Alkyl hydroperoxide reductase, F52a subunit, FAD/NAD(P)-binding; Serves to protect the cell against DNA damage by alkyl hydroperoxides. It can use either NADH or NADPH as electron donor for direct reduction of redox dyes or of alkyl hydroperoxides when combined with the AhpC protein; Belongs to the class-II pyridine nucleotide-disulfide oxidoreductase family.

Glutathione oxidoreductase; Maintains high levels of reduced glutathione in the cytosol; Belongs to the class-I pyridine nucleotide-disulfide oxidoreductase family.

Alkyl hydroperoxide reductase, F52a subunit, FAD/NAD(P)-binding; Serves to protect the cell against DNA damage by alkyl hydroperoxides. It can use either NADH or NADPH as electron donor for direct reduction of redox dyes or of alkyl hydroperoxides when combined with the AhpC protein; Belongs to the class-II pyridine nucleotide-disulfide oxidoreductase family.

Glutaredoxin 1, redox coenzyme for ribonucleotide reductase (RNR1a); The disulfide bond functions as an electron carrier in the glutathione-dependent synthesis of deoxyribonucleotides by the enzyme ribonucleotide reductase. In addition, it is also involved in reducing some disulfide bonds in a coupled system with glutathione reductase; Belongs to the glutaredoxin family.

Alkyl hydroperoxide reductase, F52a subunit, FAD/NAD(P)-binding; Serves to protect the cell against DNA damage by alkyl hydroperoxides. It can use either NADH or NADPH as electron donor for direct reduction of redox dyes or of alkyl hydroperoxides when combined with the AhpC protein; Belongs to the class-II pyridine nucleotide-disulfide oxidoreductase family.

Catalase HPII, heme d-containing; Decomposes hydrogen peroxide into water and oxygen; serves to protect cells from the toxic effects of hydrogen peroxide.

Alkyl hydroperoxide reductase, F52a subunit, FAD/NAD(P)-binding; Serves to protect the cell against DNA damage by alkyl hydroperoxides. It can use either NADH or NADPH as electron donor for direct reduction of redox dyes or of alkyl hydroperoxides when combined with the AhpC protein; Belongs to the class-II pyridine nucleotide-disulfide oxidoreductase family.

Catalase-peroxidase HPI, heme b-containing; Bifunctional enzyme with both catalase and broad-spectrum peroxidase activity. Displays also NADH oxidase, INH lyase and isonicotinoyl-NAD synthase activity; Belongs to the peroxidase family. Peroxidase/catalase subfamily.

Alkyl hydroperoxide reductase, F52a subunit, FAD/NAD(P)-binding; Serves to protect the cell against DNA damage by alkyl hydroperoxides. It can use either NADH or NADPH as electron donor for direct reduction of redox dyes or of alkyl hydroperoxides when combined with the AhpC protein; Belongs to the class-II pyridine nucleotide-disulfide oxidoreductase family.

Oxidative and nitrosative stress transcriptional regulator; Hydrogen peroxide sensor. Activates the expression of a regulon of hydrogen peroxide-inducible genes such as katG, gor, ahpC, ahpF, oxyS (a regulatory RNA), dps, fur and grxA. OxyR expression is negatively autoregulated by binding to a 43 bp region upstream of its own coding sequence. OxyR is inactivated by reduction of its essential disulfide bond by the product of GrxA, itself positively regulated by OxyR. Has also a positive regulatory effect on the production of surface proteins that control the colony morphology and auto- [...]

Alkyl hydroperoxide reductase, F52a subunit, FAD/NAD(P)-binding; Serves to protect the cell against DNA damage by alkyl hydroperoxides. It can use either NADH or NADPH as electron donor for direct reduction of redox dyes or of alkyl hydroperoxides when combined with the AhpC protein; Belongs to the class-II pyridine nucleotide-disulfide oxidoreductase family.

Superoxide dismutase, Mn; Destroys superoxide anion radicals which are normally produced within the cells and which are toxic to biological systems; Belongs to the iron/manganese superoxide dismutase family.

Alkyl hydroperoxide reductase, F52a subunit, FAD/NAD(P)-binding; Serves to protect the cell against DNA damage by alkyl hydroperoxides. It can use either NADH or NADPH as electron donor for direct reduction of redox dyes or of alkyl hydroperoxides when combined with the AhpC protein; Belongs to the class-II pyridine nucleotide-disulfide oxidoreductase family.

