There are numerous definitions of naturalism. Here is one definition with some additional observations from infidels.org:
As defined by philosopher Paul Draper, naturalism is “the hypothesis that the natural world is a closed system” in the sense that “nothing that is not a part of the natural world affects it.” More simply, it is the denial of the existence of supernatural causes. In rejecting the reality of supernatural events, forces, or entities, naturalism is the antithesis of supernaturalism.
As a substantial view about the nature of reality, it is often called metaphysical naturalism, philosophical naturalism, or ontological naturalism to distinguish it from a related methodological principle. Methodological naturalism, by contrast, is the principle that science and history should presume that all causes are natural causes solely for the purpose of promoting successful investigation. The idea behind this principle is that natural causes can be investigated directly through scientific method, whereas supernatural causes cannot, and hence presuming that an event has a supernatural cause for methodological purposes halts further investigation.
http://infidels.org/library/modern/nontheism/naturalism/
For the purposes of this discussion, I’m not going to be too insistent on particular definitions, but it seems to me this captures the essence of naturalism: “More simply, it [naturalism] is the denial of the existence of supernatural causes.”
Personally, I’d be on the side of naturalists or at least agnostic if I felt the origin of life question were satisfactorily resolved. So although I have sympathy for the naturalistic viewpoint, I find insistence on it too closed-minded. I don’t think reality operates in a completely law-like, predictable fashion, it only does so mostly, but not always.
The word “natural” can be equivocated to death and is often equated with “ordinary” or “typical” when it should not be. So if someone insists that naturalism is true but wishes to also be fair with the facts and avoid such equivocations, when they comment on the origin of life, they might say:
The origin of life was an atypical and unique event far from ordinary expectation, but many of us presume it happened naturally since supernatural events are not observed in the lab.
That would be the an accurate way to characterize the state of affairs, but this not what is usually said by advocates of naturalistic origins of life. Most origin-of-life proponents insinuate that the origin of life event was not terribly extraordinary, that OOL fits well within “natural” expectation, even though by accepted laws of physics and chemistry and current knowledge, such an event violates the ordinary (dare I say “natural”) expectation that non-living things stay non-living.
Turning to evolution, if someone insists on naturalism, but is at least fair with our present day knowledge, they might say:
It is NOT typical for something as complex as an animal to emerge from a single-celled organism, but we presume it happened naturally since animals share some DNA with single celled creatures.
Again, that would be the an accurate way to characterize the state of affairs, but this is not what is usually said by advocates of naturalistic evolution of life from the first cell. Evolutionists insinuate that the necessary events to evolve an animal from a single cell must not have been terribly extraordinary because animals and single-celled creatures share some similar DNA — the idea is insinuated even though it is a non-sequitur because something can share DNA via extraordinary or atypical events, at least in principle.
Darwin and his supporters argue that most evolution of complex function proceeded via a mechanism which Darwin labeled “natural selection”. However, if Darwin’s claims actually entail highly atypical events rather than ordinary ones, then his label of “natural selection” for how things evolved would be a false advertising label. If major evolutionary changes require highly atypical events, then “highly atypical events almost indistinguishable from miracles” would be a far more appropriate label for Darwin’s proposed mechanism of evolution. Instead, Darwin’s label of “natural” is presumptuous and unproven at best and completely false at worst. For all we know, natural selection prevents major evolutionary change. Michael Lynch points out:
many genomic features could not have emerged without a near-complete disengagement of the power of natural selection
Michael Lynch
opening, The Origins of Genome Architecture
Many? How about most? No one knows for sure, and thus Darwin’s label of “natural” for “natural selection” is presumptuous. For all we know the correct theory of evolution could be “evolution of significant novel forms by highly exceptional events”.
Animals and single-celled creatures share some DNA, but from all that we know, the transition from single-celled creatures to something as complex as a multi-cellular animal is highly atypical and so far from natural expectation that something of that order of change might likely not happen again in the history of the universe.
If naturalism can accommodate any atypical or extraordinary event as a matter of principle, no matter how improbable, then naturalism can accommodate events that would otherwise be indistinguishable from miracles.
Whether there is a theological dimension with atypical events is a separate question. Can there be an event atypical enough that it warrants supernatural explanations? That’s a philosophical question with probably no formal resolution.
