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Author
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Topic: Back to the Topo II - where does it end?
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David L. Rice III
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Member # 648
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posted 25. April 2003 11:02
Hello again - A realization just hit me as I sit here in my chair. I put up a previous post on the Topo II enzyme a little while back. After reading through the comments that were made to that string I began seeing something very interesting emerge. The first thing that I noticed in the postings was that none of the responses in defence of Topo II's evolvability were seeking to satisfy the requirements of the principal of continuity (a la Paul Nelson). I urged folks to NOT FORGET ABOUT THE ORGANISM. It must be capable of at minimum two things. 1) Viability and 2)Reproduction throughout the postulated evolutionary transition. But that was not what really was at stake for the postulated transition. What was at stake for the postulated transition was the ability to assess an existing system and see if other systems may or may not be in existence that are simpler. What's the problem? The problem is that the simpler system is not judjed on its ability to satisfy the prinicipal of continuity - It's judged on it's ability to satisfy the principal of simplicity. So in other words the message that I was getting was that continuity is not what ultimately decides the validity of a postulated transistion it was in the ability to postulate a simpler system (that could have given rise to the Topo II in this case). But here's the kicker - How do we know that the proposed simpler system was capable of living and reproducing? Any takers??
[ 25. April 2003, 11:17: Message edited by: Moderator ]
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yersinia
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posted 25. April 2003 14:38
quote:
But here's the kicker - How do we know that the proposed simpler system was capable of living and reproducing? Any takers??
Um...when it exists in extant organisms? Sometimes, but not always, this criterion can be met (when it is, the issue is settled).
Unfortunately, most things that have ever lived are extinct, so for things like pre-last common ancestor evolution, which is where the origin of Topoisomerase II occurred, we are stuck with reasoning out what would have been viable and what wouldn't, aided by whatever ancillary data we can gather from modern organisms and lab research. This is precisely what Cavalier-Smith was doing in the quotes I quoted in the other thread. In essence he pointed out that:
1) You don't need topoisomerase if the DNA is in a short, non-circular strand, as there will be no twisting strain to remove.
2) The evolutionary distance between a non-topoisomerase and topoisomerase is quite short, as TCS notes that a topoisomerase was produced from a single amino acid change.
I would imagine that the first topoisomerases actually evolved as non-circular DNA strands gradually grew longer (a sufficiently long strand might still have twisting issues; someone should look at the extant bacteria with linear rather than circular chromosomes), and that the circular chromosome came after it was made possible by the pre-existing topoisomerases. This is a helpful-part-becomes-a-required-part-later-on explanation.
In the context of the above, the ball is now in the IDists' court to show "we know that the proposed simpler system was [not] capable of living and reproducing".
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Nel
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Member # 614
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posted 30. April 2003 20:42
Nic,
I have some questions before I fully comment on this thread. Can you show me an organism with a short, linear DNA strand that does not require the topoisomerase? Also, you may have misread your reference when it discusses the "evolutionary distance" between nuclease and topoisermerase. TCS does not note that a topoisomerase was produced from a single amino acid change. What the paper notes is that NaeI endonuclease is changed to a "stand alone" topoisomerase/recombinase by a single amino acid change. In fact what they are suggesting is that they evolved from a quite a few common ancestor or a more complex ancestor (which might be consistent with IC, but we can get into all that):
quote:
Here we show that Topo IA and Topo II share a structurally conserved domain involved in DNA strand breakage and rejoining not only with one another, but also with the DnaG-type primases, a family of ATP-dependent nucleases and a family of DNA repair proteins. These observations suggest a previously unsuspected, deep mechanistic analogy between such superficially different processes as primer formation, DNA breakage and rejoining by topoisomerase and DNA cleavage by certain nucleases. We hypothesize that at a very early stage of evolution, topoisomerases and primases could have evolved from a single ancestral enzyme that might have had multiple functions in replication and repair.
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David L. Rice III
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posted 01. May 2003 12:02
Unfortunately, most things that have ever lived are extinct, so for things like pre-last common ancestor evolution, which is where the origin of Topoisomerase II occurred, we are stuck with reasoning out what would have been viable and what wouldn't, aided by whatever ancillary data we can gather from modern organisms and lab research. This is precisely what Cavalier-Smith was doing in the quotes I quoted in the other thread. In essence he pointed out that:
1) You don't need topoisomerase if the DNA is in a short, non-circular strand, as there will be no twisting strain to remove.
