Flagellum evolution – how’s your German?


Junker_Scherer_2009_edition6.jpgI just came across what is apparently a major online revision to the German creationist textbook Evolution - ein kritisches Lehrbuch, by Reinhard Junker and Siegfried Scherer. The section is section 9.4. There is an HTML summary (original German, google translation) and a 32-page PDF is here (apparently too long for google to translate).

Sadly, while I took German in high school, most of what I remember involves beer-drinking songs, which doesn’t help me out much here. Clearly Matzke (2003/6) and Pallen & Matzke (2006) and perhaps other commentary on flagellum evolution got deep under their skin – most of the chapter seems to be taken up with attempting to refute the evolutionary model for the origin of the flagellum! Regardless, I can tell there are a few issues – they cite the 2003 critiques of the flagellum evolution model by the pseudonymous “Mike Gene”, without noting that several later scientific developments caused Mike Gene to substantially improve his opinion about even the most radical part of Matzke 2003, which was the idea that a good chunk of the flagellum was homologous to the F1Fo-ATPase and relatives. (The original seems to be lost to the internet ghosts, but Ed Brayton blogged it, see: “Mike Gene Admits Matzke was Right”)

Anyway, if anyone knows of a source that can translate PDFs, or if there are any German speakers up for summarizing their main points, it would be interesting to hear if they’ve come up with anything new. I mean, there’s 32 whole pages, so maybe they will actually acknowledge that Luskin & numerous DI sources were wildly wrong about the number of required, flagellum-unique proteins in the flagellum. And actually, it does look kind of like Junker & Scherer are advancing some argument that relies on the idea that the flagellum parts are not unique, but instead were designed to serve multiple independent functions (see Figure 4). How conveniently like evolutionary cooption!


You should be able to cut and paste from the PDF into a text file, which you can then feed to an online translation service.

Looks like you can just upload the whole PDF here… http://translate.google.com

…produces OK translation, better than I thought…

An algorithm for creationist argumentation.

..Enter ObservationA

..While ObservationA = TRUE

.…Print Observation A, “proves God designed living creatures.”

.…If EvidenceSubroutine(ObservationA) = FALSE, then ObservationA = not(ObservationA)


For example, spontaneous generation. When it was thought to be true, it was undeniable proof of God’s creation. Now that we know it to be false, it is *lack* of spontaneous generation that is undeniable proof of God’s creation.

At least this PDF is further proof that creationism isn’t just an American lunacy. Takes the pressure off … a little bit.

Chris Lawson said:

For example, spontaneous generation. When it was thought to be true, it was undeniable proof of God’s creation. Now that we know it to be false, it is *lack* of spontaneous generation that is undeniable proof of God’s creation.

Good shot CL, I didn’t think of it that way.

I have no doubt that it WAS thought to be proof of creation, but do you have any references to back that up? Not challenging you, just looking for ammo.

MrG said:

At least this PDF is further proof that creationism isn’t just an American lunacy. Takes the pressure off … a little bit.

Actually, I look at it more along the lines of metastasis.

Chris Lawson said:

When it was thought to be true, it was undeniable proof of God’s creation. Now that we know it to be false, it is *lack* of spontaneous generation that is undeniable proof of God’s creation.

Sort of like interpreting the Bible, and coming up with innumerable denominations based upon diametrically opposed ‘inspirations’, wouldn’t you say?

Stanton said:

Actually, I look at it more along the lines of metastasis.

The spread of the disease is of course not welcome, but at least Americans are not uniquely prone to it.

John Vanko said:

Sort of like interpreting the Bible, and coming up with innumerable denominations based upon diametrically opposed ‘inspirations’, wouldn’t you say?

Aw c’mon, we’re not going to get into a dispute over scriptural interpretation on THIS thread now, are we?

MrG said:

Stanton said:

Actually, I look at it more along the lines of metastasis.

The spread of the disease is of course not welcome, but at least Americans are not uniquely prone to it.

True, alas.

Look at the various science departments at schools in the Middle East.

Stanton said:

Look at the various science departments at schools in the Middle East.

Ur. We could be doing worse for ourselves. From some notes I took on a survey of the Arab world run in THE ECONOMIST in early 2008:

Similarly, the focus on tradition tends to promote xenophobia and reaction, not an interest in new ideas and ways of doing things. That hidebound mentality is reflected in a commonly-quoted statistic that more foreign literature is translated every year into Spanish than has been translated into Arabic for a millennium. The low quality of Arab schools similarly reflects this narrowness. A study performed by a university in Shanghai ranking the world’s 500 best universities included one, repeat one, Arab university. The list included seven Israeli universities.

How conveniently like evolutionary cooption!

Well sure, why do you think it’s true that life looks designed?

It’s because all of the evidence predicted by evolutionary theory is actually evidence for design.

You just think that evolution makes predictions different from those of design. The lack of foresight, rationality, or thinking outside of the taxonomic category are all predictions of design rightly constructed (namely, after it becomes irrefutable), not evidence of a mindless process at all!

Haven’t you evilutionists gotten that yet? We’ll just say it millions of more times, and then you’ll have to concede that ID is right.

Glen Davidson

Glen Davidson said:

Well sure, why do you think it’s true that life looks designed?

Even bet that certain easily-excited PTers don’t recognize this as a Loki troll.

Sadly, while I took German in high school, most of what I remember involves beer-drinking songs, which doesn’t help me out much here.

I would think that drinking songs would be very helpful in dealing with this garbage.

Karen S. said:

I would think that drinking songs would be very helpful in dealing with this garbage.

Ellen Degeneres once had a line about sorting her CD collection while stoned – and finding out the next day that she’d put The Doors, The Carpenters, and Nine-Inch Nails together.

I had to think about that one for a second. Some things do make more sense when under the influence than the do sober.

Drinking songs may indeed be helpful…particularly reading creationist criticisms as provided through Google Translate… here’s what I got. Not great but you can get the gist of it…

The formation of the bacterial rotary motor is Unknown

Siegfried Scherer

Completing and updating the section IV.9.4

“Development of a molecular machine by evolution?” From “Evolution - a critical textbook”

Stand: April 2010

© 2010 Community word study and knowledge e. V.


In this text, an in-depth discussion of the issue of macro-evolution of molecular machines on the example of the bacterial rotary motor is presented. It supplements Section 9.4 of Junker & Scherer (2006). Reason for this is inter alia a speculative evolutionary scenario (Matzke, 2006) Nicholas Matzke1 that in drafting Section 9.4 was not known. Although this scenario is still not part of the scientific literature, but was published only in discussion forums and private websites, and despite the highly speculative nature, it is interesting for two reasons. First, before Matzke proposes a hypothetical way in which he can imagine the emergence of bacteria engine without all had to be essential parts of an irreducible complex machine simultaneously. This is significant. Second, it is m.W. still the only one on a mechanistic level proposal put to the emergence of a bacterial rotary motor.

Junker and Scherer (2006, p. 162 review), that 16 proteins were needed for a bacterial motor, which must also be present. This view should be questioned in view of Matzke’s model of evolution critically. If Matzke model the evolution of the bacterial motor model describes the issues raised by critics of evolutionary gaps in the imaginary evolution of the bacterial motor would be significantly reduced. That would be - all set out below, serious problems of Matzke’s hypothesis - first of all a positive step evolutionary model regarding the formation irreducible complex biological structures.

After a general introduction to the problems noted that the similarity relations a vast variety of bacteria engines casually referred to a descent from one or a few original, but already complex motors can be interpreted. Then, to explain why it is the bacteria Motor undoubtedly one irreducible complex structure, consisting of at least 20, but is probably more different proteins. On the other hand is represented differently from the popular, particularly in the U.S. ID-literature represented position, why this property of a biological structure is in itself a conclusive argument against evolution based on undirected processes of the bacterial motor.

In the main part of the amazing multi-functionality of individual substructures of the bacterial motor, and the fact-based model of evolution are critically analyzed by Matzke. In the following analysis focuses on representing a single evolutionary step in the postulated formation of the bacterial motor, namely the co-opt an adhesion protein. This evolutionary step has been chosen because this is one of the easiest steps in Matzke’s model. Only a single protein must be in the process of evolution by co-option and variation will be gained. Other steps in the hypothetical scenario Matzke are far more complex. The result of this detailed discussion is that it is unknown if and how co-option and by mutation in the course of the hypothetical formation of the bacterial motor, the gain would have a single adhesion protein may occur. This conclusion and the reasons were in terms of Matzke’s model in the spring of 2008 on an interdisciplinary colloquium at the University of Regensburg for the first time presented (Scherer, 2009). Section 10 of the following text is largely from this source. In addition, to explain why the mechanisms of evolutionary channeling and limiting the variability of multiple functions by

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Occupied biological structures give rise to the presumption that postulated Matzke stages of evolution - even if they should be selektionspositiv itself - not easily represent basic functional states, leading from a primitive type 3 secretion via the smallest of steps towards a bacterial rotary motor.

Matzke’s model is generally not reliable and convincing hypothesis to evolution of the bacterial motor. Consequently, she was introduced today in the scientific literature not yet discussed. Matzke themselves have chosen not to present his hypothesis in his publication for the bacterial motor, which was published in a refereed scientific journal, (Pallen & Matzke 2006).

The detailed discussion of the various changes that for a co-opted an adhesin protein are probably required, there is evidence of specific research projects that might help to solve a postulated evolutionary path of the emergence of bacteria engine are carried out. Whether a decrease based on experimental data and expected future progress of knowledge of existing problems or declaration will increase is not to say at present. The result of this discussion highlighted a gap in knowledge evolutionary research. Elsewhere, it was explained why such gaps are no compelling arguments against the evolution of a bacterial rotary motor, or the existence of a designer are (Scherer, 2009).

It is striking how much has been increasing in recent years the use of concepts from the engineering sciences in molecular biology. Mike Gene (2007) has described in detail. Already nearly 10 years, Lowe (2000) follows this fact to the point:

“The molecular machinery of nature outperforms anything that mankind currently knows how to construct with conventional manufacturing technology by many orders of magnitude. … Almost without exception, there exist analogues of conventional functional biomolecular devices, including structural components, wires, motors, drive shafts, pipes, pumps, production lines and programmable control systems. “

Regarding the intestinal bacterium Escherichia coli, says Howard Berg (1999): “In addition to rotary engines and propellers, E. coli’s standard accessories include particle counters, rate meters, and gear boxes. This microorganism is a nanotechnologist’s dream. “

The term “molecular machine” has now become so familiar to biological functions of the cell to beschreiben2 that he is indispensable in the literature. These machines are ribosomes Splicosomen, degradosome, protein complexes in DNA replication play a role (eg, helicase and DNA polymerase), the F1/F0-ATPase, the kinesin-machinery and much more (for B. Gene 2007). A look at modern textbook of biochemistry (Berg et al. 2007, Lodish et al. 2007) and Cell Biology (Alberts et al. 2008) is sufficient to be convinced of this fact.

The bacterial flagellum is the molecular machine with the greatest name recognition, as it has played in the U.S. in recent years a prominent role in social policy discussions. Their structure and hypotheses for their formation are the occasion of the court processes to intelligent design has been discussed worldwide. A molecular geneticist, who has looked a whole life with this engine researcher put it, already nearly 20 years (Macnab & Parkinson 1991):

“We need to think almost in engineering terms about transmission shafts, mounting plates and bushings - unfamiliar grounds for the microbial geneticicst.” Today is not such an unusual mode of expression, but the rule. For example, two years ago, a work relating to the motor in bacteria Journal of Bacteriology, entitled “Fine structure of a fine

[p. 4]

Hazard, an advantage. Many bacteria can move actively in various ways (Jarrell & McBride 2008) and some provide for this purpose on a rotary motor. Each engine requires a controller. These include sensor proteins (which may, for example, nutrient molecules such as sugar seen in the cell environment, is there a certain extent to the “nose” of the bacteria), signaling proteins transport (they received environmental signal to the motor) and control proteins (for direct control of the motor). Bacteria were found in engines of different type of construction. The E. coli motor is tested for genetic and biochemical level best. We now know that it included installation of cellular proteins (which help in the assembly of the engine, see Chevance & Hughes 2008) of about 40 proteins is formed (but see Box 1). The control contained by chemotaxis (overview eg in Wadhams & Armitage 2004) is carried by less than 10 proteins. With the help of molecular biology and electron process could explain the basic structure of the molecular motor (Fig. 1). A bacterial motor function consists of five basic elements: the filament (flagellum) or the “propeller”. By rotation of the filament flexible VorMöglicherweise the number of proteins in the synthesis or function of the bacterial motor play a role is underestimated. This is clear from a study by the investigation of a yeast two-hybrid test interactions of known motor proteins with other proteins in Treponema pallidum (the causative agent of syphilis), Campylobacter jejuni and Escherichia coli. Surprisingly, there was evidence of more than 100 proteins that interact with motor proteins.

