Here is one reason I don’t think life as we know it is the result of ordinary processes.
From Wiki:
https://en.wikipedia.org/wiki/Stop_codon
In the genetic code, a stop codon (or termination codon) is a nucleotide triplet within messenger RNA that signals a termination of translation.[1] Proteins are based on polypeptides, which are unique sequences of amino acids. Most codons in messenger RNA (from DNA) correspond to the addition of an amino acid to a growing polypeptide chain, which may ultimately become a protein. Stop codons signal the termination of this process by binding release factors, which cause the ribosomal subunits to disassociate, releasing the amino acid chain. While start codons need nearby sequences or initiation factors to start translation, a stop codon alone is sufficient to initiate termination.
Now what happens when there is no stop codon?
A nonstop mutation is a point mutation that occurs within a stop codon. Nonstop mutations cause the continued translation of an mRNA strand into an untranslated region. Most polypeptides resulting from a gene with a nonstop mutation are nonfunctional due to their extreme length.
….
Nonstop mutations have been linked with several congenital diseases including congenital adrenal hyperplasia,[15] variable anterior segment dysgenesis,[16] and mitochondrial neurogastrointestinal encephalomyopathy.
In other words, it would be bad juju if there are no means of reading of DNA and recognizing where one gene ends and the other begins. In fact, without stop codons, it looks like a DNA-RNA-protein-based life on Earth would be dead.
One could postulate a DNA-RNA-protein-based life that had an alternate stopping mechanism that eventually evolved a stop codon. But that just moves the problem elsewhere in as much as a DNA translation system that contains multiple genes needs a gene delimiting mechanism. A stopping mechanism needs proteins to implement it, but without a stopping mechanism to implement proteins, there is no stopping mechanism. We have then a chicken and egg paradox.
One could postulate proteins arose by a method outside of DNA translation and somehow recruited DNAs and RNAs and then defied all probability and somehow figured out how to code the next generation of proteins using DNAs that just happen to be coding the proteins like the ones that miraculously recruited them. At some point, such scenarios are so out of the ordinary they are not distinguishable from miracles.
Some will argue Darwinian evolution in the origin of life. That’s problematic for at least two reasons.
1. even most evolutionists don’t view the origin of life and origin of the protein translation cycle as part of typical evolutionary theory. So in that sense of the word “evolution”, stop codons didn’t evolve.
2. something dead can’t evolve by Darwinian mechanisms, and if this is an origin of life scenario we’re dealing with dead pools of chemicals.
So Darwinian evolution isn’t a solution. Chemistry isn’t a solution. Physical laws aren’t a solution. Probability isn’t a solution. In fact what we know of physical process would work against evolution of stop codons, not for it. Hence stop codons and life that depend on stop codons did not arise out of ordinary physical processes.
stcordova,
Only if it’s part of a multicellular body. Where do the blood cell’s proteins come from?
This is one of the sillier arguments I’ve encountered, and there is some stiff competition.
Why don’t you fuck off and die?
stcordova,
No, you have determined without evidence that proteins are believed to have assembled abiotically from a soup containing 19 chiral L alpha-amino acids plus their D isomers plus glycine. This is not a plausible scenario. There are actually several hundred possible amino acids, and not just those with the alpha linkage. You could bust your calculator coming up with hokey scenarios, but really the peptide bond is thermodynamically unfavourable anyway in solution. Rather than indulging a Hoyle-style taste for numeroproctology, you could just look at the chemistry. I simply don’t think any of this happened in open solution in a non-living system. RNA is a different kettle of fish, and it does have properties that peptides lack and which could be key: thermodynamically favourable polymerisation and self-selecting hybridisation. Those are my favoured bet, though I’m sure you have a quote mine ready to roll telling me how impossible RNA is.
All you need for homochiral acids is a homochiral template and a stereospecific ribosome – which is an inevitable consequence of the handedness of ribose. That’s like finding 500 coins all heads when you can only hold them one way; hardly ’22 sigma’. The one-handedness of ribose itself derives from the greater stability of homochiral double strands.
It’s not strictly relevant to origins, but what makes you think mixed-enantiomer proteins cannot have catalytic activity? What’s needed is repeat specification, not repeat specification of L isomers only.
