Tetracycline binds the small subunit of bacterial ribosomes and blocks aminoacyl tRNA entry, yet physicians prescribe it with limited harm to patient translation. What makes this selectivity possible?

Core Concept

Antibiotic specificity exploits structural differences between prokaryotic 70S ribosomes and the 80S ribosomes of eukaryotic cytosol. The tetracycline binding pocket recognizes features of the bacterial decoding center absent from the larger eukaryotic particle, so host protein synthesis continues nearly unaffected. Residual side effects trace largely to mitochondrial ribosomes, which retain prokaryotic ancestry.