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). 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. 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. Probably forms a homodimer in the absence of MazF; binds DNA as a homodimer (PubMed:25564525, PubMed:12533537). Forms a heterohexamer composed of alternating toxin and antitoxin homodimers MazF(2)-MazE(2)-MazF(2). 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). Degraded by the ClpPA and Lon proteases. Decreased sensitivity to dramatic intracellular increases of ppGpp. Double mazE-mazF disruptions survive high temperature, various DNA-damaging agents and H(2)O(2) exposure better than wild-type cells. They produce more P1 phage than wild-type cells, while introduction of lysogens into a growing non-lysogenic disruption culture is lethal (PubMed:15316771). Double mazE-mazF disruptions show reduced biofilm formation, and survive antibiotic treatment in log phase better than wild-type cells. Cells missing mazE-mazF survive hydroxyurea treatment better than wild-type; further disruption of relE-relB and tonB yields even better survival (PubMed:20005847). Belongs to the PemI family.