The Genetic Code and Universal Common Ancestry

Well since you ended up by dismissing it as insufficient, what else is that but to say it doesn’t count? The question we were considering is the potential evidence for a simpler pre-LUCA stage of life, and I have a hard time seeing how, if such a stage has not left any descendants with a similar level of complexity, we could ever hope to obtain evidence of such a stage if you are going to use the lack of homology between cellular structures or systems(or the actual lack of that structure or system) as evidence of separate ancestry.

What would evidence for simpler life look like? Well, fewer ancestral genes, missing ancestral genes, simpler ancestral genes? But if these entail the lack of a defining attribute of cellular life as we know it, you take it to imply separate ancestry rather than simpler life. But then what would evidence of simpler life have to look like? In the absence of surviving descendant with a similar level of complexity, it seems you have made it impossible for such evidence to exist.

I think this is a good illustration of the distinction between an observation and one’s interpretation of it.:

Observation: The membranes of archaea and bacteria have distinct chemistries and the respective enzymes of their lipid biosynthesis show no sign of homology.

Design interpretation: Archae and bacteria were independently designed.

Non-design interpretation: The common ancestor of archaea and bacteria did not have a membrane.

Right, but there’s no observation for which one could not come up with an almost infinite number of different interpretations. There is no pattern we could observe you could not account for with some ad-hoc hypothesis. You could say every imaginable collection of data, or any imaginable pattern is just a remarkable coincidence, or that it was designed to be the way it is because the designer desired that specific outcome.

Things fall down to the ground not because there’s a mutual forces of attraction between objects with mass, but because invisible pixies are pushing them around. Or they’re actually all moving around in random directions, it’s just a remarkable coincidence that some of them seem to systematically fall down. Or even worse, the data is an illusion, we’re in a sort of simulation and it only appears to us af if they fall down. In fact they remain stationary, or they don’t even exist.

One can have specific reasons for favoring one interpretation over the other. Personally, my own holistic view of the cell as a complex, integrated system leads me to favor the design interpretation.

Me, I like consistency, parsimony, explanatory power and scope. That’s why I don’t suddenly stop thinking ancestral convergence and consilience of independent phylogenies is evidence for common ancestry right before we hit the final node in the tree of all known life.

And one can use one’s preference for a particular interpretation as an impetus for further investigations in order to pry the two hypotheses apart. For example, the hypothesis of an independent design of archaea and bacteria would predict that other similar discontinuities between the two cell types would exist.

Why? It’s not clear to me why that would be the case. Why would the designer not just re-use the same basic designs in both the bacterial and archaeal clade? It doesn’t look like a prediction to me, it looks like a sort of ad-hoc rationalization that’s supposed to make it compatible with the already collected evidence, which you’re now trying to sell as a prediction.

I’m not buying it. You don’t have any model that actually predicts this. Where is your model? What are it’s mechanisms, what are it’s starting conditions? I want to verify that it predicts what you say. Can I implement it in a computer and see that yes, in fact, on your design model the designer will come to produce organisms with “similar discontinuities”?

I think evidence that would convince everyone is an unrealistic standard. I get that there has to be some sort of criterion by which to judge whether the evidence is good or bad, persuasive or not, but there will be some inherent subjectivity to that and all we can do is argue about it.

The sense-antisense complementarity between the conserved cores of Class I and Class II aminoacyl-tRNA synthetases is certainly something we would expect to see if the two superfamilies ultimately derive from the opposite strands of the same ancestral gene. It would be entirely rational for a researcher to take this result as an impetus to further investigate the hypothesis.

But I don’t see this as evidence that must compel accept of the hypothesis in everyone, in the sense that one would have to drop one’s own investigation of a competing hypothesis. One of the reviewers of the paper makes an interesting point: (… )A design hypothesis would predict that the sense-antisense complementarity is the result of some functional/structural constraint. This suggests an avenue for further research and shows that design thinking can lead to expectations that differ from those of the non-design approach.

This is where I think your alternative theory runs into inconsistency and arbitrariness. Why suddenly invoke the potential for a structure/function constraint criterion at the final node in the tree just because it potentially implies a lack of some later evolved structure?

Presumably the two next nodes in the bacterial tree (say) also imply a lack of later evolved structures, yet you don’t posit separate ancestry there. At that taxonomic level you would be fine(?) with accepting ancestral convergence and consilience of independent phylogenies as evidence for common ancestry, and you might even allow yourself to rationalize that some putative lack of a homologous key gene can be explained by either a lack of conservation allowing you to detect a homologous relationship, or gene loss, or replacement in one or both clades. But not at the final node.

Yet you could have invoked the same criterion as an argument for separate ancestry at any node in the tree. Reconstructed ancestral nodes in the tree of primates exhibits ancestral convergence to the reconstructed ancestral node in the tree of rodents because of some sort of structural or functional constraint, or by mere remarkable coincidence(what could not be taken to be a mere remarkable coincidence in this fashion? Homology itself could be claimed to just be a remarkable coincidence). Yet presumably you don’t think so and are fine with taking that as evidence for common descent. At every other node in the tree, except the final one.

