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Author Topic:   An ID hypothesis: Front-loaded Evolution
Granny Magda
Member (Idle past 4 days)
Posts: 2300
From: UK
Joined: 11-12-2007


(1)
Message 181 of 216 (654158)
02-27-2012 11:13 AM
Reply to: Message 175 by Genomicus
02-27-2012 3:48 AM


Re: The Role Of Chance
That depends on the amount of evidence the other hypotheses have.

Given that your primary competition is the Theory of Evolution, probably the best evidenced theory in all science, that would seem to leave you high and dry.

Mike Gene formulated the front-loading hypothesis.

So your primary source for this is a single pseudonymous blogger? One who admits that he is not a biologist? That's even more perplexing. Also, given the fact that Gene is a major contributor to Telic Thoughts - a blog that is lousy with theism - this does little to counter the charges of stealth theism. This absolutely is an ID hypothesis, whether its originator has differences with the mainstream ID movement or not.

Actually, the predictions would differ. If modern prokaryotes were front-loaded from previous prokaryotes, and eukaryotes were not front-loaded, we would not predict that prokaryotic homologs of protein components of the eukaryotic flagellum would be more highly conserved in sequence identity than the average prokaryotic protein, for example.

I think you're wrong about that. In fact that would be a necessity of your argument.

For starters, we would expect the eukaryote line to be more conserved, because prokaryotes generally mutate faster than prokaryotes, engage in LGT, etc.

If the genes in prokaryotes that you describe as homologous to eukaryote genes are functional, then it is perfectly possible that they have achieved the aim of the front-loader with that function. The continuing presence of the same gene sequences in eukaryotes is simply a result of the front-loading and its conservation mechanism (whatever that might be). You can't assume that the flagellum is the function that was front-loaded; it might just as easily be the homologous function in the prokaryote.

If the proteins in prokaryotes have been preserved by some sequence preservation mechanism, then that mechanism would have to be present in the eukaryote as well, given their common heritage. Either that or you have a situation where the preservation mechanism gets switched off in later lineages and that seems like a huge stretch of the imagination.

I've already responded to this claim, but here it is again:

In other words, homologs of the core, necessary IFT proteins would be designed into the first genomes. They�d be given a function, such that their basic 3D shape is conserved over deep-time. If they were given a function where their 3D shape would be substantially changed over deep-time, then the front-loading designer couldn�t possibly hope that when these proteins associated, their shapes would complement each other correctly such that a cilium could arise.

But if they are performing a vital function in prokaryotes, then the ToE does indeed predict that they would be highly conserved. They have a function after all.

From here, we can develop our FLE prediction. The non-telic hypothesis for the origin of the cilium does not require or predict that the prokaryotic homologs of IFT proteins be well-conserved in sequence identity. In fact, it�s certainly possible that the non-telic hypothesis predicts that most of the prokaryotic homologs of the core IFT proteins will be loosely conserved in sequence identity: a protein that is not under stringent functional constraints will be more likely to be co-opted into a novel role by chance without being deleterious.

But they are performing a function, that was a requirement of the kind of proteins we're talking about.

In your model, these sequences are conserved because they are front-loaded with a function.

In the standard model they are highly conserved simply because they have evolved a function.

You can't point to proteins that you yourself claim to be functional and then say "Look! They're highly conserved! That's not what we would expect under the ToE if they had no function". They have a function. That's enough to explain why they are conserved. We're talking about some of the most ancient adaptations for multicellularity after all. What's more, defective IFT proteins specifically are associated with a raft of hideous maladies, so that would seem to provide ample reason that they should be conserved in either model.

Thus, under the front-loading hypothesis, we would predict that important proteins in eukaryotes, animals, and plants will share deep homology with unnecessary but functional proteins in prokaryotes.

I don't see anything that prevents that from being equally true the other way around.

I don't see what's to prevent such an astonishingly proficient entity from creating a whole ecosystem; clearly they are superlative gene-engineers, why impose arbitrary limits upon them?

The suggestion made by Bluegenes would also make sense. Why not start with a simple eukaryote? That would be pretty robust and it would avoid the need for chancy freak events like the origins of mitochondria or chloroplasts.

