Scientific hypotheses make empirical predictions

No, I’m pointing out that YOU are gaming by using vague terms to begin, then moving the goalposts when challenged. That’s the antithesis of a scientific approach.

So am I, but I am focusing only the weakness of your claims about a single particular class! But you’re just talking and not offering any hypotheses that make empirical predictions.

And I am pointing out that such a sweeping and vague statement is poorly conceived because it is full of untenable assumptions. You’ll tactically convert it to a much more specific one if you are challenged.

Let’s do science and convert your rude claim into a testable scientific hypothesis.

If I manipulate E. coli K12 so that translation of 8% of protein-encoding genes occurs improperly–specifically, a bulky tryptophan residue is inserted instead of stopping, will the bacterium live or die?

Do you see how the prediction is clear and entirely empirical?

Understood. I thought you were talking about the function of tRNA suppressors to bypass early termination caused by a nonsence mutation to a stop codon, but yes, such tRNAs can also produce readthrough past the normal stop in some cases. And some of those proteins will be viable and active, others not. So technically you are right. in that Biosemiotics statement is not universally true. But by that token one could say the same about the majority of biochemical mechanisms in cells, since for every rule in cell biology there seem to exist exceptions.

Thanks for your clear and direct answers. I can only speculate that perhaps if you had given such an answer to Biosemiotics, a lot of the energy and argument above might have been avoided. Then again, I realize that I am not aware of the full history of this discussion, so I am only speculating.

[quote=“Sy_Garte, post:88, topic:4328”]
And some of those proteins will be viable and active, others not.[/quote]
Hello Sy,

I doubt that this is true on a gene-by-gene basis, though. I suspect that it’s true on a translation-by-translation basis, as in translation pooping out at different distances from the unrecognized stop codon. Either way, proper termination is not necessary, which provides evolution with far more ability to tinker and refine mechanisms for termination than it has for initiation. An intelligent designer would have no such constraints.

I don’t think it’s generally true, either, and there is more strong evidence against Bio’s claim.

But translation is a particularly ironic choice since has an internal control addressing this. What happens if we construct an analogous tRNA for the initiating AUG?

Thanks for your clear questions.

[quote]I can only speculate that perhaps if you had given such an answer to Biosemiotics, a lot of the energy and argument above might have been avoided.
[/quote]We can speculate, but IMO a huge problem is that Bio has far too much emotional investment in his hypothesis to subject it to anything resembling empirical testing. A less severe form of this problem even can be spotted in some NIH R01 applications, when the applicant proposes to “explore my hypothesis” instead of just testing it.

Hmmm Looks like you looked me up. Its OK. Im retired. Which is why I was able to come back to Biologos and comment freely.

Hello Sy,

I don’t see why that looks like I looked you up. I’m just relating my experiences on study sections.

See message.

Here’s another empirical test of your hypothesis: we will never observe a normal gene that requires failure of the stop function of translation for all or any part of its normal activity.

Thus, if we observe even one, your hypothesis is falsified. Do you agree?

No, I’m pointing out that YOU are gaming by using vague terms to begin

Vague terms? Here are the terms I’ve given:

1) the arrangement of bases in each codon results in alternate amino acids being presented for binding
2) the aaRS establishes the amino acid-to-anticodon association
3) the amino acid-to-anticodon association is spatially and temporally isolated from the pairing of codons to anticodons during translation.
4) the arrangement of the bases in each codon is independent of the minimum total potential energy state of mRNA.
5) the constraints of a reading-frame code (Crick) are necessary to proper translation
four examples:
5a) initiation at a specific location
5b) direction of reading
5c) stop function
5d) three bases in a codon

That constitutes 5 predicted observations, with four examples of constraints given of the 5th observation. You’ve attacked 1 of those 9 items, suggesting that it contains baked-in assumptions that falsify the claim of the test – i.e. that genetic translation is a semiotic system using spatially-oriented representations and a reading frame code.

