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AWESOME Post originally from RDF on Irreducible Complexity


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Intelligent Design and Transitional Fossils - by Calilasseia.

 

 

Let's start with so-called "irreducible complexity", shall we?

 

First of all, let's dismiss the canard that this was alighted upon by Michael Behe. It wasn't. He simply stole the concept, and tried to present it as a purported "problem" for evolutionary biology. Which becomes hilarious when you realise that the evolutionary biologist Hermann Joseph Müller alighted upon the idea of "irreducibly complex" structures not as a "problem" for evolutionary biology, but as a natural outcome of evolutionary processes. Here's how it works: it's called the Müllerian Two Step.

 

Step 1: Add a component;

 

Step 2: Make it necessary.

 

Indeed, Müller introduced this concept way back in 1918, and did so in the following scientific paper:

 

Genetic Variability, Twin Hybrids and Constant Hybrids in a Case of Balanced Lethal Factors by Hermann Joseph Müller, Genetics, 3(5): 422-499 (1918)

 

Here's the relevant quote from pages 465 and 466 of this paper, with the apposite part highlighted in boldface:

 

Most present-day animals are the result of a long process of evolution, in which at least thousands of mutations must have taken place. Each new mutant in turn must have derived its survival value from the effect upon which it produced upon the 'reaction system' that had been brought into being by the many previously formed factors in cooperation; thus, a complicated machine was gradually built up whose effective working was dependent upon the interlocking action of very numerous different elementary parts or factors, and many of the characters and factors which, when new, were originally merely an asset finally became necessary because other necessary characters and factors had subsequently become changed so as to be dependent upon the former. It must result, in consequence, that a dropping out of, or even a slight change in any one of these parts is very likely to disturb fatally the whole machinery

This was placed upon a rigorous footing by the 1930s, and evolutionary biologists refer to this in modern parlance using the term bricolage. Thus, Behe's canards were known to be canards by evolutionary biologists since before Behe was born.

 

Meanwhile, structures such as the eye and the bacterial flagellum didn't come into existence through random mutation alone - indeed, the omission of selection is another familiar creationist canard. Nick Matzke has not only published a paper in which he predicted that specific homologies would be found between flagellar proteins and those of antecedent systems, but also published a paper in which he presented a model for the selection of the relevant components. Indeed, I think it's worth reviewing the literature on the bacterial flagellum in detail, just to establish how much scientists actually do know about this structure, knowledge which would never have been acquired if they had followed Behe's lead and said "Magic Man did it, don't bother asking questions". So, sit down, and prepare for a long read, because I'm going to take you through about a dozen papers on the subject. Sitting comfortably? Good, I'll begin.

 

Those nice people over at TalkRational pointed me to a very interesting blog. Namely the blog of Mark Pallen, who was co-author with Nick Matzke of at least one peer reviewed paper in Nature] on the bacterial flagellum (and indeed probably wrote more - I just happen to be aware of the one I have saved to my hard drive). That paper is the following one:

 

From The Origin Of Species To The Origin Of Bacterial Flagella by Mark J. Pallen & Nicholas J. Matzke, Nature Reviews Microbiology, 4(10): 784-790 (October 2006).

 

I shall return to this paper shortly, but first, a little preamble is needed.

 

For those unfamiliar with the background, Nick Matzke was the author of an interesting article, namely this one, which hypothesised that the various proteins that are found in the bacterial flagellum would be found to be homologous with other proteins belonging to other metabolic systems, and that as a consequence, the bacterial flagellum would eventually be found to be the result of co-opting existing, earlier systems and re-using them for another purpose - a classic evolutionary process. Needless to say, a lot of noise was emitted by the ID brigade to the effect that Matzke's ideas were "speculation", and the rest of it, but, the point here is that Matzke made testable predictions in his article, and in doing so provided evolutionary biologists with real substance that they could pursue in the laboratory. The following quote from the abstract of Matzke's original paper is apposite:

 

A new model is proposed based on two major arguments. First, analysis of dispersal at low Reynolds numbers indicates that even very crude motility can be beneficial for large bacteria. Second, homologies between flagellar and nonflagellar proteins suggest ancestral systems with functions other than motility. The model consists of six major stages: export apparatus, secretion system, adhesion system, pilus, undirected motility, and taxis-enabled motility. The selectability of each stage is documented using analogies with present-day systems. Conclusions include: (1) There is a strong possibility, previously unrecognized, of further homologies between the type III export apparatus and F1F0-ATP synthetase. (2) Much of the flagellum’s complexity evolved after crude motility was in place, via internal gene duplications and subfunctionalization. (3) Only one major system-level change of function, and four minor shifts of function, need be invoked to explain the origin of the flagellum; this involves five subsystem-level cooption events. (4) The transition between each stage is bridgeable by the evolution of a single new binding site, coupling two pre-existing subsystems, followed by coevolutionary optimization of components. Therefore, like the eye contemplated by Darwin, careful analysis shows that there are no major obstacles to gradual evolution of the flagellum.