Or alternatively, just being patient would seem to be a better bet. The front-loader could have waited for an ecosystem to develop and then inserted his target organism.

but IMHO my argument does not answer my question to you of why the FL designers wouldn't seed the earth with modern prokaryotes in the first place - according to this alternative FL hypothesis you're "advocating."

Well I did mention nylon-eating bacteria. For a bacterium to eat nylon, some kindly metazoan must first come along create nylon. Many modern prokaryotes are every bit as environment-dependent as eukaryotes. If the target organism were nylon-eating bacteria or the latest strain of swine flu, it too would flounder on the early Earth.

This line of reasoning strikes me as all being a bit post hoc to be honest.

Mutate and Survive

Edited by Granny Magda, : No reason given.


This message is a reply to:
 Message 175 by Genomicus, posted 02-27-2012 3:48 AM Genomicus has not yet responded

    
Taq
Member
Posts: 6014
Joined: 03-06-2009
Member Rating: 3.6


(1)
Message 182 of 216 (654183)
02-27-2012 4:15 PM
Reply to: Message 174 by Genomicus
02-26-2012 10:39 PM


Re: General Response to Objections
Perhaps, but I think you'd be willing to agree that loading the first genomes with rhodopsins, globins, actins, kinesins, - or their sequence/structural homologs - that this would increase the chances of Metazoan-like life forms appearing on the scene.

What evidence do you have that a designer put these genes into organisms?

I am not "arguing that the odds of the bullet hitting where it did were increased simply because the bullet hit where it did." I am arguing that the odds of the bullet hitting where it did were increased by the aid of a sharpshooter, who, through the knowledge of the direction of the wind, the velocity of the bullet, etc., had a greater chance of hitting the target.

The problem is that you are assuming that the sharpshooter was aiming where the bullet hit. That is the Sharpshooter Fallacy.

The issue here isn't if I'd be able to predict which lineages would be the most successful; the issue here is, namely, if life was front-loaded to give rise to the major taxa we see today, then what testable predictions would this produce?

You should be able to predict what those major taxa would look like given the genomes of their ancestors. You have already admitted that you would not be able to do this. This is why I keep pointing to the Sharpshooter Fallacy. You are drawing the target around the results. You have something worse than a lack of predictions. You are using post hoc rationalizations.

I think you would agree that the type of animal life that was "chosen" by Nature requires cilia to exist.

But there is nothing in Nature that requires cilia for animal life. You want to count cilia as a target, but you are doing so after the bullet hole has already been made.

But, if FLE has occurred, it is probably our type of animal life that the front-loading designers were aiming for, and so under the FLE hypothesis, cilia was front-loaded.

That is an assumption, not a prediction. You have not shown anywhere that animals with cilia was an intended outcome. You are simply assuming that it is.

And this results in the testable prediction I described in my second essay, a prediction which, incidentally, does differ from the non-telelological model.

The non-teleological model also incorporates the modification of genes through time. There is no difference.

I'm saying that, under the FLE hypothesis, we can glean several testable predictions that do differ from the non-teleological model.

They are not predictions. They are assumptions, and untestable ones at that. How did you determine that the designer meant for rhodopsins to be used in eyes? You just assumed it because it is found in eyes. That is the Sharpshooter Fallacy.


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Trixie
Member (Idle past 1057 days)
Posts: 1011
From: Edinburgh
Joined: 01-03-2004


(1)
Message 183 of 216 (654185)
02-27-2012 4:23 PM
Reply to: Message 174 by Genomicus
02-26-2012 10:39 PM


Re: General Response to Objections
Genomicus writes:

Perhaps, but I think you'd be willing to agree that loading the first genomes with rhodopsins, globins, actins, kinesins, - or their sequence/structural homologs - that this would increase the chances of Metazoan-like life forms appearing on the scene.

The implications of sequence homologues is totally different from structural homologues. If homology is structural only, it suggests that the same solution has been hit on by different organisms independently of each other. If homology is seen in the DNA sequences it suggests relatedness and descent.

