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hipB | Antitoxin of HipAB toxin-antitoxin system; Antitoxin component of a type II toxin-antitoxin (TA) system. Neutralizes the toxic effect of cognate toxin HipA. Also neutralizes the toxic effect of non-cognate toxin YjjJ. Binds to operator sites with the consensus sequence 5-'TATCCN(8)GGATA-3' to repress the hipBA operon promoter ; binding of HipB(2) to DNA induces a 70 degree bend. This forces HipA dimerization, which blocks HipA's active site and thus its toxic action. May play a role in biofilm formation. (88 aa) | ||||
relE | 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 [...] (95 aa) | ||||
relB | 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 [...] (79 aa) | ||||
cbtA | 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 [...] (124 aa) | ||||
yefM | Antitoxin of the YoeB-YefM toxin-antitoxin system; Antitoxin component of a type II toxin-antitoxin (TA) system. Antitoxin that counteracts the effect of the YoeB toxin. YefM binds to the promoter region of the yefM-yeoB operon to repress transcription, YeoB acts as a corepressor. (83 aa) | ||||
zipA | FtsZ stabilizer; Essential cell division protein that stabilizes the FtsZ protofilaments by cross-linking them and that serves as a cytoplasmic membrane anchor for the Z ring. Also required for the recruitment to the septal ring of the downstream cell division proteins FtsK, FtsQ, FtsL and FtsN. ZipA overproduction protects FtsZ from degradation by ClpP by preventing recognition by ClpX. Does not affect the GTPase activity of FtsZ. (328 aa) | ||||
mazF | mRNA interferase toxin, antitoxin is MazE; Toxic component of a type II toxin-antitoxin (TA) system. A sequence-specific endoribonuclease it inhibits protein synthesis by cleaving mRNA and inducing bacterial stasis. It is stable, single- strand specific with mRNA cleavage independent of the ribosome, although translation enhances cleavage for some mRNAs. Cleavage occurs at the 5'-end of ACA sequences, yielding a 2',3'-cyclic phosphate and a free 5'-OH, although cleavage can also occur on the 3'-end of the first A. Digests 16S rRNA in vivo 43 nts upstream of the C- terminus; this remove [...] (111 aa) | ||||
mqsA | Antitoxin for MqsR toxin; Antitoxin component of a type II toxin-antitoxin (TA) system. Labile antitoxin that binds to the MqsR mRNA interferase toxin and neutralizes its endoribonuclease activity. Overexpression prevents MqsR-mediated cessation of cell growth and inhibition of cell proliferation. Initially reported to act as a cotranscription factor with MqsA. Following further experiments, the MqsR-MqsA complex does not bind DNA and all reported data are actually due to a small fraction of free MqsA alone binding DNA. Addition of MqsR to a preformed MqsA-promoter DNA complex causes d [...] (131 aa) | ||||
mqsR | GCU-specific mRNA interferase toxin of the MqsR-MqsA toxin-antitoxin system; Toxic component of a type II toxin-antitoxin (TA) system. Plays a significant role in the control of biofilm formation and induction of persister cells in the presence of antibiotics. An mRNA interferase which has been reported to be translation-independent. It has also been reported to be translation-dependent. Cleavage has been reported to occur on either side of G in the sequence GCU. Also reported to cleave after C in GC(A/U) sequences. There are only 14 genes in E.coli W3110 (and probably also MG1655) tha [...] (98 aa) | ||||
higA | Antitoxinof the HigB-HigA toxin-antitoxin system; Antitoxin component of a type II toxin-antitoxin (TA) system. Functions as an mRNA interferase antitoxin; overexpression prevents HigB-mediated cessation of cell growth and inhibition of cell proliferation. (138 aa) | ||||
