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Topic: The Other Flagellum
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Moderator
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posted 04. August 2003 12:39
Pim, Mike,
Analysis of "metaphysical needs" is off-limits for ISCID. Please refrain from referring to poster's motives, desires, and psychological motivations.
Pim: either put up the evidence for your claim or stop talking. Mike is making a reasonable request, and you're not contributing to clarity of thought or furthering the discussion with this post (above).
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Pim van Meurs
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posted 04. August 2003 13:13
Moderator:
Pim: either put up the evidence for your claim or stop talking. Mike is making a reasonable request, and you're not contributing to clarity of thought or furthering the discussion with this post (above).
It seems that the moderator misunderstands my claim and I apologize for the confusion my claim may have caused. Mike made, without much evidence, the claim that the two gene duplications had to be concurrent. I provided a reasonable or at least plausible scenario that would not require such concurrency. Perhaps the first step would be to ask Mike to provide evidence for his claim, although I would not require him to stop talking if he couldn't. Seems like a reasonable request to me.
So lets further the discussion:
Mike, when you stated that "The kinesin and dynein motors could be explained by gene duplication. Yet here we would seem to require concurrent duplications, as both motors are essential for flagellar assembly."
Could you explain why concurrency is a requirement as opposed to a scenario in which the Kinesin mechanism arose first followed by the dynein mechanism? In other words, is concurrency a requirement or a possibility?
[ 04. August 2003, 13:15: Message edited by: Pim van Meurs ]
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Mike Gene
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posted 04. August 2003 18:14
PvM,
I guess I’m not making myself clear enough, as I already answered your objection:
quote:
They become relevant once we get the faintest hint that the story is more than an ad hoc response. Note that I said “we would seem to require.” That is, there isn’t anything in the data that would lead us to choose the gradual explanation you favor (and is required by the Darwinian perspective). The data show that cells require (at least) two different motors to assemble and maintain the flagellum. You need data that shows where eukaryotes use kinesin to export things out of a cell that in someway, foreshadows flagella. Without this, you don’t even have a just so story.
But let me try again.
You write: Mike made, without much evidence, the claim that the two gene duplications had to be concurrent. I provided a reasonable or at least plausible scenario that would not require such concurrency.
Let’s consider what I wrote:
quote:
The kinesin and dynein motors could be explained by gene duplication. Yet here we would seem to require concurrent duplications, as both motors are essential for flagellar assembly. If you knock out the kenesin-II (also known as fla10), no flagella assemble (the phenotype of called “bald”), as the machine for moving the material into the flagellum is missing. If you knock out the transport dynein, stumpy, non-functional flagella form, as material (including the kinesins) is not trucked out of the flagella and thus accumulate into a disordered tangle.
Note, I did not claim the two gene duplications had to be concurrent. I claimed that we would seem to require concurrent duplications. I already anticipated the type of response you provided and this is why I did not make the strong claim of “had to be.” Consider your “plausible” scenario:
quote:
Lets presume that initially the use of kinesin export was not to build a flagellum but rather to export proteins (toxins?) such as for instance the type III secretion?
I’m sorry, but this doesn’t even qualify as a “scenario.” You raise only a possibility. And as you write on ARN, “Sure, anything is a possibility but where's the beef?” To progress from the realm of mere possibility to the realm of plausibility, you should do as I suggested:
quote:
The next step is to determine if your scenario is grounded in reality. You seemed to recognize this, but unfortunately, appealing to type III systems in bacteria are not relevant. A good place to start is to find an example where eukaryotes use kinesin to export things out of a cell that in someway, foreshadows flagella. Either that, or put a little bit more detail on your story.
Perhaps I can rephrase my original paragraph -
quote:
The kinesin and dynein motors could be explained by gene duplication. But unless there is evidence that these motors arose and functioned independently, we would seem to require concurrent duplications, as both motors are essential for flagellar assembly. If you knock out the kenesin-II (also known as fla10), no flagella assemble (the phenotype of called “bald”), as the machine for moving the material into the flagellum is missing. If you knock out the transport dynein, stumpy, non-functional flagella form, as material (including the kinesins) is not trucked out of the flagella and thus accumulate into a disordered tangle. As I noted, we need two different motors to assemble and maintain flagella.
