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Author Topic:   An ID hypothesis: Front-loaded Evolution
Genomicus
Member (Idle past 2020 days)
Posts: 852
Joined: 02-15-2012


Message 151 of 216 (653784)
02-24-2012 6:06 AM
Reply to: Message 149 by Tangle
02-24-2012 5:59 AM


Re: General Response to Objections
So your dice doesn't always roll a six but only 7 time out of 10? Doesn't your certainty only depend then on how many times the dice is rolled?
Eh, would you mind elaborating?

This message is a reply to:
 Message 149 by Tangle, posted 02-24-2012 5:59 AM Tangle has replied

Replies to this message:
 Message 154 by Tangle, posted 02-24-2012 6:48 AM Genomicus has replied

  
Genomicus
Member (Idle past 2020 days)
Posts: 852
Joined: 02-15-2012


Message 161 of 216 (654062)
02-26-2012 4:40 PM
Reply to: Message 153 by Dr Adequate
02-24-2012 6:17 AM


Re: The Role Of Chance
Speaking as an onlooker trying to figure out what you mean, no, that was not remotely clear. That was obscure. Next time you try to explain your idea to someone, do not call it front-loaded evolution, and explain from the very start that you believe that the evolution of humans (for example) was a matter of mere chance rather than foreordained necessity.
Well, under the FLE hypothesis, the origin of eukaryotes and Metazoa and plants and animals was not a matter of mere chance, but a matter of chance and direction. In other words, the first genomes anticipated the rise of these taxa and this increased the likelihood of their origin. Chance does play a role in FLE, but so too do other factors - the initial states are what channel evolution in specified directions.

This message is a reply to:
 Message 153 by Dr Adequate, posted 02-24-2012 6:17 AM Dr Adequate has replied

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 Message 162 by Granny Magda, posted 02-26-2012 5:35 PM Genomicus has replied
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Genomicus
Member (Idle past 2020 days)
Posts: 852
Joined: 02-15-2012


Message 163 of 216 (654074)
02-26-2012 5:51 PM
Reply to: Message 154 by Tangle
02-24-2012 6:48 AM


Re: General Response to Objections
So a front loaded single roll of the dice may be chance (depending on how heavily loaded it is) but a loaded dice rolled many times is a certainty.
Front-loading would not be a fully loaded dice, where there is absolute certainty. But the dice are loaded in favor of pre-planned outcomes, nonetheless.

This message is a reply to:
 Message 154 by Tangle, posted 02-24-2012 6:48 AM Tangle has replied

Replies to this message:
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Genomicus
Member (Idle past 2020 days)
Posts: 852
Joined: 02-15-2012


Message 164 of 216 (654076)
02-26-2012 5:54 PM
Reply to: Message 155 by Theodoric
02-24-2012 9:08 AM


Re: A summary
Still think he is making an agnostic argument?
I am. When the human species has the capability to design life, that won't make us gods, now will it?

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Genomicus
Member (Idle past 2020 days)
Posts: 852
Joined: 02-15-2012


Message 165 of 216 (654077)
02-26-2012 6:00 PM
Reply to: Message 162 by Granny Magda
02-26-2012 5:35 PM


Re: The Role Of Chance
You appear to be kind of assuming your conclusion here.
Of course, I could hazard an educated guess at why ID/front-loading enthusiasts prefer to think that metazoans are the intended outcome, but you won't like it...
In my first essay, I stated that a premise of the FLE hypothesis is that eukaryotes and Metazoa were front-loaded. This is the premise of the front-loading, and the one from which we can draw testable predictions.
And no, I don't think I'd particularly care for your guess about why the FLE posits this as an initial premise, precisely because you'd guess that it's because of theology. That's simply not true. It's based on the notion that if humans were to seed a planet and front-load, we would almost certainly choose to front-load Metazoa and try to front-load intelligent life forms, would we not?
You've shown homologies between modern prokaryotes and modern eukaryotes, but why should it then follow that the eukaryotes are the ones that the front-loader is interested in? Why can't it be the other way around and the modern prokaryotes are the intended outcome?
Ummm, because prokaryotes were around for about a billion years before eukaryotes came on the scene.
Edited by Genomicus, : No reason given.