Superoxide dismutase, Cu, Zn, periplasmic; Destroys radicals which are normally produced within the cells and which are toxic to biological systems.

Ammonium transporter; Involved in the uptake of ammonia; Belongs to the ammonia transporter channel (TC 1.A.11.2) family.

RNA polymerase, sigma 54 (sigma N) factor; Sigma factors are initiation factors that promote the attachment of RNA polymerase to specific initiation sites and are then released. This sigma factor is responsible for the expression of enzymes involved in arginine catabolism. The open complex (sigma-54 and core RNA polymerase) serves as the receptor for the receipt of the melting signal from the remotely bound activator protein GlnG(NtrC).

CP4-44 prophage; Antitoxin component of a type IV toxin-antitoxin (TA) system. Antitoxin that counteracts the effect of its cognate toxin CbtA (YeeV). It does not bind to the toxin but instead binds to MreB and FtsZ (the toxin targets), enhancing their polymerization by forming higher-order bundles; it is probably retained in the MreB and FtsZ filament bundles. The mechanism has been proposed to require intergenic DNA, in cis, between the cbeA (yeeU) and cbta (yeeV) genes. The intergenic region was not found to be necessary in another study. Also counteracts the morphological defects c [...]

CP4-44 prophage; Toxic component of a type IV toxin-antitoxin (TA) system. Acts as a dual toxin inhibitor that blocks cell division and cell elongation in genetically separable interactions with FtsZ and MreB. Interacts with cytoskeletal proteins FtsZ and MreB; inhibits FtsZ GTP-dependent polymerization and GTPase activity as well as MreB ATP-dependent polymerization. Binds to both the N- and C-terminus of FtsZ, likely blocking its polymerization and localization, leading to blockage of cell division. Overexpression results in inhibition of growth in liquid cultures and decrease in col [...]

CP4-44 prophage; Antitoxin component of a type IV toxin-antitoxin (TA) system. Antitoxin that counteracts the effect of its cognate toxin CbtA (YeeV). It does not bind to the toxin but instead binds to MreB and FtsZ (the toxin targets), enhancing their polymerization by forming higher-order bundles; it is probably retained in the MreB and FtsZ filament bundles. The mechanism has been proposed to require intergenic DNA, in cis, between the cbeA (yeeU) and cbta (yeeV) genes. The intergenic region was not found to be necessary in another study. Also counteracts the morphological defects c [...]

Antitoxin of the RelE-RelB toxin-antitoxin syste; Antitoxin component of a type II toxin-antitoxin (TA) system. Counteracts the effect of cognate toxin RelE via direct protein-protein interaction, preventing RelE from entering the ribosome A site and thus inhibiting its endoribonuclease activity. An autorepressor of relBE operon transcription. 2 RelB dimers bind to 2 operator sequences; DNA- binding and repression is stronger when complexed with toxin/corepressor RelE by conditional cooperativity. Increased transcription rate of relBE and activation of relE is consistent with a lower l [...]

CP4-44 prophage; Antitoxin component of a type IV toxin-antitoxin (TA) system. Antitoxin that counteracts the effect of its cognate toxin CbtA (YeeV). It does not bind to the toxin but instead binds to MreB and FtsZ (the toxin targets), enhancing their polymerization by forming higher-order bundles; it is probably retained in the MreB and FtsZ filament bundles. The mechanism has been proposed to require intergenic DNA, in cis, between the cbeA (yeeU) and cbta (yeeV) genes. The intergenic region was not found to be necessary in another study. Also counteracts the morphological defects c [...]

Qin prophage; Toxic component of a type II toxin-antitoxin (TA) system. A sequence-specific, ribosome-dependent mRNA endoribonuclease that inhibits translation during amino acid starvation (the stringent response). In vitro acts by cleaving mRNA with high codon specificity in the ribosomal A site between positions 2 and 3. The stop codon UAG is cleaved at a fast rate while UAA and UGA are cleaved with intermediate and slow rates. In vitro mRNA cleavage can also occur in the ribosomal E site after peptide release from peptidyl- tRNA in the P site as well as on free 30S subunits. In vivo [...]

CP4-44 prophage; Antitoxin component of a type IV toxin-antitoxin (TA) system. Antitoxin that counteracts the effect of its cognate toxin CbtA (YeeV). It does not bind to the toxin but instead binds to MreB and FtsZ (the toxin targets), enhancing their polymerization by forming higher-order bundles; it is probably retained in the MreB and FtsZ filament bundles. The mechanism has been proposed to require intergenic DNA, in cis, between the cbeA (yeeU) and cbta (yeeV) genes. The intergenic region was not found to be necessary in another study. Also counteracts the morphological defects c [...]