Is that better?
Anyway, things get even more interesting. Kinesin-II is not a single polypeptide chain. It functions as a heterotrimeric complex consisting of an 85, 90, and 100 kDa subunits. The two smaller proteins are FLA10 and FLA10H, the motor subunits. The largest subunit is CrKAP, a nonmotor subunit. Above, I mentioned the temp sens data using FLA10, demonstrating the importance of this subunit. But essentially the same effect is seen with a temp sens mutant of CrKAP (AFAIK, FLA10H has not been tested this way). This suggests more rounds of concurrent gene duplication just to get the kinesin II motor.
[ 04. August 2003, 18:15: Message edited by: Mike Gene ]
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Mesk
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posted 05. August 2003 00:22
quote:
Mike Gene:
I’m not demanding/expecting that axopodia evolve into the typical 9+2 eukaryotic flagellum. Any form of analogous wiggling motility structure would do.
And again, I'll point out that there is not necessarily any reason to anticipate that there is a strong selective pressure which would favour the gradual development of such a structure. But I'll go into this in more detail below.
quote:
Mesk:
You suggest that the fact that axopodia have not evolved into flagella suggests that co-option cannot readily explain flagellar evolution, but in fact there is a far more straightforward explanation from an evolutionary point of view: for many protozoons, flagellar-like motion is not required and axopodia serve their purposes admirably.
Mike:
Actually, what I am trying to point out regarding axopodia, cooption, and flagella is that the cooption story may be misleading as a function of its vagueness. Here we have a biological example with all the ingredients of the cooption story. Taking the cooption story at face value, we would predict these structures would evolve into more robust motility structures.
Actually, I for one would not immediately predict this, for at least two reasons: (1) we know nothing about whether or not there are any selective pressures which would favour the generation of such a structure (and this is by no means a foregone conclusion); and (2) even if there were, I actually believe that the evolution of structures such as the flagellum is incredibly rare, and would require a number of precursor structures to be fortuitously present in a single lineage. I would predict that where there is selection for greater motility, in the vast majority of cases such motility will evolve using comparatively simple structures.
quote:
Mike:
Now, there are two possible evolutionary explanations. There is the environmental explanation that you propose – flagella failed to evolve because the right type of selective pressure never arose. There is also the biological explanation. Flagella failed to evolve for the same reason mice never evolved an exoskeleton – there are intrinsic developmental/genetic constraints.
I suspect it is a combination of both. In most cases where motility is favoured, simple structures will evolve fairly rapidly to provide that motility and will thus alleviate the force of selection. If those structures happen to be able to combine with other cellular structures, over time, to form more complex structures which are more advantageous then this might occur - but it will be comparatively rare. Complex, integrated structures such as flagella arise via a long and (viewed in hindsight) highly improbable series of evolutionary events.
quote:
Mike:
While the environmental explanation you propose is plausible, it has a couple of things that count against it (in my mind).
First, improved motility would seem to provide a selective advantage across a wide range of environments, given this function would feed into several basic life events – finding mates, catching prey, dispersal, escaping predators. It would be surprising, that over the last millions (billions?) of years, none of the axopodia-containing lineages ever explored these niches given it would be so easy to evolve flagella (as predicted by the cooption story).
I would be staggered to discover that at least some members of the axopodia-containing lineages (particularly the predators) do not possess some means of regulated motility. However, I would also be quite surprised if structures as complex as the flagellum were shown to have evolved independently in a large number of lineages. I fundamentally disagree with your claim that the cooption story somehow makes flagella "easy to evolve" - this is absolutely not the case. The series of cooption events that occurred must have been of extremely low probability, but the end product of this series was so advantageous that the lineage which possessed it went on to persist and diversify.
quote:
Mike:
Secondly, the environmental explanation seems to take us out of the realm of testing. Raphidiophrys don’t have flagella because there was never selective forces working to make one. How do we know this? Because they don’t have flagella? But many diverse eukaryotes have flagella becaue there were selective forces that worked to make it. How do we know this? Because they have flagella? How can we test the environmental explanation?