Now, note that specific predictions were made with respect to the homologies involved, namely that homologies would be found between flagellar proteins and those of the Type 3 Secretory System, plus an enzyme called F1F0-ATP synthetase. I'll leave the latter enzyme aside for a moment, but return to it because this one turns out to play an important role. Stay tuned for the fun revelations!

 

Now, first of all, the paper from Nature Reviews Microbiology I cited above by Matzke & Pallen itself dispenses wholesale with the idea of the bacterial flagellum being "irreducibly complex", because, lo and behold, there are bacteria with flagella that are missing numerous components. From that paper, I copy the following details with respect to the presence or absence of specific flagellar proteins in various bacteria possessing flagella:

 

FlgA (P ring) - Absent from Gram-Positive bacteria

FlgBCFG (Rod) - universal

FlgD (Hook) - universal

FlgE (Hook) - universal

FlgH (L Ring) - Absent from Gram-Positive bacteria

FlgI (P Ring) - Absent from Gram-Positive bacteria

FlgJ (Rod) - FlgJ Rod N-terminal domain absent from some systems

FlgK (Hook-Filament Junction) - universal

FlgL (Hook-Filament Junction) - universal

FlgM (Cytoplasm & Exterior) - Absent from Caulobacter

FlgN (Cytoplasm) - Undetectable in some systems

FlhA (T3SS apparatus) - universal

FlhB (T3SS apparatus) - universal

FlhDC (Cytoplasm) - Absent from many systems

FlhE (Unknown) - Mutant retains full motility

FliA (Cytoplasm) - Absent from Caulobacter

FliB (Cytoplasm) - Absent from Escherichia coli

FliC (Filament) - universal

FliD (Filament) - Absent from Caulobacter

FliE (Rod/Basal Body) - universal

FliF (T3SS apparatus) - universal

FliG (Peripheral) - universal

FliH (T3SS apparatus) - Mutant retains some motility

FliI (T3SS apparatus) - universal

FliJ (Cytoplasm) - Undetectable in some systems

FliK (Hook/Basal Body) - universal

FliL (Basal body) - Mutant retains full motility

FliM (T3SS apparatus) - universal

FliN (T3SS apparatus) - universal

FliO (T3SS apparatus) - Undetectable in some systems

FliP (T3SS apparatus) - universal

FliQ (T3SS apparatus) - universal

FliR (T3SS apparatus) - universal

FliS (Cytoplasm) - Absent from Caulobacter

FliT (Cytoplasm) - Absent from many systems

FliZ (Cytoplasm) - Absent from many systems

MotA (Inner membrane) - universal

MotB (Inner membrane) - universal

 

So, the mere fact that there are in existence bacteria with missing proteins from the above list whose flagella still function rather makes a mockery of the "irreducible complexity" assertion to begin with. But, this is only part of the story. The same paper continues with the following:

 

Many paths to motility

 

Although the evolution by random mutation and natural selection of something as complex as a contemporary bacterial flagellum might, in retrospect, seem highly improbable, it is important to appreciate that probabilities should be assessed by looking forward not back [2]. For example, from studies on protein design it is clear that creating proteins from scratch that, like flagellin, self-assemble into filaments is not very difficult [39,40]. Furthermore, it is clear that there are many other filamentous surface structures in bacteria that show no apparent evolutionary relationship to bacterial flagella [41,42]. In other words, there are plenty of potential starting points for the evolution of a molecular propeller. Evolution of something like the flagellar filament is therefore far less surprising than it might at first seem. In fact, microorganisms have adopted other routes to motility besides the bacterial flagellum [43]. Most strikingly, although archaeal flagella superficially resemble bacterial flagella, in that they too are rotary structures driven by a proton gradient, they are fundamentally distinct from their bacterial counterparts in terms of protein composition and assembly.

 

Intermediate forms

 

What about intermediate forms between bacterial flagella and other biological entities? Darwin encountered a similar argument about gaps in the fossil record, and in response he pointed out how improbable fossilization was, so that little of any extinct biosphere could ever be expected to appear in the fossil record [14]. Although fossils are of no use in reconstructing flagellar evolution, similar arguments might be made at the molecular level. Despite a decade of bacterial genome sequencing, we have scarcely begun to sample the molecular diversity of the biosphere. Yet even with the scant coverage of genome sequence data to date, several curiosities have already been revealed. For example, there is growing evidence that flagellin and the flagellar filament are homologous to the NF T3SS protein EspA and the EspA filament, respectively [35,44–48]. The EspA filament therefore provides a model for how the ancestral flagellar filament might have functioned for purposes other than locomotion (adhesion or targeted protein secretion). Furthermore, the EspA protein from E. coli initially seemed to be one of a kind. However, thanks to genome sequencing, related proteins have been identified in several bacteria occupying diverse niches, including: S. typhimurium, Edwardsiella ictaluri, Shewanella baltica, Chromobacterium violaceum, Yersinia frederiksenii, Yersinia bercovieri and Sodalis glossinidius. In addition, proteins that resemble flagellar components but that are encoded in the genomes of bacteria that do not engage in flagellar motility have also been identified. The first example of these potential ‘missing links’ came from the chlamydias [49]. More recently, flagellar-related genes have been detected in the genome of the soil bacterium Myxococcus xanthus, which uses gliding rather than flagellar motility [35]. It seems likely that other examples of potential evolutionary intermediaries will be found as we sequence an increasing proportion of the biosphere.

