Deep Homology and Front-loading

In a previous thread, I have discussed the concept of front-loaded evolution as a testable teleological hypothesis. This caused a good bit of disagreement, as many of you are quite adamant that FLE doesn’t make any exclusive predictions. Contrary to this, I think FLE does, in fact, make a prediction that the current evolutionary paradigm does not.

Before beginning, let me explain exactly what the front-loading hypothesis is, as some of you have misconceptions about it.

Front-loading is all about designing future states through the present. Here’s how Mike Gene, the guy who first conceived of the idea of front-loading, defines it:

“Front-loading is the investment of a significant amount of information at the initial stage of evolution (the first life forms) whereby this information shapes and constrains subsequent evolution through its dissipation. This is not to say that every aspect of evolution is pre-programmed and determined. It merely means that life was built to evolve with tendencies as a consequence of carefully chosen initial states in combination with the way evolution works.
Front-loading does not allow for a prediction of specific outcomes, at a specific time and place, but does allow that specified outcomes can be made much more likely...” (The Design Matrix, p. 147).

According to the front-loading hypothesis, one of the objectives of front-loading was the rise of eukaryotes and multicellular life forms. And if multicellular life forms were front-loaded, this can serve as a springboard from which we can make several predictions.

So, how would a designer(s) front-load multicellular life forms through unicellular life forms? You’d simply have to load the first genomes with proteins that would later be utilized by the multicellular life forms. For example, histones seem to be universally required by eukaryotes. Thus, loading the first genomes with histones (or their analogs) would make the appearance of eukaryotes more likely (and front-loading is all about “stacking the deck” in favor of the appearance of multicellular life forms). Without histones in the first genomes, the evolution of eukaryotes is left solely to the blind watchmaker’s tinkering. And without specific information to guide and constrain the path of evolution, such that it is “nudged” in the direction of eukaryotes, there’s no guarantee that histones will evolve. Consequently, the likelihood that eukaryotes would evolve drops considerably. A front-loading designer can make the evolution of eukaryotes much more likely by packing the first genomes with eukaryotic proteins (or their analogs), such that evolution will build around these proteins, eventually producing the objective.

From here we can make a prediction: key eukaryotic proteins will share deep homology with functional but unnecessary prokaryotic proteins.

The homologous protein in prokaryotes will be functional because if the designer loads up the genome with proteins that will only find function millions of years later, these proteins will decay into oblivion, eliminating the whole purpose of front-loading. But if these homologous proteins are unnecessary in that they are not required for the basic prokaryotic cell, then we have a successful prediction of front-loading. Non-teleological evolution does not make this prediction.

This is because, under non-telic evolution, the LUCA’s genome could easily have been a minimal genome that only encodes the proteins absolutely necessary for the existence of a prokaryote cell. Non-teleological evolution does not require this; but nor does it require that the LUCA’s genome encodes more than is necessary. We can summarize this state of affairs thusly: non-teleological evolution makes no predictions regarding the gene/protein content of the LUCA, other than the obvious fact that it would have to encode the proteins necessary for its existence. On the other hand, front-loading specifically predicts that the LUCA will contain more proteins than is necessary for prokaryotic existence. If the front-loader only designed the LUCA such that it encoded the bare minimum required for life (about 250 genes or so), there’s no “stacking of the deck” in favor of the evolution of multicellularity. In short, front-loading, by its very definition, requires the loading of the LUCA’s genome with unnecessary (but functional!) proteins – proteins that are required for the rise of eukaryotes and multicellularity.