Bacterial rhodopsins, according to Wikipedia "While all microbial rhodopsins have significant sequence homology to one another, they have no detectable sequence homology to the G-protein-coupled receptor (GPCR) family to which animal visual rhodopsins belong." Additionally, they serve a purpose in prokaryotes.

Globins are found all over the place, but the important thing about those found in prokaryotes is that they serve a function in prokaryotes.

Actin, according to Wikipedia "is one of the most highly conserved throughout evolution because it interacts with a large number of other proteins, with 80.2% sequence conservation at the gene level between Homo sapiens and Saccharomyces cerevisiae (a species of yeast), and 95% conservation of the primary structure of the protein product." In addition "All non-spherical prokaryotes appear to possess genes such as MreB, which encode homologues of actin; these genes are required for the cell's shape to be maintained." So, again, actins are serving a purpose in prokaryotes.

Kinesins don't seem to have any representation in Prokaryota. Using the rat kinesin Kif18B mRNA sequence (Accession Number NM_001039019.1) I carried out a BLASTn search - that's a search looking for "somewhat" similar sequences - so that the search was as broad as possible and searched in "prokaryotes (taxid:2157)".

Matches covered from 1% down to 0% of the sequence and E values were at lowest 3e-5 (Aeropyrum pernix K1 DNA, complete genome), the next E value was 0.68 (Halorubrum lacusprofundi ATCC 49239 chromosome 1, complete sequence, Metallosphaera sedula DSM 5348, complete genome, Pyrobaculum arsenaticum DSM 13514, complete genome) Coming in with an E value of 2.4 are Vulcanisaeta moutnovskia 768-28, complete genome, Acidilobus saccharovorans 345-15, complete genome and Methanocaldococcus vulcanius M7, complete genome.

Finally the last 11 which I'm not going to bother identifying have E values of 8.3. When I carried out the same search in prokaryotes (taxid:2) I got a total of four hits, all as feeble as the above.

I think this is sufficient to show that kinesins don't have a counterpart in prokaryotes so how on earth can you cite them as evidence for front loading?

The prediction made by front-loading is that we would find something in prokaryotes which has absolutely NO function below the Metazoa, but has a distinct function above that point. So far you haven't been able to provide a single example of this.

I'd like to add that what I did with the BLASTn search is something you should have done before making your claim, just as the sequence analysis I and others did which refuted your claims for PAX6.


This message is a reply to:
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Replies to this message:
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Blue Jay
Member (Idle past 49 days)
Posts: 2843
From: You couldn't pronounce it with your mouthparts
Joined: 02-04-2008


Message 184 of 216 (654186)
02-27-2012 4:33 PM
Reply to: Message 183 by Trixie
02-27-2012 4:23 PM


Re: General Response to Objections
Hi, Trixie.

Trixie writes:

If homology is structural only, it suggests that the same solution has been hit on by different organisms independently of each other.

Can there even be such a thing as a "structural homolog"?


-Bluejay (a.k.a. Mantis, Thylacosmilus)

Darwin loves you.


This message is a reply to:
 Message 183 by Trixie, posted 02-27-2012 4:23 PM Trixie has responded

Replies to this message:
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Trixie
Member (Idle past 1057 days)
Posts: 1011
From: Edinburgh
Joined: 01-03-2004


Message 185 of 216 (654188)
02-27-2012 4:50 PM
Reply to: Message 184 by Blue Jay
02-27-2012 4:33 PM


Re: General Response to Objections
It's a bit of a stretch, but we're talking about similar 3 dimensional structure coupled with similarity of function.
This message is a reply to:
 Message 184 by Blue Jay, posted 02-27-2012 4:33 PM Blue Jay has not yet responded

  
Dr Jack
Member
Posts: 3500
From: Leicester, England
Joined: 07-14-2003


Message 186 of 216 (654189)
02-27-2012 4:54 PM
Reply to: Message 175 by Genomicus
02-27-2012 3:48 AM


Unnecessary but functional
Thus, under the front-loading hypothesis, we would predict that important proteins in eukaryotes, animals, and plants will share deep homology with unnecessary but functional proteins in prokaryotes.