Towards a plausible evolutionary model

 

From the above discussions of sequence homologies and modularity, it is clear that designing an evolutionary model to account for the origin of the ancestral flagellum requires no great conceptual leap. Instead, one can envisage the ur-flagellum arising from mergers between several modular subsystems: a secretion system built from proteins accreted around an ancient ATPase, a filament built from variants of two initial proteins, a motor built from an ion channel and a chemotaxis apparatus built from pre-existing regulatory domains (FIG. 1). As we have seen, each of these function in a modular fashion and share ancestry with simpler systems — thereby answering the question ‘what use is half a flagellum?’ Furthermore, it is not hard to envisage how an ancestral crude and inefficient flagellum, if it conferred any motility at all, could function as the starting material for natural selection to fashion today’s slicker flagellar apparatus.

 

However, one could still question how, from such bricolage, natural selection could lock on to an evolutionary trajectory leading to an organelle of motility in the first place, when none of the components alone confer the organism with a selective advantage relevant to motility. The key missing concept here is that of exaptation, in which the function currently performed by a biological system is different from the function performed while the adaptation evolved under earlier pressures of natural selection [50]. For example, a bird’s feathers might have originally arisen in the context of selection for, say, heat control, and only later have been used to assist with flight [51,52]. Under this argument, a number of slight but decisive functional shifts occurred in the evolution of the flagellum, the most recent of which was probably a shift from an organelle of adhesion or targeted secretion, such as the EspA filament, to a curved structure capable of generating a propulsive force.

 

Now, as a slight tangential diversion, which along the way provides yet more evidence for evolutionary hypotheses, one avenue of attack being considered with respect to the development of the bacterial flagellum is the reconstruction of earlier, more ancient versions of the proteins responsible for the construction of this structure. Precedents already exist with respect to the reconstruction of ancient genes, and the following four papers are examples thereof:

 

Crystal Structure Of An Ancient Protein: Evolution By Conformational Epistasis by Eric A. Ortlund, Jamie T. Bridgham, Matthew R. Redinbo and Joseph W. Thornton, Science, 317: 1544-1548 (14 September 2007)

 

Resurrecting Ancient Genes: Experimental Analysis Of Extinct Molecules by Joseph W. Thornton, Nature Reviews: Genetics, 5: 366-375 (5 May 2004)

 

Resurrection Of DNA Function In Vivo From An Extinct Genome by Andrew J. Pask, Richard R. Behringer and Marilyn B. Renfree, PLoS One, 3(5): e2240 (online version, May 2008)

 

The Past As The Key To The Present: Resurrection Of Ancient Proteins From Eosinophils by Steven A. Benner, Proc. Natl. Acad. Sci. USA., 99(8): 4760-4761 (16 April 2002)

 

From the paper by Pask et al above, we have:

There is a burgeoning repository of information available from ancient DNA that can be used to understand how genomes have evolved and to determine the genetic features that defined a particular species. To assess the functional consequences of changes to a genome, a variety of methods are needed to examine extinct DNA function. We isolated a transcriptional enhancer element from the genome of an extinct marsupial, the Tasmanian tiger (Thylacinus cynocephalus or thylacine), obtained from 100 year-old ethanol-fixed tissues from museum collections. We then examined the function of the enhancer in vivo[ Using a transgenic approach, it was possible to resurrect DNA function in transgenic mice. The results demonstrate that the thylacine Col2A1 enhancer directed chondrocyte-specific expression in this extinct mammalian species in the same way as its orthologue does in mice. While other studies have examined extinct coding DNA function in vitro, this is the first example of the restoration of extinct non-coding DNA and examination of its function in vivo. Our method using transgenesis can be used to explore the function of regulatory and protein-coding sequences obtained from any extinct species in an in vivo model system, providing important insights into gene evolution and diversity.

So scientists are already resurrecting ancient proteins and testing their functionality in model organisms. Indeed, one of the results in the scientific literature comes courtesy of this paper:

 

Resurrecting The Ancestral Steroid Receptor: Ancient Origin Of Oestrogen Signalling by J.W. Thornton, E. Need and D. Crews, Science, 301: 1714-1717 (2003)

 

in which the scientists determined that the modern receptors for steroid hormones in modern organisms are traceable to an ancestral receptor dating back 600 million years, and reconstructed the ancestral steroid receptor in the laboratory to determine that it worked.