OK, at this point I have to admit that my knowledge of the phylogenetic distribution of the flagellum is essentially nonexistent. Is there evidence that the flagellum has evolved independently in a number of separate lineages? I would be somewhat surprised if there was.
I see your point about the difficulties of testing for the presence or absence of selection favouring flagellar evolution, and I'll have to have a think about that.
quote:
Mike:
The advantage of the biological explanation is we can test it. Let’s dissect the axopodia and compare/contrast to the flagellum. Are axopodia “dead ends” with regard to flagella evolvability? One way to do some serious damage to the biological explanation is to dissect the flagella of Dimorpha. If they are structurally different from the typical eukaryotic flagellum, such that we can infer they evolved independently, yet also similar to the axopodia, the argument of biological constraint has been handed a serious blow. BTW, this is just more of the type of reseach that ID theorists could do.
Sure, and I'd be interested to see the results.
This post hasn't been as well thought-out as I would have liked, but I have a few things on at the moment which are distracting me. Hopefully I'll get the chance to add more later.
Mesk.
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Mike Gene
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posted 05. August 2003 14:04
Before continuing, I thought I would share another impressive feature of the eukaryotic flagellum. Let’s consider the mechanism behind the motility.
Behe does a nice job explaining the business end, where dynein heads interact with adjacent microtubules to impose a sliding motion that is constrained by the linkers. The basic mechanism is oddly similar to the sliding filament mechanism of muscle contraction using a different filament and a different motor. But what’s the deal with the spokes and central tubules? Here’s a picture that somewhat captures the complexity of the flagellum:
The spokes are represented by the alternating white and yellow structure that look like thumb tacks. The globular heads face the central pair of microtubules. Let’s cut down on the complexity and take a slice of the flagellum:
When I first learned about this structure, it was basically assumed that the central pair and spokes played more of a scaffolding role, imposing form on the structure. This may be partially true, but the form that is imposed is more functional.
Y’see, buried within the sliding microtubule mechanism is a rotary mechanism. It turns out the central pair rotate when the flagellum oscillates. And it turns out that the central pair structure is actually asymmetrical (unlike the picture above). Thus, when the central pair rotate, they specifically interact with one set of spokes, which in turn, specifically interact with one set of dynein motors. Put simply, the central pair acts like a distributor, coordinating the discharge of motor activity along the microtubule. And people thought the bacterial flagellum was cool! ![[Smile]](smile.gif)
I’ll say more in due time. For example, someone’s probably jumping up and down saying, “what about the 9+0 flagella?” Indeed.
P.S. Mesk, I’ll pick up our exchange as soon as I get some time. I have some serious obligations coming up in a few days.
[ 05. August 2003, 14:05: Message edited by: Mike Gene ]
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Mike Gene
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posted 05. August 2003 23:12
Here’s some more on the rotating central pair and the way it influences dynein activity.
These are a couple of figures from the following paper:
Matthew J. Wargo and Elizabeth F. Smith. 2003. Asymmetry of the central apparatus defines the location of active microtubule sliding in Chlamydomonas flagella.PNAS 100:137-142
Fig. 1. (A) Transverse section of flagellar axoneme. The outer and inner dynein arms (ODA, IDA) and radial spokes (RS) are attached to the outer doublet microtubules. The central apparatus is enlarged and offset. Central pair projections are labeled according to Mitchell and Sale. (B) Electron micrograph and accompanying diagram, axoneme transverse section after microtubule sliding. The C1 and C2 microtubules of the central pair are labeled. The arrow defines the orientation of the central pair. The point at which the arrow intersects the circumference of the doublets is indicated by a dot on the accompanying diagram. The position of active microtubule sliding includes the area lightly shaded. The inactive area includes the remainder of the axoneme (dark shading).
