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Author | Topic: An ID hypothesis: Front-loaded Evolution | |||||||||||||||||||||||||||||||||||||||
Dr Jack Member (Idle past 123 days) Posts: 3514 From: Immigrant in the land of Deutsch Joined:
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I'm afraid I must disagree with your contention. At the deep level of relationship we're talking about here, protein similarity is much more appropriate to look at than DNA sequence. DNA changes much faster so expecting any kind of base-by-base similarity is unreasonable and would likely be meaningless anyway.
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Genomicus Member (Idle past 2190 days) Posts: 852 Joined: |
General Response to Objections
Instead of getting bogged down with replying to every one of you, here I will address the objections to the FLE hypothesis that I think are surfacing the most frequently. The objections I will address here are (a) front-loading specific objectives (e.g.,eyes or blood) is not very feasible, (b) the branching problem raised by Dr Adequate, (c) the issue of predictions made exclusively by the front-loading hypothesis, that is, predictions made by the FLE model but not made by conventional evolutionary theory. Keeping perspective in mindMy objective here is not in the slightest to win the debate or anything like that. I freely admit that there are problems with the FLE hypothesis; the human species has little experience in anything like directed panspermia or front-loading, so I imagine that these problems will start disappearing once we really start getting serious about panspermia and directing evolution with unicellular organisms. My real objective here is to refine the front-loading hypothesis so that when the proper time comes, it can be submitted to the scientific community for review. Front-loading Specific ObjectivesThe gist of this objection can best be summarized by this statement by Bluejay: The more specific the objective, the less likely the objective is to be met at all using a crude technique like front-loading. I find it highly dubious to suggest that something as specific as an eye could feasibly be front-loaded at all for this exact reason.
I’d like to point out that the argument I can’t imagine how the eye could have been front-loaded, therefore it could not have been isn’t really all that valid.It’s also important to understand something here: front-loading does not necessarily entail directly front-loading something like the eye. Front-loading is stacking the deck (to borrow from Mike Gene) such that the evolution of certain features becomes much more plausible. For example, if we design rhodopsin in a bacterial genome, we could predict that when eyes evolve, rhodopsin will be used. This would make the evolution of the eye much more plausible, since rhodopsin would not have to evolve from a non-rhodopsin-like precursor. Similarly, if we loaded the first genomes with globins, then we could predict that when animals do arrive on the scene, their blood will be built around hemoglobin. Designing the initial genomes with hemoglobins (or hemoglobin homologs) encourages the evolution of blood. Another example will be cited here. If we designed cilia into simple eukaryotes, this could help channel the evolution of more complex eukaryotes like animals. This is because the cilia would encourage the evolution of organisms with tissues like that seen in complex animals. This is an example of course, and this needs to be emphasized before anyone starts saying that I think the first eukaryotes were directly designed instead of front-loaded. Thus, front-loading is largely about stacking the deck, encouraging the evolution of certain biological features through initial designed states and making the evolution of those features more plausible. Furthermore, convergent evolution has effectively demonstrated that the front-loading of specific biochemical systems is indeed feasible. For instance, hemoglobin has evolved independently in lampreys and all other vertebrates. It thus seems plausible that specific proteins can be front-loaded from initial states. A more dramatic example comes from the evolution of C4 photosynthesis. This biochemical pathway is thought to have evolved independently more than 45 times (see this review by Sage, 2003: The evolution of C4 photosynthesis). And C4 photosynthesis is mediated by four different enzymes (see figure; taken from MetaCyc): pyruvate orthophosphate dikinase, NADP malic enzyme, phosphoenolpyruvate carboxylase (PEPC), and malate dehydrogenase. Figure. A diagram of the C4 photosynthesis pathway, taken from MetaCyc. If I were to propose that a specific biochemical pathway like C4 photosynthesis was front-loaded, one might be tempted to argue that this is extremely infeasible. In short, while front-loading a biochemical pathway isn’t like front-loading an organ such as the eye, one could still argue that I find it highly dubious to suggest that something as specific as a C4 photosynthesis pathway could feasibly be front-loaded at all. Yet C4 photosynthesis has evolved independently many, many times, proving the feasibility of front-loading a specific biochemical pathway. Why does this prove the feasibility of front-loading? Precisely because it proves that fairly specific targets can be reached