Many prokaryotic species generate hydrogen sulfide (H₂S) in their natural environments. However, the biochemistry and physiological role of this gas in nonsulfur bacteria remain largely unknown. Here we demonstrate that inactivation of putative cystathionine β-synthase, cystathionine γ-lyase, or 3-mercaptopyruvate sulfurtransferase in Bacillus anthracis, Pseudomonas aeruginosa, Staphylococcus aureus, and Escherichia coli suppresses H₂S production, rendering these pathogens highly sensitive to a multitude of antibiotics. Exogenous H₂S suppresses this effect. Moreover, in bacteria that normally produce H₂S and nitric oxide, these two gases act synergistically to sustain growth. The mechanism of gas-mediated antibiotic resistance relies on mitigation of oxidative stress imposed by antibiotics.

Transcription and Translation in Train: In bacteria, translation of messenger RNA into proteins by the ribosome usually begins soon after the ribosome binding site emerges from RNA polymerase. Now there is evidence for direct coupling between transcription and translation in bacteria. Proshkin et al. (p. 504 ; see the Perspective by Roberts ) show that the trailing ribosome controls the rate of transcription by preventing RNA polymerase from spontaneous backtracking, which allows precise adjustment of transcriptional yield to translational needs under various growth conditions. Burmann et al. (p. 501 ; see the Perspective by Roberts ) provide a potential mechanism for coupling by showing that the transcription factor NusG, which binds RNA polymerase through its amino-terminal domain, competitively binds either a ribosomal protein or the Rho transcription termination factor through its carboxy-terminal domain. Rho binding might occur after release of the ribosome from messenger RNA, thus linking termination of transcription and translation.

It's a Gas: Many antibiotics, including beta-lactams, aminoglycosides, and quinolones, kill bacteria (at least in part) by oxidative stress.Gusarovet al.(p.1380) show that nitric oxide (NO) produced by bacterial NO synthases (bNOS) protects bacteria, includingStaphylococcus aureusandBacillus anthracis, against toxic agents they may encounter in the soil or in host organisms. Thus, bNOS activity is specifically induced in response to antibiotics and, in turn, activates the expression of another key antioxidant enzyme: superoxide dismutase. Hence, NO-mediated antibiotic resistance not only operates by direct chemical modification of toxic molecules, but also alleviates oxidative stress caused by naturally occurring antibiotics.