Fig. 5. As the central apparatus rotates clockwise, the C1 microtubule contacts specific radial spokes, which in turn relay a regulatory signal to the dynein arms on specific subsets of doublet microtubules. The doublets and associated dynein arms actively engaged in microtubule sliding are indicated by light shading. In each subsequent transverse section (left to right), microtubule sliding is visualized as progressive loss of doublet microtubules from the axoneme.
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This mechanism looks vaguely familiar to me. Although it’s in a completely different, unrelated system. Let’s see. An asymmetric central structure that spins such that a rotating "bump" coordinates the firing of ATP-binding domains that surround it in circular pattern....
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yersinia
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posted 08. August 2003 18:18
A few random comments:
(1) I agree that Behe was relatively clear that what he meant by "the cilium is IC" is that tubulin, dynein and linkers (nexin I guess) were required, rather than the 9+2. However, this kind of subtle distinction is rather easy to miss as neither Behe nor any of his followers has been particularly clear about the definition of IC, what constitutes a "part", what effect cross-taxa variation in a system is supposed to have on the IC definition or the IC argument, and whether ICness is (a) conceptual (stator-motor-paddle) (b) empirical #1 (knockout tests, protein lists), (c) empirical #2 (universally present, protein lists), (d) the system or a subset of it, etc. When the main concept under discussion is complexity that cannot be reduced, it's pretty natural to look at the canonical system, depicted in Behe's book without notation of variations, and see if it can be reduced or not.
Also, Behe's inspiration, Denton (1986), *does* say explicitly that the 9+2 pattern is invariant.
(2) I don't particularly see a need to imagine the simultaneous development of cilium-specific dynein (proximal-moving IIRC) and kinesin (distal-moving IIRC) -- although, since it has come up, such a thing might even be possible by duplication of a chromosomal segment, which is then up-regulated, producing a primitive protrusion from the rest of the cytoskeleton.
My basic point is that kinesin and dynein are actively used in all kinds of cellular transport and cytoskeletal processes. The cilium is basically an extension of the cytoskeleton.
(3) More specifically, it seems that the cilium is an extension of the mitotic apparatus. In single-celled eukaryotes we see much variation from the "standard" mitosis of "higher" eukaryotes. "Pleuromitosis" is the buzzword, there isn't much on the net, but here is an article that discusses it briefly. Some of the differences:
- the spindle is embedded in the nuclear membrane, which does not disappear during mitosis (IIRC)
- on the outer side of the nuclear membrane, microtubular bundles extend out to the cellular membrane to attach the splitting nucleus to the correct halves of the splitting cell
- the flagellum is (IIRC) an extension of this extranuclear bundle, and a connection between the cilium base, mitotic apparatus, and nucleus is commonplace in many very different eukaryotes
- this already solves several of Behe's alledged problems for the origin of the cilium, e.g. how a bundle would get perpendicular to the cell membrane.
(4) thus it seems that the source of the pre-cilial protrusion was probably just an extension of the mitotic apparatus, which is regularly sending microtubules and MT bundles in every direction anyhow
(5) possible advantages of non-motile protrusions include: increasing surface area, decreasing sinking rate, increasing probability of prey intercept or surface attachment, raising the cell above the substrate, or defense against other eukaryote predators
(6) probably the key step in the origin of crude motility (or motile feeding appendage) was a mutation in part of a dynein complex (maybe not the actual dynein chains) that made some of the dyneins transporting stuff down the MTs instead get attached to another MT. Thus these dyneins could "walk" a little ways down an MT, but then would get stuck because the rest of the complex would be attached to another MT. This would create wiggling which could help with random dispersal, suspension, stirring the medium to increase diffusion, and/or attaching to prey floating by.