Because such tests can give false-positive results, an experimental analysis of the predicted interactions is necessary. For Escherichia coli, this analysis was performed on a Deletionsmutantenbank and found 159 deletion strains that showed a Motilitätsdefekt. Among the affected genes, there were 43 known Motilitätsproteine. The significance of the remaining 100 genes for the synthesis, structure and function of the engine is often unclear. There may be unknown, in addition to motor proteins, to genes that have an indirect effect on motor function (eg via the formation of energy-proton). Maybe it has to do with the fact that the fumarate reductase in Escherichia coli Respirationsprotein interacts unexpectedly with the control of the bacterial motor.

From such data one must conclude that we know about the bacteria engine not much. All speculation about the evolution of such a structure are regarded with skepticism for that reason. This also applies to the statements in this article.

machine “provided (Blair 2006) and recently the same group a” coupling “of the bacteria, Gram positive bacteria found in motor (Blair et al. 2008). One can hardly avoid the impression as if the phenomena of life on a biochemical and cell biological level could best be described in terms of engineering and computer science (eg, Nurse 2008). I think it is an open question whether life is at its molecular function relationships without such concepts at all, to adequately determine kann.3 The philosopher of technology Mutschler HD has this problem discussed in detail and pointed (Mutschler, 2002, Mutschler 2003).

Bacteria are dependent for their growth, absorb nutrients from their environment. This may prove advantageous if the cell can move in a concentration gradient in the direction of a nutrient source. On the other bacteria are exposed to negative environmental influences, such as toxins. Here, too, is an active movement, away in this case by the

[p. 5]

operation of the bacterium produces, it is mainly from about 20,000 copies of the protein flagellin built. This protein in turn consists of several hundred amino acids, its amino acid sequence and the corresponding gene sequence is known. This filament is coupled by a bend (link element) to a rotation axis which is of camps in the cytoplasmic membrane and the cell wall of bacteria cell held in place. The genes that code for proteins of the axle and the bearing are largely unknown. The rotation axis and thus the bacterial flagellum is placed on drive proteins into rotation. The engine is driven by the energy that is stored in the proton gradient across the cytoplasmic membrane. This proton gradient generated outside the cytoplasm to a positively charged environment. The potential gradient (= membrane potential) of approximately 0.2 V. Figuratively speaking, the bacterial cell is a “0.2 volt battery, which can drive these” NanoElektromotor.

Important reviews on the structure, biosynthesis and function of the bacterial motor comes from eubacterial Macnab (Macnab 2003, 2004, Jarrell 2009). A very brief but informative overview is given in Berg (2008). This work also shows how much of the bacteria engine not yet be Michael Behe has the bacterial rotary motor known as a clear example that one could make the work of an intelligent designer of biological phenomena sense pin down (Behe, 1996): A bacterial motor is irreducible complex and therefore could not result from a natural process of evolution. On the contrary, the existence of such a structure could be the inference to an intelligent designer. Behe has put forward “Darwin’s Black Box,” a popular science book, which is an important foundation for the aspirations of the Discovery Institute in Seattle was to bring the perspective of Intelligent Design (hereinafter abbreviated as ID) in the curricula of public schools. Thus, the “bacterial outboard” of some bacteria become an unexpected popularity.

In the wake of this popularity, a number of biologists contradicted the views of Behe: The bacteria engine is neither irreducible complexity, yet it is unclear how it arose. On the contrary, could the evolution of this biological nanomachine by known evolutionary mechanisms now explained very well and not be questioned more reasonable (eg Musgrave 2006; Miller 2007; Pallen & Gophna 2007). This view was reflected hasty and not very popular in the literature included (eg, Hemminger, 2007, Jones 2008). The most important design publication, which Behe criticized on a scientific level is provided by Matzke (2006), because the model is the only sufficiently specific to a mechanistic, theoretical examination accessible. Pallen & Matzke (2006) also have a readable critique of Behe argued that in much, however, arguments from comparative

Figure 1 Schematic drawing of the bacterial motor of Escherichia coli associated with some of the structural proteins (from Junker & Scherer, 2006).

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Biology is based and discuss any questions mechanisms. Sikorski (2009) took the model of Matzke without any critical debate, in this respect rightly, however, the observations of Junker and Scherer (2006) on the evolution of the bacterial motor in question. Musgrave (2006), Miller (2007) as well as bracing and Gophna (2007) criticize the view that the flagellum irreducible complexity and therefore be understood only by intelligent design, but the above arguments focus on the multifunctionality of the flagellum, as well as on findings from the comparative biology and in the core of Matzke (2006) and Pallen and Matzke (2006) summarized. For this reason, in this paper mainly discusses the latter two works.

ID proponents have defended their position on the flagellum, for example, Behe (2004). The work of Smart and Bracht (Smart 2003), but especially the extensive analysis by Mike Gene5 (2003) are scientifically very well over Behes also quite popular text that can be criticized no doubt with good reason. Mike Gene’s work is about the size of a 100-page book and sets the standard by which all scientific discussion based on the origin of the bacterial motor needs. While I know of no case, where Mike Gene’s been critical, purely scientific explanations of evolution representatives are discussing, but I should have overlooked a text published on the Internet, I am grateful for a hint. (The discussion in Internet forums is confused and hardly manageable, and make many contributions even miss rudimentary skills.)

First, it is gratifying that the dispute from both sides now with technical arguments are held. I write “well” because I can not help but talk about the surprise my style of some colleagues to give expression. Not infrequently, speech and argument are a strikingly emotional, polemical, and sometimes even personally insulting, sometimes you even think of having to exercise fanatic traits. That goes for both sides - and, unfortunately, this style is already arrived in Germany. One may explain the fact that basic philosophical issues are under discussion. An apology is not tolerated and certainly not for the failure of editors that such a level of argumentation would never dürfen6.

On different occasions I have expressed my wish that the drift of the discussion on an ideological level, at least in Germany might still be prevented. Criteria for what makes an ideological argument, I have called elsewhere (Scherer 2006b). This wish, I can only repeat, together with the regretful conclusion that the counterparty in the U.S. in this respect is not a good role model sind7. From the few, on a scientific level, limiting work to

1st What are the consequences of the barely manageable variability of different bacterial motors for its existence?

2nd Is a specific bacteria engine from a specific bacterial species in general a non-reducible complex structure?

3rd If it would be possible to establish credible for a given biological structure, the non-irreducible complexity: Does it follow necessarily that they can not arise through evolutionary processes?

4th How important is the fact that some proteins of the bacteria Motors similarities to proteins that carry out elsewhere in the cell a different function?

5th What is the significance of multifunctionality of the bacterial motor or its components for hypotheses about its evolution?

6th Can the probability of formation of a bacterial motor can be estimated?

7th Behes critics have a reliable, plausible theory for the evolutionary origin of a bacterial rotary motor proposed?

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Formation of a bacterial engine results in a series of questions, which are summarized in Text Box 2. These are treated separately to allow maximum clarity. The main objections to these questions will be taken up and discussed briefly. The reader should be familiar with the contents of the chapter “Molecular mechanisms of evolution” (Junker & Scherer, 2006).

Pallen & Matzke (Pallen & Matzke 2006) right when they write: “There is no such thing as, the ‘bacterial flagellum.” We now know - and not just since complete genome sequencing - to the almost unmanageable diversity of different bacteria motors ( Jarrell & McBride 2008).

4.1 Verschiedene engine types in eubacteria

Bacterial motor proteins can be extremely diverse with the same basic blueprint of the engine. This goes to the point that some motors are driven by proton gradient and other Natriumionengradienten (Asai et al. 2003). Both engine types are sometimes in a single cell before (Paulick et al. 2009). Na +-driven motors turn with much greater speed than Protonengetriebene engines and can be up to 100,000 rpm quickly.

The protein FliL is another example. The exact function of the protein is still unknown, but it is essential for the SchwärmerPhänotyp Salmonella and E. coli (Attmannspacher et al. 2008). First, it is striking that this protein is highly variable. For example, Caulobacter crescentus FliL proteins of Escherichia coli and have only about 25% similarity (Yu & Shapiro 1992). Obviously, the functions of the proteins are different, because E. coli does not result in a knockout of the gene to a significant impairment of locomotion (see above), while a knockout of C. crescentus has FliL in a non-motile (immovable) phenotype (Jenal et al. 1994). Proteus mirabilis has not motile and this one, or otherwise disturbed phenotype when FliL is turned off (Belas & Suvanasuthi 2005). For Caulobacter and Proteus - but not for Escherichia! - Obviously belongs to this protein complex irreducible Kernproteinset of the engine. This points to different versions of the engine type.

In the Eubacteria8 a rotary motor has been found in 8 of 19 phyla (tribes). All Enterobacteriaceae (which include, for example, E. coli and Samonella) have a similar type of engine. But beyond the construction of engines Gram negative and Gram positive bacteria is significantly different. The functional necessity of this is immediately obvious because the former have an outer membrane of the latter are not. Still other rotary engines are found in the spirochetes, which their flagellum between cytoplasmic membrane and outer membrane around the cell body wrap ““, these allow for a total of rotation and the entire bacterium is similar to a screwdriver, very effectively through the medium winds (Murphy et al. 2006). These bacteria and molecular motors are built quite differently. Table 1 and in bracing Matzke (2006) illustrates this fact very clearly.

There is now good evidence that different bacteria, although not in the core proteins of the engine (see below), but differ greatly in “accessory” Motilitätsproteinen (eg Rajagopala et al. 2007). Overall, the variability of bacterial rotary engines to be unmanageable.

4.2 Comparison of homologous motor proteins

In principle, all eubacterial flagella share a common basic structure. However, subject to all parts of engines of evolutionary variation. This means that point mutations, deletions, duplications, the exchange of genes with other bacteria through horizontal gene transfer (Ren et al. 2005) and more intended. An introduction to such evolutionary processes is in Junker and Scherer (2006, Chapter 9.1) given. Within a single engine type it is therefore likely to be uncounted millions of variants. Individual motor proteins can change very quickly if they are recognized by the immune system of the host and thus subject to extreme selection pressure. An example is flagellin, the main protein of the filament

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(Beatson et al. 2006). However, especially some of mechanically not as heavily used, outward-facing domains of Flagellinproteins are so variable. Sometimes even come in a single bacterium in different flagellin (Ely et al. 2000, McQuiston et al. 2008), which can be explained by diversifying selection after gene duplication or horizontal gene transfer (see disruptive selection, Junker & Scherer 2006, p. 70 ). This finding graded similarity applies not only to the flagellin, but for all motor proteins.

In fact, it looks as if the homologous sequences of key proteins of the flagellar motor is a continuum of different eubacteria show sequence similarity. This finding can be explained by an evolutionary relationship suggests - more precisely: it is a direct consequence of the evolutionary origins hypothesis. A mechanistic objection, for example, that today would have been flagellins from a common Vorfahrenprotein (which, however, already part of a complex motor), are formed by gradual evolution seems not to lie, at least at hand. Maybe dip the problems only appear when one examines such a question in detail. Whether all of today’s engines have eubacterial rotation by known evolutionary processes can develop from a common ancestor, but is not part of the current discussion. This is about where the “first” engine comes in this ancestor.

The observed, graded similarity of motor proteins from different species can be interpreted well by evolutionary descent.

4.3 similarity of motor proteins with proteins of other function

Another similar argument relates to proteins of the bacterial motor, which are not similar to proteins of another engine, but to other proteins function. Pallen & Matzke (2006) have led a series of examples. is an illustration of this point, singled out one case (see also Chapter 8). Central to the flagellar motor is the implementation of the proton gradient across the cytoplasmic membrane energy stored in a rotational movement of the motor shaft. Therefore, the two motor proteins MotA and MotB are responsible. Several MotAB complexes are arranged in a ring around the motor axis (Fig. 2A). They belong to the stator of the motor and are anchored to the cell wall via MotB. MotAB part of the complex is a proton channel, which converts the energy of the proton in a conformational change of MotA. This is then transferred to the axis of rotation of the engine and put the axle in rotation (Fig. 2B).

The sequences of MotA and MotB are known. The comparative search in sequence databases showed that MotAB have a low but detectable sequence similarity with the proteins TolA and TolQ and ExbD / TonB. These proteins are also anchored in the cytoplasmic membrane, have a proton channel and have binding affinities to the outer membrane or the cell wall. TolAQ play a role in cell division, while ExbD / TonB are transport proteins (Cascales et al 2000, Cascales et al. 2001, Gerding et al. 2007, Zhai et al 2003). If one assumes TolAQ or ExbD / TonB than initially, then one could speculate that these proteins have been co-opted for the construction of an engine. Whether such, from similarities of developed process of evolution is mechanistic at all possible, however, was never investigated (see Section 10).

Figure 2 Schematic representation of the arrangement of the drive elements MotAB to the hollow motor shaft (A) and sketch to explain how a conformational change is converted into MotAB in a rotational movement of the motor shaft.