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Genomicus
Member (Idle past 2020 days)
Posts: 852
Joined: 02-15-2012


Message 167 of 216 (654079)
02-26-2012 6:24 PM
Reply to: Message 166 by Granny Magda
02-26-2012 6:17 PM


Re: The Role Of Chance
But you're just asserting that. There is no reason to assume it.
It's the premise of the FLE. We can draw testable predictions from it; if confirmed, it would no longer be an assumption.
It may not be true for you personally, but the fact remains that the purpose of the ID movement is not the way you seem to want to paint it. I fear that you have been had. If you are truly interested in unbiased scholarship, then the ID lobby are not your fellow travellers.
I am perfectly aware that the ID movement has a religious agenda. Did I say the ID lobby were my fellow travelers? The problem, though, is that the FLE hypothesis was not proposed by the ID movement. The ID movement guys would far rather prefer intelligent intervention over front-loading, IMHO. Anyways, I'm not a part of the ID movement, I don't share their obvious (and awfully unscientific) religious agenda, so the point is...?
Maybe the front-loader aimed for bacteria, got what he wanted and life has progressed on its own terms since that time, no front-loading required.
Yes, maybe it did. What predictions would you propose for this idea? You can advocate that idea if you wish; personally, based on various factors, I'm not inclined to advocate that idea (e.g., why didn't the front-loader put modern prokaryotes on earth from the start?).
Edited by Genomicus, : No reason given.

This message is a reply to:
 Message 166 by Granny Magda, posted 02-26-2012 6:17 PM Granny Magda has replied

Replies to this message:
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Genomicus
Member (Idle past 2020 days)
Posts: 852
Joined: 02-15-2012


Message 169 of 216 (654081)
02-26-2012 6:36 PM
Reply to: Message 168 by jar
02-26-2012 6:29 PM


Re: The Role Of Chance
Front-loading is an ID hypothesis: intelligent design is involved. Feel free to have your laugh, jar

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 Message 168 by jar, posted 02-26-2012 6:29 PM jar has replied

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Genomicus
Member (Idle past 2020 days)
Posts: 852
Joined: 02-15-2012


Message 174 of 216 (654111)
02-26-2012 10:39 PM
Reply to: Message 158 by Taq
02-24-2012 1:45 PM


Re: General Response to Objections
You are painting the target around the bullet hole. If we had a time machine and were transported back in time to the era where the first life appeared (by whatever mechanism) I really, really doubt you could have predicted which proteins would be deeply conserved through life. Referring back to the Sharpshooter fallacy, you are arguing that the odds of the bullet hitting where it did were increased simply because the bullet hit where it did.
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 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. In this case, the "sharpshooter" is the initial states that constrained subsequent evolution, channeling it in specified directions.
Even more importantly, it may just be happenstance that certain lineages were as successful as they were. I really doubt that if we travelled back in time that you would be able to pick which species would give rise to successful lineages. It is only thorugh hindsight that we know which lineages were the most successful.
Quite right, but I think you might be viewing life through non-telic lenses. 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?
This is a perfect example of the Sharpshooter fallacy. I see no reason why the evolution of animals requires cilia. Yes, modern metazoans do require cilia, but there is no fundamental physical law that requires ambulatory organisms to have cilia. It seems to me that it is entirely happenstance that cilia became an important function in the lineage that gave rise to modern metazoa. Other proteins could have evolved just as much importance, but they didn't.
Again, you're looking at life with non-telic lenses. I think you would agree that the type of animal life that was "chosen" by Nature requires cilia to exist. Thus, if the front-loading designers wished to front-load the type of animal life that live on our planet, they'd have to front-load cilia. If they chose some other animal life forms, they'd probably have to use another type of molecular machine. 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. And this results in the testable prediction I described in my second essay, a prediction which, incidentally, does differ from the non-telelological model.
Let's look at the game Jenga. IMHO, it is a great analogy for biological interdependence. As you move more and more blocks to the top of the stack you will find that certain blocks are absolutely vital to keep the stack upright. However, there is no way you could have predicted ahead of time which blocks those would be. These vital blocks only become vital as time moves forward. No one had to stack the deck to make these blocks vital. It just happens. Evolution is the same way. Certain proteins will start towards the "top of the stack" and are not a vital function. However, as more and more functions become dependent on that function (i.e. more blocks are stacked on top of it) it becomes a vital function. You want to say that this requires foresight and planning, but I see no reason why it does and you have offered no evidence as to why it would.
No, I'm not saying that at all. Evolution can make proteins necessary over deep-time, without the input of foresight and planning. I'm saying that, under the FLE hypothesis, we can glean several testable predictions that do differ from the non-teleological model. I'm really not quite sure where in my essay you got the inspiration to go on what seems to me to be a bit of a tangent, IMHO.
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.
Edited by Genomicus, : No reason given.
Edited by Genomicus, : No reason given.

