close
> >enough to any other novel system beyond the 1000 fsaar threshold. In
> >other words, show me two novel systems of function that are
> >qualitatively unique in function, both require at least 1000 fsaar to
> >work, and yet are within only a handful of mutational differences from
> >each other. Do you know of any such examples? Or, show me any other
> >system that is within dozens of mutational differences from a
> >flagellar system. Or, show me any subsystem or proposed steppingstone
> >system within the proposed evolutionary pathway of the flagellar
> >system where any two steppingstones are within striking distance of
> >your evolutionary mechanism - i.e., this side of trillions of years of
> >time on average.
>
> Let me see now. Molecules don't fossilize. Therefore we don't have
> fossils of the evolutionary precursors to the bacterial flagellum.
How convenient for you. You have no evidence, but you know it must
have been there because you know your mechanism must have done the
job?! Don't you realize that you just removed your theory from the
real of potential falsification and therefore from the realm of
science into the realm of fairytale just-so story telling?
> We do
> have numerous fossils of organisms that *do* fossilize, and they all
> pretty much seem to indicate that evolution proceeds by a long series of
> small changes to structures and processes.
You think the changes were small? How small where they? Can you
actually demonstate this small gap size for any system beyond the 1000
fsaar threshold level? Hmmmm?
You see, what appears to be a small morphologic difference is often
based on a very large underlying genetic difference. So, "small" is a
relative term. Please, how "small" is small? Some real data here
would be nice - something specific this time . . .
> We also know of existing
> systems like the type three secretion system that have similar
> functionality.
Not remotely. The TTSS has no similar functionality to a flagellar
motility system at all. It is a secretory system with no motility
functionality whatsoever. In fact, it only requires around 10
proteins to produce while a flagellar motility system requires around
40 proteins according to the arguments of Kenneth Miller. Beyond
this, it has recently been proven that the TTSS subsystem evolve from
the flagellar motility system by a removal of 30 of the 40 parts.
That's right, the TTSS system degenerated from the fully formed
flagellar system - not the other way around.
Come on now. Surely you can do better than this!
> But there's no fossilized flagella. You ignore the fact
> that molecules don't fossilize and that therefore it's completely
> fatuous to conclude from this fact that the flagellum had no similar
> precursors.
It is the best currently available evidence that we have. There
simply are no known precursors that are remotely similar enough to the
flagellum for the mechanism of RM/NS to have produced it in a
reasonable amount of time. You are basing everything on your bald
assumption that these precursors must have existed because of your
assurance, blind as it is, that this mechanism must have done the
job. Yet, you are the one with absolutely no evidence to support this
assumption of small gaps beyond very low levels of functional
complexity. Yet, you think you have "science" on your side? You are
blind my friend. All you really have are bald assertions and just-so
story telling. The best available evidence that is actually known is
against you.
> You conclude that there were no precursors. You deduce that,
> in the absence of evolutionary precursors, an intelligent designer must
> have created the flagellum completely de novo. You regard your procedure
> as scientifically valid. Others regard it as God of the gaps.
All science is based on leaps of faith of some sort. That is the
nature of science - to leap across gaps in knowledge that are not and
cannot be completely known due to limited amounts of available
information. So, science is all about the "god of the gaps"
argument. That is science.
> >If you can show me any such examples, you will effectively falsify my
> >position. Good luck!
>
> No thanks. I'm not, like you, assuming that organisms have no closely
> similar ancestors. If they have similar ancestors, they don't require
> your molecular saltations.
Yes indeed. If they have similar ancestors that are similar enough,
they certainly don't or didn't require the crossing of large gaps.
But, that's a big "if". What are the odds that your "if" stories are
true? Have any idea at all? Where are your odds analyzes? Where is
your predictive value? Where is your "science"?
> >> >I ask you, what is it that limits the evolutionary progress of the
> >> >mechanism of RM/NS so that there are no examples evolution in action
> >> >beyond such very low levels of functional complexity? - not a single
> >> >example in all of literature?
>
> >> It's because these huge jumps don't occur and are not needed.
>
> >Again, I'm not proposing huge steps. The 1000 fsaar threshold isn't a
> >mutational step. It is a description of the final product. If your
> >staring point happens to be within one point mutation of such a
> >system, then evolution across this threshold would be very easy. All
> >you have to do now is to find that such a small gap between what
> >exists in any genome and what might exist to some beneficial level is
> >actually a very small gap size. That's your goal here.
>
> No, it's not my goal, Sean. You see, I don't share your view that
> evolution is shooting at specified targets within some vast universe of
> potential functions.
That's not my view. The mechanism of RM/NS isn't shooting at anything
in particular at all. However, it is shooting and the odds of it
hitting something are based on the ratio of potentially beneficial vs.
non-beneficial sequences in sequence space.
> It's just stepping from one functional system to
> another that may be slightly different. Over great spans of time the
> little changes sometimes add up to something substantially different,
> but there never was any improbable "search."
How do you know? Where are your examples of such closely spaced
systems beyond the 1000 fsaar threshold level of functional
complexity? Seems to me like you simply assume that these gaps were
small at all levels of complexity without a single higher level
example. And you think you have real science on your side? I call
what you are doing just-so story telling. It is a fairytale. That's
all. It's not science. It has no predictive value or potential
falsifiability. In short, it cannot be tested in a falsifiable manner.
> >> Complex
> >> biological systems develop from slightly modified precursors.
>
> >That's a lovely story. Prove it. Or, at least produce some
> >statistical basis for this bald assertion beyond very very low levels
> >of functional complexity.
>
> Go ahead and ignore the entire fossil record. Ignore the nested
> hierarchy of species which conforms to the pattern generated by
> branching evolutionary processes.
Ah, the arguments for common descent. You do realize that arguments
for common descent are not the same thing as arguments for the
mechanism of RM/NS?
> Ignore it all and then demand proof
> that such evidence exists. Stick with your own claims, although you
> can't adduce a scrap of evidence to support their validity or relevance.
> Heck, it's your life; you can do with it as you please.
Hey, I've just asked you to support your stories with at least some
testable potentially falsifiable evidence. All you've done is present
arguments for common descent and numerous pejoratives. Where is your
evidence for the mechanism of RM/NS beyond very low levels of
functional complexity? Where are these small gaps that you speak of?
> >> There's
> >> not a lick of evidence, so far as I can tell, that your molecular
> >> saltations have ever occurred. So you don't really need an intelligent
> >> designer to account for them.
>
> >Large molecular mutations do occur - quite often. It is just that
> >they don't ever end up producing higher level systems of function.
>
> Well, genes get duplicated sometimes, producing a redundant gene that
> may then undergo slight modifications that eventually alter its
> function. As for "higher levels of function," I don't think you have any
> more idea what that means than I do.
If you have no idea how to define a level of functional complexity,
you're not doing science. All I ask is for you to present some
evidence that your gaps at higher levels are indeed as small as you
imagine them to be or have been. And no, arguments for common descent
are not the same thing as arguments for small enough gaps for the
mechanism of RM/NS to cross.
Sean Pitman
www.DetectingDesign.com
Seanpit
> On May 5, 12:57 pm, Seanpit <sean...@gmail.com> wrote:
>
> > On May 5, 12:04 am, "R. Baldwin" <res0k...@nozirevBACKWARDS.net>
> > wrote:
>
> > > It seemed clear that Dryden understood and dismissed your argument as
> > > vacuous. ORFs reach a "selectable level of usefulness" at far shorter
> > > lengths than 1000 aa.
>
> > Of course, that is because they don't have a minimum structural
> > threshold requirement that is greater than 1000 fsaars. That is why
> > they are in fact on a lower level of functional complexity.
>
> does anyone know what 'functional complexity' is? a 300aa protein
> enzyme that catalyzes complex reactions is somehow 'less' complex than
> a flagellum that rotates? looks like a meaningless distinction.
There is nothing "complex" about the reactions catalyzed by a 300aa
enzyme if these reactions only require a system with no more than 300
fsaars.
It is obviously ludicrous to argue that a flagellar motility system is
somehow on the same level as any single protein enzyme. That's so
silly that it really deserves a Chez Watt nomination - even though
someone like Dryden actually made such a idiotic argument.
> > How do you not understand this concept?
>
> wrong question. how do YOU understand a concept that NO ONE thinks is
> valid?
Just answer one question: Do all systems of function have the same
minimum structural threshold requirements?
> > The definition of a level of
> > functional complexity is defined as the *minimum* structural threshold
> > requirement for a system to work. If you find that the minimum
> > requirement for a particular system is far less than 1000 fsaars, then
> > that system is on a far low level of functional complexity.
>
> uh...why? if the system WORKS then the LENGTH of the protein is
> irrelevant BY YOUR OWN DEFINITION.
Just because it works doesn't mean it is a high level function. Lots
of low-level systems work just fine. Try getting a flagellar motility
system to "work" with less than 1000 fsaars.
> sean's argument is a hodgepodge of mis-applied ideas, 7th day
> adventist nonsense, distortions of real work and complete disregard
> for the methods of science. other than that it's great stuff.
I've just presented a few simple questions. They aren't difficult to
understand. All you have to do is answer them.
Sean Pitman
www.DetectingDesign.com
wf3h
> On May 5, 10:11 am, wf3h <w...@vsswireless.net> wrote:
>
>
> >
> > does anyone know what 'functional complexity' is? a 300aa protein
> > enzyme that catalyzes complex reactions is somehow 'less' complex than
> > a flagellum that rotates? looks like a meaningless distinction.
>
> There is nothing "complex" about the reactions catalyzed by a 300aa
> enzyme if these reactions only require a system with no more than 300
> fsaars.
who says? if the system works, what makes it non-complex?
if a system performs a very simple function and is long, is that more
'complex' than one that performs a convoluted function and is short>
>
> It is obviously ludicrous to argue that a flagellar motility system is
> somehow on the same level as any single protein enzyme. That's so
> silly that it really deserves a Chez Watt nomination - even though
> someone like Dryden actually made such a idiotic argument.
IOW it doesnt fit your creationist argument so it's not true. gee. to
a chemist, catalyzing reactions is a VERY COMPLEX process. but, i
suppose if you're a creationist and just get to make stuff up, it
seems very simple because you guys don't know much about science.
>
> > > How do you not understand this concept?
>
> > wrong question. how do YOU understand a concept that NO ONE thinks is
> > valid?
>
> Just answer one question: Do all systems of function have the same
> minimum structural threshold requirements?
\
what is a 'system of function'?
and you answer a question: what proof is there that 'systems of
function' are deterministically related to protein size?
>
> > > The definition of a level of
> > > functional complexity is defined as the *minimum* structural threshold
> > > requirement for a system to work. If you find that the minimum
> > > requirement for a particular system is far less than 1000 fsaars, then
> > > that system is on a far low level of functional complexity.
>
> > uh...why? if the system WORKS then the LENGTH of the protein is
> > irrelevant BY YOUR OWN DEFINITION.
>
> Just because it works doesn't mean it is a high level function. Lots
> of low-level systems work just fine. Try getting a flagellar motility
> system to "work" with less than 1000 fsaars.
so now you're saying that if it works it's not complex unless you say
it's complex. as dryden pointed out, many of the aa's in proteins are
non-functional. it doesn't matter which aa is in the chain so there
are plenty of ways to build a chain if the links can be made of
anything at all.
and, again, your creationist viewpoint skips over its own failure to
describe ANY method for doing ANYTHING in biochemistry at all.
creationism can't even explain SIMPLE systems let alone COMPLEX
systems
if your idea is so powerful you should be able to specify an
OBSERVABLE mechanism of how creationism builds a protein of 1000aa's.
you can't.
you should be able to point at the transition between 'simple' and
'complex' systems and say HERE is where the creationist mechanism
takes over. you can't.
IOW there's NOTHING in your model at all...NOTHING that is testable or
observable. it's a complete failure from the viewpoint of science.
just as the rest of your creationist nonsense has been for 2000 years.
>
> > sean's argument is a hodgepodge of mis-applied ideas, 7th day
> > adventist nonsense, distortions of real work and complete disregard
> > for the methods of science. other than that it's great stuff.
>
> I've just presented a few simple questions. They aren't difficult to
> understand. All you have to do is answer them.
>
i did. and i presented my own questions
which you will completely ignore. because that's what creationism
does. ignore evidence. that's why it's not science
Perplexed in Peoria
> On May 5, 12:04 am, "R. Baldwin" <res0k...@nozirevBACKWARDS.net>
> wrote:
> > If you paid attention to his explanation, you would understand why
> > systems having short sequences sufficient.You should have focused on
> > "Nature takes the domain modules and puts them together to make novel
> > structures and functions," and contemplated what that means with respect
> > to your model. Evolution is not exploring a space the size of 20^N when
> > combining domain modules. You should consider the subspace defined by
> > the combinations of domain modules.
> You're mistaken. A combination of domain modules does in fact explore
> a larger sequence space and has the potential to land upon a system
> that is on a higher level of functional complexity - i.e., a system
> with greater minimum size and specificity requirements. It is just
> that the odds of this actually happening ...
In my opinion, this is the key issue in the never-ending Pitman debate.
Sean's simple model says that novel functions arise by chance and then
are refined by NS. Sean's critics point out that there is evidence (in
sequence databases) that novel functions may have arisen by the pasting
together of smaller domains. Sean then usually claims that the
pasting-together mode of mutation provides a path to functionality
which is no more likely to succeed in hitting one of those elusive
'islands' than does starting with a big random sequence and mutating
it. At least that is what he usually claims. And he is right, if the
two things that got pasted together were random sequences. But,
of course, in the evolutionist model, they are not random sequences.
They are copies of existing functional domains - sequences of amino acids
which fold in a stable and useful way. And the evolutionists claim
that the odds of hitting an 'island' by gluing together two already tested
and refined domains is MUCH higher than the odds of hitting an 'island'
by gluing together two random sequences. As far as I know, Sean has
never addressed this point.
However, it may be unfair of me to ask him to address it here, because
he is apparently making some other argument here - an argument I neither
recognize nor understand. Let us see what he actually says:
> ... the odds of this actually happening are exponentially lower than
> the odds of such a combination landing upon a lower level system. The
> reason for this is due to the exponentially reduced ratio of higher
> level vs. lower level system in sequence space.
Correct me if I am wrong, Sean, but it seems to me that you are saying
that the odds of hitting, say, a minimal flagellum are smaller than the
odds of hitting, say, cytochrome C (but a bloated variant of cytochrome
C which is much larger than it absolutely needs to be).
Is this what you are saying, Sean? And if so, why is it relevant?
Steven L.
We've already explained that to you before.
A flagellum isn't THAT much different from other microbial structures,
such as the type III secretory system. It's a molecular motor that is
used to inject toxins into prey cells.
http://www.millerandlevine.com/km/evol/design2/article.html
The important thing about it is that it can use the energy of a cell to
do mechanical work. And with only a few tweaks to its structure, it can
produce a spinning motion instead of an injecting motion.
What looks like a large *qualitative* difference to you in
functionality, can be produced with just a few tweaks of the molecular
structure.
I think that's the point you are missing. You're assuming that a
qualitative change in functionality must necessarily require a large
change in structure (and hence a large number of mutations). Not so.
>
> If you are successful in this, you will be the first. Certainly there
> are no such observations of evolution in action and there are no
> relevant statistical predictions either - regarding the creative power
> of the mechanism of RM/NS.
Then I don't understand what your alternative theory is: If evolution
of species has never occurred, then are you suggesting that an
Intelligent Agency or Intelligent Designer had intervened to produce
each and every one of the millions of species that have existed on
Earth? Each and every one is a special creation by this Intelligence?
Indeed, your focus on the bacterial flagellum suggests that you believe
that every *structure* of every life form had to be specially designed.
So the Intelligent Designer is keeping pretty busy: He has to sculpt
every nucleus, every cilium, every flagellum, every ribosome, of every
type of cell of every life form that ever existed. Is THAT what you're
arguing for????
Most recently, the Intelligent Designer must have created HIV around the
beginning of the 20th century. To paraphrase what you said: Certainly
there are no observations of Intelligent Design of HIV in action.
--
Steven L.
Email: sdli...@earthlinkNOSPAM.net
Remove the NOSPAM before replying to me.
Steven L.
I agree with you that there are levels of complexity in the
functionality of any complex system. But where I part company with you
is your assumption that higher levels of functional complexity require
larger structural changes (and hence many more mutations). Not
necessarily. It all depends on how the system is structured.
It doesn't take a big structural change to produce a qualitative
functional change. In the case of the bacterial flagellum, only a few
molecular "tweaks" change it from spinning to a back-and-forth motion,
and a few more "tweaks" leave it completely inoperative. That's been
proven already.
Steven L.
> It is obviously ludicrous to argue that a flagellar motility system is
> somehow on the same level as any single protein enzyme.
Why??? WHY???
Just because a flagellum spins, and spinning looks cool to the
laypersons who are the real target of the ID proponents, rather than
biologists who know better?
A wheel spins. Is the *structure* of the wheel complex? No, it's based
on a circle, which is a very *simple* curve. Was it hard for primitive
man to invent the wheel? Not if he first noticed that a tree trunk that
was lying on the ground could be rolled. Then all it took to make a
wheel was to take a horizontal slice of that tree trunk.
I don't understand why a flagellum is your "model organism" for
complexity. You've been told already that the components of the
flagellum responsible for spinning are similar to NON-spinning
structures found in other species of microbes. You ignored that.