Secretion injectisome axis of rotation

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4.4 Interpretation of similarities

After Pallen and Matzke (Pallen & Matzke 2006), the variability of the eubacterial rotary engines as well as these common basic structure have described, they come first to the conclusion that intelligent design have difficulties to explain the presence of different engine types. You ask how many procedures the designer one should assume for now if you wanted to postulate a Schöpfungsereignis11 for each engine type. Or if one does not need to accept based on these data, that all rotary engines have diversified from an ancestor through evolution, because “all show sequence similarity flagellin indicative of common ancestry (homology). Pallen & Matzke question is justified and indicates a serious problem of ID: a concrete, coherent and scientific criteria and interpretation of diverse variable bacterial rotary engines as part of Intelligent Design (or a “creation model”) as an alternative to a descent of the day this flagellar motors of one or a few ancestors has not been submitted.

The underlying problem is the lack of a “General Theory for Organic Design” and is generally applicable to biological observation of nature. The theme has also Paul Nelson as an important representative of ID: “Easily the biggest design challenge facing the ID community is to develop a full-fledged theory of biological. We do not have such a theory right now, and that’s a problem. Without a theory, it’s very hard to know where to direct your research focus. Right now, we’ve got a bag of powerful intuition, and a handful of notions such as ‘irreducible complexity’ and ‘specified complexity’ - but, as yet, no general theory of biological design. “(Nelson 2004) Pallen and Matzke (2006) ask further, now that they postulate an on core proteins (see below) reduced Urflagellum:

“This reduced flagellum is still a challenge to explain, but if one accepts that all current flagellar systems diverged from their common ancestor last (the ur-flagellum), why stop there?”

The first question is justified and will be discussed below. Is there a tangible difference between the biological hypothesis of the origin of today’s Flagellenmotorvarianten a Urflagellum and the emergence of a Urflagellums from unknown precursor structures?

Michael Behe has proposed that it is the bacteria engine is a non-reducible complex structure. He defined a non-reducible complex system, first as follows:

“… a single system composed of several well-matched, interacting parts that contribute to the basic function, wherein the removal of any one of the parts causes the system to effectively cease functioning. “(Behe 1996)

In other words, all belonging to a non-reducible complex structural parts necessary for its function, other functions of sub-structures of irreducible complexity are therefore not excluded.

1.5 Arguments for the irreducible Complexity of the bacterial motor of the experimental molecular genetics

The experimental proof that a specific biological structure is indeed irreducible complexity, and above all to answer the question of how complex it actually is quite expensive. In a simple structure based on a targeted mutation approach is then successful if (a) of the genetic blueprint of the structure sufficiently precisely known and (b) of the organism genetic engineering is available. When bacterial motor of enterobacteria, Escherichia coli and Salmonella which are, in principle, both conditions are met. That means you can turn off individual genes coding for the engine, by targeted mutagenesis in several ways. Such mutants also called “knockout mutants. When the engine no longer works (“non-motile phenotype”), was the gene for the motor function is essential.

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Sometimes a deliberately turned off Motorgen not lead to loss of motility. Either it really was not essential. But it could have been replaced by another protein of the cell. The simplest explanation for the latter would be that the relevant gene or segment of the chromosome is duplicated and the duplicate in a knockout mutant may take over the function. We have recently found the pathogen Yersinia enterocolitica that there are duplications of genes and knock out mutants of Flagellenoperons individual genes do not always function. The importance of such duplications, which are also found in some strains of E. coli, but hardly studied.

On the other hand it could be that the function of motor proteins selectively turned off by such proteins in the cell, so to speak “over makeshift” that have a remotely similar function. Paul et al. (2008) constructed a five-knockout mutant, which three ATPase / secretory fliHIJ lack of the flagellum, but it also contained two ATPase-related protein type 3 secretion systems (INVC and Sansandi). The mutant was slightly Schwärmassay Motil, but far less than the wild type. If these three motor proteins that are not essential for motor function? Galan (2008) discusses this issue and advises caution, because it could be that other ATP hydrolyzing proteins from the cell coupled to the secretion apparatus and cause a partial complementation of protein. In Beau’s meaning could be the exciting findings of Minamino et al. suggest that in the Zweifachmutante DfliHI found a partial Suppressormutation, which turned out to be a point mutation at the protein FlhB. This protein is part of the “lock” of the secretion injectisome, bind to the FliH and FliI may. A mutation in this protein might bind the imperfect one unknown, complementing protein to improve the secretion apparatus and thus lead to “partial repair” the secretion of motor proteins. Additional mutations would probably lead to further optimization (the principle is in Junker and Scherer 2006, p. 143ff) explains at the end could be a successful co-option of an existing protein. However, this scenario is highly speculative and the Declaration of Suppressormutation could also be quite different, even to remain in the comparison of the phenotypes of the different mutants constructed some questions unanswered.

These and similar processes (one could cite many other examples) are often referred to by evolutionary biologists with the rather negative-sounding term “patchwork”. One can formulate the findings also positive and understood as an expression of a widely interconnected and highly robust system that has a high degree of built-in potential variability, providing maximum security, so that the cell survival even under adverse conditions still kann.10 The Most of the genes encoding the bacterial motor, were in this way, but initially found by chance. It has been collected previously immovable mutants and to investigate in which genes they were mutated. This engine had to be genes. Today it is partially targeted before, identifies possible engine genes by sequence similarity and then turn them out in order to investigate its effect on the motor structure and motor function. In most cases it is found that has the engine off of an immovable phenotype result in genes. Set an example Chaban et al. (2007). The authors work with the Methanococcus maripaludis Archaebakterium9. Because the genome sequence of a suspected Flagellenoperon was identified. The authors targeted the genes switched FlaB1, flaB2, flac, FlAF, flag, and FLAI flah directed by deletion (loss) and found that all mutants were motionless and showed under the electron microscope no hostages. The genes were therefore essential for motor function. A similar experiment reported (Allan et al. 2000) for the pathogen Helicobacter pylori, the genes Flife, Flis, flhB, fliQ, FliG and FliI also proved to be essential. A comprehensive such experiment conducted (Rajagopala et al. 2007 through), they found in Escherichia coli more than 100 genes that influence the motility (see text box 1).

Overall, through such experiments that many genes of a specific bacteria are essential engine, but there are definitely exceptions. (Yokoseki et al. 1995) show, for example, surprised that were motile after knockout mutants of genes flis engine and flit as before, although there is agreement about the fact that these genes are part of the bacterial motor. This can have two causes: either these genes are not

[p. 11]

essential. Then they do not belong to the potentially non-reducible complex structure, it would thus be built was easier than expected, perhaps. But it could also be that the rejected genes are replaced by other genes of the bacterial cell, in other words, the cell is about the function of such genes redundant. Then no safe conclusion would be possible if the protein is essentially turned off or not (see Box 3).

Of particular interest are mutants in which the mobility is not turned off, but is reduced. An example of this type Attmannspacher et al. (2008) for Salmonella enterica. These authors have eliminated the protein FliL, which is localized in the flagellum basal body (shown graphically in Figure 8 of Attmannspacher et al. 2008). They report that the mutants have only a limited ability to swim in liquid medium, it can no longer swarm (in schools refers to the flagella caused by movement on viscous agar surfaces). Undoubtedly fliL not an essential gene of the engine, although it is the first gene in a central Motoroperon. Presumably, it contributes to the mechanical stability of the engine at under high-viscosity conditions.

Another example is the gene flaB3 the above aforementioned Methanococcus maripaludis (Chaban et al. 2007). A deletion of this gene led to the movement in circles, the targeted nature of the movement was so disturbed. The electron microscopic analysis showed that flagella were trained, who lacked the “hook” structure (the elbow). The Geißelfilament was with these mutants have been grown directly on the axis of rotation, which has not resulted in a completely inoperative engine. In evolutionary terms this is a very interesting finding. flaB3 is therefore not essential for a rotation of the engine. Does this engine, which only leads to a stochastic motion of the cell, perhaps a selection advantage over the mutant cells isogenischen result, the engine can no longer be made? If you could clarify this experimentally, and if the answer was positive, one could imagine the irreducible complex Motorstrukt ur simply a gene.

In most cases, including in the case of a specific bacteria Motors, can probably be said only ensures that a biological structure with regard to a given function contains a non-reducible complex core. The term “irreducible core” is by Dembski, who developed the definition of Behe on, but again a very popular level (Dembski 2007). Joshua Smart has applied this definition clearly detailed on a bacterial engine (Smart 2003). Mike Gene has brought the argument to be a subject-specific level (Gene 2003). This enhancement of the Beheschen argument was in a case known to me also recognized by evolutionary biologists (Musgrave 2004).

How many genes includes such a core, in the case of a specific bacteria could be estimated experimentally accurate engine, but only at high costs (Box 4).

Overall, one can first say that the assertion, a concrete biological structure is non-reducible complex in principle be experimentally tested by knockoutMutanten. If one second, the feature “irreducible complexity” by Behe (above) defines and applies to bacteria engines, then contain an irreducible complex core structure of several essential components, because many proteins that form a given bacterial motor, can not be eliminated definitively, without the motor function is completely destroyed (see below for other functions). How many essential proteins could contain a given bacterial motor, is discussed in the next section. 5.2Argumente the irreducible complexity of the bacterial motor from comparative biology through comparisons of different structures with similar functions (“similarity search”) you can get important information about the necessary ingredients for a real function. Pallen & Matzke write:

“Despite this diversity, it is clear that all (bacterial) flagella share a conserved core set of proteins. Of the forty or so proteins in the flagellum of S. typhimurium standard strain LT2 or E. coli K-12, only about half universally seem to be necessary. “(Pallen & Matzke, 2006)

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Mike Gene (2003) three years earlier a similar analysis is undertaken and concludes that 21 proteins may have belonged to a core set hypothetical original flagellum. He calls this the flagellum “UR-IC-flagellum,” which set in about the “core” of non-reducible complex structure of all eubacterial bacteria could reflect motors. Liu & Ochman (2007b) come in a recent study found that the core set consists of 24 genes.

Liu & Ochman (2007b) show in the supplementary material of their PNAS article (see below more on this article) a table with the analysis of 41 fully sequenced bacterial genomes, which contain flagellar genes. I have plotted the number of flagellar against the total number of genes in the respective chromosomes (Fig. 3). It is clear that no correlation between genome size and number of flagellar exists. Given the well-founded assumption that small genomes reductive evolution is likely, which avoids non-essential genes by deletion, and this result suggests that the complexity of today’s (!) Bacterial rotary motor can not fall below a certain threshold. Analyses must take into account, however, that are found by homology search, not all the genes necessary for motor function, so that the number of genes essential engine may be underestimated.

The small group of genomes with about twice the number of motor genes indicates cases in which motor genes were duplicated, or where two different engines available per cell. The fact that both can occur has been demonstrated experimentally. Liu and Ochman have recently been presented to a vergleichendbiologische analysis showing that there has been duplication of the flagellum genes after a much different, line-specific evolutionary disintegration of these genes (Liu & Ochman 2007a).

Such comparisons are fraught with some methodological problems to which there can not be discussed in more detail, but at least they allow some basic insights. One can state that there is an extraordinarily large number of quite different bacteria eubacterial engines, and that these contain a common set of proteins.

Probably has the number so obtained merely indicates a lower limit of the complexity of today’s bacteria engines. The methodology requires only the proteins associated with a core set, which occur in all investigated engines. This comparative method (can not decide a) whether the other form, for each engine belonging to different proteins and essential components that are designed differently for different motors. You can (2) decide not even decide whether in the given case, all 20 proteins of a Core sets are really essential. These questions can only be clarified through a research program carried out separately for each engine type (see text box 4). Of the combination with the knockout experiments discussed in Section 5.1 for the construction of functionless mutants it would not be surprising if 20 proteins are essential for a given motor are bacteria. It does not matter at first whether the Filamentkonstruktion or protein secretion or other important function of the motor is affected by the mutation.

Today, existing bacteria motors contain a non-reducible complex core of about 20 essential proteins, as defined by Mike Behe. It is not easy to determine the exact number of essential proteins, and it could be different for different types of bacteria.

Figure 3 Number of bacterial genes in motor function of the genome size of different bacteria. Data from Liu & Ochman (2007)

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The transported popular core argument of ID is a direct conclusion about the existence of a non-reducible complex system to its non-Evolvable. Mike Behe wrote:

“An irreducibly complex system can not be produced directly by numerous, successive, slight modifications of a precursor system, because any precursor to an irreducibly complex system that is missing a part is by definition non-functional. …. Since natural selection can only choose systems that are already working, then if a biological system can not be produced gradually it would have to arise as an integrated unit, in one fell swoop, for natural selection to have anything to act on. “(Behe 1996 )

In further steps the ID concept then includes the gradual non-Evolvable a structure to the existence of a designer. Although it may be true that an irreducible complex structure like the bacterial motor can not arise through evolution, and although it may be true that the bacteria engine can come only through “design” into existence, both conclusions are mE not in the horizon of scientific knowledge analysis (Scherer 2008b, see also footnote 11). The question of Evolvable a non-reducible complex structure is central to the historical evolution and should generally be answerable with the results of causal theories of evolution, which is further discussed below.

