Sean Pitman M.D.
This exchange discusses the existence of various levels of functional complexity when it comes to protein function and what levels of function can and cannot be evolved.
The comments of Bill Rogers are marked by: > > >
The comments of Von Smith are marked by: >
My comments are marked by > > and no carats
From: Sean Pitman (firstname.lastname@example.org)
Subject: Re: All Functions... Sean Pitman = Used Car Salesman
View: Complete Thread (28 articles)
Date: 2003-07-15 14:04:43 PST
email@example.com (Von Smith) wrote in message news:<firstname.lastname@example.org>...
> email@example.com (Sean Pitman) wrote in message news:<firstname.lastname@example.org>...
Bill Rogers > > > For instance one of his main issues is the rate of evolution.
> > > He either gets it much to fast or the reverse.
Sean Pitman > > You don't seem to understand my point here. If there were no neutral
> > gaps or if they were relatively small as you and most other
> > evolutionists in this forum seem to suggest, then the rate of
> > evolution would proceed extremely fast. Millions of years would not
> > be required to achieve the diversity of life forms that we see today.
> > However, if the neutral gaps really are there and do in fact expand
> > exponentially with increasing complexity as I suggest, then the
> > evolution of multi-protein systems would indeed take far longer than
> > even the theory of evolution has time for (i.e., trillions upon
> > trillions upon zillions of years).
Von Smith > On the other hand, if your whole neutral gaps model is nonsense, then
> none of your estimates of rates of evolutionary change are worth
> anything. I have seen you repeatedly assert your "neutral gap"
> argument, but I have never seen you support it, here or on your web
> page. You just seem to take it as an article of faith that they are
What then would you call my use of experiments like Barry Hall's work
with E. coli and my descriptions of antibiotic resistance and the
evolution of various enzymatic type functions? I have demonstrated as
ladder of complexity that clearly gets more complex as one moves up
the ladder. On the lowest rungs of the ladder one can find the most
simple functions of antibiotic resistance and other types of drug
resistance that rely upon the interference with or destruction of
other pre-established functions/interactions. The neutral gaps on
this level are very small because the ratio of interfering sequences
as compared to neutral or non-interfering sequences is very high.
Many mutations will cause at least some sort of beneficial
interference. And, in real life, this is exactly what happens.
Antibiotic resistance to just about any antibiotic is evolved in very
short order in just about any bacterial colony that is exposed to a
particular antibiotic. However, as one moves up the ladder of
complexity to the next higher rung of complexity the neutral gaps
increase significantly. Single protein enzymes have been shown to
evolve in real time, but they are far less common and far more
difficult to demonstrate than those functions on the lower rung of
complexity. The reason for this is that the function of enzymes is
not dependent upon the interference with or destruction of a
pre-established function or interaction. This means that the ratio of
what will yield a particular enzymatic function compared with the
total number of potential sequences that will not yield this type of
enzymatic function is far lower than the ratio of antibiotic producing
sequences. Still, the ratio is fairly high compared with the next
rung up the ladder of complexity which includes those functions that
required multiple proteins all working together at the same time
(i.e., bacterial motility systems and the like). At this level of
functional complexity there simply are no real time examples. The
reason for this is that the ratio of what will work in a beneficial
way compared with what will not work is extremely tiny. Such a minute
ratio creates a large neutral gap between what will work and anything
else of that level of complexity. This neutral gap destroys the
power of natural selection and evolution stalls out. Not even
billions or trillions upon trillions of years can save evolution when
it comes to such levels of complexity.
This is not blind faith at all. This hypothesis can be demonstrated
in real life. It has a very high predictive value and is very well
supported by repeated experimentation. Please, you are the one with
the great faith, not I. I do admire your faith, but I simply cannot
accept something so irrational as Darwinian evolution that goes
against all statistical probabilities.
> > > He says that what he asks for can't be shown, therefore
> > > biology is wrong.
> > If it can't be shown, then your theory of no-neutral gaps must be
> > wrong.
> > > Von Smith promptly provided a couple of examples.
> > Von Smith did no such thing.