 

So, given that precedents already exist for the successful reconstruction of ancient proteins and the genes coding for them, this avenue of attack is likely to prove highly instructive with respect to the bacterial flagellum. Indeed, Pallen & Matzke make this very observation in their paper:

But obviously, one cannot model millions of years of evolution in a few weeks or months. So how might such studies be conducted? One option might be to look back in time. It is feasible to use phylogenetic analyses to reconstruct plausible ancestral sequences of modern-day proteins, and then synthesize and investigate these ancestral proteins. Proof of principle for this approach has already been demonstrated on several NF proteins [69–75]. Similar studies could recreate plausible ancestors for various flagellar components (for example, the common ancestor of flagellins and HAP3 proteins). These proteins could then be reproduced in the laboratory in order to examine their properties (for example, how well they self-assemble into filaments and what those filaments look like). An alternative, more radical, option would be to model flagellar evolution prospectively, for example, by creating random or minimally constrained libraries and then iteratively selecting proteins that assemble into ever more sophisticated artificial analogues of the flagellar filament. Another experimental option might be to investigate the environmental conditions that favour or disfavour bacterial motility. The fundamental physics involved (diffusion due to Brownian motion) is mathematically tractable, and has already been used to predict, for example, that powered motility is useless in very small bacteria [76,77].

Now, back in 2006, Pallen & Matzke listed some known homologies, and once again, I reproduce their results from the table in the paper:

 

FlgA (P ring) - CpaB

FlgBCFG (Rod) - FlgBCEFGK

FlgD (Hook) - none specified

FlgE (Hook) - FlgBCEFGK

FlgH (L Ring) - none yet known

FlgI (P Ring) - none yet known

FlgJ (Rod) - none yet known

FlgK (Hook-Filament Junction) - FlgBCEFGK

FlgL (Hook-Filament Junction) - FliC

FlgM (Cytoplasm & Exterior) - none yet known

FlgN (Cytoplasm) - none yet known

FlhA (T3SS apparatus) - LcrD/YscV

FlhB (T3SS apparatus) - YscU

FlhDC (Cytoplasm) - Other activators

FlhE (Unknown) - none specified

FliA (Cytoplasm) - RpoD, RpoH, RpoS

FliB (Cytoplasm) - none specified

FliC (Filament) - FlgL, EspA

FliD (Filament) - none yet known

FliE (Rod/Basal Body) - none yet known

FliF (T3SS apparatus) - YscJ

FliG (Peripheral) - MgtE

FliH (T3SS apparatus) - YscL, AtpFH

FliI (T3SS apparatus) - YscN, AtpD, Rho

FliJ (Cytoplasm) - YscO

FliK (Hook/Basal Body) - YscI

FliL (Basal body) - none yet known

FliM (T3SS apparatus) - FliN, YscQ

FliN (T3SS apparatus) - FliM, YscQ

FliO (T3SS apparatus) - none

FliP (T3SS apparatus) - YscR

FliQ (T3SS apparatus) - YscS

FliR (T3SS apparatus) - YscT

FliS (Cytoplasm) - none yet known

FliT (Cytoplasm) - none yet known

FliZ (Cytoplasm) - none yet known

MotA (Inner membrane) - ExbB, TolQ

MotB (Inner membrane) - ExbD, TolR, OmpA

 

Now, as Pallen states in his blog entry as linked above, out of this list of proteins, only two were listed as being both essential to all bacterial flagella AND possessing no known homologues in 2006. Those proteins were FliE and FlgD. From the 2006 update of Matzke's original 2003 paper, we read:

Many of the homologous and/or inessential proteins found in Table 1 of Pallen and Matzke 2006 were cited in the 2003 paper, but the 2006 table is an authoritative update and supercedes what is said here. The important overall point, as discussed in my blog post, is that of the 42 proteins in Table 1 of Pallen and Matzke, only two proteins, FliE and FlgD, are both essential and have no identified homologous proteins. This is substantially more impressive than the situation in 2003, and means that the evidence for the evolutionary origin of the flagellum by standard gene duplication and cooption processes is even stronger than in 2003. Important specific updates include: a homolog of FlgA has been confirmed (along the lines that I suggested in 2003); FliG has no homolog in NF-T3SS or the Exb/Tol systems, rather it may be homologous to the magnesium transporter MgtE; and the flagellar filament protein FliC (and its sister FlgL) is probably homologous to EspA and other pilus proteins found in NF-T3SS. I still suspect that all of the axial proteins (including FliE and FlgD) are homologous to each other and therefore to pilus proteins in NF-T3SS, but only the confirmed homologies are reported in Pallen and Matzke 2006.

At least, this was the situation back in 2006. However, science moves on!