2) The evolutionary distance between a non-topoisomerase and topoisomerase is quite short, as TCS notes that a topoisomerase was produced from a single amino acid change.
I would imagine that the first topoisomerases actually evolved as non-circular DNA strands gradually grew longer (a sufficiently long strand might still have twisting issues; someone should look at the extant bacteria with linear rather than circular chromosomes), and that the circular chromosome came after it was made possible by the pre-existing topoisomerases. This is a helpful-part-becomes-a-required-part-later-on explanation.
In the context of the above, the ball is now in the IDists' court to show "we know that the proposed simpler system was [not] capable of living and reproducing".
To the above response: The issue has not been settled. The statement "if the DNA is in a short, non-circular strand" places the burden of proof on the individual to provide a case where such DNA actually existed. From everything I know about prokaryotes and eukaryotes there is no short DNA like that. It seems to me that long DNA (long chromosomes) are a requirement for viability and reproduction and that short DNA chromosomes are not (simply because there is no evidence that they existed in living organisms). The question still remains "How do we know that that these postulated short chromosomes actually existed rather than assuming that they did exist?" The first step in the hypothesis has no evidence in it's favor.
This goes back to my original point that the principal of continuity is not being applied as it should and that the test should reflect that. Has the principal of continuity been violated? And more importantly CAN the principle of continuity be violated?
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yersinia
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posted 01. May 2003 13:52
Unfortunately I don't have time at the moment to get into a whole debate about standards of evidence, on whom the burden of proof falls, and what are legitimate inferences about plausibility when the organisms we are hypothesizing are extinct (which is quite literally a requirement of the definition of pre-Last Common Ancestor, which is what we're talking about). The original argument was that topoisomerases were required, and I showed that they are required only if the unwinding is required, which it would not be with short linear chromosomes (which just happens to be the favored original state of DNA in OOL scenarios for various other independent reasons, see Cavalier-Smith for details; another place with a good discussion of the origin of chromosomes and circular chromosomes is Szathmary & Maynard Smith's Major Transitions in Evolution, a book consistently ignored by IDists).
FWIW, though, many viruses, bacteria, and plasmids encode their genes in linear chromosomes of widely varying lengths. E.g. Borrelia burgdorferi, aka Lyme disease,
quote:
has a genome composed of a linear chromosome that is approximately 1 Mb and multiple linear and circular plasmids. The telomeres of the linear chromosome and linear plasmids consist of covalently closed singlestranded hairpin loops and short inverted terminal repeats (Barbour and Garon 1987; Hinnebusch and Barbour 1991; Casjens et al. 1997b). The complete nucleotide sequence of the linear chromosome and of 21 plasmids from the B. burgdorferi–type strain B31 has been determined (Fraser et al. 1997; Casjens et al. 2000). Its 12 linear plasmids and nine circular plasmids constitute >40% of the genetic material of the cell, and it has been proposed that Borrelia plasmids are minichromosomes (Barbour 1993).
(source
[ 01. May 2003, 15:50: Message edited by: yersinia ]
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Nel
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posted 01. May 2003 14:58
Nic,
The B. burgdorferi example worsens your case, since they still require the topoisomerase:
quote:
B. burgdorferi has one type I topoisomerase (topA) and two type II topoisomerases (gyrase and topoisomerase IV) for DNA topology management and chromosome segregation, despite its linear chromosomal structure. This suggests that topoisomerase IV may be required for more than the separation of circular DNAs during segregation.
Nature 390, 580 - 586 (1997)
In fact, topoisomerases may be indispensible for replication. Viruses and plasmids seem to post-date bacteria.
[ 01. May 2003, 15:04: Message edited by: Nelson_Alonso ]
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yersinia
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posted 01. May 2003 15:48
Ah, but do small linear plasmids, which contain a substantial chunk of this bug's genome, require topoisomerase?
As you recall, I hypothesized that small linear strands would not need topoisomerase, but that larger and larger linear chromosomes would have a greater and greater need for it. Once it evolved then circular chromosomes would be possible, and then topoisomerase would be essential.