Seanpit
>
> >> Your arguments have been obliterated by someone who
> >> unlike you has the training and the talent to do the
> >> math. You aren't going to restore your arguments by
> >> just repeating more loudly and unchanged.
>
> > First off, why do you highlight every single one of your posts by
> > changing the topic heading? It is very annoying . . .
>
> > Beyond this, where is your own definition of levels of functional
> > complexity?
>
> I agree with you that there are levels of complexity in the
> functionality of any complex system. But where I part company with you
> is your assumption that higher levels of functional complexity require
> larger structural changes (and hence many more mutations). Not
> necessarily. It all depends on how the system is structured.
>
> It doesn't take a big structural change to produce a qualitative
> functional change. In the case of the bacterial flagellum, only a few
> molecular "tweaks" change it from spinning to a back-and-forth motion,
> and a few more "tweaks" leave it completely inoperative. That's been
> proven already.
It is easy to produce a quantitative loss of function with a few very
small mutational "tweaks". That's easy. It is also easy to
quantitatively improve a particular type of function once it is
realized to at least some level of selectable benefit. What is not so
easy is to discover a qualitatively novel beneficial functional system
via random mutations.
Of course, it is theoretically possible to find such a system with one
or two small mutations, but what is possible isn't always likely. The
fact that there are no such examples beyond the 1000 fsaar threshold
level of functional complexity should tell you something about the
odds. No small tweaks actually end up producing anything close to
this level. There isn't a single example in all of literature. Now
why might that be considering that there are many of examples of this
sort of thing happening at the level of only a few hundred fairly
specified residues or lower? Why are there so many lower level
examples, but no higher level examples? - not even one? What does
that tell you about the odds of small tweaks actually producing
something useful at higher and higher levels?
> Steven L.
> Email: sdlit...@earthlinkNOSPAM.net
> Remove the NOSPAM before replying to me.
Sean Pitman
www.DetectingDesign.com
NA Sides
wrote:
>On May 5, 8:31 am, NA Sides <nongo1...@sonic.net> wrote:
<snip>
>> You conclude that there were no precursors. You deduce that,
>> in the absence of evolutionary precursors, an intelligent designer must
>> have created the flagellum completely de novo. You regard your procedure
>> as scientifically valid. Others regard it as God of the gaps.
>
>All science is based on leaps of faith of some sort. That is the
>nature of science - to leap across gaps in knowledge that are not and
>cannot be completely known due to limited amounts of available
>information. So, science is all about the "god of the gaps"
>argument. That is science.
Then tell me the inferences you've drawn about the nature of the
intelligent designer or designers. Can you say anything about their
motives for creating more efficient pathogens?
>> >If you can show me any such examples, you will effectively falsify my
>> >position. Good luck!
>>
>> No thanks. I'm not, like you, assuming that organisms have no closely
>> similar ancestors. If they have similar ancestors, they don't require
>> your molecular saltations.
>
>Yes indeed. If they have similar ancestors that are similar enough,
>they certainly don't or didn't require the crossing of large gaps.
>But, that's a big "if". What are the odds that your "if" stories are
>true? Have any idea at all? Where are your odds analyzes? Where is
>your predictive value? Where is your "science"?
I'm extremely pleased to find out that God of the gaps is science! I'm
even thinking of becoming an intelligent design proponent. Please advise
me on how I can find out more about the designer's identity, methods and
motives. Should I expect it, or them, to have been active throughout the
history of life on earth? Where do I go about looking for signs that
they've been around? Do you think they've been here all along, or do
they visit us using faster than light travel? Do they have an especial
fondness for beetles? I can't wait to find out how you've investigated
all this and dispensed with just-so stories!
<snip>
NAS
>Sean Pitman
>www.DetectingDesign.com
wf3h
which, of course, is wrong. what differentiates a 'quantitative
improvement of a function' vs a 'novel' function? is an eyespot better
than no eyespot? the quantitative differences between eye types...is
that an 'improvement' or a 'novel beneficial function' if it is a
major change in characteristics?
sean tries, it seems, to make a distinction without a difference
>
> Of course, it is theoretically possible to find such a system with one
> or two small mutations, but what is possible isn't always likely. The
> fact that there are no such examples beyond the 1000 fsaar threshold
> level of functional complexity should tell you something about the
> odds.
an irrelevant argument. functionality is not deterministically linked
to protein length.
No small tweaks actually end up producing anything close to
> this level. There isn't a single example in all of literature
and in 2000 years there's not a single example of creationism ever
being anything but wrong. it's one thing to say evolution has unknown
causes. it's another to say a WRONG idea is right.
sean's argument ultimately fails both for scientific AND historical
reasons.
Seanpit
> Seanpit wrote:
>
> > Ok, have any examples of this? - beyond your just-so stories that such
> > a thing actually happens via the specific mechanism of RM/NS? Produce
> > a single example of your mechanism producing a novel functional system
> > that requires at least 1000 fsaars to work. For example, the rotary
> > flagellar motility system requires several thousand fairly specified
> > coded residue positions, at minimum, to work as a motility system.
> > Care to provide any statistical basis for how long it should take your
> > mechanism to produce such a system starting with any historically non-
> > flagellate gene pool? Good luck.
>
> We've already explained that to you before.
>
> A flagellum isn't THAT much different from other microbial structures,
> such as the type III secretory system. It's a molecular motor that is
> used to inject toxins into prey cells.
>
> http://www.millerandlevine.com/km/evol/design2/article.html
>
> The important thing about it is that it can use the energy of a cell to
> do mechanical work. And with only a few tweaks to its structure, it can
> produce a spinning motion instead of an injecting motion.
Oh really? You think just a couple mutations are all that are needed
to take the next step in the proposed evolutionary pathway? Care to
detail how many mutational steps you think are likely to be involved
here? It is easy to make the bald assertion that the mutational
changes would be minimal. It is another thing entirely to back this
assertion up.
You do realize, of course, that it has been demonstrated that the TTSS
system is not the evolutionary precursor of the bacterial flagellum.
It is actually the other way around. The flagellar system gave rise
to the TTSS system. That's right. The TTSS system is a degerative
system that devolved from the flagellar motility system - not the
other way around.
> What looks like a large *qualitative* difference to you in
> functionality, can be produced with just a few tweaks of the molecular
> structure.
What "few tweaks"? If you think they are so few, what are they?
> I think that's the point you are missing. You're assuming that a
> qualitative change in functionality must necessarily require a large
> change in structure (and hence a large number of mutations). Not so.
Care to support this assertion of yours with some actual evidence? -
fill in a few specific details? So far, I only see this as just-so
story telling on your part together with several bald assertions.
Certainly such a thing has never been demonstrated in real time -
which is very surprising given the truth of your assertions of such a
small gap distance.
> > If you are successful in this, you will be the first. Certainly there
> > are no such observations of evolution in action and there are no
> > relevant statistical predictions either - regarding the creative power
> > of the mechanism of RM/NS.
>
> Then I don't understand what your alternative theory is: If evolution
> of species has never occurred, then are you suggesting that an
> Intelligent Agency or Intelligent Designer had intervened to produce
> each and every one of the millions of species that have existed on
> Earth? Each and every one is a special creation by this Intelligence?
I think the definition for "species" is too subjective. However, I
will say that every single qualitatively unique beneficial system of
function that requires more than 1000 fsaars was the result of
deliberate design.
> Indeed, your focus on the bacterial flagellum suggests that you believe
> that every *structure* of every life form had to be specially designed.
That's right.
> So the Intelligent Designer is keeping pretty busy: He has to sculpt
> every nucleus, every cilium, every flagellum, every ribosome, of every
> type of cell of every life form that ever existed. Is THAT what you're
> arguing for????
Yes . . .
> Most recently, the Intelligent Designer must have created HIV around the
> beginning of the 20th century. To paraphrase what you said: Certainly
> there are no observations of Intelligent Design of HIV in action.
What I said was that such viruses, like the TTSS system, are likely
degenerative in origin - not the result of deliberate design.
> Steven L.
> Email: sdlit...@earthlinkNOSPAM.net
> Remove the NOSPAM before replying to me.
Sean Pitman
www.DetectingDesign.com
Seanpit
>
> > > It doesn't take a big structural change to produce a qualitative
> > > functional change. In the case of the bacterial flagellum, only a few
> > > molecular "tweaks" change it from spinning to a back-and-forth motion,
> > > and a few more "tweaks" leave it completely inoperative. That's been
> > > proven already.
>
> > It is easy to produce a quantitative loss of function with a few very
> > small mutational "tweaks". That's easy. It is also easy to
> > quantitatively improve a particular type of function once it is
> > realized to at least some level of selectable benefit. What is not so
> > easy is to discover a qualitatively novel beneficial functional system
> > via random mutations.
>
> which, of course, is wrong. what differentiates a 'quantitative
> improvement of a function' vs a 'novel' function? is an eyespot better
> than no eyespot?
In certain environments - yes. An eyespot is better than no eyespot.
However, the simplest beneficially functional eyespot is at a very
high level of functional complexity. It is therefore very unlikely to
evolve via RM/NS this side of many trillions of years of time.
> the quantitative differences between eye types...is
> that an 'improvement' or a 'novel beneficial function' if it is a
> major change in characteristics?
The differences between various types of eyes isn't just quantiative,
but qualitative. That is why evolution between various types of eyes
is not realized in observable time nor is it remotely likely to be
realized in trillions of years of time if you actually consider the
mutational differences needed to cross the gaps between one type of
eye and the next proposed steppingstone in the proposed pathways of
eye evolution.
http://www.detectingdesign.com/humaneye.html
> sean tries, it seems, to make a distinction without a difference
You don't understand the difference between and change in quantity vs.
quality of a function?
> > Of course, it is theoretically possible to find such a system with one
> > or two small mutations, but what is possible isn't always likely. The
> > fact that there are no such examples beyond the 1000 fsaar threshold
> > level of functional complexity should tell you something about the
> > odds.
>
> an irrelevant argument. functionality is not deterministically linked
> to protein length.
Yes it is. All functional systems have minimum size and specificity
requirements.
> > No small tweaks actually end up producing anything close to
> > this level. There isn't a single example in all of literature
>
> and in 2000 years there's not a single example of creationism ever
> being anything but wrong. it's one thing to say evolution has unknown
> causes. it's another to say a WRONG idea is right.
>
> sean's argument ultimately fails both for scientific AND historical
> reasons.
This is about at least human-level intelligent design - which is a
very natural level of intelligence that is seen in action all the time
and is a big part of many scientific disciplines.
Sean Pitman
www.DetectingDesign.com
Spil...@gmx.net
> On May 5, 11:44 am, "Steven L." <sdlit...@earthlink.net> wrote:
> > Then I don't understand what your alternative theory is: If evolution
> > of species has never occurred, then are you suggesting that an
> > Intelligent Agency or Intelligent Designer had intervened to produce
> > each and every one of the millions of species that have existed on
> > Earth? Each and every one is a special creation by this Intelligence?
>
> I think the definition for "species" is too subjective. However, I
> will say that every single qualitatively unique beneficial system of
> function that requires more than 1000 fsaars was the result of
> deliberate design.
>
> > Indeed, your focus on the bacterial flagellum suggests that you believe
> > that every *structure* of every life form had to be specially designed.
>
> That's right.
>
> > So the Intelligent Designer is keeping pretty busy: He has to sculpt
> > every nucleus, every cilium, every flagellum, every ribosome, of every
> > type of cell of every life form that ever existed. Is THAT what you're
> > arguing for????
>
> Yes . . .
Your idea has just a little flaw. For it to work there has to be a
designer. If it is shown (as I have done) that there never was a
designer under the premises of the design argument, then your idea is
falsified.
Best regards,
Lark
Seanpit
First off, the structure of the functional flagellar motility system
is not remotely similar to any of the subsystems you've mentioned -
certainly no the TTSS system which only uses 10 of the 40 or so
proteins of the flagellar system and from which the TTSS system is
derived (not the other way around).
Secondly, to describe the flagellar motility system as nothing more
than a simplistic spinning wheel is very naive. It is a very complex
machine that requires a large number of parts at minimum in order to
work to produce rotary flagellar motility. Without all of these
parts, it simply wouldn't work at all to produce this type of
functionality. It is not the simplistic system that you and Dryden
have described. It is more than ludicrous to even try to argue along
these lines when the complexity of the system is so blatantly obvious
to anyone with a candid mind. It seems like you and even Dryden would
describe the Space Shuttle as a "simple" machine if it would help to
support Darwinian thinking.
In short, the job might seem to you to be a simple job. But, the
machine itself is not simple. It requires a great many parts all
working together in a very specific arrangement at the same time.
Such a machine cannot be described as "simple" or comparable to a
single protein enzyme by any stretch of the imagination - at least not
with a straight face.
> Steven L.
> Email: sdlit...@earthlinkNOSPAM.net
> Remove the NOSPAM before replying to me.
Sean Pitman
www.DetectingDesign.com
Seanpit
>
> Your idea has just a little flaw. For it to work there has to be a
> designer. If it is shown (as I have done) that there never was a
> designer under the premises of the design argument, then your idea is
> falsified.
Designers exist Lark. Human-level intelligence does exist and has not
been falsified. Your arguments concern the ultimate origin of all
things - which is not known or knowable from either the naturalistic
or creationists or IDist perspective. Knowing who or what created the
designer is really a non-issue relative to this particular topic.
> Best regards,
> Lark
Sean Pitman
www.DetectingDesign.com
Seanpit
wrote:
That's not true. Starting with non-random sequences does improve the
odds of success - but this improvement does not solve the problem of
the linearly expanding gap distances.
> And he is right, if the
> two things that got pasted together were random sequences.
I'm right even if the pasted sequences are fully functional
sequences.
> But,
> of course, in the evolutionist model, they are not random sequences.
That's right. They start out as functional islands. I've never
argued otherwise. The problem isn't because of a random starting
point. The problem is that even if the starting points are not
random, the same problem occurs.
> They are copies of existing functional domains - sequences of amino acids
> which fold in a stable and useful way. And the evolutionists claim
> that the odds of hitting an 'island' by gluing together two already tested
> and refined domains is MUCH higher than the odds of hitting an 'island'
> by gluing together two random sequences. As far as I know, Sean has
> never addressed this point.
I've addressed this point many times in this forum. I've even devoted
an entire section to this particular argument in my discussion of how
to calculate the odds of success:
http://www.detectingdesign.com/flagellum.html#starting
> However, it may be unfair of me to ask him to address it here, because
> he is apparently making some other argument here - an argument I neither
> recognize nor understand. Let us see what he actually says:
>
> > ... the odds of this actually happening are exponentially lower than
> > the odds of such a combination landing upon a lower level system. The
> > reason for this is due to the exponentially reduced ratio of higher
> > level vs. lower level systems in sequence space.
>
> Correct me if I am wrong, Sean, but it seems to me that you are saying
> that the odds of hitting, say, a minimal flagellum are smaller than the
> odds of hitting, say, cytochrome C (but a bloated variant of cytochrome
> C which is much larger than it absolutely needs to be).
> Is this what you are saying, Sean?
Yes - that's exactly what I'm saying.
> And if so, why is it relevant?
Because, the odds of finding lower level functional systems are much
greater than the odds of finding higher level systems due to the
difference in the ratios of one compared to the other within sequence
space. This is in fact why we actually see many examples of RM/NS
actually coming up with lower-level systems, but have yet to see a
single higher level example of evolution in action beyond the 1000
fsaar level of functional complexity.
Sean Pitman
www.DetectingDesign.com
'Rev Dr' Lenny Flank
seen and laughed at a thousand times already?
Anything?
Anything at all?
pol...@msx.dept-med.pitt.edu
> On May 5, 1:41 pm, wf3h <w...@vsswireless.net> wrote:
>
> > > > It doesn't take a big structural change to produce a qualitative
> > > > functional change. In the case of the bacterial flagellum, only a few
> > > > molecular "tweaks" change it from spinning to a back-and-forth motion,
> > > > and a few more "tweaks" leave it completely inoperative. That's been
> > > > proven already.
>
> > > It is easy to produce a quantitative loss of function with a few very
> > > small mutational "tweaks". That's easy. It is also easy to
> > > quantitatively improve a particular type of function once it is
> > > realized to at least some level of selectable benefit. What is not so
> > > easy is to discover a qualitatively novel beneficial functional system
> > > via random mutations.
Too bad for you that REALITY is replete with such findings - nylonase
and other systems.
By your 'math', the 'odds' that a 100 amino acid sequence having a
selectable function OF any sort is 20^ln(100)/20^100 - about 1 in
10^124. The function in this case is beneficial and novel (since it
wasn't present before).
Examination of REALITY shows the odds at 1 in 10^9 to 1 in 10^15.
More than 100 orders of magnitude more likely.
Blubbering 'but, but - those are LOW levels of complexity !!!!!!!!!'
doesn't cut the mustard, since those are the odds of ANY function
arising (the 'demand' that it be 'high complexity/specificity/novel'
is a deranged add-on you apply when reality contradicts your silly
models)
> > which, of course, is wrong. what differentiates a 'quantitative
> > improvement of a function' vs a 'novel' function? is an eyespot better
> > than no eyespot?
>
> In certain environments - yes. An eyespot is better than no eyespot.
> However, the simplest beneficially functional eyespot is at a very
> high level of functional complexity.
You 'determined' that HOW ? Oh, right - 'Lord Pitman SAYS so !!'
> It is therefore very unlikely to
> evolve via RM/NS this side of many trillions of years of time.
RiiIIiiiIIiight ! It is true because your simpering numerology SAYS
so, right ? Because Lord Pitman DECREES that selection is 'all or
nothing' - there is absolutely NO function until every single amino
acid matches his target sequence, right ?
