| IED ID |
IndEnz0002002591 |
| Enzyme Type ID |
protease002591 |
| Protein Name |
Antitoxin MazE
|
| Gene Name |
mazE chpAI chpR b2783 JW2754 |
| Organism |
Escherichia coli (strain K12) |
| Taxonomic Lineage |
cellular organisms
Bacteria
Proteobacteria
Gammaproteobacteria
Enterobacterales
Enterobacteriaceae
Escherichia
Escherichia coli
Escherichia coli (strain K12)
|
| Enzyme Sequence |
MIHSSVKRWGNSPAVRIPATLMQALNLNIDDEVKIDLVDGKLIIEPVRKEPVFTLAELVNDITPENLHENIDWGEPKDKEVW |
| Enzyme Length |
82 |
| Uniprot Accession Number |
P0AE72 |
| Absorption |
|
| Active Site |
|
| Activity Regulation |
|
| Binding Site |
|
| Calcium Binding |
|
| catalytic Activity |
|
| DNA Binding |
|
| EC Number |
|
| Enzyme Function |
FUNCTION: 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 MazE are coexpressed. Both MazE and MazE-MazF bind to the promoter region of the mazE-mazF operon to inhibit their own transcription (PubMed:8650219). There are 3 operators to which MazE binds (PubMed:12533537). MazE has higher affinity for promoter DNA in the presence of MazF (PubMed:25564525). {ECO:0000269|PubMed:11071896, ECO:0000269|PubMed:12123459, ECO:0000269|PubMed:12533537, ECO:0000269|PubMed:19707553, ECO:0000269|PubMed:21419338, ECO:0000269|PubMed:25564525, ECO:0000269|PubMed:8650219}.; FUNCTION: Cell death governed by the MazE-MazF and DinJ-YafQ TA systems seems to play a role in biofilm formation, while MazE-MazF is also implicated in cell death in liquid media. {ECO:0000269|PubMed:15576778, ECO:0000269|PubMed:19707553}.; FUNCTION: Might also serve to protect cells against bacteriophage; in the presence of MazE-MazF fewer P1 phage are produced than in a disrupted strain. For strain K38 most wild-type cells are killed but not by phage lysis; it was suggested that MazE-MazF causes P1 phage exclusion from the bacterial population. This phenomenon is strain dependent. {ECO:0000269|PubMed:15316771}. |
| Temperature Dependency |
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| PH Dependency |
|
| Pathway |
|
| nucleotide Binding |
|
| Features |
Beta strand (4); Chain (1); Domain (1); Helix (1); Mutagenesis (2) |
| Keywords |
3D-structure;DNA-binding;Reference proteome;Repressor;Toxin-antitoxin system;Transcription;Transcription regulation |
| Interact With |
|
| Induction |
INDUCTION: Expressed in exponentially growing cells. Induction has been reported to occur after amino acid starvation in a ppGpp-independent fashion and to be Lon protease-dependent (PubMed:12972253), but also to not occur after amino acid starvation and to be regulated by ppGpp (PubMed:8650219). MazE alone and in combination with MazF, represses transcription of the mazE-mazF operon. Fis activates transcription. Part of the relA-mazE-mazF-mazG operon, there is also a second mazE-mazF specific promoter which is negatively autoregulated. This operon induced by ectopic expression of toxin RelE; induction of this operon by amino acid starvation requires the relBEF operon (PubMed:23432955). {ECO:0000269|PubMed:11071896, ECO:0000269|PubMed:12972253, ECO:0000269|PubMed:16390452, ECO:0000269|PubMed:23432955, ECO:0000269|PubMed:8650219}. |
| Subcellular Location |
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| Modified Residue |
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| Post Translational Modification |
PTM: Degraded by the ClpPA and Lon proteases. {ECO:0000269|PubMed:12972253, ECO:0000269|PubMed:24375411, ECO:0000269|PubMed:8650219}. |
| Signal Peptide |
|
| Structure 3D |
NMR spectroscopy (2); X-ray crystallography (4) |
| Cross Reference PDB |
1MVF;
1UB4;
2MRN;
2MRU;
5CQX;
5CQY;
|
| Mapped Pubmed ID |
16606699;
27026704;
|
| Motif |
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| Gene Encoded By |
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| Mass |
9,356 |
| Kinetics |
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| Metal Binding |
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| Rhea ID |
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| Cross Reference Brenda |
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