CP4-57 prophage; Toxic component of a type IV toxin-antitoxin (TA) system. Acts as a dual toxin inhibitor that blocks cell division and cell elongation in genetically separable interactions with FtsZ and MreB. Overexpression results in inhibition of growth in liquid cultures. Overexpression leads to formation of lemon-shaped cells; inactivated by overexpression of cognate antitoxin YfjZ but not when the 2 genes are coexpressed from the same plasmid. Also neutralized by overexpression of non-cognate antitoxins YafW and CbeA.

CP4-44 prophage; Toxic component of a type IV toxin-antitoxin (TA) system. Acts as a dual toxin inhibitor that blocks cell division and cell elongation in genetically separable interactions with FtsZ and MreB. Interacts with cytoskeletal proteins FtsZ and MreB; inhibits FtsZ GTP-dependent polymerization and GTPase activity as well as MreB ATP-dependent polymerization. Binds to both the N- and C-terminus of FtsZ, likely blocking its polymerization and localization, leading to blockage of cell division. Overexpression results in inhibition of growth in liquid cultures and decrease in col [...]

CP4-44 prophage; Antitoxin component of a type IV toxin-antitoxin (TA) system. Antitoxin that counteracts the effect of its cognate toxin CbtA (YeeV). It does not bind to the toxin but instead binds to MreB and FtsZ (the toxin targets), enhancing their polymerization by forming higher-order bundles; it is probably retained in the MreB and FtsZ filament bundles. The mechanism has been proposed to require intergenic DNA, in cis, between the cbeA (yeeU) and cbta (yeeV) genes. The intergenic region was not found to be necessary in another study. Also counteracts the morphological defects c [...]

CP4-44 prophage; Toxic component of a type IV toxin-antitoxin (TA) system. Acts as a dual toxin inhibitor that blocks cell division and cell elongation in genetically separable interactions with FtsZ and MreB. Interacts with cytoskeletal proteins FtsZ and MreB; inhibits FtsZ GTP-dependent polymerization and GTPase activity as well as MreB ATP-dependent polymerization. Binds to both the N- and C-terminus of FtsZ, likely blocking its polymerization and localization, leading to blockage of cell division. Overexpression results in inhibition of growth in liquid cultures and decrease in col [...]

Serine/threonine-protein kinase toxin HipA; Toxic component of a type II toxin-antitoxin (TA) system, first identified by mutations that increase production of persister cells, a fraction of cells that are phenotypic variants not killed by antibiotics, which lead to multidrug tolerance. Persistence may be ultimately due to global remodeling of the persister cell's ribosomes. Phosphorylates Glu-tRNA-ligase (AC P04805, gltX, on 'Ser-239') in vivo. Phosphorylation of GltX prevents it from being charged, leading to an increase in uncharged tRNA(Glu). This induces amino acid starvation and [...]

CP4-44 prophage; Toxic component of a type IV toxin-antitoxin (TA) system. Acts as a dual toxin inhibitor that blocks cell division and cell elongation in genetically separable interactions with FtsZ and MreB. Interacts with cytoskeletal proteins FtsZ and MreB; inhibits FtsZ GTP-dependent polymerization and GTPase activity as well as MreB ATP-dependent polymerization. Binds to both the N- and C-terminus of FtsZ, likely blocking its polymerization and localization, leading to blockage of cell division. Overexpression results in inhibition of growth in liquid cultures and decrease in col [...]

mRNA interferase toxin, antitoxin is MazE; Toxic component of a type II toxin-antitoxin (TA) system. A sequence-specific endoribonuclease it inhibits protein synthesis by cleaving mRNA and inducing bacterial stasis. It is stable, single- strand specific with mRNA cleavage independent of the ribosome, although translation enhances cleavage for some mRNAs. Cleavage occurs at the 5'-end of ACA sequences, yielding a 2',3'-cyclic phosphate and a free 5'-OH, although cleavage can also occur on the 3'-end of the first A. Digests 16S rRNA in vivo 43 nts upstream of the C- terminus; this remove [...]