higB | mRNA interferase toxin of the HigB-HigA toxin-antitoxin system; Toxic component of a type II toxin-antitoxin (TA) system. A probable translation-dependent mRNA interferase. Overexpression causes cessation of cell growth and inhibits cell proliferation via inhibition of translation; this blockage is overcome by subsequent expression of antitoxin HigA. Overexpression causes cleavage of a number of mRNAs in a translation-dependent fashion, suggesting this is an mRNA interferase. mRNA interferases play a role in bacterial persistence to antibiotics; overexpression of this protein induces p [...] (104 aa) | ||||
mreB | 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 [...] (347 aa) | ||||
chpS | Antitoxin of the ChpBS toxin-antitoxin system; Antitoxin component of a type II toxin-antitoxin (TA) system. May be involved in the regulation of cell growth. It acts as a suppressor of the endoribonuclease (inhibitory function) of ChpB protein. Both ChpS and ChpB probably bind to the promoter region of the chpS-chpB operon to autoregulate their synthesis. (83 aa) | ||||
chpB | Toxin of the ChpB-ChpS toxin-antitoxin system; Toxic component of a type II toxin-antitoxin (TA) system. ChpB is a sequence-specific mRNA and (weak) tmRNA endoribonuclease that inhibits protein synthesis and induces bacterial stasis. Cleavage is independent of the ribosome. Cleavage occurs at ACY sequences where Y is not C. The endoribonuclease activity is not as strong as that of MazF. The endoribonuclease activity (a toxin) is inhibited by its labile cognate antitoxin ChpS. Toxicity results when the levels of ChpS decrease in the cell, leading to mRNA degradation. Both ChpS and ChpB [...] (116 aa) | ||||
hicA | mRNA interferase toxin of the HicAB toxin-antitoxin system; Toxic component of a type II toxin-antitoxin (TA) system. A probable translation-independent mRNA interferase. Overexpression causes cessation of cell growth and inhibits cell proliferation via inhibition of translation; this blockage is overcome (after 90 minutes) by subsequent expression of antitoxin HicB. Overexpression causes cleavage of a number of mRNAs and tmRNA, in a translation-independent fashion, suggesting this is an mRNA interferase. mRNA interferases play a role in bacterial persistence to antibiotics ; Belongs t [...] (58 aa) | ||||
yoeB | Toxin of the YoeB-YefM toxin-antitoxin system; Toxic component of a type II toxin-antitoxin (TA) system. Its mode of function is controversial; it has been proposed to be an mRNA interferase but also an inhibitor of translation initiation. When overproduced in wild-type cells, inhibits bacterial growth and translation by cleavage of mRNA molecules while it has a weak effect on colony forming ability. Overproduction of Lon protease specifically activates YoeB-dependent mRNA cleavage, leading to lethality. YefM binds to the promoter region of the yefM-yeoB operon to repress transcription [...] (84 aa) | ||||
mazE | Antitoxin of the ChpA-ChpR toxin-antitoxin system; Antitoxin component of a type II toxin-antitoxin (TA) system. Labile antitoxin that binds to the MazF endoribonuclease toxin and neutralizes its endoribonuclease activity. Is considered to be an 'addiction' molecule as the cell dies in its absence. Toxicity results when the levels of MazE decrease in the cell, leading to mRNA degradation. This effect can be rescued by expression of MazE, but after 6 hours in rich medium the overexpression of MazF leads to programmed cell death. Cell growth and viability are not affected when MazF and M [...] (82 aa) | ||||
dnaK | Chaperone Hsp70, with co-chaperone DnaJ; Plays an essential role in the initiation of phage lambda DNA replication, where it acts in an ATP-dependent fashion with the DnaJ protein to release lambda O and P proteins from the preprimosomal complex. DnaK is also involved in chromosomal DNA replication, possibly through an analogous interaction with the DnaA protein. Also participates actively in the response to hyperosmotic shock. (638 aa) | ||||
ftsZ | 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. (383 aa) | ||||
