node1 | node2 | node1 accession | node2 accession | node1 annotation | node2 annotation | score |
dinQ | ghoT | b4613 | b4559 | UV-inducible membrane toxin, DinQ-AgrB type I toxin-antitoxin system; Belongs to the DinQ family. | Toxin of GhoTS toxin-antitoxin pair; Toxic component of a type V toxin-antitoxin (TA) system. Causes membrane damage when induced by MqsR, slowing cell growth and increasing the formation of dormant persister cells; involved with GhoS, its antitoxin, in reducing cell growth during antibacterial stress. Overexpression causes cell lysis, forming ghost cells; both effects are neutralized by expression of GhoS. Overexpression in the presence of ampicillin increases persister cell formation (persister cells exhibit antibiotic tolerance without genetic change). Overexpression causes about 90 [...] | 0.540 |
dinQ | hokB | b4613 | b4428 | UV-inducible membrane toxin, DinQ-AgrB type I toxin-antitoxin system; Belongs to the DinQ family. | Toxic polypeptide, small; Toxic component of a type I toxin-antitoxin (TA) system (Probable). When overexpressed kills cells within minutes; causes collapse of the transmembrane potential and arrest of respiration. Expression leads to membrane depolarization; when protein levels are high enough depolarization probably leads to lowered metabolic activity which in turn induces some cells to enter the persistent state in which they transiently survive antibiotic exposure. Its toxic effect is probably neutralized by antisense antitoxin RNA SokB, which is encoded in trans on the opposite DN [...] | 0.730 |
dinQ | ibsC | b4613 | b4665 | UV-inducible membrane toxin, DinQ-AgrB type I toxin-antitoxin system; Belongs to the DinQ family. | Toxic membrane protein. | 0.806 |
dinQ | ldrD | b4613 | b4453 | UV-inducible membrane toxin, DinQ-AgrB type I toxin-antitoxin system; Belongs to the DinQ family. | Toxic polypeptide, small; Toxic component of a type I toxin-antitoxin (TA) system. Overexpression causes rapid cell killing and nucleoid condensation of the host cell. Overexpression induces stress-response and a number of membrane protein genes. May inhibit ATP synthesis due to its insertion in the cell inner membrane (By similarity). | 0.817 |
dinQ | ralR | b4613 | b1348 | UV-inducible membrane toxin, DinQ-AgrB type I toxin-antitoxin system; Belongs to the DinQ family. | Rac prophage; Toxic component of a type I toxin-antitoxin (TA) system. Upon overexpression inhibits growth and reduces colony-forming units in both the presence and absence of the Rac prophage, cells become filamentous. Has deoxyribonuclease activity (probably endonucleolytic), does not digest RNA. Its toxic effects are neutralized by sRNA antitoxin RalA, which is encoded in trans on the opposite DNA strand. Has RAL-like activity. | 0.809 |
dinQ | shoB | b4613 | b4687 | UV-inducible membrane toxin, DinQ-AgrB type I toxin-antitoxin system; Belongs to the DinQ family. | Toxic membrane protein; Toxic component of a type I toxin-antitoxin (TA) system. May be a toxic protein; overexpression causes cessation of growth and rapid membrane depolarization. Overexpression induces stress-response and a number of membrane protein genes. | 0.897 |
dinQ | symE | b4613 | b4347 | UV-inducible membrane toxin, DinQ-AgrB type I toxin-antitoxin system; Belongs to the DinQ family. | Toxic peptide regulated by antisense sRNA symR; Toxic component of a type I toxin-antitoxin (TA) system. Involved in the degradation and recycling of damaged RNA. It is itself a target for degradation by the ATP-dependent protease Lon. Belongs to the SymE family. | 0.818 |
dinQ | tisB | b4613 | b4618 | UV-inducible membrane toxin, DinQ-AgrB type I toxin-antitoxin system; Belongs to the DinQ family. | Toxic membrane persister formation peptide, LexA-regulated; Toxic component of a type I toxin-antitoxin (TA) system (Probable). Overexpression causes cessation of growth, induces stress-response, a number of membrane protein genes, and leads to cell death. Inhibits ATP synthesis, ATP levels drop drastically quickly after induction. Part of the programmed response to DNA damage; damage leads to increased accumulation of the protein which slows or stops bacterial growth, probably allowing DNA repair before cells continue to grow. | 0.900 |
ghoT | dinQ | b4559 | b4613 | Toxin of GhoTS toxin-antitoxin pair; Toxic component of a type V toxin-antitoxin (TA) system. Causes membrane damage when induced by MqsR, slowing cell growth and increasing the formation of dormant persister cells; involved with GhoS, its antitoxin, in reducing cell growth during antibacterial stress. Overexpression causes cell lysis, forming ghost cells; both effects are neutralized by expression of GhoS. Overexpression in the presence of ampicillin increases persister cell formation (persister cells exhibit antibiotic tolerance without genetic change). Overexpression causes about 90 [...] | UV-inducible membrane toxin, DinQ-AgrB type I toxin-antitoxin system; Belongs to the DinQ family. | 0.540 |