by the blind watchmaker independently and multiple times— this means that FLE is feasible — given certain initial states.I like the example of C4 photosynthesis because I think it’s a good illustration of how initial states can shape subsequent evolution, such that the blind watchmaker stumbles upon a certain target. For the record, I do not think that C4 photosynthesis was front-loaded. But it’s a good example of how feasible FLE could be. Sage, 2003, describes the initial states that must be present before C4 photosynthesis can evolve (see figure; from Sage, 2003). Figure. In this figure, Sage describes the initial states that are required before C4 photosynthesis can evolve. Thus, if we designed a plant genome such that it is prone to many gene duplication events (and we would have to design the right genes into this genome), and designed the plant such that it has closed veins and its bundle sheath organelles are enhanced, and we placed this plant on another planet (supposing this planet was not hostile to plant life, of course!), then we could predict that when we visit this planet many centuries later, C4 photosynthesis will have evolved in this plant species. Botanists et al., please don’t quibble about my lack of a discussion on how we would need many plants with this designed genome, etc. Thus, it seems to me that specific proteins can be front-loaded — as evidenced by the independent evolution of hemoglobin; specific biochemical pathways can be plausibly front-loaded, as demonstrated by the multiple, independent evolution of C4 photosynthesis; and furthermore, specific molecular machines could be front-loaded: this is evidenced by the independent evolution of two protein export systems from the bacterial flagellum — namely, the type III secretion system and a protein export system in Buchnera very similar to the TTSS, and one that is also derived from the bacterial flagellum — but evolved independently.Given the above considerations, I really do think that to argue that an organ like the eye — or an analogous organ — couldn’t be feasibly front-loaded is a gaps argument. If specific proteins can be front-loaded, and if specific molecular machines and specific biochemical pathways can be front-loaded, you’re just pushing the goal-posts back and demanding that I explain how something like the eye could be front-loaded. Admittedly, at the present moment, this is a difficult question to answer — and this would be a good line of research, but as the evidence shows, specific biological objectives can be feasibly front-loaded. The Branching ProblemThis objection to FLE was raised by Dr Adequate, who stated: According to your hypothesis, LUCA must have had genes to turn it into a whale, and a spider, and an oak tree, and a camel. So what decides which it will actually do?
This question is a bit flawed to begin with. I am not proposing that specific species or genera or families or orders were front-loaded. The initial genomes would not, therefore, contain the genomic information necessary to give rise to oaks and camels and whales and spiders.However, I do propose that the first genomes were capable of front-loading the appearance of both animals and plants. How would this be possible? Recall that front-loading is about stacking the deck such that the appearance of certain biological features becomes much more plausible. Consider an analogy from a game of cards (say, poker). If we loaded a deck of cards with aces, such that 25% of the card deck contains aces, it would be very likely that we’d get a hand with four aces — far more likely than if we didn’t tamper with the deck. Similarly, if we loaded a deck of cards with queens, so that another 25% of the deck contains queens, we would be very likely to get a hand with four queens. Importantly, it would be very probable that one person will get a hand with four queens, while another gets a hand with four aces. We’ve front-loaded the appearance of four queens and four aces so that these combinations are far more likely than with a standard deck. Note that, with this analogy, it is perfectly feasible for one person to get four aces (I shall call this front-loading objective x) and for another to get four queens (front-loading objective y) - even though this would be a branching pattern, where both front-loading objectives x and y have been realized. So, the first genomes could be loaded with genes necessary for plant development and function and with genes necessary for animal development and function. And thus the origin of both plants and animals would be effectively anticipated by the first genomes. It’s not like an evolving animal lineage must use plant genes; nor does an evolving plant lineage have to use animal genes. I’m going to use another example here, albeit a hypothetical one. Suppose we designed plant that (a) was prone to many gene duplication events, had closed veins, its bundle sheath organelles were enhanced, and had a photorespiratory CO2 pump, and (b) had globin proteins that could, in a number of mutational steps, be converted to hemoglobin. In effect, a population of these designed plants would be poised to evolve the C4 photosynthesis pathway and the hemoglobin molecule — front-loading both biological features. If Dr Adequate’s objection is indeed valid, then we must believe that this hypothetical plant