How Comfortable is Naturalism with Highly Atypical Events?

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.

530 thoughts on “How Comfortable is Naturalism with Highly Atypical Events?

  1. stcordova,

    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.

    But you have seemingly ignored the logical possibility that the event itself is quite routine (the actual origination of replicators) but that ecology and finite resources prevent the retention of multiple origins indefinitely. It doesn’t much bother me if it’s ‘atypical’ or not, but I don’t see that we are in a position to say that the probability of the event is reliably indicated by the number of origins that can now be detected.

  2. stcordova,

    Those discussion can be carried out with a modest degree mathematical precision when considering chemistry and physics involved.

    Only if one insists that the probabilities are independent, and biology does not even come into it.

  3. stcordova,

    It makes a mess of things.

    In a modern organism, where a 20-acid table has been in existence for something like 3 billion years, and several thousand proteins are made, it makes a mess of things. This is not a good reason to assume perennial brittleness in codon assignment from the word go.

  4. Why pick proline?

    It is interesting that the fault tolerance of the genetic code – the ability of ‘accidental’ substitutions to be tolerated – is felt to be indicative of Design, and yet the code is held to be so brittle that those self-same substitutions cannot occur.

  5. Allan Miller:

    Why pick proline?

    It was the most a-typical, next to Glycine.

    Although I must admit I have a special place in my heart for Lysine. But of late I’m starting to warm to Serine, Threeonine, and Histidine too. 🙂

    Proline acts as a structural disruptor in the middle of regular secondary structure elements such as alpha helices and beta sheets;

    I chose Proline as an example because it made the point more forcefully than any other random amino acid change. Randomly putting Prolines due to tRNA or codon table assignments won’t be good. We might be able to say the same of Glycine (Ramachandaran Plot depicted below):

    So, at the very least we need a tRNA table that is stable with respect to Proline, imho. Can’t mess with that one. Probably same with Glycine. One shouldn’t put such a loose cannon randomly on a protein.

  6. stcordova,

    It was the most a-typical, next to Glycine.

    Exactly. So you pick that most favourable to your case. If all acids were as different in effect from each other as Proline is from the rest, you might have a case. But “substitutability is highly improbable because – well, look at Proline!” does not really do it.

  7. I should point out, there is a quite a lot of opportunity to suppose not all amino acids are essential since there are the terms “essential” an “non-essential” amino acids.

    https://en.wikipedia.org/wiki/Essential_amino_acid

    An essential amino acid, or indispensable amino acid, is an amino acid that cannot be synthesized de novo (from scratch) by the organism, and thus must be supplied in its diet. The nine amino acids humans cannot synthesize are phenylalanine, valine, threonine, tryptophan, methionine, leucine, isoleucine, lysine, and histidine (i.e., F V T W M L I K H).[1][2]

    Six other amino acids are considered conditionally essential in the human diet, meaning their synthesis can be limited under special pathophysiological conditions, such as prematurity in the infant or individuals in severe catabolic distress.[2] These six are arginine, cysteine, glycine, glutamine, proline, and tyrosine (i.e. R C G Q P Y). Five amino acids are dispensable in humans, meaning they can be synthesized in the body. These five are alanine, aspartic acid, asparagine, glutamic acid and serine (i.e., A D N E S).[2]

    So the word “dispensible” or “non-essential” doesn’t really mean what one may think it means in terms of making proteins!

  8. Allan Miller:

    But you have seemingly ignored the logical possibility that the event itself is quite routine (the actual origination of replicators)

    Something can be routine but still far from ordinary expectation. God can specially create millions of creatures. It might be part of his “routine”.

    If what you are really saying is that it complex replicators routinely emerge well within ordinary chemical expectation, then we clearly see no evidence of that in the lab. By complex, I mean something that reads a blue print, and self-replicates from that blue print. I’m not referring to replicators like salt-crystals or autocatalytic reactions. There are lots of automatic chemical replicators (replicators that don’t read, translate, and then make copies of themselves), but replicators that can break down if a blueprint breaks down.

    But you have seemingly ignored the logical possibility that the event itself is quite routine (the actual origination of replicators) but that ecology and finite resources prevent the retention of multiple origins indefinitely. It doesn’t much bother me if it’s ‘atypical’ or not, but I don’t see that we are in a position to say that the probability of the event is reliably indicated by the number of origins that can now be detected.

    We can make inferences based on chemistry. RNA synthesis is a chemists nightmare as a matter of principle. In contrast, the hydrolysis of amino acid peptides in water is ordinary and expected.

