KaladinsSenseOfHumourSpren

There are a few conceptual mix-ups in your argument.
It’s reasonable to say anticodons play a role in assembling a polypeptide, but they don’t originate the sequence. The ordering of amino acids is encoded in the mRNA codons, but tRNA anticodons simply recognize those codons and bring the corresponding amino acids. So anticodons are part of the translation machinery, not the primary drivers of sequence information.
The larger issue is with the stop codon point. A stop codon does not correspond to tertiary structure at all. As I mentioned previously, it signals the end of translation, meaning the ribosome releases the completed primary structure (the linear amino acid chain). Tertiary structure arises later through protein folding driven by chemical interactions, not from anything the stop codon specifies. E.g., pure ribosome assembly doesn't produce tertiary structures, and there is no direct correlation.

There’s also a terminology slip: “quaternary polypeptides” isn’t accurate. Quaternary structure refers to a protien composed of multiple polypeptide chains, like hemoglobin. Each chain is synthesized separately (each with its own stop codon), and only afterward do they assemble into a functional complex, hrough folding and chemcial bonding (e.g. Covalent, Hydrogen bonding, etc)

What are you trying to argue?
 

Nerds/with love

'Twas enjoyable.