False.
It could (and does) work without all the tRNAs, using less than 21 amino-acids.
It could (and possibly did) work without any DNA sequences, using only RNA templates.
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It doesnât matter how many times you repeat your flawed logic, it will never become unflawed.
{p(X) and q(X) and p(Y)} -/-> q(Y).
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I think that analogy is rather exaggerated.
Youâve been shown evidence that the ribosomal core is highly similar to tRNA, and that their sequence similarity increases as we go deeper in the nodes of their phylogenetic trees (back in time), which implies they share a common ancestor, and youâve been shown evidence that the PTC center can function as a peptide bonding ribozyme by first self-assembling from a molecule highly similar to tRNA into a dimer, entirely in the absense of ribosomal proteins, the absense of all the rest of rRNA, and the small ribosomal subunit.
Youâve also been shown evidence that the two families of aminoacyl-tRNA-synthetases, today comprising 64 distinct enzymes, derive from one ancestral gene.
All of this implies an era in which almost the entirety of the rest of the translation system was missing (including all the ribosomal proteins and the small ribosomal subunit), and this common ancestral molecule had an entirely different function, or alternatively was dimerizing into something like the PTC and was more or less only stringing mino acids together in an uncoded fashion.
None of this seems to correspond all that well to the idea that youâve just been given a one-propeller and two-propeller airplane.
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And yet we have evidence the system evolved so your statement seems to have no capacity to explain the data we see or how the system came to exist.
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Yes but first of all, the problem is youâre just saying that, while offering no explanation for any of the data that indicates that the genetic code evolved.
And second, the inference that âlike other digital codes, the product of an intelligent mindâ is an inductive inference from the observed which @Faizal has already addressed.
Presumably you are trying to argue that we should think the genetic code was intelligently designed, because other digital codes we know of have been intelligently designed. But as Faizal points out, another just as well-supported inductive inference from observation is that intelligent minds require the genetic code, thus implying a contradiction between the two inductive arguments. The genetic code cannot have come into existence without having already existed in the intelligent designer that created the code. So one or both of the inductive inferences must be false.
It just so happens we have good reason to think both statements are false. There is evidence the genetic code evolved, and we know of other digital codes that werenât designed (tree rings), and thereâs good reason to think intelligent designers can be machines for example.
This idea that the translation system was more or less created as-is in any particular organism by some instance or process of intelligent design has no explanatory power when it comes to the data we have about the translation system and itâs various components in many different organisms. This data is however well explained by the hypothesis that the system is the product of an evolutionary process, because this hypothesis can explain why the data looks the way it does. Itâs also a useful basis for doing research aiming to understand how the code evolved, because it has yielded numerous curious insights into how the code functions (and would have functioned at earlier stages).
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Why not answer my question with a simple âyes,â in that expecting a Wikipedia-level understanding is not possible?
No, you still donât know what youâre talking about, and your pasting of a large block of text only illustrates that.
What is shows is that it is not arbitrary. If you have so much faith in your position, why all of the painfully obvious goalpost moving?
Youâre ignoring the âorâ in the definition you posted:
1b: based on or determined by individual preference or convenience rather than by necessity or the intrinsic nature of something.
Again, this gets back to your abject failure to understand what catalysts are incapable of doing. Enzymes donât perform magic.
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Straw man. They were predicted by the hypothesis that the genetic code (no reason to capitalize anything) evolved.
You, on the other hand, have multiple false predictions of your hypothesis piling up that you tacitly acknowledge by moving the goalposts and changing definitions.
You literally reject the scientific method. Testing empirical predictions is simply how science works. Youâre desperately trying to misrepresent science as mere after-the-fact explanations.
More scientifically, much of it was predicted by the existence of that era.
Interestingly, we know manyâprobably mostâof these things because, unlike IDcreationist rhetoricians, real scientists tested and confirmed many of these predictions with the goal of improving human health, something the rhetoricians apparently donât care about.
I wonder if those claiming to understand the big picture better than we do even know how these things are relevant to medicine.