    The chemistry of life (any life) proceeding from a random mix of chemicals that involves reading of a blue print, doesn’t seem within ordinary expectation, and specifically a self-replicating 3D printer that uses DNA-RNA-Proteins in the replication cycle.

    One thing I should add, the reason gradualism and selection is not indicated is because of the quantum mechanics and particle physics that is expressed in the science of chemistry itself and iconified by the periodic table (below).

    There is not a gradual transition from one atom to another, but rather discrete (dare I say digital), transition. In comparable manner, there isn’t really a gradual transition from one chemical species to another. We might only gradually change concentrations, but not fundamental chemistries. Though DNA is similar to RNA by removing an oxygen (hence then prefix “de-oxy” in DNA), it is still a different chemical species and will entail discrete changes.

    The more things that are tied to a particular molecule or reaction mechanism, the more an all-of-the-sudden transformation is indicated as a matter of principle. I alluded to one such case regarding the codon/aa-tRNA assignment of proline. If we substituted Methionine start codon with proline, that would not be good and would entail global change in the way to do business, assuming business could even proceed in the first place.

    Look at the 10 steps of the glycolosis cycle. In the first step a glucose is phosphorylated. Glucose is either phosphorylated or it’s not, there is no gradual step in between in practical terms. The reaction pathway requires ATP to power the reaction. There might be other ways power the phosphorylation of glucose other than ATP, but the point is, the emergence of those pathways as far as the reactants is discrete — the reactant is either there or it’s not, there is not much sense in saying it’s half there. Now if the Gibbs energy profile is favorable, then an enzyme is not strictly speaking required to eventually move the reaction forward, providing the reactants don’t themselves self-degrade. But to the extent the reaction must take place according to a schedule, then the enzyme must be present.

    But in any case, there are definitely aspects of biology that don’t lend themselves to gradualistic transformations because those transformations happen at the molecular level where things are effectively digitized and tranformations are punctuated as a matter of principle.

  9. stcordova: But in any case, there are definitely aspects of biology that don’t lend themselves to gradualistic transformations because those transformations happen at the molecular level where things are effectively digitized and tranformations are punctuated as a matter of principle.

    Therefore…..

  10. stcordova,

    If what you are really saying is that it complex replicators routinely emerge well within ordinary chemical expectation, then we clearly see no evidence of that in the lab.

    ‘The lab’ is hardly the best place to look. The conditions where life emerged were likely very dirty and involved a complex mixture of chemical and physical conditions. The fantasy ‘if OoL were possible it would happen in a lab’ is just that; a fantasy. We are talking about a planet 10,000 miles across, with a vast array of different physical conditions with perhaps half a billion years to play with, vs – how many, exactly? – labs going to great pains to decompose the problem in an experimentally repeatable setup – ie, eliminating as much mess as possible. This is hardly a broad sample of the space of possibilities.

    We can make inferences based on chemistry. RNA synthesis is a chemists nightmare as a matter of principle. In contrast, the hydrolysis of amino acid peptides in water is ordinary and expected.

    In your answer, you just ignore biology, again. Sure, I haven’t solved the problems. No-one has. Nonetheless, replicators could perfectly conceivably be popping out of vents on an almost daily basis, and no-one would ever know. Because they aren’t looking. What would be the signal, and how long would it last before something ate it?

    Look at the 10 steps of the glycolosis cycle

    Like I already said, glycolysis is an irrelevance, many years beyond a realistic OoL scenario. The modern cycle is peptide catalysed. It’s not going to be a primordial source of ATP, and ATP has in any case a fundamental feature: its stereochemistry, which is selected by its role in RNA, not by its role in enzymatic catalysis. The chicken-and-egg problem does not involve time machines shuttling the products of glycolysis back to synthesise the RNA that makes the peptides that catalyse the reactions that specifiy and make themselves. OoL researchers are not completely stupid.

  11. stcordova,

    But in any case, there are definitely aspects of biology that don’t lend themselves to gradualistic transformations because those transformations happen at the molecular level where things are effectively digitized and tranformations are punctuated as a matter of principle.

    Yeah, you seem to have wandered off the page a bit there …

  12. Mung:
    That periodic table of the elements looks remarkably atypical and naturalism appear comfortable with that.

    Except for the fact naturalism cannot account for atoms. I would think that would make it very uncomfortable

  13. Mung,

    That periodic table of the elements looks remarkably atypical and naturalism appear comfortable with that.

