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| Author | Topic: An ID hypothesis: Front-loaded Evolution | |||||||||||||||||||||||||||||||||||||||||||||||
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RAZD Member (Idle past 514 days)  Posts: 20714 From: the other end of the sidewalk Joined: |
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Genomicus Member (Idle past 1051 days)  Posts: 852 Joined: |
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RAZD Member (Idle past 514 days) Posts: 20714 From: the other end of the sidewalk Joined: |
Hi Genomicus, excuse the length - we may need to break this down into subtopics if this goes on growing.
Please note that I added a section on derived traits and a question about convergent evolution before I saw your reply:
The weak link is your completely unevidenced assumption of an intelligence and that the process is directed and designed to front-load the system, and in this your thesis is considerably different from "plain ole' panspermia" or FLU ... PLUS your FLE relies entirely on this being true: that is your extremely weak link.
Been there, hence my comment being what it was. quote: They are not positively identified as interstellar cells or the remains of them. The possibility of constructs like buckyballs were not known by Hoyle and Wickramasinghe when they published in the 70's: quote: And likely many other patterns are possible for forming hollow shells, with the ones observed being more stable. I would expect that a dodecahedron pattern would also be stable and larger geodesic shapes may also be possible. The graph used by Hoyle and Wickramasinghe
As NASA's recent evidence for buckyballs is the same kind of evidence as the 40+ year old evidence used by Hoyle and Wickramasinghe, and is much more discrete in analyzing the signal (two peaks instead of one), my money is on fullerenes rather than cells as the more accurate explanation. Furthermore, fullerenes are now known to clump together into larger particles: quote: Stacked like a crystalline structure using buckyballs as the matrix molecules ... could we see superbuckyballs made of buckyballs? In addition, there are other problems for them being dried shells of bacteria: they are not necessarily living organisms (or spores) nor do they necessarily have functional DNA inside - the pattern is for hollow shells, not living cells --- that has to be assumed for your thesis. Do a google on buckyball panspermia and see how many advocates are trying to cram panspermia inside the buckyballs.
Yes, it makes mine more complete and comprehensive, while yours still rests on certain incompletely defined assumptions being true without any objective evidence in this area.
Because (a) otherwise the FLE is unnecessary and (b) the inability to produce results would tend to invalidate the concept of abiogenesis by "natural (FLU/NFLU) laws" - leaving the field open for life being "salted" on earth.
But it makes assumptions about the origin of the cells and their delivery to the earth, assumptions that are just assumed to be true without testing or validation.
First, we may see evidence in life occurring today of "key eukaryotic proteins sharing deep homology with functional but unnecessary prokaryotic proteins." Seeing as all these forms are current living organisms they do not necessarily make any claim about early life. We also know that unicellular life is rife with horizontal transfer of material from one organism to another, even across the designations of the major domains of life (the cells don't care what they are). The laws of an FLU would allow this horizontal transfer, but it should be completely unnecessary and certainly is not predicted by an FLE that has a complete package in the initial life. quote: Curiously, I would expect that the FLE would predict a single unequivocal tree structure at the roots of life without Horizontal Gene Transfer (HGT), including genes for the production of proteins. Second, proteins are proteins, they don't depend on any specific branch of life to exist, they just need to be combined from amino acids in roughly the same order by any type of cell so we would expect (deep) homologies from shared ancestors along with some variation accumulated over time. If they serve little or no function in the fully developed cell at this stage in the game of existence (3.5 billion years after the first life) we can assume that some variation would occur, such that the proteins are not as homologous across domains as they are within domains. quote: Similar but different, just as should be expected. Note also that we have {p, b, a}, {p, b, nota}, {p, notb, a}, and {notp, b, a} homologies, which looks a lot more like horizontal transfer than front-loading to me.
Curiously, you appear to using evidence that is known prior to the hypothesis formation as a validation test, when this is properly included in your review of the current state of knowledge in forming an hypothesis in order to explain all the known objective empirical evidence. That is not a true prediction of the hypothesis, instead it is a demonstration of consilience between the known objective evidence and the hypothesis. A proper prediction is for something not already known, something new, and preferably something that cannot occur without the hypothesis or theory.
But there isn't -- see above. There is objective evidence that cilia exist. The proper approach is to take your example of your purported FLE instance (cilia exist), show that this could not occur in a NFLE world, and then form your your hypothesis test. Unfortunately, for you, you have done the opposite - shown how the NFLE would work.
Disagree all you want, but show me the evidence. You're going to have to provide me with more information than this hopefully from professional journals such as you have already used for this "discussion" you have asserted. I'm betting it is about details rather than yes or no.
