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 tri
saccharide 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.