As for the relative age of viruses, plasmids, and bacteria, it's not relevant since we're arguing about possibility here, but I'd like to see you cite some evidence to back up your assertion. Both viruses and plasmids go both to and from genomes with regularity, I doubt there is any way to do any overall phylogeny of it. However, the origin of selfish genetic elements is easiest to understand if they have been coevolving with life ever since the precellular stage.
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yersinia
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posted 01. May 2003 15:58
Nelson, regarding your comments about the TCS quote, what he says is pretty clear:
quote:
The distinction between a nuclease and a DNA topoisomerase can be evolutionarily slight. Thus the restriction endonuclease NaeI can be converted into a topoisomerase II (unrelated to the natural ones) by a single amino acid substitution (Huai et al, 2000). The fact that early eukaryotes evolved a DNA topoisomerase I entirely unrelated in sequence or 3D structure (hence called Ib) to topoisomerases Ia and II also indicates that it is mechanistically relatively easy to evolve a topoisomerase from other enzymes: topoisomerase Ib is related to the site-specific integrase (sometimes called recombinase) of phage (Aravind et al, 1998).
So he and Huai make 2 points: (1) a topoisomerase was produced by a single aa substitution, which indicates that such things are not that difficult, and (2) in addition to being remarkable in itself, this is a bit of evidence for ancient kinship of various enzymes. You seemed to be obscuring #1 by focusing on #2.
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Nel
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posted 01. May 2003 17:10
Nic,
If you can show me a small linear plasmid that does not require a topoisomerase then we can discuss that, however, as far as viruses and plasmids are concerned, I think that they are largely irrelevant as they seem to post-date bacteria. Note this is not just about possibility. Viruses require extra machinery to replicate and thus it is quite unlikely that they represent a "stand alone" simpler ancestral version of the machinery, although the point may be moot anyway since I've never seen a virus or plasmid that does not require topoisomerase, but I wouldn't be surprised.
Regarding the Huai paper, again, the data does not show that a topoisomerase can be "produced" by 1 amino acid change, the data shows that an endonuclease can act as a toposomerase if you change 1 amino acid. This bears no relevance on the ability of natural selection nor does it bear any relevance on the requirement of topoisomerase, however, it does point to the possibility of a more complex ancestor.
[ 01. May 2003, 17:13: Message edited by: Nelson_Alonso ]
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Rex Kerr
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Member # 632
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posted 01. May 2003 21:05
Small linear chromosomes are vulnerable to degradation at the ends. Why would we expect any such organisms to be alive any more, faced with stiff competition from their circularized, more robust counterparts? Furthermore, one might expect topoisomerase to speed DNA replication as it would help avoid tangling of the linear strand.
Anyway, if topoisomerase is so useful, is it reasonable to expect any organisms to not have it, at this point?
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Pim van Meurs
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Member # 541
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posted 02. May 2003 00:21
Nelson seems to be missing the point here. First of all the examples given by Nic are very relevant to the question of mutation and natural selection being able to lead to a topoisomerase. The example showed how a single mutation to an existing gene was sufficient. Secondly in order to address the issue of likelihood one seems to need to understand the likelihood of an evolutionary pathway, which needs to include the scenario of short linear chromosomes. To require that examples are given of such chromosomes in presently living creatures misses the point as Rex points out.
The question is: Can Nelson assign probabilities to the pathway proposed? Lacking such probabilities, it seems too early to accept topoisomerase as IC.
Which reminds me to respond to Micah's request about criticisms of CSI/IC/design inference.
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Nel
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posted 03. May 2003 12:24
Rex,
The problem that no organism exists with small linear chromosomes may indicate a few of things:
1. They existed at one point but went extinct due to competition.
2. They never existed because such a simpler version is non-viable and the the first organisms were designed with the more complex version.
3. The simpler version may or may not be viable, but RM&NS is incapable of building any version, we only see the complex version because that is what the organism began with (it was designed with the requirement of topoisomerase).
