NITROSATIVE STRESS - ACTIVATION OF THE TRANSCRIPTION FACTOR OXYR

Hydrogen peroxide (H2O2) imposes an oxidative stress to Escherichia co li that is manifested by oxidation of glutathione and related redox-se nsitive targets. OxyR is a thiol-containing transcriptional activator whose oxidation controls the expression of genes involved in H2O2 deto xification. Here we report that certain S-nitrosothiols (RSNOs) impose what we term a ''nitrosative stress'' to E. coli, evidenced by loweri ng of intracellular thiol and the transcriptional activation of OxyR b y S-nitrosylation. This cellular and genetic response determines the m etabolic fate of RSNOs and thereby contributes to bacterial rescue fro m stasis. Our studies reveal that signaling by S-nitrosylation can ext end to the level of transcription and describe a metabolic pathway tha t constitutes an adaptation to nitrosative stress.