| node1 | node2 | node1 accession | node2 accession | node1 annotation | node2 annotation | score |
| 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 |
| kilR | racR | b1352 | b1356 | Rac prophage; inhibitor of ftsz, killing protein; 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; dna-binding transcriptional repressor racr; Repressor protein for rac prophage | 0.737 |
| kilR | ralR | b1352 | b1348 | Rac prophage; inhibitor of ftsz, killing protein; 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; 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 | 0.927 |
| kilR | recE | b1352 | b1350 | Rac prophage; inhibitor of ftsz, killing protein; 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; exonuclease viii, ds dna exonuclease, 5' --> 3' specific; Is involved in the RecE pathway of recombination. Catalyzes the degradation of double-stranded DNA. Acts progressively in a 5' to 3' direction, releasing 5'-phosphomononucleotides. Has a strong preference for linear duplex substrate DNA and appears to be unable to initiate degradation from single-stranded breaks in DNA | 0.813 |
| kilR | ydaC | b1352 | b1347 | Rac prophage; inhibitor of ftsz, killing protein; 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; double-strand break reduction protein; 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 | 0.832 |
| kilR | ydaQ | b1352 | b1346 | Rac prophage; inhibitor of ftsz, killing protein; 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; excisionase; Uncharacterized protein YdaQ; Putative lambdoid prophage Rac excisionase | 0.528 |
| kilR | ydaT | b1352 | b1358 | Rac prophage; inhibitor of ftsz, killing protein; 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; protein ydat; Uncharacterized protein YdaT; Phage or Prophage Related | 0.800 |
| kilR | ydcX | b1352 | b1445 | Rac prophage; inhibitor of ftsz, killing protein; 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 | DUF2566 family protein; Acts as an orphan toxin which is important for maintaining cell fitness during stress related to the stringent response (decreased amino acid, purine and thymidine availability). Overexpression inhibits cell growth and increases the formation of persister cells. Causes 99.9% of cells to undergo bacterial lysis within 2 hours after induction; nucleoids condense, the cytoplasm seems empty and the periplasmic space enlarges. The intracellular ATP level decreases about 27-fold suggesting the membrane potential may be disrupted | 0.475 |
| racR | kilR | b1356 | b1352 | Rac prophage; dna-binding transcriptional repressor racr; Repressor protein for rac prophage | Rac prophage; inhibitor of ftsz, killing protein; 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 | 0.737 |
| racR | ralR | b1356 | b1348 | Rac prophage; dna-binding transcriptional repressor racr; Repressor protein for rac prophage | 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 | 0.782 |
| racR | ydaC | b1356 | b1347 | Rac prophage; dna-binding transcriptional repressor racr; Repressor protein for rac prophage | Rac prophage; double-strand break reduction protein; 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 | 0.560 |
| racR | ydaT | b1356 | b1358 | Rac prophage; dna-binding transcriptional repressor racr; Repressor protein for rac prophage | Rac prophage; protein ydat; Uncharacterized protein YdaT; Phage or Prophage Related | 0.952 |
| racR | ydcX | b1356 | b1445 | Rac prophage; dna-binding transcriptional repressor racr; Repressor protein for rac prophage | DUF2566 family protein; Acts as an orphan toxin which is important for maintaining cell fitness during stress related to the stringent response (decreased amino acid, purine and thymidine availability). Overexpression inhibits cell growth and increases the formation of persister cells. Causes 99.9% of cells to undergo bacterial lysis within 2 hours after induction; nucleoids condense, the cytoplasm seems empty and the periplasmic space enlarges. The intracellular ATP level decreases about 27-fold suggesting the membrane potential may be disrupted | 0.702 |
| ralR | ghoT | b1348 | b4559 | 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 | 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 [...] | 0.811 |
| ralR | kilR | b1348 | b1352 | 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 | Rac prophage; inhibitor of ftsz, killing protein; 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 | 0.927 |
| ralR | racR | b1348 | b1356 | 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 | Rac prophage; dna-binding transcriptional repressor racr; Repressor protein for rac prophage | 0.782 |
| ralR | recE | b1348 | b1350 | 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 | Rac prophage; exonuclease viii, ds dna exonuclease, 5' --> 3' specific; Is involved in the RecE pathway of recombination. Catalyzes the degradation of double-stranded DNA. Acts progressively in a 5' to 3' direction, releasing 5'-phosphomononucleotides. Has a strong preference for linear duplex substrate DNA and appears to be unable to initiate degradation from single-stranded breaks in DNA | 0.835 |
| ralR | shoB | b1348 | b4687 | 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 | 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 | 0.782 |
| ralR | tisB | b1348 | b4618 | 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 | 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 | 0.784 |
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