(2) and (3) are consistent with ID. I'm leaning towards (2) since all organisms have at least one topo IA and one topo II. For an organism to at least be viable, they might need a type II, and thus, this thread (I'm guessing). I consider this hypothesis stronger since it carries with it no need to "imagine" a simpler organism with a short chromosome that doesn't require any topoisomerase, I can only imagine what I can test scientifically, and what the evidence shows is that topo II is essential for viability, although the issue of viability may be a seperate one from whether natural selection and random mutation can build the IC system in the first place. The issue of viability may be a question of minimal function of the irreducibly complex system.
[ 03. May 2003, 12:59: Message edited by: Nelson_Alonso ]
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Nel
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posted 03. May 2003 12:48
Pim,
The example that Nic shows is about a group of researchers that mutated Leu43 to Lys of NaeI and showed the mutant acts as a topo I. The crystal structures showed that NaeI contains an endonuclease domain at the N-terminus and a topoisomerase at the C-terminus (from the Huai paper). This is not production of a topo I from a single mutation, although, it is not clear where the topoisomerase activity arrives from, it could be in the N or C-terminus or both could accomplish the topoisomerase activity. For sure, the N-terminal domain is responsible for the endonuclease activity.
Now if the likelihood of an evolutionary scenario depends crucially on short linear chromosomes, then asking for an organism with short linear chromosomes seems to be exactly on point. The burden of proof here is no longer on the IDer, since the IDer can show that topoisomerase is IC and essential for replication. Although burden of proof seems moot here, we both have different ways of looking at this data and thats fine. But I see no reason to accept the Darwinian side just because an organism could possibly get by with a small linear chrosome without the need for topoisomerase doesn't mean that one existed and that present organisms arose from those.
Whether an organism existed did not need topo because it had a small chrosome seems to me to be irrelevant to whether the topo II is IC. I don't need flagella to move, heck I don't even need it to reproduce no matter what niche I'm in, and I still think the bacterial flagellum is irreducibly complex.
Note also, for a pathway to be given a probability, a pathway needs to be given in the first place. No pathway is given here, simply an imagined organism. It's as David Rice says in his OP:
quote:
The problem is that the simpler system is not judged on its ability to satisfy the prinicipal of continuity - It's judged on it's ability to satisfy the principal of simplicity.
It is the job of the Darwinist and the IDer together, to come up with some calculations and experimental data attempting to show which hypothesis carries the most weight. For now, it seems that the IDer's hypothesis is based on testable data. Remove topo and you don't have replication, and it usually results in death.
[ 03. May 2003, 13:04: Message edited by: Nelson_Alonso ]
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Pim van Meurs
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posted 03. May 2003 14:51
Nelson: The example that Nic shows is about a group of researchers that mutated Leu43 to Lys of NaeI and showed the mutant acts as a topo I.
Indeed, thus showing how a single mutation can 'create' topoisomerase. From an evolutionary perspective, the finding that a simple mutation in a pre-existing gene can lead to new activity is quite relevant.
Your question about living creatures with linear chromosomes is a red herring as shown by Rex.
Nelson: It is the job of the Darwinist and the IDer together, to come up with some calculations and experimental data attempting to show which hypothesis carries the most weight.
Exactly but so far ID seems to fail to propose any hypothesis of its own. In fact Intelligent Design seems to be depending on elimination rather than on proposing their own hypotheses.
If ID's hypothesis is merely that TOPO removal stops replication then I would like to hear the relevance of this obvious finding to ID. Perhaps Nelson could explain to us why this should be considered to be an ID hypothesis rather than something expected from present scientific thought?
What is the ID hypothesis? Surely it is more than "TOPO removal stops replication"? Nothing intelligent or design about that.
Nelson seems to have pointed out that it may be time for ID to propose its own hypotheses that go beyond "x could not have happened" and propose something relevant to ID rather than try to falsify an endless series of hypotheses without proposing its own.
IMHO of course...
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Nel
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posted 03. May 2003 15:29
Pim,
Again, the change did not "create" a topo I, again, what the example showed was that NaeI contains an endonuclease domain at the N-terminus and a topoisomerase at the C-terminus. Your post contains nothing but assertions that I already addressed.
As far as proposing hypothesis, ID, in my opinion, might propose that living organisms show a state that might have been a more complex ancestral state, or with a minimal requirement of topo II and topo I. This certainly runs contradictory to a hypothesis where an organism can replicate without topo activity.
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