Your issues with chirality also betray an amusing failure to grasp stereospecificity in molecular biology. Do you that any biological process ever looked for a molecule of a particular molecular weight or stoichiometric composition, and was confused by stereoisomers? It’s hilarious. The D isomer of any L acid has a hydrogen where the L has its side chain. That’s more than enough to allow discard of all D isomers – they look like Glycine at that position, and are therefore as distinct as that is. If you can discard Glycine, you can discard all D acids.
What I mean by that is your terrible misrepresentations are beyond the pale, and the arrogance you display alongside your ignorance is very ugly Sal. So, you know, what I said just now.
No , because as I pointed out in my essay, the problem proceeds from the simple fact Dawinian process eliminates diversity. One can’t create diversity by eliminating it. Darwin’s dumb idea. He should have titled his book, “Elimination of Species by Means of Natural Selection”, and that would have made more sense.
I’ll say then in the future, Lynch disdains the worship of Darwinian selection than Darwinian selection itself. Thank you for helping me improve the expression of my essay and discovering Janet Browne was the historian that noted how thrilled Darwin was to be a liar ever since childhood.
I’ll try to mention you in the acknowledgement section of some of my future essays. Thanks for your free-of-charge peer review. 🙂
I gave a favorable scenario to show the absurdity of assuming proteins can assemble abiotically. Your objections just make the odds in more remote.
Yes it is not plausible, so the improbability of the proteins assembling pre-biotically is worse than my scenario, not better!
Thanks for giving even more reason to say OOL did not happen by ordinary processes.
His name will live forever, as long as there are Humans we will know Darwin’s name. Your lot, not so much.
Mung,
Boom! I’ve taught biochemistry classes, and no I’m not going to give you the answer. Every IDIot screed reads as if it’s the first time anyone has ever thought of the “problem.”
stcordova,
Not if it includes a means of adding new variation. Does it? Why yes, it does.
stcordova,
Yes, precisely. You did read my post didn’t you? It looks like my point completely passed you by, if you feel the need to lengthen the odds as if you just though of it. Since I don’t buy that scenario in the first place, I don’t actually give a shit how remote the odds are. Add a few billion noughts if you like. Do you understand basic chemical thermodynamics? That’s the deal-breaker, not some ridiculous mechanism no-one proposes where some system reaches into a bag and peptide-bonds the contents one at a time. Classic example of the manner in which religion corrodes the intellect.
You’re welcome … hang on, what ‘ordinary processes’? Where have you ever come across the notion that peptide bonding occurs spontaneously? Why are we compelled to assume that proteins are essential for life?*** Or that L acids and D sugars are the only possible components of living systems? Are these the ONLY WAYS in which the OoL could have happened? Argumentum ad lackofimaginationum
*** Of course, there are no non-protein-coders now. They were wiped out.
Got round to addressing my point on the carbon content of limestone yet?
Mutation, Sal. Mutation creates diversity, selection eliminates that which doesn’t work. It doesn’t eliminate everything, only that which reduces fitness. And even then, it usually takes multiple generations before that happens, so other things can happen in the mean time, like more mutations and epistatic effects between them.
I’m trying to like Mung. But when he gets into specifics it all tends to fall over. This seems common for IDers, unhappy with things they’ve not bothered examining.
I am often impressed by creationist skills at self-delusion.
From the OP:
This is completely arse ways about. A STOP codon indicates the absence of a corresponding tRNA. You seem to be proposing a system with all the tRNAs assigned, which then evolves a gap. God knows where the tRNAs are supposed to have come from, but if we did have such a start point, loss of a tRNA would be seen as a ‘loss-of-function’ mutation … But hardly a massive counter-physical leap.
But a more likely start point is that everything is a STOP – there are no tRNAs initially. The length of early peptides was constrained by being tiny islands in a sea of STOPs which gradually became assigned. But they could still grow by tandem repeat.
Mutation, the great homogenizer.
Sal,
It seems pointless, and almost dishonest to debate biochemical minutae that would be relevant to proto-life billions of years ago when you actually believe that life only came into existence on earth about 10,000 years ago? Am I correct that this is your belief?
If life is 10,000 years old then ool and evolution couldn’t have occurred and all supposed evidence for them must be false. The argument for young-life would trump all evidence for ool and evo – so why do you bother with these other arguments? Make your case for young-life.
Exactly. I’m glad to see you reminding Sal of their real problem here.
