The Ladder of Increasing Functional Complexity

And The Limits of How High Evolutionary Processes Can Climb


Sean Pitman M.D.

July 2003



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 (

Subject: Re: All Functions... Sean Pitman = Used Car Salesman

View: Complete Thread (28 articles) 

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Date: 2003-07-15 14:04:43 PST (Von Smith) wrote in message news:<>...

> (Sean Pitman) wrote in message news:<>...




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

> there.


Sean Pitman


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: <> I

> cited the following:


> begin quote



> Message-ID: <>



> 'Johnson GR, Jain RK, Spain JC. "Origins of the 2,4-dinitrotoluene

> pathway."

> 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

USA 95:6854-6859).


> 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

> theories.


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

following excerpt:


"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.


> That's

> 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

> editions.


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.