population could not front-load the appearance of both C4 photosynthesis and hemoglobin (I am, of course, supposing that there’d be a selective advantage to both of these biological features). If I understand his objection correctly, he’s suggesting that only one of these features could be front-loaded. But this obviously not logical; as we have seen, it wouldn’t be very hard to front-load the C4 photosynthesis pathway, nor would it be difficult to front-load the appearance of hemoglobin. Nothing is stopping the front-loading of both of these features. Furthermore, it would be indeed possible to front-load hemoglobin and C4 photosynthesis such that they do not occur in the same population. All that would be needed is for this plant population to split into two populations, say A and B. A simple deletion event of the globin gene in population A would lead to the appearance of only C4 photosynthesis; deletion of the four enzymes involved in C4 photosynthesis in population B would lead to the appearance of only hemoglobin. This simple example shows how Dr Adequate’s objection is answered: there is no conceptual problem with different lineages being front-loaded. Predictions of the FLE HypothesisIt 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-loadingI 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. P.S. Often in lengthy essays like this, typos will be a bit frequent. I’m sure all of you will forgive any typos Also note, again, in this thread I do not intend to discuss whether the predictions of front-loading have been confirmed to any degree. I intend to discuss whether these are indeed valid predictions of FLE. Edited by Genomicus, : No reason given. Edited by Genomicus, : No reason given. Edited by Genomicus, : No reason given. Edited by Genomicus, : No reason given. Edited by Genomicus, : No reason given. Edited by Admin, : Reduce image width, change image background to white, remove link to image, center caption. It's a poor quality image, even at full size.
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Genomicus Member (Idle past 2190 days) Posts: 852 Joined: |
Massimo Di Giulio (2001) argues that this actually makes approaches such as Freeland's tautological since the nature of the genetic code has had a significant effect on the distribution of amino acid substitutions making it far from an independent measure of the optimisation of that code. Quite right. Freeland et al. (The Case for an Error Minimizing Standard Genetic Code), 2004, responds to this argument thusly:Attempts to obviate this problem by measuring similarity directly from estimates of the frequencies with which amino acids substitute for one another within real proteins do suggest the code to be close to a global optimum (Ardell, 1998; Freeland et al., 2000a), but have been criticized as tautologous given a correlation between the code and patterns of substitution (Di Giulio, 2001b), though the flow of causality in this correlation is yet to be determined. Encouragingly, a recent attempt to derive a multidimensional measure of amino acid similarity that is truly independent from the code supports the counter criticism: the more sophisticated our representation of similarity, the better the code appears (Gilis et al., 2001). For the record. Edited by Genomicus, : No reason given.
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Genomicus Member (Idle past 2190 days) Posts: 852 Joined: |
Wait ... scientists are disagreeing about something? This has hardly ever happened before. Actually, it happens all the time. Investigators do disagree on the origin of the type III secretion system, for example (i.e., there is a good bit of disagreement on whether the TTSS and the bacterial flagellum are sister groups or whether the TTSS descended directly from the flagellum).
According to your hypothesis (if you fudge it a bit) it would be jolly nice if the genetic code was globally optimal. But no-one has proved this to be the case. Not meaning to quibble over semantics here, but science isn't so much about proving things as it is about providing evidence. And evidence has been presented by various researchers that the genetic code is very close to being globally optimal for error-minimization - it is an extremely optimal code.
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Genomicus Member (Idle past 2190 days) Posts: 852 Joined: |
I just performed the same search, on the NCBI site limiting the search to the Prokaryota, and there were indeed hits below the 1e-05 level, a grand total of three of them and all from the same thing, a putative paired box domain protein from the protobacteria Methylocystis. I imagine that the sequence similarity is why this is identified as a putative paired box domain protein in the first place. The region that comes up only covers 23% of the submitted amino acid sequence and has a maximum identity of 30% and less than 50% for positive (BLOSUM62 compatible) sites. If this was what he got then I'm not surprised Genomicus didn't want to go into any more detail about the results since they are so weak. That the matches have >30% identity isn't that bad at all, when you factor in E-values. You can have a database match to your query sequence that has little over 20% sequence identity, but if the match is accompanied by a good E-value, it's still significant.