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Exactly. And what are you using? The opposite of knowledge?
Yes, I think everyone here understands this. And, as has been repeatedly explained to you, you have not demonstrated that this is sufficient reason to conclude that something is âdesigned.â
I reject the assertion, made by ID proponents and other creationists, that whether something is âdesignedâ is determined by inherent characteristics like âirreducible complexityâ, âspecified informationâ or âcodeâ. It is determined, rather, through our knowledge of whether something is produced naturally or requires human beings to manufacture it.
Well, I would disagree that the statement âAll swans are whiteâ is not scientific. It would be a perfectly fine conclusion to draw thru inductive reasoning if the empirical evidence was such that millions of swans had been observed and none of them were any colour other than white. It is, however, a false statement, since we know that black swans exist. Thatâs how science works.
Similarly, my statement would be falsified if we witnessed a god or angel or demon or some other being that did not require DNA and could create a code.
But, more to the point, the statement, âEvery intelligent being that can create a code requires the genetic code to existâ is at least as strongly supported by evidence as is your assertion âEvery code requires an intelligent being to create it.â And you have yet to provide any rational reason that you accept one premise and not the other. It is quite apparent to me that the only reason is because you believe one statement supports your religious beliefs, and the other refutes it. That is not a rational reason, but one of personal prejudice.
IOW, you still do not understand the evidence and arguments that have been provided. If anyone wants to try explaining it some other way, they are welcome to try. Though I suspect many are coming to the conclusion that it is a lost cause.
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Thereâs no explaining the scientific method to those who reject it.
Again, hereâs my challenge to @theaz101 and @appsandorgs:
What I find remarkable about religion-driven rejection of science is how little real faith backs it up.
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Why then, did you describe genetic code as digital information (or any other base), if that is irrelevant to it being the product of an intelligent mind?
So I think we are finally agreed on this point about base; it is irrelevant. Therefore your conclusion should be that ALL INFORMATION is the product of an intelligent mind, not just that genetic code. (This is where you inject the supernatural.)
No doubt you will object. You might reasonably counter by providing an example of information, using your definition, that is not the product of an intelligent mind? You might have used tree rings, but then you wrote âŚ
If ânaturally occurring informationâ is tree rings, then it isnât digital information.
But if the base is irrelevant then tree rings must be information in the same sense as genetic code is information.
What is really going on here, is that I have imposed the same definition of coded Information on tree rings as you have imposed on the genetic sequences. The only intelligent minds at work here are ourselves.
[Bolded for reasons which will become apparent]
It seems obvious you are doing just that - appealing to the supernatural. Otherwise, where is the explanatory power in such a claim?
âŚas a cause of a chemical reaction.
If you are not appealing to the supernatural as a cause of a chemical reaction, or arranging or sequencing of DNA bases at the time that life originated, then what are you appealing to?
Other have already noted this moving of the goalposts.
By this, do you concede that the genetic code has evolved from an ancestral state?
Do you agree this is unlike any human designed code, which do not change themselves?
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Thatâs also my understanding that the history of the ribosome is surprisingly obvious from itâs structure alone. Before one stage, the precursors of the two subunits could not interact with one another which is necessary for translation. So what did these things do before translation? They made polymers, peptides probably but perhaps also other kinds of polymers, but these were not encoded (i.e. template directed sequences). In the absence of coding, that does mean that the modern complex folds that we see in proteins today were not available to these early peptides, and the nature of their sequences were highly statistical, producing a collection of similar sequences instead of one specific sequence from one gene: the âStatistical ensemblesâ as hypothesized by Carl Woese. The folds of these sequences would also be rather simple, but as translation was established and fidelity increased over time we would expect that peptides would have attained more complex folds correspondingly. It turns out that this history of protein folding is also recorded in the structure of the ribosome and ribosomal proteins. The peptide strands which interact with deeper and older parts of the ribosome are simpler and donât fold, but as you go to more younger parts of the ribosome, the peptides attain more complex folds.