There are single celled organisms with eyespots - like Euglena. It
does not require a high level of complexity to detect light - a few
proteins with a common chemical attached does the job for everything
from Euglena and Volvox to humans.
Is there a DIFFERENT designer for each type of eye in existence, or
just one ? And WHERE did something complex enough to design eyes come
from ?
> > the quantitative differences between eye types...is
> > that an 'improvement' or a 'novel beneficial function' if it is a
> > major change in characteristics?
>
> The differences between various types of eyes isn't just quantiative,
> but qualitative.
You 'determined' that how, exactly ? You 'determined' that the known
processes of evolution are NOT up to the task HOW ? (oh, right -
divine fiat).
> That is why evolution between various types of eyes
> is not realized in observable time
Translation : If Lord Pitman didn't see it happen right before his
eyes, IT CANNOT HAPPEN !!
Too bad for you that REAL events produce REAL, OBSERVABLE effects. If
you see a pile of smouldering rubble where your house used to be, does
the fact that you didn't witness the fire mean there was no fire ?
> nor is it remotely likely to be
> realized in trillions of years of time if you actually consider the
> mutational differences needed to cross the gaps between one type of
> eye and the next proposed steppingstone in the proposed pathways of
> eye evolution.
You 'determined' that HOW, exactly ?
Oh, right - your pathological need for a Magical Sky Pixie/External
Intelligence to exist so you can justify your posturing arrogance
leads you to decree that all sorts of things can't happen inside of
'zillions of years'.
And you've 'considered' the mutational differences needed to cross the
gaps ? Or did you just invoke your simpering numerology and
'calculate' the odds of an eye falling together all at once PURELY by
chance (like you always do), decree that the odds are too high, then
just drop to your knees and start gibbering about Magical Sky Pixies/
Intelligent Designers (like you always do) ? Or just your nigh
infinite incredulity - 'if Lord Pitman can't/won't figure it out, then
the ONLY possible explanation is direct divine intervention' ?
> > sean tries, it seems, to make a distinction without a difference
>
> You don't understand the difference between and change in quantity vs.
> quality of a function?
As both are amenable and explainable via KNOWN processes of mutation
and selection, there is no real need to invoke the unknowable whim of
unknowable beings to somehow do stuff (your pathological need to
grovel before them notwithstanding, of course !)
> > > Of course, it is theoretically possible to find such a system with one
> > > or two small mutations, but what is possible isn't always likely. The
> > > fact that there are no such examples beyond the 1000 fsaar threshold
> > > level of functional complexity should tell you something about the
> > > odds.
Maybe because nature is under no obligation to meet your silly-arsed
criteria ?
Or perhaps your 'requirement' that it happen in 'observable time'
limits what can be done ?
By that 'logic', we can't really be sure those sequoia sapling
ACTUALLY grow into sequoia trees, since the growth doesn't
happen fast enough to suit Lord Pitman.
There are examples, but you just reach up your colon and pull out
irrelevant 'limits'.
The atrazine degradation pathway evolved within the last few decades,
and is 3 proteins representing 1200 amino acids working together to
produce the FUNCTION of atrazine digestion. NOWHERE IN your 'math' is
there a factor or a need for them to be stuck together in any way - a
single 1200 aa protein is just as 'likely' as 3 400 amino acid
proteins evolving to perform a function.
By your 'math', the 'odds' of even one of those proteins arising is
20^ln(300)/20^300. By your 'logic', atrazine degradation SHOULD take
'zillions and zillions of years' to arise.
Yet it didn't.
Did your Magical Sky Pixie/External Intelligence somehow reach into
the genomes of those bacteria and install the function ? Or are
evolution and reality beyond your willfully stunted comprehension ?
> > an irrelevant argument. functionality is not deterministically linked
> > to protein length.
>
> Yes it is. All functional systems have minimum size and specificity
> requirements.
Determined by you AFTER the fact, apparently. If a function arises
and it is beneficial, selection will tune it.
End result after untold generations - a highly 'specified/complex'
system.
Then blithering IDiots stagger in, note how 'complex/specified' the
system is, then perform numerology on it ('the odds of this system
arising PURELY BY CHANCE is 1 to 10^gadzookillions to one against !!),
then decree that since the 'odds' are so long, the ONLY 'explanation'
is the whim of an unknown External Intelligence. Then howl in rage
when other people don't believe them ...
> > > No small tweaks actually end up producing anything close to
> > > this level. There isn't a single example in all of literature
>
> > and in 2000 years there's not a single example of creationism ever
> > being anything but wrong. it's one thing to say evolution has unknown
> > causes. it's another to say a WRONG idea is right.
>
> > sean's argument ultimately fails both for scientific AND historical
> > reasons.
>
> This is about at least human-level intelligent design - which is a
> very natural level of intelligence that is seen in action all the time
> and is a big part of many scientific disciplines.
Where did this human-level intellect come from, Lord Pitman ?
If something like a flagellum MUST have a designer, that designer must
be as complex (if not more so) than the flagellum.
And since the flagellum was designed, its Designer MUST have been
designed by an even more complex Designer.
And so on ad infinitum.
How, EXACTLY, do you escape the infinite regress of designers again,
you Most Bellicose Lord ?
Oh, right - fiat ! ALL complex things MUST be designed - EXCEPT my
more-complex-than-everything-else Designer !
'Rev Dr' Lenny Flank
> Your argument here makes it very clear that both you and Dryden
> misunderstand the very concept of levels of functional complexity.
> You just don't get it - even after all of this time. Yet, it is such
> a simple concept. How is it that you cannot seem to grasp it?
Indeed, Sean, it seems that NOBODY grasps your wonderful sciency mathy
argument. NOBODY. In fact, it certainly seems as though EVERYONE WHO
HAS EVER HEARD IT has, uh, misunderstood it and failed to grasp it.
Why do you suppose that is, Sean? Why do you suppose that everyone
who has heard your wonderful science-destroying world-shattering
paradigm-shifting Scientific Discovery Of All Time, thinks it's just a
load of bullshit?
Is it because you are so much more brilliant than the rest of the
world and the rest of the world is just too stupid to appreciate your
singular genius?
Is it because you are too incompetent and dumb to explain your
wonderful mathy science in such a way that people can understand it
and grasp its genius?
Or is it just because your entire argument really IS just a load of
bullshit?
How many dozens or hundreds or thousands of people need to
consistently and unfailingly "not understand" and "not grasp" your
"simple argument" before you begin to suspect that, uh, maybe it's NOT
EVERYONE ELSE's FAULT that nobody seems to grasp its
genius . . . . . . . . ? Maybe the fault lies with . . . uh . . .
YOU?
Or are you, uh, just too arrogant and self-important to consider that
possibility . . . . . . ?
(snicker) (giggle) <---- Yes, Sean, I am laughing at you. Again.
Seanpit
> On Tue, 5 May 2009 10:57:11 -0700 (PDT), Seanpit <sean...@gmail.com>
Ask SETI scientists. They'll tell you that you don't need to know the
actual identity, methods, or motives of the proposed ETI's before you
can in fact detect the need for at least human-level intelligent input
to explain certain types of phenomena - be those phenomena certain
types of radio signals or certain patterns of DNA or certain types of
functional systems. You just don't need to know about any other than
the system in question and that it is within the realm of at least
human level creativity and technology but is well beyond the realm of
any known non-deliberate non-intelligent force of nature. That is the
basis of SETI and also other sciences like forensics and
anthropology.
Now, what about your just-so stories? Come up with any statistical
analysis or predictive value to back them up yet? Where is your
*science*?
> NAS
Sean Pitman
www.DetectingDesign.com
Seanpit
Why do you keep reposting this cut-n-paste when I've already pointed
out to you that your strawman misrepresentations are just that -
starwman arguments that don't remotely represent my actual arguments?
Why do you keep posting your nonsense about enzymatic cascades when
I've explained them to you dozens of times? - that their parts are not
specified in arrangement and are therefore no more complex than their
most specified single protein part?
Sean Pitman
www.DetectingDesign.com
'Rev Dr' Lenny Flank
Well, Sean, for the same reason *I* keep repeating my simple questions
over and over and over again -- because you don't answer them. You
evade them, you belittle them, you bemoan them, but you never ANSWER
them.
And I want everyone here to see you do that. Repeatedly. As often as
possible.
You are a bullshitter, Sean. Nothing more, nothing less, nothing
else.
> when I've already pointed
> out to you that your strawman misrepresentations are just that -
> starwman arguments that don't remotely represent my actual arguments?
Hey Sean, why is it that NOBODY seems to be able to grasp your "actual
arguments"?
Is it because the whole world is too stupid to understand you?
Is it because YOU are too stupid to explain your "actual arguments" to
people?
Or is it just because your "actual arguments" are all nothing but hand-
waving bullshit?
Why won't you answer that simple question from me, Sean?
(snikcer) (giggle) <--- yes Sean, I am laughing at you. Again.
'Rev Dr' Lenny Flank
(snip)
> the TTSS system which only uses 10 of the 40 or so
> proteins of the flagellar system and from which the TTSS system is
> derived (not the other way around).
You do seem to be the only person saying so . . . .
Nevertheless, you never answered my simple question:
How did this portion of the flagellum manage to get unattached from a
bacterium's ass and get incorporated into an utterly novel structure
with an utterly unrelated function? How did the appearence of that
utterly new novel complex function, from parts of an uterly different
unrelated system, manage to beat your astronomical mathy statisticy
probability odds, Sean?
I'd tell you to be careful how you answer that, Sean --- but the
simple fact that you repeatedly WON'T answer it indicates to me that
you already know the big oozing sticky tarpit that it opens up for
you . . . . . . . . .
You are a bullshitter, Sean. Nothing more, nothing less, nothing
else.
And the fact that you refuse to answer this simple question, indicates
to me that you KNOW you are just bullshitting.
pol...@msx.dept-med.pitt.edu
EVASION NOTED.
Your actual 'arguments' are nothing but gibbering numerology.
Mathematical delusions based on the silly idea that reality MUST
conform to your silly ideas. That there are targets that evolution
MUST find purely by staggering through random sequence space. Your
'model' is indeed the 'tornado thru a junkyard' delusion - it is the
ONLY way to generate numbers as large as you keep tossing out.
By your 'math', the 'odds' of a 100 amino acid sequence having a
function (which for the population WOULD be novel and beneficial) is 1
in 10^124; REALITY shows the odds are only 1 in 10^9 to 1 in 10^15.
Given that your model is off by over 100 orders of magnitude for even
the simplest and smallest proteins, WHY should anyone take your model
seriously ?
Oh, right - negative argumentation ! If you can burn enough evo-
strawmen, your 'model' will be accepted as valid without you needing
to DEMONSTRATE that it is actually better. Or relevant. Or conforms
to reality.
WHY are your numbers so high ? Because they are calculated as falling
together all at once PURELY by chance to match one predetermined
sequence (hence the 'odds of THIS sequence arising goes as 1/20^N').
As this is not representative of evolution in any way, your model doth
suck.
That exponential bloating of the 'beneficial/non-beneficial ratio'
that you CLAIMED made making 7-letter words near impossible (as well
as pretty much everything else) only happens if the non-beneficials
are not removed each generation; in other words, pulling 7 Scrabble
tiles out of a hat and having them be a valid word.
The only way to bloat the ratio is to NOT remove non-beneficial
sequences from the pool. Generally don't see non-beneficial sequences
staying in a population for very long for more realistic simulations
of evolution.
Oh, wait - your entire 'argument' is based on that silly bloating of
the 'beneficial/non-beneficial' ratio, isn't it ?
> Why do you keep posting your nonsense about enzymatic cascades when
> I've explained them to you dozens of times?
Because you keep posting your nonsense about how it is so
'IMPROBABLE !!!!!!!' for anything to evolve when your math is
obviously crap, based on many erroneous ideas.
You've blubbered, blithered, waved your hands and screamed, but you've
NEVER explained WHY a three protein cascade does not qualify (you have
yet to JUSTIFY that your 'conditions' are relevant).
Once again, simpleton : for atrazine degradation, there is NO FUNCTION
until ALL PROTEINS ARE THERE. Your math does not differentiate
between 1 1200 aa, 3 400 aa or 6 200 amino acid proteins. Mainly
because such a consideration is irrelevant.
Initiating standard howling :
> - that their parts are not
> specified in arrangement and are therefore no more complex than their
> most specified single protein part?
Once again, simpleton : THERE IS NO SELECTABLE FUNCTION UNTIL ALL
THREE PROTEINS ARE PRESENT.
'Arrangment' is one of your standard crimson whales you vomit up to
evade the FACT that cascades do qualify (and thus refute your silly
'there are no examples of 1000fsaar systems arising').
Who 'specifies' the arrangement ? Are you seriously DERANGED enough
to 'think' the 'specification' exists OUTSIDE of the system, and had
to be imposed upon it ?
Arrangement is amenable to selection - if sticking together a certain
way helped, that configuration would become more common. Thus your
blubbering 'THEY NOT CONFORM TO *MY* SPECIFICATIONS, THEREFORE THEY
NOT COUNT !!' evasion can be ignored.
If there was no atrazine degradation until AtzA stuck to AtzB a
certain way in the presence of AtzC, the FACT that atrazine
degradation arose would MEAN that AtzA stuck to AtzB the 'correct' way
to generate the observed function; your 'specification' was derived
AFTER THE FACT.
Which seems to be a serious problem with you - your 'math' PRESUMES
that the sequences observed today were the 'target' of evolution, and
they had to be found by random search (again, the only way to get
numbers as large as you like throwing around). Generally NOT a good
idea to calculate the 'odds' of something happening after it happened
- it makes even the most mundane events look near impossible.
Ex : a raindrop lands on the end of your nose. The odds of THAT
particular drop hitting YOU in THAT particular place at that
particular time are astronomical; would you then conclude it was
guided by an External Intelligence ?
You ARE aware that organ development is done via CASCADES, right ?
That most of the proteins in the DEVELOPMENTAL CASCADES are small, do
NOT stick to others in 'specified' ways for long ?
Which means that - by your own mewlings - development is fully
explainable by evolution, since all the players are small enough to
evolve !
wf3h
> On May 5, 1:41 pm, NA Sides <nongo1...@sonic.net> wrote:
>
>
> >
> > I'm extremely pleased to find out that God of the gaps is science! I'm
> > even thinking of becoming an intelligent design proponent. Please advise
> > me on how I can find out more about the designer's identity, methods and
> > motives. Should I expect it, or them, to have been active throughout the
> > history of life on earth? Where do I go about looking for signs that
> > they've been around? Do you think they've been here all along, or do
> > they visit us using faster than light travel? Do they have an especial
> > fondness for beetles? I can't wait to find out how you've investigated
> > all this and dispensed with just-so stories!
>
> Ask SETI scientists.
we have sean. they said you're full of shit. you say you're
misundertood. your argument has no validity. no one here accepts it.
no SETI researchers accept it. it's wrong
They'll tell you that you don't need to know the
> actual identity, methods, or motives of the proposed ETI's before you
> can in fact detect the need for at least human-level intelligent input
> to explain certain types of phenomena -
actually they'll tell you just the opposite. they'll tell you you need
to know enough about the designers to exclude natural processes
you haven't. another reason you're wrong
be those phenomena certain
> types of radio signals or certain patterns of DNA or certain types of
> functional systems. You just don't need to know about any other than
> the system in question and that it is within the realm of at least
> human level creativity and technology but is well beyond the realm of
> any known non-deliberate non-intelligent force of nature. That is the
> basis of SETI and also other sciences like forensics and
> anthropology.
creationsits get alot of mileage out of SETI. the argument is wrong.
it has no applicability for reasons explained above. so sean is
engaged in begging scientists to disregard their own work and accept
his bizarre cult beliefs
>
> Now, what about your just-so stories? Come up with any statistical
> analysis or predictive value to back them up yet? Where is your
> *science*?
and we've asked you the same question. all you come up with is 7th day
adventist manure.
NA Sides
wrote:
>On May 5, 1:41 pm, NA Sides <nongo1...@sonic.net> wrote:
Couldn't you broaden your investigation just a little? Surely the
designers would have left clues behind. If I were an intelligent design
theorist, I'd be more ambitious. It would be scientific to make some
inferences about the designer(s), wouldn't it? After all, your entire
method is based on a *lack* of physical evidence, so that shouldn't hold
you back. We can infer that they must have a very stable civilization
because they've been around for billions of years. Or maybe it's just
one guy who's immortal. They can't be naturally evolved biological
organisms because that would require the evolution of novel functional
systems that required at least 1000 fsaars, and your investigations have
shown that this could not have happened in less than zillions of years.
You may think I'm making up just-so stories, but I'm just logically
eliminating possibilities. If we eliminate the impossible, that which
remains must be the truth. I'm having a problem here, though. I've run
into an infinite regress. If the designers can't have evolved, who
designed them? You've had more experience in this area than me, Sean,
how do you deal with this problem? Any tips would be greatly
appreciated.
See? We've already made more progress than Behe has had in a decade. By
process of elimination we seem to be left with robots or supernatural
beings, though you may want to suggest other possibilities. If time
travel is involved, do you see any paradoxes?
>Now, what about your just-so stories? Come up with any statistical
>analysis or predictive value to back them up yet? Where is your
>*science*?
Nah. If I'm going to be an intelligent design theorist, I have to give
up those fairytales about organisms being descended from similar
ancestors. So, do you think every species is independently created? Have
you determined a list of molecules and molecular systems that couldn't
have evolved? If so, where can I get it? I appreciate any help you can
give.