Perhaps more relevantly all of the lower hits are from tranposon and insertion sequences, suggesting that what we are seeing is a convergent signature for DNA binding interacting activity rather than an ancestral relic of a front loaded primeval PAX gene lineage. To support this the SMART database of protein architecture identifies 3 bacterial hits for the PAX domain and all 3 are from transposase sequences. This may very well be the case. But from a non-telic perspective, do you think we'll ever find significant PAX6 sequence/structural matches in prokaryotes?
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Genomicus Member (Idle past 2190 days) Posts: 852 Joined: |
Can anyone someone lay his position out for me in laymans terms? Is he arguing that evolution was front loaded by a creator/deity? I'm arguing that evolution was front-loaded by some intelligence(s), the identity of which I haven't got the slightest idea - and for all we know, this intelligence might be extinct by now. The FLE hypothesis is not a theistic argument, and the existence of gods (or lack thereof) has no bearing on this hypothesis. It is, however, a teleological, ID hypothesis.
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Genomicus Member (Idle past 2190 days) Posts: 852 Joined: |
On another related point, if you take the mRNA coding for the sequence that Genomicus chose and blast that against the Prokaryota then you get no significant hits. Protein sequence comparisons allow us to look back over longer periods of time than DNA/mRNA sequences. Since we're talking about deep time here, I don't think it's even appropriate to do a BLAST search with an mRNA query.
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Genomicus Member (Idle past 2190 days) Posts: 852 Joined: |
For the record: I kinda buried my primary post with replies to individual comments, so my general response to objections to FLE can be found in my brief essay above.
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Dr Jack Member (Idle past 123 days) Posts: 3514 From: Immigrant in the land of Deutsch Joined: |
That the matches have >30% identity isn't that bad at all, when you factor in E-values. You can have a database match to your query sequence that has little over 20% sequence identity, but if the match is accompanied by a good E-value, it's still significant. You don't have good E-values. 1e-5 is not a good E-value, it's bordering on noise. I've been looking at the homology found by the NCBI database and I note this: what similarity exists is found only in the helix-turn-helix DNA binding motif of the better matching proteins. Do helix-turn-helix (HTH) motifs have deep evolutionary history? Yes, they likely do, but that really doesn't support your front-loading hypothesis because HTH motifs are simply a means to match specific DNA sequences, usually found in transcription factors. In other words, an HTH motif forms part of a mechanism that switches genes on or off according to circumstance. That's not any part of anything specifically eye related about pax6 but rather a faint superfamily relationship. You'll get similar results from any HTH protein you choose to pick. This freely accessible paper discusses the deep family relationships between HTH transcription factors in depth. (edit) To illustrate my point about E-values, try blasting P11388 against the prokaryotes (P11388 being human DNA topoisomerase ii-alpha), here where there is genuine, deep-rooted, homology you get E-values in the sub 1e-35 range across a stack of different bacterial species from the various branches of bacterial life. Edited by Mr Jack, : Added DNA topoisomerase ii BLASTp details
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Genomicus Member (Idle past 2190 days) Posts: 852 Joined: |
You don't have good E-values. 1e-5 is not a good E-value, it's bordering on noise. Well, consider that: a. The E-values are not 1e-05. They are a bit less than that. b. An E-value of 1e-05 is not "bordering on noise" IMHO. Various investigators have used the E-value of 1e-04 as the cutoff value, yet their findings have been accepted by the scientific community. Of course, we have to look at the broader biological context here, too. In fact, I'm more than willing that the matches don't indicate front-loading. That's why I'm curious on this: do you think we'll ever find significant structural or sequence homologs of PAX6 in prokaryotes?
To illustrate my point about E-values, try blasting P11388 against the prokaryotes (P11388 being human DNA topoisomerase ii-alpha), here where there is genuine, deep-rooted, homology you get E-values in the sub 1e-35 range across a stack of different bacterial species from the various branches of bacterial life. I'm perfectly aware about the statistics of database matches. Edited by Genomicus, : No reason given.