This seems a contradiction in terms; what do you mean by unnecessary but functional? Because I assure there are no known unnecessary but functional genes in prokaryotes (excepting, I suppose, the few molecular parasites known) under the usual meaning of these terms.


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Dr Jack
Member
Posts: 3500
From: Leicester, England
Joined: 07-14-2003


Message 187 of 216 (654190)
02-27-2012 5:05 PM
Reply to: Message 183 by Trixie
02-27-2012 4:23 PM


Re: General Response to Objections
Kinesins don't seem to have any representation in Prokaryota. Using the rat kinesin Kif18B mRNA sequence (Accession Number NM_001039019.1) I carried out a BLASTn search - that's a search looking for "somewhat" similar sequences - so that the search was as broad as possible and searched in "prokaryotes (taxid:2157)".

As I suggested earlier, I believe BLASTp is more appropriate for these searches than BLASTn. BLASTp produces an identical result, however. Nor do our sloppy searches produce results different from those in the wider literature, those interested can read two open access papers on Kinesin evolution here and here.


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 Message 183 by Trixie, posted 02-27-2012 4:23 PM Trixie has not yet responded

  
Dr Jack
Member
Posts: 3500
From: Leicester, England
Joined: 07-14-2003


Message 188 of 216 (654192)
02-27-2012 5:20 PM
Reply to: Message 174 by Genomicus
02-26-2012 10:39 PM


Re: General Response to Objections
Perhaps, but I think you'd be willing to agree that loading the first genomes with rhodopsins, globins, actins, kinesins, - or their sequence/structural homologs - that this would increase the chances of Metazoan-like life forms appearing on the scene.

I wouldn't, no. Metazoa use proteins derived from globins and actins, sure, but other proteins would have served just as well; and the broader set of hurdles to metazoan-life are sufficient to control the chances of such life.

I described two predictions made by the FLE hypothesis, one regarding levels of sequence conservation in prokaryotic homologs of cilia, and the other regarding deep homology and proteins in eukaryotes. These predictions are not made by conventional theory.

I'm afraid I missed the details of that first prediction, I'm assuming the second is this, from your opening post:

quote:
2) The front-loading hypothesis predicts that prokaryotic homologs of important eukaryotic/metazoan proteins will be more highly conserved in sequence identity than the average prokaryotic protein. This prediction makes sense from a rational design perspective because designing these prokaryotic homologs with functions that conserve their sequence identity will ensure that their 3D shapes will not be significantly changed by the blind watchmaker, preventing the appearance of eukaryotes (I realize that this prediction might sound a bit confusing its past midnight where I am so Id be more than willing to elaborate on this).

We discussed this earlier in the thread, but it's perhaps time to pick it up again, in message 47, you said:

Mr Jack writes:

Of course it does. Highly conserved proteins have higher sequence identities than average proteins whilst, conversely, proteins not under selective pressure rapidly diverge. Proteins shared between the three domains must be highly conserved and thus will tend to have higher sequence identities.


I don't see how this would be the case. If a protein has homologs in all domains of life, this does not mean that it is necessary for life per se; it means that it is beneficial. And most proteins are, of course, beneficial. This doesn't constrain their sequence identity above average.

When we're talking about sequence identity, we're talking about levels of conservation across different kinds of organisms, different species, families, phyla, domains - whatever level you're choosing - not just selection within a single group. Of course, most proteins in a given organism will be selected for in that organisms offspring, and have been selected in its ancestor, but high sequence identity between larger groups speaks to something more fundamental - it means that protein has been under substantial selection in all those organisms and all their respective ancestors right back to their joint common ancestor.

It follows, therefore, that a protein found across multiple domains will show higher sequence identity within those domains than average proteins of those domains. Otherwise it would be insufficiently conserved to have made it between domains.

A much better comparison would be to look for proteins conserved with a domain but not between domains (e.g. a protein found in all prokaryotes but in no eukaryotes) and compare the level of sequence identity of that to the sequence identity of proteins shared between domains. But, even then, you're not really comparing like to like.