    What would a typical periodic table look like?

  14. stcordova,

    If we substituted Methionine start codon with proline, that would not be good and would entail global change in the way to do business, assuming business could even proceed in the first place.

    So, we can reasonably conclude that never happens, then. Leaving us with the codon changes that aren’t start-Met->Pro.

  15. Allan Miller:

    So, we can reasonably conclude that never happens, then. Leaving us with the codon changes that aren’t start-Met->Pro.

    To clarify, there are abundant alternate start codons in biology, but these are gene specific. The issue I was highlighting was difficulty of GLOBAL codon/aa-tRNA assignment changes, not gene specific changes. Furthermore, the alternate start codons still result in the metheonine being put in the start position of the protein, so there isn’t a re-assignment of the aa-tRNA.

  16. stcordova: The issue I was highlighting was difficulty of GLOBAL codon/aa-tRNA assignment changes, not gene specific changes.

    Right, but as I pointed out, this isn’t so much a reassignment as it is the inclusion of an alternative amino acid at a low level of expression.

    There’s a reason the genetic code is now pretty much universal (and was already established in it’s extant form by the time of LUCA). Yes, even small changes to the code now will have global consequence for probably many hundreds of proteins, and this will in the vast majority of cases result in a huge fitness cost. If not lethality, depending on the organism and particular codon in question. As Francis Crick put it, the code has become “frozen”.
    It should be noted, it is not so frozen that any and all changes are lethal, even if the change is global.

    On subject, I recently read a paper detailing an experiment where a population of bacteria had every single codon which codes for Trp evolved to accept a synthetic amino acid. Over twenty thousand tryptophanes were replaced with a synthetic but chemically similar amino acid. In the end, the bacteria were able to survive and reproduce in media completely absent Trp (with the Trp biosynthesis pathway removed).

    Chemical Evolution of a Bacterial Proteome.
    Hoesl MG, Oehm S, Durkin P, Darmon E, Peil L, Aerni HR, Rappsilber J, Rinehart J, Leach D, Söll D, Budisa N.

    Abstract
    We have changed the amino acid set of the genetic code of Escherichia coli by evolving cultures capable of growing on the synthetic noncanonical amino acid L-β-(thieno[3,2-b]pyrrolyl)alanine ([3,2]Tpa) as a sole surrogate for the canonical amino acid L-tryptophan (Trp). A long-term cultivation experiment in defined synthetic media resulted in the evolution of cells capable of surviving Trp→[3,2]Tpa substitutions in their proteomes in response to the 20,899 TGG codons of the E. coli W3110 genome. These evolved bacteria with new-to-nature amino acid composition showed robust growth in the complete absence of Trp. Our experimental results illustrate an approach for the evolution of synthetic cells with alternative biochemical building blocks.

    Trp is believed to be evolution’s latest addition to the genetic code[10] and demands the highest metabolic synthesis cost of all proteinogenic amino acids. Therefore, it has relatively low abundance in proteins (~1% i.e. about 20,000 residues in the whole E. coli proteome[11]) and is encoded by a single codon (UGG). It possesses special biophysical properties which allow for its participation in numerous interactions (π→ π stacking, hydrogen bonding, cation-π interactions). Therefore, Trp plays a major role in protein stability and folding, and participates in mediation processes such as receptor-ligand interactions or enzyme-substrate binding. Thus, substitution of Trp with other cAAs can often result in misfolded proteins and inactive enzymes, ultimately causing cell death

    Suitable auxotrophic strains are a prerequisite to apply selection pressure for amino acid analog usage by the cell. We have chosen the E. coli K12 W3110 derivative CGSC# 7679.[17] In this strain, the whole Trp biosynthesis pathway is removed (ΔtrpLEDCBA). In Trp-auxotrophic E. coli strains, Trp and its analogs enter the cell via transporter-mediated uptake.[18] This mechanism might be a ready-made target for the cell to shut down analog uptake and avoid disadvantageous consequences of incorporation into proteins. Therefore, our experimental setup was based on indole (Ind) and β-thieno[3,2-b]pyrrole ([3,2]Tp) (Figure 1), which enter bacterial cells by passive diffusion through the membrane.[19] To convert these precursors intracellularly into Trp and [3,2]Tpa respectively, we equipped CGSC# 7679 with the plasmid pSTB7[20], which harbors the Salmonella typhimurium Trp synthase (TrpBA), an enzyme known to efficiently convert [3,2]Tp into [3,2]Tpa.

