Understanding how bacteria resist antibiotics lies at the crux of staying ahead in the resistance game. A research group at the New York State Health Department's Wadsworth Center in Albany offers a vivid view of how a bacterial protein called Tet (0) shoves aside the antibiotic tetracycline. (C.M.T. Spahn et al., "Localization of the ribosomal protection protein Tet (0) on the ribosome and the mechanisms of tetracycline resistance." Molecular Cell, 7[5]:1037-45, May 2001.) To be an effective drug, an antibiotic must target a part of the protein synthetic machinery that is present in the bacteria cell but not in human cells. The ribosome is one such area of distinction. "Tetracycline normally binds the center of the small subunit of the ribosome and prevents binding of incoming tRNA, interfering in protein synthesis," says Christian Spahn, a postdoctoral associate in the laboratory of Joachim Frank, director of the computational biology...
Interested in reading more?
Become a Member of
Receive full access to digital editions of The Scientist, as well as TS Digest, feature stories, more than 35 years of archives, and much more!