> Yes, I did, and you have yet to respond to it.
I cannot read everything that people write much less respond to
everything that I would wish to respond too. Much of what is written
in response to my threads is redundant anyway. The same is true for
your examples, which are very similar to examples of evolution in
action that I have already responded to several times before.
> > All Smith provided where a bunch of
> > just-so-stories about how such evolution of multi-part systems "must
> > have happened." No real time examples where provided for the
> > evolution of any multi-protein system of function.
> That is untrue.
> In message ID: <email@example.com> I
> cited the following:
> begin quote
> Message-ID: <firstname.lastname@example.org>
> 'Johnson GR, Jain RK, Spain JC. "Origins of the 2,4-dinitrotoluene
> J Bacteriol. 2002 Aug;184(15):4219-32.
> '"The degradation of synthetic compounds requires bacteria to recruit
> and adapt enzymes from pathways for naturally occurring compounds.
> Previous work defined the steps in 2,4-dinitrotoluene (2,4-DNT)
> metabolism through the ring fission reaction. The results presented
> here characterize subsequent steps in the pathway that yield the
> central metabolic intermediates pyruvate and propionyl coenzyme A
> (CoA). The genes encoding the degradative pathway were identified
> within a 27-kb region of DNA cloned from Burkholderia cepacia R34, a
> strain that grows using 2,4-DNT as a sole carbon, energy, and nitrogen
> source. Genes for the lower pathway in 2,4-DNT degradation were found
> downstream from dntD, the gene encoding the extradiol ring fission
> enzyme of the pathway. The region includes genes encoding a
> CoA-dependent methylmalonate semialdehyde dehydrogenase (dntE), a
> putative NADH-dependent dehydrogenase (ORF13), and a bifunctional
> isomerase/hydrolase (dntG). Results from analysis of the gene
> sequence, reverse transcriptase PCR, and enzyme assays indicated that
> dntD dntE ORF13 dntG composes an operon that encodes the lower
> pathway. Additional genes that were uncovered encode the 2,4-DNT
> dioxygenase (dntAaAbAcAd), methylnitrocatechol monooxygenase (dntB), a
> putative LysR-type transcriptional (ORF12) regulator, an intradiol
> ring cleavage enzyme (ORF3), a maleylacetate reductase (ORF10), a
> complete ABC transport complex (ORF5 to ORF8), a putative
> methyl-accepting chemoreceptor protein (ORF11), and remnants from two
> transposable elements. Some of the additional gene products might play
> as-yet-undefined roles in 2,4-DNT degradation; others appear to remain
> from recruitment of the neighboring genes. The presence of the
> transposon remnants and vestigial genes suggests that the pathway for
> 2,4-DNT degradation evolved relatively recently because the extraneous
> elements have not been eliminated from the region."
> end quote.
> 2,4-DNT is a synthetic chemical that has only been around for a few
> decades, and the microorganisms described in this article use it as
> their sole carbon, energy, and nitrogen source. Either these bacteria
> have been carrying around a useless metabolic pathway all this time
> that just happens to be ideal for 2,4-DNT, or the bacteria acquired
> the pathway since 2,4-DNT has appeared in their environment, meaning
> that it did indeed evolve "real time". That is not a just so story,
> that is a conclusion based on observation.
> I'll ask the question again: how is this not an example of recent
> evolution of a novel multi-protein function?
In this particular study the authors themselves note that the "De novo
evolution of genes for nitrotoluene degradation during the short
period seems unlikely. Instead, it is more plausible that the pathways
evolve by recruiting genes that encode degradative enzymes for other
compounds to assemble a functional pathway." In other words, the
genes and enzymes themselves did not evolve much at all, but were
already there. Because of this, very few mutations were required to
achieve this relatively simple *cascade-type* enzymatic function. In
fact, three recombinant strains showed activity for all three of the
required enzymes, and the cosmids carried by the strains were
designated pJS314, pJS315, and pJS316.
