In the Drosophila gut, reactive oxygen species (ROS)‐dependent immunity is critical to host survival. This is in contrast to the NF‐κB pathway whose physiological function in the microbe‐laden epithelia has yet to be convincingly demonstrated despite playing a critical role during systemic infections. We used a novel in vivo approach to reveal the physiological role of gut NF‐κB/antimicrobial peptide (AMP) system, which has been ‘masked’ in the presence of the dominant intestinal ROS‐dependent immunity. When fed with ROS‐resistant microbes, NF‐κB pathway mutant flies, but not wild‐type flies, become highly susceptible to gut infection. This high lethality can be significantly reduced by either re‐introducing Relish expression to Relish mutants or by constitutively expressing a single AMP to the NF‐κB pathway mutants in the intestine. These results imply that the local ‘NF‐κB/AMP’ system acts as an essential ‘fail‐safe’ system, complementary to the ROS‐dependent gut immunity, during gut infection with ROS‐resistant pathogens. This system provides the Drosophila gut immunity the versatility necessary to manage sporadic invasion of virulent pathogens that somehow counteract or evade the ROS‐dependent immunity.

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Periodic evolution of H 2 S during aerobic chemostat culture of Saccharomyces cerevisiae resulted in ultradian metabolic oscillation via periodic inhibition of respiratory activity. To understand the nature of periodic H 2 S evolution, we investigated whether oxidative stress is associated with H 2 S production. The cellular oxidative states represented by intracellular level of lipid peroxides oscillated out of phase with the oscillation of dissolved O 2 . Pulse addition of antioxidant, oxidative agent or inhibitor of antioxidation enzymes perturbed metabolic oscillation producing changes in H 2 S evolution. Analysis of H 2 S production profiles during perturbation of oscillation revealed that the amount of H 2 S production is closely linked with cellular oxidative states. Based on these results and our previous reports, we suggest that oxidative stresses result in periodic depletion of glutathione and cysteine, which in turn causes stimulation of the sulfate assimilation pathway and H 2 S production. ß

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