I will now briefly address the objections that I’ve come across so far:

1. If evolution can explain something happening, it also predicts that it can happen (source: Dr Adequate). The modern evolutionary theory might be able to explain some biological feature, while an ID hypothesis would predict that biological feature. If the prediction is confirmed, this is evidence for that ID hypothesis, regardless of whether non-telic evolution can explain it or not. Science is built upon a track record of successful predictions, not on whether some alternative model can explain the feature under consideration. Consider the following example. Evolution predicts that if the bacterial flagellum evolved, a number of its components will share similarity with proteins that are more ancient than the bacterial flagellum. Can the hypothesis that the flagellum was engineered explain this? Yes. Engineers very often re-use parts in different systems. But the ID hypothesis does not predict that the flagellar components will share similarity with more ancient proteins. This is because engineers can also design from scratch. So, while ID can explain this, it does not predict it. Which means that, when it comes to similarity, evolution is the superior explanation.

2. Why would the LUCA have a minimal set of genes ? Wouldn't it be expected to have more than the absolute minimum ? Given evolution, rather than design (source: PaulK). In my humble opinion, evolutionary theory – that is, the current biological paradigm – doesn’t make a prediction either way regarding the gene content of the LUCA. Under evolutionary theory, LUCA would not be expected to have more genes than necessary any more than it would be expected to have only the bare minimum. This is because, under non-teleological evolution, the LUCA could have been simply a self-replicating molecule, encoding only a few genes. This population of self-replicating molecules would then diverge, producing different domains of life. But under front-loading, the LUCA would have to have more genes than necessary because there’s no reason to suppose that a minimum gene set could specifically evolve into multicellular life forms, given that there are many directions in which this minimum gene set could evolve. Only a few of the paths consist of multicellular life forms of the type we see today, while the vast majority of possible evolutionary trajectories does not consist of the multicellular life forms we see today. So, to front-load these life forms, you’d need to load the LUCA’s genome with genes that would make the appearance of these life forms more probable.

One more point. I’d like to correct something I stated earlier. Previously, I said something to the effect that these functional but unnecessary proteins in prokaryotes would be so unnecessary that deleting them wouldn’t significantly affect fitness. This is not correct. Deleting them might kill the organism under consideration. Nevertheless, if a given gene is required for one prokaryote, this does not mean that it is required by all prokaryote life forms. So, by “unnecessary but functional” I mean a gene that is not required by the basic prokaryote cell plan but does carry out a functional role in the LUCA.

If the homologues are sufficiently useful that natural selection would conserve them, then they will in fact be conserved, and their conservation is in fact predicted by the ToE.

Yes, but that's not the issue here at all. I said that the FLE would predict that proteins crucial to eukaryotes will share deep homology with proteins in prokaryotes. That's the whole issue here, not whether a protein will be conserved in one lineage or another. In other words, the ToE doesn't predict the existence of histones in prokaryotes; it can explain the existence of histones in prokaryotes, but it doesn't predict it.

Well, so does Darwinian evolution. How could they not?

Two points here:

1) Darwinian evolution (that is, the current paradigm) does not predict that crucial proteins in eukaryotes will share deep homology with functional but unnecessary proteins in prokaryotes. By unnecessary I do not mean a protein that offers only little fitness advantage. I simply mean a protein that is not necessary for the basic prokaryotic cell plan. For example, although histones are found in a number of prokaryotes, and are fully functional, they are not required for the existence of prokaryotes. In a world without histones, we'd still have prokaryotes.

2) Unlike front-loading, Darwinian evolution does not necessarily predict that eukaryotic histones will share deep homology with prokaryotic proteins. Why? Proteins not only evolve from coding sequences, but they can also be pieced together from non-coding sequences. A cool example of this is T-urf13, which, IIRC, evolved from rRNA sequences and other non-coding sequences. In short, T-urf13 didn't evolve from any protein-coding gene. It was pieced together from different non-coding sequences. Thus we see that Darwinian evolution could expect that histones (or analogous counterparts) would only be homologous with non-coding regions. In other words, there's no reason, from a Darwinian perspective, why the existence of histones in eukaryotes implies the existence of histones in prokaryotes. Taking this from a Darwinian point of view, the presence of histones in eukaryotes only means that it will be homologous with different chunks of DNA/RNA sequences in prokaryotes - DNA/RNA sequences that are not necessarily functional. This goes against the expectations of front-loading, because you can't really front-load histones by depending on chance to cobble together a histone from "scratch" (i.e., non-coding sequences).