    This is nothing short of astonishing.

    But it is also a fact that there’s a strong phylogenetic signal in the aaRS enzymes and tRNAs that reflect the evolutionary history of the code and translation system, pre-LUCA. There are many interesting and curious facts surrounding the translation system and the charging of tRNA’s with their cognate amino acids.

    As I described earlier, the code is thought to have evolved some of the way to it’s “universal” form, in some small part at least, by promiscous aaRS activity, charging tRNAs with multiple (but usually chemically similar) amino acids. This facilitates code expansion by allowing duplications of the aaRS and associated tRNA to diverge from their “ancestors” (allowing both to become specific for the new amino acid), while the originals becomes specific for the “old” amino acid. The new tRNA then replaces the function of an already existing redundantly used codon, or possibly takes up a new unused one. Needless to say, this would have had to happen at a time when the genome of the organism was small, in that it contained relatively few protein coding genes compared to modern organisms, and had smaller amino acid alphabets, facilitating a greater beneficial effect from including a new amino acid, to compensate for the fitness cost of an occasionally mistranslated protein (which is further compensated for by the promiscous side-activity of the aaRS being low).

    In is an interesting fact that the rate of duplication of aaRS (and tRNA) genes is very high. As far as I can gather, researchers don’t even know why, but they’re duplicated at an unusually high rate and it seems to result in interesting functions. See for example: Trans-oligomerization of duplicated aminoacyl-tRNA synthetases maintains genetic code fidelity under stress.

    Gene duplication is thought to have played a major role in the evolution of aminoacyl-tRNA synthetases (aaRSs), a family of essential enzymes that provide the aminoacyl-tRNAs substrates for protein synthesis at the ribosome. Contemporary aaRSs are partitioned in two classes called class I and class II (3). Enzymes of each class have evolved from two unrelated ancestral proteins that arose previous to the last universal common ancestor (LUCA) and are thought to have had a broad specificity for tRNAs and amino acids (4,5). Generation of the current aaRSs was proposed to have occurred by multiple successive events of gene duplication and diversification, paralleled by a progressive narrowing of specificity for tRNAs and amino acids by the newly arising enzymes (4,6). Whereas these events are ancient, predating the apparition of the LUCA, other more recent events have sprinkled genomes of the three domains of life with duplicated aaRSs genes of which only a few have been empirically characterized (7–9). These duplicated aaRSs were observed to have diverged evolving distinct features. In some other cases, divergence has originated truncated aaRS paralogs that do not conserve the original aminoacylation function and have adopted new roles (10–12).

    It is an interesting fact that there are organisms living now, today, with promiscous aaRS enzymes that misincorporate the “wrong” amino acid on their tRNAs. And as expected, since this is probably strongly deleterious if not lethal, these organisms have ways of fixing this, though strange and unconventional. For example, I recently read about this bacterium that some times mischarges tRNA with Asp instead of Asn due to a “defective” promiscous aaRS^Asn enzyme. The organism deals with this by having another enzyme chemically convert the Asp amino acid charged on tRNA, into the correct Asn one, before it goes on to partake in translation.

    What a strange and convoluted way to “fix” this. The organism has both an aaRS^Asn and aaRS^Asp, but as stated one of them is promiscous and will accept both Asp and Asn when it chargest tRNA. It would seem a much simpler fix that the aaRS simlpy worked correctly. But no, this organism seems to have evolved an entirely new enzymes just to compensate for this promiscous aaRS.

    Why am I telling you all this in response to what you said? The point is to get you to think about how things could be different from how they are now. These systems, whether translation system, flagellums, the ribosomes, membrane transporter proteins or what have you. They didn’t evolve by modern protein X, binding to modern protein Y, then accidentally and luckily inserting in fortuitous position in the membrane or whatever.
    It is not just that back in time, before LUCA, that for example the translation system just had fewer parts, the parts it DID have were also different from how they are now (and through phylogenetic methods such as ancestral sequence reconstruction), provably so. Different in a way that compensates for the absense of components we now detect as essential to these system’s modern function.

  17. stcordova,

    The issue I was highlighting was difficulty of GLOBAL codon/aa-tRNA assignment changes, not gene specific changes.

    I got that, but you were picking the most extreme example to do it. This is SOP, and it is much the same as the ‘many mutations are deadly, therefore they can never be beneficial’ schtick one sees. There is not an equiprobable distribution of damage caused by GLOBAL codon reassignment throughout the table, nor throughout evolutionary history.