For Sal, IF IDists could prove that origin of life absolutely required and did have a designed/created/supernatural intervention, so what? When everything else remains the same, when we still have an entire universe full of consilient evidence for big bang, stellar evolution, billions of years, followed by all the accessible evidence on our planet for billions of years of life leaving traces and fossils from the very simplest, through surges of diversification and mass extinctions, till now … what is Sal going to gain when it’s all an illusion to him anyways? No matter whether OoL required a divine kickstart or not, it still happened about 4 billion years ago on our planet, and Sal is still in deep shit with his dopey belief in the impossibly young Earth.
Either he admits Earth actually is as old as it has been determined to be by every sane geologist (including three centuries of faithful christian geologists), or he pretends it might be possible for every single one of them to be in on some conspiracy to manufacture the literal tons of old-age evidence (keeping in mind that conspiracy would have to involve three centuries of christian geologists as well as the “evil” modern materialists). OR, he believes his Lord god is a wicked liar who created a young Earth will all the evidence of great age. In that case it could not possibly matter one bit if life appears designed or if life appears evolved, because all appearances are total lies. No point in arguing about the fine details of the lies of a lying liar like Sal’s god.
Sal should probably remember that before he goes to post any more “biological minutae”.
Welcome to TSZ, flandestiny, and I agree with your concern.
@ stcordova
Sal, have you any proper training in science and been awarded any recognised qualification? Do you have any training or expertise in teaching? How old are the kids you are teaching? Are you getting paid for it?
I think he’s referring to the person following his website, if such a person exists.
That’s a relief!
I’m not sure that this is correct. I could be wrong, but I think that Sal, like me, might be a grad student somewhere. I’m sure he can elaborate on this, if he so desires.
Dave Carson, flandestiny,
Sal attended Johns Hopkins part-time and got a masters in applied physics a few years ago.
I doubt very much that he has any kind of official teaching position. I know he’s involved with campus ministries and ID clubs, so that’s probably what he means when he refers to his “ID students”.
Thanks for the correction and info, Keiths!
But here you are with a chance to discuss science with an ID proponent and this is the best you can come up with. That’s why I support ID.
That you have “students” is the most concerning part of this post. Teachers who refuse to teach. Not getting paid enough? Against union rules?
Well, we knew it wasn’t for a good reason.
Glen Davidson
Still smarting from the last thread you started? You know, the one where I took six specific instances of alleged contradictions in the bible and showed how they were not in fact contractions, that the two sources were not even speaking of the same thing?
That’s ok, I’m trying to like you too. 🙂
I know folks here won’t want to think it even possible, but I was disagreeing with Sal. Far be it for me to ever disagree with Salvador!
There was something fundamentally wrong with his scenario about how polypeptides are generated.
Allan addresses it here.
There is no corresponding tRNA for a stop codon. So peptide synthesis does not just proceed ad infinitum. But I’ve never taught a course in biochemistry myself.
Mung, I think you may have just articulated a new and important epistemological methodology: in order to weigh the truth claims of two competing view points, count up the number of times that proponents of each view have been rude on the internet, and then whichever has the smaller number is declared to be the truth! Granted, this will heavily favor minority opinions (since they presumably have fewer adherents who might potentially be rude on the internet), but those are just pesky details that will be worked out in time. This could change EVERYTHING!
Well, there are other benefits. 😉
ok, so now I need to come up with a web scraper and a real time indication of who is right or wrong. That way people who want to be on the side of consensus can easily find the right thing to say. Got to find a way to turn this into cash.
🙂
I bet you favor lying to others over lying to self. Whatever works, right?
You are pragmatist, aren’t you?
Oh yes, this will be worth…billions. Especially to those like us who can get in on the ground floor!
Money may not be able to buy happiness, but we can show that it can buy truth!
Mung,
You support ID because one person lost his rag with [YEC] Sal Cordova? ‘Kay.
No, I asked you here why you were an ID supporter and you said
And in case you missed it, Sal does not discuss science.
Anyone interested in how things might happen, rather than determined to show they cannot, might be interested to note that the smallest catalytic peptide is also the smallest possible peptide, ie a dipeptide.
Also that catalysis is by no means the only function of peptides. They can serve to regulate cell pressure, as structural components, as moppers-up of free radical damage, as motors, as filtration channels, as signals and labels. So there could readily be a role for short peptides in early non-protein cells from which the longer catalysts are derived.