CP4-44 prophage; Toxic component of a type IV toxin-antitoxin (TA) system. Acts as a dual toxin inhibitor that blocks cell division and cell elongation in genetically separable interactions with FtsZ and MreB. Interacts with cytoskeletal proteins FtsZ and MreB; inhibits FtsZ GTP-dependent polymerization and GTPase activity as well as MreB ATP-dependent polymerization. Binds to both the N- and C-terminus of FtsZ, likely blocking its polymerization and localization, leading to blockage of cell division. Overexpression results in inhibition of growth in liquid cultures and decrease in col [...]

Antitoxin of the RelE-RelB toxin-antitoxin syste; Antitoxin component of a type II toxin-antitoxin (TA) system. Counteracts the effect of cognate toxin RelE via direct protein-protein interaction, preventing RelE from entering the ribosome A site and thus inhibiting its endoribonuclease activity. An autorepressor of relBE operon transcription. 2 RelB dimers bind to 2 operator sequences; DNA- binding and repression is stronger when complexed with toxin/corepressor RelE by conditional cooperativity. Increased transcription rate of relBE and activation of relE is consistent with a lower l [...]

CP4-44 prophage; Toxic component of a type IV toxin-antitoxin (TA) system. Acts as a dual toxin inhibitor that blocks cell division and cell elongation in genetically separable interactions with FtsZ and MreB. Interacts with cytoskeletal proteins FtsZ and MreB; inhibits FtsZ GTP-dependent polymerization and GTPase activity as well as MreB ATP-dependent polymerization. Binds to both the N- and C-terminus of FtsZ, likely blocking its polymerization and localization, leading to blockage of cell division. Overexpression results in inhibition of growth in liquid cultures and decrease in col [...]

Qin prophage; Toxic component of a type II toxin-antitoxin (TA) system. A sequence-specific, ribosome-dependent mRNA endoribonuclease that inhibits translation during amino acid starvation (the stringent response). In vitro acts by cleaving mRNA with high codon specificity in the ribosomal A site between positions 2 and 3. The stop codon UAG is cleaved at a fast rate while UAA and UGA are cleaved with intermediate and slow rates. In vitro mRNA cleavage can also occur in the ribosomal E site after peptide release from peptidyl- tRNA in the P site as well as on free 30S subunits. In vivo [...]

Chromate reductase, Class I, flavoprotein; Catalyzes the reduction of quinones. Acts by simultaneous two-electron transfer, avoiding formation of highly reactive semiquinone intermediates and producing quinols that promote tolerance of H(2)O(2). Quinone reduction is probably the primary biological role of ChrR (By similarity). Can also reduce toxic chromate to insoluble and less toxic Cr(3+). Catalyzes the transfer of three electrons to Cr(6+) producing Cr(3+) and one electron to molecular oxygen without producing the toxic Cr(5+) species and only producing a minimal amount of reactive [...]

RNA polymerase sigma E factor; Sigma factors are initiation factors that promote the attachment of RNA polymerase (RNAP) to specific initiation sites and are then released. Extracytoplasmic function (ECF) sigma-E controls the envelope stress response, responding to periplasmic protein stress, increased levels of periplasmic lipopolysaccharide (LPS) as well as heat shock and oxidative stress; it controls protein processing in the extracytoplasmic compartment. The 90 member regulon consists of the genes necessary for the synthesis and maintenance of both proteins and LPS of the outer me [...]

Multicopper oxidase (laccase); Probably involved in periplasmic detoxification of copper by oxidizing Cu(+) to Cu(2+) and thus preventing its uptake into the cytoplasm. Possesses phenoloxidase and ferroxidase activities and might be involved in the production of polyphenolic compounds and the prevention of oxidative damage in the periplasm.

Copper-responsive regulon transcriptional regulator; Regulates the transcription of the copA and cueO genes. It detects cytoplasmic copper stress and activates transcription in response to increasing copper concentrations.

Multicopper oxidase (laccase); Probably involved in periplasmic detoxification of copper by oxidizing Cu(+) to Cu(2+) and thus preventing its uptake into the cytoplasm. Possesses phenoloxidase and ferroxidase activities and might be involved in the production of polyphenolic compounds and the prevention of oxidative damage in the periplasm.

Zinc, cobalt and lead efflux system; Confers resistance to zinc, cadmium and lead. Couples the hydrolysis of ATP with the export of zinc, cadmium or lead, with highest activity when the metals are present as metal-thiolate complexes. Can also bind nickel, copper, cobalt and mercury. Belongs to the cation transport ATPase (P-type) (TC 3.A.3) family. Type IB subfamily.