Proponents of naturalistic emergence of biological complexity desperately pretend the sequence of necessary events are not atypical, but rather within the realm of ordinary expectation. Hence they try to render the question of supernatural origins as moot as the question of whether supernatural causes are needed to make ice melt on a hot day.
But imho, efforts to characterize emergence of biological complexity as “not that out of the ordinary” are failing. The more we learn of life’s complexity the more it seems highly atypical events were involved to create them. Perhaps these events were so atypical that they are virtually indistinguishable from miracles of supernatural creation.
I’m certainly not alone in those sentiments:
If we do not accept the hypothesis of spontaneous generation, then at this one point in the history of evolution we must have recourse to the miracle of a supernatural creation
Ernst Haeckel, 1876
Pasteur’s experiments and those followed from 1862 disproved spontaneous generation. Ernst Haeckel’s 1876 quote shows how false ideas like spontaneous generation die a slow death. Haeckel’s quote symbolizes how naturalism seems inherently uncomfortable with anything that suggests a highly atypical event actually happened somewhere in the past.
stcordova,
You can’t make RNA if there is no ATP. So it’s reasonable to suppose that, if there is an RNA precursor to full protein synthesis, there is ATP.
Clearly, there are chemical situations that prevent denaturation of RNA. The Thermophilus bacteria from which we obtain PCR polymerase survive perfectly happily. I don’t think they have a mechanism of mRNA or tRNA repair. Eukaryotes can keep RNAs intact for days. The fact that there are some situations where high temperature is a difficulty, or RNA survival is limited, does not mean that all are.
You keep missing the point. Hot, mineral-laden water emerges from vents at temperatures up to 460°C. But it mixes immediately and turbulently with water down near 0°C. High enough temperatures for reactivity juxtaposed with temperatures low enough for stability.
So I was looking in my copy of Essential Cell Biology for what it had to say about ribonuclease and came up empty. Does anyone else have a copy and can verify this?
Thank you
Additional codons evolve from promiscous activity of tRNA’s and aaRS enzymes, not by new mRNA codons evolving first. The other way around. To begin with, one of the existing codons accepts a tRNA carrying a new amino acid.
In other words, the aminoacyl-tRNA-synthetase enzymes were less discriminatory, and could aminoacylate tRNA’s encoded by the same gene, with multiple different, but probably chemically similar amino acids.
Over time, both the tRNA encoding genes, and the aaRS encoding genes, were duplicated, leaving both copies to become more specific towards their particular cognate amino acid. The new aaRS could become specific for the new amino-acid, and the new tRNA coevolve with it, leaving the original tRNA and aaRS to become more specific towards the originally encoded amino acid.
The new amino acid, while not strictly necessary at this stage, was beneficial to include in one or some of the already existing proteins encoded by the organism’s genome for many reasons (which could be anything from more stable proteins to greater catalytic repertoire of enzymes), causing the retaining and enhancement of the duplicated tRNA and aaRS genes.
Basically, new amino acids find their way into the genetic code through the aminoacyl-tRNA-synthetase enzymes first, not through the sudden emergence of a new codon in mRNA.
There was never a point where an organism carried around a useless and redundant tRNA molecule (with an associated mRNA codon that results in stalling), primed for accepting a new amino acid, but never receiving it because the associated aaRS had yet to evolve.
That’s not how it happened. I’m sorry, but you give the impression of a person who’s never been in contact with the literature on the origin of the translation system. Rather, your posts read to me like someone taking basic molecular biology, having come to understand the basics of modern translation, and now thinks he’s in a position to starts speculating on how an ancient translation system would have looked. For example, your post shows zero awareness of the fact that some aminoacyl-tRNA-synthetases can aminoacylate tRNA with several distinct but chemically related amino acids.
I don’t have that book, I have Molecular Cell Biology (5th edition). Anything in particular you’re looking for? I also have a biochemistry textbook that speaks more specifically about RNase A and how it works.
Nothing in particular. Just wanted to read up. The wiki article mentioned that some cells secrete RNase but gave no reference.
Which biochem textbook, Stryer, Lehninger?