 

First, take a look at atpsynthase.info, which is the site devoted to ATP synthase. Now, one of the homologies that Matzke originally hypothesised was that at least one of the flagellar proteins would prove to be homologous to proteins in the ATP synthase group, in particular the awkwardly named F1F0-ATP synthetase. Now it turns out that ATP synthases are themselves complex entities, and indeed F1-ATPase rotates on an axis as it performs its synthesis! However, as this paper:

 

Axle-Less F1-ATPase Rotates In The Correct Direction by Shou Furuike, Mohammad Delawar Hossain, Yasushi Maki, Kengo Adachi, Toshiharu Suzuki, Ayako Kohori, Hiroyasu Itoh, Masasuke Yoshida and Kazuhiko Kinosita, Jr., Science, 319: 955-958 (No. 5865, 15 February 2008)

 

reveals very succinctly, dismantling this structure so that it no longer has an axle to rotate about does not stop it from functioning! Here's the abstract:

F1–adenosine triphosphatase (ATPase) is an ATP-driven rotary molecular motor in which the central γ subunit rotates inside a cylinder made of three α and three β subunits alternately arranged. The rotor *****, an antiparallel α-helical coiled coil of the amino and carboxyl termini of the γ subunit, deeply penetrates the central cavity of the stator cylinder. We truncated the ***** step by step until the remaining rotor head would be outside the cavity and simply sat on the concave entrance of the stator orifice. All truncation mutants rotated in the correct direction, implying torque generation, although the average rotary speeds were low and short mutants exhibited moments of irregular motion. Neither a fixed pivot nor a rigid axle was needed for rotation of F1-ATPase.

Another blow to "irreducible complexity" sensu Behe (Hermann Müller would doubtless have smiled wryly over this!), but this isn't all. Returning to Pallen's blog, we find this:

Since the early 1990s, it has been known, from sequence comparisons, that the flagellar ATPase (FliI) is homologous to the alpha and beta subunits of the F-type ATPase, a transmembrane protein complex (see figure) found in bacteria, mitochondria and chloroplasts (see http://www.atpsynthase.info).

 

In 2003, Nick Matzke (then at the NCSE and so a couple of years later science adviser to the plaintiffs in the Dover trial) wrote an essay summarising plausible evolutionary scenarios for the origin of the bacterial flagellum. He noted a couple of previous suggestions that the proto-flagellum might have originated from the F-type ATPase. Crucially, he predicted that additional homologies would be found between components of the F-type ATPase and the flagellar protein export apparatus, for example between the b subunit of the ATPase and FliH and between the delta subunit and FliJ.

 

In 2006, I confirmed one of Nick's hunches through homology searches, showing that part of FliH was homologous to the b subunit. However, things turned out slightly different from Nick's predictions in that FliH is actual of a fusion of domains homologous to the b subunit and the delta subunit.

 

Last year Namba's group published the structure of FliI and confirmed the striking homology with the F-type ATPase enzymatic subunits. At that stage in the game, it had become clear that the ATPase was a universal component not just of flagellar export systems but also of non-flagellar type III secretion systems. Also, if it was also clear that if one knocked out the gene for FliI, one abolished flagellar biosynthesis. Thus, just about everyone in the field accepted that FliI was an essential component of the flagellar apparatus and that it energised secretion of proteins through the protein export system. In other words, if there were anything to the idea, put forward by Behe and others in the ID movement, that the flagellum showed "irreducible complexity", even experts might have accepted that FliI was one of the "irreducible" components!!

 

BUT earlier this year, Minamino and Namba (and independently a team headed by Kelly Hughes in the US) overturned all our assumptions by showing that it was perfectly possible to make flagella without FliI--what you needed to do was knock out FliH at the same time. Somehow or other FliH, which usually interacts with FliI, gums up the export apparatus in the absence of FliI. So, bang goes another pillar of support for the ID argument! In fact, it appears that flagellar protein export is powered not primarily by the ATPase but by the proton-motive force.

So, the FliI protein appeared on the face of it to be essential, because knocking out the gene for FliI synthesis destroyed flagellar biosynthesis. But, and here's the part that really throws the spanner into "irreducible complexity" as espoused by Behe, if you knock out the gene coding for FliI, but in addition knock out the gene for FliH, flagellar biosynthesis returns! This rather buggers up Behe's version of "irreducible complexity" in a spectacular manner.

 

Yet even this is not the whole story. Believe it or not, there is more! Returning to Pallen's blog, we read:

Namba and colleagues have now solved the structure of FliJ, another protein that interacts with FliI and FliH. And what they found was clear evidence of homology with yet another protein from the F-type ATPase--the gamma subunit!

 

So, now we have deep and broad homologies between the flagellum and the F-type ATPase, just as Nick predicted. This provides another nail in the coffin of the idea that flagellum was intelligently designed. If the flagellum were the product of intelligent design, particularly by an omniscient deity, the designer could have custom-built it from scratch, so it need not resemble anything else in nature. By contrast, the processes of evolution tends to cobble together and tweak already existing components (something Francois Jacob called bricolage)--and slowly but steadily it is become clear that the flagellum has been built this way.

 

Incidentally, the paper covering the homology between FliI and the alpha and beta subunits of the F-type ATPase is this paper:

 

Salmonella typhimurium Mutants Defective In Flagellar Filament Regrowth And Sequence Similarity Of FliI to F0F1, Vacuolar, And Archaebacterial ATPase Subunits by Alfried P. Vogler, Michio Homma, Vera M. Irikura and Robert M. McNab, Journal of Bacteriology, 173(11): 3564-3572 (June 1991) [Full paper downloadable]

 

so this homology had actually been known even before Behe made his assertions about "irreducible complexity", something he would have known if he had bothered to perform a basic literature search. After all, he has institutional access, whereas I don't currently, yet I was able to find this paper once pointed in the right direction. This paper also covers the knocking out of the gene for FliI and the effect on flagellar biosynthesis.

