HIV can be safely classified as a hypermutator and its been around for over a hundred years. It has a short generation time and accumulates humongous numbers of mutations. The HIV data is enough to test GE and GE crashes its in face.
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E. coli turn on hypermutation via the so called âSOS responseâ when under stress, where they use low fidelity polymerases over high fidelity to obtain more mutations.
The fact that E. coli want MORE mutations under stress conditions directly refutes genetic entropy.
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Not if this is a specific deterministic process independent of mutations solely due to reproduction errors.
What part of âlow fidelity DNA polymeraseâ do you not understand?
How would you determine whether a process was deterministic or not?
What is your definition of genetic entropy?
If an organism turns up mutation rates to improve fitness, it directly refutes genetic entropy.
Genetic entropy claims that there is an inexorable decline in fitness over time of an organism due to mutations.
If more mutations can cause a fitness benefit than fewer, then GE is debunked.
Genetic entropy implies that a higher fidelity DNA polymerase MUST ALWAYS be better than low fidelity DNA polymerase under ALL scenarios.
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As far as I understand it GE is targeted at mutations that occur during replication and are not fixed by error correction. This could be a real problem and it may be premature to rule out the idea of GE.
Hypermutation from the adaptive immune system is different and used in immune response is a biological process to keep the organism healthy against pathogens.
The targeted use of hypermutation is different than the random mutation from reproduction which can happen almost anywhere in the genome.
If you think that more mutations cause fitness benefit, I suggest that you treat yourself with radiations or certain mutagenic chemicals 
It is supposed to apply to all mutations that occur in a cell and are passed on to any offspring cell. Somatic cell line should in principle to be subject to GE too, if GE was a real thing, as these too should gradually decay to accumulating mutations as they go through many consecutive replications.
It seems to me that if GE was true and adaptive mutations were overwhelmingly rare, of overwhelmingly small effect when and if they occur, and basically all other mutations were deleterious, then we naively might expect hyper-speed antibody decay with the million-fold increase in the mutation rate, rather than highly successful antibody adaptation.
I will happily agree this question depends on the exact values for things like population size, mutation rate, and the DFE for antibody mutations, but without these numbers we canât just self-servingly assume the concept of GE is compatible with the adaptive immune system.
Only in the sense that the mutational target is restricted to a particular gene encoding antibodies. If it was really true that the vast, vast, vast majority of mutations were weakly deleterious, and that there is only an infinitesimal small minority of mostly weak-effect beneficial mutations, itâs just not clear to me why that should nevertheless make affinity maturation a plausible exception to the concept of GE.
What kinds of population sizes are we dealing with when the immune system adapts, and what are the selection coefficients of the adaptive mutations that occur then? Iâm not asking you these questions because I expect you to know and answer them. But I think it should lead anyone who is a proponent of GE, and who has genuine curiosity about the subject, with more unsolved questions and potential issues that need to be sorted out.
And we donât need just more verbal excuses that can be invoked to just handwave away all questions and criticisms. Again, someone needs to do some actual math here and show, using real values garnered from experiments and observation, how and why GE should be considered compatible with the process of antibody affinity maturation and somatic hypermutation.
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Nobody is suggesting that GE is targeted at mutations that do not occur. Iâm not sure what your intention is here.
Simply to clarify the definition of genetic entropy. Rum is discussing somatic mutations. WD includes mutations during the adaptive immune process.
The only thing that makes logical sense are mutations during reproduction as those are potentially fixed in the population.
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The reason it is so abundant is that Raoultâs methods have not been satisfactory in 22 of his previous papers.
Furthermore, his own publisherâs review stated that his HcQ paper had âgross methodological shortcomings.â
Kindly explain to me, Gilbert, why you are a better judge of Raoultâs methodology than the publisherâs review?
Have you actually read â with care â the publisherâs review or the detailed examination of his publications by Elisabeth Kis?
Best,
Chris Falter
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Several of the papers give explanations of the mutations from ancient sequence to current sequence, as indicated by my comments. Is that what youâre looking for?
One example I had in mind was the CERN Higgs Boson experiments. The outcome of particle collisions is non-deterministic due to quantum effects (and perhaps other factors, I welcome elucidation from physicists!). But the standard particle model indicated that the existence of the Higgs Boson would be associated with a certain distribution of outcomes over thousands of experiments. When that distribution was found, the Higgs Boson was considered confirmed by physicists.
String theory is not at all what I had in mind; it is an attempt to mathematically unify relativity and quantum mechanics.
Regards,
Chris
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Clown.
During stress-induced hypermutation mutations happen in other parts of the genome as well, some of them unselectable (which is what GE wants right, although it prefers them deleterious?)
Mutations that occur during hypermutation are due to replication errors.
What is needed is a model how this happens that can be generalized. The common descent claim to be robust needs to explain differences.
This is a very interesting idea and a good point for discussion. The difference here is you are trying to explain the existence of a particle and not its origin. We observe functional information or functional sequences in biology. Explaining their origin is a much more difficult problem and may be beyond the reach of science. Hence the suggestion to take this burden away from the model.
This is a distinction without a difference, in my opinion.
Quantum physicists theorize to explain the origin of their observations. Often, the origin is a series of interactions between particles.
This is not fundamentally different than the work of evolutionary biologists; itâs just in a different branch of science.
