First off, I would like to say that you definately have made some interesting points, and I would like to keep discussing the TTSS and the bacterial flagellum.
He, S. Y., 1998. Type III protein secretion in plant and animal pathogenic bacteria. Annual Reviews in Phytopathology. 36, 363-392., doi:10.1146/annurev.phyto.36.1.363.
Macnab, R. M., 1999. The bacterial flagellum: reversible rotary propellor and type III export apparatus. J Bacteriol. 181 (23), 7149-7153.
Kim, J. F., 2001. Revisiting the chlamydial type III protein secretion system: clues to the origin of type III protein secretion. Trends Genet. 17 (2), 65-69., doi:10.1016/S0168-9525(00)02175-2.
Plano, G. V., Day, J. B. and Ferracci, F., 2001. Type III export: new uses for an old pathway. Mol Microbiol. 40 (2), 284-293., doi:10.1046/j.1365-2958.2001.02354.x.
Nguyen, L., Paulsen, I. T., Tchieu, J., Hueck, C. J. and Saier, M. H., Jr., 2000. Phylogenetic analyses of the constituents of Type III protein secretion systems. J Mol Microbiol Biotechnol. 2 (2), 125-144.
The fact that known nonflagellar type III secretion systems are restricted to proteobacteria, and that these systems are mostly virulence systems specializing on eukaryotes (which are probably far younger than flagella), lead Macnab (1999) as well as others (He, 1998; Kim, 2001; Plano et al., 2001) to conclude that the flagellar pathway is probably the older one, and that type III virulence systems are derived from flagella. Although some apparently avirulent type III secretion systems have been discovered (e.g., in the legume symbiote Rhizobium; see Marie et al., 2001), and the phylogenetic distribution of type III secretion systems has been widened somewhat by their discovery in Chlamydiales (Kim, 2001), these data still support the conclusion that type III virulence systems are derived eukaryote-interaction systems, rather than phylogenetically basal homologs. Phylogenetic analysis of type III secretion systems seemed to confirm the case (Nguyen et al., 2000).
I bolded the sentence which reiterates what I said earlier: type III secretory systems extend well beyond gram-negative bacteria. They extend beyond the wider class of proteobacteria, as their presence in Chlamydia shows. In fact, every major clade of bacteria with members displaying flagella also has members displaying the TTSS.
Other bacteria, such as the archaea, have flagella, but they are homologous to type IV secretory systems, not type III.
The article does correctly note that TTSS-equipted bacteria can infect eukaryotes
in general, not just plants and animals. Your earlier articles did not note this fact. This is quite important to the issue of which system came first because eukaryotes are considerably more ancient than metazoans and plants.
Also, the phylogenetic analysis in the article I provided above is from 2003 (Gophna) and is considerably more extensive: 20 TTSS and 25 flagellar gene sets are compared for the four most homologous genes. The finding was that TTSS is not a branch on the flagellum phylogenetic tree nor vice versa: both systems diverged from a common ancestor.
Nguyen's conclusion has been challenged by Gophna (2003), when he demonstrated with the gene trees of Flha, FliI, FliP, and FliO that the type III virulence system do not nest within flagellar systems. This supports the view that the two systems diverged from a common ancestor, which could plausibly have been a type III export system functioning in a nonflagellar, nonpathogenic context. However, Gophna et al. (2003) are not able to exclude the possibility that virulence systems evolve more rapidly, or that the frequent lateral transfer of type III virulence system genes (Nguyen et al., 2000; Gophna et al., 2003) might have increased the rate of sequence divergence.
Sorry, I should have read ahead and seen that you have referenced Goghna's findings on the phylogenetic morphology.
As long as known nonflagellar type III secretion systems are phylogenetically restricted and only function as specialized systems for eukaryote penetration, the suspicion will remain that they are derived from flagella. This view is strengthened by the fact that type III virulence systems have homologs of proteins like FliG, which only have an obvious function in the flagellar motor and may be essentially vestigial in type III virulence systems.
Yes, one can make the argument that flagella could have been present before eukaryotes and therefore before TTSS. On the other hand, TTSS are the simpler system, which would favor their evolving first. Most plausible to me, both evolved from a common ancestor system which either has not yet been identified or has become extinct.
It is useful to examine the Type IV secretory system (TFSS) for analogies with the Type III. The TFSS is used by bacteria to invade eukaryotes, just as with Type III. TFSS are built from a baseplate and a hollow needle, all made of protein subunits. Again, this is analogous to TTSS. So, there are strong functional and structural correlations between TTSS and TFSS.
The Type IV secretory system contains proteins homologous to the archaea flagellum. The TFSS is present in many eubacteria pathogens. Like the TTSS, the TFSS is used by bacteria to invade a host eukaryote cell.
In one very interesting example, the TFSS is used by the typhus-causing bacteria Rickettsia to invade and parasitize eucharyotes. One strain of Rickettsia, Rickettsia prowazeki, can invade single celled protists as well as metazoans. In fact, the genome of this bacteria is the closest match to the mitochondria genome found in virtually all eukaryotes!