Hi Nes
The simple to complex process forming new arrangements is an assumption as there is little if any empirical evidence to support this critical assumption that is required for the claim that similarities alone can support the evolutionary paradigm.
The similarities donât come âalone.â The similarities come in nested hierarchies.
That is one of the many reasons why the evidence for âthe evolutionary paradigmâ is so overwhelmingly compelling.
Those nested hierarchies are also surrounded by the piles and piles of compelling CONSILIENCE OF EVIDENCE from many many fields of science.
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7 posts were merged into an existing topic: Side Comments: Is there really information being conveyed within a cell?
This is all great stuff, thanks for posting these treasures. I just read a paper that features some of the new(ish) ways that structural biologists are capturing enzymes âin the act,â and thatâs interesting by itself but I learned more about the way that biophysicists talk about protein structural dynamics and itâs changed how I visualize/conceptualize enzymes and active sites. Here are a few sentences from their Introduction:
Enzymes, like all proteins, exist in conformational ensembles corresponding to multiple populated minima in their potential energy landscapes (4, 5). Protein dynamics are a combination of motions within these minima and transitions among them. The conformations that compose an ensemble can have intrinsically different catalytic proficiencies, permitting sampling of optimal conformations during catalysis (6, 7), in the laboratory (8, 9), or through evolution (10â12). Because the catalytic cycle transiently changes the underlying protein energy landscape, enzyme conformational ensembles also change during catalysis (7, 13, 14).
This seems conceptually similar (just a bit) to the âstatistical ensemblesâ idea. It undermines the highly simplistic views of poorly informed biochemists like Behe and archaic rigid views of Axe (unless heâs actually read some papers in the last couple of years), but to be fair to those lost souls, simple views of protein structure are ubiquitous in textbooks and in the old slogans of previous eras of biochemistry. âLock and keyâ is a useful simplification for the first step of explaining a binding site and/or an active site to a beginner, but like all such simplifications, it is all too easily co-opted by apologists who need the world to be simple.
The paper is from one year ago, is open access, and includes some nice rabbit trails references. The concept of âenzyme ensemblesâ is not new, but I think (could be wrong) the phrasing is recent. The authors cite this really interesting 2016 Nature Chemical Biology paper for its exhaustive experimental evolutionary analysis of a protein evolving in the lab, and that paper doesnât use the phrase.
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Your post and the link was fascinating to me. Entertaining, even. And yes, Iâm one of those people entirely outside of the field who still thinks in simple âlock and keyâ termsâbut I know just enough about the basics of enzymes and protein folding to not be a bit surprised that new discoveries of the complexities and their explanatory mechanisms are dazzling to behold.
Yet again, every time we turn around, the consilience of evidence for evolutionary processes just gets more and more compelling. And goes deeper. And richer. And very beautiful.
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There actually is a lot of empirical evidence to support this, and in this case we are not talking about so-called âsimilaritiesâ here. We arenât doing phylogenetics and trying to reconstruct evolutionary history. The origin of the ribosome is before LUCA, and thus phylogenetics doesnât go back far enough to help us (except in the case of ancient paralogs).
If you look at this paper which I linked previously, one of the things they focus on is the A-minor motifs. These are RNA-structural interactions formed when you have one RNA helix with a stack of nucleotides (usually adinosines) that turn outward and fit into a minor-groove of another RNA helix. This is one of the inter-molecular interactions that âlatchesâ the ribosome together. Here below is an example o A-minor motifs.
Now, notice how this interaction is assymetric; one fits into the other. It is inherently directional. This likely means that one is structurally dependent on the other to exist, but not the other way around. Most likely the helix that donates the adenosines is dependent and thus younger than the helix that accepts it into its minor groove. If this is the case, then we would expect that all the A-minor motifs in the ribosome all have one direction, which is really useful in figuring out which parts of the ribosome are predate the other parts. See this figure below from this paper. This is regarding the large sub unit of the ribosome. Red arrows indicate the directions of A-minor interactions. Black arrows indicate another structural dependency, wherein the removal of the part at the start of the arrow before the part at the end of the arrow would break the structure in half. Notice how the PTC is at the bottom and structurally independent to all the other domains (more on that later).