Sal is articulating a widespread view, tracing at least back to the highly intelligent ignoramus Fred Hoyle that, because modern cells cannot function without long catalytic peptides, no cell can, making it an OoL problem. There is certainly no logical necessity that this be the case, nor a chemical necessity, although proof-of-concept is tricky precisely because Design is so inadequate!
The absence of modern non-protein-coders is readily explained, in principle at least, by the ecological superiority of derived protein-coders. They are aggressive and efficient moppers-up of organic molecules, including those presently residing in the cells of others.
Well yes, and the synthesis of RNA nucleotides is also thermodynamically unfavorable.
But…
Energetics of Amino Acid Synthesis in Hydrothermal Ecosystems
J. P. Amend, E. L. Shock
“[…] The energy yield from the autotrophic synthesis of amino acids in a 100°C mixed hydrothermal fluid (see Table 3) may ultimately be used to overcome the energy requirements of protein synthesis. To calculate this energy yield, we combined sequence data for thermophilic proteins with the thermodynamic evaluation discussed above. For example, from the sequence of rubredoxin from the hyperthermophilic Archaeon Pyrococcus furiosus (53 residues) and the values of ΔGr for all 20 amino acids (Table 3), we computed that, in a 100°C mixed hydrothermal solution, the net synthesis of the amino acids constituting 1 mol of this protein releases 722 kJ. The values of ΔGr for the net amino acid synthesis of this and eight other thermophilic proteins (Table 4) are all negative (exergonic). Combined with the conclusion that peptide bond formation is energetically favored with increasing temperature (12), an argument can be made that thermophilic chemoautotrophs, such as those occupying the deepest branches in the universal tree of life, expend considerably less energy for the synthesis of macromolecules, such as proteins, than do their mesophilic counterparts. Depending on the amino acid composition of the protein, the synthesis of the monomers from CO2, H2, and other inorganic precursors in hot, reduced aqueous solutions may provide substantial surplus energy that can be harnessed to drive intracellular synthesis of enzymes and other polymers.”
Lawyers, anyway. And apopogists. But it doesn’t seem to fill ID journals like Bio-Complexity with research articles.
Rumraket,
Yes, peptide monomers are easier to synthesise than nucleic acid monomers. But the latter polymerise more readily and they have the bonus of being ‘self-selecting’. You don’t need crystal surfaces or whatever – complementary random oligonucleotides find each other with quite remarkable specificity. In doing so the single strands stabilise each other, preferentially in homochiral 3′-5′ linked configurations, reducing the exposure to 2′ -OH attack by reducing strand flexion, as well as providing a lattice to permit re-ligation should chain hydrolysis occur. Peptides, not so much.
OK, you’ve created a single peptide molecule in exotic conditions – now what you going to do … ? Hydrolysis and monomer decomposition increase with temperature, and there is no obvious mechanism for repeat synthesis in any case, and no replicating beneficiary of the catalysed reaction.
I think sequence flows from nucleic acid to peptides for fundamental reasons.
Rumraket,
Just digging a little more, it’s not clear how the authors envisage coupling the energy output of monomer synthesis to protein synthesis. Monomer synthesis would release heat, I’d have thought, not useful chemical energy.
Additionally, their observation that peptide bonds form more readily at high temperatures, coupled with observations from elsewhere that hydrolysis also occurs more readily, argues for a change in the shape of the reaction energy profile. Although bonds form more readily, they will break more readily too, giving a dynamic equilibrium. This doesn’t matter in many simpler reactions where it does not affect the net yield, since the same product is reformed, but in the case of a ‘useful peptide’, you lose the sequence you want, to say nothing of generating ectopic linkages with amine/carboxyl side chains.
Also of interest. It seems that singleton acids are hard to glue to anything else, probably because they wibble about so much. Once you get some links, it becomes easier to join multi-residue lengths.
Hey thanks for the great insight. I was obviously referring to DNA stop codons not mRNA as you can see listed here:
https://en.wikipedia.org/wiki/DNA_codon_table
I should add not just the DNA stop codon but the associated termination sequences in the DNA, not the mRNA. But to avoid confusion in the future, I’ll try to add some things to help clarify when I’m talking of the Stop Codon in DNA vs. RNA.
I’ll try to mention in the Acknowlegements section of future versions of this essay for helping me improve what I wrote.
Thanks. Couldn’t have done it without you.
A more charitable reading would have not cause you to blow a gasket. That said, future incarnations of this essay will be worded to avoid such confusion.