  18. The error tolerance of the codon table to non-silent substitutions is often held to be evidence of its ‘design’. An accidental substitution of one codon position often results in a chemically similar acid, such that the product is about as useful as the ‘properly’ translated version.

    This just affects one position in one protein molecule, but this fault tolerance is itself supportive of the possibility of global reassignment. Given that global substitution is acknowledged to be more likely damaging than not, the least damaging would involve subdivision of a codon group between two acids of similar property. Add in the stochastic and mechanistic variation of codon usage – codons are not each represented a precise 1/64th of the time – and you have a circumstance where occasional substitutions could be tolerated, for similar acids in little-used codons, without it being an everyday occurrence.

    For example…

    Glutamic acid and aspartic acid differ only by an extra -CH2 in the chain of the former. This has a mild effect on certain parameters, and on the shape because the extra atoms cause some slight distortion. But clearly, a global change from a precursor where the entire codon group coded for one, and then purine-pyrimidine distinction led to a subdivision, is not exactly out of the question. Numerous 1st / 2nd-position substitutions can be likewise identified, though the arrangement of the table in that image only highlights the 3rd.

    And, as if by magic, a constraint on global substition gives a misread-tolerant code, for free.

    People would have it that the acids are 20 completely different things, hence all that 20^xxxxx nonsense repeatedly paraded. They aren’t.

  19. Rumraket:

    On subject, I recently read a paper detailing an experiment where a population of bacteria had every single codon which codes for Trp evolved to accept a synthetic amino acid. Over twenty thousand tryptophanes were replaced with a synthetic but chemically similar amino acid. In the end, the bacteria were able to survive and reproduce in media completely absent Trp (with the Trp biosynthesis pathway removed).

    Chemical Evolution of a Bacterial Proteome.
    Hoesl MG, Oehm S, Durkin P, Darmon E, Peil L, Aerni HR, Rappsilber J, Rinehart J, Leach D, Söll D, Budisa N.

    That’s one of the best comments I’ve seen in a long time. Thanks for the input.

    Why am I telling you all this in response to what you said? The point is to get you to think about how things could be different from how they are now

    Yes indeed. To the extent I’m in error, I’m indebted to you. To the extent I was still generally right, I’m still indebted to you for those two papers which you provided, especially the first on synthetic biology.

    I will have to think upon these things, and furthermore, at least for now, it motivates me to learn more.

    About the only thing perhaps we can agree on is that synthetic biology is interesting, and it gives us understanding in ways we may not have expected. Thank you for helping expand my knowledge base.

    Thank you for the thoughtful and well-researched response.

    Cheers.

  20. The tryptophan thing is interesting. In the graphic I linked earlier, Trp is right next to a STOP. Almost all codon groups where the 3rd position matters, are subdivided on a purine/pyrimidine distinction. This is one of the few places where all 3 matter precisely. As I mentoned earlier, it is (in principle) far easier to convert a STOP to an assignment than to convert an assignment to a STOP, or one assignment to another.

    My bet is that TGG was, until recently-ish (but still pre-LUCA), a STOP codon. I’d be interested to know if it is overrepresented toward the ends of peptides, which might account for its comparative ease of substitution. UGG does group with STOP codons for releasing synthesised peptides from the mRNA-ribosome complex, even in humans.

  21. Allan Miller: My bet is that TGG was, until recently-ish (but still pre-LUCA), a STOP codon. I’d be interested to know if it is overrepresented toward the ends of peptides, which might account for its comparative ease of substitution.

    What you’re suggesting is that there should be a detectably higher frequency of codons that are only one or two substitutions away from a stop-codon, near the ends of peptides. This is a very interesting suggestion and seems to me a genuine prediction of code evolution through stop codon reassignment.

  22. Rumraket,

    You might find this interesting, then. Ciliates are a particularly extravagant group, breaking many of the ‘rules’ of genetics. Among them is a species that has no STOP codons. All 64 triplets have a cognate tRNA. But those that are, in other organisms, true STOPs, function as STOPs toward the poly-A tail, a bit like the dual role of the initial AUG, and the human UGG I mentioned.

    There’s a general bimodal distribution of these not-quite-STOPs between species: more in the body of the peptide, then a sparse region, then more again towards the poly-A tail. Almost as if there were selection against their presence in an ambigous ‘grey area’ where there is potential uncertainty about whether to stick an acid in or initiate release.

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