"Inferences from the comparison of the structural genes of the 2,4-DNT
pathway suggest that the pathway came together from three sources. The
initial dioxygenase appears to have originated from a naphthalene
degradation pathway like that of strain U2. A large portion of the
salicylate hydroxylase oxygenase component is retained but is not
functional. The MNC monooxygenase was probably derived from a pathway
for degradation of chloroaromatic compounds. The presence of the
vestigial (with respect to 2,4-DNT degradation) ortho-ring fission
dioxygenase is consistent with its recruitment from a pathway for
chloroaromatic compounds. The true ring fission enzyme for 2,4-DNT
degradation has a different origin. The sequence of DntD is quite
dissimilar to all other described meta-ring fission enzymes, including
those from naphthalene and chloroarene degradative pathways. The
distinctive sequence of the ring cleavage enzyme reflects the
substrate specificity observed for the THT oxygenase. The distant
relationship between homogentisate dioxygenase and DntD and the
association with homologs from amino acid metabolism (dntE and dntG)
indicate that the lower pathway operon arose from a gene cluster for
amino acid degradation."
Enzymatic activities are relatively simple to achieve. If all the
needed enzymes are already being made to break down a particular
molecular construct in at least some selectably beneficial way
(synthetic or natural), then obviously not much change or evolution is
required to be able to use this 2,3-DNT molecule for energy. Unlike
bacterial motility systems, enzymatic cascades need not self-assemble
themselves in any *particular* way. All that needs to happen is for
all the required enzymes to be present in the intracellular
environment (in any order/arrangement). This is not the case for
other non-cascading functions (i.e., bacterial motility) where all the
protein parts are required to be in a *particular order* all working
together at the same time before the function in question will be
realized. The order of protein parts is not so important in cascading
enzyme functions. Only the presence of the parts is important, but
not so much their order.
However, even though cascading systems of enzymatic function are
relatively simple because of a lack of required specified order of the
individual parts, cascades are still fairly complex. Without the
original enzymes being there preformed, multi-enzyme cascades will
most likely not evolve even in billions of years. As in the case of
2,3-DNT utilization, if all the original enzymes are preformed, some
refining mutations will no doubt contribute to a more effective
interaction with and breakdown of this molecule. However, without the
original genes and enzymes in place to begin with, even this
relatively simple enzymatic function would most likely never have
evolved - even in billions of years. The authors themselves state as
much when they note that the "De novo evolution of genes for
nitrotoluene degradation during the short period of time seems
What I am proposing is that even with billions of years available,
such evolution of even this relatively simple cascading enzymatic type
function would still be unlikely if the required enzymes were not
already there preformed. Another thing is that these scientists did
not demonstrate the evolution of this function in real time.
Certainly I am not saying that this function did not evolve in real
time. It obviously did. However, these scientists were not able to
reproduce the actual evolution of this function in the lab. They came
to their conclusions by studying the pre-existing genes and functions
in those bacteria that had already evolved this function. They made
comparisons between the existing genes and other known genes in other
types of bacteria. Because of this, their hypothesized pathways and
series of mutational events are limited in that several gaps in
knowledge are involved. One of these gaps involves the gene encoding
the methylhydroxyquinone reductase for the 2,4-DNT pathway - which has
not been identified. As such, this experiment is not only limited in
its explanatory value over a real time demonstration, but even what it
proposes to explain doesn't even come close to an explanation of a
multi-protein system where each of the parts work together at the same
time (i.e., where a specific internal order of the individual protein
parts is important).
Thank-you though for the referral to this most interesting article. I
don't see how it helps your evolutionary position out much, but it was
very interesting none-the-less.
> And of course, there is the by-now classic example of the
> pentachlorophenol pathway.
As already noted above, cascades are different. The individual
proteins/enzymes that make up a cascade do not work together at the
same time. Because of this, the function of the cascade will not be
completely destroyed if one of the start proteins is removed. The
rest of the cascade will still function just fine. An enzymatic
cascade is even simpler since a specified order of the required
enzymes is not so important. As long as all of the required enzymes
are there floating around randomly, the sequential degradation of the
substrate will take place just fine. You see, a specified order of
the enzymes is not needed. They can be in any order here. However, if
a function is dependent upon multiple proteins all working together at
the same time, as in the case of bacterial motility systems like the
flagellar apparatus, then the ballgame is a bit different.