Thanks for the editorial suggestions. But that doesn’t overturn the basic point, if there isn’t a termination mechanism in reading the multigene genetic strand, the thing dies, hence there is no evolution.
But if you find any more minutia you want to whale about, I would actually be grateful and take it into serious consideration.
Yet if you do whale, you’re going to be in a lot of trouble with the law.
Glen Davidson
stcordova,
Good grief. What’s a ‘DNA STOP codon’ do other than cause termination of translation after transcription into mRNA and passing through a ribosome? Obviously, the listed codon becomes an anticodon. Other than that, the one is pretty much the other. There isn’t a separate ‘DNA STOP’ mechanism at triplet level.
The DNA STOP has no effect on transcription, so yes, you’d need to be clearer if you were talking about things that affected transcription instead of things that didn’t (like STOP codons). Termination sequences aren’t codons.
To avoid confusion in the future, take a basic biochemistry course. There is no significant distinction.
Yeah, sarcasm noted.
OK, I apologise if my wording was overly robust. But when people pontificate loftily about subjects they know little about, it does tend to grate.
Therefore protein transcription and translation both need termination. So? I don’t see termination at either step as unavailable to evolution, provided non-protein-coding replicators are possible. I see no reason to think they aren’t. In an (admittedly hypothetical) RNA-only life form you would not even need transcription. All you’d need is one or more STOP codons, which you’d be bound to have if you only had 1 tRNA.
Yes there is in terms of operation.
The termination at the DNA level is not driven by the DNA stop codon only, but termination sequences. Somewhat understood for prokaryotes with rho dependent and rho independent termination, not so well understood for eukayrotes. I actually didn’t realize that until your comment made me give the DNA stop codon a second look.
The RNA Polymerase just happily transcribes the DNA until it reaches the termination sequence with the stop codon presumably the last transcribed part, but the DNA stop codon is not the termination signal, the termination sequence is. Apparently, something I have to check, it seems the polymerase reads the stop codon and transcribes it (substituting RNA Uracils for DNA Thymines), but what really causes transcription termination is the termination sequence, not the DNA stop codon.
You mentioned just having a missing tRNA would cause a stop. But this makes the problem worse, not better. Take any of the other 63 codons. If there is any missing tRNA, oh well, the gene translation halts mid stream since now any DNA codon without a corresponding tRNA becomes a stop codon — organism dead, end of story.
Seriously, I took incarnations of this essay to 4 other venues trying to get some substantive criticism, and you were the first to make something substantive, you found a glaring error on my part. “Stop codon” is the proper term for termination of mRNA translation, “termination sequence” is the more proper term for termination of the polymerase transcription of DNA to mRNA, even though there is a DNA stop codon.
The rest of the responses from others was kinda not as sophisticated in understanding as yours. Thanks.
Unnecessarily surfacing from the lurking depths here, especially considering Allan has already pointed out the problem with your original post but…
The main problem with your argument is your ignorance of basic biochemistry.
Your original post is talking about translational termination (both wiki quotes are in reference to translation, stop codons are only relevant to translational termination). It’s not an issue of being charitable in interpreting things, anyone who understands these processes would assume you meant translation. If that’s not what you meant, that’s a problem with how you wrote things.
Now you’re saying you meant transcription termination. First off, the stop codon whether in DNA or RNA has nothing to do with transcriptional termination, nor does it mark off where the mRNA stops (look up 3′-UTR). Second, transcriptional termination isn’t necessary for ensuring separate protein products, many genes can all be on one transcript (look up polycistronic mRNA), what separates protein products are the stop codons, so we’re right back at Allan’s points.
As for premature termination being an issue – this is silly. First off, there are 3 stop codons, not 1 as you assume, and some of those already get suppressed by non-standard tRNAs to code for rare amino acids (look up selenocysteine), so the number of stop codons is already variable. Plus you are assuming that early genes would have all 61 other codons in use using all 20 amino acids, so any stop codon reassignments would lead to internal termination sites. They wouldn’t. We don’t know how protein translation emerged, but it very likely used a reduced codon set and a reduced amino acid set. Proteins don’t need all 20 amino acids to function.