Biologists also observe the mechanisms for new functional information and functional sequences. These observed mechanisms make the problem scientifically tractable, and I am puzzled why anyone would think otherwise.
I think you would learn a lot by reading the summary article I recommended in post 57, along with its key citations. You will need to invest some time, of course, but since you are clearly interested in the issue, Iâm sure you will find it worthwhile.
Best,
Chris
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I deleted the previous post because I managed to reply to my first post instead of editing it.
Heredity is not a law of chemistry or physics, which is why it doesnât refute my claim.
First of all, Iâm not switching anything. My initial responses were aimed at the âwhat is information?â question within the ID argument. Abiogenesis is the answer to the âwhen does the ID argument first apply?â question.
Secondly, you are changing my statement of âno chemical lawâ to âno natural processesâ.
Donât blame your poor reading comprehension on me.
Heredity is a natural process guided by chemical and physical principles which is why it soundly refutes your claim.
Irrelevant. I never responded to your definition of information within the context of ID, but to your claim that no chemical or physical laws could explain the exact order of nucleotide sequences in extant organisms.
You should really blame your inability to write clearly.
Itâs true there is no âlawâ that says what the order of bases has to be, but your latter claim doesnât follow from the former, and itâs wrong. There is no âlawâ that says what tomorrowâs weather will be, but tomorrowâs weather is still due to physics and chemistry. The nature of atoms and molecules (of all the atoms that make up the solar system, the Sun, the Earth, and the atmosphere) is what determines tomorrowâs weather through their mutual interactions through all the fundamental forces of nature. And the nature of atoms and molecules that make up a string of DNA and itâs chemical and physcial surroundings explains why we have a particular string of DNA: and yes we call that explanation heredity.
It certainly refutes your claim that "The chemical nature of atoms and molecules does not require or impose any particular order of the bases, because the chemical nature of atoms and molecules of the ancestral DNA molecule and those of itâs surrounding environment strongly determines the descendant sequence
Thereâs going to be a physical explanation for why any particular piece of genetic material comes out the way it does even if not derived through complementary basepairing from some ancestral template, just like thereâs a physical and chemical explanation for Earthâs weather pattern going back before even the origin of the planet.
I think I understand it perfectly well, thanks. Itâs all just based on the idea that some particular arrangement is just one out of all possible arrangements(be it order of bases in a sequence of DNA, letters in a sentence, atoms in some structure) and if there are lots of possible arrangements it would be very unlikely to pick the specified one by chance in one or a few attempts.
Thatâs basically all ID arguments about information ever.
Sequence information is not the only kind of specified complexity. The arrangments of the atoms that make up the mountain can take an innumerable number of other forms only one of which is the Mt Everest.
Thatâs specified complexity, by definition. You just specified it. Thatâs literally what specified complexity is, complexity you specify. You having now specified that sequence, it would be extremely unlikely to blindly and randomly pick it from the total set of all possible letter sequences of equal length.
Of course those kinds of after-the-fact probabilities are meaningless. They donât tell us how anything came to be. Finding a DNA sequence and then specifying it, and then pretending because itâs low odds for a blind and random sampling of all sequences of equal length to find it, doesnât tell us anything about how it came to be. The Mt Everest didnât emerge through a blind random sampling of the total structure space of an equal number of the same types of atoms, thereâs no reason to think thatâs how the first genetic polymer had to originate either.
The act of specifiying it is what makes it specified complexity, as opposed to just complexity. Nobody was specifying some sequence of DNA or amino acids before we sequenced them as best we can tell.
Thatâs a false trichotomy, since clearly there is another way in which physics and chemistry can explain how and why some particular complex arrangement came to be, even if that does not reduce to some particular law of physics, but rather has to do with the interactions between a large number of atoms and molecules through their mutual forces of attraction and repulsion, strongly contingent on prior(and initial) conditions of the system.
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A thousand times yes. This whole notion of âspecifiedâ complexity as used in IDC is just another way of presupposing the conclusion: if something was specified, there must have been someone who specified it. But the existence and activity of âsomeone who specified itâ is precisely what IDC has to show, and cannot be shown by any of the methods offered. Itâs like Beheâs constant conflation of âfunctionâ and âpurpose.â
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Agreed. @DaveB, do you know of any exceptions? Letâs get a prediction from âID Theory.â
I have a library of random, 110-residue protein sequences that are juxtaposed essentially as dimers, but very constrained to fit in (and not disrupt) a particular structural motifâthe immunoglobulin fold.
@DaveB, how many of those dimers do you predict that one would have to screen to get immunoglobulins with measurable beta-lactamase activity?
@DaveB, do you now see the circularity of your argument?
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Even William Dembski cannot explain CSI in any meaningful way (See Dembski 2005). First itâs a probability, then itâs an upper bound on probability, but he still uses it when the probability is great then 1.0 (which is nonsensical). Dembski calls it an Information Measure, but it is not. The CSI value is -2*log(p) where p is supposed to be a probability but isnât. Ignoring those problems and a host of more serious troubles (See Elsberry and Shallit 2011, and Devine 2014), a high value of CSI indicates simplicity not complexity - the opposite of his claim. Dembski uses Kolmogorov Information as a measure of complexity, but the scale is backwards: Low KI means high CSI and vice versa. Either way, Dembski never establishes a connection between this measure and biological complexity, and never published corrections.
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