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Genomicus
Member (Idle past 2020 days)
Posts: 852
Joined: 02-15-2012


Message 175 of 216 (654133)
02-27-2012 3:48 AM
Reply to: Message 171 by Granny Magda
02-26-2012 6:43 PM


Re: The Role Of Chance
But there's absolutely no reason to prefer it over any other hypothesis, right?
That depends on the amount of evidence the other hypotheses have.
So whose idea was it exactly? Where does it originate?
Mike Gene formulated the front-loading hypothesis. Here's how much he's part of the ID movement: http://www.designinference.com/...ents/2002.07.Mike_Gene.htm.
Exactly the same as you cite for eukaryote front-loading; conserved sequences and such. The real problem is that the evidence that one would expect for prokaryote front-loading would not differ one iota from what you predict for eukaryote front-loading.
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.
nor would either differ in the least from what we would expect for normal evolution.
I've already responded to this claim, but here it is again:
It is important for a hypothesis to make testable predictions. Here, I will try to briefly describe how the FLE hypothesis makes predictions that are not made by conventional theory. Before beginning, however, I would like to point out that, in this thread, I do not intend to discuss in depth the issue of whether some of these predictions have, in fact, been confirmed. In this thread, I am primarily interested in discussing if these predictions differ from those generated by conventional theory.
Let me begin with a prediction concerning the origin of molecular machines like cilia. Intra-flagellar transport (IFT) particles are involved in ciliary function in most eukaryotes. These proteins contribute to ciliary function, and any eukaryotes that lack these IFT proteins — such as Plasmodium -- are probably degenerate cilia and do not represent the structure of the last cilia common ancestor.
The point is this: under the non-teleological framework, co-option events are primarily responsible for the origin of this motility organelle and its IFT proteins. Under this model, random co-option events of proteins in the cell resulted in the functional association of different proteins, which would have been preserved by natural selection — and over time, through repeating this step, finally a cilium arose. This is, in essence, the non-teleological hypothesis for the origin of the eukaryotic flagellum.
Given that the existence of Metazoa seems to require the existence of cilia, under the FLE model, cilia were front-loaded. How would cilia be front-loaded? The FLE hypothesis is only at its beginning stages, so one should not expect, at the present moment, a rigorous FLE model for the origin of the cilium. However, I can offer a cursory model for the FLE origin of the cilium. In this model, the first genomes would be designed with components that would later be used by the cilium. 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.
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. For example, H4 histone is one of the most highly conserved proteins in eukaryotes. To me, at least, it seems that it would be much more likely that if H4 histone was duplicated and then co-opted into an entirely novel function a non-adaptive effect would occur than if a fibrinopeptide, for example (which are not at all highly conserved), were co-opted into this novel role. This would be an interesting line of research, but I don’t intend to explore this argument further, because the fact remains: the non-telic hypothesis for the origin of the cilium does not require or predict that the prokaryotic homologs of core IFT proteins be well-conserved in sequence identity, while the FLE hypothesis for the origin of the cilium predicts that the prokaryotic homologs of core IFT proteins would be well-conserved in sequence identity, more so than the average prokaryotic protein. This is a testable prediction: we would need to find a prokaryotic homolog of a core IFT protein, and then conduct pairwise comparisons of that IFT homolog with its prokaryotic orthologs, and check its degree of sequence conservation. There is nothing in the non-telic hypothesis that predicts this hypothetical prokaryotic homolog will be highly conserved in sequence identity, more so than the average prokaryotic protein. You will not find anything like this prediction in the scientific literature. IMHO, this is an exclusively teleological/FLE prediction.
Deep Homology and Front-loading
I argue that the FLH predicts that proteins of major importance in eukaryotes and advanced multi-cellular life forms (e.g., animals, plants) will share deep homology with proteins in prokaryotes. I have discussed this prediction with various critics of the FLH, and the most common objection seems to be that non-teleological evolution also makes this prediction. I disagree, so let me explain.