Well, ATP (Adenosine Tri Phosphate) is itself an RNA with 3 phosphate groups attached is it not? Adenosine is an RNA. Now I’m not saying that we just take a pre-existing RNA and attach phosphate groups to it. In biology, the pathway is a little more nuanced than that.
Take glycolysis which creates net 2 ATP, there are 10 steps, with several enzymes (proteins) needed. Here are a list of some of the enzymes:
hexokinase
phosphoglucose isomerase
phosphofructokinase
fructose-bisphosphate aldolase
triosephosphateisomerase
glyceraldehyde phosephate dehydrogenase
phosphoglycerate kinase
phosphoglycerate mutase
enolase
pyruvate kinase
The article on glycolysis points out:
https://en.wikipedia.org/wiki/Glycolysis
Then there is the citric acid cycle, etc.
There are probably other ways to make ATP, but none of them strike me as trivial. In all biological cases anyway, there is a need for pre-existing enzymes (proteins). So the chicken and egg problem emerges yet again.
So where would ATP come around in an OOL context to synthesize RNA?
Belated Merry Christmas.
The point is however if it goes to 0 C, then it can’t do things like peptide synthesis. Part of the reason for the heat is to circumvent the need of ATP.
One can’t fix one problem without creating others. That’s the real point.
And Happy New year!
The point you still seem to be missing is there is a gradient (not smooth but turbulent) You have water at over 450°C and you have water near 0°C. That means you have water at every temperature in between. It means reactions can take place at an optimum temperature if it lies anywhere between those limits and reactants can be stabilised in cooler water. Animals that inhabit the zone around hydrothermal vents live on a knife-edge between being too warm and too cold.
That’s often true. On the other hand we shouldn’t angst over problems that aren’t there.
Merry Christmas.
I’ve read the absurdities, my lack of accepting them and promoting them doesn’t mean I’ve not had familiarity with them.
The point of specific aaRS enzymes is to speed aminoacylation process up so that effectively there IS discrimination and there aren’t random peptides synthesized. The scenario you describe is synthesis of random junk.
So to fix the problem of a stalled ribosome, one creates a ribosome that generates junk, or maybe at best irrelevant parts. What good is a random protein like hemoglobin or insulin in a primitive prokaryotic cell that has no need for them, much less a junk peptide. Would you expect a cell to be viable if it’s peptides are synthesized with random aminoacyl tRNAs?
Lest you think I’m making this up:
Perhaps random? How about almost certainly random.
The author says:
Ok, let’s throw random peptide in a soup of RNAs, do we think they’ll somehow become more functional?
And how about this for a victory dance as far as a “solution”
Beg to differ, the RNA world sounds more absurd now that we know more. But even granting it were plausible, the problem is “extremely difficult”, ergo not ordinary, not typical chemistry. The trend has not been less mystery, but more.
It began with Haekel’s spontaneous generation in the present. When that failed, they moved to spontaneous in the past (aka abiogenesis).
But now we see as a matter of principle, a self-replicator that involves reading of blueprints to re-create itself (as opposed to salt-crystal replication or autocatalytic replication) is not driven to exist like common chemical reactions. These are algorithmic replicators. Algorithmic replicators are not driven solely by chemistry from general conditions, but only by highly specific conditions. At some point, conditions that are rare and specific enough can be deemed atypical or extraordinary.
Emergence of life is atypical.
As if OOL researchers are in a better position to speculate in total absence of facts, especially since they’ve had a 100% track record of failure.
I don’t care if you accept them. There’s a difference between accepting them and IGNORING them. I don’t accept any of the proposed scenarios for the origin of the translation system (because they’re speculative and untested), but that’s not the same as saying they’re all likely to be false because of [this particular difficulty I myself imagined for a scenario I pulled out of my arse].
What part of some aaRS enzymes are known to promiscously incorporate noncanonical amino acids is escaping your comprehension here? You’re not a stupid man, so what gives?
You can’t just ignore a concrete empirical fact like this and (ironically) Intelligently Designing some (seemingly) deliberately unworkable scenario for code-evolution.
Yes, that’s what aaRS enzymes DO. That’s not how new aaRSs incorporating novel amino acids emerge. Setting aside the origin of the translation system and the ribosome, we know of cases where novel amino acids were incorporated in the canonical genetic code. Knowing about how this happens will give you important and useful information about how the translation system is actually known to be malleable.