NAS
>Sean Pitman
>www.DetectingDesign.com
wf3h
because he accurately represents your position: your ridiculous
qualifications of evolution and creationism are models that no one
believes happen. you're simply wrong.
> Why do you keep posting your nonsense about enzymatic cascades when
> I've explained them to you dozens of times? - that their parts are not
> specified in arrangement and are therefore no more complex than their
> most specified single protein part?
and THAT particular mechanism happens again and again in
evolution...even with VERY complex systems.
so, again, you're wrong
wf3h
>
>
>
> >
> > which, of course, is wrong. what differentiates a 'quantitative
> > improvement of a function' vs a 'novel' function? is an eyespot better
> > than no eyespot?
>
> In certain environments - yes. An eyespot is better than no eyespot.
> However, the simplest beneficially functional eyespot is at a very
> high level of functional complexity. It is therefore very unlikely to
> evolve via RM/NS this side of many trillions of years of time.
no one knows what this means. what is 'very high level of functional
complexity'? it's a meaningless term that seems to depend on what you
believe to be true.
you've said that protein LENGTH is DETERMINISTICALLY causal to
functional complexity. prove it. go ahead. you made the claim. prove
it.
and we can SEE the eye evolving across different species...see
different mechanisms for eyes. the octopus eye is different than the
human eye. as dryden pointed out, if the structure of proteins is so
flexible that MANY structures can perform a function then your
argument is wrong
and teh ONLY reason you CONTINUE to make a wrong argument is because
of your trailer park religious beliefs.
>
> > the quantitative differences between eye types...is
> > that an 'improvement' or a 'novel beneficial function' if it is a
> > major change in characteristics?
>
> The differences between various types of eyes isn't just quantiative,
> but qualitative. That is why evolution between various types of eyes
> is not realized in observable time nor is it remotely likely to be
> realized in trillions of years of time if you actually consider the
> mutational differences needed to cross the gaps between one type of
> eye and the next proposed steppingstone in the proposed pathways of
> eye evolution.
nonsense. there are MANY types of eye structures. we can see their
development across species. this is explained by evolution
it is NOT explained by creationism. creationism fails even at the
SIMPLE level. it can not explain the SIMPLEST proteins let alone
COMPLEX proteins. your view of science is EXACTLY backwards. you
pretend to explain the complex while failing at the simple. that's
going backwards.
and that's what creationism is: a regression. it can't explain
ANYTHING about nature.
in addition EVERY MIND we've EVER observed is material...brains. YOU
exclude brains in favor of some easter bunny running around the
universe pulling species out of hats...
>
> http://www.detectingdesign.com/humaneye.html
>
> > sean tries, it seems, to make a distinction without a difference
>
> You don't understand the difference between and change in quantity vs.
> quality of a function?
i understand when an argument is wrong. when it's
ambiguous...vague...meaningless....when it invokes non existent
requirements....that's what you've done. dryden explained it. wolpert
explained it. SETI scientists explained it. everyone gets it except
for you creationsits with your junior high school science educations.
>
> > > Of course, it is theoretically possible to find such a system with one
> > > or two small mutations, but what is possible isn't always likely. The
> > > fact that there are no such examples beyond the 1000 fsaar threshold
> > > level of functional complexity should tell you something about the
> > > odds.
>
> > an irrelevant argument. functionality is not deterministically linked
> > to protein length.
>
> Yes it is. All functional systems have minimum size and specificity
> requirements.
which is meaningless. you insist on making meaningless statements. i
made a claim above: there is no relationship between complexity of
function and protein length. a catalyst is just as complex as a
flagellum if not moreso. you havent been able to quantify a difference
YOU say exists.
your argument is nonsense and based solely in religion of an
intellectually backward church.
>
> > > No small tweaks actually end up producing anything close to
> > > this level. There isn't a single example in all of literature
>
> > and in 2000 years there's not a single example of creationism ever
> > being anything but wrong. it's one thing to say evolution has unknown
> > causes. it's another to say a WRONG idea is right.
>
> > sean's argument ultimately fails both for scientific AND historical
> > reasons.
>
> This is about at least human-level intelligent design - which is a
> very natural level of intelligence that is seen in action all the time
> and is a big part of many scientific disciplines.
human level design REQUIRES a MATERIAL brain.
does your designer have a MATERIAL brain, sean?? because, to use YOUR
qualifier, we have NEVER, in the literature, seen a NON MATERIAL mind.
ever
so if YOUR DESIGN requires a designer that has 'human level'
intelligence based on the literature THEN your designer MUST be
MATERIAL.
are you saying that??
-
Seanpit
>
> > > > It is therefore very unlikely to
> > > > evolve via RM/NS this side of many trillions of years of time.
>
> > > RiiIIiiiIIiight ! It is true because your simpering numerology SAYS
> > > nothing' - there is absolutely NO function until every single amino
> > > acid matches his target sequence, right ?
>
> > > There are single celled organisms with eyespots - like Euglena. It
> > > does not require a high level of complexity to detect light - a few
> > > proteins with a common chemical attached does the job for everything
> > > from Euglena and Volvox to humans.
>
> > > Is there a DIFFERENT designer for each type of eye in existence, or
> > > just one ? And WHERE did something complex enough to design eyes come
> > > from ?
>
> > > > > the quantitative differences between eye types...is
> > > > > that an 'improvement' or a 'novel beneficial function' if it is a
> > > > > major change in characteristics?
>
> > > > The differences between various types of eyes isn't just quantiative,
> > > > but qualitative.
>
> > > You 'determined' that how, exactly ? You 'determined' that the known
> > > processes of evolution are NOT up to the task HOW ? (oh, right -
> > > divine fiat).
>
> > > > That is why evolution between various types of eyes
> > > > is not realized in observable time
>
> > > eyes, IT CANNOT HAPPEN !!
>
> > > Too bad for you that REAL events produce REAL, OBSERVABLE effects. If
> > > you see a pile of smouldering rubble where your house used to be, does
> > > the fact that you didn't witness the fire mean there was no fire ?
>
> > > > nor is it remotely likely to be
> > > > realized in trillions of years of time if you actually consider the
> > > > mutational differences needed to cross the gaps between one type of
> > > > eye and the next proposed steppingstone in the proposed pathways of
> > > > eye evolution.
>
> > > You 'determined' that HOW, exactly ?
>
> > > Oh, right - your pathological need for a Magical Sky Pixie/External
> > > Intelligence to exist so you can justify your posturing arrogance
> > > leads you to decree that all sorts of things can't happen inside of
> > > 'zillions of years'.
>
> > > And you've 'considered' the mutational differences needed to cross the
> > > gaps ? Or did you just invoke your simpering numerology and
> > > 'calculate' the odds of an eye falling together all at once PURELY by
> > > chance (like you always do), decree that the odds are too high, then
> > > just drop to your knees and start gibbering about Magical Sky Pixies/
> > > Intelligent Designers (like you always do) ? Or just your nigh
As I've already explained, you're misquoting my argument and your own
numbers are not based on systems that have minimum structural
threshold requirements of at least 100 fairly specified amino acid
residues. Your numbers are based on any functional system that uses
100aa of less regardless of any level of sequence specificity. That's
a very big difference in functional complexity.
> Given that your model is off by over 100 orders of magnitude for even
> the simplest and smallest proteins, WHY should anyone take your model
> seriously ?
You aren't actually evaluating *levels* of functional complexity
here. You're lumping all levels that use less than 100aa into one
category.
> Oh, right - negative argumentation ! If you can burn enough evo-
> strawmen, your 'model' will be accepted as valid without you needing
> to DEMONSTRATE that it is actually better. Or relevant. Or conforms
> to reality.
>
> WHY are your numbers so high ? Because they are calculated as falling
> together all at once PURELY by chance to match one predetermined
> sequence (hence the 'odds of THIS sequence arising goes as 1/20^N').
> As this is not representative of evolution in any way, your model doth
> suck.
You're mistaken. My model producing a calculation of the likely ratio
of beneficial vs. non-beneficial sequences at various levels of
functional complexity. You're model doesn't do this.
> That exponential bloating of the 'beneficial/non-beneficial ratio'
> that you CLAIMED made making 7-letter words near impossible (as well
> as pretty much everything else) only happens if the non-beneficials
> are not removed each generation; in other words, pulling 7 Scrabble
> tiles out of a hat and having them be a valid word.
I've never drawn the line of essential impossibility at 7-character
sequences within any language system. I've specifically drawn the
line at systems that require at least1000-characters where there is
also a fairly degree of minimum specificity.
> The only way to bloat the ratio is to NOT remove non-beneficial
> sequences from the pool. Generally don't see non-beneficial sequences
> staying in a population for very long for more realistic simulations
> of evolution.
>
> Oh, wait - your entire 'argument' is based on that silly bloating of
> the 'beneficial/non-beneficial' ratio, isn't it ?
>
> > Why do you keep posting your nonsense about enzymatic cascades when
> > I've explained them to you dozens of times?
>
> Because you keep posting your nonsense about how it is so
> 'IMPROBABLE !!!!!!!' for anything to evolve when your math is
> obviously crap, based on many erroneous ideas.
>
> You've blubbered, blithered, waved your hands and screamed, but you've
> NEVER explained WHY a three protein cascade does not qualify (you have
> yet to JUSTIFY that your 'conditions' are relevant).
>
> Once again, simpleton : for atrazine degradation, there is NO FUNCTION
> until ALL PROTEINS ARE THERE. Your math does not differentiate
> between 1 1200 aa, 3 400 aa or 6 200 amino acid proteins. Mainly
> because such a consideration is irrelevant.
>
> Initiating standard howling :
Do you not understand the concept of specificity? The proteins in
this cascade example you've listed do not require specific orientation
relative to each other. This system is therefore not specified with
regard to the arrangement of its parts. That means that it is no more
complex that the part of the system that is actually specified.
As I've explained to you dozens of times, it is far more likely to
roll triple sixes at least five times at some point in 100 rolls of
three dice compared to the odds of rolling triple sixes five times in
a row given 100 rolls of the three dice. Specificity of arrangement
makes all the difference when it comes to the odds of finding a
particular sequence or system.
> > - that their parts are not
> > specified in arrangement and are therefore no more complex than their
> > most specified single protein part?
>
> Once again, simpleton : THERE IS NO SELECTABLE FUNCTION UNTIL ALL
> THREE PROTEINS ARE PRESENT.
In any arrangement . . . not specified.
> 'Arrangment' is one of your standard crimson whales you vomit up to
> evade the FACT that cascades do qualify (and thus refute your silly
> 'there are no examples of 1000fsaar systems arising').
How do cascades qualify for the requirement that there be a fair
degree of specificity for the system?
> Who 'specifies' the arrangement ? Are you seriously DERANGED enough
> to 'think' the 'specification' exists OUTSIDE of the system, and had
> to be imposed upon it ?
The system itself defines its own need for specificity. A flagellar
system would not work at all unless all of its parts both exist at the
same time and are also specifically arranged relative to each other at
the same time. Both features are required. Simply having all your
parts exist doesn't qualify them as being specifically arranged.
> Arrangement is amenable to selection - if sticking together a certain
> way helped, that configuration would become more common.
That's right.
> Thus your
> blubbering 'THEY NOT CONFORM TO *MY* SPECIFICATIONS, THEREFORE THEY
> NOT COUNT !!' evasion can be ignored.
What are you talking about? Some systems will not work unless all of
their parts are specifically arranged. Not all systems are like
this. Cascading systems are not likely this. And, therefore, they
aren't high level systems compared to those systems that do have this
requirement for the specific arrangement of all of their protein
parts.
> If there was no atrazine degradation until AtzA stuck to AtzB a
> certain way in the presence of AtzC, the FACT that atrazine
> degradation arose would MEAN that AtzA stuck to AtzB the 'correct' way
> to generate the observed function; your 'specification' was derived
> AFTER THE FACT.
The enzymes in your cascade work sequentially on the substraight.
They are not required to be in specific arrangement with the other
enzymes in the cascade to produce their collective function.
> Which seems to be a serious problem with you - your 'math' PRESUMES
> that the sequences observed today were the 'target' of evolution, and
> they had to be found by random search (again, the only way to get
> numbers as large as you like throwing around). Generally NOT a good
> idea to calculate the 'odds' of something happening after it happened
> - it makes even the most mundane events look near impossible.
>
> Ex : a raindrop lands on the end of your nose. The odds of THAT
> particular drop hitting YOU in THAT particular place at that
> particular time are astronomical; would you then conclude it was
> guided by an External Intelligence ?
>
> You ARE aware that organ development is done via CASCADES, right ?
> That most of the proteins in the DEVELOPMENTAL CASCADES are small, do
> NOT stick to others in 'specified' ways for long ?
>
> Which means that - by your own mewlings - development is fully
> explainable by evolution, since all the players are small enough to
> evolve !
It is the final product that is important here. The odds of this
product being put together where all of its parts are required to be
in a specific arrangement relative to all the other parts become more
and more remote, exponentially so, with each increase in the minimum
structural threshold requirements - which include specificity.
I tell you what, explain to me why cascading systems can evolve in
observable time but no specified system of equivalent size has ever
been observed to evolve? Why might that be - do you think? Do you
have an explanation for this observation?
Sean Pitman
www.DetectingDesign.com
Seanpit
> On May 5, 5:44 pm, Seanpit <sean...@gmail.com> wrote:
>
> (snip)
>
> > the TTSS system which only uses 10 of the 40 or so
> > proteins of the flagellar system and from which the TTSS system is
> > derived (not the other way around).
>
> You do seem to be the only person saying so . . . .
>
> Nevertheless, you never answered my simple question:
>
> How did this portion of the flagellum manage to get unattached from a
> bacterium's ass and get incorporated into an utterly novel structure
> with an utterly unrelated function? How did the appearence of that
> utterly new novel complex function, from parts of an uterly different
> unrelated system, manage to beat your astronomical mathy statisticy
> probability odds, Sean?
>
> I'd tell you to be careful how you answer that, Sean --- but the
> simple fact that you repeatedly WON'T answer it indicates to me that
> you already know the big oozing sticky tarpit that it opens up for
> you . . . . . . . . .
I've already answered this for you many times Lenny. Why not actually
respond to my answers instead of repeating this very same question as
if I've never responded to it dozens of times before?
Again, the answer is that it is much much easier to remove parts and
maintain the function of an intact pre-formed subsystem structure than
to go the other way around. It is easy to maintain the function of a
car's radio even though the engine and drive shaft are removed. The
very same thing is true of the TTSS system. It is very easy to remove
the parts of the higher level system, one at a time, and still
maintain the function of the underlying system as a toxin injector.
In fact, Kenneth Miller has argued that the flagellar system itself
can function as a toxin injector as well.
> You are a bullshitter, Sean. Nothing more, nothing less, nothing
> else.
>
> And the fact that you refuse to answer this simple question, indicates
> to me that you KNOW you are just bullshitting.
>
> ================================================
> Lenny Flank
> "There are no loose threads in the web of life"
>
> Editor, Red and Black Publishershttp://www.RedandBlackPublishers.com
Sean Pitman
www.DetectingDesign.com
Seanpit
> On Tue, 5 May 2009 15:15:09 -0700 (PDT), Seanpit <sean...@gmail.com>
Yes yes, the standard "infinite regress" argument. The fact of the
matter is that SETI scientists don't have to know the origin of their
proposed ETIs before they can adequately propose the need for
intelligent input to explain their artifactual radio signals. You
simply don't have to answer the question of "Who made the designer?"
before you can detect the need for ID.
Beyond this, mainstream scientists also have the same infinite regress
problem. Where did the first material come from? What made the big
bang? No one knows. And, no one has to know in order to know, with a
very high degree of predictive power, that regardless of where matter
or the first designer came from, higher level functional information
is not produced in this universe without the outside input of even
higher level functional information.
> See? We've already made more progress than Behe has had in a decade. By
> process of elimination we seem to be left with robots or supernatural
> beings, though you may want to suggest other possibilities. If time
> travel is involved, do you see any paradoxes?
There's always paradoxes in science because of the problem that
science is only useful when there is limited information - and
therefore apparent paradoxes.
> >Now, what about your just-so stories? Come up with any statistical
> >analysis or predictive value to back them up yet? Where is your
> >*science*?
>
> Nah. If I'm going to be an intelligent design theorist, I have to give
> up those fairytales about organisms being descended from similar
> ancestors. So, do you think every species is independently created? Have
> you determined a list of molecules and molecular systems that couldn't
> have evolved? If so, where can I get it? I appreciate any help you can
> give.
I've already given you examples of higher level systems. Others
include ATPase, transcription and translation, amoeboid movement, the
function of various organells, and ultimately entire multicellular
organ systems and organisms - anything that requires more than 1000
fsaar working together at the same time.
> NAS
Sean Pitman
www.DetectingDesign.com
'Rev Dr' Lenny Flank
> On May 5, 3:56 pm, "'Rev Dr' Lenny Flank" <lfl...@yahoo.com> wrote:
>
>
>
>
>
> > On May 5, 5:44 pm, Seanpit <sean...@gmail.com> wrote:
>
> > (snip)
>
> > > the TTSS system which only uses 10 of the 40 or so
> > > proteins of the flagellar system and from which the TTSS system is
> > > derived (not the other way around).
>
> > You do seem to be the only person saying so . . . .
By the way, is this just another example of everybody else
misunderstanding you and failing to grasp your argument . . . ?