Except that these are, as already noted, predicted by ToE and our current knowledge of early life and horizontal transfer among unicellular life. In no case have you provided evidence of something predicted that was not previously known. That is not a prediction, it is a claim of consilience between the known objective evidence and the hypothesis. Seeing as any new hypothesis must explain all current known existing evidence, demonstration of consilience with that evidence is not the result of prediction, rather this is a necessary part of the effort, the homework, that needs to go into the formation of a new hypothesis - checking to see that it is consilient with all known data. What you need to predict is something not already known, something new, and preferably something that cannot occur without FLE.
See above where I explain how "conventional theory" does in fact predict "deep homologies" ... (and derived traits in the added sections of the previous message noted above, along with the question of convergent evolution). Curiously, the ToE makes no prediction that preserved elements need to be functional or necessary, just that they not be deadly.
Again, see above where I explain why ToE does predict the patterns of deep homologies regardless of how specific they are. You have not shown a specific instance of any element that cannot occur by "conventional theory" and in fact have said so ("This is, in essence, the non-teleological hypothesis for the origin of the eukaryotic flagellum").
If you can then show me how. I'm open to evidence based logical argument.
Repeating your assertion does not make it any more valid. Using A you make a prediction that you have not made by B So which is more valid? The function of a hypothesis or a theory is to explain the evidence, it doesn't matter if the evidence is new or old, predicted or covered by the mechanics that went into the development of the hypothesis or theory. The function of a prediction test is to predict something not already known, something new, and preferably something that cannot occur without the hypothesis or theory.
Really? A "flagellum second" hypothesis would be a counter hypothesis (antithesis) to the "flagellum first" hypothesis and it would predict that TTSS would be more prevalent than the flagellum, which would be a proper falsification test for the "flagellum first" hypothesis. This test failed to falsify "flagellum first" -- it's simple cladistics: | This is why I talk about having a notA prediction to validate your hypothesis. Passing this test (and others as the testing progresses) makes the hypothesis stronger than not being tested. It doesn't make it true, as no amount of testing can accomplish that, and it doesn't make other hypothesis invalid unless they are mutually exclusive. What horizontal gene transfer would predict is that both the flagellum and TTSS could be transfered via HGT from bacteria that posses these trait to ones that don't. Natural selection says that these with the transfered gene would be preserved if they expressed the gene and it provided survival and reproductive benefit. This would predict that we would have some "flagellum first" and some "flagellum second" bacteria (and that this could muddy the evidence). It would also predict that all the species of bacteria where the gene originated would have the gene but not all species of bacteria that received the transfer would (however, those 'with' would likely be classified as a new species that would all have the gene). Thus these hypothesis are not incompatible or exclusive, and both hypothesis could be working at the same time. HGT is not invalidated here as the explanation (and it has been validated elsewhere as occurring), and it's prediction is not tested. The true answer probably lies with a combination of both hypothesis to explain all the evidence. This puts the "sister group" hypothesis in the same position as String Theory (really an hypothesis) compared to the "standard model" in physics, ... and your hypothesis. An hypothesis that is tested by passing invalidation tests is stronger than one that has not. This applies to "the standard model" the "flagellum first" hypothesis, common descent and the ToE, but it does not apply to String Theory, the "sister group" hypothesis, ... or your hypothesis. Your hypothesis is still not tested by a proper prediction. You can't predict something already known to exist, you can just show how the hypothesis explains it.
Curiously, that's not what I said. What I said was that
A falsification test for common ancestry is the genetic data: specifically there should be no ERV's of the same kind in the same locations in the genes. The genetic analysis not only shows these occurring, but occurring with "deep homologies" in a nested clade hierarchy pattern, just as predicted by the ToE. You don't have a proper invalidation test, and you don't have a prediction for something not already known, something new, and preferably something that cannot occur without the hypothesis or theory.
Except that (a) the "creationism model" pretends to do science after "special creation" rather than whole sale tweaking of every piece of evidence (a position they are forced into by the increasing evidence for ToE), (b) that the existence of NHP alone does not explain the existence of ERV sharing, and when the "goddunnit" card gets played every time the "creationism model" runs into problems, then it is constantly being revised to include more "goddunnit" and less natural processes validating the model. This means overall validation by objective evidence is shrinking rather than growing, and (c) invalidation of one hypothesis or theory does not make a single other hypothesis or theory more valid. Enjoy (1) - NHP as in Non-Human Primate? by our ability to understand Rebel American Zen Deist ... to learn ... to think ... to live ... to laugh ... to share. • • • Join the effort to solve medical problems, AIDS/HIV, Cancer and more with Team EvC! (click) • • •
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Genomicus Member (Idle past 1051 days) Posts: 852 Joined: |
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RAZD Member (Idle past 514 days) Posts: 20714 From: the other end of the sidewalk Joined: |
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Taq Member (Idle past 81 days)  Posts: 8488 Joined: |
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