It is first noted that Behe, like many writers of textbooks of evolution, only the Darwinian mechanism of evolution by mutation and selection considered. Of which will be discussed later. But even under this restriction, the situation turns out to be complex, which Behe, however, has recognized for over 10 years himself, when he writes: “not demonstrate that a system is irreducibly complex is a proof that there is absolutely no gradual route to its production . Although irreducibly complex system can not be to produced directly, one can not definitively rule out the possibility of an indirect, circuitous route. “(Behe 1996) In other words, there is no way around it, is concrete thoughts about the plausibility to make possible evolutionary paths that can range from very simple structures with well-known variation processes to so you do not yet say exactly how many essential proteins includes a specific bacteria engine. In principle, this number could be estimated but experimental. The research needed for this would include approximately the following steps:

-Choose one specific organism, such as Escherichia coli

-Identify (based on experimental data or in silico) all the genes involved in synthesis of the E. coli flagellum might play a role.

-Create from any putative flagellum a markerless gene deletion in a Einfachmutation.

Lay-down experimental procedure to test the functionality of the bacterial motor (eg, light microscopic observation, Motilitätsassay, swarming assay, electron microscopic analysis).

-Define a standard by which a cell as a portable, movable or reduced non-mobile will be classified.

-Diagnosis of any mutant on mobility: (i) the mutant motionless, then the gene was essential. (Ii) If the motion in whole or in limited availability, then the gene could not be essential.

-Check if a mutant, whose mobility is not or only partially destroyed, possibly another gene has taken over the function of the deleted gene (eg duplicated genes engine).

-Check whether limited mobility has a selective advantage to immobility. I could carry out such a research program in my department, the necessary molecular genetic methods are well established, but it would be a significant human and material resources necessary.

[p. 14]

complex structures like the bacterial motor lead. This is a painstaking process. Michael Behes provocative theses were the direct reason that such a model concepts by Matzke (see Section 9 have been formulated). No matter how plausible they are as individuals, we must recognize, first, that Behes stimulates critical arguments have the scientific debate. This is true even if he should not be right.

Although all bacteria engines a non-reducible complex containing core set of proteins, it does not follow necessarily that, through gradual evolution, therefore resulting in principle can not.

In a highly regarded publication have Liu & Ochman (2007b) proposed a core set of 24 proteins, which occurs in all previously genomsequenzierten eubacteria (see above). These core proteins were then examined in detail on their sequence similarities. The authors say that all the core proteins of the supposed “great-engine” each other more or less similar. From these similarities, they conclude that these proteins have emerged from a joint development by numerous, successive Duplikationsprozesse and that at the beginning of a single motor protein was original. However, the authors claim not believe that this motor protein has already exerted a motor function. Because the molecular motor proteins, and the pedigrees of the parties agree to some bacterial species, and because the motor genes are widespread on the eubacteria, Liu & Ochman conclude that the core proteins were created of the motor before the diversification of the eubacteria. Science, in its online magazine commented immediately positive (Cutraro 2007). First you have to state that similarity explained by common descent kann11 that one but it must not close to common ancestry. The primary literature in textbooks and many interpreted as convergences similarities highlight the problem. It is undisputed similarity, not by descent, but must be caused functional and it is obvious that this is the case at the molecular level. It would however be too long to reopen the homology discussion here, see for example, Junker and Scherer (2006), Junker (2002) and Fehrer (2009). A potential cause of functional similarity in the sense of convergence is by Liu & Ochman not even mentioned as a vague possibility.

Surprisingly, this model of evolution unexpectedly harsh and basic criticism is met by evolutionary scientists. These relate to one part of the methodological errors of the work and the other on conceptual problems. A comprehensive collection of arguments and of links added Nick Matzke at Panda’s Thumb collected (Matzke, nd), he himself rejects the model of Liu & Ochman from as well. Meanwhile, a correction has been published (Liu & Ochman 2007c), but it is not a smear given at the basic statement. In October 2007, commented M.Y. Galperin with respect to Panda’s Thumb this publication: “… what is true in the paper by Liu and Ochman is not new, and what is new is not true “(Galperin, 2007). More friendly sounding, but its content clearly the violent criticism of Doolittle12 that rejects for various reasons the speculation by Liu & Ochman (Doolittle & Zhaxybayeva 2007).

I think the main criticism that m. in the literature W. is no discussion, however, but is located on a completely different level: Liu & Ochman no mechanistic model offer for what it is supposed to have been as functionally possible that a rotary motor function is said to have formed gradually on the basis of ongoing gene duplication. Only such a hypothesis would be testable at least conceptually. This is not to say that the approach of the authors is entirely worthless. It would certainly important to recognize actually existing similarities between proteins and to ask for possible familial or functional causes. In conclusion, the speculation (of a model can not talk seriously) by Liu &

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Ochman no contribution to understanding the evolution of a bacterial engine delivers. Why such a weak one in many ways could appear in an article of the world’s highest-ranking scientific journals, is the secret of the responsible editor Francisco J. Ayala. Much more interesting than the work of Liu & Ochman are approaches which, though hypothetical, but nevertheless represent intermediates containing evolutionary paths for discussion, as presented in biology didactics Nicholas Matzke. Before these are discussed, however, is its basis are presented, which is situated in the fascinating discovery of the multi-functionality of many biological structures.

With increasing sequence data on the one hand, and increasing molecular insights on the other hand it is increasingly clear that biological structures can also have multiple functions. Particularly impressive is the very long-known and surprising finding that eye lens proteins (Crystalline), both structure and function can have enzymatic functions (Piatigorsky 1992, Piatigorsky 2003). Also very interesting, and of growing importance is the existence of overlapping genes (Chung et al. 2007, Liang and Landweber 2006, Loessner et al. 1999, Scherer 2008a), ie a nucleic acid sequence encodes several different proteins. Known to what extent a plausible mechanism for the evolutionary origin of these dual functions is to be discussed elsewhere.

Also for the flagellum have been described other than the motor function as other functions. The flagella of the transmitted mainly by food pathogens Campylobacter jejuni and C. coli practice next to the motor function also functions in the secretion of virulence factors, the autoagglutination, the micro-colony formation / biofilm formation and the defense by the innate immune response (Guerry, 2007).

In Figure 4, four functions are called. This includes the observation of multi-functionality of sub-components based model of evolution of bacteria engine as the core of the idea of evolution by mutation and co-option “(Gene 2003). This model is particularly caused by the discovery that the proteins of the bacterial motor by a similar mechanism of cytoplasmic membrane, cell wall and outer membrane

Figure 4 A bacteria engine is a complex molecular machine consisting of several closely interacting small molecular machines or functions. In this picture, four functions are shown, there exist others: proton transport, ATP-cleavage, secretion and adhesion (adhesion is a simple function, not a machine). Mapping of the engine model with approval (Protonic nanomachines Project, Japan, http://www.fbs.osakau.ac.jp/labs/namba/npn/ top.html).

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to be transported, as was in the type 3Sekretionssystemen (T3SS), found 13 of pathogenic bacteria (eg (Blocker et al. 2003, 2008 Galan, Galan & Wolf-Watz, 2006, Journet et al. 2005, Pallen & Matzke 2006 ). In this he is particularly well studied because it is an important virulence factor. It is sort of a molecular syringe, with a pathogen toxins can be directly injected into a host cell (“Injektisom”).

T3SS proteins but can also give directly to the cell environment. In Figure 5 is a schematic model of the type 3 secretion system of the pathogen E. coli shown 0157th It consists of about 10 proteins, is thus relatively complex. We know that the engine for bacteria belonging to the building and can secrete essential T3SS proteins that do not belong to the bacterial motor. Of particular interest is the new discovery that the protein transport T3SS not ATP, but is driven proton and thus fed by the same energy source as the rotation of the flagellum is (Galan 2008).

It can therefore be speculated that not a complex bacterial motor was at the beginning, but that the simpler the structure of a “primitive” type 3 secretion system (without motor function) decline, which in many evolutionary stages additional, already receives co-opted into the cell existing proteins and altered by mutation, until finally led to the current, complex motor function (Musgrave 2004, Matzke 2006). The objection that the type 3-derived secretion apparatus and the bacteria could be original engine should not be further discussed. In addition, there is evidence of a number of other sub-functions of the bacterial motor, such as Virulenzgenregulation (Belas & Suvanasuthi 2005) or the perception of moisture (Wang et al. 2005) .14 It seems as if the flagellum also have gene regulatory functions (Anderson et al. 2009).

Such dual functions do not contradict the assumption that the flagellum is not irreducibly complex, because the destruction of Proteinsekretionsapparates of the flagellum leads to loss of motor function, because the engine can not be assembled. One could even imagine that the entirety of the core proteins of each bacteria engine with regard to motor function is a non-reducible complex structure, and that the contained secretion apparatus terms of protein secretion also one - but simpler structure - non-reducible complex structure (with a different function) be could. Although the existence of secondary functions of biological structures for the modeling of potential evolutionary paths is extremely important (Fig. 5, see Schematic representation of the type three secretion system of pathogenic Escherichia coli cell (below). The pathogen attaches itself to an intestinal epithelial cells of the host (above) to . The secretion consists of an apparatus that in the cytoplasm of E. coli-synthesized proteins transported first through cytoplasmic membrane, periplasm and outer membrane. constructed by a molecular “needle” (mainly from the protein EspA), headed from the proteins and EspD EspB in the cytoplasmic membrane of the host cell inserts, go effector proteins (eg EspH, EspG) in their cytoplasm and enslave “the human cell. The disease can in extreme cases lead to death. Schema of Angelika Sell, changed, from different sources collected.

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below). Their mere existence means but not (unfortunately, the argument is quite familiar), so that the evolution of non-reducible structures had already been fully clarified. Secondary functions of parts of the bacteria motors are not an argument against the fact that these engines in their current form, one - included in terms of their motor function - substantial complex irreducible core set of proteins. Secondary functions may however serve as a basis for the development of hypothetical models with evolutionary intermediates.

There is no doubt that not a bacteria engine “from nowhere” can arise through evolution. If the bacteria has emerged evolutionary engine, then there must have been intermediates, which were either fixed through selection or through neutral evolution in bacterial populations. These intermediates have to be built on existing structures, as they also can not arise de novo. A cognitive progress can be expected only if such intermediates proposed concrete and transitions between them are analyzed. The discovery that bacteria engage parts of the motor secondary functions, was an important step in this direction. Of particular importance in this context, the already mentioned ability of the bacteria in the secretion of motor proteins.

We know then that the T3SS is true today for the irreducible complex motor, however, that this apparatus also has another function that is independent from the rotary engine, and could therefore arise independently. One can speculate that an entirely independent of the engines were, preliminary T3SS was used to build an engine. would in other words, the emergence of a “primitive” so that a functional T3SS, intermediate stabilized by selection on the way to the formation of the bacterial motor, and so a significant simplification of its evolution. Such intermediates were also known as basic functional states (Junker & Scherer 2006, Scherer 1983).

It is the merit of Matzke (2006), the m. W. have proposed so far only speculative scenario for the evolution of the bacterial motor of which is detailed enough to be testable. In this scenario, an evolution story is told, which is well suited to be initially examined theoretically. I have Matzke evolutionary steps to this end, graphically in Figure 6 together gefasst15. Designed by Matzke scenario is a fantastic story (which is not meant pejoratively, any science thrives on creative hypotheses, more in section 12). It is based on the postulate of thought of many intermediates in a hypothetical evolutionary selektionspositiver (cumulative selection). However, the fact or the presumption is that a new or modified structure increases the fitness of its bearer, a true notwendige16, but by no means a sufficient condition to ensure that they can develop through evolution. You have such stories, therefore submit a “reality check”. This is the only way aussehen17 that the various necessary conditions identified for a postulated evolutionary step as accurately as possible and the chances of evolutionary transitions can be estimated taking into account molecular and population genetic framework.

The principal merit of Matzke is that you, the individual may consider him postulated evolutionary steps 1-11 (Fig. 6) in principle to known experimental data. As an example, I choose evolution step 4, and this is because it can be very good reasons: First, has the bacteria on a motor Sekretionsfunktion. This is intended to be already created some unknown way and as a starting point. Second, the scourge of a Adhäsionsfunktion, ie, the bacterial cell to bind with the scourge of surfaces. This was for various eubacteria such as Escherichia (Giron et al.