Additionally, the first paper also discusses so-called âinsertional fingerâ prints, which mark sites where folded RNA structure have been known to expand and grow. So when they combined all these empirical evidence, they get a very detailed view of the ribosome. The two subunits are constructed in layers, and layer-by-layer they remains compact internally stabilized structures such that each layer is independent from the one(s) on top of it. This gives us a very straight forward picture of the history of the ribosome. Deeper and independent predate the ones that are structurally dependent on them. This is the striking model that they propose detailing six phases; with each phase representing a structural layer.
And thatâs just discussing the empirical evidence of the ribosomal RNA. If we look empirical observations of ribosomal proteins and look at the protein strands that interact with each of these six phases, we get this picture below. The first two phases donât interact with any peptides, but the 3rd phase interacts with random coils, the 4th phase interacts with secondary structures like beta-sheets, and the 5th and 6th phases interact with peptides that fold into complex globular structures.
Well ainât that peculiar? Ribosomal peptides that interact with older parts of the ribosome are simpler, while those that interact with younger parts are more complex. Also notice that the phase where proteins first acquire complex folds (phase 5-6) is also the phase where the ribosome is predicted to have acquired the capacity to perform translation.
But we are not done yet. Remember the PTC (peptidyl transferase center)? That structure appeared at phase 2, which often called the âprotoribosomeâ (see picture below). It is a semi-symmetrical structure composed of stemâelbowâstem structural motifs, which is an ancient RNA fold found in tRNAs as well. What could this small core of the ribosome possibly do? Itâs certainly not capable of translation. However, the PTC is the catalytic site that forms peptide bonds. So we can predict that this proto-ribosome would do something similar. Lo and behold, it actually does! More empirical evidence.
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Very interesting, but I think my reference of âensemblesâ is different form this. Your citation refers to conformation, i.e. if you produce many many copies of one enzyme, these enzymes do not all have identical folds. They populate multiple energetic minima, and each copy constantly changes confirmation from one minima to another. Thatâs indeed an important fact that is often overlooked in the âmachineâ view of life that minimizes the importance of the statistical noise that dominates the molecular world.
However, when I was referring to âensemblesâ, I was talking about the sequences of the peptides. Not their confirmations. Today, one encoded enzyme has a highly predictable sequence because translation fidelity is high. Of course the folded structure changes confirmation constantly (as previously mentioned) but the amino acid sequences remain near constant. That was not the case prior to the origin of translation, during which only ensembles of sequences were available: sets of similar but still highly variable sequences. At least, thatâs how I understand the argument made by Carl Woese. These could have performed some functions, but thatâs an area of research that needs to be explored further. I have seen that even random peptide sequences of 80-100 amino acids, they can still acquire a folded structures at a fairly high probabilities (5-20%). Regarding functions, I have also seen mentions of âpeptide nestsâ that can bind onto phosphates, sulfates, carbonates and ironâsulfur clusturs which are important in metabolism. Some of these ânestsâ are still present in some of the most ancient protein motifs (e.g. Rossmann and Walker-A). Here is a good review paper on this.
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Yep, which is why I wrote ââŚconceptually similar (just a bit)âŚâ
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Iâm not ignoring the âorâ. If the âintrinsic natureâ of the codon/amino acid was capable of specifying the nucleotide sequences of the translation system, then it (the âintrinsic natureâ of the codon/amino acid) would necessitate the mapping. Necessity and intrinsic nature would both be non-arbitrary.
What you need to do is explain how the intrinsic nature of the codon/amino acid pairing is capable of arranging the nucleotide sequences that code for the translation system.
Catalysts simply speed up a chemical reaction. They donât arrange nucleotide sequences in any particular order. Thatâs what you need to explain.