(probably any nonmotile bundle must have linkers already in order to stick together)
Unfortunately, putting together a FAQ like Matt Inlay's immune system FAQ about the cilium is very difficult, because the details of many of the above points are very difficult to research in detail because (1) most of the literature is based on light- and electron- microscopy of the pre-genomic age and is locked up in old obscure paper journals, (2) many of the workers were German, Russian, etc., (3) the names of the critters are constantly changing, (4) the taxonomy is in continual chaos, (5) the whole lot of single-celled eukaryotes is very poorly studied and is almost the definition of obscurity, (6) it's not even clear that we have much more than a beginner's understanding of the details of mitosis, cilial assembly, protozoan diversity, and several other crucial topics.
End of ramble. But IMO discussions of the evolution (or non-evolution) of the cilium aren't really in the ballpark unless they discuss the above points.
[ 09. August 2003, 04:03: Message edited by: yersinia ]
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nosivad
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posted 10. August 2003 07:14
I cannot imagine in my wildest dreams that the eukaryotic flagellum resulted from an incremental evolutionary process. Of course I could claim the same for a host of other universal cellular structures for which intermediates are completely unknown. I agree with Otto Schindewolf who claimed that we might as well stop looking for missing links as they never existed. That seems to be the case not only in the fossil record but also in the domain of molecular biology.
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Nel
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posted 10. August 2003 14:13
I am admittedly still digesting the OP. Something tells me though that Mike has already addressed a lot of Yersinia's post.
And some he has not. Particularly the following.
First, there are plenty of posts here and ARN that show IDers define IC, and then effectively utilize it. Of course there are no precise definition of parts, but thats true of all Biological definitions. This is not to say of course, that people are not working on more precise definitions of IC particularly with regard to the machine concept. This is analogous (pun intended) to the work currently being done on the definition of "homologous".
Nic writes:
quote:
Also, Behe's inspiration, Denton (1986), *does* say explicitly that the 9+2 pattern is invariant.
AFAIK, Denton-1986 mentions the 9+0 pattern on page 108 (don't have the book on me right now so not sure if thats the correct page number).
Nic writes:
quote:
My basic point is that kinesin and dynein are actively used in all kinds of cellular transport and cytoskeletal processes. The cilium is basically an extension of the cytoskeleton.
the spindle is embedded in the nuclear membrane, which does not disappear during mitosis (IIRC)
on the outer side of the nuclear membrane, microtubular bundles extend out to the cellular membrane to attach the splitting nucleus to the correct halves of the splitting cell
Actually, there is no evidence that the spindle is embedded in the nuclear membrane. MTs can be nucleated at SPBs that are not actual components of the nucelar envelope. MTs can also enter through apertures in the nuclear envelope.
Also, trypanosomes show that MTs can be built inside the mitotic nucleus.
nic writes:
quote:
- the flagellum is (IIRC) an extension of this extranuclear bundle, and a connection between the cilium base, mitotic apparatus, and nucleus is commonplace in many very different eukaryotes
Basal bodies in Trypanosome doesn't seem to have any function in mitosis. Also, S. pombe and S. cerevisae have cytoplasmic MTs that interface with spindle pole bodies but they don't assemble a basal body/cilium.
I don't know if Mike would agree with this or not, but it seems that eukaryotic flagella fits a view of frontloading higher organisms. Interestingly, some cystic diseases and left-right symmetry in higher organisms may be linked to mutations in proteins associated with the dynein complex.
[ 22. February 2006, 12:45: Message edited by: Nel ]
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yersinia
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posted 10. August 2003 23:09
Hey Nelson,
FWIW, I wasn't saying that all eukaryotes had such a cilium-spindle-nucleus connection, just some of them. There is alot of diversity among protozoans in the spindle etc., many of which don't fit the patterns in common model organisms. (And its also good to keep in mind that terminology varies -- for centrioles/basal bodies etc. it is wildly inconsistent)
I don't know much about trypanosomes, but according to this page they have some of the weird features I was talking about:
quote:
Ultrastructurally, the flagellum consists of a canonical 9+2 microtubule axoneme and a lattice like structure termed the Paraflagellar Rod (PFR) -- this latter structure is restricted to a set of ancient unicellular eukaryotes including trypanosomes.
