The antibiotic streptomycin inhibits initiation and causes misreading of mRNA in prokaryotes (bacteria). Very effective against Mycobacterium tuberculosis, the "bug" causing tuberculosis, but also used in veterinary medicine and against plant infections.
Streptomycin is produced by Streptomyces griseus and contains three groups: N-methyl-L-2-glucosamine, a methyl pentose and an inositol derivative with two guanidyl residues (therefore I'm not even trying to draw it here).

This trisaccharide interferes with the binding of formylmethionyl-tRNA to ribosomes, therefore the mRNA that arrives at the ribosomes with the intention to be translated into a protein never occurs. But if it gets that far for the translation to start, misreading occurs because the streptomycin causes isoleucine (with triplet AUU) to be build in too, when only a phenylalanine (UUU) is ment to go into the polypeptide chain, resulting in a "wrong" protein.

Well, this for the good old days of sensitivity to antibiotics. Because initially only several bacteria were resistant to streptomycin, it was fairly easy to find out the trick of the resistant bacteria. It appeared to be just one point mutation, the so-called 30S subunit of the ribosome. Even more precisely: the protein S12 is the key to sensitivity. Transfer of the resistance between bacteria occurs via the R-plasmids.

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