Edited by Genomicus, : No reason given.

We don't know that there isn't a minimal gene set that would enable evolution into something of equivalent complexity to modern animals and plants in the time available. It only seems likely that this is true.

Would you care to elaborate on this? With a LUCA that has a minimal gene set, there's really no reason to suppose that complex life forms could arise. You'd have to guarantee the rise of mitochondria before you can get complex life forms. And, IMHO, there's no reason to suspect that a minimal gene set consisting of just essential proteins - i.e., DNA replication proteins, ribosomes, key metabolic pathway proteins, and the like - is all that likely to "just happen" to evolve in specific directions that would allow the evolution of mitochondria. In the absence of mitochondria, you won't have complex life forms.

But if we accept that the LUCA is a community of simple organisms sharing genes it is vanishingly unlikely that evolution would only have a minimal gene set to work with.

What does horizontal gene transfer have to do with a minimal gene set? I.e., sure, this LUCA community could be transferring genes, but these genes would be part of the minimal gene set.

Even taken as a vague idea, ignoring what we know about the development of early life this seems false. How can a simple self-replicating chemical have genes ?

A self-replicating RNA molecule could specify a protein sequence.

If we take into account the fact that DNA seems to be a relative latecomer (and ask yourself why we would have evidence pointing to this if life on Earth started with artificial prokaryotes)...

I haven't found any convincing evidence that DNA evolved from RNA. I am aware of a number of papers on the subject, but I'll (hopefully!) discuss this evidence in another thread (so we don't get sidetracked here).

...any LUCA you could find by investigating the homology of genes would necessarily be the product of considerable evolution, with DNA and a gene set already in place...

Yes, but under the FLH, the LUCA isn't the product of considerable evolution. Maybe I'm not getting your point with this statement?

So the emphasis is on functional but unnecessary?

Yes.

But then you could say the same of front-loading. What is there in FLE that says that by the modern era, the only homologous proteins won't be those absolutely necessary to both lineages?

If I understand your question correctly, the answer is: if you loaded the first genomes on earth with proteins "in waiting" that will find their intended function only later, when complex life forms have arisen, then, in the modern era, you can trace this homology back in time. Naturally, these proteins "in waiting" will carry out a function such that it isn't likely that they will be weeded out by natural selection.

How likely, though, is a complete turnover of genes?

Well, it's likely enough to happen.

Could you clarify --- do you think that this, and things like it, actually happened?

Yes. That's what the evidence indicates happened in the case of T-urf13.

You haven't addressed my point about front-loading. What is there in the concept of FLE as such which stops the LUCA from having two non-intersecting sets of genes, one for eukaryotes, one for prokaryotes? Now, I know the evidence is that the LUCA wasn't like that, but if there's nothing to stop a designer from doing something like that, then there's no prediction, is there?

Well, in this case, we'd have an either/or prediction. In other words, FLH predicts either that the LUCA will have functional and unnecessary genes or that the LUCA will have non-intersecting sets of genes.

But where does FLE predict that some things that are essential to eukaryotes are merely useful to prokaryotes? Is not FLE consistent with the idea that everything that is essential to eukaryotes is also essential to prokaryotes?

Let's take a look at calmodulin (CaM) as an example. Calmodulin binds to calcium and is found universally among eukaryotes. This fact, coupled to the observation that its sequence identity is exceptionally conserved across taxa, suggests that eukaryotes require calmodulin for their existence. In a world without calmodulin (or a functional analog), would eukaryotes exist? Probably not.

Now, it appears to me that you're saying "is not FLE consistent with the idea that calmodulin is also essential to prokaryotes?"

