node1 | node2 | node1 accession | node2 accession | node1 annotation | node2 annotation | score |
cbeA | cbtA | b2004 | b2005 | CP4-44 prophage; Antitoxin component of a type IV toxin-antitoxin (TA) system. Antitoxin that counteracts the effect of its cognate toxin CbtA (YeeV). It does not bind to the toxin but instead binds to MreB and FtsZ (the toxin targets), enhancing their polymerization by forming higher-order bundles; it is probably retained in the MreB and FtsZ filament bundles. The mechanism has been proposed to require intergenic DNA, in cis, between the cbeA (yeeU) and cbta (yeeV) genes. The intergenic region was not found to be necessary in another study. Also counteracts the morphological defects c [...] | CP4-44 prophage; Toxic component of a type IV toxin-antitoxin (TA) system. Acts as a dual toxin inhibitor that blocks cell division and cell elongation in genetically separable interactions with FtsZ and MreB. Interacts with cytoskeletal proteins FtsZ and MreB; inhibits FtsZ GTP-dependent polymerization and GTPase activity as well as MreB ATP-dependent polymerization. Binds to both the N- and C-terminus of FtsZ, likely blocking its polymerization and localization, leading to blockage of cell division. Overexpression results in inhibition of growth in liquid cultures and decrease in col [...] | 0.977 |
cbeA | ftsZ | b2004 | b0095 | CP4-44 prophage; Antitoxin component of a type IV toxin-antitoxin (TA) system. Antitoxin that counteracts the effect of its cognate toxin CbtA (YeeV). It does not bind to the toxin but instead binds to MreB and FtsZ (the toxin targets), enhancing their polymerization by forming higher-order bundles; it is probably retained in the MreB and FtsZ filament bundles. The mechanism has been proposed to require intergenic DNA, in cis, between the cbeA (yeeU) and cbta (yeeV) genes. The intergenic region was not found to be necessary in another study. Also counteracts the morphological defects c [...] | GTP-binding tubulin-like cell division protein; Essential cell division protein that forms a contractile ring structure (Z ring) at the future cell division site. The regulation of the ring assembly controls the timing and the location of cell division. One of the functions of the FtsZ ring is to recruit other cell division proteins to the septum to produce a new cell wall between the dividing cells. Binds GTP and shows GTPase activity. Polymerization and bundle formation is enhanced by CbeA. | 0.908 |
cbeA | mreB | b2004 | b3251 | CP4-44 prophage; Antitoxin component of a type IV toxin-antitoxin (TA) system. Antitoxin that counteracts the effect of its cognate toxin CbtA (YeeV). It does not bind to the toxin but instead binds to MreB and FtsZ (the toxin targets), enhancing their polymerization by forming higher-order bundles; it is probably retained in the MreB and FtsZ filament bundles. The mechanism has been proposed to require intergenic DNA, in cis, between the cbeA (yeeU) and cbta (yeeV) genes. The intergenic region was not found to be necessary in another study. Also counteracts the morphological defects c [...] | Cell wall structural complex MreBCD, actin-like component MreB; Forms membrane-associated dynamic filaments that are essential for cell shape determination. Acts by regulating cell wall synthesis and cell elongation, and thus cell shape. A feedback loop between cell geometry and MreB localization maintains elongated cell shape by targeting cell wall growth to regions of negative cell wall curvature. Filaments rotate around the cell circumference in concert with the cell wall synthesis enzymes. The process is driven by the cell wall synthesis machinery and does not depend on MreB polyme [...] | 0.937 |