You haven’t even begun to falsify that claim, what you have done is assumed that the cell’s capacity to control protein length isn’t necessary to function - whereas I do not make that assumption because it’s both unnecessary and contrary to the evidence. The processes that the cell uses to control protein length are an observable reality of the system, both in transcription and translation. My view is based on the removal of those processes. Your view allows the cell to continue with those processes intact, and then you point out isolated instances of specific transcripts that are themselves controlled in length. You have further demonstrated that this less-than-earnest view is the only view you are willing to entertain.

I am not obliged to overlook the processes that the cell uses to control protein length – and I have no intentions of doing so. I’m not obligated to ignore that improper length often ends in non-function and disease. But even if you demand that you are correct under your terms, it doesn’t falsify the test. At the very most, it would only show that the observation of a reading-frame code doesn’t turn on controlling protein length, and so, the stop function shouldn’t be included among the examples given. This is clearly evidenced by the fact that you can’t attack any of the other examples in item #5, nor any of the observations 1 though 4. I expect that you will continue to ignore those remaining predictions.

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your rude claim

You can talk to me about rude claims when you deal with the ridiculous hit piece you wrote as the OP. After you sift through the pedantic nonsense, you can recant your claim that my argument doesn’t make predictions that are empirically verifiable.

By the way…

You’ve suggested that the observations I’ve provided for the test don’t actually predict anything at all, they are, as you say “post-hoc rationalizations”. But if the predictions just end up describing the existing system, then you are effectively saying that the descriptions I’m giving are already established facts. So I would just ask: then why are you not accepting them? Instead, you lecture me about what real scientists do.

Do you understand the problem with that? If you are not accepting them, then they are predictions - to you. They are predictions to anyone who doubts them. Anyone who would attack them as you have, and me for bringing them up.

So let us just say the material facts are not the problem. It’s the observation you don’t like. You believe in empirical evidence; it’s a thing of value to you, and you don’t want it to show that the translation system can be physically identified, and then found nowhere else but in language and mathematics.

That’s what this thread is about. And you are right about physical evidence, it is a great value.

One more thing … Marshall Nuremberg’s real name is Marshall Nirenberg, and the methodology he used to decipher the genetic code was to manipulate the input and document the output. And what he documented at the output could not be derived from the input, even in principle. The relationships had to be demonstrated. They exist as a part of the necessary discontinuity between the input and output of the system.

(clipped)

There is a formidable line at the origin of life, where a representational organization necessarily comes into being. This line has been repeatedly described in the scientific literature. Pattee refers to it in terms of an “epistemic cut” between rate-independent genetic symbols and the rate-dependent dynamics they control. Johnson refers to it in terms of the necessary contingency instantiated in a physical medium. Barbieri states that any description of the living world requires objective observables that are otherwise not measurable. Yockey speaks of the symbolic nature and immateriality of the biological message recorded in monomers. Abel refers to it in terms of the primacy of formalism over function. Crick required it in the adapter hypothesis. Nirenberg demonstrated it in the ribosome. And the late British-Hungarian polymath John von Neumann wrote of it in terms of non-dynamic “quiescent descriptions” required in the logic of self-replication.

cheers

Please, Upright, this is absurd. None of those are anything you can directly observe.

You, probably unintentionally, stumbled onto an actual empirical prediction:

Instead of pretending to know my view and putting words in my mouth, why don’t you ask me? More importantly, why don’t you make an empirical prediction and search the literature to see if one of the doers has done what you dream about?

[quote=“Biosemiosis.org, post:96, topic:4328”]
You’ve suggested that the observations I’ve provided for the test don’t actually predict anything at all, they are, as you say “post-hoc rationalisations”.[/quote]
Correct. There’s no such thing as “observations provided for the test.” That’s more word salad.

Then they aren’t predictions at all! They are descriptions!

You need to have the courage to predict something you don’t know, or in your case what you think you know.

No, I’ve pointed out that at least one of your major descriptions is anything but an established fact.

Because some of them are wrong, and I’m focusing on your ignorance of translation stops.

[quote]Instead, you lecture me about what real scientists do.
[/quote]Real scientists test the empirical predictions of their hypotheses. You appear to have zero interest in doing anything of the sort.