The problem is that, simply put, calmodulin is not essential to prokaryotes. The basic prokaryotic cell plan does not require calmodulin. You could design a prokaryotic cell that requires calmodulin, but the basic prokaryotic cell architecture does not require the existence of calmodulin. And this is the key point. This means that saying "is not FLE consistent with the idea that calmodulin is also essential to prokaryotes" doesn't really make sense, because we know that calmodulin isn't essential to prokaryotes.

If you believe that Darwinian evolution is sufficient to produce a complete turnover of a genome...

Well, first of all, you said "turnover of genes;" I didn't think you meant a complete genome. And, come to think of it, the terminology "turnover of genes" is kinda vague in this context. Care to elaborate?

You apparently believe in Darwinian evolution plus front-loaded evolution.

I'm not sure how you're defining Darwinian evolution.

So if you believe that a complete turnover of the genome is "likely enough to happen" given Darwinian evolution, then you believe that it is "likely enough to happen". In which case, where is your prediction? If you admit that given FLE, it is "likely enough to happen", then FLE has no prediction that it wouldn't happen.

No, because FLE has an objective, while non-telic evolution does not. Thus, non-telic evolution could stitch together a protein from non-coding segments of a genome, "just happening" to produce a new protein. In short, if FLE relies on the cobbling together of proteins to reach an objective, it is extremely unlikely that a specific, intended outcome will be produced, given that there are trillions of different possible configurations for pieces of DNA sequences. Non-telic evolution has no goal, so it can cobble stuff together, and stumble on novel functions. Meanwhile, FLE has an objective, and since there are many more possible functions than the FLE objective, it is vanishingly unlikely that the FLE objective will be found. To remedy this, you simply need to load the first cells with proteins that are nearby in sequence space to the objective (or are the objectives themselves).

We can't actually look at LUCA, can we?

Yes, we can. Not directly, of course, but indirectly.

You say you have an "either/or prediction". Well, how does that differ from the "either/or prediction" of Darwinism in terms of the phenomena that we can actually observe?

Well, Darwinian evolution "predicts" that either the LUCA will have a minimal genome, or the LUCA will have more than a minimal genome. Confirmation of any of these "predictions" is compatible with Darwinian evolution. It should be noted that something that predicts every scenario isn't really predicting anything, and this seems to be the case with non-telic evolution when it comes to the gene content of the LUCA. However, FLE is not compatible with the former scenario (that of a minimal genome). Thus, if we find that the LUCA actually did have a minimal genome, FLE will have been falsified. Which means its testable, and that it makes a specific prediction Darwinian evolution does not make.

Edited by Genomicus, : No reason given.

Edited by Genomicus, : No reason given.

But is there anything in FLE that predicts that such a thing should exist? Would it not be compatible with FLE that everything that's essential to eukaryotes should also be essential to prokaryotes? Where does FLE rule that out?

Huh? It's not FLE that rules that out, it's basic observations that rule it out. And the FLE hypothesis is built around biological observations, such as the fact that not everything that is essential to the eukaryotic cell structure is required for the existence of the prokaryotic cell structure. I'm not arguing in favor of this hypothesis on the basis of what ifs, such as "what if everything that is essential to eukaryotes is also essential to prokaryotes?" It's on the basis of known biological facts that this hypothesis is constructed upon.

Well, suppose that prokaryotes started off with a certain set of genes, let's call them genes 1 ... 1000. Then gene 1001 arises by the mechanisms you suggest, and substitutes for gene 1 and displaces it, and then gene 1002 arises by the mechanisms you suggest, and substitutes for gene 2 and displaces it ... and so on until every gene in LUCA has been substituted by a gene arising by the mechanisms you postulate.

I'm not suggesting anything like that happened. I'm saying that some key eukaryotic proteins, under the non-telic model, could have evolved through patching together different chunks of non-coding sequences.

You believe, do you not, in random mutation and in natural selection?

Quite right.

Therefore, you believe in "non-telic evolution" don't you?