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Dr Adequate Member Posts: 16113 Joined: |
If Dr Adequate’s objection is indeed valid, then we must believe that this hypothetical plant population could not front-load the appearance of both C4 photosynthesis and hemoglobin (I am, of course, supposing that there’d be a selective advantage to both of these biological features). If I understand his objection correctly, he’s suggesting that only one of these features could be front-loaded. No, no, you misunderstand me. Let's hypothesize that they're both front-loaded. Fine. But at some point branching has to take place. One lineage has to go one way and do photosynthesis, while the other goes the other way and does hemoglobin. Now this itself, on the face of it, cannot be preprogrammed. The reason why one lineage develops one way and another develops in another way cannot be the result of their common genetic heritage. So what, in your scheme, does explain it?
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Dr Adequate Member Posts: 16113 Joined: |
I’d like to point out that the argument I can’t imagine how the eye could have been front-loaded, therefore it could not have been isn’t really all that valid. Actually, I think it is. Now, it is perfectly true that if someone claims that such-and-such a thing occurs, or has occurred, then it is not a conclusive argument against this claim to point out that they have no theory explaining how it occurred. To take a trivial example, I've seen Penn and Teller do their bullet-catching trick. I have no idea how they did it. I'm still certain that I've seen them do it. But this is not like the situation that we are in. We agree on what happened: life evolved by radiation from a common ancestor. What you are trying to do is produce a theory explaining that fact. So it is actually a valid criticism of your theory to point out that it does not in fact explain the things that it's meant to explain. That's the whole point of a theory, that's what theories are meant to do. They're meant to explain the facts. If it doesn't do that, it's no good.
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PaulK Member Posts: 17906 Joined: Member Rating: 7.2 |
quote: It was valid enough that Darwin thought it to be worth answering. The usual problem is that creationists quote the argument but ignore the response, giving a deeply misleading impression of what Darwin was saying. I think that recognising the problems with front-loading, even if they are expressed a little vaguely is an important part of this discussion.
quote: Now this is where we see problems with your arguments. Does designing rhodopsin into the first life significantly increase the chance of eyes evolving ? Nothing you say really addresses this point. You say it does, but it really isn't clear why you think that. Can we really say that rhodopsin specifically would be used ? It's available for co-option, sure, but is it the only possibility ? How likely is it to be the only possibility or even the most available option when eyes do evolve ? We do need to be careful to avoid thinking that the way things work now is the only possible way, especially in the context of this discussion since it would bias the argument in favour of front-loading. According to Wikipedia (not the best source, I know but usually OK on science and more accessible to the lay public) bacterial rhodopsins may have an evolutionary relationship with visual rhodopsins, but they may not. Doesn't this make it a rather poor example of possible "front-loading" ?
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Genomicus Member (Idle past 2190 days) Posts: 852 Joined: |
No, no, you misunderstand me. Let's hypothesize that they're both front-loaded. Fine. But at some point branching has to take place. One lineage has to go one way and do photosynthesis, while the other goes the other way and does hemoglobin. Now this itself, on the face of it, cannot be preprogrammed. The reason why one lineage develops one way and another develops in another way cannot be the result of their common genetic heritage. Yes, but front-loading isn't about pre-programming something. It's about "stacking the deck," and anticipating the rise of plants and animals, for example. Simply put, if we start with an origin population of cells, which contain genes necessary for the development/function of plants and animals; next, this initial population separates into two populations. Then, deletion events in one population removes the animal genes, say, so that we just end up with plants. Alternatively, the front-loading designers could have designed such a population from the start: where some cells have genes for plants, and others have genes for animals.
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Genomicus Member (Idle past 2190 days) Posts: 852 Joined: |
Actually, I think it is. Well, not when seen in the context of other biological features. In my little essay, I showed how (a) it is feasible for specific proteins to be front-loaded; (b) it is feasible for specific molecular machines to be front-loaded; and (c) how specific biochemical pathways can plausibly front-loaded. Thus, demanding that I explain the origin of the eye through FLE seems to be pushing the goal-posts back. The FLE hypothesis is just in its infancy; demanding that we produce a teleological hypothesis for the origin of the eye, at this point, seems a little premature, to me at least.
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