Endogenous protein S-Nitrosylation in E. coli: regulation by OxyR.
Summary of "Endogenous protein S-Nitrosylation in E. coli: regulation by OxyR."
Endogenous S-nitrosylation of proteins, a principal mechanism of cellular signaling in eukaryotes, has not been observed in microbes. We report that protein S-nitrosylation is an obligate concomitant of anaerobic respiration on nitrate in Escherichia coli. Endogenous S-nitrosylation during anaerobic respiration is controlled by the transcription factor OxyR, previously thought to operate only under aerobic conditions. Deletion of OxyR resulted in large increases in protein S-nitrosylation, and S-nitrosylation of OxyR induced transcription from a regulon that is distinct from the regulon induced by OxyR oxidation. Furthermore, products unique to the anaerobic regulon protected against S-nitrosothiols, and anaerobic growth of E. coli lacking OxyR was impaired on nitrate. Thus, OxyR serves as a master regulator of S-nitrosylation, and alternative posttranslational modifications of OxyR control distinct transcriptional responses.
Affiliation
Institute for Transformative Molecular Medicine and Department of Medicine, Case Western Reserve University School of Medicine and University Hospitals Case Medical Center, Cleveland, OH 44106, USA.
Journal Details
This article was published in the following journal.
Name: Science (New York, N.Y.)
ISSN: 1095-9203
Pages: 470-3
Links
- PubMed Source: http://www.ncbi.nlm.nih.gov/pubmed/22539721
- DOI: http://dx.doi.org/10.1126/science.1215643
Medical and Biotech [MESH] Definitions
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Src-family Kinases
A PROTEIN-TYROSINE KINASE family that was originally identified by homology to the Rous sarcoma virus ONCOGENE PROTEIN PP60(V-SRC). They interact with a variety of cell-surface receptors and participate in intracellular signal transduction pathways. Oncogenic forms of src-family kinases can occur through altered regulation or expression of the endogenous protein and by virally encoded src (v-src) genes.
Enterohemorrhagic Escherichia Coli
Strains of ESCHERICHIA COLI that are a subgroup of SHIGA-TOXIGENIC ESCHERICHIA COLI. They cause non-bloody and bloody DIARRHEA; HEMOLYTIC UREMIC SYNDROME; and hemorrhagic COLITIS. An important member of this subgroup is ESCHERICHIA COLI O157-H7.
Adenomatous Polyposis Coli Protein
A negative regulator of beta-catenin signaling which is mutant in ADENOMATOUS POLYPOSIS COLI and GARDNER SYNDROME.
Adhesins, Escherichia Coli
Thin, filamentous protein structures, including proteinaceous capsular antigens (fimbrial antigens), that mediate adhesion of E. coli to surfaces and play a role in pathogenesis. They have a high affinity for various epithelial cells.
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