If that's how you're defining "non-telic evolution," then yes. But when I say "non-telic evolution" I mean this whole non-teleological framework which says that planning and foresight was not involved in the origin of genetic diversity on earth (with the exception of human intervention).

But as I have pointed out before, our ability to look "indirectly" at LUCA depends crucially on accepting Darwinian evolution. That is the theory which allows us to infer LUCA. If we deny Darwinism, we have no basis on which to say what LUCA looked like.

And, in this context, what does "Darwinism" mean? Random mutation coupled to natural selection (and similar mechanisms)?

(1) There are certain proteins that are essential to eukaryotes.

Yes.

(2) These proteins have homologues in prokaryotes such that prokaryotes would not actually drop dead if deprived of these proteins, but would be significantly disadvantaged if deprived of them.

Specifically, some prokaryotes might actually drop dead because scaffolding allows an originally unnecessary protein to become essential for a given species. But this protein would not be universally required for the overall prokaryotic cell plan.

How does FLE predict this state of affairs? How would I, or you, or anyone, reason from "LUCA was front-loaded" to this conclusion?

Let me try again:

1. Front-loading, by definition, involves loading the first genomes with proteins that are unnecessary for prokaryotes but are necessary for the origin of eukaryotes and multicellular life forms.

2. Thus, front-loading predicts that the important proteins in eukaryotes will share deep homology with proteins in prokaryotes which are unnecessary for the existence of prokaryotes. These functional but unnecessary proteins in prokaryotes are the descendants of the original proteins that were loaded into the first genomes.

Possibly I'm not being clear enough.

If so, doesn't the prevailing view imply that random mutations that are NOT seriously damaging to the chance of reproduction get retained?

Not all neutral mutations will be retained by a population. Only some.

The real question is whether it is possible to engineer a minimal gene set which would encourage the formation of complex life. Given the size of the minimal gene set that you suggest, it seems that that is at least something that could plausibly be true.

The minimal genome would be around 250 genes. You're basically suggesting that the designers take calmodulin and fashion it such that it is necessary for the prokaryotic cell plan, are you not?

Wouldn't it make a lot more sense to engineer eukaryotes with artificial mitochondria - if the engineers chose the symbiotic route at all?

Eukaryotes aren't very good terraformers compared to prokaryotes, and FL is intimately linked to terraforming. If you engineered the first bunch of cells in the right way, the origin of eukaryotes becomes quite likely. Thus we see that multicellularity has evolved independently several times, pointing to the plausibility of the evolution of multicellular life forms, given specific initial conditions.

If the LUCA is a population of organisms exchanging genes it would be expected to have a greater diversity of genes than if it were a single individual organism. And thus far more likely to have more than a minimal genome (in aggregate).

Yes, but the LUCA could also be a self-replicating RNA molecule, with - as you correctly point out - small amounts of molecular machinery needed for the formation of primitive proteins.

For the purposes of this discussion it is going to be better if you at least take the leading views of the origin of DNA as possibilities that have to be considered. To the best of my knowledge, the RNA World hypothesis is widely accepted among researchers into the origins of life.

Yes, but if I accept the RNA world hypothesis - that is, the thesis that life evolved from compounds on earth - my front-loading hypothesis is blown out of the water, effectively. So, when you suggest that I take the leading view that DNA evolved from RNA, you're essentially saying that I should take the leading view that teleology has not played a role in the history of life on earth.

I was merely doing my best to answer your question, jar. No need to get slightly snarky over it

Look, suppose you said that giraffes confirm FLE because FLE predicts giraffes. And then I come back saying: "But is there anything in FLE that predicts that giraffes should exist? Would it not be compatible with FLE that there should be no giraffes? Where does FLE rule that out?" And then you riposte with: "Huh? It's not FLE that rules that out, it's basic observations that rule it out." These "basic observations", of course, being that we can see giraffes. Don't you see that in order for a theory to predict X, it has to rule out not-X? You can't say: "My theory predicts X ... OK, I grant you it doesn't rule out not-X ... but we can see that X". Well in that case your theory hasn't made a prediction. We've just seen X.