Life seems to require a minimum of about 250 genes (Koonin, Eugene V. How Many Genes Can Make a Cell: The Minimal-Gene-Set Concept, 2002. Annual Reviews Collection, NCBI) — a proto-cell would not require that many genes. Thus, it would be perfectly acceptable, under the non-teleological model, that the last common ancestor of all life forms had approximately 250 genes, add or take a few. From this small genome, gene duplication events would have occurred, subsequently followed with mutations in the new genes, would lead to a novel protein. Over time, then, and through gene and genome duplication/random mutation, this small genome would evolve into larger genomes. This model is perfectly acceptable with the non-teleological hypothesis, and the non-teleological hypothesis does not predict otherwise. However, this model — where a minimum genome gradually evolves into the biological complexity we see today, through gene duplication, genome duplication, natural selection, and random mutation — is not compatible with the front-loading hypothesis. This is because front-loading requires that the first genomes have genes that would be used by later, more complex life forms. Of the 250 or so genes required by life, none of them could encode proteins that would be used later in multicellular life forms (excluding the proteins that are necessary to all life forms). A front-loading designer couldn’t possibly hope to stack the deck in favor of the appearance of plants and animals, for example, by starting out with a minimal genome.
Look at it this way. With a minimal genome of 250 genes that are involved in metabolism, transcription, translation, replication, etc., evolution could tinker with that genome in any way imaginable, so that you couldn’t really front-load anything at all with a minimal genome. You couldn’t anticipate the rise of animals and plants. Such a genome would not shape subsequent evolution. If the last common ancestor of all life forms had a minimal genome, and if you ran the tape of life back, and then played it again, a totally different course of evolution would result. But if you loaded LUCA with genes that could be used by animals and plants, you could predict that something analogous to animals and plants would arise. If you loaded this genome with hemoglobin, rhodopsin, tubulin, actin, epidermal growth factors, etc. — or homologs of these proteins — something analogous to animal life forms would probably result over deep-time.
Given that you couldn’t really front-load anything with a minimal genome consisting of about 250 genes, under the front-loading hypothesis, it is necessary that LUCA contain unnecessary (but beneficial) genes that would later be exploited by more complex life forms. Non-teleological evolution does not require this. It has no goal, unlike front-loading. It tinkers with what is there — and if a minimal genome was all that was there, it would tinker around, eventually producing endless forms most beautiful as Darwin so famously put it. On the other hand, front-loading is goal-oriented: a minimal genome does not allow one to plan the origin of specific biological objectives.
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.
Non-teleological evolution does not predict this. Non-teleological evolution could explain that observation, but it does not predict this. And this is the important point to understand. There is nothing in non-teleological evolution that requires multi-cellular proteins to share deep homology with unnecessary prokaryotic proteins — but front-loading demands this. There is nothing in non-teleological evolution that requires that LUCA have a genome larger than the minimum genome size — but for front-loading to occur, this must be the case. I conclude, then, that this prediction is made by the front-loading hypothesis, but it is not made by non-teleological evolution, and so front-loading is certainly testable.
That said:
Is that question only just occurring to you? Genomicus, we might as well ask why the "front-loader" didn't just go straight for the blue-footed boobies, day one. Why bother with any of this?
Prokaryotes are far more survivable, and would be far more likely to survive on the early, hostile earth, than eukaryotes. Sure, the front-loading designers could have dropped a population of cows right from the start, but this would fail miserably. You need a whole biosphere for the existence of complex life forms. That's the answer to your question; 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."
Edited by Genomicus, : No reason given.