When new aaRS enzymes emerge, they also aren’t just completely random and incorporates anything and everything at equiprobable rates. I’m sorry, this is a fantasy of your own making that ignores how the actual biochemistry works.
No it isn’t. That’s your take on it, because you don’t know enough. (Or maybe you DO know it, which raises the question why you don’t bring it up and reflect on it? In academic settings, such as writing a thesis, or discussing an issue in a publication, not including known counterexamples and arguments to your own case and discussing them can ruin your fucking career for good reason. It’s effectively a form of lying by omission).
We are talking about a situation where a new amino acid is incorporated in a simpler genetic code encoding fewer amino acids, not about a fully random code. This is the very premise you laid out when you suggested that expansion of the code entailed emergence of a new mRNA codon lacking an associated aaRS enzyme.
Even in this scenario of your own concoction, there’s a genetic code established, encoding multiple amino acids. 6, 8, 10 or however many you like. How does a new amino acid get added to such a code? That’s what I’m describing. Using knowledge of how the genetic code that exists NOW is known to be malleable.
The established codons in this scenario aren’t random (just like now), and the single one that has some promiscous activity due to a less discriminatory aaRS, is still not effectively 50/50 (as you seem to imagine). That’s just not how it works. You really need to get over this silly idea that these things are equiprobable.
Why aren’t they? – you might ask. Because when a new enzymatic function emerges in an already existing enzyme, the new activity is almost always very low compared to the extant one (for well known structural reasons). Meaning, in the case of a mutant aaRS with promiscous activity, the new amino acid is maybe incorporated at a rate of 1 in every 50, 100 or 1000 aminoacylated tRNAs. The point is, the new amino acid being incorporated is rare.
To pick an example using two chemically similar amino acids (serine and cysteine), if 1 out of every 100 codons that code for serine, incorporates a cysteine (a chemically and structurally close one), the overall result of this on translation is not “random junk”. The entirety of the rest of the protein is the same. In fact, depending on how many serine-codons are used for that particular protein, it might even come out at only 1 in every 10 proteins produced, comes with a single cysteine incorporated. None of those 10 proteins are “random junk” by any stretch of the imagination except if, by sheer chance, that particular residue results in lethality if changed (which is quite unlikely).
But if that cysteine is beneficial, selection can work on enhancing the activity of that duplicated aaRS towards more frequent cysteine incorporation. From here on, the codon and the associated tRNA+anticodon can also be honed by selection.
Merry christmas and a happy new year. 🙂
stcordova,
Thanks Sal, same to you 🙂
phoodoo,
I don’t know what you mean by ‘signalling molecules that recognise RNA sequences’, and I’m not sure you do either.
stcordova,
Ouch. ATP is an RNA monomer. Two of the phosphates are cleaved off when RNA is synthesised. The energy of that cleavage drives the reaction forward. You can’t make RNA with AMP. ATP is primordial IMO.
No, don’t. Glycolysis is almost certainly a secondary pathway for ATP synthesis, from long after the origin of RNA. You do raise a relevant point – activated Adenosine molecules appear, in the form of NAD and FAD and Acetyl CoA, all over the energetic pathways, not just as ATP.
But here’s the fundamental question: why Adenosine? What’s special about ATP? Answer: it can stack in a coiled polymer when paired with a pyrimidine chain oriented antiparallel. Adenosine sticks into the centre of the helix as a planar molecule, allowing these molecules to be stacked one above the other, and because of specific atoms on the edges of the purines and pyrimidines, it allows the hydrogen bonding of classical Watson-Crick base pairing. This has nothing to do with its energetic role – that’s mainly the phosphates. Many a molecule could be stuck on the other end and serve just as well. ATP has this central role because it is an RNA monomer. This makes it primordial, in my view.
So how can we test the claim that stochastic processes produced ATP synthase?
He’s probably referring to something like this:
Ribonucleases (RNases) III, P, F cut at definite positions, producing pre-16S, 23S and 5S rRNAs, as well as pre_tRNAs.
Biochemical Pathways p. 212
Looks like the RNases are pretty specific. They don’t just go around willy-nilly snipping at RNA.