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On a related note, if you think the ancestral convergence towards opposite strand complementarity is due to some sort of functional constraint by a mere coincidence, you still have to reason that the last common ancestor of all bacteria, and the last common ancestor of all archaea, each must have independently evolved all twenty aminoactyl-tRNA-synthases from two ancestral genes that were merely coincidentally exhibiting ancestral strand complementarity, perhaps due to functional constraint.

All the extant enzymes in the bacterial class I aaRS enzymes are homologous and belong to the same family that you now must rationalize evolved in some bacterial lineage before the last common bacterial ancestor. So the last common bacterial ancestor itself has a substantial prior evolutionary history, and was once simpler and had a simpler genetic code. Same goes with the bacterial class II enzymes of course.

And in parallel then, the same thing happened in the archaeal clade. They too must have started out (been designed) initially with just two enzymes that coincidentally appears to be opposite-strand complementary, from which the archaeal class I and class II families evolved prior to the last archaeal common ancestor.

Or I suppose you can again just invoke the two classes of enzymes only appear to belong to a homologous family by remarkable coincidence of structural/functional constraint, so they never even evolved from common ancestral genes at all but show nesting hiearchical structure by coincidence too.

It seems to me that the monophyly of all known cellular life is a simpler hypothesis. The evolutionary expansion of the class I and II enzyme superfamilies only happened once in the lineage leading to LUCA, by which time they had expanded to all twenty members, which all subsequent life inherited.

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does evolution explain how this protein evolved in the first place? such a protein need at least 2-3 sites. a site for binding trna and a site to bind amino acid:

(image from https://www.mun.ca/biology/desmid/brian/BIOL2060/BIOL2060-22/CB22.html)

also note that the genetic code need at least several of them to form a code. a code base on a single amino acid suppose to be non functional.

That’s a distinction without a difference.

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We may never know the evolutionary histories of the earliest proteins.

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the problem is that i think its true for almost any protein. there is no real scenario for a well known protein like hemoglobin for instance. just assumptions.

Origin of antifreeze genes in fish:

https://www.pnas.org/content/94/8/3485

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im not sure about that case since it may be a simple function. this is why i mention the hemoglobin. do we have a stepwise explanation for the evolution of a globin from non globin protein?

No. There will always be proteins that we may not have a specific evolutionary history for. Why is that a problem? A scientific theory is never going to be a complete explanation since humans are not omniscient.

In principle, it can. It’s just that we don’t know which of many possible options occurred in actual history, because it happened too long ago to determine. What little evidence from that early period that is left behind is not good enough to determine what happened to spawn these proteins in the first place.

The discussion has gotten quite lengthy, and I may not have the time to reply to the latest round of replies. But let me just quickly note the irony that the entire scientific community, with all its bright minds and laboratories around the world, may never find the evolutionary history of the earliest proteins - whereas little old me, discussing this in my spare time, has to explain every single feature of early life from a design perspective.

There is the additional irony of ID/creationists demanding step by step processes for how genes evolved, and yet supply none of that evidence for how genes were designed.

You also claim that features shared by modern organisms can be used to construct the genomes of the first life forms. That argument needs to be supported.

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I don’t think your characterization here portrays the situation accurately. First of all it is certainly true to say that scientists might never find the evolutionary history of the first proteins. But there is certainly a desire to know it, and if they can’t provide the evolutionary history of the first proteins, there is a desire for them to at least come up with some plausible history for the first proteins. How it could have happened, not necessarily that they prove how it did actually happen.

I don’t see how anyone have suggested you are under any greater or more difficult to meet degree of obligation here.

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And if you provide such a step by step account, they call it a just-so story and dismiss it as a baseless fantasy invented because of your Darwinist-atheistic materialistic bias and fear and hate of God yadda yadda.

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I’m only asking you to explain the utter stupidity of the design of the start codon, which is painfully obvious if one uses the stop codons as intelligently-designed controls. It makes perfect sense if it evolved.

You keep falsifying that claim. How come?

As a human of human-like intelligence, I see no engineering reason for such a fundamental difference between the start and stop codons.

I’ve seen you say this before ( Code as an Analogy of DNA? - #205 by Mercer for instance) but could you explain this just a bit more? I read a bit on start and stop codons, so I see there are differences. Are you saying that you wouldn’t expect there to be any difference if they were engineered? I would think that they would have to have some difference to be distinguishable. Or are you saying that you expect different differences, or something else entirely?

The start codon puts a mandatory methionine at the N-terminus. The stop codons allow any amino-acid residue at the C-terminus.

If stop codons are intelligently designed, start codons are stupidly designed.

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are you saying that you are able to detect bad design? if so what do you think about the eye design?

Are you saying you’re not?

That’s another of those inadvertent admissions of ignorance.

Anyone with even the slightest familiarity with zoology, biology or evolution knows that there are about half-a-dozen different ‘designs’ of eye across animals, each of which comes in a wide variety of shapes, sizes, colours and other variants.

Only some-one who’s knowledge is limited to out-of-context Darwin quotes would refer to “the eye design”.

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