This message is a reply to:
 Message 171 by Granny Magda, posted 02-26-2012 6:43 PM Granny Magda has replied

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Genomicus
Member (Idle past 2020 days)
Posts: 852
Joined: 02-15-2012


Message 177 of 216 (654136)
02-27-2012 4:17 AM
Reply to: Message 176 by Tangle
02-27-2012 4:13 AM


Re: General Response to Objections
How many times are you allowing your front loaded genome(s) to be rolled? Assuming billions of years, that would be multiple billions of rolls.
I question the relevance of the dice analogy. Take a deck of cards, load it with aces, such that, say, 30% of the deck consists of aces. You'll be far more likely to get a hand of four aces than if you had not tampered with the deck of cards. That's front-loading, in a nutshell.

This message is a reply to:
 Message 176 by Tangle, posted 02-27-2012 4:13 AM Tangle has replied

Replies to this message:
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 Message 189 by Percy, posted 02-28-2012 9:13 AM Genomicus has replied

  
Genomicus
Member (Idle past 2020 days)
Posts: 852
Joined: 02-15-2012


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 replied

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Genomicus
Member (Idle past 2020 days)
Posts: 852
Joined: 02-15-2012


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.

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Genomicus
Member (Idle past 2020 days)
Posts: 852
Joined: 02-15-2012


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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Genomicus
Member (Idle past 2020 days)
Posts: 852
Joined: 02-15-2012


Message 198 of 216 (654363)
02-29-2012 5:35 PM
Reply to: Message 196 by Percy
02-29-2012 8:44 AM


Re: General Response to Objections
You already presented your clue in Message 1, the genetic code - nobody's buying it.
It's debatable.
And you also described your testable predictions - the first wasn't a prediction, the second is already accounted for by evolution.
And I clearly explained exactly why evolution does not make those predictions in my second essay (and incidentally, both are predictions - I explained that in my second essay). The only responses so far are: (a) that I'm using the Sharpshooter fallacy - this is not in any way equivalent to showing that these predictions are also made by conventional theory, and (b) that the prediction regarding the cilium is also made by the modern synthesis. And I will respond to that claim.

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 Message 196 by Percy, posted 02-29-2012 8:44 AM Percy has replied

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 Message 200 by Percy, posted 02-29-2012 10:14 PM Genomicus has seen this message but not replied

  
Genomicus
Member (Idle past 2020 days)
Posts: 852
Joined: 02-15-2012


Message 199 of 216 (654365)
02-29-2012 5:54 PM
Reply to: Message 183 by Trixie
02-27-2012 4:23 PM