(snicker) (giggle)
>
> > Nevertheless, you never answered my simple question:
>
> > How did this portion of the flagellum manage to get unattached from a
> > bacterium's ass and get incorporated into an utterly novel structure
> > with an utterly unrelated function? How did the appearence of that
> > utterly new novel complex function, from parts of an uterly different
> > unrelated system, manage to beat your astronomical mathy statisticy
> > probability odds, Sean?
>
> > I'd tell you to be careful how you answer that, Sean --- but the
> > simple fact that you repeatedly WON'T answer it indicates to me that
> > you already know the big oozing sticky tarpit that it opens up for
> > you . . . . . . . . .
>
> I've already answered this for you many times Lenny.
No you haven't. You evaded it. Which you will now do again . . . .
> Again, the answer is that it is much much easier to remove parts and
> maintain the function of an intact pre-formed subsystem structure than
> to go the other way around.
But my dear Sean, taking a piece of a cellular secretory system and
using it as a bacterial tail, or vice versa, is NOT "maintaining the
function of an intact pre-formed subsystem". They are two entirely
different structures with two entirely different functions.
But you already knew that, didn't you . . . . .
>It is easy to maintain the function of a
> car's radio even though the engine and drive shaft are removed.
But my dear Sean, this is NOT a matter of simply removing a car's
engine and drive shaft and finding a car radio left. It is a matter
of taking a car part out of the car and using it as a part in an
AIRPLANE instead.
But of course, you already knew that.
> The
> very same thing is true of the TTSS system. It is very easy to remove
> the parts of the higher level system, one at a time, and still
> maintain the function of the underlying system as a toxin injector.
But my dear Sean, a "toxin injector" is NOT the same thing as a
cellular motility tail. It is a NOVEL FUNCTION, Sean. One that
didn't exist before. And it was made by taking a piece out of
something totally unrelated that already existed, and modifying it for
a new purpose.
Hmmmm . . . do you think this might have some, I dunno, applicability
to the assembly of larger complex structures from smaller pre-existing
units . . . . . ?
Another question for you to evade, Sean --- since the secretory system
has parts that are not found in the flagellum, and since the flagellum
has parts that are not found in the secretory system -- no matter
WHICH formed from which, the question remains ------------> where did
the rest of the parts come from? How'd they get there, Sean?
Careful how you answer that, Sean . . . IF you answer it . . . . .
> In fact, Kenneth Miller has argued that the flagellar system itself
> can function as a toxin injector as well.
>
And a mousetrap spring can function as a tie clip very well, too.
I can use a rock as a pretty good imitation of a hammer, too.
Indeed, Sean, THAT IS EXACTLY HOW EVOLUTION WORKS. It takes bits and
pieces out of unrelated things and cobbles them together in whatever
way happens to get the job done. Does it need to be perfect? Nope.
It just needs to work "good enough".
Exactly like (as yolu say) your flagellum got taken off of some
bacterium's ass and (according to your, uh, singular hypothesis) was
modified to serve as a part of an excretary apparatus--an utterly
novel complex system with an utterly novel function.
Notice that the secretory apparatus did NOT, repeat NOT, as in N-O-T,
appear by being assembled all at once from single fs-whatever units
like a 747 being made in a junkyard from spare parts by a tornado.
Which means that your entire mathy sciencey argument is . . .
well . . . bullshit. And you yourself have pointed out why it's
bullshit.
> > You are a bullshitter, Sean. Nothing more, nothing less, nothing
> > else.
>
> > And the fact that you refuse to answer this simple question, indicates
> > to me that you KNOW you are just bullshitting.
>
Just as does the fact that you simply evaded it yet again with more
arm-waving.
NA Sides
wrote:
>On May 5, 4:20 pm, NA Sides <nongo1...@sonic.net> wrote:
Are you saying I can make inferences about the designer(s)? If so, you
must have spotted a flaw in my logic. Using your own claims, I logically
concluded that designer(s) can't have been naturally evolved biological
organisms. If you see a flaw, what is it? Or are you claiming that I
can't legitimately apply logical reasoning to draw such inferences? If
so, what prohibits me from doing so?
>Beyond this, mainstream scientists also have the same infinite regress
>problem. Where did the first material come from? What made the big
>bang? No one knows. And, no one has to know in order to know, with a
>very high degree of predictive power, that regardless of where matter
>or the first designer came from, higher level functional information
>is not produced in this universe without the outside input of even
>higher level functional information.
That's irrelevant to my own particular study of the designer(s)' nature.
I merely eliminated one possibility as to who the designer might be. Do
you doubt that I've done this? If so, what leads you to think my
inference is false? You shouldn't discourage me in this, you know. I'm
the first intelligent design theorist to scientifically investigate the
nature of the designer. You can criticize my logic or you can criticize
the claim that evolution of novel functional systems that require at
least 1000 fsaars. Since it was initially your own claim, I don't think
you're going to take the second course. Are you going to respond at all?
Are you going to help me in my sincere attempt to narrow down the
possibilities as to who or what the intelligent designer could be?
>> See? We've already made more progress than Behe has had in a decade. By
>> process of elimination we seem to be left with robots or supernatural
>> beings, though you may want to suggest other possibilities. If time
>> travel is involved, do you see any paradoxes?
>
>There's always paradoxes in science because of the problem that
>science is only useful when there is limited information - and
>therefore apparent paradoxes.
You forgot to say whether you think time travel might have been
involved, but you seem to be implying that it's a viable possibility and
that any paradoxes will be only apparent. Do you think the intelligent
designers could have been time travelers?
>> >Now, what about your just-so stories? Come up with any statistical
>> >analysis or predictive value to back them up yet? Where is your
>> >*science*?
>>
>> Nah. If I'm going to be an intelligent design theorist, I have to give
>> up those fairytales about organisms being descended from similar
>> ancestors. So, do you think every species is independently created? Have
>> you determined a list of molecules and molecular systems that couldn't
>> have evolved? If so, where can I get it? I appreciate any help you can
>> give.
>
>I've already given you examples of higher level systems. Others
>include ATPase, transcription and translation, amoeboid movement, the
>function of various organells, and ultimately entire multicellular
>organ systems and organisms - anything that requires more than 1000
>fsaar working together at the same time.
Roger. Got it. Just one more question for now. Do you believe that all
species were created at once, or is it more likely that the process
occurred over a period of billions of years? Thanks for all your help!
>
>> NAS
>
>Sean Pitman
>www.DetectingDesign.com
Perplexed in Peoria
> On May 5, 11:35 am, "Perplexed in Peoria" wrote:
> > "Seanpit" <sean...@gmail.com> wrote:
>
> > > ...A combination of domain modules does in fact explore
> > > a larger sequence space and has the potential to land upon a system
> > > that is on a higher level of functional complexity - i.e., a system
> > > with greater minimum size and specificity requirements. It is just
> > > the odds of such a combination landing upon a lower level system. The
> > > reason for this is due to the exponentially reduced ratio of higher
> > > level vs. lower level systems in sequence space.
> >
> > Correct me if I am wrong, Sean, but it seems to me that you are saying
> > that the odds of hitting, say, a minimal flagellum are smaller than the
> > odds of hitting, say, cytochrome C (but a bloated variant of cytochrome
> > C which is much larger than it absolutely needs to be).
> > Is this what you are saying, Sean?
>
> Yes - that's exactly what I'm saying.
>
> > And if so, why is it relevant?
>
> Because, the odds of finding lower level functional systems are much
> greater than the odds of finding higher level systems due to the
> difference in the ratios of one compared to the other within sequence
> space.
You are not making sense, Sean. The odds of finding nothing at all
are even greater yet. We are already calculating and dealing with
the fact that the odds are small of finding something big and useful.
The fact that the odds of finding something else are larger is totally
irrelevant. We are looking for the plausibility that one organism
in a big population over a long period of time comes up with the
'right' mutation. What all of the other organisms are coming up with
just doesn't matter in this argument.
R. Baldwin
news:8abe10fd-76c7-4c60...@v1g2000prd.googlegroups.com:
> On May 5, 12:04�am, "R. Baldwin" <res0k...@nozirevBACKWARDS.net>
> wrote:
>> Seanpit <sean...@gmail.com> wrote
>> innews:47c29c43-bfe4-4c16-838c-7b1423e7
> 04...@f41g2000pra.googlegroups.com:
>>
>>
>>
>>
>>
>> > Regarding the following paper by David Dryden:
>>
>> >http://rsif.royalsocietypublishing.org/content/5/25/953.long
>>
>> [snip]
>>
>> >> I am probably going to write far too much but if you want the
>> >> conclusion, it is that Sean Pitman is completely and utterly wrong
>> >> in everything he says in his comments and displays a great
>> >> ignorance of proteins and their structure and function. However, I
>> >> do hope he will read on.
>>
>> > I think you simply don't understand my argument, or the nature of
>> > the concept of increasing levels of functional complexity. �It
>> > seems like your understanding of functional complexity is based on
>> > how interesting you think the function in question is. �My
>> > definition of functional complexity, in comparison, is not based on
>> > how interesting various systems may or may not be, but in the
>> > minimum structural threshold requirements needed to build a system
>> > so that it will work to at a selectable level of usefulness.
>>
>> It seemed clear that Dryden understood and dismissed your argument as
>> vacuous. ORFs reach a "selectable level of usefulness" at far shorter
>> lengths than 1000 aa.
>
> Of course, that is because they don't have a minimum structural
> threshold requirement that is greater than 1000 fsaars. That is why
> they are in fact on a lower level of functional complexity.
>
> How do you not understand this concept? The definition of a level of
> functional complexity is defined as the *minimum* structural threshold
> requirement for a system to work. If you find that the minimum
> requirement for a particular system is far less than 1000 fsaars, then
> that system is on a far low level of functional complexity.
Yes, I understand that is how you have defined this term. I do not agree
that your definition constrains reality, or even has anything to do with
reality. I also do not agree that biologists recognize or use this term,
or that any research has been conducted to verify its correspondence
with reality. It is your own peculiar definition, created out of your
own imagination.
>
> Your argument here makes it very clear that both you and Dryden
> misunderstand the very concept of levels of functional complexity.
> You just don't get it - even after all of this time. Yet, it is such
> a simple concept. How is it that you cannot seem to grasp it?
>
I disagree that you have established any relationship between sequence
length and structural complexity.
>> Since there is no goal, there is no minimum
>> structural threshold to worry about. A flagellar motility system
>> isn't a goal. It just happens to be where things ended up for a
>> particular genome. A sequence either does something biologically
>> interesting, or it doesn't. Your functional complexity concept is
>> meaningless.
>
> There is a goal for evolutionary progress - and that is to actually
> find novel beneficial systems.
No, that is not a goal. That is just what results.
> If the system in question has a very
> low minimum structural threshold requirement it is exponentially more
> likely to be found vs. a system that has a higher minimum structural
> threshold requirement. That is why single protein enzymes which
> require no more than a few hundred fairly specified amino acid
> residues are found all the time by RM/NS. Yet, no system, to include
> multi-protein systems, which have more than a 1000 fsaar minimum
> structural threshold requirement are ever found by RM/NS - regardless
> of the starting points within any gene pool you wish to consider. It
> just doesn't happen, has never happened, and statistically is
> extremely unlikely to happen this side of trillions of years of
> time.
This is simply an assertion you keep making without evidence. Your math
is not based on reality, so there is no reason to accept your
conclusion.
>
>> >> He has failed to recognise that we wished to establish limits on
>> >> the amount of sequence space explored.
>>
>> > But I do recognize and even agree with your estimates on the limits
>> > of the amount of sequence space that can be explored over a given
>> > time limit. �But that isn't the main problem here. �The main
>> > problem is
> how
>> > much time it takes to actually find novel beneficial sequences that
>> > go beyond the very very low levels of minimum structural threshold
>> > requirements noted in your paper. �You only deal with systems that
>> > have, at minimum, very very low level structural thershold
>> > requirements - less than 100aa or "characters" at minimum.
>>
>> If you paid attention to his explanation, you would understand why
>> systems having short sequences sufficient.You should have focused on
>> "Nature takes the domain modules and puts them together to make novel
>> structures and functions," and contemplated what that means with
>> respect to your model. Evolution is not exploring a space the size of
>> 20^N when combining domain modules. You should consider the subspace
>> defined by the combinations of domain modules.
>
> You're mistaken. A combination of domain modules does in fact explore
> a larger sequence space and has the potential to land upon a system
> that is on a higher level of functional complexity - i.e., a system
> with greater minimum size and specificity requirements. It is just
> that the odds of this actually happening are exponentially lower than
> the odds of such a combination landing upon a lower level system. The
> reason for this is due to the exponentially reduced ratio of higher
> level vs. lower level system in sequence space.
>
No, the odds are not exponentially lower, and they are unrelated to the
ratio of "higher level vs. lower level system in sequence space." If
sequences of domain modules are concatenated (fused), the sequence
length does not matter. A rich complexity is accessible with a small
number of mutations.
>> >> �It is very important
>> >> to note that in many cases such folding does not require complete
>> >> specification of the sequence but only maintenance of the pattern
>> >> of amino acid categories (polar, non-polar etc). Many domains do
>> >> interesting things but a recurring theme is to then bring
>> >> collections of the domains together either as separate subunits to
>> >> form quaternary structure or to string them together into one
>> >> single chain by making them via a single gene. This latter process
>> >> is how one makes a 1000 amino acid protein. Nature takes the
>> >> domain modules and puts them together to make novel structures and
>> >> functions. (Note that very few long protein chains are found as
>> >> their synthesis is tricky due to increasing chances of errors in
>> >> gene replication, transcription or translation. These problems
>> >> were recognised by Francis Crick if I recall correctly in the
>> >> 1960�s. The average protein size is around 500 amino acids.) The
>> >> number of domains with unique folds appears to be limited to
>> >> around 1000 to 10,000 (certainly less than a million) and it is
>> >> becoming rare for science to find new ones. This means that
>> >> whatever sequence you have, you get one of these folds
>>
>> > Good so far.
>>
>> >> (but note that
>> >> there is a relatively new discovery of �natively-unfolded� protein
> s
>> >> which are unfolded until they bind to their target molecule at
>> >> which point they fold up. How much of sequence space is occupied
>> >> by these fully functional proteins is unknown).
>>
>> > While it is true that the exact ratio of functional vs.
>> > non-functional proteins is not known, an upper limit on the ratio
>> > can be determined to a useful degree of certainty based on the idea
>> > that the vast majority of potential protein folds are not stable
>> > and therefore would not make viable proteins. �This ratio of
>> > potentially viable vs. non- viable folds decreases exponentially
>> > with each increase in the size of the protein sequence under
>> > consideration.
>>
>> How many non-stable sequences do you really need to worry about if
>> you are combining stable domain modules to form a larger stable
>> sequence? �
>
> I've already explained to you that the vast majority of possible
> combinations of stable domains will be unstable. How do you not grasp
> this concept? It is like trying to randomly combine meaningful words
> and phrases and expecting the majority of combinations to be
> meaningfully beneficial as well. That's a ludicrous assumption and is
> demonstrably false when it comes to protein combinations.
You have asserted that, not explained it. If you fuse two stable
sequences, why would the result be unstable?
>
>> >> The number of protein types in
>> >> any organism also appears to be very limited from several hundred
>> >> in the bacteria with very small genomes to perhaps of the order of
>> >> 10,000 in multicellular organisms. These proteins still contain
>> >> the same domains. These limited numbers of proteins perform a
>> >> limited number of reactions (again totalling hundreds to thousands
>> >> of such reactions as detailed in standard biochemistry textbooks).
>> >> The important thing to produce different species is how all these
>> >> reactions are controlled (mostly) by proteins each built using the
>> >> same structural principles as already detailed. This area of
>> >> control is often referred to as part of EvoDevo or evolutionary
>> >> development and it is where the real discussions of complexity are
>> >> going on. That�s not my speciality so I will return now to
>> >> proteins.
>>
>> > So far so good . . .
>>
>> >> Hopefully it is clear that we have considerable understanding of
>> >> protein structure and how they function and that they are not so
>> >> complex that we cannot possibly explain them (and even design them
>> >> ourselves. David S Goodsell has published an excellent book on
>> >> �Bionanotechnology� showing what Nature has achieved and how our
>> >> understanding of it lets us design new experiments). We could if
>> >> we wished define a structural space and a functional space in the
>> >> same way as a sequence space. From the foregoing, it should be
>> >> clear that neither of these spaces is particularly large when
>> >> compared to the possible size of sequence space.
>>
>> > This is because you are only dealing with sequence spaces for
>> > protein- based systems that are made up of single proteins - and
>> > small ones at that. �The real problems come when you start
>> > considering multi-protei
> n
>> > systems where all the protein parts, and therefore all of their
>> > individual residues, are required to be in a fairly specific
>> > arrangement relative to each other at the same time for the
>> > function in question to be realized.
>>
>> Who cares about the "function in question"? There IS no function in
>> question. An ensemble of proteins either has a combined function, or
>> not. This teleological goal of finding a particular function exists
>> only in your mind.
>
> It is not a teleological goal as far as a specific type of function is
> concerned. However, if no novel functionally beneficial sequences are
> ever discovered by RM/NS evolution does not occur. While it is true
> that evolution doesn't have to occur at any level of functional
> complexity, that isn't the issue. The issue is what it takes for
> evolution to occur at various levels of functional complexity - what
> are the odds? What is the predicted time that it should take to find
> any type of functional system at any given *level* of functional
> complexity. That's the question here.