Yes, but you're saying that FLE doesn't rule out the possibility that all essential proteins in eukaryotes will be essential in prokaryotes. I don't know how I can make this clear, but think of it like this:

The theory of common descent predicts that organisms that share a common ancestor will share the same ERV insertion spots. But does common descent rule out the possibility that ERV insertions are non-random? It does not, and therefore, using your logic, one could argue that since common descent doesn't rule out this possibility, it doesn't predict that closely related species will share the same ERV insertion sites. Do you get the idea?

But unless you claim that it is a prediction of Darwinism that there should most likely have been a complete genomic turnover, then you must acknowledge that it is a prediction of Darwinism that there should be homologies.

The non-teleological model predicts both (a) that eukaryotic proteins will share homology with prokaryotic proteins, and (b) that eukaryotic proteins will share homology with non-coding regions of prokaryotic genomes. On the other hand, FLE exclusively predicts the former.

Challenge: find a universally widespread protein among eukaryotes that has been cobbled together from different non-coding regions of prokaryotic genomes.

But if you admit that Darwinian evolution can and does take place, then none of your predictions can be based on the premise that it can't and it didn't.

Again, if by Darwinian evolution you simply mean random mutation and natural selection (and other mechanisms), then yes, of course Darwinian evolution happens. But my prediction is based on the two different models for the origin of life's diversity: the teleological, front-loading model and the non-teleological model.

Therefore, you must admit that FLE permits anything that ToE permits. In which case FLE can never be more specific in its predictions than ToE.

No, I disagree, precisely because FLE doesn't permit the LUCA's genome to consist of little more than a minimal gene set.

No. That is not the definition of front-loading.

Actually, by definition, FL does involve the loading of a genome with proteins that the basic prokaryotic cell architecture doesn't require but the eukaryotic cell plan does.

I'm suggesting that it is plausible that there is a set of 250 genes that would encourage the evolution of complex life.

Yes, if this set of 250 genes encoded stuff like calmodulins, histones, tubulin, dynein, etc. But such a set of genes wouldn't be something that is required by all life forms. And this is where we get our FL prediction: at minimum, the LUCA would have consisted of 250 genes (actually, fewer, given that LUCA didn't have to have a complex prokaryotic cell organization). But a minimum gene set consisting of the genes absolutely required for life doesn't allow you to front-load anything. That's why you'd need to load the genome with unnecessary - but functional - proteins.

I don't see that as very plausible, unless you assume that the LUCA was engineered.

Under the RNA world hypothesis, how did the first proteins originate? They would have originated long before the origin of the LUCA, and prior to the LUCA you'd have very simple cells (under the non-telic model) - possibly consisting of primitive membranes such as lipid bubbles - and these cells wouldn't require 250 genes.

I am not asking you to believe in the RNA world. I am saying that you have to accept it as an important part of a serious opposing position.

Absolutely. There are many problems and challenges facing the FL hypothesis. It's a shaky hypothesis at the moment.

Edited by Genomicus, : No reason given.

Edited by Genomicus, : No reason given.

And I should like you to answer that point rather than another one.

I answered your point by bringing up the example of ERVs.

Where does it do that?

*sigh*

I think I've already answered this question, but here goes:

Front-loading basically doesn't work if it must rely on some of the important eukaryotic proteins evolving purely through the chance stitching together of random DNA sequences. This is because the odds of this process generating a specified target is next to nil.

But so far as I can see, you believe in both.

Earlier, I defined what I meant by the "non-teleological model." Let me define it again for you:

By "non-teleological model" I mean the scenario wherein all of the diversity of life arose without the input of teleology at some stage in life's history. So, no, I don't accept the non-teleological model.

In which case your range of predictions includes anything that Darwinism says is possible, and so cannot have greater specificity than Darwinism.