But, even such enzyme cascades are very difficult to evolve from
scratch. If only one or two point mutations are needed to proteins
that are already available to the cell, then such evolution is not a
problem, even if multiple proteins are involved (as was the case with
Hall's E. coli lactase evolution experiments where at least two
independent mutations were required before the lactase function could
be realized). However, if the genes in question are removed
completely, the evolution of even a simple multi-enzyme cascade will
never take place in anyone's lifetime – or even millions of years.
Also, I wouldn't call the genetic engineering in this case natural
evolution by random mutation and natural selection. A fair amount of
intelligent design was involved in this process. As it turns out, the
original wild-type bacteria did in fact have the ability to oxidize
polychlorinated benzenes to at least some degree to begin with. Many
chlorophenol products are known to be degraded by various
microorganisms, and therefore the CYP101 mutants could form the basis
of novel bioremediation systems for polychlorinated benzenes. The
genes encoding the three proteins of the CYP101 system can be
genetically introduced into chlorophenol-degrading micro-organisms to
convert chlorinated benzenes into phenols, which are then degraded by
natural pathways in the host organism. However, you will note that
these three genes are not "evolved" in these organisms, but are placed
there fully formed by intelligent design. A few subsequent mutations
are used later to refine their desired function, but the fact remains
that these required genes did not evolve from scratch at all. I mean,
certainly if Hall's E. coli could not evolve a relatively simple
lactase function from scratch without the ebg or lac genes previously
in place, I don't think that a function that required three complete
genes is going to just spring into existence in a single lifetime or
even in billions or trillions of years. The statistics are just too
much to overcome by purely mindless processes.
> "Molecular analysis of pentachlorophenol degradation", Orser CS, Lamae
> CC, Biodegradation 5:277 Dec 1994
> > This position of mine is clearly falsifiable. All one would have to
> > do is to evolve a multi-protein function (just two or three proteins
> > working together from scratch), and my theory would be falsified.
> Why do they have to be from scratch? Evolution is generally proposed
> to work on what is already there.
Yes, this is what the theory of evolution proposes, but this is what
has not been demonstrated in real time or even theorized in a
statistically significant way. Even if the genes and proteins are
fully formed to begin with, they simply do not self-assemble
themselves to form just any beneficial function that requires all the
proteins to work together at the same time. Examples of cascading
systems do not solve this problem - as described above.
> Even new genes as often as not are
> simply duplications of older ones that have subsequently mutated to
> serve a different function.
Where are the real time examples of this? Besides, a duplicated gene
is basically redundant, and if anything, a negative selective factor
for the organism who must support this duplication with more energy.
Also, a duplicated gene still has the problem of crossing the neutral
gaps that grow exponentially as one moves up the ladder of complexity.
> At any rate, the 2,4-DNT pathway is a
> multi-enzyme function that has, as far as anyone can tell, has
> appeared within a single human lifetime.
The 2,4-DNT pathway is a cascading multi-enzyme function in which the
required enzymes were already present preformed in the organism's
ancestors. Some modifying mutations were subsequently realized, but
the basic enzymes and the beneficial function were already available
to these bacteria to begin with - before this synthetic molecule came
> > On
> > the other hand, no evolutionist in this forum has offered a way in
> > which the theory of evolution might be falsified genetically.
> One way could be to demonstrate that various genes are sui generis,
> are isolated from all others by considerable "neutral gaps", and do
> not nest robustly into families and super-families.
Nesting does not disprove isolation since the nests themselves can be
isolated from other nests. Also, such nests are generally built using
single protein sequences. This method fails to take into account
those functions that require multiple proteins - all working together
at the same time. In order to calculate the nest size for such
functions, much longer sequence analysis would need to be employed and
compared to other sequences of equivalent multi-gene length. I am
betting that the gaps between the coded sequences for such
multi-protein functions would be much wider than many currently
realize. Also, nesting can equally be explained by the theory of
intelligent design. Your goal is to explain the differences, not so
much the similarities. Only in and explanation of the differences can
the theory of evolution be supported over the theory of intelligent
So you see, the simple demonstration of nesting is not a falsifiable
hypothesis. A falsifiable hypothesis presents a prediction that can
be tested and disproved. To say that nesting is present is not a
prediction, but an observation. You need to make a prediction based
on your current ideas of how genetic evolution is supposed to work
that can actually be disproved. For example, I have predicted that
the devo evolution of a multi-protein system of function where all the
proteins work together at the same time will never be demonstrated in
real time. This is a hypothesis that can be tested and disproved.