Here we go:

  1. If I manipulate E. coli K12 so that translation of 8% of protein-encoding genes occurs improperly–specifically, a bulky tryptophan residue is inserted instead of stopping, will the bacterium live or die?

  2. We will never observe a normal gene that requires failure of the stop function of translation for all or any part of its normal activity.

[quote=“Biosemiosis.org, post:97, topic:4328”]
One more thing … Marshall Nuremberg’s real name is Marshall Niremberg,[/quote]

Good point. Let’s do science!

Hypothesis: my Mac’s autocorrect made the change and I missed it.
Empirical prediction: if I type “Nirenberg,” my Mac will change it to “Nuremberg.”
Experiment: my hypothesis was supported by the empirical observation.

See how easy it is?

But his predictions for the output were empirical, that is, merely that one homopolymer would increase the cpm from one particular labeled amino acid over control, but the others would not.

Nothing more. Read the paper. No silly demands that anyone do anything like yours. They tested their hypothesis. What are you afraid of?

[quote]And what he documented at the output could not be derived from the input, even in principle.
[/quote]You’re very mistaken there. That’s what went into the design of the experiments, something you also seem to be afraid to do.

1) the arrangement of bases in each codon results in alternate amino acids being presented for binding
2) the aaRS establishes the amino acid-to-anticodon association
3) the amino acid-to-anticodon association is spatially and temporally isolated from the pairing of codons to anticodons during translation.
4) the arrangement of the bases in each codon is independent of the minimum total potential energy state of mRNA.
5) the constraints of a reading-frame code (Crick) are necessary to proper translation
four examples:
5a) initiation at a specific location
5b) direction of reading
5c) stop function
5d) three bases in a codon
.

Benkirk: None of those are anything you can directly observe.

When someone defends their position by suggesting that universal experience is disallowed in science, that person is not practicing science. The insults and pedantic referencing of the scientific method is icing on the cake.
.

“ genetic translation is a semiotic system using spatially-oriented representations and a reading frame code.”

Show me a physical system that produces function in the living kingdom, where:

  • where a finite set of iterative objects evoke alternate products in the output of the system
  • where a second set of objects determines what the products will be
  • where the arrangement of the iterative objects is energy rate-independent (Pattee)
  • where permutations (combinatorial expansion) controls the product

… that isn’t also a semiotic system using spatially-oriented representations and a reading-frame code. You can’t do that and neither can anyone else. It’s called universal experience (the backbone of science).

.
Empirical science isn’t the issue, Ben. You just don’t want the observations to be made. But the people who study such things are respected (often venerated) members of the scientific community. They’ve made the observations, and those observations don’t disappear because you ignore them. You only have the power to obfuscate knowledge, not make it go away.

And what he documented at the output could not be derived from the input, even in principle.

Benkirk: You’re very mistaken there.

Nirenberg tagged the amino acids, introduced a known input, and documented the output. He demonstrated the relationship of poly-U to phenylalanine. By no other means would we know the genetic code.

This is intentional deception on your part. Like I said earlier, you don’t need me around for that.

I’m pointing out that observations have been made that you are ignoring.

Again, your hypothesis:

If stop functions are NECESSARY as stated in the hypothesis, a SINGLE exception is sufficient to falsify the hypothesis, correct?

It took me literally 30 seconds to find the relevant empirical literature.

Not at all. If something you claim to be necessary really isn’t, it tells us a lot about how it likely evolved and was not designed.

There’s no deception. Try to state Nirenberg’s work as he saw it: a brilliant example of multiple hypothesis testing (most of which were falsified), one huge step in a long, iterative process. And the output is simply empirical, cpm in experimental vs. control. They baked everything in before they knew the results.

Where are your empirical predictions?

More deception.

You are deceiving yourself Ben. I provided 9 observables in a test, and you were only able to attack one of those, and in that one instance you were forced to make a massively unwarranted assumption which no biologist in the world would make (i.e. since xyz protein can survive stop codon anomaly, the living cell does not need to control protein length). And after multiple corrections on this point, you persist with the deception, as you wrap yourself in the flag of science. You had an intellectual choice of addressing the issue in earnest, or continuing with your deception for rhetorical purposes. You failed to make the right choice.

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