Your "levels of functional complexity" are meaningless and not founded
in reality.
>
>> >> Given the small sizes of the spaces of domain structure, chemical
>> >> reactivity, and biochemical function, or perhaps I could refer to
>> >> them as toolboxes, it does not seem to be too much of a guess that
>> >> the last common ancestor of all life on earth would be equipped
>> >> with all of these toolboxes. This is why we decided to determine
>> >> the limits of use of these toolboxes and calculate the upper and
>> >> lower limits starting from way back in time. The tools may not
>> >> have been fully utilised or explored by that stage (or even by
>> >> bacteria today), but later when multicellular organisms appeared,
>> >> these tools were ready to be used and even reconfigured.
>>
>> >> So we return to the problem of how big is sequence space? It is
>> >> not 20 raised to the power of the number of amino acids in the
>> >> sequence but much less as we discussed in our paper. There is no
>> >> need to have 20 different types of amino acid each with unique
>> >> properties or sequence lengths greater than around 100. This is
>> >> due to the physical similarities between amino acids and the
>> >> limited range of folded structures. Only a few amino acids in any
>> >> protein are crucial for its function. Changing these ones will
>> >> sometimes do almost nothing to the function. However, some will
>> >> change the function to something new while maintaining structure,
>> >> and a very few will change the protein structure (and hence its
>> >> original function) altogether but in all probability still confer
>> >> a new function. Even if the original structure is destroyed by a
>> >> mutation and the protein does not fold, the possibility of a new
>> >> function is not lost as evidenced by the discovery of natively
>> >> unfolded proteins which acquire fold and function upon binding to
>> >> a target.
>>
>> > It is very clear that protein-based systems do indeed contain a
>> > degree of flexibility where many mutations can be tolerated without
>> > a significant loss of the function in question. �It is also agreed
>> > that a smaller alphabet of amino acids would be able to do the job.
>> > However, there are several problems with the assumptions behind
>> > this argument. �One problem is the assumption that the minimum size
>> > requirement for a system would not increase given a smaller
>> > alphabet. One might be able to build a flagellar motility system
>> > with an alphabet of only two characters, but most likely the system
>> > would require far more characters, at minimum, than if a
>> > 20-character alphabet were used.
>>
>> You seem to have made an assumption that most of the characters in
>> the sequence are contributing to what the function of the protein
>> actually is. Otherwise, you could easily accept Dryden's explanation
>> which is based on what the molecles are actually doing. What is the
>> basis for your assumption? WHY do you believe that all those
>> characters are vital?
>
> Most of the characters in the sequence are contributing to at least
> some degree. That's a fact. This is the reason why that each
> additional character change that is realized at the same time produces
> an exponentially increased risk of a total loss of functionality of
> the system in question.
If this is a fact, where is the fact in evidence? Please provide the
cites.
Spil...@gmx.net
Please read carefully. I wrote: "...there never was a designer *under
the
premises of the design argument*..."
Yes, humans exist. Yes, humans design things. Yet, from the premise of
the design argument - namely the claim, that complex life cannot
result from undirected processes - follows, as I have shown, that
humans don't exist. This is an obvious contradiction.
Conclusion: The premise of the design argument is false.
I'm not talking about the "ultimate origin of all things". I'm talking
about the possible ultimate origin of the first designer, a discrete
event in time and space well after the big bang, after the first
habitable planet was formed. There's nothing fundamentally unknowable
about that, and nothing that is unassessable by logic. Furthermore I'm
not talking about who or what designed the designers, apart from the
fact that they have to be designed in order to exist, according to the
premises of the design argument. And if they are designed, they
logically have to have a desiner, and so on, which leads you to the
paradoxical situation, that you need a first designer, but the first
designer needs a designer himself because he cannot have come to be on
his own, according to the premise, and hence isn't the first designer.
I'm only talking about points, that you yourself brought up, and
follow them through to see, if they are consistent. Unfortunately,
they are not.
Argument contra design:
http://newsgroups.derkeiler.com/Archive/Talk/talk.origins/2009-04/msg04103.html
If you find any flaw in my argumentation, please show, where I am
wrong.
Best regards,
Lark
Burkhard
But SETI, as far as I know, does not evoke your "law of information
preservation" which is at the heart of your infinite regress, so it
only applies to you, not them.
Perplexed in Peoria
> I'm not talking about the "ultimate origin of all things". I'm talking
> about the possible ultimate origin of the first designer, a discrete
> event in time and space well after the big bang, after the first
> habitable planet was formed. There's nothing fundamentally unknowable
> about that, and nothing that is unassessable by logic. Furthermore I'm
> not talking about who or what designed the designers, apart from the
> fact that they have to be designed in order to exist, according to the
> logically have to have a desiner, and so on, which leads you to the
> paradoxical situation, that you need a first designer, but the first
> designer needs a designer himself because he cannot have come to be on
Hmmm. I'm not sure there is a contradiction.
Observation: Complex things exist.
Premise: Complex things require an Intelligent Designer.
Conclusion: An Intelligent Designer exists.
Hypothesis: The Intelligent Designer is itself designed.
Failure: You can't prove that unless you know the Intelligent
Designer is complex:
Ok, then try this:
Observation: All known intelligent things are complex.
Hypothesis: The Intelligent Designer is complex
Failure: You can't prove that because the Intelligent Designer
is not a *known* intelligent thing.
The best you can do with the "Who designed the Designer?"
ploy is to show that the hypothetical Designer must be very
different from anything we have experience of.
Of course, there is something very suspicious about the
idea of using logic and experience to prove the existence
of something which we have no experience of.
Burkhard
wrote:
That would be a way out (I had suggested on another tread an
intelligent blue shadow that does not have anything like DNA), but
only I think if Sean drops his "law of information preservation" which
is an additional constraint.
Steven L.
> On 5 Mai, 22:49, Seanpit <sean...@gmail.com> wrote:
>> On May 5, 11:44 am, "Steven L." <sdlit...@earthlink.net> wrote:
> [snip]
>>> Then I don't understand what your alternative theory is: If evolution
>>> of species has never occurred, then are you suggesting that an
>>> Intelligent Agency or Intelligent Designer had intervened to produce
>>> each and every one of the millions of species that have existed on
>>> Earth? Each and every one is a special creation by this Intelligence?
>> I think the definition for "species" is too subjective. However, I
>> will say that every single qualitatively unique beneficial system of
>> function that requires more than 1000 fsaars was the result of
>> deliberate design.
>>
>>> Indeed, your focus on the bacterial flagellum suggests that you believe
>>> that every *structure* of every life form had to be specially designed.
>> That's right.
>>
>>> So the Intelligent Designer is keeping pretty busy: He has to sculpt
>>> every nucleus, every cilium, every flagellum, every ribosome, of every
>>> type of cell of every life form that ever existed. Is THAT what you're
>>> arguing for????
>> Yes . . .
> [snip]
>
> Your idea has just a little flaw. For it to work there has to be a
> designer. If it is shown (as I have done) that there never was a
> designer under the premises of the design argument, then your idea is
> falsified.
Really? Point me in the direction of that proof, please.
--
Steven L.
Email: sdli...@earthlinkNOSPAM.net
Remove the NOSPAM before replying to me.
Steven L.
> On May 5, 11:52 am, "Steven L." <sdlit...@earthlink.net> wrote:
>>>> Your arguments have been obliterated by someone who
>>>> unlike you has the training and the talent to do the
>>>> math. You aren't going to restore your arguments by
>>>> just repeating more loudly and unchanged.
>>> First off, why do you highlight every single one of your posts by
>>> changing the topic heading? It is very annoying . . .
>>> Beyond this, where is your own definition of levels of functional
>>> complexity?
>> I agree with you that there are levels of complexity in the
>> functionality of any complex system. But where I part company with you
>> is your assumption that higher levels of functional complexity require
>> larger structural changes (and hence many more mutations). Not
>> necessarily. It all depends on how the system is structured.
>>
>> It doesn't take a big structural change to produce a qualitative
>> functional change. In the case of the bacterial flagellum, only a few
>> molecular "tweaks" change it from spinning to a back-and-forth motion,
>> and a few more "tweaks" leave it completely inoperative. That's been
>> proven already.
>
> It is easy to produce a quantitative loss of function with a few very
> small mutational "tweaks". That's easy. It is also easy to
> quantitatively improve a particular type of function once it is
> realized to at least some level of selectable benefit. What is not so
> easy is to discover a qualitatively novel beneficial functional system
> via random mutations.
And thereby hangs the tale.
This is the crux of the matter:
You think of the flagellum as a *qualitatively novel* function.
Yet you have no models, no theories, no metrics for deciding when one
function is more "qualitatively novel" than another.
As far as I can tell, you and the other ID proponents glommed onto the
spinning of the bacterial flagellum just because it looks cool. But
spinning is NOT a complex function; mathematically it's simple.
As Dryden explained, there are enzyme systems whose functionality is
qualitatively far more complex than spinning functionality.
Steven L.
>>>> functional change. In the case of the bacterial flagellum, only a few
>>>> molecular "tweaks" change it from spinning to a back-and-forth motion,
>>>> and a few more "tweaks" leave it completely inoperative. That's been
>>>> proven already.
>>> It is easy to produce a quantitative loss of function with a few very
>>> small mutational "tweaks". That's easy. It is also easy to
>>> quantitatively improve a particular type of function once it is
>>> realized to at least some level of selectable benefit. What is not so
>>> easy is to discover a qualitatively novel beneficial functional system
>>> via random mutations.
>> improvement of a function' vs a 'novel' function? is an eyespot better
>> than no eyespot?
>
> In certain environments - yes. An eyespot is better than no eyespot.
> However, the simplest beneficially functional eyespot is at a very
> high level of functional complexity.
The heart of the eyespot mechanism is a photoreceptor enzyme, which when
activated by certain wavelengths of light catalyzes ATP.
What makes this a "high level of functional complexity"? It's a
light-activated enzyme, that's all.
Spil...@gmx.net
Sure, that would be a way out. But Sean claims that information
ultimately flows downhill, see his "law of information preservation",
and additionally Sean takes the fact that humans, which are above
Seanpits complexity border of 1000 fsaars, "designed" an artificial
bacterium as evidence that it is possible for at least human-level
intelligence to design complex life forms. There is no evidence of
life forms that are completely below Seanpits border of 1000 fsaars
capable of designing other life forms. So that would hurt the design
argument, too.
Lark
Spil...@gmx.net
> Remove the NOSPAM before replying to me.
Sure: http://newsgroups.derkeiler.com/Archive/Talk/talk.origins/2009-04/msg04103.html
Lark
Steven L.
Your argument is nonsense.
The Designer of life on Earth need not have been designed Himself.
Your assumption that every Designer must have been designed by some
other Designer is just false.
I can imagine other alternatives: A Designer that exists outside of
time and space of this Universe, for example. In which case it could
have always existed.
Or, the Designer of life on Earth itself arose from natural processes
elsewhere in this Universe, or in some other Universe.
--
Steven L.
Email: sdli...@earthlinkNOSPAM.net
Seanpit
Useful vision, as a function, isn't just the result of a single light-
activated enzyme. In short, you don't automatically gain vision if
you produce such an enzyme. Read my discussion of useful vision, even
of a single eyespot, on my website dealing with eye evolution.
> Steven L.
> Email: sdlit...@earthlinkNOSPAM.net
> Remove the NOSPAM before replying to me.
Sean Pitman
www.DetectingDesign.com
Seanpit
Sure I do. Compare a flagellar motility system with a lactase
enzymatic system. One is not simply a quantitatively different
function relative to the other. Simply adding increased lactase
activity to the lactase enzyme isn't going to get you flagellar
motility. Why not? Because there is a qualitative, not just a
quantitative, difference. This is an easy concept. Don't try to make
this difficult. It isn't.
> As far as I can tell, you and the other ID proponents glommed onto the
> spinning of the bacterial flagellum just because it looks cool. But
> spinning is NOT a complex function; mathematically it's simple.
Structurally, it isn't simple and it cannot be made to be simple when
it comes to useful rotary flagellar motility. All such systems would
require thousands of basic building blocks in specific arrangement to
be useful for this type of function.
> As Dryden explained, there are enzyme systems whose functionality is
> qualitatively far more complex than spinning functionality.
A small single protein enzyme is not structurally more complex when it
comes to its minimum structural threshold requirements. It therefore
occupies a much smaller sequences space, has an island footprint with
an exponentially higher ratio within sequence space, and is therefore
exponentially easier to find via a random search process within
sequence space.
Drydens assertion that such a simple enzyme is actually qualitatively
more complex is subjective nonsense. He has not actually defined what
it means to be functionally complex in any sort of scientific sense
that is usefully testable and measurable - and neither have you.
> Steven L.
> Email: sdlit...@earthlinkNOSPAM.net
> Remove the NOSPAM before replying to me.
Sean Pitman
www.DetectingDesign.com
Seanpit
wrote:
> "Seanpit" <sean...@gmail.com> wrote:
> > On May 5, 11:35 am, "Perplexed in Peoria" wrote:
> > > "Seanpit" <sean...@gmail.com> wrote:
>
> > > > ...A combination of domain modules does in fact explore
> > > > a larger sequence space and has the potential to land upon a system
> > > > that is on a higher level of functional complexity - i.e., a system
> > > > with greater minimum size and specificity requirements. It is just
> > > > that the odds of this actually happening are exponentially lower than
> > > > the odds of such a combination landing upon a lower level system. The
> > > > reason for this is due to the exponentially reduced ratio of higher
> > > > level vs. lower level systems in sequence space.
>
> > > Correct me if I am wrong, Sean, but it seems to me that you are saying
> > > that the odds of hitting, say, a minimal flagellum are smaller than the
> > > odds of hitting, say, cytochrome C (but a bloated variant of cytochrome
> > > C which is much larger than it absolutely needs to be).
> > > Is this what you are saying, Sean?
>
> > Yes - that's exactly what I'm saying.
>
> > > And if so, why is it relevant?
>
> > Because, the odds of finding lower level functional systems are much
> > greater than the odds of finding higher level systems due to the
> > difference in the ratios of one compared to the other within sequence
> > space.
>
> You are not making sense, Sean. The odds of finding nothing at all
> are even greater yet.
Absolutely. There are odds for finding nothing useful - which are
extremely good. Then there are odds for finding low level beneficial
systems and higher level beneficial functional systems. The odds are
different for each one of these levels. And, when it comes to the
odds of finding a beneficial sequence, the odds of finding a lower
level functional system are exponentially greater than the odds for
finding a higher level system.
> We are already calculating and dealing with
> the fact that the odds are small of finding something big and useful.
> The fact that the odds of finding something else are larger is totally
> irrelevant. We are looking for the plausibility that one organism
> in a big population over a long period of time comes up with the
> 'right' mutation. What all of the other organisms are coming up with
> just doesn't matter in this argument.
There are lots of "right" mutations PiP. Not all "right" mutation are
created equal. The odds that the "right" mutation or the discovered
beneficial target will be a lower level target are exponentially
greater than the odds that the beneficial target will actually be a
higher level target. This is true regardless of the gene pool of
starting points you choose - and regardless of the various levels of
functional complexity that already exist preformed within your chosen
gene pool of options or starting points.
Sean Pitman
www.DetectingDesign.com
Seanpit
>
> > Yes yes, the standard "infinite regress" argument. The fact of the
> > matter is that SETI scientists don't have to know the origin of their
> > proposed ETIs before they can adequately propose the need for
> > intelligent input to explain their artifactual radio signals. You
> > simply don't have to answer the question of "Who made the designer?"
> > before you can detect the need for ID.
>
> But SETI, as far as I know, does not evoke your "law of information
> preservation" which is at the heart of your infinite regress, so it
> only applies to you, not them.
SETI scientists do believe in the law of certain types of information
never being produced by systems with lower level informational
complexity. They do in fact believe that higher level outside
informational input was required. That is why they think themselves
able to detect the need or the requirement for at least human level
intelligent input to explain certain types of radio signals. If the
information needed to produce these types of signals could be derived
from lower level informationally inferior systems, like random weather
patterns and the like, the concept of SETI would be hopeless.
Sean Pitman
www.DetectingDesign.com
Seanpit
>
> Your argument is nonsense.
>
> The Designer of life on Earth need not have been designed Himself.
>
> Your assumption that every Designer must have been designed by some
> other Designer is just false.
>
> I can imagine other alternatives: A Designer that exists outside of
> time and space of this Universe, for example. In which case it could
> have always existed.
>
> Or, the Designer of life on Earth itself arose from natural processes
> elsewhere in this Universe, or in some other Universe.
Exactly. The "who made the maker" argument is futile and ultimately
irrelevant to the ability to detect the need for outside intelligent
or higher level informational input to explain certain types of
phenomena.
> Steven L.
> Email: sdlit...@earthlinkNOSPAM.net
> Remove the NOSPAM before replying to me.
Sean Pitman
www.DetectingDesign.com
Seanpit
No it's not. The flagellum can also function as a toxin injector,
just like the TTSS system. It is just that the TTSS system is cheaper
to maintain since it is less complex than the flagellar system. The
parts of the flagellar system can therefore be lost, one at a time,
while maintaining the toxin injector function the entire time.
Again, the TTSS system isn't novel in function or structure - both
existed at the time the fully formed flagellar motility system
existed.
> Notice that the secretory apparatus did NOT, repeat NOT, as in N-O-T,
> appear by being assembled all at once from single fs-whatever units
> like a 747 being made in a junkyard from spare parts by a tornado.
>
> Which means that your entire mathy sciencey argument is . . .