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Percy
Member
Posts: 15491
From: New Hampshire
Joined: 12-23-2000
Member Rating: 4.3


(5)
Message 189 of 216 (654226)
02-28-2012 9:13 AM
Reply to: Message 177 by Genomicus
02-27-2012 4:17 AM


Re: General Response to Objections
Hi Genomicus,

Much of the objection to your FLE hypothesis seems to be that it's really just ID, and I think the discussion has taken this turn because of one key quality it shares with ID: lack of evidence. You could stop the accusations of "FLE is ID" by producing evidence that requires an FLE interpretation.

But what you're instead doing is the same thing creationists and IDists before you have done: attempting to develop scenarios that are not contradicted by existing evidence while at the same time de-emphasizing the lack of positive evidence.

In essence your FLE hypothesis is another celestial teapot.

--Percy


This message is a reply to:
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Replies to this message:
 Message 190 by Genomicus, posted 02-28-2012 5:08 PM Percy has responded

    
Genomicus
Member
Posts: 781
Joined: 02-15-2012
Member Rating: 4.6


Message 190 of 216 (654273)
02-28-2012 5:08 PM
Reply to: Message 189 by Percy
02-28-2012 9:13 AM


Re: General Response to Objections
I'm cooking up a response to the rest of you guys and gals, but I want to make a quick response to Percy.

Much of the objection to your FLE hypothesis seems to be that it's really just ID...

As is obvious by the title of my O.P., the FLE hypothesis is an ID hypothesis in that intelligent design is involved. Does that mean it's part of the ID movement? Not at all.

...and I think the discussion has taken this turn because of one key quality it shares with ID: lack of evidence. You could stop the accusations of "FLE is ID" by producing evidence that requires an FLE interpretation.

But what you're instead doing is the same thing creationists and IDists before you have done: attempting to develop scenarios that are not contradicted by existing evidence while at the same time de-emphasizing the lack of positive evidence.

In essence your FLE hypothesis is another celestial teapot.

Actually, I have purposefully not gone into detail on the evidence for the FLE hypothesis: remember the point of my discussion? My main objective, in this thread, is to establish the predictions made by the FLE hypothesis. I can hardly go into detail on the evidence for the FLE hypothesis if we can't even agree on what would be considered evidence for the FLE hypothesis. Thus, it is imperative that we first establish what predictions FLE makes that are not made by conventional theory.

Edited by Genomicus, : No reason given.


This message is a reply to:
 Message 189 by Percy, posted 02-28-2012 9:13 AM Percy has responded

Replies to this message:
 Message 192 by Dr Adequate, posted 02-28-2012 8:19 PM Genomicus has acknowledged this reply
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Genomicus
Member
Posts: 781
Joined: 02-15-2012
Member Rating: 4.6


Message 191 of 216 (654276)
02-28-2012 5:31 PM
Reply to: Message 183 by Trixie
02-27-2012 4:23 PM


Re: General Response to Objections
Several points here, Trixie:

The implications of sequence homologues is totally different from structural homologues. If homology is structural only, it suggests that the same solution has been hit on by different organisms independently of each other. If homology is seen in the DNA sequences it suggests relatedness and descent.

You do, I suppose, realize that the phrase "if homology is structural only, it suggests that the same solution has been hit on by different organisms independently of each other" is a contradiction? I really don't mean to be pedantic, but I'd just like to clarify something here. Homology, by definition, means common evolutionary ancestry. So, to say that "if [common evolutionary ancestry] is structural only, it suggests that the same solution has been hit on by different organisms independently of each other" is simply a contradiction. Don't worry about it, though - I've made that mistake, too, here:

Perhaps, but I think you'd be willing to agree that loading the first genomes with rhodopsins, globins, actins, kinesins, - or their sequence/structural homologs - that this would increase the chances of Metazoan-like life forms appearing on the scene.

What I really meant was sequence/structural analogs.