Re: General Response to Objections
Hi Trixie,
This will be my follow-up response to your post on your BLASTn searches.
You quoted this statement of mine:
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.
Your response to this comment completely missed the point, unfortunately. In this comment of mine, I was not arguing that we can find traces of sequence/structural homologs of these proteins in prokaryotes. I was merely pointing out that if the first genomes were loaded with these proteins - or their analogs - that the chances of Metazoan-like life forms appearing on the scene are increased.
Also, you often implicitly said that "such-and-such a protein is a serving a function in prokaryotes, so how can you cite that as evidence for the FLE hypothesis?" The fact is that of course they would be serving a function - otherwise the front-loading designers couldn't possibly hope for their basic 3D structure to be preserved over deep-time.
Of course, you will object that evolutionary theory also makes this prediction. But I have responded to that claim already:
I argue that the FLH predicts that proteins of major importance in eukaryotes and advanced multi-cellular life forms (e.g., animals, plants) will share deep homology with proteins in prokaryotes. I have discussed this prediction with various critics of the FLH, and the most common objection seems to be that non-teleological evolution also makes this prediction. I disagree, so let me explain.
Life seems to require a minimum of about 250 genes (Koonin, Eugene V. How Many Genes Can Make a Cell: The Minimal-Gene-Set Concept, 2002. Annual Reviews Collection, NCBI) — a proto-cell would not require that many genes. Thus, it would be perfectly acceptable, under the non-teleological model, that the last common ancestor of all life forms had approximately 250 genes, add or take a few. From this small genome, gene duplication events would have occurred, subsequently followed with mutations in the new genes, would lead to a novel protein. Over time, then, and through gene and genome duplication/random mutation, this small genome would evolve into larger genomes. This model is perfectly acceptable with the non-teleological hypothesis, and the non-teleological hypothesis does not predict otherwise. However, this model — where a minimum genome gradually evolves into the biological complexity we see today, through gene duplication, genome duplication, natural selection, and random mutation — is not compatible with the front-loading hypothesis. This is because front-loading requires that the first genomes have genes that would be used by later, more complex life forms. Of the 250 or so genes required by life, none of them could encode proteins that would be used later in multicellular life forms (excluding the proteins that are necessary to all life forms). A front-loading designer couldn’t possibly hope to stack the deck in favor of the appearance of plants and animals, for example, by starting out with a minimal genome.
Look at it this way. With a minimal genome of 250 genes that are involved in metabolism, transcription, translation, replication, etc., evolution could tinker with that genome in any way imaginable, so that you couldn’t really front-load anything at all with a minimal genome. You couldn’t anticipate the rise of animals and plants. Such a genome would not shape subsequent evolution. If the last common ancestor of all life forms had a minimal genome, and if you ran the tape of life back, and then played it again, a totally different course of evolution would result. But if you loaded LUCA with genes that could be used by animals and plants, you could predict that something analogous to animals and plants would arise. If you loaded this genome with hemoglobin, rhodopsin, tubulin, actin, epidermal growth factors, etc. — or homologs of these proteins — something analogous to animal life forms would probably result over deep-time.
Given that you couldn’t really front-load anything with a minimal genome consisting of about 250 genes, under the front-loading hypothesis, it is necessary that LUCA contain unnecessary (but beneficial) genes that would later be exploited by more complex life forms. Non-teleological evolution does not require this. It has no goal, unlike front-loading. It tinkers with what is there — and if a minimal genome was all that was there, it would tinker around, eventually producing endless forms most beautiful as Darwin so famously put it. On the other hand, front-loading is goal-oriented: a minimal genome does not allow one to plan the origin of specific biological objectives.
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.
Non-teleological evolution does not predict this. Non-teleological evolution could explain that observation, but it does not predict this. And this is the important point to understand. There is nothing in non-teleological evolution that requires multi-cellular proteins to share deep homology with unnecessary prokaryotic proteins — but front-loading demands this. There is nothing in non-teleological evolution that requires that LUCA have a genome larger than the minimum genome size — but for front-loading to occur, this must be the case. I conclude, then, that this prediction is made by the front-loading hypothesis, but it is not made by non-teleological evolution, and so front-loading is certainly testable.
Please respond specifically to the arguments I make in the above paragraph, where I suggest that the FLE hypothesis makes a prediction regarding deep homology that non-teleological evolution does not make.
That said - and Mr Jack has already raised this point - but for any of you who do BLAST searches, understand that protein sequence comparisons allow us to look back over longer periods of time than nucleic acid sequence comparisons - BLASTn searches are not appropriate for deep-time searches, so use BLASTp. Hopefully, that's clearer now
Edited by Genomicus, : No reason given.
Edited by Genomicus, : No reason given.

This message is a reply to:
 Message 183 by Trixie, posted 02-27-2012 4:23 PM Trixie has not replied

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 Message 201 by Taq, posted 03-01-2012 11:47 AM Genomicus has seen this message but not replied

  
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