The general answer as to what happens when a ribosome encounters an unrepresented triplet is that extension stops. What I’m not clear on is why this is regarded as a killer problem in a primitive system. If there were only one amino acid, and one codon for it (yes, there are functional roles for monotonous peptides)), then it would be rather mutation-sensitive. Instead of substituting another acid, we would get truncated peptides. But the organisms without the mutation would continue to do what they do. Mutation is not fatal to the unmutated. And it does create a potential selective scenario where addition of a second codon reduces the incidence of these premature STOPs, at a small cost (see below).
It is noteworthy that all bar one of the variable codon positions (of which there are just 13 out of a possible 64) is a STOP in at least one species. The suggestion is that STOP is the ancestral position. It is much less damaging to make a wholesale change of STOP->acid than acid -> STOP or acid 1 -> acid 2. The first merely adds a tail whose average length is related by a simple formula to the fraction of codons already assigned. The fewer the STOPs, the longer the tail, so in a primitive code this is milder in a mature one.
Nucleases catalyze the cleavage of phosphodiester bonds in DNA (DNases) or RNA (RNAses). … Nucleases either remove terminal nucleotides (exonucleases) or act inside of the nucleic acid molecule.
Biochemical Pathways p. 156
Mung,
Some do, some don’t. The ones that produce mature functional RNAs within the cell are likely specific. The ones that degrade mRNA etc less so. The ones that coat the cell and protect from viruses etc are much more general and scattergun in their approach.
fifthmonarchyman,
Even if you had, you can’t turn that into an event probability, for reasons extensively discussed in this very thread. And even if you could do that, you can’t include all the asteroids and rocks …
We don’t need any probabilities. All we need is your failure to make a positive case along with your failure to tell us how to test your position’s claims.
There are many different RNases, such as RNase A, B, C, D, II, III and so on. Many of them are specific and used in post-transcriptional regulation and processsing (modifying ribosomal RNA, tRNA and other things).
RNase A has very little specificity and cuts at all pyrimidine nucleotides. Meaning it will cut next to any U and C. Which pretty much means any RNA it comes near will be cut into tiny fragments.
From Principles of Biochemistry 5th Ed:
The p’s are phosphodiester linkages.
I didn’t write it, Rumraket did. Maybe he doesn’t know what it means
phoodoo,
So you want the answer to a question you don’t understand? ‘kay…
There is an unappreciated contradiction in the parallel threads being pursued here – on the one hand, that RNA is such an unstable molecule, its half life can sometimes be measured in seconds. Yet on the other, that its hydrolysis is WAAAY beyond the reach of simple enzymatic catalysis.
Nuclease function – like its complement, ligase – is likely to be pretty fundamental. An enzyme such as topoisomerase combines both. Some very important nucleases are actually derivatives of topoisomerase with the ligase function disabled – eg spo11: a ‘loss-of-function’ topoisomerase derivative that initiates crossover in meiosis, something with very far-reaching effects.
“Where did topisomerase come from?”, I hear the cry. Combination of a nuclease and a ligase, perhaps? “OK, where did … ?”. The brow of Zeus, of course.
<
blockquote cite=”comment-156138″>
Allan Miller:
phoodoo,
So you want the answer to a question you don’t understand? ‘kay…
Gee Allan, why are you quote mining. Are you intentionally being misleading. I wrote:
QUOTE:
“What does it even mean that “they recognize” something?”
I guess Rumraket has no idea what he is talking about. he also dodged the question. Unfortunately you didn’t realize someone on your own team wrote that. I am sure now you will claim it makes perfect sense. Team player you are.
phoodoo,
You still appear not to understand the question you are asking. You want me to explain where something Rumraket said comes from, without YOU really knowing what he meant. So I have to find that out in order to answer it – this question you don’t actually understand, relating to something I did not even say. Go, phoodoo, go! You’re doing great, you really are.
phoodoo,
OK, the quote in full was “Want to take a stab at where signaling molecules that recognize RNA sequences came from?”. Pretty hard to quote mine, though I realise in your world “signaling molecules that recognize RNA sequences” is one.
phoodoo,
What I would understand by ‘recognise’ would be differential binding affinity. Some proteins and nucleic acids have greater affinity for some sequences than for others. But I didn’t – and still don’t – understand what YOU mean when you use the term, whether or not you were parroting Rumraket.