cbeA | relB | b2004 | b1564 | CP4-44 prophage; Antitoxin component of a type IV toxin-antitoxin (TA) system. Antitoxin that counteracts the effect of its cognate toxin CbtA (YeeV). It does not bind to the toxin but instead binds to MreB and FtsZ (the toxin targets), enhancing their polymerization by forming higher-order bundles; it is probably retained in the MreB and FtsZ filament bundles. The mechanism has been proposed to require intergenic DNA, in cis, between the cbeA (yeeU) and cbta (yeeV) genes. The intergenic region was not found to be necessary in another study. Also counteracts the morphological defects c [...] | Antitoxin of the RelE-RelB toxin-antitoxin syste; Antitoxin component of a type II toxin-antitoxin (TA) system. Counteracts the effect of cognate toxin RelE via direct protein-protein interaction, preventing RelE from entering the ribosome A site and thus inhibiting its endoribonuclease activity. An autorepressor of relBE operon transcription. 2 RelB dimers bind to 2 operator sequences; DNA- binding and repression is stronger when complexed with toxin/corepressor RelE by conditional cooperativity. Increased transcription rate of relBE and activation of relE is consistent with a lower l [...] | 0.457 |
cbeA | relE | b2004 | b1563 | CP4-44 prophage; Antitoxin component of a type IV toxin-antitoxin (TA) system. Antitoxin that counteracts the effect of its cognate toxin CbtA (YeeV). It does not bind to the toxin but instead binds to MreB and FtsZ (the toxin targets), enhancing their polymerization by forming higher-order bundles; it is probably retained in the MreB and FtsZ filament bundles. The mechanism has been proposed to require intergenic DNA, in cis, between the cbeA (yeeU) and cbta (yeeV) genes. The intergenic region was not found to be necessary in another study. Also counteracts the morphological defects c [...] | Qin prophage; Toxic component of a type II toxin-antitoxin (TA) system. A sequence-specific, ribosome-dependent mRNA endoribonuclease that inhibits translation during amino acid starvation (the stringent response). In vitro acts by cleaving mRNA with high codon specificity in the ribosomal A site between positions 2 and 3. The stop codon UAG is cleaved at a fast rate while UAA and UGA are cleaved with intermediate and slow rates. In vitro mRNA cleavage can also occur in the ribosomal E site after peptide release from peptidyl- tRNA in the P site as well as on free 30S subunits. In vivo [...] | 0.600 |
cbeA | rnlB | b2004 | b2631 | CP4-44 prophage; Antitoxin component of a type IV toxin-antitoxin (TA) system. Antitoxin that counteracts the effect of its cognate toxin CbtA (YeeV). It does not bind to the toxin but instead binds to MreB and FtsZ (the toxin targets), enhancing their polymerization by forming higher-order bundles; it is probably retained in the MreB and FtsZ filament bundles. The mechanism has been proposed to require intergenic DNA, in cis, between the cbeA (yeeU) and cbta (yeeV) genes. The intergenic region was not found to be necessary in another study. Also counteracts the morphological defects c [...] | CP4-57 prophage; Antitoxin component of a type II toxin-antitoxin (TA) system. A labile antitoxin (half-life of 2.1 minutes) that inhibits the endonuclease activity of cognate toxin RnlA but not that of non-cognate toxin LsoA. | 0.471 |
cbeA | ykfI | b2004 | b0245 | CP4-44 prophage; Antitoxin component of a type IV toxin-antitoxin (TA) system. Antitoxin that counteracts the effect of its cognate toxin CbtA (YeeV). It does not bind to the toxin but instead binds to MreB and FtsZ (the toxin targets), enhancing their polymerization by forming higher-order bundles; it is probably retained in the MreB and FtsZ filament bundles. The mechanism has been proposed to require intergenic DNA, in cis, between the cbeA (yeeU) and cbta (yeeV) genes. The intergenic region was not found to be necessary in another study. Also counteracts the morphological defects c [...] | Toxin YkfI; Toxic component of a type IV toxin-antitoxin (TA) system. Acts as a toxin inhibitor that blocks cell division and cell elongation via FtsZ and possibly also MreB (although no interaction with MreB has been proven). Overexpression results in inhibition of growth in liquid cultures and a decrease in colony formation. These effects are overcome by concomitant expression of cognate antitoxin YafW, which leads to toxin loss by an unknown mechanism. Overexpression leads to formation of lemon-shaped cells and cell lysis; inactivated by overexpression of cognate antitoxin YafW but [...] | 0.734 |