ghoT | hipA | b4559 | b1507 | Toxin of GhoTS toxin-antitoxin pair; Toxic component of a type V toxin-antitoxin (TA) system. Causes membrane damage when induced by MqsR, slowing cell growth and increasing the formation of dormant persister cells; involved with GhoS, its antitoxin, in reducing cell growth during antibacterial stress. Overexpression causes cell lysis, forming ghost cells; both effects are neutralized by expression of GhoS. Overexpression in the presence of ampicillin increases persister cell formation (persister cells exhibit antibiotic tolerance without genetic change). Overexpression causes about 90 [...] | 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 [...] | 0.644 |
ghoT | hokB | b4559 | b4428 | Toxin of GhoTS toxin-antitoxin pair; Toxic component of a type V toxin-antitoxin (TA) system. Causes membrane damage when induced by MqsR, slowing cell growth and increasing the formation of dormant persister cells; involved with GhoS, its antitoxin, in reducing cell growth during antibacterial stress. Overexpression causes cell lysis, forming ghost cells; both effects are neutralized by expression of GhoS. Overexpression in the presence of ampicillin increases persister cell formation (persister cells exhibit antibiotic tolerance without genetic change). Overexpression causes about 90 [...] | Toxic polypeptide, small; Toxic component of a type I toxin-antitoxin (TA) system (Probable). When overexpressed kills cells within minutes; causes collapse of the transmembrane potential and arrest of respiration. Expression leads to membrane depolarization; when protein levels are high enough depolarization probably leads to lowered metabolic activity which in turn induces some cells to enter the persistent state in which they transiently survive antibiotic exposure. Its toxic effect is probably neutralized by antisense antitoxin RNA SokB, which is encoded in trans on the opposite DN [...] | 0.784 |
ghoT | ldrD | b4559 | b4453 | Toxin of GhoTS toxin-antitoxin pair; Toxic component of a type V toxin-antitoxin (TA) system. Causes membrane damage when induced by MqsR, slowing cell growth and increasing the formation of dormant persister cells; involved with GhoS, its antitoxin, in reducing cell growth during antibacterial stress. Overexpression causes cell lysis, forming ghost cells; both effects are neutralized by expression of GhoS. Overexpression in the presence of ampicillin increases persister cell formation (persister cells exhibit antibiotic tolerance without genetic change). Overexpression causes about 90 [...] | Toxic polypeptide, small; Toxic component of a type I toxin-antitoxin (TA) system. Overexpression causes rapid cell killing and nucleoid condensation of the host cell. Overexpression induces stress-response and a number of membrane protein genes. May inhibit ATP synthesis due to its insertion in the cell inner membrane (By similarity). | 0.523 |
ghoT | ralR | b4559 | b1348 | Toxin of GhoTS toxin-antitoxin pair; Toxic component of a type V toxin-antitoxin (TA) system. Causes membrane damage when induced by MqsR, slowing cell growth and increasing the formation of dormant persister cells; involved with GhoS, its antitoxin, in reducing cell growth during antibacterial stress. Overexpression causes cell lysis, forming ghost cells; both effects are neutralized by expression of GhoS. Overexpression in the presence of ampicillin increases persister cell formation (persister cells exhibit antibiotic tolerance without genetic change). Overexpression causes about 90 [...] | Rac prophage; Toxic component of a type I toxin-antitoxin (TA) system. Upon overexpression inhibits growth and reduces colony-forming units in both the presence and absence of the Rac prophage, cells become filamentous. Has deoxyribonuclease activity (probably endonucleolytic), does not digest RNA. Its toxic effects are neutralized by sRNA antitoxin RalA, which is encoded in trans on the opposite DNA strand. Has RAL-like activity. | 0.785 |
ghoT | symE | b4559 | b4347 | Toxin of GhoTS toxin-antitoxin pair; Toxic component of a type V toxin-antitoxin (TA) system. Causes membrane damage when induced by MqsR, slowing cell growth and increasing the formation of dormant persister cells; involved with GhoS, its antitoxin, in reducing cell growth during antibacterial stress. Overexpression causes cell lysis, forming ghost cells; both effects are neutralized by expression of GhoS. Overexpression in the presence of ampicillin increases persister cell formation (persister cells exhibit antibiotic tolerance without genetic change). Overexpression causes about 90 [...] | Toxic peptide regulated by antisense sRNA symR; Toxic component of a type I toxin-antitoxin (TA) system. Involved in the degradation and recycling of damaged RNA. It is itself a target for degradation by the ATP-dependent protease Lon. Belongs to the SymE family. | 0.603 |