Now that we've clarified our terms, let me respond to your points. You argue that if structural similarity is the only thing we're going by, two proteins may very well not be homologous. However, IMHO this is only true if we're talking about a moderate degree of structural similarity. If we're talking about fairly significant structural similarity, the two structures are probably homologous. And it's not just plain ole' me saying this:

A fundamental observation is that a single function, such as catalysis of a specific enzymatic reaction, is often performed by two or more proteins that have unrelated structures. In 2.2.5, we discuss this phenomenon in some detail and present several specific examples. These observations indicate that the same function does not necessarily require significantly similar structures, which means that, as a rule, there is no basis for convergent evolution of extensive sequence and structural similarity between proteins. This is not to say that unrelated enzymes that catalyze the same reaction bear no structural resemblance whatsoever. Indeed, subtle similarities in the spatial configuration of amino acid residues in the active centers are likely to exist, and these are precisely the kind of similarity that is expected to emerge due to functional convergence. These similarities, however, do not translate into structural and sequence similarity detectable by existing methods for comparison of proteins (at least in the overwhelming majority of cases). By inference, we are justified to conclude that whenever statistically significant sequence or structural similarity between proteins or protein domains is observed, this is an indication of their divergent evolution from a common ancestor or, in other words, evidence of homology. We will revisit the issue of convergence versus divergence when discussing the deepest structural connections between proteins. (Emphasis not added)

From "Sequence - Evolution - Function: Computational Approaches in Comparative Genomics," Koonin EV, Galperin MY.

I'll respond to your other points later. At the moment, suffice it to say that all your arguments completely missed the point of my statement.


This message is a reply to:
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Dr Adequate
Member
Posts: 15474
Joined: 07-20-2006
Member Rating: 3.9


Message 192 of 216 (654279)
02-28-2012 8:19 PM
Reply to: Message 190 by Genomicus
02-28-2012 5:08 PM


Re: General Response to Objections
Actually, I have purposefully not gone into detail on the evidence for the FLE hypothesis: remember the point of my discussion? My main objective, in this thread, is to establish the predictions made by the FLE hypothesis.

Unless you're trying to come up with predictions that you think are false, this would be a distinction without a difference.


This message is a reply to:
 Message 190 by Genomicus, posted 02-28-2012 5:08 PM Genomicus has acknowledged this reply

  
Percy
Member
Posts: 15491
From: New Hampshire
Joined: 12-23-2000
Member Rating: 4.3


Message 193 of 216 (654288)
02-28-2012 9:35 PM
Reply to: Message 190 by Genomicus
02-28-2012 5:08 PM


Re: General Response to Objections
Hi Genomicus,

People who have evidence talk about evidence. People who don't have evidence claim that they first require a lot of prelude.

Threads here usually end around 300 messages (generally not while active and productive discussion is still ongoing). You're 2/3 through, you might want to pick up the pace, though of course there can always be follow-on threads.

--Percy


This message is a reply to:
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Genomicus
Member
Posts: 781
Joined: 02-15-2012
Member Rating: 4.6


Message 194 of 216 (654296)
02-28-2012 11:08 PM
Reply to: Message 193 by Percy
02-28-2012 9:35 PM


Re: General Response to Objections
People who have evidence talk about evidence. People who don't have evidence claim that they first require a lot of prelude.

Again, the objective of my discussion - in this particular thread - is not to present evidence for the FLE hypothesis. Instead, my objective is to: (a) describe the testable predictions made by the FLE hypothesis, (b) describe what the FLE hypothesis is all about, and (c) offer some responses to objections to the FLE hypothesis. In a follow-up thread, I will present the clues in favor of the FLE hypothesis.

Edited by Genomicus, : No reason given.


This message is a reply to:
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Replies to this message:
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Trixie
Member (Idle past 1057 days)
Posts: 1011
From: Edinburgh
Joined: 01-03-2004


Message 195 of 216 (654305)
02-29-2012 3:48 AM
Reply to: Message 194 by Genomicus
02-28-2012 11:08 PM


Re: General Response to Objections
You've already proposed some predictions made by your FLE hypothesis and then provided evidence which you claim fulfills the predictions. So far none have stood up to scrutiny, in fact they seem to be evidence against your FLE.
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