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2002, Monteiro-Neto et al. 2003, Nather et al. 2006, Parthasarathy et al. 2007), Aeromonas (Gavin et al. 2003, Kirov et al. 2004), Pseudomonas (Lillehoj et al. 2002), Clostridium (Tasteyre et al. 2001) and Shewanella (Caccavo & Das 2002) is shown. Even in archaebacteria was one of the flagella Adhäsionsfunktion described (Nather et al. 2006), but these structures are entirely different than the eubacterial flagellum (Jarrell et al. 2009). A Adhäsionsfunktion is a selective advantage under certain conditions and could therefore establish by Darwinian evolution, function occurs before the rotation of the apparatus. Thirdly, this is only the co-option (transfer to a new context), and mutation of a single protein. Less than one protein can not be co-opted, we have here is a minimal Kooptionsschritt before us. Fourth, one could imagine that a not yet optimal Adhäsionsfunktion can perhaps be generated by a small number of mutations in a protein preadapted. Fifth, one might then speculate that from this initial adhesin by consecutive (following) mutations later developed the multimeric flagellins (building blocks of the Scourge). Evolutionary step 4, which is illustrated in Figure 7 graphically simplistic, I think one of the links on its evolutionary path described in Figure 6, which realize at first glance seem the easiest.

What processes must be postulated to occur to ensure successful co-opt it? Matzke did not deal with molecular details. Especially this is crucial to a meaningful assessment, however, so I will add Matzke and in the following example to argue at this level. In Figure 8, the necessary requirements for are shown in Figure 6 outlined evolutionary step.

10.1 Präadaption of Vorläufergens

should first follow the precursor protein, which is to be co-opted, some requirements so that the evolutionary process is likely. I assume therefore that this protein was pre-adapted (for example, the concept of Präadaption Junker & Scherer, 2006, and Ridley 2004). So that it possessed some structural features that target this protein to some extent for the necessary adhesion protein. These include, first, that there was a secretion, which can be detected by a secretion apparatus, this precursor protein should therefore belong to those who have evolved through the unknown way, “primitive” type 3Sekretionssystem were secreted. The second is to assume that the overall structure of the protein to a one Präadaption Adhäsionsfunktion brought. On einfachsten18 it would be that the origin of protein already had a vorangepasste domain

Figure 6 Evolution of the bacterial motor by co-option and mutation by Matzke (2006). Co-option of existing proteins are shown in blue, with here are also mutations necessary. Mutation events without Kooptionsereignis ngegeben are in red. The co-opt an adhesin by a type three secretion apparatus is highlighted with a red arrow and is used here as an example to examine the requirement for this evolutionary step.

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was the only convert to a new Adhäsionsspezifität. This is not unreasonable, for example for each enzymatic function is also a binding of the substrate needed to be split. Must create a completely new Adhäsionsdomäne by mutation, but an existing substrate binding must be transformed in only a Adhäsionsfunktion.

2.10 mutations in Vorläufergen (1): gene duplication

In general and for good reason it is assumed that new genes arise by duplication of existing genes, in particular, maintaining the original function and the duplicated copy is free to accept mutations by a modified or new function, without the old function is destroyed ( statements such as (Hughes 1994, Ohta 1989, Roth et al. 2007, Zhang 2003, Lynch 2002). Bergthorsson et al (2007) have described a way how a new function from a previously existing page function (so to speak a “preadaptation”) in a population could be established. In more recent work is the emergence of a new position in duplicate also called Neofunktionalisierung (eg Beisswanger & Stephan, 2008, Teshima and Innan 2008). gene duplications are frequently observed events, but it is relatively likely that as a result of either a functionless pseudogene arises or that a subfunctionalization begins. This refers to a parallel change in the function of the original and the duplicated gene, so that both run together the function of the original gene (Hittinger & Carroll, 2007, Hovav et al. 2008, Lynch et al. 2001). Neofunktionalisierung but could possibly also run through subfunctionalization (He & Zhang, 2005, Rastogi & Liberles 2005). I postulate here that a preadapted Vorläufergen of the adhesion protein was first duplicated and then by mutations in a copy of a Adhäsionsfunktion has won it (Fig. 7).

3.10 mutations in Vorläufergen (2): Formation of an adhesion function

How is it in duplicate, Vorläufergen preadapted to form a Adhäsinfunktion? One might think that this secreted protein precursor dietary sources of the bacterium opens (complex polysaccharides, proteins, nucleic acids) and showed for this purpose an appropriate enzymatic function. Thus polymers are broken down into monomers, which may be included. Such secreted, polymer-degrading proteins could also serve to destroy other cells. A number of such enzymes is eliminated, for example in phytopathogenic microorganisms by type 2 secretion, for example, Jha et al. (2005).

The advantage is, therefore, that the precursor protein would already have a binding site. This should now only be reconstructed so that a reliable bond occurs without enzymatic activity. The selective advantage of the binding of a bacterium to an abiotic substrate or a plant surface is obvious.

Is it possible to estimate the number of required mutations at the origin of protein? As a simple model, I see a polysaccharidabbauendes enzyme (those secreted enzymes are common). It has an enzymatic function, the polysaccharides into monomers or oligomers disassembled. This includes substrate binding, this domain could be converted into a Adhäsionsdomäne. If there are very similar substrates, the binding specificity or the affinity to polysaccharides by single point mutations can be changed (for Polysaccharidbindungsproteine see eg Simpson et al 2000; for enzymatic activity, there are many such cases, see Junker & Scherer 2006, page 143f).

Figure 7 co-opt a preadapted adhesion protein and mutation of an existing type three secretion apparatus. The presumed secretion apparatus is very simplified blue outlines the preadapted protein, which is formed in the cytoplasm and then secreted through the Sekretionspparat is shown in yellow. It should already have a precursor Adhäsionsdomäne. According to co-opt and mutation in an adhesin binding protein now transformed to a protein on the outside of the secretion apparatus (black dumbbell) and can attach themselves out from there to an extracellular substrate.

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If you want to recreate a Polysaccharidbindungsstelle a bond for other types of carbohydrate, then there is the requisite number of mutations, however, 4:00 to 10:00 amino acid changes (Gunnarsson et al. 2004). Conditions for success in the considered here example are that (i) the enzymatic function is destroyed, (ii) maintain the binding function at the same time remains, and (iii) is such that it has a sufficiently high affinity for the substrate receives a fixed to ensure binding of the bacteria. Alternatively, one can imagine that bind an intracellular “adhesin”, which may be bacterial polysaccharides konnte19 converted into a Adäsin was that recognizes an extracellular polysaccharide matrix. Perhaps the transformation to achieve the active site of the protein by only two point mutations on one or the other way. These are m. W. Although no experiments known. Such conduct might be, however, this assertion testen.20

4.10 mutations in Vorläufergen (3):

Coupling of the Adhäsinproteins Sekretionsmaschine (co-option)

A free adhesion protein is of no selective advantage for the cell, the protein must be linked to the cell surface. This later postulated a further evolution for the bacterial motor can be coupled to the one lying on the outside of the cell proteins of the existing Type 3 secretion apparatus erfolgen21. The issue is the reappearance of a very stable, noncovalent protein-protein coupling. How many mutations are required? The generation of new binding specificity in proteins by laboratory evolution has developed on the basis of biotechnological interest to a booming area of research (overviews in Bersthein & Tawfik, 2008, Singh & Sharma, 2006). Here the cases of interest, which is produced in a precursor structure that has already binding capacity (so-called scaffold22, Skerra 2007) a new binding domain, which in the present context only pure random processes are considered, ie the initial formation of a binding function. Optimizing Darwinian evolution, which would build on those already established functions and alter selection driven, inevitably in the course of evolution to be expected.

In a series of recent works have been from existing scaffold genes frequently mutated gene libraries stochastic and won, which contains up to 1013 different variants. Hence the individuals were selected that have a new binding activity. This shows that binding domains in the sequence space are not too rare, and in respect of some bound substrates even occur relatively frequently. A few examples may be mentioned, I begin with the formation of protein binding domains that couple to medium determinants (we know very much about it, because that is biotechnologically relevant). If you Lipocalinscaffold the basis sets, then new binding domains for digoxygenin of about 15 new amino acids built up (Schlehuber et al. 2000), also from 1416 to phthalic new amino acids (Mercader & Skerra 2002), which requires about the same for fluorescein number of new amino acids (Best et al. 1999).

The coupling to the secretion apparatus adhesin a high affinity protein-protein coupling is required. Also one has been won on the basis of Lipocalinscaffolds (Xu et al. 2002), about 20 new amino acids were involved. On another scaffold could be shown that a protein binding domain arising from a Polysaccharidbindungsscaffold also from 9-12 new Aminosäuscher forces.

Figure 8 Composition of the conditions and changes that are being discussed for the co-option, and mutation of a precursor protein for a preadapted adhesin in the text.

[p. 21]

It must be remembered that contribute to binding of a bacterium to a solid substrate, even with slight movements enormous train and shear forces on the secretion apparatus, because its size relative to total cell mass is very small. This is true even when a cell forms multiple copies of the secretion apparatus. The various protein-protein interactions within the secretion apparatus are certainly not designed for these tensile forces, this problem would probably be offset by compensatory mutations.

How many such compensatory mutations are needed? The answer to this question no one knows, the experimental verification would be difficult, and therefore can only be preliminary at this point a question mark.

10.6 Regulation of expression of the adhesin

This creates an overall operational construct, it is necessary that the control of gene expression of the duplicated and mutated adhesin is reasonably fit. The new adhesin must be produced at about the right time and in roughly the right amount (optimizations by subsequent Darwinian evolution is no fundamental problem). The associated regulatory elements have to arise by mutation at the same time. How many changes in the promoter structure of the duplicated gene notre created for it (can Gunnarsson et al. 2004).

These results must be considered in the present context, however, differentiated. From the gene libraries because of the experimental approach only höchstaffine variants were isolated. One can certainly assume that were included in the libraries even less affinity variants, which use less new amino acid changes. However, the required power in our context from the beginning to be quite stable because the binding of the bacteria to a surface by the adhesin that would otherwise be swept away by the secretion apparatus. I propose as a working hypothesis that a sufficiently strong, bind to the novel secretion apparatus only five amino acid changes in the precursor protein requires. It must be noted also that amino acid changes that lead to the coupling to the secretion apparatus, does not change the adhesion sites of the protein to the external substrate. Perhaps the number is taken five more deeply.

Mutations in the secretion apparatus 10.05

The adhesion protein that is coupled to the secretion apparatus. This has a number of consequences, which are summarized in Figure 9.

First, the binding of a protein to another protein inhibits the function of the first protein is often what is used in molecular biology for years, proving that a protein carries a very specific function (eg inhibition of a response by antibody binding). This would be unacceptable in our case, because of the secretion apparatus is essential to remain functional. It is therefore proposed that the secretion apparatus is first changed in the affected protein coupling by mutations so that the function of this protein is not impaired too much. Furthermore, these changes the function of other proteins of the secretion apparatus may, the binding partners of the affected secretory, are being affected too much. Perhaps this additional mutations are needed? Mutations that abolish the negative result of a previous mutation, are known as compensatory mutations (overview eg Ferrer-Costa et al. 2007). An additional complication is expected by the appearance of not acting far mechaniwendig are currently can not be estimated data-driven.

Figure 9 Interactions of the secretion apparatus / adhesin with the substrate for adhesion and subsequent interactions and their importance for the interaction of various proteins of the secretion apparatus (schematic diagram), details in text

[p. 22]

Other hand, we postulate that the duplicated gene is transferred through nichthomologe, intrachromosomal recombination in an operon of the secretion apparatus, so that would be at the same time the temporal expression control and perhaps the quantity produced so happens to be true to some extent. How common is such a locally appropriate, double intrachromosomal recombination? Reliable data on such frequencies exist m. W. it, but I guess at less than 10-9 per cell per replication (Hülter & Wackernagel 2008).

7.10 Fixing of the two new loci in the population

Often remains unmentioned in the narrative of evolutionary history a further important detail. Assuming all of the above changes are somehow come about: Well the data has to bacterial cell has yet to fulfill its competitors. This will only succeed on the one hand, if the positive selection coefficient is sufficiently strong. But regardless, there is a significant chance that, despite a positive selection coefficient of the new construction by random genetic drift disappears before she had the chance to assert itself by selection.

The fixation of mutations in a population can also be made by neutral evolution, and so initially without Darwinian selection. For this reason, by multiplying the individual probabilities can be given only the probability of the emergence of a structure per cell and per generation. The potential of neutral evolution is discussed in Junker and Scherer (2006, p. 139f and 162F) and Scherer (2011, in preparation). There are reasons why the neutral theory of evolution - it is so important for the understanding of evolutionary processes - mE currently no convincing solution to the problem of macro-evolution has on the molecular basis.