ghoT | tisB | b4559 | b4618 | Toxin of GhoTS toxin-antitoxin pair; Toxic component of a type V toxin-antitoxin (TA) system. Causes membrane damage when induced by MqsR, slowing cell growth and increasing the formation of dormant persister cells; involved with GhoS, its antitoxin, in reducing cell growth during antibacterial stress. Overexpression causes cell lysis, forming ghost cells; both effects are neutralized by expression of GhoS. Overexpression in the presence of ampicillin increases persister cell formation (persister cells exhibit antibiotic tolerance without genetic change). Overexpression causes about 90 [...] | Toxic membrane persister formation peptide, LexA-regulated; Toxic component of a type I toxin-antitoxin (TA) system (Probable). Overexpression causes cessation of growth, induces stress-response, a number of membrane protein genes, and leads to cell death. Inhibits ATP synthesis, ATP levels drop drastically quickly after induction. Part of the programmed response to DNA damage; damage leads to increased accumulation of the protein which slows or stops bacterial growth, probably allowing DNA repair before cells continue to grow. | 0.884 |
hipA | ghoT | b1507 | b4559 | 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 [...] | Toxin of GhoTS toxin-antitoxin pair; Toxic component of a type V toxin-antitoxin (TA) system. Causes membrane damage when induced by MqsR, slowing cell growth and increasing the formation of dormant persister cells; involved with GhoS, its antitoxin, in reducing cell growth during antibacterial stress. Overexpression causes cell lysis, forming ghost cells; both effects are neutralized by expression of GhoS. Overexpression in the presence of ampicillin increases persister cell formation (persister cells exhibit antibiotic tolerance without genetic change). Overexpression causes about 90 [...] | 0.644 |
hipA | hokB | b1507 | b4428 | 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 [...] | Toxic polypeptide, small; Toxic component of a type I toxin-antitoxin (TA) system (Probable). When overexpressed kills cells within minutes; causes collapse of the transmembrane potential and arrest of respiration. Expression leads to membrane depolarization; when protein levels are high enough depolarization probably leads to lowered metabolic activity which in turn induces some cells to enter the persistent state in which they transiently survive antibiotic exposure. Its toxic effect is probably neutralized by antisense antitoxin RNA SokB, which is encoded in trans on the opposite DN [...] | 0.474 |
hipA | symE | b1507 | b4347 | 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 [...] | Toxic peptide regulated by antisense sRNA symR; Toxic component of a type I toxin-antitoxin (TA) system. Involved in the degradation and recycling of damaged RNA. It is itself a target for degradation by the ATP-dependent protease Lon. Belongs to the SymE family. | 0.483 |
hipA | tisB | b1507 | b4618 | 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 [...] | Toxic membrane persister formation peptide, LexA-regulated; Toxic component of a type I toxin-antitoxin (TA) system (Probable). Overexpression causes cessation of growth, induces stress-response, a number of membrane protein genes, and leads to cell death. Inhibits ATP synthesis, ATP levels drop drastically quickly after induction. Part of the programmed response to DNA damage; damage leads to increased accumulation of the protein which slows or stops bacterial growth, probably allowing DNA repair before cells continue to grow. | 0.812 |
hokB | dinQ | b4428 | b4613 | Toxic polypeptide, small; Toxic component of a type I toxin-antitoxin (TA) system (Probable). When overexpressed kills cells within minutes; causes collapse of the transmembrane potential and arrest of respiration. Expression leads to membrane depolarization; when protein levels are high enough depolarization probably leads to lowered metabolic activity which in turn induces some cells to enter the persistent state in which they transiently survive antibiotic exposure. Its toxic effect is probably neutralized by antisense antitoxin RNA SokB, which is encoded in trans on the opposite DN [...] | UV-inducible membrane toxin, DinQ-AgrB type I toxin-antitoxin system; Belongs to the DinQ family. | 0.730 |