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 | 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 | 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 |
kilR | racC | b1352 | b1351 | Killing protein, Rac prophage; Causes inhibition of cell division. At high levels of expression, can also abolish the rod shape of the cells. Division inhibition by KilR can be relieved by overexpression of the cell division protein FtsZ. | RacC protein. | 0.940 |
kilR | ralR | b1352 | b1348 | Killing protein, Rac prophage; Causes inhibition of cell division. At high levels of expression, can also abolish the rod shape of the cells. Division inhibition by KilR can be relieved by overexpression of the cell division protein FtsZ. | 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. | 0.949 |
kilR | recT | b1352 | b1349 | Killing protein, Rac prophage; Causes inhibition of cell division. At high levels of expression, can also abolish the rod shape of the cells. Division inhibition by KilR can be relieved by overexpression of the cell division protein FtsZ. | Rac prophage; Binds to single-stranded DNA and also promotes the renaturation of complementary single-stranded DNA. Function in recombination. Has a function similar to that of lambda RedB. | 0.645 |
kilR | ydaC | b1352 | b1347 | Killing protein, Rac prophage; Causes inhibition of cell division. At high levels of expression, can also abolish the rod shape of the cells. Division inhibition by KilR can be relieved by overexpression of the cell division protein FtsZ. | DUF1187 family protein, Rac prophage; Helps to maintain the integrity of the chromosome by lowering the steady-state level of double strand breaks. This region of DNA acts as an antitoxin to toxin RalR, a DNase, but it seems to be sRNA RalA that has the antitoxin activity and not this putative protein. Therefore the identity of this as a protein-coding gene has been cast into doubt. | 0.958 |
kilR | ydaQ | b1352 | b1346 | Killing protein, Rac prophage; Causes inhibition of cell division. At high levels of expression, can also abolish the rod shape of the cells. Division inhibition by KilR can be relieved by overexpression of the cell division protein FtsZ. | Rac prophage; Putative lambdoid prophage Rac excisionase. | 0.798 |
racC | kilR | b1351 | b1352 | RacC protein. | Killing protein, Rac prophage; Causes inhibition of cell division. At high levels of expression, can also abolish the rod shape of the cells. Division inhibition by KilR can be relieved by overexpression of the cell division protein FtsZ. | 0.940 |
racC | ralR | b1351 | b1348 | RacC protein. | 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. | 0.798 |
racC | recT | b1351 | b1349 | RacC protein. | Rac prophage; Binds to single-stranded DNA and also promotes the renaturation of complementary single-stranded DNA. Function in recombination. Has a function similar to that of lambda RedB. | 0.559 |
racC | ydaC | b1351 | b1347 | RacC protein. | DUF1187 family protein, Rac prophage; Helps to maintain the integrity of the chromosome by lowering the steady-state level of double strand breaks. This region of DNA acts as an antitoxin to toxin RalR, a DNase, but it seems to be sRNA RalA that has the antitoxin activity and not this putative protein. Therefore the identity of this as a protein-coding gene has been cast into doubt. | 0.917 |
racC | ydaQ | b1351 | b1346 | RacC protein. | Rac prophage; Putative lambdoid prophage Rac excisionase. | 0.533 |
ralR | dinQ | b1348 | b4613 | 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. | UV-inducible membrane toxin, DinQ-AgrB type I toxin-antitoxin system; Belongs to the DinQ family. | 0.809 |