node1 | node2 | node1 accession | node2 accession | node1 annotation | node2 annotation | score |
flu | recE | b2000 | b1350 | Novel sRNA, CP4-44; Controls colony form variation and autoaggregation. May function as an adhesin. | Rac prophage; 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. | 0.693 |
flu | recT | b2000 | b1349 | Novel sRNA, CP4-44; Controls colony form variation and autoaggregation. May function as an adhesin. | 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. | 0.665 |
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 | recE | b1352 | b1350 | 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; 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. | 0.639 |
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 |
ralR | kilR | b1348 | b1352 | 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. | 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. | 0.949 |
ralR | recE | b1348 | b1350 | 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. | Rac prophage; 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. | 0.713 |
ralR | recT | b1348 | b1349 | 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. | 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. | 0.789 |
ralR | ydaC | b1348 | b1347 | 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. | 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. | 0.969 |
ralR | ydaQ | b1348 | b1346 | 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. | Rac prophage; Putative lambdoid prophage Rac excisionase. | 0.917 |
recA | recE | b2699 | b1350 | DNA recombination and repair protein; Required for homologous recombination and the bypass of mutagenic DNA lesions by the SOS response. Catalyzes ATP-driven homologous pairing and strand exchange of DNA molecules necessary for DNA recombinational repair. Catalyzes the hydrolysis of ATP in the presence of single-stranded DNA, the ATP-dependent uptake of single- stranded DNA by duplex DNA, and the ATP-dependent hybridization of homologous single-stranded DNAs. The SOS response controls an apoptotic-like death (ALD) induced (in the absence of the mazE-mazF toxin-antitoxin module) in resp [...] | Rac prophage; 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. | 0.880 |
recA | recF | b2699 | b3700 | DNA recombination and repair protein; Required for homologous recombination and the bypass of mutagenic DNA lesions by the SOS response. Catalyzes ATP-driven homologous pairing and strand exchange of DNA molecules necessary for DNA recombinational repair. Catalyzes the hydrolysis of ATP in the presence of single-stranded DNA, the ATP-dependent uptake of single- stranded DNA by duplex DNA, and the ATP-dependent hybridization of homologous single-stranded DNAs. The SOS response controls an apoptotic-like death (ALD) induced (in the absence of the mazE-mazF toxin-antitoxin module) in resp [...] | Gap repair protein; The RecF protein is involved in DNA metabolism; it is required for DNA replication and normal SOS inducibility. RecF binds preferentially to single-stranded, linear DNA. It also seems to bind ATP. | 0.959 |
recA | recO | b2699 | b2565 | DNA recombination and repair protein; Required for homologous recombination and the bypass of mutagenic DNA lesions by the SOS response. Catalyzes ATP-driven homologous pairing and strand exchange of DNA molecules necessary for DNA recombinational repair. Catalyzes the hydrolysis of ATP in the presence of single-stranded DNA, the ATP-dependent uptake of single- stranded DNA by duplex DNA, and the ATP-dependent hybridization of homologous single-stranded DNAs. The SOS response controls an apoptotic-like death (ALD) induced (in the absence of the mazE-mazF toxin-antitoxin module) in resp [...] | Gap repair protein; Involved in DNA repair and RecF pathway recombination; Belongs to the RecO family. | 0.952 |
recA | recT | b2699 | b1349 | DNA recombination and repair protein; Required for homologous recombination and the bypass of mutagenic DNA lesions by the SOS response. Catalyzes ATP-driven homologous pairing and strand exchange of DNA molecules necessary for DNA recombinational repair. Catalyzes the hydrolysis of ATP in the presence of single-stranded DNA, the ATP-dependent uptake of single- stranded DNA by duplex DNA, and the ATP-dependent hybridization of homologous single-stranded DNAs. The SOS response controls an apoptotic-like death (ALD) induced (in the absence of the mazE-mazF toxin-antitoxin module) in resp [...] | 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. | 0.836 |
recA | ssb | b2699 | b4059 | DNA recombination and repair protein; Required for homologous recombination and the bypass of mutagenic DNA lesions by the SOS response. Catalyzes ATP-driven homologous pairing and strand exchange of DNA molecules necessary for DNA recombinational repair. Catalyzes the hydrolysis of ATP in the presence of single-stranded DNA, the ATP-dependent uptake of single- stranded DNA by duplex DNA, and the ATP-dependent hybridization of homologous single-stranded DNAs. The SOS response controls an apoptotic-like death (ALD) induced (in the absence of the mazE-mazF toxin-antitoxin module) in resp [...] | Single-stranded DNA-binding protein; Plays an important role in DNA replication, recombination and repair. Binds to ssDNA and to an array of partner proteins to recruit them to their sites of action during DNA metabolism. Acts as a sliding platform that migrates on DNA via reptation. SSB or its 10 C-terminal amino acids stimulates the ATPase activity of RadD. | 0.927 |
recE | flu | b1350 | b2000 | Rac prophage; 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. | Novel sRNA, CP4-44; Controls colony form variation and autoaggregation. May function as an adhesin. | 0.693 |
recE | kilR | b1350 | b1352 | Rac prophage; 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. | 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. | 0.639 |
recE | ralR | b1350 | b1348 | Rac prophage; 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. | 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. | 0.713 |