Importantly for our studies the trypanosome cell has a useful attribute -- it possesses one flagellum and builds a new flagellum during the cell cycle. Thus, observation of a trypanosome late in the cell cycle reveals one old (the anterior) and one new (the posterior) flagellum.
And, knowing very little about trypanosomes, I'd be willing to bet that the separation of the cilial basal bodies coincides with (or *is*) the separation of the nucleation centers for the mitotic spindle.
The Denton quote is,
quote:
No cilia are known which possess, for example, 3, 5 or 7 filaments or possess the filaments in any other but the typical 9+2 arrangement.
'Tis on page 108. Strangely, he does mention "the absence of the two central filaments in one or two cases, such as in the tail of certain spermatazoa" two sentences previously (strangely because he then says there is no variation from the 9+2 structure).
But 3+0 (and I think 5+0 and 7+0) flagella were well-known even in 1986, discussed here among other places:
Afzelius BA. The flagellar apparatus of marine spermatozoa: evolutionary and functional aspects. Symp Soc Exp Biol. 1982;35:495-519.
PS: BTW, here's an interesting-looking article that popped up from the same issue as the above (Cavalier-Smith's 1982 article is also in there):
quote:
Symp Soc Exp Biol. 1982;35:521-32.
The evolution of the sperm tail.
Baccetti B.
In this paper the evolution of the sperm tail is discussed. The primitive motile apparatus is assumed to be a conventional '9 + 2' axoneme which persists in all aquatic phyla having external fertilisation. Where internal fertilisation has evolved in association with terrestrial life, the sperm tail has a '9 + 9 + 2' pattern: it has acquired new accessory proteins and has become enormously elongated. A subsequent trend is towards diminished motility, owing perhaps to the excessive development of skeletal structures and sophisticated copulatory organs. This is marked by unusual axoneme patterns and a lack of dynein arms. Aflagellate spermatozoa seem to represent a high evolutionary level. Finally, it appears that in the sperm of some groups motility has been regained. However, the axoneme never reappears: motility is produced instead by the spermatid manchette or an actin system.
[ 10. August 2003, 23:26: Message edited by: yersinia ]
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yersinia
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posted 10. August 2003 23:48
Here is the kind of thing I was talking about regarding cilium-mitosis connections.
(Note: the phylogeny of things like Trichomonads is controversial IIRC)
quote:
J Parasitol. 1999 Apr;85(2):203-7.
Flagellar duplication and migration during the Trichomonas vaginalis cell cycle.
Zuo Y, Riley DE, Krieger JN.
Department of Urology, School of Medicine, University of Washington, Seattle 98195, USA.
Trichomonas vaginalis is a flagellated protozoan, a representative of 1 of the earliest known eukaryotic lineages. Trichomonas vaginalis lacks centrioles but possesses basal bodies. We report here the cell cycle-dependent flagellar dynamics of T. vaginalis. By immunofluorescence, we found that T. vaginalis flagella duplicated during S-phase, segregated toward the nuclear poles, and then emanated from the spindle poles at mitosis. This behavior strongly parallels that of centrioles and other spindle pole-associated structures variously termed centrosomes, spindle pole bodies, or microtubule organizing centers. These observations support the hypothesis that flagellar forces may have provided motile forces for spindle pole alignment in an ancestral eukaryote.
Or a related article with a somewhat different story on some of the details:
quote:
J Eukaryot Microbiol. 2000 Sep-Oct;47(5):481-92. Related Articles, Links
Contributions of the axostyle and flagella to closed mitosis in the protists Tritrichomonas foetus and Trichomonas vaginalis.
Ribeiro KC, Monteiro-Leal LH, Benchimol M.