You need to come up with something equivalent.
> Phylogenists have
> tested their methods on random data, and have an idea what the results
> look like. If genetic sequences looked like that, instead of
> generally falling into nested families and superfamilies, you would
> have a point.
Not so. My position of ID also predicts nested hierarchies of genes
and protein sequences. You must therefore support your position over
my position with something that explains the differences. It is
erroneous for you to assume, without basis, that if life were
intelligently designed that no nesting would exist. The basis for
your theory must rest on an explanation of the differences in a
falsifiable manner. What falsifiable genetic test can you present
that supports your explanation of the differences as one moves up the
ladder of genetic complexity?
> But as Lilith has pointed out to you, genes fit onto phylogenetic
> trees just as organisms do; not only that, but the shape of the trees
> makes evolutionary sense.
Just because something makes "sense" or seems logical does not mean
that it is true. You must be able to make falsifiable predictions
based on this evidence that explains the differences. Also, these
trees do not always make so much sense. Genetic phylogeny is often
very contradictory to classical morphologic classification schemes.
"Animal relationships derived from these new molecular data sometimes
are very different from those implied by older, classical evaluations
of morphology. Reconciling these differences is a central challenge
for evolutionary biologists at present." (Maley, Laura E. and Charles
R. Marshall. 1998. The Coming of Age of Molecular Systematics. Science
"A year ago, biologists looking over newly sequenced genomes from more
than a dozen microorganisms thought these data might support the
accepted plot lines of life's early history. But what they saw
confounded them. Comparisons of the genomes then available not only
didn't clarify the picture of how life's major groupings evolved, they
confused it. And now, with an additional eight microbial sequences in
hand, the situation has gotten even more confusing . . . Many
evolutionary biologists had thought they could roughly see the
beginnings of life's three kingdoms . . . When full DNA sequences
opened the way to comparing other kinds of genes, researchers expected
that they would simply add detail to this tree. But "nothing could be
further from the truth," says Claire Fraser, head of The Institute for
Genomic Research (TIGR) in Rockville, Maryland. Instead, the
comparisons have yielded many versions of the tree of life that differ
from the rRNA tree and conflict with each other as well . . . "
(Elizabeth Pennisi, "Is It Time to Uproot the Tree of Life?" Science,
vol. 284, no. 5418, 21 May 1999, p. 1305 -
"As morphologists with high hopes of molecular systematics, we end
this survey with our hopes dampened. Congruence between molecular
phylogenies is as elusive as it is in morphology and as it is between
molecules and morphology. . . . Partly because of morphology's long
history, congruence between morphological phylogenies is the exception
rather than the rule. With molecular phylogenies, all generated
within the last couple of decades, the situation is little better.
Many cases of incongruence between molecular phylogenies are
documented above; and when a consensus of all trees within 1% of the
shortest in a parsimony analysis is published structure or resolution
tends to evaporate." (Patterson, Colin, and others. 1993. Congruence
Between Molecular and Morphological Phylogenies. Annual Review of
Ecology and Systematics 24:153-188).
"No consistent organismal phylogeny has emerged from the many
individual protein phylogenies so far produced. Phylogenetic
incongruities can be seen everywhere in the universal tree, from its
root to the major branchings within and among the various taxa to the
makeup of the primary groupings themselves." (Woese, Carl. 1998. The
Universal Ancestor. Proceedings of the National Academy of Sciences
> The trees show that genes with relatively
> specialized functions have branched off from genes with more general
> core biological functions, such as the various opsins in our eyes
> tracing back to more fundamental cell membrane proteins, or various
> factors in the blood-clotting cascade nesting as if they had
> progressively branched off from some sort of trypsin, a serine
> protease whose function, unlike those in the clotting cascade, is not
> predicated on a vertebrate's high-pressure circulation system.
