Background:

Spectinomycin is an aminocyclitol antibiotic produced by S. spectabilis with activity against gram-negative bacterial species. Spectinomycin has been used for the treatment of gonorrhea, where it inhibits microbial protein synthesis by binding to the 30S ribosomal subunit, protects the N‐7 position of E. coli 16S rRNA residue G1064 from methylation by dimethyl sulfate. Binding of spectinomycin at this location is thought to stabilize helix 34, inhibiting the binding of elongation factor G, thereby blocking translocation of peptidyl‐ RNAs from the ribosomal A site to the P site [1].

Spectinomycin selectively inhibited protein synthesis in cells and in extracts of E. coli. Mutations to high-level resistance to this antibiotic map close to the streptomycin locus, and the site of action of spectinomycin, like that of streptomycin, is the 30S ribosomal subunit, as shown by experiments with reconstituted 70S ribosomes containing subunits from sensitive and from resistant ribosomes [2].

参考文献:
[1] Zimmerman J M, Maher L J.  In vivo selection of spectinomycin‐inding RNAs[J]. Nucleic acids research, 2002, 30(24): 5425-5435.
[2] Davies J, Anderson P, Davis B D.  Inhibition of protein synthesis by spectinomycin[J]. Science, 1965, 149(3688): 1096-1098.