cbeA | ypjF | b2004 | b2646 | CP4-44 prophage; Antitoxin component of a type IV toxin-antitoxin (TA) system. Antitoxin that counteracts the effect of its cognate toxin CbtA (YeeV). It does not bind to the toxin but instead binds to MreB and FtsZ (the toxin targets), enhancing their polymerization by forming higher-order bundles; it is probably retained in the MreB and FtsZ filament bundles. The mechanism has been proposed to require intergenic DNA, in cis, between the cbeA (yeeU) and cbta (yeeV) genes. The intergenic region was not found to be necessary in another study. Also counteracts the morphological defects c [...] | CP4-57 prophage; Toxic component of a type IV toxin-antitoxin (TA) system. Acts as a dual toxin inhibitor that blocks cell division and cell elongation in genetically separable interactions with FtsZ and MreB. Overexpression results in inhibition of growth in liquid cultures. Overexpression leads to formation of lemon-shaped cells; inactivated by overexpression of cognate antitoxin YfjZ but not when the 2 genes are coexpressed from the same plasmid. Also neutralized by overexpression of non-cognate antitoxins YafW and CbeA. | 0.864 |
cbtA | cbeA | b2005 | b2004 | CP4-44 prophage; Toxic component of a type IV toxin-antitoxin (TA) system. Acts as a dual toxin inhibitor that blocks cell division and cell elongation in genetically separable interactions with FtsZ and MreB. Interacts with cytoskeletal proteins FtsZ and MreB; inhibits FtsZ GTP-dependent polymerization and GTPase activity as well as MreB ATP-dependent polymerization. Binds to both the N- and C-terminus of FtsZ, likely blocking its polymerization and localization, leading to blockage of cell division. Overexpression results in inhibition of growth in liquid cultures and decrease in col [...] | CP4-44 prophage; Antitoxin component of a type IV toxin-antitoxin (TA) system. Antitoxin that counteracts the effect of its cognate toxin CbtA (YeeV). It does not bind to the toxin but instead binds to MreB and FtsZ (the toxin targets), enhancing their polymerization by forming higher-order bundles; it is probably retained in the MreB and FtsZ filament bundles. The mechanism has been proposed to require intergenic DNA, in cis, between the cbeA (yeeU) and cbta (yeeV) genes. The intergenic region was not found to be necessary in another study. Also counteracts the morphological defects c [...] | 0.977 |
cbtA | ftsZ | b2005 | b0095 | CP4-44 prophage; Toxic component of a type IV toxin-antitoxin (TA) system. Acts as a dual toxin inhibitor that blocks cell division and cell elongation in genetically separable interactions with FtsZ and MreB. Interacts with cytoskeletal proteins FtsZ and MreB; inhibits FtsZ GTP-dependent polymerization and GTPase activity as well as MreB ATP-dependent polymerization. Binds to both the N- and C-terminus of FtsZ, likely blocking its polymerization and localization, leading to blockage of cell division. Overexpression results in inhibition of growth in liquid cultures and decrease in col [...] | GTP-binding tubulin-like cell division protein; Essential cell division protein that forms a contractile ring structure (Z ring) at the future cell division site. The regulation of the ring assembly controls the timing and the location of cell division. One of the functions of the FtsZ ring is to recruit other cell division proteins to the septum to produce a new cell wall between the dividing cells. Binds GTP and shows GTPase activity. Polymerization and bundle formation is enhanced by CbeA. | 0.740 |
cbtA | kilR | b2005 | b1352 | CP4-44 prophage; Toxic component of a type IV toxin-antitoxin (TA) system. Acts as a dual toxin inhibitor that blocks cell division and cell elongation in genetically separable interactions with FtsZ and MreB. Interacts with cytoskeletal proteins FtsZ and MreB; inhibits FtsZ GTP-dependent polymerization and GTPase activity as well as MreB ATP-dependent polymerization. Binds to both the N- and C-terminus of FtsZ, likely blocking its polymerization and localization, leading to blockage of cell division. Overexpression results in inhibition of growth in liquid cultures and decrease in col [...] | 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. | 0.522 |