10.8 Can the probability of formation of a bacterial motor can be estimated?

As the above discussion has shown, the evolutionary history of Matzke be told clearly detailed. This allows only a still very rough reality check of history. Some things you can assess this data-driven, others for lack of data on the other hand still?) not (. The conclusion is m. E. obvious that the total probability considered for the evolutionary step is very small. How small? Behe writes: “However, as the complexity of an interacting system increases, the likelihood of such an indirect route drops precipitously. And as the number of unexplained, irreducibly complex biological systems increases, our confidence that Darwin’s criterion of failure has been met Skyrockets toward the maximum that science allows. “(Behe 1996)

That is a steep proposition. Can the “probability” or “improbability” of the evolution of a bacterial motor call a number? One could take the number of mutations estimated to be independent of each other, multiplying their individual abundances of it, and then would get a vanishingly tiny number for the simultaneous occurrence of events in a cell in one generation. Apart from the problem of neutral evolution, which makes such an assessment impossible (Junker & Scherer 2006, page 162F) that figure would imply an unrealistic accuracy of the result. You might also suggest the conclusion of this result is the evolution of the evolutionary process under discussion is refuted. Both is not my intention.

It should be pointed out again that selected from evolutionary history to the formation of the bacterial motor (Fig. 6) one of the simplest and most justifiable action became aware of this discussion. The other postulated evolutionary steps are sometimes more complex. My conclusion from the discussion held in this section is therefore:

It is unknown as by co-option and mutation in the course of the hypothetical formation of the bacterial motor, the gain would have an adhesin can run.

[p. 23]

Among other things, for the following reasons, Matzke Kooptionshypothese turns to the evolution of the eubacterial flagellum mE not as reliable scientific hypothesis.

11.1 All models are intermediates in Matzke selektionspositiv?

Some of Matzke postulated evolutionary stages, it remains questionable whether the postulated evolutionary steps actually have a selective advantage. Whether, for example, the steps 5-8 in Figure 6 are selektionspositiv, reveals itself at least not at first glance, but this question should be discussed in detail.

11.2 The problem of the fundamental reconstruction of structures by mutations

If one wants to assess whether a postulated evolutionary step could have something like this actually take place, then you have to enter more deeply into molecular genetics, mechanistic details, as has happened in Matzke (2006). Matzke from evolutionary history to the formation of the bacterial motor (Fig. 3) was one of the simplest and most justifiable action is selected and analyzed for the presumably necessary modifications in the structures involved. This results in a number of serious, unresolved problems. My conclusion from this discussion is: It is unknown as by co-option and variation in the course of the hypothetical formation of the bacterial motor, the gain would have an adhesin can run. Nevertheless, it could be that important factors were overlooked and that the co-option of a one adhesion protein secretion apparatus was somehow in another way. Perhaps further analysis will solve the problem. Then the problem would result as described below.

11.3 The problem of evolutionary canalization

If the selection coefficient is high enough, a primitive, initial Adhäsionsfunktion prevail in a population and is also in the further course of evolution by the Darwinian selection mechanism, which is a biological law, need to be optimized. This will gradually be made by individual mutations in the binding site and elsewhere in the adhesin and the secretion apparatus. The further optimization of this process, the more difficult it is to couple to this function later, a new property, such as Pilusbildung with channel or rotation.

It follows that a Adhäsionsfunktion (should they arise for) in an evolutionary dead end must lead in terms of the formation of a rotating flagellum.

11.4 The problem of the limitation of the variational space by multiple functions

From Matzke is postulated that several adhesins coupled together and to enable more Adhäsinkomplexe that increase the binding function (Matzke 2006, step 3b). So that the secretion is not it impair its function, one must postulate with Matzke that the monomeric adhesins aggregate into a multimeric ring on * secretion apparatus, forming a pore through which secreted proteins find their way to the outside can. That would be a completely unnecessary and would Adhäsionsfunktion but an unknown number of additional changes to the Adhäsinproteinen need so that they bind to each other and to the secretion apparatus and can form the secretion injectisome.

An increase in the number of Adhäsinproteine would be much easier to reach by the binding of adhesins to cell surface structures that affect not the Sekretionsfunktion.

The underlying general problem is the limitation of space, and therefore the evolutionary variation possibilities when structures must perform a dual function (or will run later) - here a single protein that (a) an adhesion

[p. 24]

is already functional exercises, and (2) also form a secretion injectisome and (3 rotate) later. Either will be optimized to increase the adhesion point, or to form a secretion injectisome. Both are also very unlikely to be worthwhile because the dual role required only a few mutations. On the other hand, there will be many mutations that improve a Adhäsionsfunktion. Of the Darwinian selection process built in “optimization constraint” will not lead to the formation of an adhesive secretion injectisome, but to an optimized adhesion. But should be made contrary to the Darwinian selection theory, a secretion injectisome, the variation of room for future rotation is the same the more restricted (evolutionary channeling).

5.11 Darwinian evolution is contrary to the flagella-Evolution

Evolutionary channeling and multiple functions of individual components lead to the following adhesion to a stage of evolution represents the evolution in real Adhäsinrings course not a realistic option. The problem is illustrated in Figure 10. The coupled to a Sekretionsmaschine adhesin will initially operate sub-optimal and the Sekretionsfunktion should be disturbed at first, because you must start it so, as few mutations have that first one still “primitive creates” new function. All the available experimental data on the evolution of bacteria consistently show that in this case an optimization and finally perfecting the still suboptimal functions by single point mutations. This is the evolutionary path that points in Figure 10 below. The better the optimization is, the farther away the structure in the area of the mutation actually desired new function of the secretion injectisome (which also has no obvious selective advantage). The formation of a built up from Adhäsinmonomeren secretion injectisome is associated with a significant number of changes in the secretion, the adhesins and the regulation of their expression. Such a multifactorial event will occur very, very rare, and it is in constant competition with the frequent occurrences of optimizing existing adhesin / Sekretionsfunktion. The Darwinian selection mechanism as a biological law will therefore need to ensure that the “wrong” evolutionary path is taken. Regarding the evolution of a flagellum leads to Darwinian evolution, which follows a hypothetical origin of the adhesin / secretion system, whose inevitable optimization in a selektionspositive impasse.

6.11 Hidden teleology

The example of the above described formation of an initial secretion injectisome of a ring of Adhäsinproteinen is clear that

Figure 10 Evolutionary sewer crosses the biological law of the Darwinian mechanism of evolution inevitably to the optimization of hypothetical, newly formed adhesin / secretion apparatus and power (thick black arrow) and away from the actually required to Flagellum evolutionary path (dotted red arrow to the right). The Matzke after lying on the evolutionary path “Adhäsionsring” (right box), also exhibits no better selection advantage.

[p. 25]

Matzke this ring is placed just so mentally cope, has so he can use it later as the basis for the further polymerization of Adhäsinproteinen to form a flagellum. In other words, Matzke has (not only for this step) and an unnamed reader ignorant hidden teleological (ie targeted) component is hidden in his evolutionary model in order to make the model plausible at all can. Such a thing is in the context of a naturalistic evolutionary biology actually is strictly prohibited.

7.11 Matzke model is not discussed in the literature to date

As far as I know, was Matzke evolutionary model in the refereed literature and microbiological still not diskutiert.23 This is surprising because the evolution of the bacterial flagellum, the prime example in the public debate about Intelligent Design in the United States. In addition, alternative mechanistic (and hence theoretically testable mW) Evolution models for the bacterial motor not proposed until now. Can we conclude that the experts - if they ever took note of it - Matzke model holds little convincing?

8.11 Matzke waived the discussion of his own evolution model

Together with Mark Pallen Matzke presented a comprehensive and readable publication in a leading journal on microbiological evolution of the bacterial motor (Pallen & Matzke 2006). connected Matzke relevant, above-discussed model of evolution, the two authors in their own work discussed but not yet as an argument benutzt.24 Nevertheless, Johannes Sikorski has recently Matzke model without any criticism or modification fully and it “impressive and resilient model for the evolution of the bacterial Flagellensystems “praised (2009, 278). This assessment corresponds to the available data (not so) and is used by the experts at least not yet supported.

In Junker & Scherer (2006, pages 157-163) it was assumed that a “primitive” type 3-secretion apparatus is converted by the conversion of 16 pre-adapted proteins in a simple bacterial rotary motor, and for the conversion of a protein 10 mutations were estimated. This figure was derived from experimental work on the change of function of proteins and is about the lessons on the basis of other sources number of changes which are in Figure 8 of this work for the example of the co-option of the adhesin collected. The core allegation of Matzke model now is that these 16 proteins were not co-exist, if the evolution process can be divided into different stages selektionspositive. In Junker & Scherer (2006, page 158) were selektionspositiven intermediates such “basic functional states” mentioned. If Matzke true model, then two selektionspositive basis states would be much less far apart as in Junker and Scherer (2006, Seite162) was adopted. While they were still so far apart that remains unknown, as the distance could be overcome between the two selektionspositiven states by known factors of evolution, but that does not change the fact that to overcome gap would be much smaller than from Junker & Scherer adopted.

While it is doubtful whether Matzke’s model is basically effective. This is related to the angle shown in 11.3 and 11.4 facts of evolutionary canalization and the multiple functions of structures. Matzke assumes two things: First, should all be given for intermediate selektionspositiv. That would be examined in detail thoroughly (see 11.1). Secondly, Matzke assumes that upon reaching a level (for example, the co-opt an adhesin) the subsequent stage (the initial secretion injectisome Adhäsinring as) an undirected by the evolutionary process actually selectable option. However, this is in the specific example discussed just not the case - Matzke shall establish here a teleological element. This is not a viable co-opt an adhesin precursor to the formation

[p. 26]

a rotating flagellum (see Section 03/11 to 05/11) but in this respect is an evolutionary dead end. It looks at the current Argumentationsstand m. E. look as if Matzke model does not readily selektionspositive basis function describes conditions that lead from a primitive type 3 secretion via the smallest steps towards a bacterial rotary motor.

Let there be no mistake: Despite the criticism is noted with appreciation that there is always a great merit of Matzke’s model to have raised the argument to a qualitative new level. The affected section of Junker & Scherer will therefore be in a planned remake along the argument presented here, which would not exist without Matzke model reformulated.

We know m. E. not far may have evolved by which evolutionary path a bacterial motor. Instead of reasonable scientific theories in such cases, sometimes ad hoc speculations voiced and considered a sufficient explanation. It does appear, particularly among amateurs, but is sometimes observed in the scientific literature. The argument often goes in the direction that a structure has adopted an assumed precursor structure to a selective advantage, which should make the whole process of evolution appear to have completely plausible. Egbert Leigh sat down with the still widely held view that the mere enumeration of hypothetical selection benefits sufficiently explain the evolution of life, a critical look (Leigh 1999). He cites first Antnonovics (1987): “Too many biologists behaved as if to imagine a use for an organ is … equivalent to explaining its origin by natural selection without further inquiry “and then Gould & Lewontin (1979), this approach” adaptive storytelling “services. Gould and Lewontin made with that name probably a little fun of the “omnipotence claim” to the selection theory, as for example, particularly stark in Dawkins (1987, 2008), but not just appear there. Lynch (2007) comments on Dawkins acting religious absolutism rather ironically:

“Dawkins’ agenda to spread the word on the awesome power of natural selection has been quite successful, but it has come at the expense of reference to any other mechanisms, a view that is in some ways profoundly misleading.”

The concept of Molecular Evolutionary Story Telling will be here on the problem of the evolution of the bacteria used motor. This is not meant disparagingly. Only today’s knowledge of the biology of bacterial transport systems and flagella allow the molecular basis of it all, such ad hocGeschichten to tell in acceptable detail. That was not even possible 10 years ago. There is a wealth of detailed biological knowledge to relate to such evolutionary histories so that we can derive testable hypotheses and research programs.

That is a significant step forward not only of microbiology, but also in evolutionary biology: The more specifically an evolutionary story can be told, that is, the more subdued by Experimentalwissen molecular and genetic details can be incorporated into the story, the better they can on a theoretical or, much more be important, also tested on an experimental level. In that sense, I think Matzke evolutionary history (Matzke 2003) - for all substantive criticism - for helpful and wichtig.25

The molecular tools are always available to these and other stories told from the resulting experimental questions (for example, by stochastic protein libraries and targeted mutagenesis) to klären.26 Evolutionary story telling is by no means obsolete. It is on the contrary, an important element not only in evolutionary biology, but of the scientific research process insgesamt27. Regarding the evolution of the flagellum, today we can at least tell stories so far substantiated that one can examine these theoretically or experimentally. As shown, such an examination leads so far not satisfactory to a result. We currently do not know whether there is any plausible evolutionary paths, to allow a primitive flagellum or precursor thereof produced through natural processes.

[p. 27] is to be hoped, however, Delt by no means a final argument in this matter. The presented preliminary conclusions are always subject to revision, if this is required by substantive arguments. The claim that the evolution of the bacterial motor was a settlement in principle, because of scientific data is not covered. This does not appear that an evolution of the bacterial motor would be fundamentally impossible.