Agree, ATP must be primordial.
With respect to RNA polymerizations, biologically speaking the reaction goes like this:
(NMP)n + NTP –> (NMP)n+1 + PPi
https://en.wikipedia.org/wiki/RNA_polymerase
NMP = Nucleoside Monophosphate (adenosine monosphate (AMP), guanosine monosphate (GMP), cytidine monophosphate (CMP), uridine monosphate (UMP)).
NTP = Nucleoside Monophosphate (adenosine triphosphate (ATP), guanosine triphosphate(GTP, cytidine triphosphate (CTP), and uridine triphosphate (UTP)).
PPi = Phosphate Phosphate Inorganic
Szostak was able to create polymers in his ribozyme engineering experiments. When he said RNAs, it wasn’t clear what was attached to them.
Here is the paper.
https://www.cs.duke.edu/courses/spring04/cps296.4/papers/BS93.pdf
Anyway a diagram for the benefit of the readers. It has two RNAs connected together. It shows in principle how they can create long plolymer strands of RNAs.
“BASE” refers to the actual distinguishing part of the RNA A, C, G, U…
I didn’t write the term, to recognize. Rumraket wrote the term, to recognize. So I asked him what it meant, no answer. I asked you, if you care to take a stab at what it means to recognize-then you ask me what I meant when I wrote the term.
I wonder what you mean by what do I mean. If I had to guess I would say you mean you are trying to be the best team player you can be, and deflect the criticism towards Rumraket-by claiming it is me misusing a term, when I asked what the heck it means to say that.
Team MVP trophies will be handed out at the end of the year. You have a tough fight this year, with Alan doing his best to decide preemptively who is right and who can say what.
Larry Moran mentions my former professor of Quantum mechanics, James Trefil while Trefil was at George Mason University. Trefil is better known for his work on cosmology and astrophysics than OOL. Moran nonetheless praises Trefil’s work on OOL.
In any case, here are Larry’s comments:
http://sandwalk.blogspot.com/2009/05/metabolism-first-and-origin-of-life.html
Larry says:
Nevertheless, Trefil argues elsewhere in a book about Extra Terrestrials (or lack thereof) that we live on a privileged planet — therefore it would be an atypical argument. He was rather horrified when I informed him ID proponents hailed many of his works on Dark Matter and the privileged planet. He was famous for saying:
phoodoo,
You asked me the question with no attribution to Rumraket. No quotes round the phrase, no nothing. I’m not about to re-read entire threads just in case the words you use are not your own. Your clarification that they were not your words, and you didn’t understand them anyway, merely confirms what I said.
Would it be too much to ask that you grow up a little in 2017?
phoodoo,
You will note that I actually did both.
stcordova,
Likewise, Moran argues elsewhere that […]. Selective endorsement by Authority X is a double edged sword.
Allan Miller,
You asked me what I meant by Rumraket saying that signaling molecules recognize RNA sequences, and now you are saying I should grow up?
Gee, if I didn’t know better I think you might be trying to rile me up there ol boy.
Do you have an online cite for the full context of this quote?
Phoodoo is not aware that I put him back on ignore it seems. I’m only aware of the fact that he’s still trying to argue in this thread because Allan Miller is responding to him. I will not waste my time with taking him off ignore again.
I will give a quick elaboration on what I meant by a signaling molecule that recognizes RNA (and how it does so).
In eukaryotes, transcription encompasses the conversion from mRNA to so-called mature mRNA. This is described as post-transcriptinal modification and involves anything from after producing the transcript, through splicing out introns, to adding the special 5´-5´ GTP cap. Once this has been done, this special bond is recognized (by it’s shape and properties of attraction and repulsion) by special transporter proteins that “marks” the mature mRNA for transport to the endoplasmic reticulum, where the ribosomes are located. That “marking” of the mRNA by transporter proteins, which in a sense tell the cell where these mRNA molecules are supposed to go, is what I call signaling molecules. That’s it.
How do molecules recognize each other? Structure and charge. They fit together, and opposite charges attract each other. They’re not like, sentient, or have eyes.