yafQ | mRNA interferase toxin of toxin-antitoxin pair YafQ/DinJ; Toxic component of a type II toxin-antitoxin (TA) system. A sequence-specific mRNA endoribonuclease that inhibits translation elongation and induces bacterial stasis. Cleavage occurs between the second and third residue of the Lys codon followed by a G or A (5'AAA(G/A)3'), is reading-frame dependent and occurs within the 5' end of most mRNAs. Ribosome-binding confers the sequence specificity and reading frame- dependence. When overexpressed in liquid media YafQ partially inhibits protein synthesis, with a reduction in growth rat [...] (92 aa) | ||||
dinJ | Antitoxin of YafQ-DinJ toxin-antitoxin system; Antitoxin component of a type II toxin-antitoxin (TA) system. A labile antitoxin that counteracts the effect of cognate toxin YafQ. YafQ and DinJ together bind their own promoter, and repress its expression. There are 2 operators with imperfect inverted repeats (IR) in the dinJ promoter, YafQ-(DinJ)2-YafQ only binds to the first (most upstream) of them to repress transcription; binding to a single IR is sufficient for activity in vivo and in vitro. DinJ alone is as potent a transcriptional repressor as the heterotetramer and also only need [...] (86 aa) | ||||
yafN | Antitoxin of the YafO-YafN toxin-antitoxin system; Antitoxin component of a type II toxin-antitoxin (TA) system. Functions as an mRNA interferase antitoxin; overexpression prevents YafO-mediated cessation of cell growth and inhibition of cell proliferation. (97 aa) | ||||
yafO | mRNA interferase toxin of the YafO-YafN toxin-antitoxin system; Toxic component of a type II toxin-antitoxin (TA) system. A translation-dependent mRNA interferase. Overexpression causes cessation of cell growth and inhibits cell proliferation via inhibition of translation; this blockage is overcome by subsequent expression of antitoxin YafN. Overexpression causes cleavage of a number of mRNAs in a ribosome-dependent fashion. YafO binding to the 50S ribosomal subunit in the translation complex induces mRNA cleavage 3' to the region protected by the ribosome; YafO alone is not able to di [...] (132 aa) | ||||
dacA | D-alanyl-D-alanine carboxypeptidase (penicillin-binding protein 5); Removes C-terminal D-alanyl residues from sugar-peptide cell wall precursors. (403 aa) | ||||
mrdA | Penicillin-binding protein 2, transpeptidase involved in peptidoglycan synthesis; Catalyzes cross-linking of the peptidoglycan cell wall. Responsible for the determination of the rod shape of the cell. Is probably required for lateral peptidoglycan synthesis and maintenance of the correct diameter during lateral and centripetal growth. Belongs to the transpeptidase family. MrdA subfamily. (633 aa) | ||||
pgaD | Biofilm PGA synthase PgaCD, regulatory subunit; Required for the synthesis of poly-beta-1,6-N-acetyl-D- glucosamine (PGA), a biofilm adhesin polysaccharide. May assist the glycosyltransferase PgaC in the polymerization of PGA. (137 aa) | ||||
hicB | Antitoxin for the HicAB toxin-antitoxin system; Antitoxin component of a type II toxin-antitoxin (TA) system. Functions as an mRNA interferase antitoxin; overexpression prevents HicA-mediated cessation of cell growth and inhibition of cell proliferation. (138 aa) | ||||
hipA | Serine/threonine-protein kinase toxin HipA; Toxic component of a type II toxin-antitoxin (TA) system, first identified by mutations that increase production of persister cells, a fraction of cells that are phenotypic variants not killed by antibiotics, which lead to multidrug tolerance. Persistence may be ultimately due to global remodeling of the persister cell's ribosomes. Phosphorylates Glu-tRNA-ligase (AC P04805, gltX, on 'Ser-239') in vivo. Phosphorylation of GltX prevents it from being charged, leading to an increase in uncharged tRNA(Glu). This induces amino acid starvation and [...] (440 aa) |