 

More pertinently, the following paper:

 

Evolutionary Links Between FliH/YscL-Like Proteins From Bacterial Type III Secretion Systems And Second-Stalk Components Of The F0F1 And Vacuolar ATPases by Mark J. Pallen, Christopher M. Bailey and Scott A. Beatson, Protein Science, 15: 935-941 (2006) [Full paper downloadable]

 

is the one containing the confirmation by Pallen of one of Matzke's predictions as cited above. Another homology was confirmed courtesy of this paper:

 

Structural Similarity Between The Flagellar Type III ATPase FliI And F1-ATPase Subunits by Katsumi Imada, Tohru Minamino, Aiko Tahara and Keiichi Namba, Proceedings of the National Academy of Sciences of the USA, 104(2): 485-490 [Full paper downloadable]

 

This paper:

 

Distinct Roles Of The FliI ATPase And Proton Motive Force In Bacterial Flagellar Protein Export by Tohru Minamino and Keiichi Namba, Nature, 451: 485-489 (24th January 2008) [Full paper downloadable]

 

is the paper that covers the knocking out of FliH and FliI resulting in restoration of flagellar biosynthesis.

 

So, now the only two proteins remaining to find homologies for are FliE and FlgD, and you can bet that this is being worked upon as I type this.

 

What was that about "evolution couldn't produce the bacterial flagellum" again? Looks like someone needs to spend time reading some real science instead of creationist websites.

 

Oh, and as for the "no transitional fossils" canard, allow me to present:

 

Here's a sequence of fossils covering the tetrapod lineage, namely:

 

Eusthenopteron ... 385 million years ago

Panderichthys ... 380 million years ago

Tiktaalik ... 375 million years ago

Acanthostega ... 365 million years ago

Ichthyostega ... 362.5 milllion years ago

Hypnerpeton] ... 360 million years ago

 

Several other taxa have been added since I compiled that list.

 

Indeed, Tiktaalik was predicted to exist before it was found. Not only was it predicted to exist, but it was predicted to possess specific features and to exist in a particular geological stratum before it was found. Moreover, the fossil was found where it was predicted to exist, and upon detailed examination, was found to possess the precise anatomical features that were predicted in advance by evolutionary biologists and palaeontologists. Here are some nice illustrations of anatomical comparisons (click on links to view):

 

Comparative anatomy of tetrapods

 

So, since scientists knew what to look for in advance, found the fossil of Tiktaalik where it was predicted it would exist, and found that Tiktaalik possessed the anatomical features it was predicted to possess on the basis of it being an intermediate step between earlier creatures and later creatures in the sequence, we can consider this confirmed set of predictions validated by real world evidence to be yet more support for the existence of a sequence of organisms in various stages of development between Rhipidistian fishes and land-dwelling tetrapods, as if, of course, all the other fossils cited above weren't enough to begin with.

 

Moving on to the theropods, here's a nice list of relevant fossils which exhibit a brace of features that any trained comparative anatomist would regard as "transitional":

 

Shuvuuia ... 81 million years ago

Protarchaeopteryx ... 122 million years ago

Sinosauropteryx ... 122 million years ago

Sinornithosaurus ... 122 million years ago

Caudipteryx ... 125 million years ago

Beipiaosaurus ... 125 million years ago

Yixianosaurus ... 125 million years ago

Jinfengopteryx ... 125 million years ago

Sinocalliopteryx ... 125 million years ago

Cryptovolans ... 130 million years ago

Dilong ... 130 million years ago

Microraptor ... 130 million years ago

Archaeopteryx ... 155 million years ago

Pedopenna ... 160 million years ago

Epidendrosaurus ... 170-120 million years ago (date yet to be more precisely determined)

Scansoriopteryx ... 170-120 million years ago (date yet to be more precisely determined)

 

An interesting scientific paper is this one which contains an extensive family tree of theropods and pre-Avian dinosaurs, namely:

 

A Basal Dromaeosaurid And Size Evolution Preceding Avian Flight by Alan H. Turner, Diego Pol, Julia A. Clarke, Gregroy M. Erickson and Mark A. Noreli, Science, 317: 1378-1381 (7th September 2007)

 

This paper includes a good number of illustrations of the fossils of a recent discovery among the Dromaeosaurids, namely Mahakala omnogovae - indeed, the paper describes the holotype.

 

What was that about "no transitional fossils" again?

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One variable always left out is water. No aspect of the evolutionary process can happen without water being present. We are leaving out this other half the equation of life, which represents most of the atoms of life. What is left does not contain all the logic needed for pure reason, causing us to remain in empirical mode by default.