So, mitochondria are very likely the result of a rickettsia TFSS invasion of the ancestors to eukaryotes, followed by the establishment of an symbiotic relationship between host and parasite. This pushes back the age of TFSS systems to the dawn of eukayotes themselves, roughly 2 billion years ago.
As mentioned above, the TFSS is related to the flagellum of archaea bacteria. The TFSS is also related to the bacterial conjugative pilus used in "bacterial sex".
The conjugative pilus is used to transmit loops of DNA called
plasmids from one bacteria to another, even between different species. The conjugative pilus is a hollow tube, just like the flagellum and TFSS. The genes for the pilus are also carried on a plasmid, called the F-plasmid. A bacterium with an F-plasmid can build a pilus tube, attach the tube to a second bacterium, and transmit a copy of the F-plasmid to the second bacterium.
Sometimes other plasmids besides the F-plasmid get transmitted when the conjugative pilus is in operation. This is how many disease genes get transmitted between bacteria, on so-called "pathogenicity island" plasmids. In fact plasmids containing the genes for both TFSS and TTSS have been found.
So here we have three related systems: the TFSS, the archaea flagellum, and the conjugative sex pilus (F-plasmid). All three are hollow tubes. All three share homologous proteins. Did one system come first, or did they co-evolve by borrowing parts from one another?
The F-plasmid pilus is the simplest of the three systems, suggesting it may be the earliest. Also, the F-plasmid, with it's ability to spread genes between many species of bacteria, would help increase the speed of evolution of the other two related systems.
This raises an interesting question concerning the TTSS and eubacteria flagellum, which are also related tube systems like the TFSS, F-plasmid, and archaea flagellum. Was there once a conjugative pilus related to the TTSS and its homologous flagellum?
It worthy of mentioning that I am researching this very subject at the moment with my professor here at Winthrop University (Julian Smith), because I may get the chance as an undergraduate research student to look at this very complex information rich structure.
I primarily fund research in gene regulation systems, so the complex assembly sequences of flagellum, secretory systems, and conjugative pili are of interest to me.
Behe argues that natural selection and random mutation cannot produce the irreducibly complex bacterial flagellar motor with its ca. forty separate protein parts, since the motor confers no functional advantage on the cell unless all the parts are present. Natural selection can preserve the motor once it has been assembled, but it cannot detect anything to preserve until the motor has been assembled and performs a function. If there is no function, there is nothing to select. Given that the flagellum requires approximately around 50 genes to function, how did these arise?
The flagellum proton motor is not unique to flagellum. In fact a similar cross-membrane proton drive is used to generate ATP in mitochondria and related bacteria.
Not only does this flagellum share many base proteins with the TTSS, the needle complex of the TTSS has the same helical structure as the flagellum basal hook structure. Furthermore, the same signalling system is used to activate both the TTSS and the flagellum. In TTSS, export of infection proteins is activated. In flagellum, export of flagellum proteins (FlgA, etc) is activated.
Comparing the flagellum and TTSS.
So, it is the functional gap between these two similar systems that evolution must bridge. This is much more plausible than building an entire flagellum from scratch, as Behe insists is the only way possible.
Connecting the two systems further, some flagellum can even export TTSS infection proteins! Functional flagellum are needed for some bacteria pathogens to invade their hosts, so they are in fact acting as TTSS systems.
By the way, what proteins are you including in your count of fifty?
Some argue that natural selection could have "co-opted" the functional parts from the TTSS and earlier simple systems to produce the flagellar motor. The TTSS contains eight-ten proteins that are also found in the forty protein bacterial flagellar motor.
Don't forget that the gene regulation and chaperone systems of TTSS and flagellum are highly similar as well. The genes for these are included in the gene-count you gave above.
Co-option of genes for unrelated fuctions is well known. There are highly homologous protein modules which are used in dozens of different applications. Think of the protease regulators, g-proteins, membrane-channel proteins, etc.
However, the TTSS generate more complications than solutions to this question. The problem occurs when there are multiple TTSSs, because they cause interference. If not segregated one or both systems are lost. Additionally, the other thirty proteins in the flagellar motor (that are not present in the TTSS) are unique to the motor and are not found in any other living system. From whence, then, were these protein parts co-opted?
Some inaccuracies here. There are bacteria with multiple TTSS and flagellum active at the same time, so where is the interference problem of which you speak? And what thirty other proteins do you mean? The last count I saw showed a total of 32-33 proteins in flagellum, not 30 in addition to the ones homologous with TTSS.
Also, Minnich argues that, "even if all the protein parts were somehow available to make a flagellar motor during the evolution of life, the parts would need to be assembled in the correct temporal sequence similar to the way an automobile is assembled in factory."
The construction sequence regulation is already present in the TTSS. Both systems are regulated in a highly homologous way. In fact, the initial structure of the flagellum looks just like a TTSS.
Yet, to choreograph the assembly of the parts of the flagellar motor, present-day bacteria need an elaborate system of genetic instructions as well as many other protein machines to time the expression of those assembly instructions. Arguably, this system is itself irreducibly complex. In any case, the co-option argument tacitly presupposes the need for the very thing it seeks to explain
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Topic: Irreducible Complexity: Behe's Argument (Read 8559 times)