node1 | node2 | node1 accession | node2 accession | node1 annotation | node2 annotation | score |
dinQ | hokB | b4613 | b4428 | Uv-inducible membrane toxin, dinq-agrb type i toxin-antitoxin system; Belongs to the DinQ family | 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 DNA strand | 0.821 |
dinQ | ralR | b4613 | b1348 | Uv-inducible membrane toxin, dinq-agrb type i toxin-antitoxin system; Belongs to the DinQ family | Rac prophage; endodeoxyribonuclease toxin ralr; 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 | 0.738 |
dinQ | shoB | b4613 | b4687 | Uv-inducible membrane toxin, dinq-agrb type i toxin-antitoxin system; Belongs to the DinQ family | Small toxic protein shob; 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 | 0.871 |
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 | 0.876 |
ghoT | hipA | b4559 | b1507 | 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-fold reduction in cellular ATP lev [...] | 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 the stringent response via RelA/SpoT and in [...] | 0.731 |
ghoT | hokB | b4559 | b4428 | 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-fold reduction in cellular ATP lev [...] | 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 DNA strand | 0.854 |
ghoT | hokD | b4559 | b1562 | 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-fold reduction in cellular ATP lev [...] | Qin prophage; toxic protein hokd; Toxic component of a type I toxin-antitoxin (TA) system (Probable). When overexpressed kills cells within 2 minutes; causes collapse of the transmembrane potential and arrest of respiration | 0.520 |
ghoT | hokE | b4559 | b4415 | 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-fold reduction in cellular ATP lev [...] | Toxic polypeptide, small; Toxic component of a type I toxin-antitoxin (TA) system; if it expressed it could be neutralized by antisense antitoxin RNA SokE | 0.607 |
ghoT | ralR | b4559 | b1348 | 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-fold reduction in cellular ATP lev [...] | Rac prophage; endodeoxyribonuclease toxin ralr; 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 | 0.811 |
ghoT | tisB | b4559 | b4618 | 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-fold reduction in cellular ATP lev [...] | 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 | 0.873 |
hipA | ghoT | b1507 | b4559 | 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 the stringent response via RelA/SpoT and in [...] | 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-fold reduction in cellular ATP lev [...] | 0.731 |
hipA | hokB | b1507 | b4428 | 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 the stringent response via RelA/SpoT and in [...] | 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 DNA strand | 0.626 |
hipA | tisB | b1507 | b4618 | 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 the stringent response via RelA/SpoT and in [...] | 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 | 0.871 |
hokB | dinQ | b4428 | b4613 | 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 DNA strand | Uv-inducible membrane toxin, dinq-agrb type i toxin-antitoxin system; Belongs to the DinQ family | 0.821 |
hokB | ghoT | b4428 | b4559 | 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 DNA strand | 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-fold reduction in cellular ATP lev [...] | 0.854 |
hokB | hipA | b4428 | b1507 | 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 DNA strand | 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 the stringent response via RelA/SpoT and in [...] | 0.626 |
hokB | hokD | b4428 | b1562 | 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 DNA strand | Qin prophage; toxic protein hokd; Toxic component of a type I toxin-antitoxin (TA) system (Probable). When overexpressed kills cells within 2 minutes; causes collapse of the transmembrane potential and arrest of respiration | 0.609 |
hokB | hokE | b4428 | b4415 | 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 DNA strand | Toxic polypeptide, small; Toxic component of a type I toxin-antitoxin (TA) system; if it expressed it could be neutralized by antisense antitoxin RNA SokE | 0.676 |
hokB | mokB | b4428 | b1420 | 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 DNA strand | Putative regulatory protein mokb; Overlapping regulatory peptide whose translation enables hokB expression | 0.922 |
hokB | obgE | b4428 | b3183 | 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 DNA strand | An abundant, essential GTPase which binds GTP, GDP and ppGpp with moderate affinity. Has high guanosine nucleotide exchange rate constants for GTP and GDP, and a relatively low GTP hydrolysis rate stimulated by the 50S ribosomal subunit. It is estimated there are 34000 molecules in log-phase cells and 5600 molecules in stationary- phase cells. Required for chromosome segregation. Plays a role in the stringent response, perhaps by sequestering 50S ribosomal subunits and decreasing protein synthesis , and a non-essential role in the late steps of ribosome biogenesis, perhaps acting as a [...] | 0.789 |