> well . . . bullshit. And you yourself have pointed out why it's
> bullshit.
The TTSS system, to include structure and function, existed from the
beginning. It isn't novel in any sense of the word except in the loss
of extra baggage that wasn't needed to produce the toxin injector
function in particular. It is less expensive to keep the injector
function and let the motility function go away given that the
nutritional needs of the organism can be adequately met in a given
environment without the motility system.
> > > You are a bullshitter, Sean. Nothing more, nothing less, nothing
> > > else.
>
> > > And the fact that you refuse to answer this simple question, indicates
> > > to me that you KNOW you are just bullshitting.
>
> Just as does the fact that you simply evaded it yet again with more
> arm-waving.
>
> ================================================
> Lenny Flank
> "There are no loose threads in the web of life"
>
Rodjk #613
Its futile because creationist like you have their heads too far up
their ass to hear anything.
Rodjk #613
'Rev Dr' Lenny Flank
Here, Sean, let me rem ind you one more time what an expert in the
field (which you are not) said wehen you presented him with this
blizzard of bullshit:
On May 2, 10:54 am, david.dry...@ed.ac.uk wrote:
"If you want the conclusion, it is that Sean Pitman is completely and
utterly wrong in everything he says in his comments and displays a
great ignorance of proteins and their structure and function."
Any questions, Sean . . . . . ?
'Rev Dr' Lenny Flank
Didn't read the part below, did you Sean.
Tell me, Sean, is a cellular excretory apparatus THE SAME THING as a
cellular motility tail?
Yes or no, Sean.
You are jsut bullshitting everyone again.
> > One that
> > didn't exist before. And it was made by taking a piece out of
> > something totally unrelated that already existed, and modifying it for
> > a new purpose.
>
> > Hmmmm . . . do you think this might have some, I dunno, applicability
> > to the assembly of larger complex structures from smaller pre-existing
> > units . . . . . ?
>
Well, Sean? Do you . . . . . ?
> > Another question for you to evade, Sean --- since the secretory system
> > has parts that are not found in the flagellum, and since the flagellum
> > has parts that are not found in the secretory system -- no matter
> > WHICH formed from which, the question remains ------------> where did
> > the rest of the parts come from? How'd they get there, Sean?
>
> > Careful how you answer that, Sean . . . IF you answer it . . . . .
And, surprise of all surprises, you didn't answer it. Color me
shocked. Shocked, I say.
No problem. I'll keep asking until you do.
>
> > > In fact, Kenneth Miller has argued that the flagellar system itself
> > > can function as a toxin injector as well.
>
> > And a mousetrap spring can function as a tie clip very well, too.
>
> > I can use a rock as a pretty good imitation of a hammer, too.
>
> > Indeed, Sean, THAT IS EXACTLY HOW EVOLUTION WORKS. It takes bits and
> > pieces out of unrelated things and cobbles them together in whatever
> > way happens to get the job done. Does it need to be perfect? Nope.
> > It just needs to work "good enough".
>
> > Exactly like (as yolu say) your flagellum got taken off of some
> > bacterium's ass and (according to your, uh, singular hypothesis) was
> > modified to serve as a part of an excretary apparatus--an utterly
> > novel complex system with an utterly novel function.
>
> Again, the TTSS system isn't novel in function or structure
Yes it is. It ain't a bacterial flagellum and it doesn't function as
one.
>- both
> existed at the time the fully formed flagellar motility system
> existed.
No shit, Sherlock.
The point is that they are DIFFERENT FUNCTIONS, and one was built by
using PARTS FROM A DIFFERENT FUNCTION. Exactly as I said (and you
ignored) above.
I don't think even YOU can be so obtuse as to not see that,m so I can
only conbclude that you are just bullshitting us again, Sean.
>
> > Notice that the secretory apparatus did NOT, repeat NOT, as in N-O-T,
> > appear by being assembled all at once from single fs-whatever units
> > like a 747 being made in a junkyard from spare parts by a tornado.
>
> > Which means that your entire mathy sciencey argument is . . .
> > well . . . bullshit. And you yourself have pointed out why it's
> > bullshit.
>
> The TTSS system, to include structure and function, existed from the
> beginning.
No shit. YOU are trhe one claiming the TTSS came from the bacterial
flagellum, Sean. Make up your goddamn mind. Which line of bullshit
is it?
The simple point, one more time -- YOU YOURSELF have declared that new
functional parts can be formed by taking pieces out of pre-existing
DIFFERENT parts. Which means that all of your "747 in a tornado"
mathy stuff, is pure bullshit. See how simple that is?
> It isn't novel in any sense of the word except in the loss
> of extra baggage that wasn't needed to produce the toxin injector
> function in particular.
Bullshit, Sean. Cellular secretatory apparatuses are not bacterial
motility devices, Sean. They are entirely unrelated functions.
So explain to me one more time how parts from one function got used to
make parts of an entirely differnet and new function that did not
exist before.
> It is less expensive to keep the injector
> function and let the motility function go away given that the
> nutritional needs of the organism can be adequately met in a given
> environment without the motility system.
So what, Sean.
That doesn't cvhange the fact in the slightest that (1) the motility
system wasn't there before, (2) the motility system appeared as a new
function, and (3) it was built using parts from an already-existing
system that had an entirely unrelated function.
Which makes all your mathy stuff, bullshit.
>
> > > > You are a bullshitter, Sean. Nothing more, nothing less, nothing
> > > > else.
>
> > > > And the fact that you refuse to answer this simple question, indicates
> > > > to me that you KNOW you are just bullshitting.
>
> > Just as does the fact that you simply evaded it yet again with more
> > arm-waving.
>
And then evaded it again.
I await your explanation of where the "extra parts" in the bacterial
flagellum and/or the secretoary system, came from, Sean. And I'll
keep asking till I get one.
Seanpit
> Seanpit <sean...@gmail.com> wrote innews:8abe10fd-76c7-4c60...@v1g2000prd.googlegroups.com:
>
>
>
> > On May 5, 12:04 am, "R. Baldwin" <res0k...@nozirevBACKWARDS.net>
> > wrote:
> >> Seanpit <sean...@gmail.com> wrote
> >> innews:47c29c43-bfe4-4c16-838c-7b1423e7
In that case, it should be easy for you to point to an example of
evolution in action that ends up producing any system that has a
minimum structural requirement beyond 1000 fairly specified amino acid
residues (fsaars). If you cannot find such a system, upon what basis
do you argue that my definition has nothing to do with predicting
reality?
> I also do not agree that biologists recognize or use this term,
> or that any research has been conducted to verify its correspondence
> with reality. It is your own peculiar definition, created out of your
> own imagination.
It is very clear that systems with larger or more specified structural
requirements, to include multiprotein systems, do not evolve in
observable time. That is very clear - even to mainstream biologists.
What has not been done by mainstream biologists or scientists in
general, is to attempt to predict at what level the mechanism of RM/NS
should be expected to work given a certain span of time. In other
words, there has been no attempt to develop a statistical basis to
support the theory behind the very mechanism of evolution. It's
activity at various levels of functional complexity is based on
nothing but just-so story telling, bald assertions, and wishful
thinking. There is no science here. There hasn't even been an
attempt at a real scientific basis when it comes to the proposed
mechanism of RM/NS.
There is a very good reason for this. Obviously, if such an attempt
where ever seriously entertained, it would quickly become clear to all
who even attempt such an effort that the evolutionary mechanism is
simply untenable beyond very very low levels of functional complexity.
To give credit where credit is due, at least Dryden has attempted to
address this issue - which is something. Unfortunately, he hasn't
really defined a useful concept of levels of functional complexity.
He has actually classified many different levels all together into one
group and thought that by demonstrating the tenability of evolution at
very low levels that this could easily be extrapolated to all levels
of functional complexity. This last assumption of his simply isn't
true. But, at least he tried. At least he is considering, sort of,
the right questions. That's more than I can say for most contributors
to this forum.
> > Your argument here makes it very clear that both you and Dryden
> > misunderstand the very concept of levels of functional complexity.
> > You just don't get it - even after all of this time. Yet, it is such
> > a simple concept. How is it that you cannot seem to grasp it?
>
> I disagree that you have established any relationship between sequence
> length and structural complexity.
Ok, show me how to build a rotary bacterial flagellar motility system
with just 1000aa in any arrangement you choose. If you cannot do
this, how can you say that you see no relationship between certain
types of functional systems and minimum structural threshold
requirements? This relationship is downright obvious. You have to be
deliberately blind not to see it. I'm sorry, but that's a fact.
> >> Since there is no goal, there is no minimum
> >> structural threshold to worry about. A flagellar motility system
> >> isn't a goal. It just happens to be where things ended up for a
> >> particular genome. A sequence either does something biologically
> >> interesting, or it doesn't. Your functional complexity concept is
> >> meaningless.
>
> > There is a goal for evolutionary progress - and that is to actually
> > find novel beneficial systems.
>
> No, that is not a goal. That is just what results.
LOL - whatever man. If this doesn't result, there is no evolution.
We are talking about what it takes for evolution to happen here. Of
course evolution doesn't have to happen, but that's not the issue.
The issue is what it takes for it to happen.
> > If the system in question has a very
> > low minimum structural threshold requirement it is exponentially more
> > likely to be found vs. a system that has a higher minimum structural
> > threshold requirement. That is why single protein enzymes which
> > require no more than a few hundred fairly specified amino acid
> > residues are found all the time by RM/NS. Yet, no system, to include
> > multi-protein systems, which have more than a 1000 fsaar minimum
> > structural threshold requirement are ever found by RM/NS - regardless
> > of the starting points within any gene pool you wish to consider. It
> > just doesn't happen, has never happened, and statistically is
> > extremely unlikely to happen this side of trillions of years of
> > time.
>
> This is simply an assertion you keep making without evidence. Your math
> is not based on reality, so there is no reason to accept your
> conclusion.
It isn't just an assertion. It is a testable potentially falsifiable
theory. Where is your evidence that falsifies my theory?
The minimum sequence length and specificity for a higher level system
does matter when it comes to successful fusions of lower level systems
to produce higher level systems. The odds of a successful random
fusion depend greatly on the minimum size and specificity requirements
of the larger system. Why? Because there are vastly more ways to
produce useless fusions relative to the very few ways there are to be
successful in the concatenations.
I've explained this to you dozens of times. By definition the
majority of ways that two smaller stable sequences could be fused
would not be stable. You're notion that such fusions would have to be
stable just because the original smaller sequences were stable is
simply not true. This is even explained in mainstream literature as
I've already shown you . . .
< that's all for now >
Sean Pitman
www.DetectingDesign.com
Burkhard
> On May 6, 6:23 am, Burkhard <b.scha...@ed.ac.uk> wrote:
>
>
>
> > > Yes yes, the standard "infinite regress" argument. The fact of the
> > > matter is that SETI scientists don't have to know the origin of their
> > > proposed ETIs before they can adequately propose the need for
> > > intelligent input to explain their artifactual radio signals. You
> > > simply don't have to answer the question of "Who made the designer?"
> > > before you can detect the need for ID.
>
> > But SETI, as far as I know, does not evoke your "law of information
> > preservation" which is at the heart of your infinite regress, so it
> > only applies to you, not them.
>
> SETI scientists do believe in the law of certain types of information
> never being produced by systems with lower level informational
> complexity. They do in fact believe that higher level outside
> informational input was required.
Ehh, no. We know what types of signals are produced by natural ways,
and we haven't found any that have a very narrow bandwith yet. so
finding one of these is a good strating point. Functional complexity
does not enter this. See the SETI FAQ on their website
complexity does That is why they think themselves
> able to detect the need or the requirement for at least human level
> intelligent input to explain certain types of radio signals. If the
> information needed to produce these types of signals could be derived
> from lower level informationally inferior systems, like random weather
> patterns and the like, the concept of SETI would be hopeless.
Nature can be very complex, man made signals very simple. And that is
not even touchig on the possibility that the Milky Way is nothing but
a love poem written by an intergalactic species to his neighbour.
>
> Sean Pitmanwww.DetectingDesign.com
Perplexed in Peoria
---------------------
PiP: And again I have to ask, what is the relevance of this observation?
It is almost as if you were arguing that evolution can not be the
explanation for a universe in which the bacterial flagellum was
invented before nylonase. Only a Designer would have done things
in that order.
And a suggestion. Every time you are tempted to write the word
'exponentially', first write down an equation of the form y = k e^rx
where y is the variable which increases exponentially with x and
in which k and r are parameters. Then ask yourself whether your
reader can reasonably be expected to write down the same
equation. If not, then find some other way of communicating
besides using that word 'exponentially'.
R. Baldwin
news:087390ff-5aed-4a97...@d7g2000prl.googlegroups.com:
> On May 5, 7:18�pm, "R. Baldwin" <res0k...@nozirevBACKWARDS.net> wrote:
>> Seanpit <sean...@gmail.com> wrote
>> innews:8abe10fd-76c7-4c60-9e62-abafaf8c
> 4d...@v1g2000prd.googlegroups.com:
Well, this for example:
"it has been known for more than 20 years that neutral substitutions in
evolutionarily related proteins are scattered randomly along the chain
in accordance with Poisson statistics except for perhaps 5-20% of the
residues which are invariant and strongly conserved"
White, S. & R. Jacobs, "Statistical distribution of hydrophobic residues
along the length of protein chains: Implications for protein folding and
evolution" Biophysical Journal, Vol 57, April 1990.
http://www.ncbi.nlm.nih.gov/pubmed/2188687
This directly contradicts your "fairly specified" concept and suggests
that most of an ORF is random. Sequence length is therefore not a good
predictor of functional complexity.
>
>> I also do not agree that biologists recognize or use this term,
>> or that any research has been conducted to verify its correspondence
>> with reality. It is your own peculiar definition, created out of your
>> own imagination.
>
> It is very clear that systems with larger or more specified structural
> requirements, to include multiprotein systems, do not evolve in
> observable time. That is very clear - even to mainstream biologists.
Since "more specified structural requirements" is the result of your own
imagination, not research, it is not clear at all.
> What has not been done by mainstream biologists or scientists in
> general, is to attempt to predict at what level the mechanism of RM/NS
> should be expected to work given a certain span of time. In other
> words, there has been no attempt to develop a statistical basis to
> support the theory behind the very mechanism of evolution.
Certainly, there has. Such data is important to protein designers. It is
simply that the data doesn't correspond to your irrelevant model.
Most of the articles about this you have to buy, and since I'm not in
the trade I'm not going to buy them just for the pleasure of refuting
you.
But, according to this news article about research published in Nature,
gene recombination in yeast occurs at a rate of 150 per meiosis event.
http://esciencenews.com/articles/2008/07/10/zooming.genetic.shuffling
> It's
> activity at various levels of functional complexity is based on
> nothing but just-so story telling, bald assertions, and wishful
> thinking. There is no science here. There hasn't even been an
> attempt at a real scientific basis when it comes to the proposed
> mechanism of RM/NS.
Oh yes there has. You just choose to ignore it. Try starting by
reviewing all the articles cited by the Wikipedia article "protein
domain." There are about 100 or so if you include the key papers. You
might start with:
Apic, G. et. al. "An insight into domain combinations." Bioinformatics
Vol 17 Suppl 1 2001.
http://bioinformatics.oxfordjournals.org/cgi/reprint/17/suppl_1/S83
>
> There is a very good reason for this. Obviously, if such an attempt
> where ever seriously entertained, it would quickly become clear to all
> who even attempt such an effort that the evolutionary mechanism is
> simply untenable beyond very very low levels of functional complexity.
Actually, the converse happened. It became clear that domain swapping
neatly solves the Levinthal peradox you are so fond of pushing.
>
> To give credit where credit is due, at least Dryden has attempted to
> address this issue - which is something. Unfortunately, he hasn't
> really defined a useful concept of levels of functional complexity.
> He has actually classified many different levels all together into one
> group and thought that by demonstrating the tenability of evolution at
> very low levels that this could easily be extrapolated to all levels
> of functional complexity. This last assumption of his simply isn't
> true. But, at least he tried. At least he is considering, sort of,
> the right questions. That's more than I can say for most contributors
> to this forum.
This "levels of functional complexity" exists in your mind.
>
>> > Your argument here makes it very clear that both you and Dryden
>> > misunderstand the very concept of levels of functional complexity.
>> > You just don't get it - even after all of this time. �Yet, it is
>> > such a simple concept. How is it that you cannot seem to grasp it?
>>
>> I disagree that you have established any relationship between
>> sequence length and structural complexity.
>
> Ok, show me how to build a rotary bacterial flagellar motility system
> with just 1000aa in any arrangement you choose. If you cannot do
> this, how can you say that you see no relationship between certain
> types of functional systems and minimum structural threshold
> requirements? This relationship is downright obvious. You have to be
> deliberately blind not to see it. I'm sorry, but that's a fact.
The relationship is not obvious, is not established fact, and is
contradicted by research. See the White & Jacobs quote above.
>
>> >> Since there is no goal, there is no minimum
>> >> structural threshold to worry about. A flagellar motility system
>> >> isn't a goal. It just happens to be where things ended up for a
>> >> particular genome. A sequence either does something biologically
>> >> interesting, or it doesn't. Your functional complexity concept is
>> >> meaningless.
>>
>> > There is a goal for evolutionary progress - and that is to actually
>> > find novel beneficial systems. �
>>
>> No, that is not a goal. That is just what results.
>
> LOL - whatever man. If this doesn't result, there is no evolution.
> We are talking about what it takes for evolution to happen here. Of
> course evolution doesn't have to happen, but that's not the issue.