cbtA | mreB | b2005 | b3251 | CP4-44 prophage; Toxic component of a type IV toxin-antitoxin (TA) system. Acts as a dual toxin inhibitor that blocks cell division and cell elongation in genetically separable interactions with FtsZ and MreB. Interacts with cytoskeletal proteins FtsZ and MreB; inhibits FtsZ GTP-dependent polymerization and GTPase activity as well as MreB ATP-dependent polymerization. Binds to both the N- and C-terminus of FtsZ, likely blocking its polymerization and localization, leading to blockage of cell division. Overexpression results in inhibition of growth in liquid cultures and decrease in col [...] | Cell wall structural complex MreBCD, actin-like component MreB; Forms membrane-associated dynamic filaments that are essential for cell shape determination. Acts by regulating cell wall synthesis and cell elongation, and thus cell shape. A feedback loop between cell geometry and MreB localization maintains elongated cell shape by targeting cell wall growth to regions of negative cell wall curvature. Filaments rotate around the cell circumference in concert with the cell wall synthesis enzymes. The process is driven by the cell wall synthesis machinery and does not depend on MreB polyme [...] | 0.785 |
cbtA | ralR | b2005 | b1348 | CP4-44 prophage; Toxic component of a type IV toxin-antitoxin (TA) system. Acts as a dual toxin inhibitor that blocks cell division and cell elongation in genetically separable interactions with FtsZ and MreB. Interacts with cytoskeletal proteins FtsZ and MreB; inhibits FtsZ GTP-dependent polymerization and GTPase activity as well as MreB ATP-dependent polymerization. Binds to both the N- and C-terminus of FtsZ, likely blocking its polymerization and localization, leading to blockage of cell division. Overexpression results in inhibition of growth in liquid cultures and decrease in col [...] | 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. | 0.546 |
cbtA | relB | b2005 | b1564 | CP4-44 prophage; Toxic component of a type IV toxin-antitoxin (TA) system. Acts as a dual toxin inhibitor that blocks cell division and cell elongation in genetically separable interactions with FtsZ and MreB. Interacts with cytoskeletal proteins FtsZ and MreB; inhibits FtsZ GTP-dependent polymerization and GTPase activity as well as MreB ATP-dependent polymerization. Binds to both the N- and C-terminus of FtsZ, likely blocking its polymerization and localization, leading to blockage of cell division. Overexpression results in inhibition of growth in liquid cultures and decrease in col [...] | Antitoxin of the RelE-RelB toxin-antitoxin syste; Antitoxin component of a type II toxin-antitoxin (TA) system. Counteracts the effect of cognate toxin RelE via direct protein-protein interaction, preventing RelE from entering the ribosome A site and thus inhibiting its endoribonuclease activity. An autorepressor of relBE operon transcription. 2 RelB dimers bind to 2 operator sequences; DNA- binding and repression is stronger when complexed with toxin/corepressor RelE by conditional cooperativity. Increased transcription rate of relBE and activation of relE is consistent with a lower l [...] | 0.525 |
cbtA | relE | b2005 | b1563 | CP4-44 prophage; Toxic component of a type IV toxin-antitoxin (TA) system. Acts as a dual toxin inhibitor that blocks cell division and cell elongation in genetically separable interactions with FtsZ and MreB. Interacts with cytoskeletal proteins FtsZ and MreB; inhibits FtsZ GTP-dependent polymerization and GTPase activity as well as MreB ATP-dependent polymerization. Binds to both the N- and C-terminus of FtsZ, likely blocking its polymerization and localization, leading to blockage of cell division. Overexpression results in inhibition of growth in liquid cultures and decrease in col [...] | Qin prophage; Toxic component of a type II toxin-antitoxin (TA) system. A sequence-specific, ribosome-dependent mRNA endoribonuclease that inhibits translation during amino acid starvation (the stringent response). In vitro acts by cleaving mRNA with high codon specificity in the ribosomal A site between positions 2 and 3. The stop codon UAG is cleaved at a fast rate while UAA and UGA are cleaved with intermediate and slow rates. In vitro mRNA cleavage can also occur in the ribosomal E site after peptide release from peptidyl- tRNA in the P site as well as on free 30S subunits. In vivo [...] | 0.784 |
