| node1 | node2 | node1 accession | node2 accession | node1 annotation | node2 annotation | score |
| ARQ73966.1 | ARQ73968.1 | B6D87_07015 | B6D87_07025 | Cell division inhibitor SulA; Component of the SOS system and an inhibitor of cell division. Accumulation of SulA causes rapid cessation of cell division and the appearance of long, non-septate filaments. In the presence of GTP, binds a polymerization-competent form of FtsZ in a 1:1 ratio, thus inhibiting FtsZ polymerization and therefore preventing it from participating in the assembly of the Z ring. This mechanism prevents the premature segregation of damaged DNA to daughter cells during cell division. | Hypothetical protein; Derived by automated computational analysis using gene prediction method: GeneMarkS+. | 0.575 |
| ARQ73966.1 | ARQ73969.1 | B6D87_07015 | B6D87_07030 | Cell division inhibitor SulA; Component of the SOS system and an inhibitor of cell division. Accumulation of SulA causes rapid cessation of cell division and the appearance of long, non-septate filaments. In the presence of GTP, binds a polymerization-competent form of FtsZ in a 1:1 ratio, thus inhibiting FtsZ polymerization and therefore preventing it from participating in the assembly of the Z ring. This mechanism prevents the premature segregation of damaged DNA to daughter cells during cell division. | TetR family transcriptional regulator; Derived by automated computational analysis using gene prediction method: Protein Homology. | 0.570 |
| ARQ73966.1 | lexA | B6D87_07015 | B6D87_07020 | Cell division inhibitor SulA; Component of the SOS system and an inhibitor of cell division. Accumulation of SulA causes rapid cessation of cell division and the appearance of long, non-septate filaments. In the presence of GTP, binds a polymerization-competent form of FtsZ in a 1:1 ratio, thus inhibiting FtsZ polymerization and therefore preventing it from participating in the assembly of the Z ring. This mechanism prevents the premature segregation of damaged DNA to daughter cells during cell division. | Repressor LexA; Represses a number of genes involved in the response to DNA damage (SOS response), including recA and lexA. In the presence of single-stranded DNA, RecA interacts with LexA causing an autocatalytic cleavage which disrupts the DNA-binding part of LexA, leading to derepression of the SOS regulon and eventually DNA repair. | 0.906 |
| ARQ73966.1 | nagZ | B6D87_07015 | B6D87_07035 | Cell division inhibitor SulA; Component of the SOS system and an inhibitor of cell division. Accumulation of SulA causes rapid cessation of cell division and the appearance of long, non-septate filaments. In the presence of GTP, binds a polymerization-competent form of FtsZ in a 1:1 ratio, thus inhibiting FtsZ polymerization and therefore preventing it from participating in the assembly of the Z ring. This mechanism prevents the premature segregation of damaged DNA to daughter cells during cell division. | beta-N-acetylhexosaminidase; Plays a role in peptidoglycan recycling by cleaving the terminal beta-1,4-linked N-acetylglucosamine (GlcNAc) from peptide- linked peptidoglycan fragments, giving rise to free GlcNAc, anhydro-N- acetylmuramic acid and anhydro-N-acetylmuramic acid-linked peptides. Belongs to the glycosyl hydrolase 3 family. NagZ subfamily. | 0.404 |
| ARQ73968.1 | ARQ73966.1 | B6D87_07025 | B6D87_07015 | Hypothetical protein; Derived by automated computational analysis using gene prediction method: GeneMarkS+. | Cell division inhibitor SulA; Component of the SOS system and an inhibitor of cell division. Accumulation of SulA causes rapid cessation of cell division and the appearance of long, non-septate filaments. In the presence of GTP, binds a polymerization-competent form of FtsZ in a 1:1 ratio, thus inhibiting FtsZ polymerization and therefore preventing it from participating in the assembly of the Z ring. This mechanism prevents the premature segregation of damaged DNA to daughter cells during cell division. | 0.575 |