Universidade Estadual do Norte Fluminense, LBCT, Rio de Janeiro, Brazil.
Tritrichomonas foetus and Trichomonas vaginalis are protists that undergo closed mitosis: the nuclear envelope remains intact and the spindle remains extranuclear. Here we show, in disagreement with previous studies, that the axostyle does not disappear during mitosis but rather actively participates in it. We document the main structural modifications of the cell during its cell cycle using video enhanced microscopy and computer animation, bright field light microscopy, confocal laser scanning microscopy, and scanning and transmission electron microscopy. We propose six phases in the trichomonad's cell cycle: an orthodox interphase, a pre-mitotic phase, and four stages during the cell division process. We report that in T. foetus and T. vaginalis: a) all skeletal structures such as the costa, pelta-axostyle system, basal bodies, flagella, and associated filaments of the mastigont system are duplicated in a pre-mitotic phase; b) the axostyle does not disappear during mitosis, otherwise playing a fundamental role in this process; c) axostyles participate in the changes in the cell shape, contortion of the anterior region of the cell, and karyokinesis; d) flagella are not under assembly during mitosis, as previously stated by others, but completely formed before it; and e) cytokinesis is powered in part by cell locomotion.
[ 10. August 2003, 23:53: Message edited by: yersinia ]
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Nel
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posted 11. August 2003 18:59
Nic writes:
quote:
FWIW, I wasn't saying that all eukaryotes had such a cilium-spindle-nucleus connection, just some of them.
It is true that some have structural connections between the basal body and the nucleus, but I can't find much information on their structure/function.
Nic writes:
quote:
And, knowing very little about trypanosomes, I'd be willing to bet that the separation of the cilial basal bodies coincides with (or *is*) the separation of the nucleation centers for the mitotic spindle.
I'd bet the separation of the basal bodies is related to the separation of the nucleation centers with respect to timing, but that both are completely seperate events. When the basal bodies in trypanosomes already fully replicate and become seperate, the nuclease by this time is only starting the metaphase and kinetoplast still hasn't divided.
Nic writes:
quote:
But 3+0 (and I think 5+0 and 7+0) flagella were well-known even in 1986, discussed here among other places:
Afzelius BA. The flagellar apparatus of marine spermatozoa: evolutionary and functional aspects. Symp Soc Exp Biol. 1982;35:495-519.
Hmm, I can't find the abstract to this paper and I don't have access to it. However, it mentions spermatozoa, could it be discussing only the 9 + 0 structure? I'm not being hardheaded just giving Denton the benefit of the doubt. I do this because he references two articles that point to what he is saying:
quote:
Each cilium could be seen to consist primarily of a sheaf of filaments...arranged in what came to be called the 9 +2 pattern
and
quote:
all the phyla...are of the 9 + 2 pattern.
From Peter Satir and Frey-Wyssling respectively.
Since he mentions the variation, I think Denton is emphasizing only that it is the most ubiquitous (which is true) and not necessarily it's invariance. Thats just my devil's advocate interpretation of course. It's kind of hard to reconcile the claim that Denton is arguing the 9 + 2 pattern is invariant when he mentions the 9 + 0 pattern.
I find this statement to be intersting in your references:
quote:
d) flagella are not under assembly during mitosis, as previously stated by others, but completely formed before it
[ 11. August 2003, 20:26: Message edited by: Nelson-Alonso ]
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yersinia
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posted 11. August 2003 20:18
Howdy,
I have that 1982 Azfelius paper somewhere, I know he specifically makes a long list of variants. I vaguely recall quoting it somewhere online (ARN?) eons ago (like 2000), but I can't dig it up at the moment.
Miller references other pre-1986 papers on 3+0 etc. in Finding Darwin's God, so its not just Azfelius.
Denton does bring up the cilium in his typology-type discussion rather than in his proto-IC discussion later in the book (where the bacterial flagellum, orchid complexities, etc. are discussed), but he does make similar claims in the cilium bit.