cbtA | rnlA | b2005 | b2630 | CP4-44 prophage; Toxic component of a type IV toxin-antitoxin (TA) system. Acts as a dual toxin inhibitor that blocks cell division and cell elongation in genetically separable interactions with FtsZ and MreB. Interacts with cytoskeletal proteins FtsZ and MreB; inhibits FtsZ GTP-dependent polymerization and GTPase activity as well as MreB ATP-dependent polymerization. Binds to both the N- and C-terminus of FtsZ, likely blocking its polymerization and localization, leading to blockage of cell division. Overexpression results in inhibition of growth in liquid cultures and decrease in col [...] | CP4-57 prophage; Toxic component of a type II toxin-antitoxin (TA) system. A stable (half-life 27.6 minutes) endoribonuclease that in the absence of cognate antitoxin RnlB causes generalized RNA degradation. Degrades late enterobacteria phage T4 mRNAs, protecting the host against T4 reproduction. Activity is inhibited by cognate antitoxin RnlB and by enterobacteria phage T4 protein Dmd. Targets cyaA mRNA. | 0.529 |
cbtA | rnlB | b2005 | b2631 | CP4-44 prophage; Toxic component of a type IV toxin-antitoxin (TA) system. Acts as a dual toxin inhibitor that blocks cell division and cell elongation in genetically separable interactions with FtsZ and MreB. Interacts with cytoskeletal proteins FtsZ and MreB; inhibits FtsZ GTP-dependent polymerization and GTPase activity as well as MreB ATP-dependent polymerization. Binds to both the N- and C-terminus of FtsZ, likely blocking its polymerization and localization, leading to blockage of cell division. Overexpression results in inhibition of growth in liquid cultures and decrease in col [...] | CP4-57 prophage; Antitoxin component of a type II toxin-antitoxin (TA) system. A labile antitoxin (half-life of 2.1 minutes) that inhibits the endonuclease activity of cognate toxin RnlA but not that of non-cognate toxin LsoA. | 0.624 |
cbtA | yafW | b2005 | b0246 | CP4-44 prophage; Toxic component of a type IV toxin-antitoxin (TA) system. Acts as a dual toxin inhibitor that blocks cell division and cell elongation in genetically separable interactions with FtsZ and MreB. Interacts with cytoskeletal proteins FtsZ and MreB; inhibits FtsZ GTP-dependent polymerization and GTPase activity as well as MreB ATP-dependent polymerization. Binds to both the N- and C-terminus of FtsZ, likely blocking its polymerization and localization, leading to blockage of cell division. Overexpression results in inhibition of growth in liquid cultures and decrease in col [...] | CP4-6 prophage; Antitoxin component of a type IV toxin-antitoxin (TA) system. Antitoxin that counteracts the effect of cognate toxin YkfI. It does not seem to bind to the cognate toxin but instead induces toxin loss by an unknown mechanism. Co-overexpression of toxin YkfI and antitoxin YafW leads to formation of elongated cells. | 0.813 |
cbtA | yfjZ | b2005 | b2645 | CP4-44 prophage; Toxic component of a type IV toxin-antitoxin (TA) system. Acts as a dual toxin inhibitor that blocks cell division and cell elongation in genetically separable interactions with FtsZ and MreB. Interacts with cytoskeletal proteins FtsZ and MreB; inhibits FtsZ GTP-dependent polymerization and GTPase activity as well as MreB ATP-dependent polymerization. Binds to both the N- and C-terminus of FtsZ, likely blocking its polymerization and localization, leading to blockage of cell division. Overexpression results in inhibition of growth in liquid cultures and decrease in col [...] | CP4-57 prophage; Antitoxin component of a type IV toxin-antitoxin (TA) system. Antitoxin that counteracts the effect of cognate toxin YpjF. Also counteracts the effect of non-cognate toxins CbtA and YfkI. | 0.807 |
dicB | ftsZ | b1575 | b0095 | Qin prophage; Involved in cell division inhibition; this function can be repressed by DicA and DicC proteins as well as antitoxin CbeA (yeeU). | GTP-binding tubulin-like cell division protein; Essential cell division protein that forms a contractile ring structure (Z ring) at the future cell division site. The regulation of the ring assembly controls the timing and the location of cell division. One of the functions of the FtsZ ring is to recruit other cell division proteins to the septum to produce a new cell wall between the dividing cells. Binds GTP and shows GTPase activity. Polymerization and bundle formation is enhanced by CbeA. | 0.730 |