| ARQ73968.1 | ARQ73969.1 | B6D87_07025 | B6D87_07030 | Hypothetical protein; Derived by automated computational analysis using gene prediction method: GeneMarkS+. | TetR family transcriptional regulator; Derived by automated computational analysis using gene prediction method: Protein Homology. | 0.720 |
| ARQ73968.1 | lexA | B6D87_07025 | B6D87_07020 | Hypothetical protein; Derived by automated computational analysis using gene prediction method: GeneMarkS+. | Repressor LexA; Represses a number of genes involved in the response to DNA damage (SOS response), including recA and lexA. In the presence of single-stranded DNA, RecA interacts with LexA causing an autocatalytic cleavage which disrupts the DNA-binding part of LexA, leading to derepression of the SOS regulon and eventually DNA repair. | 0.584 |
| ARQ73968.1 | mtnP | B6D87_07025 | B6D87_07040 | Hypothetical protein; Derived by automated computational analysis using gene prediction method: GeneMarkS+. | Methylthioadenosine phosphorylase; Catalyzes the reversible phosphorylation of S-methyl-5'- thioinosine (MTI) to hypoxanthine and 5-methylthioribose-1-phosphate. Involved in the breakdown of S-methyl-5'-thioadenosine (MTA), a major by-product of polyamine biosynthesis. Catabolism of (MTA) occurs via deamination to MTI and phosphorolysis to hypoxanthine. | 0.419 |
| ARQ73968.1 | nagZ | B6D87_07025 | B6D87_07035 | Hypothetical protein; Derived by automated computational analysis using gene prediction method: GeneMarkS+. | beta-N-acetylhexosaminidase; Plays a role in peptidoglycan recycling by cleaving the terminal beta-1,4-linked N-acetylglucosamine (GlcNAc) from peptide- linked peptidoglycan fragments, giving rise to free GlcNAc, anhydro-N- acetylmuramic acid and anhydro-N-acetylmuramic acid-linked peptides. Belongs to the glycosyl hydrolase 3 family. NagZ subfamily. | 0.435 |
| ARQ73969.1 | ARQ73966.1 | B6D87_07030 | B6D87_07015 | TetR family transcriptional regulator; Derived by automated computational analysis using gene prediction method: Protein Homology. | Cell division inhibitor SulA; Component of the SOS system and an inhibitor of cell division. Accumulation of SulA causes rapid cessation of cell division and the appearance of long, non-septate filaments. In the presence of GTP, binds a polymerization-competent form of FtsZ in a 1:1 ratio, thus inhibiting FtsZ polymerization and therefore preventing it from participating in the assembly of the Z ring. This mechanism prevents the premature segregation of damaged DNA to daughter cells during cell division. | 0.570 |
| ARQ73969.1 | ARQ73968.1 | B6D87_07030 | B6D87_07025 | TetR family transcriptional regulator; Derived by automated computational analysis using gene prediction method: Protein Homology. | Hypothetical protein; Derived by automated computational analysis using gene prediction method: GeneMarkS+. | 0.720 |
| ARQ73969.1 | lexA | B6D87_07030 | B6D87_07020 | TetR family transcriptional regulator; Derived by automated computational analysis using gene prediction method: Protein Homology. | Repressor LexA; Represses a number of genes involved in the response to DNA damage (SOS response), including recA and lexA. In the presence of single-stranded DNA, RecA interacts with LexA causing an autocatalytic cleavage which disrupts the DNA-binding part of LexA, leading to derepression of the SOS regulon and eventually DNA repair. | 0.603 |
| ARQ73969.1 | mtnP | B6D87_07030 | B6D87_07040 | TetR family transcriptional regulator; Derived by automated computational analysis using gene prediction method: Protein Homology. | Methylthioadenosine phosphorylase; Catalyzes the reversible phosphorylation of S-methyl-5'- thioinosine (MTI) to hypoxanthine and 5-methylthioribose-1-phosphate. Involved in the breakdown of S-methyl-5'-thioadenosine (MTA), a major by-product of polyamine biosynthesis. Catabolism of (MTA) occurs via deamination to MTI and phosphorolysis to hypoxanthine. | 0.507 |