1 For a person of Nick Matzke see http://en.wikipedia.org/wiki/Nick_Matzke

2 On the macroscopic level of biology you come across the same phenomenon, such as the lavishly-equipped works “Bionics” show of Nightingale & Blüchel or “fascination Bionics - the intelligence of the Creation” impressive.

3 It would be really interesting to see whether such an attempt succeeds or whether it ends like trying to describe an angel as a “winged year-end figure.

4 eubacteria and archaebacteria have a plethora of variants of the rotary engine.

5 Mike Gene is neither creationist nor a representative of the usual ID course which is known from U.S..

6 example, there are numerous, very negative and often personally disparaging comments on Mike Behe on the Internet, in journals and newspapers, especially book reviews. This is for the following two reasons not addressed: First, they generally contain no or no new scientific arguments. Secondly, I have decided, personally offensive publications regardless of their scientific merits in principle not to quote.

7 The North American public discussion of the bacterial motor can really only be understood against the political-religious background of the United States. The often consciously, but quite wrongly, as creationists have designated representatives of the Intelligent Design (though similar to creationism), aims to anchor its intuition and in classes in state schools. I think that is not appropriate. To achieve this goal, it would be intelligent design a scientific alternative to evolutionary theory. I do not believe that to be generated research will shed more light on this problem.

Nevertheless: A story is not the reality, a speculative evolutionary history should not be confused with a scientific explanation, it may not considered a substitute for evolutionary research, and should be collected at least as verbal immunization against objective criticism. Stories are initially only just stories and highlight gaps statement. If they are good, they will stimulate the imagination and generate experiments that permit an assessment of their plausibility. In the end, one could initially only fictional, imaginative story prove to be plausible model for a process, which may be of this or similar actually played in the past. Or it turns out after a thorough examination as a fairy tale penned in biological terminology without parallel in the empirically tangible reality.

Lynch (2007) is to agree when he remarks with regard to the causal theory of evolution, “Evolutionary biology is not not a story-telling exercise, and the goal of population genetics is to be inspiring, but to be explanatory.” However, the explanatory power of evolutionary theories regarding the origin of novelties (macro evolution) at the molecular detail, ultimately prove.

The bacteria engine has proven to date in this regard as quite bulky. Total lies neither in the scientific primary literature nor in the popular literature, even in a plausible mechanistic approaches, scientifically resilient model for the initial formation of the bacterial rotary motor. The claim that the evolution of the bacterial motor is basically clarified (Doolittle & Zhaxybayeva 2007, Liu & Ochman 2007b, Matzke 2006, Miller 2004, Musgrave 2004, Pallen & Matzke 2006, Wong et al. 2007, Sikorski, 2009) is not because of scientific data gedeckt.28 This is not to show that an evolution of the bacterial motor would be fundamentally impossible. It is not the intention of this paper, nor is it even possible to draw such conclusions.

This work will be seen as another step in the critical discourse on the origin of the bacterial rotary motor. It han-that this is the case and have the justified elsewhere (Scherer, 2009).

[p. 28]

8 archaebacteria contain a completely different type of engine, the is far less known than about the eubacterial flagellum. About its origin can be hardly justified under discussion due to lack of functional analysis.

9 The rotary engine of the archaebacteria is very different from that of eubacteria, but the same rules apply to the experimental search for essential genes of the engine as in eubacteria.

10 I do not hesitate to call cellular systems such as “brilliant”, knowing that this is a border crossing that leads from the field of scientific terminology out.

11 Of course, it is also possible that similarity was caused by the operation of a designer. Even if that were true in the case of the bacterial motor, the argument would not belong in a scientific discussion:

The work of a designer is not reproducible and not examinable process and the adoption of a designer is not falsifiable, therefore, lies beyond the horizon of scientific knowledge.

12 It should be known to the fact that Doolittle is one of the world’s recognized authorities in the field is the bacterial evolution.

13 Among the prokaryotes a number of different secretion systems are known that the extrusion of proteins through the cytoplasm and possibly allow the outer membrane. Basically, these are relatively complex procedures.

14 Both functions are biologically meaningful connections with the motor function, but this leads at this point too far.

15 A corresponding to the lay stunningly convincing sounding and no problems leave open evolutionary history is at http:// www. youtube.com / watch? v = SdwTwNPyR9w available. Basically, this video is adjacent to a dumbing down of the unfortunately ignorant viewer.

Here’s 16 of Darwinian evolution, the speech, neutral evolution is an important, but among the laity is still no course concept and is discussed elsewhere (Junker & Scherer 2006, p. 139f and p. 162; and Scherer, 2010, formation of the bacterial motor by Neutral evolution? In preparation)

17 On these facts, I would point in 25 years, see Scherer 1983rd

18 Yet it would be easier if you already have a functional adhesion protein would be co-opted. However, this would then have been otherwise have been established, which is known by various adhesins in the outer membrane. In this case, the change in the secretion apparatus, however, would not include new functionality and thus do not lead to greater fitness.

Maybe in the 19 Mureinzellwand? We know a number of polysaccharide-binding domains of bacterial enzymes.

20 This is an example of this is to bring as evolutionskritische analyzes the evolution of research forward.

21 If one asks what it did, as the narrator of the story, of course this still does not need current date in mind that the evolutionary path must lead towards the flagellum.

22 In “scaffold” (scaffold) means a protein which has a total construction has essential features that are new for the important function to be constructed. A scaffold is a sense preadapted protein, although it is not in the biotechnological usage so called.

23 The same goes for me the only previous known case, cited in the text in Internet Matzkes a refereed journal (Pallen et al. 2006). If there is other work, I am grateful for a hint.

24 Matzke’s model is not even cited as a reference in the text there is no relation, only the title of Matzke’s work is mentioned in the notes under “Further Information”.

My 25 made on Matzke constructive, further spun and much more detailed evolutionary history told me quite well.

26 you have to know that such work will need huge research funds.

27 Those who work experimentally know that many major scientific discoveries have begun with some adventurous and imaginative stories.

28 I am well aware that this conclusion is completely unacceptable, regardless of the reasons for those biologists for whom the term “evolution criticism from fundamentalist reasons basically a taboo.


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I’m going from memory about the spontaneous generation. Will try to find some direct quotes in the not too distant future.

There’s a quote I’ve been desperate to find about heart function. I remember seeing a documentary about medical history that quoted a pre-scientific anatomist saying that the function of the heart was to filter blood from one ventricle to the other. The fact that blood does not leak from one side to the other in sheep’s hearts was taken as proof of divine intervention with every heartbeat. I’ve always wanted to find that quote, but it has eluded my searches (it would help if I could remember the name of the documentary).

Chris Lawson said:

I’m going from memory about the spontaneous generation. Will try to find some direct quotes in the not too distant future.

No sweat, just curious.

Chris, you’re likely thinking of Aelius Galenus (http://en.wikipedia.org/wiki/Galen), who was undeniably important for anatomy and physiology, but postulated structures (such as the heart-filter) which simply don’t exist.

co, thanks for the Galen link. I know that Galen was an amazing scientist for his time who had the misfortune to become the Official Doctrinal Figure on medicine and thus all of his mistakes became ossified as medical canon for centuries, and now the mistakes are what he’s mostly remembered for.

I’ll have to look through Galen’s work for that quote, but I don’t know if he said it or if it was one of the many commentators who followed.

Reply to Nick Matzke’s translation:

Very nice. One thing that stood out for me was Paul Nelson’s repeating what Phillip Johnson was reported to have said some years ago:

“The theme has also Paul Nelson as an important representative of ID: “Easily the biggest design challenge facing the ID community is to develop a full-fledged theory of biological. We do not have such a theory right now, and that’s a problem. Without a theory, it’s very hard to know where to direct your research focus. Right now, we’ve got a bag of powerful intuition, and a handful of notions such as ‘irreducible complexity’ and ‘specified complexity’ - but, as yet, no general theory of biological design. “(Nelson 2004).

This still holds true today. But I’m sure those at the Dishonesty Institute’s puppet pseudo-science lab are hard at work on this very issue.

As for Behe’s comment:

“The conclusion is m. E. obvious that the total probability considered for the evolutionary step is very small. How small? Behe writes: “However, as the complexity of an interacting system increases, the likelihood of such an indirect route drops precipitously. And as the number of unexplained, irreducibly complex biological systems increases, our confidence that Darwin’s criterion of failure has been met Skyrockets toward the maximum that science allows. “(Behe 1996).

So then what is the probability of winning PowerBall? It certainly isn’t infinitely small, and someone wins every few weeks, a totally random affair. And he is basing in reasoning on what? Creationist assertions.

I know you hate to admit it Matzke, but you KNOW Behe was right.

In order to show that Behe was wrong, you need to demonstrate first, how many intermediate steps there are on the road to bacterial flagellum land ( I count at least 10 steps) and second, what the functions for each of these intermediate steps are. (I understand you may believe this to be an unfair burden to you (pl). However, it is crucial to your refutation of Behe. Note your first attempt at refutation with the assertion of T3SS secretion system as being a precursor to the b/f has failed, since it has been shown that T3SS is most likely a devolution of and not a precursor to the b/f).

For example, the b/f had to be built from the basal body outwards. The basal body is fixed to the inner membrane. So what was the function of the basal body fixed in the inner membrane before it added the C-Ring?

Next, what was the function of the basal body and the C-Ring before it added the MS-Ring?

After that, we need to know the function of the next intermediate step, the basal body + C-Ring + MS-Ring.

Moving along, what is the function of the basal body + C-Ring + MS-Rings + the newly added stators? Note for these intermediate steps in the flagelllum’s development, the new parts are placed in the periplasmic space. What advantage would the function of these intermediate configurations be considering the fact that these new parts are neither within the cell (to presumably support internal functions) nor outside of the cell (to presumably support locomotion or defense)?

Without this knowledge, how can we say with any scientific confidence that the bacterium did not contain within its genome a pre-existing program for the expression of a flagellum waiting to be triggered by an environmental cue (like cecal valves in lizards)? Why would a scientist discard such an intuition when all the observations point in this direction?

Steve P. said:

Why would a scientist discard such an intuition when all the observations point in this direction?

By the same logic, icicle formation is also impossible. In order for a water molecule to lock into a particular position, it has to be oriented just right; exactly the right amount of energy has to be removed, and it cannot be dislodged by the impact of an air molecule whizzing by.

On top of all that, the molecule has to have migrated along a path of an already improbably formed nascent icicle in order to find itself in just exactly the right position when the energy release occurs and it locks into position.

Even more fantastic is the final formation of the icicle. How could it possibly be in exactly that shape with all the various bands and wrinkles along its length and with exactly those neighboring icicles of the size and shape they have?

And this is just the simple stuff. How about superconductivity? How is it possible for a phonon to exactly coordinate the movement of two electrons, one with spin up the other with spin down? When this happens with billions upon billions of such pairs, the probability is astronomically small. Yet these billions and billions of electrons are chosen and paired off in “Cooper pairs” so that they become a collection of bosons that then condense into a superconducting state in which they flow through the solid material without any resistance whatsoever.

If they have no resistance, how do they interact with the phonons that are singling them out and pairing them off into Cooper pairs?

Ever look at the sequence of license plate numbers in the huge parking lot of a large shopping mall? What is the probability you would find that sequence? How could those cars be there; and how could those particular car owners be in that shopping mall at the same time?

According to Behe’s logic, the world doesn’t exist.

Mike Elzinga,

Paul Davies also uses the “it’s improbable therefore designed” argument as well (although he’s too sophisticated to propose an anthropomorphic designer; he’s more of a Spinozan, not that it stopped him taking the Templeton bait). A properly shuffled deck of cards has 8x10^67 possible orderings – which means by Davies/Behe logic, you can’t shuffle a pack of cards because any given combination is so unlikely.

Mr. Elzinga, I understand your viewpoint that you believe physics and chemistry account for all manner of material configurations whether they be inanimate or animate.

Yet, there are crucial differences in your icicle analogy: 1) the water molecule that accounts for the icicle is no special or particular variant of H2O. There is no difference between your water molecule in the icicle and the water that forms a pool of water in a pothole, or the water that is in the mist on Mom’s roses, or the water in my tea, or the water in tears, or the water in the ocean;

2) the icicle is formed by only one molecule- water. It is not a configuration of numerous, disparate molecules; and

3) the icicle does not exhibit function. The water molecules in the icicle do not move in any manner that represents work (the expending of energy in the transformation from one particular molecular configuration into another for a particular purpose i.e locomotion, catalysis, sensory perception, etc.

Really, we are talking apples and oranges here.

Getting back to the question, it is not the matter of the organism co-opting protein function, ie one protein is found doing more than one function in the organism.

Rather it is that one particular protein set is configured in a particular way in juxtaposition to another, albeit different protein set configured in its own particular arrangement, and this is done several times.

It seems more likely that if a bacterium over-produced a protein and had no where to store it, then the proteins would stick to the inner wall but in no particular pattern.

