Part:BBa_K4656009
Plac-tetR-Ptet-lacI-MazF
TetR, the tetracycline repressor, can inhibit the promoter Ptet. That is to say, the promoter Ptet is constitutively ON and repressed by TetR. However, TetR repression is inhibited by the addition of tetracycline(TET) or its analog, aTc. LacI can bind to the PLac promotor and PLlac0-1 hybrid promotor and inhibit transcription. IPTG (isopropyl-β-d-thiogalactoside) binds to LacI and inhibits its operation, therefore promoting transcription.
Thus, tetR's ability to inhibit Ptet is weakened when TET is present, while lacI expression products inhibit the promoter Plac to produce less tetR to repress Ptet and enable MazF behind lacI on the gene route to express. MazF, as a toxin, is an endonuclease that cuts RNA at ACA sites and acts as a reporter gene to cause microbial death[1]. MazF can be characterized in a cell density-dependent manner in E. coli.
MazE, like MazF, encodes stable non-specific ribonuclease enzymes in Bacillus subtilis that are used in combination to deliver toxin-antitoxin suicide switches under a variety of stressful conditions. In the gene route, rhamnose activates the promoter PRha, which is expressed in the downstream MazE. Because MazE is an antitoxin, it can produce the opposite effect of MazF, that is, providing exogenous rhamnoose can eventually produce an antitoxin to fight the toxin and keep the E. coli alive.
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