> The issue is what it takes for it to happen.
The distinction matters, because assuming there is a goal leads to
erroneous conclusions.
>
>> > If the system in question has a very
>> > low minimum structural threshold requirement it is exponentially
>> > more likely to be found vs. a system that has a higher minimum
>> > structural threshold requirement. �That is why single protein
>> > enzymes which require no more than a few hundred fairly specified
>> > amino acid residues are found all the time by RM/NS. �Yet, no
>> > system, to include multi-protein systems, which have more than a
>> > 1000 fsaar minimum structural threshold requirement are ever found
>> > by RM/NS - regardless of the starting points within any gene pool
>> > you wish to consider. �It just doesn't happen, has never happened,
>> > and statistically is extremely unlikely to happen this side of
>> > trillions of years of time.
>>
>> This is simply an assertion you keep making without evidence. Your
>> math is not based on reality, so there is no reason to accept your
>> conclusion.
>
> It isn't just an assertion. It is a testable potentially falsifiable
> theory. Where is your evidence that falsifies my theory?
You don't have a theory. You have a crude hypothesis based on a
simplistic model that isn't correlated to observed fact and is even
contradicted by observed fact.. A theory, on the other hand, is
validated by overwhelming independent evidence and peer review.
If you want a theory, you will have to produce mutliple lines of
biological observations that correlate to your model, have them
corroborated by independent researchers, and give it the test of time.
>> > system. �Th
> e
>> > reason for this is due to the exponentially reduced ratio of higher
>> > level vs. lower level system in sequence space.
>>
>> No, the odds are not exponentially lower, and they are unrelated to
>> the ratio of "higher level vs. lower level system in sequence space."
>> If sequences of domain modules are concatenated (fused), the sequence
>> length does not matter. A rich complexity is accessible with a small
>> number of mutations.
>
> The minimum sequence length and specificity for a higher level system
> does matter when it comes to successful fusions of lower level systems
> to produce higher level systems. The odds of a successful random
> fusion depend greatly on the minimum size and specificity requirements
> of the larger system. Why? Because there are vastly more ways to
> produce useless fusions relative to the very few ways there are to be
> successful in the concatenations.
Why do you think it is so vast? The average domain length is 100
residues. Most domains are no more than 200 residues. There are three
nucleotides per residue. Does not this put a bound on the probability
involved?
Suppose we have an overly simplistic model, where sequences split and
join at Uniformly random locations. ORFs are made up of domains having a
length of exactly 100 residues. The probility of a fusion of two split
ORF segments we will call P. The probability that a split within an ORF
happens at a domain interface is 1/300, because only 1 out of every 300
nucleotide base pairs represents the start of a domain. With a very
crude statistical approximation, we could set the probability that two
joined sequences fuse at P/(300)^2 = P(1.1E-05). This probability does
not vary with ORF sequence length, so there is no "exponentially lower"
relationship with an increase in sequence length.
Now, even if P is pretty small, the effect of "useless fusions" that you
are so worried about only reduces it by a factor of 1.1E-05, or 11 parts
per million. There are enough single celled organisms on hand to exploit
this and find the "useful fusions" amid all the useless ones.
>
>> >> >> �It is very important
>> >> >> to note that in many cases such folding does not require
>> >> >> complete specification of the sequence but only maintenance of
>> >> >> the pattern of amino acid categories (polar, non-polar etc).
>> >> >> Many domains do interesting things but a recurring theme is to
>> >> >> then bring collections of the domains together either as
>> >> >> separate subunits to form quaternary structure or to string
>> >> >> them together into one single chain by making them via a single
>> >> >> gene. This latter process is how one makes a 1000 amino acid
>> >> >> protein. Nature takes the domain modules and puts them together
>> >> >> to make novel structures and functions. (Note that very few
>> >> >> long protein chains are found as their synthesis is tricky due
>> >> >> to increasing chances of errors in gene replication,
>> >> >> transcription or translation. These problems were recognised by
>> >> >> Francis Crick if I recall correctly in the 1960�s. The average
>> >> >> protein size is around 500 amino acids.) The number of domains
>> >> >> with unique folds appears to be limited to around 1000 to
>> >> >> 10,000 (certainly less than a million) and it is becoming rare
>> >> >> for science to find new ones. This means that whatever sequence
>> >> >> you have, you get one of these folds
>>
>> >> > Good so far.
>>
>> >> >> (but note that
>> >> >> there is a relatively new discovery of �natively-unfolded� prot
Even if the majority of fusions from stable sequences are not stable,
they happen at a high enough rate to drive evolution. That is the point
you have continuously missed. That is why your explanations don't
explain.
By the way, the real world does not work by definition.
'Rev Dr' Lenny Flank
'Rev Dr' Lenny Flank wrote:
> > > Another question for you to evade, Sean --- since the secretory system
> > > has parts that are not found in the flagellum, and since the flagellum
> > > has parts that are not found in the secretory system -- no matter
> > > WHICH formed from which, the question remains ------------> where did
> > > the rest of the parts come from? How'd they get there, Sean?
> >
> > > Careful how you answer that, Sean . . . IF you answer it . . . . .
>
>
>
>
>
> And, surprise of all surprises, you didn't answer it. Color me
> shocked. Shocked, I say.
>
> No problem. I'll keep asking until you do.
>
Well, Sean? Any ideas yet?
Spil...@gmx.net
> Your argument is nonsense.
I wouldn't be so quick to dismiss it.
>
> The Designer of life on Earth need not have been designed Himself.
I don't claim that. There are several other options, some of which you
mentioned.
>
> Your assumption that every Designer must have been designed by some
> other Designer is just false.
I want to point out that it's Sean that claims, that "functionally
complex information" can ultimately only flow "downhill", i.e. from
more to less. So if the designer was functionally complex enough to
produce us, his functionally complex information has to come from a
source at least as functionally complex as himself. "Non-intelligent
natural processes cannot describe the origin of intelligence. This is
the basis of a concept related to information
theory - i.e., informational entropy. Systems with lower-level
meaningful or functional information cannot given rise to higher-
levels of meaningful/functional or "emergent" information." If I
misrepresent you, Sean, please clarify.
>
> I can imagine other alternatives: A Designer that exists outside of
> time and space of this Universe, for example. In which case it could
> have always existed.
Sure, but it would now be an argument for a supernatural designer.
That means, except you can give an example of an eternal natural
being. (preferably one of at least human-level intelligence with
access to at least 21-century-level technology, as Seanpit demands)
>
> Or, the Designer of life on Earth itself arose from natural processes
> elsewhere in this Universe, or in some other Universe.
Sure, thats what I'm arguing for, that the premise of the design
argument, that undirected natural processes cannot account for the
existence of complex life, is false. If you grant, that a designer can
come to be by unknown undirected natural processes, then what stops
complex life on earth having arisen by unknown undirected natural
processes? In this case the assumption of an designer of complex life
on earth wouldn't be contradictory, but not parsimonous.
>
> --
> Steven L.
> Email: sdlit...@earthlinkNOSPAM.net
> Remove the NOSPAM before replying to me.
Another option would be to claim that the designer isn't complex. But
since Seanpit set the conditions for complexity relatively low, at a
functional complexity of at least the equivalent of 1000 fsaars, if I
understand him right, there isn't much room for a potential designer:
"Steven L: "So the Intelligent Designer is keeping pretty busy: He
has to sculpt every nucleus, every cilium, every flagellum, every
ribosome, of every type of cell of every life form that ever existed.
Is THAT what you're arguing for"???? Seanpit: "Yes" . . . " A designer
of archaean-level complexity without a single system of the equivalent
of 1000 fsaars, of at least human-level intelligence with access to at
least 21st-century-level technology? Maybe, but this would contradict
Seans "law of information preservation": "Ok, Richard, produce an
example of functional informational complexity being produced
significantly beyond the functional informational complexity of its
source."
So the question remains, who designed the designer?
Lark
Spil...@gmx.net
> On May 6, 2:24 pm, "Steven L." <sdlit...@earthlink.net> wrote:
>
>
>
> > Spille...@gmx.net wrote:
> > > On 6 Mai, 16:39, "Steven L." <sdlit...@earthlink.net> wrote:
> > >> Spille...@gmx.net wrote:
> > >>>> On May 5, 11:44 am, "Steven L." <sdlit...@earthlink.net> wrote:
> > >>> [snip]
> > >>>>> Then I don't understand what your alternative theory is: If evolution
> > >>>>> of species has never occurred, then are you suggesting that an
> > >>>>> Intelligent Agency or Intelligent Designer had intervened to produce
> > >>>>> each and every one of the millions of species that have existed on
> > >>>>> Earth? Each and every one is a special creation by this Intelligence?
> > >>>> I think the definition for "species" is too subjective. However, I
> > >>>> will say that every single qualitatively unique beneficial system of
> > >>>> function that requires more than 1000 fsaars was the result of
> > >>>> deliberate design.
> > >>>>> Indeed, your focus on the bacterial flagellum suggests that you believe
> > >>>>> that every *structure* of every life form had to be specially designed.
> > >>>> That's right.
> > >>>>> So the Intelligent Designer is keeping pretty busy: He has to sculpt
I disagree. It is neither futile, nor irrelevant. ID depends on the
existence of a designer, so it has to answer, whether a *natural*
designer with the the proposed characteristics (for example eternal
existence) can exist. If not, the argument becomes a supernatural one.
hersheyh
What is needed is the ability to interact with other protein systems
to generate a signal. But since you reject anything but a single
structure (like the flagella) as fitting your criteria for larger
systems and *specifically* reject pathways as fitting your criteria,
you cannot move those goal posts now. In fact, like the existence of
two different types of rotary flagella, the visual *pathway* differs
(past the first two proteins) between invertebrate and vertebrate
visual systems. Both systems involve a cis-retinal molecule bound to
an opsin protein. Cis-retinal, closely related to the ubiquitous
vitA, naturally changes shape upon absorption of light. In
invertebrates, this change in shape becomes a 'nerve impulse' via a
rhodopsin/Gq/PLC pathway. In vertebrates, this pathway is rhodopsin/
transducin/phosphodiesterase pathway. But the important point is that
*both* pathways pre-exist in organisms. The only point that needs to
be "invented" is the initial linkage of the signal from the shape
change to *some* pre-existing neural signalling pathway. However,
since this represents a *pathway* rather than an interacting
*structure*, there should be no problem with it evolving, according to
your dismissal of similar enzymatic pathways meeting your bogus
criteria.
www.riken.go.jp/lab-www/library/publication/review/pdf/No_11/11_061.pdf
hersheyh
That would be comparing apples and oranges.
> One is not simply a quantitatively different
> function relative to the other.
That would be comparing apples and oranges.
> Simply adding increased lactase
> activity to the lactase enzyme isn't going to get you flagellar
> motility. Why not?
Because they are not similar in structure? But adding more efficient
rotation to a motorized rotating pore does increase flagellar
activity. And connecting a pre-existing pore plus whip to a pre-
existing motor *can* produce a motorized rotating pore. Similarly,
changing sequence on the lactase enzyme can change the efficiency of
its binding to other beta-galactioside linkages.
> Because there is a qualitative, not just a
> quantitative, difference. This is an easy concept. Don't try to make
> this difficult. It isn't.
But there is no qualitative difference between going from an enzyme
that inefficiently cleaves the beta-galactoside linkage of, say, X-
gal, to one that more efficiently cleaves X-gal but at the expense of
efficiency in cleaving lactose, on the one hand, and increasing the
efficiency of rotation of motorized rotating pore at the expense of
decreasing the efficiency of injecting toxins on the other hand.
> > As far as I can tell, you and the other ID proponents glommed onto the
> > spinning of the bacterial flagellum just because it looks cool. But
> > spinning is NOT a complex function; mathematically it's simple.
>
> Structurally, it isn't simple and it cannot be made to be simple when
> it comes to useful rotary flagellar motility.
The spinning *function* is entirely the consequence of the existence
of a linker protein between a 'motor' and a 'rotatable pore plus
whip.' That is no different than the lactase *function* being due to
the affinity of a small site for an intermediate between the intact
beta-galactoside linkage and the hydrolyzed one. Change in a single
protein is all that is required for both. The number of mutations
require is much smaller precisely *because* these protein structures
already exist in cells and do not, as you attempt to claim in your
bogus straw man probability numerology, have to be created from
scratch by a completely random process.
> All such systems would
> require thousands of basic building blocks in specific arrangement to
> be useful for this type of function.
And your evidence for this is...? We certainly can generate a
rotating flagella by two *entirely* different sequences. Both are,
however, due to the linkage of a rotatable pore and a motor which are
systems that do exist in real cells.
> > As Dryden explained, there are enzyme systems whose functionality is
> > qualitatively far more complex than spinning functionality.
A single *function* cannot be qualitatively "complex" unless it is
composed of multiple subfunctions. If the subfunctions are
potentially independently useful, aggregating them to form a new
function that is composed of the subfunction does not involve
inventing the subfunctions from scratch at the same time.
> A small single protein enzyme is not structurally more complex when it
> comes to its minimum structural threshold requirements. It therefore
> occupies a much smaller sequences space, has an island footprint with
> an exponentially higher ratio within sequence space, and is therefore
> exponentially easier to find via a random search process within
> sequence space.
And larger proteins can certainly include the function that exists in
smaller proteins and use those subfunctions to generate more complex
functions by re-shuffling those subfunctional parts.
>
> Drydens assertion that such a simple enzyme is actually qualitatively
> more complex is subjective nonsense.
Only to idiots who assume that size is a measure of complexity.
> He has not actually defined what
> it means to be functionally complex in any sort of scientific sense
> that is usefully testable and measurable - and neither have you.
Functional complexity is measureable only by counting the number of
subfunctions a system has.
Steven L.
> On May 6, 11:24 pm, "Steven L." <sdlit...@earthlink.net> wrote:
>
>> Your argument is nonsense.
>
> I wouldn't be so quick to dismiss it.
>
>> The Designer of life on Earth need not have been designed Himself.
>
> I don't claim that. There are several other options, some of which you
> mentioned.
>
>> Your assumption that every Designer must have been designed by some
>> other Designer is just false.
>
> I want to point out that it's Sean that claims, that "functionally
> complex information" can ultimately only flow "downhill", i.e. from
> more to less. So if the designer was functionally complex enough to
> produce us, his functionally complex information has to come from a
> source at least as functionally complex as himself.
That's nonsense too.
Humans have terraformed this entire planet, we've engineered structures
and mathematical concepts that are highly complex, all over the Earth.
We've created a knowledge base vastly more complex than any human
being--the Internet. We've created an entire planetary civilization,
far more complex than any single human's anatomy. How did we do this?
By inventing *writing*, which enabled our ideas to be preserved long
after our own deaths. Thus our knowledge base increased, generation
after generation, outside our own bodies.
There's no evidence that all this vast complexity "flowed downward" from
our anatomies.
So a Designer doesn't have to be as complex as the things He designs.
Sean Pitman is undoubtedly wrong.
But so are you.
For different reasons.
--
Steven L.
Email: sdli...@earthlinkNOSPAM.net
wf3h
>
> In short, the job might seem to you to be a simple job. But, the
> machine itself is not simple. It requires a great many parts all
> working together in a very specific arrangement at the same time.
> Such a machine cannot be described as "simple" or comparable to a
> single protein enzyme by any stretch of the imagination - at least not
> with a straight face.
>
and since we know evolution co-opts various functions for OTHER
processes, such machinery can evolve.
and creationism, unfortunately, has no way to explain this.
Steven L.
Indeed, once you have an eyespot that can generate a signal when light
falls on it, evolving the rest of the human eye is just a matter of
encasing that eyespot for protection, improving the ability to focus
light, muscles to move the eye around, etc. All incremental
improvements. No "irreducibly complex" changes.
--
Steven L.
Email: sdli...@earthlinkNOSPAM.net
Steven L.
Thousands???
The bacterial flagellum can be decomposed into a few basic building
blocks, which were undoubtedly reused from other applications.
It's true that each of those building block components may itself be
complex internally. But in the course of evolution, those components
could get reused (with some tweaks) and combined to form a more complex
system.
We know that cells have to have means of forced intracellular
transport--they eat, they move that food to where it can be processed,
and they excrete. Motor proteins have been discovered that can do work
like that. So once they evolved cellular motors for this purpose, why
couldn't those motors be reused for the propulsion of the entire bacterium?
Didn't you ever study the paramecium in school? It's got cellular
motors for a large number of complex functions.
So I still don't understand this obsession with spinning flagella--again
except that it wows the uninformed audiences.
>> As Dryden explained, there are enzyme systems whose functionality is
>> qualitatively far more complex than spinning functionality.
>
> A small single protein enzyme is not structurally more complex when it
> comes to its minimum structural threshold requirements. It therefore
> occupies a much smaller sequences space, has an island footprint with
> an exponentially higher ratio within sequence space, and is therefore
> exponentially easier to find via a random search process within
> sequence space.
>
> Drydens assertion that such a simple enzyme is actually qualitatively
> more complex is subjective nonsense. He has not actually defined what
> it means to be functionally complex in any sort of scientific sense
> that is usefully testable and measurable - and neither have you.
Well, if it's truly a cellular motor that spins a whip around, it's
analogous to an electric fan, which has a motor that spins a four- or
five-bladed fan around.
Now an electric fan is a very simple mechanism. That's why you can buy
one for little money.
I'm not impressed with the bacterial flagellum.
--
Steven L.
Email: sdli...@earthlinkNOSPAM.net