But that is not what we are observing. What we do observe is particular sets of proteins configured in particular patterns, and each protein configuration are themselves configured into a meta-pattern resulting in a functional organelle.

Are we to conclude that proteins only arrange themselves in circular patterns and that is why we see what we see in the b/f? But that is not the case AFAIK. So the question becomes ‘what causes proteins to align themselves in particular patterns and these patterns themselves arranged into meta-patterns (resulting in a pattern that begins to perform work) from a physics and chemistry POV?

Mike Elzinga said:

Steve P. said:

Why would a scientist discard such an intuition when all the observations point in this direction?

By the same logic, icicle formation is also impossible. In order for a water molecule to lock into a particular position, it has to be oriented just right; exactly the right amount of energy has to be removed, and it cannot be dislodged by the impact of an air molecule whizzing by.

On top of all that, the molecule has to have migrated along a path of an already improbably formed nascent icicle in order to find itself in just exactly the right position when the energy release occurs and it locks into position.

Even more fantastic is the final formation of the icicle. How could it possibly be in exactly that shape with all the various bands and wrinkles along its length and with exactly those neighboring icicles of the size and shape they have?

And this is just the simple stuff. How about superconductivity? How is it possible for a phonon to exactly coordinate the movement of two electrons, one with spin up the other with spin down? When this happens with billions upon billions of such pairs, the probability is astronomically small. Yet these billions and billions of electrons are chosen and paired off in “Cooper pairs” so that they become a collection of bosons that then condense into a superconducting state in which they flow through the solid material without any resistance whatsoever.

If they have no resistance, how do they interact with the phonons that are singling them out and pairing them off into Cooper pairs?

Ever look at the sequence of license plate numbers in the huge parking lot of a large shopping mall? What is the probability you would find that sequence? How could those cars be there; and how could those particular car owners be in that shopping mall at the same time?

According to Behe’s logic, the world doesn’t exist.

Chris Lawson Wrote:

For example, spontaneous generation. When it was thought to be true, it was undeniable proof of God’s creation. Now that we know it to be false, it is *lack* of spontaneous generation that is undeniable proof of God’s creation.

Just what one expects from a pseudoscience that tries to have everything both ways. I wish that would sink in to those who carelessly suggest that “creationism” is always about “proving” a recent 6-day creation. That may be what most American (European too?) nonscientists may infer, and it may even be what most anti-evolution activists want them to infer (even if they don’t believe it themselves), but that’s an artifact of the preconceived notions of the audience, not necessarily anything inherent in the “creationist” arguments. Even the old-style YECs base their “evidences” almost exclusively on sought and fabricated “weaknesses” of “Darwinism,” not on finding evidence that just happens to converge on their particular interpretation of Genesis.

The ID scam has completed the strategy, allowing readers to infer anything they want, even if their conclusions contradict each other’s. If there’s any doubt that ID/creationism is pseudoscience…

Nick Matzke Wrote:

…most of the chapter seems to be taken up with attempting to refute the evolutionary model for the origin of the flagellum!

Right. I’m trying to imagine a chemistry book being mostly about refuting phlogiston theory instead of supporting its own explanations. As crazy as that sounds, it would actually be far less crazy than the anti-evolution books because there really are weaknesses of phlogiston theory.

Steve P. said:

I know you hate to admit it Matzke, but you KNOW Behe was right.

In order to show that Behe was wrong, you need to demonstrate first.…



Behe claimed, rather clearly, that the flagellum was a deal breaker because getting there was impossible.

In order to refute that sweeping claim you don’t have to demonstrate that you’ve found the path, you just have to show that at least one path exists.

Once you prove it’s possible to grow a flagellum, an argument that relies exclusively on it being impossible just whithers away and dies.


You haven’t been paying attention. NCSE and similar organizations have been documenting the success of creationist movements not only in the English-speaking world but also in the German and Dutch-speaking world as well for years. I was wondering when someone like Nick would discover this Teutonic absurdity, and now he has:

MrG said:

At least this PDF is further proof that creationism isn’t just an American lunacy. Takes the pressure off … a little bit.

Steve P. said:

Why would a scientist discard such an intuition when all the observations point in this direction?

For the exact same reason scientists discard all intuitions with no evidence. An intuition is fine, have them, they often lead to good discoveries, but you cannot produce a journal paper and expect classrooms to teach it unless you have more than circumstantial evidence and your ‘intuition’.

This is what the cDesign crowd fail at. They have all these amazing intuitions and ideas, but have no evidence to back it up and they still expect to get it put into classrooms. It’s perfectly acceptable in scientific circles to say ‘We don’t know.… yet’. To add ‘Therefore god must have done it’ isn’t scientific and shouldn’t be taught in schools.

I’m sure that most people would gladly accept creationist claims in the classroom, provided that there was peer-reviewed, robust and repeatable evidences for it. There isn’t.

Steve P -

Without this knowledge, how can we say with any scientific confidence that the bacterium did not contain within its genome a pre-existing program for the expression of a flagellum waiting to be triggered by an environmental cue (like cecal valves in lizards)?

1) What would be the exact physical nature of such a “program”?

2) What would be the exact physical nature of the receptor for the environmental cue?

3) Can you look for these “programs”? Can you identifiy them and show how they are “triggered”? That would seem like a remarkably easy way for you to turn science on its ear and win a Nobel prize. Recognition of your “great genius” at last. Precisely as you constantly and obsessively fantasize. What’s stopping you?

Please note that YOU are the one who is making this vague claim, so the onus is on YOU to provide support for it.

Why would a scientist discard such an intuition when all the observations point in this direction?


Because it is not an “intuition” at all, but a desperate, vague, meaningless rationalization of science denial, which no observations whatsoever point to.

Prove me wrong by providing good answers to my questions.

Steve P. said:

Give it up, DS. It is YOU that errs in asserting that information is a physical thing. Information is not physical, but is conveyed through a physical medium. Different animals.

Nucleotides contain no information. BUT the sequence of nucleotides does. The information is only conveyed through a physical medium as it should be since the information is building a physical structure.

Just as the house in a builder’s head does not reside in a single point in his brain. However, the idea of the house he is building is conveyed through the brain, which commands his hands to form the house with physical substrates. Otherwise, the house could never achieve physical form.

Give it up Steve, you are dead wrong. There is information in the linear sequence of nucleotides in exactly the same way that there is information in the linear sequence of letters and spaces in this sentence. If you disagree, then you will have no trouble providing a definition of information that excludes DNA now will you. If you don’t think that there is any information is words and sentences, then you might as well not post anything ever again. In fact, I would recommend just that.

If you agree that there is information in a sequence of DNA, then exactly what is your problem? Can you describe the processes of transcription and translation? Why don’t you think that this is enough information to direct the synthesis and assembly of a flagellum?

You are a completely incompetent boob as anyone can plainly see. No on cares what you think because of your astonishing ignorance. I notice you still haven’t answered the multiple choice question about the structure of DNA. Until you do, no one will taker you seriously. After that, I can make no promises.

Now get to readin them references if you want to have an intelligent conversation about flagella. They should clear up many of your misconceptions.

I really cannot get my mind around this one. I think Steve is just yanking chains. I think he is trying to see how bat shit insane he can get without some calling POE.

How is it possible to reconcile the phrase:

“Information is not physical…”

With the claim in the very next paragraph:

“Nucleotides contain no information. BUT the sequence of nucleotides does.”

So, I guess the sequence of nucleotides is not a physical entity! It’s not like, you know, a real physical molecule or anything! Man, this guy really doesn’t understand the structure of DNA. How in hell does he think that the linear sequence of amino acids in proteins is determined? Oh wait, that’s right, he thinks DNA is composed of amino acids, so I guess he couldn’t have a clue about that either.

Oh and by the way, individual nucleotides can contain information as well, such as the tautomeric form they are in or whether or not they are methylated. Now why am I not surprised that Stevie did not know that either? Oh well, what can you expect from someone who claims that the genome contains a program, but there is no information in DNA. If this jackass is serious, he is seriously deluded. I’m beginning to think that he is just plain nuts and off his meds.

This is what I love.

These guys are hilarious. They say yeah sure information is not physical, but er it is in fact physical(one of Elzinga’s science lessons I bet).

You know like, “Yeah sure it looks designed but you know, er it is in fact not designed”.

I’m sure you guys have a mantra you keep mumbling to yourself like “It is NOT designed. It is NOT designed. It is NOT designed”.

How about an “Oooooohhhhhmmm” to got with that?.

Ohhhh, but you guys got me right where you want me, huh? Coming out of the woodwork in droves now.

Rave on. Got my 3-D glasses on.

Well Stevie boy seems to have finally fallen off the deep end. Maybe he finally realized that everyone was just laughing at him. Maybe he realized that he had blown all of his imaginary credibility by repeatedly claiming that DNA was composed of amino acids. Or maybe he finally realized that physical objects can indeed contain information, it isn’t just some abstract idea in someones head. It takes intelligence to interpret information, it does not take any intelligence to create it.

One last time, just to be clear, There is information in the linear sequence of nucleotides in a molecule of DNA. This information is expressed through gene regulation and transcription and translation. The information is sufficient to control all of metabolism, development and reproduction, including assembly of the flagellum. There is no magic invisible hologram. There is no consciousness or intelligence required. Real scientists understand this very well. That is why we spent three billion dollars on the human genome project. Just one more thing that Steve doesn’t understand.

In any event, his record is still intact. He still hasn’t read a single paper, even though he challenged people repeatedly to provide him with the “information”. He still hasn’t learned a single thing, including the definition of information or the structure of DNA. He still hasn’t given anyone a single reason to take him seriously about, well, anything. FIne by me.

Steve P. said:

Look at me! I so smart! I l337 creotard! Me contradict self every time me post!

Yay me!

That about sums it up.

Steve P. said:

This is what I love.

These guys are hilarious. They say yeah sure information is not physical, but er it is in fact physical(one of Elzinga’s science lessons I bet).

You know like, “Yeah sure it looks designed but you know, er it is in fact not designed”.

I’m sure you guys have a mantra you keep mumbling to yourself like “It is NOT designed. It is NOT designed. It is NOT designed”.

How about an “Oooooohhhhhmmm” to got with that?.

Ohhhh, but you guys got me right where you want me, huh? Coming out of the woodwork in droves now.

Rave on. Got my 3-D glasses on.

I’m not quite sure why you consider it to be some sort of victory when your opponents “concede” what they’ve been saying all along – that, for example, the genome encodes information. This point has not been in dispute throughout this discussion, except by one person … anyone remember who said this? (emphasis added)

Does it scare you shitless that in the 21st century, information will be ‘nailed down’ as a real entity, existing independent of matter? Why does it bother you to such an extreme?

So, when proven to be absolutely wrong about everything, Steve once again starts making shit up and laughing about how he was right all along. Well nobody else ever claimed that information could not be physical. JHFC, how in the hell does this guy think that CSI works? Like there isn’t any information in the markings on a bullet or the spatter pattern of blood! If the is no information in DNA, how in the world can it be used to identify suspects?

Perhaps this intellectually challenged primate is just trying to play word games. Perhaps he thinks that there is somehow an important distinction between claiming that DNA IS information and claiming that DNA CONTAINS information. BFD. Who cares? The point is that DNA does contain all of the information required in order to create an entire organism, including the flagella, heart, testes and anal sphincter. JHFC you can even clone animals using nothing but an enucleated egg and a transplanted nucleus. There is no magic invisible hologram. There is no semi intelligent designer watching over every flagellum in every bacteria. If the ass hat is so frickin intelligent, why the hell can’t she create a flagellum without having to supervise every time? Don’t sound very intelligent like to me.

Oh well, they say ignorance is bliss, so Steve must be the happiest guy on earth. I guess that’s what’s really important, not you know, reality. Maybe he will read those references soon. Yea, right.

Of course information can exist without matter. JHFC on a shingle, there is information in radio waves. There is information in the spectrum of the sun. There is information in the periodicity of a pulsar. How in the hell is this supposed to mean that there can be no information in DNA? How in the hell is this supposed to mean that the magic invisible hologram controls development, or the magic invisible designer puts flagella together?

Well at least you have to admit that no one else could get so much mileage out of refusing to define the term “information”. Way to go Stevie I. Wonder.

Thanks for linking to this particularly telling bit of dumbshittery, SWT:

Steve P. said:

And again, i say to you if life is inherent in the laws of physics and chemistry ONLY, then we should logically see all manner of life forms (and not necessarily carbon/water based) all over the universe. We DO NOT see this happening.

Therefore, logically we can say that life does in fact have some element in it that is not present in inanimate matter.


The stupid, it burns!

Yeah, it’s amazing how little life we’ve seen in the 99.999999… percent of the universe that we’ve never been to!

Gaebolga said:


The stupid, it burns!

It appears that the only thing he is reading is this kind of projection.

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This page contains a single entry by Nick Matzke published on August 8, 2010 6:23 PM.

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