All of these similarities can also be explained by conservation of
design. The burden of proof that would allow you to rationally
overcome the intuitively obvious designs in living systems would be
some way to explain the differences, not the similarities. What
falsifiable testable predictions can you come up with that support
your idea that random mutations and mindless natural selection can
give rise to the differences found in higher and higher levels of
functional complexity? An appeal to similarities is quite convincing
to most, but this is a logical fallacy since similarities do not
necessitate common evolutionary origin at all.
> If your South Pacific fitness landscape were the correct account of
> how functioning genetic sequences relate to one another, we shouldn't
> see any of this.
Why not? Why wouldn't we see islands of function with many different
variations depending upon many different variations in functional
needs in various local environments?
> A consistent failure to construct robust trees for
> gene families, or the frequent formation of robust trees that made no
> evolutionary sense would be a real problem for existing evolutionary
The problem is that everything can be made to make evolutionary sense.
Similar creatures living is similar environments would only be
expected to have many genetic and functional similarities as well.
Nothing lives to itself. All living things are dependent upon other
living things. If they were not molecularly and thus genetically
compatible, nothing would survive very long. The "cycle of life" is
dependent upon this fact. There would be no cycle if the basic
building blocks of the creatures involved were not interchangeable
with each other. Considering this need, it seems reasonable to
assume that those creatures that share the most similar environments,
body plans, and physiology would also have the most similar needs and
thus the most similar genetic and molecular machineries.
Biologist Leonard Brand makes this point quite eloquently in the
"Anatomy is not independent of biochemistry. Creatures similar
anatomically are likely to be similar physiologically. Those similar
in physiology are, in general, likely to be similar in biochemistry,
whether they evolved or were designed. . . An alternate,
interventionist hypothesis is that the cytochrome c molecules in
various groups of organisms are different (and always have been
different) for functional reasons. Not enough mutations have occurred
in these molecules to blur the distinct grouping evident. If we do
not base our conclusions on the a priori assumption of megaevolution,
all the data really tell us is that the organisms fall into nested
groups without any indication of intermediates or overlapping of
groups, and without indicating ancestor/descendant relationships."
(Brand, Leonard. 1997. Faith, Reason, and Earth History. Andrews
University Press, Berrien Springs, MI)
That fact of the matter is, even if such relationships did make sense,
this is not enough. If an alien from outer space came to this planet
after a nuclear holocaust where all humans had been wiped out, they
might conclude that all the various automobiles evolved from a common
ancestor over time or that all the computers evolved from a common
ancestor over time. I mean, nested hierarchies and many classifiable
similarities can be established for all of these things as well as the
books on my bookshelf. You see, many relationships can be made based
on similarities, but these similarities do not necessitate any theory
of common descent via random mutation and natural selection, however
rational that may sound at first glance. Unless the differences can
be explained, it a demonstration of classifiable similarities alone
means very little as far as an explanation of origins.
> Lilith has invited you to discuss gene phylogenies with
> her. Why don't you take her up, and explore that particular avenue of
> potential falsification?
I would be glad to discuss this with Lilith, but this is not an avenue
of potential falsification since it is a well-established observation.
The statement that it is impossible for mindless natural processes to
build a building like the Empire State Building is not falsifiable by
pointing to the Empire State Building. You must point to a
naturalistic process, not the finished product, in a falsifiable way.
The fact is, I have discussed this topic with Lilith. I find her
arguments lame and uninteresting and do not wish to spend my limited
time so much on points of debate that I have already covered
extensively and for which I have no particular interest.
> > > In fact Sean has seen at least one of them time after time.
> > Oh yeah? Which one?
> I believe Dunk is referring to the pentachlorophenol paper, although I
> do not have the message IDs handy for where you were shown this
> before. I could look if you like...
See above. . .
> > > When
> > > reminded, he says No, that doesn't count.
