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mrcB | Fused glycosyl transferase and transpeptidase; Cell wall formation. Synthesis of cross-linked peptidoglycan from the lipid intermediates. The enzyme has a penicillin-insensitive transglycosylase N-terminal domain (formation of linear glycan strands) and a penicillin-sensitive transpeptidase C-terminal domain (cross- linking of the peptide subunits); In the N-terminal section; belongs to the glycosyltransferase 51 family. (844 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) | ||||
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) | ||||
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) | ||||
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) | ||||
phoU | Negative regulator of PhoR/PhoB two-component regulator; Part of the phosphate (Pho) regulon, which plays a key role in phosphate homeostasis. Encoded together with proteins of the phosphate-specific transport (Pst) system in the polycistronic pstSCAB- phoU operon. PhoU is essential for the repression of the Pho regulon at high phosphate conditions. In this role, it may bind, possibly as a chaperone, to PhoR, PhoB or a PhoR-PhoB complex to promote dephosphorylation of phospho-PhoB, or inhibit formation of the PhoR- PhoB transitory complex. Is also part of complex networks important for [...] (241 aa) | ||||
rpmA | 50S ribosomal subunit protein L27; Protein involved in structural constituent of ribosome and translation. (85 aa) | ||||
yhaV | Toxin of the SohB(PrlF)-YhaV toxin-antitoxin system; Toxic component of a type II toxin-antitoxin (TA) system. Has RNase activity in vitro. Overexpression leads to growth arrest after 30 minutes; these effects are overcome by concomitant expression of antitoxin SohA (PrlF). Massive overexpression is toxic. Unlike most other characterized TA systems degrades rRNA, and co-folding of the both TA proteins is necessary in vitro for inhibition of the RNase activity. It is not known if it has any sequence-specificity. Acts as a transcription factor. The YhaV/PrlF complex binds the prlF-yhaV o [...] (154 aa) | ||||
prlF | Antitoxin of the SohA(PrlF)-YhaV toxin-antitoxin system; Antitoxin component of a type II toxin-antitoxin (TA) system. Labile antitoxin that binds to the YhaV toxin and neutralizes its ribonuclease activity. Also acts as a transcription factor. The YhaV/PrlF complex binds the prlF-yhaV operon, probably negatively regulating its expression. (111 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) | ||||
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) | ||||
ssnA | Putative chlorohydrolase/aminohydrolase; Protein involved in cell cycle. (442 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) | ||||
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) | ||||
rnlB | 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. (123 aa) | ||||
rnlA | 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. (357 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) | ||||
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) | ||||
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) | ||||
glsB | Putative glutaminase; Protein involved in cellular amino acid catabolic process. (308 aa) | ||||
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) | ||||
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) | ||||
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) | ||||
ybjN | Negative regulator of motility; Putative sensory transduction regulator. (158 aa) | ||||
glsA | Putative glutaminase; Protein involved in cellular amino acid catabolic process. (310 aa) | ||||
ykfI | 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 [...] (113 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) | ||||
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) | ||||
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) | ||||
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) |