PS: Yesterday I looked up one of Margulis' recent papers. Argh, she insists on using her special terms for everything. Cilium="undulipodium", etc. Why can't they all just agree on one term??
yersinia
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Mike Gene
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posted 19. August 2003 22:48
Hi Mesk,
Regarding the axopodia and their failure to evolve into flagella-like motility structures, I wrote:
quote:
Actually, what I am trying to point out regarding axopodia, cooption, and flagella is that the cooption story may be misleading as a function of its vagueness. Here we have a biological example with all the ingredients of the cooption story. Taking the cooption story at face value, we would predict these structures would evolve into more robust motility structures.
You disagreed and cited two reasons for not predicting this. First, you noted that “we know nothing about whether or not there are any selective pressures which would favour the generation of such a structure.” Sounds good. But then, this same reasoning extrapolates to the flagellum. That is, we know nothing about whether or not there were any selective pressures that would have favored the evolution of the flagellum. And this poses a very serious problem for anyone who proposes that the flagellum actually evolved by neo-Darwinian processes.
Secondly, you wrote:
quote:
even if there were, I actually believe that the evolution of structures such as the flagellum is incredibly rare, and would require a number of precursor structures to be fortuitously present in a single lineage.
Exactly. I brought this point up in my discussion of IC and how it often forces an appeal to coincidental cooption.
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Yet the most basic problem with CAF is its complete reliance on chance. If we return to the originally proposed pathway above, we are asked to believe that while A, B, C, and D have long been shaped by selection to carry out their original alternative functions, a fortuitous interaction among them all would spontaneously emerge a brand new function. Selection might be invoked to fine-tune and improve this new function, but the bottom line remains in that raw chance is being credited for the creation of a novel function. I explained this elsewhere as follows:
"Co-option is the most commonly cited non-teleological means to generate an IC system. Yet, it is essentially a return to raw coincidence to account for apparent design. The brilliance of Darwin was to minimize the role of chance in apparent design. But once we turn to the co-option explanation, we leave this explanatory appeal behind, as chance reasserts itself into a place of prominence. For it is chance that determines whether the various gene products just happen to come together to form a new functioning system, as selection was previously pruning these gene products in accord with various different functions. If one is to invoke co-option, good supporting evidence is required."
The problem of invoking chance to explain the origin of a new function is quite serious when dealing with IC molecular machines. For these machines to work, their components are usually tightly fitted into a whole through the interactions of their complementary conformations. It would be unlikely for four various proteins, pruned by selection to carry out their original functions, just happened to have sufficient conformational complementarity to assemble into a novel machine with a novel function (which explains why no one has ever observed cooption to spawn a new molecular machine).
Some might argue that the fortuitous interactions are so unlikely that they rule out cooption as a serious explanation. To make this strong point, one would have to carefully catalog the minimal number of components required to undergo the proto-flagellar-relevant interactions and the time frame within which this occurs. Whether we can ever arrive at such resolution is questionable. In the meantime, I can simply point out that a teleologist is not likely to be impressed by appeals to fortuitous interactions to explain the origin of machines.
You said that you disagreed that the cooption story makes flagella easy to evolve. Yet as stated (by PvM and yersinia), and given the almost complete lack of detail, the story does make it appear flagella would be easy to evolve – all you have to do is duplicate a few cytoplasmic gene products and allow for some messy interaction that first makes some type of cellular appendage and then causes it is wiggle ever so slightly. What’s hard about that?
I happen to think flagella would be hard to evolve. Perhaps we should arrive at a consensus on this issue first. Was the flagellum something that was easy to evolve? Or was it difficult to evolve?
Finally, you write:
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The series of cooption events that occurred must have been of extremely low probability, but the end product of this series was so advantageous that the lineage which possessed it went on to persist and diversify.
Yet the interesting questions are how many extremely low probability cooption events were required and how much form did this structure require before is becomes “so advantageous?”
[ 19. August 2003, 22:49: Message edited by: Mike Gene ]
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