| ARQ73969.1 | nagZ | B6D87_07030 | B6D87_07035 | TetR family transcriptional regulator; Derived by automated computational analysis using gene prediction method: Protein Homology. | beta-N-acetylhexosaminidase; Plays a role in peptidoglycan recycling by cleaving the terminal beta-1,4-linked N-acetylglucosamine (GlcNAc) from peptide- linked peptidoglycan fragments, giving rise to free GlcNAc, anhydro-N- acetylmuramic acid and anhydro-N-acetylmuramic acid-linked peptides. Belongs to the glycosyl hydrolase 3 family. NagZ subfamily. | 0.521 |
| lexA | ARQ73966.1 | B6D87_07020 | B6D87_07015 | Repressor LexA; Represses a number of genes involved in the response to DNA damage (SOS response), including recA and lexA. In the presence of single-stranded DNA, RecA interacts with LexA causing an autocatalytic cleavage which disrupts the DNA-binding part of LexA, leading to derepression of the SOS regulon and eventually DNA repair. | Cell division inhibitor SulA; Component of the SOS system and an inhibitor of cell division. Accumulation of SulA causes rapid cessation of cell division and the appearance of long, non-septate filaments. In the presence of GTP, binds a polymerization-competent form of FtsZ in a 1:1 ratio, thus inhibiting FtsZ polymerization and therefore preventing it from participating in the assembly of the Z ring. This mechanism prevents the premature segregation of damaged DNA to daughter cells during cell division. | 0.906 |
| lexA | ARQ73968.1 | B6D87_07020 | B6D87_07025 | Repressor LexA; Represses a number of genes involved in the response to DNA damage (SOS response), including recA and lexA. In the presence of single-stranded DNA, RecA interacts with LexA causing an autocatalytic cleavage which disrupts the DNA-binding part of LexA, leading to derepression of the SOS regulon and eventually DNA repair. | Hypothetical protein; Derived by automated computational analysis using gene prediction method: GeneMarkS+. | 0.584 |
| lexA | ARQ73969.1 | B6D87_07020 | B6D87_07030 | Repressor LexA; Represses a number of genes involved in the response to DNA damage (SOS response), including recA and lexA. In the presence of single-stranded DNA, RecA interacts with LexA causing an autocatalytic cleavage which disrupts the DNA-binding part of LexA, leading to derepression of the SOS regulon and eventually DNA repair. | TetR family transcriptional regulator; Derived by automated computational analysis using gene prediction method: Protein Homology. | 0.603 |
| lexA | nagZ | B6D87_07020 | B6D87_07035 | Repressor LexA; Represses a number of genes involved in the response to DNA damage (SOS response), including recA and lexA. In the presence of single-stranded DNA, RecA interacts with LexA causing an autocatalytic cleavage which disrupts the DNA-binding part of LexA, leading to derepression of the SOS regulon and eventually DNA repair. | beta-N-acetylhexosaminidase; Plays a role in peptidoglycan recycling by cleaving the terminal beta-1,4-linked N-acetylglucosamine (GlcNAc) from peptide- linked peptidoglycan fragments, giving rise to free GlcNAc, anhydro-N- acetylmuramic acid and anhydro-N-acetylmuramic acid-linked peptides. Belongs to the glycosyl hydrolase 3 family. NagZ subfamily. | 0.407 |
| mtnP | ARQ73968.1 | B6D87_07040 | B6D87_07025 | Methylthioadenosine phosphorylase; Catalyzes the reversible phosphorylation of S-methyl-5'- thioinosine (MTI) to hypoxanthine and 5-methylthioribose-1-phosphate. Involved in the breakdown of S-methyl-5'-thioadenosine (MTA), a major by-product of polyamine biosynthesis. Catabolism of (MTA) occurs via deamination to MTI and phosphorolysis to hypoxanthine. | Hypothetical protein; Derived by automated computational analysis using gene prediction method: GeneMarkS+. | 0.419 |
| mtnP | ARQ73969.1 | B6D87_07040 | B6D87_07030 | Methylthioadenosine phosphorylase; Catalyzes the reversible phosphorylation of S-methyl-5'- thioinosine (MTI) to hypoxanthine and 5-methylthioribose-1-phosphate. Involved in the breakdown of S-methyl-5'-thioadenosine (MTA), a major by-product of polyamine biosynthesis. Catabolism of (MTA) occurs via deamination to MTI and phosphorolysis to hypoxanthine. | TetR family transcriptional regulator; Derived by automated computational analysis using gene prediction method: Protein Homology. | 0.507 |