 

The variety of things possible via the organics of life appears limitless. While the odds that life can form from simple organic seems low. However, the main component of life, which is water, is more limited in terms of preferred states. This sets limit for life and defines preferred states; lowest energy. With water, one is not just talking about the organic odds, but an aqueous system that makes specific organic outcomes more preferred for energy reasons.

 

One is not throwing dice in a vacuum, but in a media that can interact with the dice. The six dimple side has a different drag in the water than the one dimple side of the dice, creating a prefer dice spin.

 

For example, the lipid bi-layer of the membrane is the lowest energy state of these materials, when these materials are dissolved in water. There are not an infinite number of possibilities (leave out water and assume this is done in a vacuum). Rather there is one lowest energy state because of water. Even before life or lipids appeared on earth this was still going to be the fate of the lipids because of water, even if chaos was working overtime rolling the dice for the lipids for millions of variations.

 

Although harder to demonstrate, I assume that many other milestones of life, although random to some extent, have favored states in water. Once you know what is favored in water, it eventually becomes what is optimized with selective advantage; irreducible simplicity.

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I read the entire OP through twice and still I don't see how it addresses the fundamental issue raised by Behe that there is no natural mechanism offered that at the molecular level accounts for the similarities described in the compiled summaries and more importantly no mechanism the describes how these molecular systems that he defines as having irreducible complexity actually formed in a stepwise fashion.

 

Do we suppose that the modern protein systems were derived from a common form of these similar components found in other biological systems by known processes or do we know they are related? If so, how do we know? Have we conducted experiments that confirm that the presumed processes actually occur?

 

It seems to me that citing similarities only confirms that some proteins with different functions have some sequence similarity. Several explanations for these similarities are possible.

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I agree. It provides an excellent opportunity to discuss many of the difficulties with the current models of both common ancestry and descent with modification as solutions to the diversity we observe in biology. The argument that holology or similarities of proteins in current biological organisms provides demonstration that Behe is wrong about the nature of complex biomoloecular systems is very very incomplete and it exposes a much bigger weakness in arguments that selection acting on genetic errors accounts for all of life based on homology of organisms and sequence similarity in genes.

 

A solution to the question of how biological diversity occurred cannot be answered if there is not an identified process or processes that are known to have accomplished all of the modes of changes involved. Behe agrees that there is good evidence for common descent but he argues that the mechanisms or processes that are cited are not capable of generating many of the structures we observe at the molecular level. His argument is based on the molecular processes occurring within the cell. These processes were unknown back in 1920-1930 so it is silly to argue that this was dismissed 80 years ago.

 

Systems of multiple molecular components containing specific well fitted shapes along with multiple specific coherent properly place binding sites attached together to form complex molecular machines that perform cell level functions is what he is talking about. When you properly discuss the strict definition of what Behe calls irreducible complexity such that if certain (but not just any) components is removed, the system can no longer perform at least one of its primary functions then the idea that citing sequence similarity and homology as opposed to processes one should see that the argument is far from over. Because it is far from over, and because the current models do not provide a mechanism to accomplish these molecular level changes, we can't say the mechanism for diversity is known. In fact the mechanisms currently cited are being tested experimentally and they do not generate the kinds of molecular level alterations required to derive new tertiary structures, protein-protein binding sites, gene expression, regulatory and developmental controls, and a number of other low level changes required to generate a novel functioning system of interacting protein components in a time period cited by the geologic sequence whether or not one has a ready supply of these components with similar primary amino acid sequences or not.

 

The first argument that different flagellum systems are observed with different components and therefore one can remove some components and the system will still function. Clearly that is true but that is not Behe's argument. Functioning systems can and do contain parts that improve function or reliability but are not critical to primary function. An auto engine has many of these parts, however if you remove the crank shaft you will no longer have an engine. Same with flagellum. Some components are extra but there exists a subsystem of components that are critical. Focusing on extra components and noting that extra components are extra fails to address Behe's argument.

 

The second argument makes an appeal to homologies. But noting that particular proteins display sequence similarities not not provide any insight into the process by which novel protein tertiary structures, and binding sites are formed and it is the processes that Behe argues against.

 

The third argument returns to the definition of critical subcomponents thus demonstrating that the author of the post recognizes that the first argument is logically incorrect. It note that the axle should be considered a critical sub-component and then provides a example where an ATP based hydrogen pump system lacking an axle still rotates whereby the turbine asembly serves one of the functions of an axle but only when there is no connected load. But this is not new information, engineers know of this limited and special case. However when the axle is removed, another critical function is eliminated, namely the ability to have a connected load attached and therefore the system still does not meet Behe's definition.

 

The forth argument returns to homologies, again straying very far from the actual argument, which is about the process of developing and assembling the required components as opposed to locating possible sources of similar gene sequences.

 

And then the post ends, never having addressed the argument behe makes against the inability to identify processes capable of generating such systems.