They’re sorta like very structurally complex magnets with tiny spots that attract and repel opposite charges. Some fit together very well, because the lumpy surface features of one fit very well into the grooves and valleys in another, and along this surface are those local spots of attraction and repulsion. You find a positive charge on one molecule, where it fits with another there will be a negative charge on the other molecule. Otherwise it won’t “fit”.
To say they recognize each other is of course really just a metaphor for this phenomenon of a structural and electromagnetic good “fit”.
And now phoodoo can do what this whatever he wants, I don’t care.
But he’s not a religious man, so what’s his actual opinion?
If I was a religious man, I’d say other stuff than I do. Therefore God!
Wait.. what?
Good thing there isn’t a rule about keeping comments PG13!
phoodoo,
No, I asked what you meant by it – you did not originally attribute it to anyone. Fucksake phoodoo. Anyone with a scroll wheel can see what was said, there’s no need to rehash it endlessly (I also realise that NO-ONE gives a flying fuck).
ONLINE? No, but I have the book. Trefil was actually arguing we should try to preserve our species since we might be the only intelligent life in the universe. The sense of what he was saying was that he wasn’t a particularly religious man, but that we should value life on the planet because we are so unique.
The book is:
Are we Alone
When I spoke to him, that particular quotation of him didn’t bother him as much as YEC citing his chapter in Dark Side of the Universe entitled: “The Five Reasons Galaxies Can’t Exist”. He really took exception to that.
As far as I know, he hasn’t taken exception to creationists, myself included for that quotation about him if he were a religious man.
All that said, his obvious sense of our specialness in the scheme of things drew some negative comments when he wrote this book:
Are We Unique
I mentioned Ryszard Michalski at UD here:
Pioneer of non-Darwinian Intelligent Evolutionary Design
We’re special.
On the first day of class on Quantum Mechanics, he makes a passing remark about how miraculous the structure of the universe is.
He also thinks the human soul or species is special.
Nevertheless, he’s gone on a campaign against ID.
That said in his book Are We Unique, the first chapter opens:
Mrs. Trefil told me that was her favorite book of all the books her husband wrote.
I don’t much care what Authority X or Authority Y thinks. Such quotes are as old as Creationism, but carry zero weight.
If I were a flying pig, I would not eat bacon. But would, hopefully, make it.
Maybe for you, but not for me. But the discussion is not about proving God, I was arguing whether OOL or other things are atypical, and if atypical, how far from natural expectation.
Those discussion can be carried out with a modest degree mathematical precision when considering chemistry and physics involved.
The theological dimension of atypical and extraordinary is a separate discussion.
If naturalism is comfortable with atypical events, I see no reason why we can’t as an academic exercise if we conclude something like OOL or biological evoluition progress by atypical events far from ordinary expectation. I argue that they must have proceeded by atypical and extraordinary events.
As to the question whether there must be a supernatural explanation, I remarked that I think there is no formal resolution to that question. Each person makes his own decision which explanation is most believable for sufficiently atypical events. I believe God was involved.
First of thank you for you comment as it gives me an opportunity to clarify because I see from your reaction that I was not as clear as I could be.
Even though it is true a specific protein can be modified in numerous locations without compromising primary function, in some cases probably as much as 50% or more can be changed to alanine-like amino acids, changing the codon assignments by having some random or imperfect aminoacylation of tRNAs can affect multiple amino proteins.
When a researcher is trying to determine the important parts of a protein, he mutates several amino acids, and if there is no major effect, he knows the important positions are elsewhere. But even if he can mutate 90% of the protein and still have function, he can’t randomly mutate the protein and expect it will still work.
For example say a protein has 200 residues. 180 aren’t really senstitive, but he randomly mutates 20 amino acids. Odds are he’ll hit a critical region and disable it. But let’s be generous and say he didn’t.
If there are 100 proteins, and now we change the codon assignments globabally. The result is we improve 1 proteins effectiveness, and then break at least 10. This creates a net junk situation.
Here is a specific example, involving the Beta-turn. We would not want random codon assigments randomly inserting or deleting these things. We could easily delete a critical turn in a protein by reassigning the proline amino acid due to one of those supposed global changes to codon assignments.
Also bad is putting a proline probably where an alanine-like amino acid is needed to maintain an alpha helix.
So my comment stands, the scenario you suggest of shifting codon assignment tables is like changing the syntax for software on already written software. It makes a mess of things.