> > You need to be specific here. Your simple statement that this is what
> > happened is not enough. What exactly was I reminded of? What example
> > was used - specifically? I simply do not recall anyone ever showing
> > me an example of a multi-protein function evolving in real time.
> > > Not enough proteins.
> > Not enough proteins? You've got to be kidding! No one has shown me
> > the evolution of any multi-protein system requiring anything more than
> > one protein. I've not even been shown a system of function where two
> > proteins evolved in real time.
> Yes, you have. And actually the very Hall experiments that have been
> such a debating point did precisely this, since it involved both a
> novel dehydrogenase activity and a novel transport activity.
The second mutation that was needed involved a pre-formed regulator
gene. The transport of lactose across the cell membrane was
artificially achieved by Hall including a chemical that caused
membrane permeability. In any case, both the ebg and the regulator
genes required just one point mutation each before function was
realized. Again, this is not the de novo evolution of a double
protein system of function. The ebg gene was a de novo evolution of a
brand new protein, but the regulator sequence was the original.
> two proteins right there. In fact, Behe, on his web page has
> responded to this example by acknowledging that multi-protein
> metabolic pathways can evolve, and uses this argument to argue that
> such examples are therefore not IC, which AFAICT renders his argument
> completely circular and useless. He even claims to have mentioned
> this already in Darwin's Black Box, although I cannot find the quote
> he is referring to on the pages he supplies. Must be different
What Behe is referring to is that in his book he claims that cascading
systems of function can evolve and that they are not irreducibly
complex. I agree with him when he says that some cascading systems
certainly can evolve and have evolved in real time. However, I
disagree with Behe when he says that such systems of function are not
irreducibly complex. As you know, from my previous posts, I believe
that all systems of function are irreducibly complex but that there
are different levels of complexity. The lower levels of complexity
can be evolved quite rapidly because of a relative lack of significant
neutral gaps. However, as one moves up the ladder of complexity, the
gaps become quite significant indeed and evolution stalls out.
So you see, I think that Behe has it basically right, but he could do
better if he did not limit his definition of irreducible complexity to
only those systems of function of very high complexity.
> > > I want a completely new function requiring twenty or more
> > > proteins. I want it pronto. None of this millions of
> > > years business.
> > This is a complete lie. Where did I ever say that I reqiure the
> > demonstration of the evolution of a twenty protein function? I require
> > no such thing at all. The fact is though that the more parts that are
> > required for the realization of a particular level of function, the
> > time required will increase exponentially. The evolution of a
> > 20-protein function where all of the parts are all working together at
> > the same time would require googols of years to evolve spontaneously.
> > The time and population required simply boggles the imagination. But
> > hey, even a two or three protein system would require astronomical
> > amounts of time.
> And yet the 2,4-DNT pathway seems to have evolved in no more than a
> few decades.
And yet, the 2,4-DNT pathway is a cascading system where all the
required enzymes were already there and did not required any internal
specified order to perform this particular hydrolytic function.
> > And again, if you think that neutral gaps are not a problem, then why
> > do you still need millions of years?
> Why wouldn't you? You've never justified this conclusion, you have
> merely asserted it, so I don't see what argument there is to answer.
If there were no neutral gaps, there
would be nothing to slow evolution down. Without neutral gaps just
about any mutation would quickly produce new functions. Given the
very high mutation rates of living organisms, new functions would
rapidly poof into existence. For example, if a given bacterium would
be benefited by the ability to gain motility in a particular
competitive environment, the motility function would rapidly poof into
existence - if there were no neutral gaps. This problem is in fact
well recognized. It even has a name. According to John Harshman this
problem can be overcome by assuming (based on the fossil record etc.)
that the gap is "just right" to slow evolution down just enough to
make millions of years the time required to produce the changes that
we see around us today. Harshman suggests the name, "The Baby Bear
Theory" for this assumption. Well, I don't know about the Baby Bear
Theory, but it is encouraging to know that at least some, like
Harshman, actually seem to understand the problem even if they don't
have much of a solution.
> Von Smith
> Fortuna nimis dat multis, satis nulli.