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Life on earth formed in water. The properties of water, which is the most anomalous of all chemicals, are still limited in scope. The theoretical organic complexity, on the other hand, appears almost limitless. When we combine both, to form life, the limitations of water reduce the organic complexity, to a greatest hits set, since only certain situations can take full advantage of the properties of water; certain organic things offer selective advantage in terms of the entire system water/organic.

 

If we assume the organics evolved without water, then it looks like there are infinite possibilities and random/chance limited the set. If we add water, random/chance is replaced by the potentials and properties of water, molding what is optimized in the system water/organic. If we know water, we know how organics need to align in fundamental ways, if the goal is to fully take advantage of the potential that water has to offer; selective advantage.

 

Here is the analogy. A person is in charge of a summer camp of small children (water). As the leader (organics), you can initiate any type of activity. Although the possibilities are almost endless, not all activities will allow the camp of children to get the most out of the camp experience. For example, although cliff diving is possible, very few can or will be able to participate; there no selective advantage for the group. However, there are a more limited number of activities that will allow the entire group to participate, giving all the best experience. With life, some theoretical organic complexity is like cliff diving and will not work very well in water. But there are certain things that work perfectly.

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Is it really necessary to refute specific allegations of irreducible complexity as obstacle to evolution? There is always going to be something we haven't figured out yet, and creationists will always point to such things as evidence that it could only have been intentional. That's how arguments from ignorance work. Once upon a time the anger of the gods was "the only possible explanation" for lightning and earthquakes.

 

Rather than directly refuting whatever the current specific claim is, make a general response.

1) Tell them to look up "argument from ignorance."

2) Tell them to look up "exaptation."

3) Go back to doing real science.

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Life on earth formed in water. The properties of water, which is the most anomalous of all chemicals, are still limited in scope. The theoretical organic complexity, on the other hand, appears almost limitless. When we combine both, to form life, the limitations of water reduce the organic complexity, to a greatest hits set, since only certain situations can take full advantage of the properties of water; certain organic things offer selective advantage in terms of the entire system water/organic.

 

If we assume the organics evolved without water, then it looks like there are infinite possibilities and random/chance limited the set. If we add water, random/chance is replaced by the potentials and properties of water, molding what is optimized in the system water/organic. If we know water, we know how organics need to align in fundamental ways, if the goal is to fully take advantage of the potential that water has to offer; selective advantage.

 

Here is the analogy. A person is in charge of a summer camp of small children (water). As the leader (organics), you can initiate any type of activity. Although the possibilities are almost endless, not all activities will allow the camp of children to get the most out of the camp experience. For example, although cliff diving is possible, very few can or will be able to participate; there no selective advantage for the group. However, there are a more limited number of activities that will allow the entire group to participate, giving all the best experience. With life, some theoretical organic complexity is like cliff diving and will not work very well in water. But there are certain things that work perfectly.

 

 

HB, this is the key to your problem

Life on earth formed in water.
Life on earth HB, while it is the only life we know of there is reason to think that water may not be the only working fluid of life. Life on the Earth is based in water life on Venus might be based in concentrated sulfuric acid, life on mars might be based in hydrogen peroxide, life on titan might be based in liquid methane. we have one data point, we cannot derive a curve based on one data point, your idea of life is only based in water is just that, an idea, one data point, nothing to back it up but the one data point.... and what does water have to do with the OP of irreducible complexity?
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Is it really necessary to refute specific allegations of irreducible complexity as obstacle to evolution? There is always going to be something we haven't figured out yet, and creationists will always point to such things as evidence that it could only have been intentional. That's how arguments from ignorance work. Once upon a time the anger of the gods was "the only possible explanation" for lightning and earthquakes.

 

Rather than directly refuting whatever the current specific claim is, make a general response.

1) Tell them to look up "argument from ignorance."

2) Tell them to look up "exaptation."

3) Go back to doing real science.

 

Of course it is necessary. It is part of the process of validating scientific theories and in some cases it is more serious than simply that there are some things that have not been figured out. Whether Behe is correct or not about why diversification of life occurred and regardless of how you care to describe his metaphysical beliefs or how you characterize his motivation, there is a serious issue with the present description of how diversification might have occurred. With Irreducible Complexity, Behe provides a simple illustration of the problem that the modern evolutionary theory faces namely that it seems to have wrong, at least some of the processes under which significant diversification occurred.

 

A good scientific explanation of past events requires a causally adequate mechanism, which requires that a process in observation today must be known to have accomplished similar events. As Behe notes, the current processes do not explain how these molecular systems came to be. Homology and/or similarity does not explain how and in the case of Behe he even agrees that these similar systems provide evidence of the feedstock for the systems, he correctly points out the these similarities are silent about the process under which the hypothetical feedstock was employed.

 

I agree that genetic error and natural selection is a good mechanism to generate adaptive systems but it seems not able to derive the types of precursors required for novel form and function. Behe make this case. There must be a different more causally adequate process that has not been uncovered. ID proponents note that genetic engineers are getting very close to demonstrating that design is a causally adequate explanation, but I think there may well be a natural mechanism that is able to derive the kinds of systems Behe describes.

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