Okay, I think I understand what you mean with this one. All FLE predictions (that I am aware of) include things that are possible under "Darwinism." However, there are some possible scenarios in Darwinian evolution that isn't allowed by FLE. And this allows us to make predictions from an FLE standpoint, predictions that Darwinian evolution does not make but predictions that can be explained by Darwinian evolution.

WE CAN'T SEE LUCA.

To which I respond that, yes, we can see LUCA, through phylogenomics and similar approaches.

I understand that this can get frustrating, since it's difficult for us to get into the mind of the other. Still, let me try yet again, using the true/false method.

True or False: You cannot front-load multicellular life forms with just a minimal genome, since there'd be no "stacking of the deck" in favor of multicellular life forms, and "stacking the deck" is the essence of front-loading.

True or False: In order to "stack the deck" in favor of multicellularity, you'd need to load the first genomes with something more than just the required minimum. You'd need to load the first genomes with proteins that would be used by multicellular life forms, allowing their origin.

True or False: Front-loading therefore predicts that the first genomes, and consequently the genome of the LUCA, had more proteins than is necessary for the existence of a cell. In other words, FL requires that the LUCA was needlessly complex.

True or False: We can detect this needless complexity by comparing the genomes of different species, allowing us to track back over deep time.

Edited by Genomicus, : No reason given.

So long as it encourages the development of complex life forms, it doesn't matter what the genes code for. They need not be analogs of proteins used by known life.

True, but proteins that encourage the development of multicellularity and Metazoa etc. aren't likely to be found in a minimal gene set, because such genes only encode the bare necessity, which means there'd be no "front-loading." There's a difference between simply designing the first life forms and specifically engineering it such that it front-loads the appearance of complex life forms.

That is the very assertion that I am disagreeing with. Given 250 distinct proteins it is simply not clear that they would be insufficient for front loading, given the modest goals assumed.

Yes, but you're forgetting that these 250 distinct genes would also have to be part of a minimal gene set. So, you'd need to get one of the genes necessary say, for the Krebs cycle, and engineer it such that it actually does nudge evolution in the direction of complex life forms. Or you could take SecY, which AFAIK is a necessary protein for life, and engineer it so that it biases evolution in favor of multicellular life. But then, once you do that, there's no reason to suspect that we'd have something that looks like SecY anymore. And, unless you have evidence suggesting otherwise, there's nothing inherent in SecY that would bias evolution towards the development of complex life forms, is there?

No, that's where you ducked my point.

Elaborate, if you please.

For example, what's to stop LUCA from having two parallel sets of genes, one for prokaryotes and one for eukaryotes?

I already explained this: we have an either/or prediction in this case. Under front-loading, either the LUCA has more than a minimal genome, or LUCA has two parallel gene sets.

Darwinian evolutionary models also generate either/or predictions. For example, the specific evolutionary hypothesis that the bacterial flagellar system arose from the type III secretory system predicts that either the type III secretory system is a pre-cursor to the flagellum and thus pre-dates the origin of the flagellum, or both systems share a common ancestral system that is essentially a type III secretory system.

Okay, I think I understand what you mean with this one. All FLE predictions (that I am aware of) include things that are possible under "Darwinism." However, there are some possible scenarios in Darwinian evolution that isn't allowed by FLE. Which? Mutation still happens, doesn't it? And natural selection? And lateral gene transfer? And recombination? Anything that can happen under Darwinian mechanisms can happen under the FLE hypothesis, since it does not deny the existence of those mechanisms.

You will note that I said "there are some possible scenarios in Darwinian evolution that isn't allowed by FLE." At this point, I wasn't talking about mechanisms. I was talking about scenarios. And one scenario that is perfectly acceptable under Darwinian evolution is that the LUCA had only a minimal genome. Such a scenario is not, however, compatible with FLE.

False.

Really? Why?

Edited by Genomicus, : No reason given.