Demarcating protein-coding genes would not have been the hard part of evolving translation. Getting a proto-ribosome to stop or terminate is easy, and the same goes for transcription – its easy to find sequences that cause transcription to stop, and the more primitive the polymerase the more common this sort of thing would be.
stcordova,
The termination at the DNA level is not driven by the ‘DNA stop codon’ at all. Use of the term ‘codon’ independent of the ribosome is extremely misleading. That’s your basic error, right in the title of the OP. If you are talking of STOP codons, you are talking of a triplet with no corresponding tRNA. If you are talking of termination of transcription, you aren’t talking of STOP codons.
David,
Thank you for setting me straight on the biochemistry.
Btw, I did not assume 1 codon. I even provided a table that showed 3. But unfortunately I said 63 not 61 other codons, so that is a mistake. Thank you for correcting my 1st grade math error.
However, the following isn’t biochemistry, this is total conjecture that makes little sense and I will point out one error.
Even with reduced number of amino acids and corresponding tRNAs, if the code is a triple code there will be 64 codons (4^3). It will still stop midstream for missing tRNA if the mechanism of stop is missing tRNA. There is of course the hypothetical ter-Trna’s of Ivanov, but no need to go there at this time.
Assuming Allan’s missing tRNA as the mechanism of stop, then my point stands.
The other things you said were most certainly informative, but without transcript termination (nor regulation) of the transcripts, the fate of the cell is not very promising. That would be the case if the entire genome generated one big polycistronic strand. So the termination sequences of DNA are important, the existence of some polycistronic transcripts does not imply DNA termination is un-necessary.
Most certainly it is both a problem with what I wrote and my understanding of biochemistry which you have thankfully enlightened me on.
I’m sorry I have to beg to differ. If the mapping of the tRNAs do not conform in a meaningful way with the DNA codons, gibberish comes out, and part of that mapping is the demarcations. I pointed out the problem of premature demarcation, and that doesn’t go a way merely because of a reduced number of amino acids. The only way that might possibly work without creating undesirable stop codons is with higher degeneracies of the codons mapping to a small set of amino acids which doesn’t exactly make an evolutionary scenario that much more plausible since one has to then account for how the degeneracy was reduced as more of the 20 amino acids were added without killing the organism along the way.
Yes, by killing it for sure. But getting it to stop in the right place, not so easy, and if that surely won’t happen in functional way if there is not a means of terminating transcription, especially presuming a cell will express on gene far more abundantly than others.
Thank you anyway for correcting my errors in understanding biochemistry. This has been one of the most productive and enlightening exchanges. Sorry I must disagree with you on the ease of evolving a system.
The empirical evidence is surely on the side that the proposed evolutionary scenarios would be out of the ordinary because if they were ordinary they would have been observed in the lab. One might argue it happened but it just doesn’t happen frequently enough to be observed. Well, that supports my claim it would not be an ordinary event, but an exceptional one.
Oh, what’s that, your killer argument against a non-miraculous version of OOL turned out to be just your ignorance?
What a total surprise.
Oh, I see you’ve learnt no lesson after all. But that’s something of a record, admit your ignorance after you make a mistake then go on in the same comment to make exactly the same mistake.
stcordova,
Weeeelll …… It is true that evolution from an assigned codon to a STOP will chop the organism’s proteins into smaller pieces, which would be fatal, so we can probably discount that.
But can you seriously not see a way out of this apparent dilemma? I don’t know how you think an organism is going to evolve 60-odd assignments without going through a period when those assignments were STOPs. Assignment of STOP is essentially irreversible in an organism with a significant protein repertoire. But this does not mean you can never have STOP codons. STOP is the default.
There are variant genetic codes. Only 9 positions out of the 64 possibles vary in modern life. In every variation but one (to my knowledge), the triplet is a STOP in at least one of the variants. This suggests permissible evolutionary activity this far down the protein-coding line is restricted to STOP reassignments. As you correctly say, loss of a tRNA is very unlikely. But assigning STOP->tRNA isn’t, since all it does is add a short tail to the protein, through translation to the next real STOP. The average distance to this STOP, and hence the length of the tail, depends on the percentage of the codon matrix currently assigned. It is much easier to go STOP->tRNA when there are few tRNAs, because the tails will be short, if anything. The more assignments there are, the more likely it is to be disruptive – but that just means it will become rarer, not non-existent. The code gradually becomes frozen in place. But around the edges (as we can see from the variant codes) post-LUCA STOP variants still occur from time to time, almost certainly by assignment of a tRNA rather than loss.
stcordova,
Let me be clear: I was talking about a tRNA that never existed, not one that was lost.